Gastro Intestinal problems by Muhammad Shakeel Talat

SURGERY Gastro-Intestinal Problems First Edition

Muhammad Shuja Tahir Awais Shuja Faisal Bilal Lodhi SURGERY - GASTRO-INTESTINAL PROBLEMS

ISBN 969-8295-12-7

FIRST EDITION 2009

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Muhammad Shuja Tahir All rights are reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form by any means without prior permission of the copy write owner.

Price : 30 US $

Published by:

Independent Publishing House

Jinnah Colony, Faisalabad. Tel: 092-41-2617122-24, 2623412, Fax: 092-41-2623413 http://www.theprofesional.com publication@theprofesional.com editor@theprofesional.com

SURGERY - GASTRO-INTESTINAL PROBLEMS

SURGERY Gastro-Intestinal Problems First Edition

Muhammad Shuja Tahir FRCS (Edin), FCPS Pak (Hon) Professor of Surgery

Awais Shuja MRCS Assistant Professor of Surgery

Faisal Bilal Lodhi FCPS Associate Professor of Surgery

Published by:

Independent Publishing House

Jinnah Colony, Faisalabad. Tel: 092-41-2617122-24, 2623412, Fax: 092-41-2623413 http://www.theprofesional.com publication@theprofesional.com editor@theprofesional.com

SURGERY - GASTRO-INTESTINAL PROBLEMS

iii

Dedicated to general surgeons who love to innovate and perform Surgery

SURGERY - GASTRO-INTESTINAL PROBLEMS

Foreword

FOREWORD Surgery is more about dealing with gastro intestinal problems as most of other surgical problems have already been specialized into separate fields. Even gastrointestinal problems have further specialized into many fields of its own as Biliary, Pancreatic and Colo-rectal surgery. The subjects of surgery have been described in problem based manner. The practical and economical approach has been followed in dealing with various surgical problems. The description is simple and up to date. It will definitely help readers to understand the problems and find easy solutions. Professor Shuja Tahir has motivated younger colleagues to write and present various subjects of gastro intestinal surgery in new and better style for students and doctors. The book has been composed beautifully and gives a fresh look. Its a joy to read this book. I have liked the presentation and am sure that it will not only help the readers but writers as well. I am sure that students of surgery will have no problem in understanding surgery after reading this book.

Muhammad Iqbal Khan MBBS, FRCS Professor of Surgery

SURGERY - GASTRO-INTESTINAL PROBLEMS

Preface

PREFACE I decided to write simple solutions to various problems of gastro-intestinal tract few years ago. Unfortunately it took much more time than expected to complete it. It has been edited for easy and quick understanding. I have tried to make it simple and logical as much as I could. I hope my efforts are an effective contribution to the existing text. I have been successful and lucky enough to establish a team of dedicated teachers, both seniors and juniors, surgeons and trainees, postgraduates and undergraduates to read the manuscript and give their feed back. Most of the text has been accepted by most of my colleagues. It is up-to-date and nothing significant has been missed out from the text. I pray to God Almighty that my colleagues will continue to contribute more in logical and evidence based management regimens in future also. I am anxiously waiting for the changes and improvements in the book (next edition) from my colleagues. I hope students and teachers will like it and I hope it is useful to the medical community as a whole. Amen! Shuja Tahir

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Acknowledgment

ACKNOWLEDGMENT I decided to write simple solutions to various problems of gastro-intestinal tract few years ago. Colleagues and friends were requested to help and join in this joyful venture. Many surgeons and teachers helped to read, reread, edit and improve various chapters. It was most satisfying hard work. Every change was worth the trouble and every moment spent on finalizing the manuscript was productive. I am highly obliged to all of my colleagues, both seniors and juniors for their help. When I sit back and think, it becomes very clear that it was impossible to complete this book without their help. I have nothing else to say to them other than "Thank you very much". God bless them all. Some of them are named here; Dr. Mahnaaz Roohi

Dr. Abid Bashir

FRCOG Professor of Gynaecology and obstetrics Punjab Medical College, Faisalabad.

FCPS Assistant Professor of Surgery Independent Medical College Faiaslabad.

Muhammad Yousaf Shah

Dr. Irfan Ahmad Mughal

FRCS Professor of surgery Punjab Medical College, Faisalabad.

MBBS, M.Phil, Ph.D. Professor of Anatomy Independent Medical College, Faisalabad.

Dr. Muhammad Ramzan

Dr. Faisal Bilal Lodhi

FCPS Specialist surgeon Kingdom of Saudia.

Dr. Tariq Mahmood FCPS Specialist surgeon Aziz Fatima Trust Hospital.

SURGERY - GASTRO-INTESTINAL PROBLEMS

FCPS Associate Professor of Surgery Punjab Medical College, Faisalabad.

Dr. Sohail Amir FCPS Assistant Professor of Surgery Punjab Medical College, Faisalabad.

Acknowledgment

Dr. Awais Shuja

Dr. Badar Bashir

MRCS (U.K) Assistant Professor of Surgery Independent Medical College, Faisalabad.

FCPS Assistant Professor Independent Medical College, Faisalabad.

Dr. Syyad Tajammal Hussain Shah

Dr. Anwar Saood Saqib

FCPS Assistant Professor Independent Medical College, Faisalabad.

MBBS DMJ Assistant Professor Independent Medical College, Faisalabad.

Dr. Quddus-ur-Rahman

Dr. Muhammad Ashraf Siddiqui

FCPS Assistant Professor Independent Medical College, Faisalabad.

MBBS MD

Dr. Shamoona Rashid MBBS

Dr. Usman Latif FCPS Assistant Professor Independent Medical College, Faisalabad.

Dr. Nadia Hasnain

Dr. Jaweeria Mujahid MBBS

Dr. Saadia Anwar MBBS

MBBS

I am also grateful to my typing, composing and designing team for their efforts and dedicated work. The team has really worked hard to make this work worthwhile. Muhammad Shakeel Talat Muhammad Mohsin Imran Ali Muhammad Qasim Faqeer Hussain

Shuja Tahir

SURGERY - GASTRO-INTESTINAL PROBLEMS

Contents

CONTENTS GASTRO-INSTESTINAL TRACT S.NO. 01 02

PAGE Embryology of gasto-intestinal tract Anatomy of gastro-instestinal tract

01 07

OESOPHAGUS 03 04

Dysphagia Carcinoma of Oesophagus

23 33

STOMACH & DUODENUM 05 06 07 08 09

Blood supply and Lymphatic Drainage of Stomach Pyloric Stenosis Complications of Peptic Ulcer Haematemesis and Melaena Carcinoma of Stomach

49 53 61 69 77

SPLEEN 10 11

Splenic Trauma Splenectomy

91 101

LIVER 12 13 14

Liver Abscess Hydatid Cyst of liver Liver Trauma

SURGERY - GASTRO-INTESTINAL PROBLEMS

111 119 127

Contents

GALL BLADDER & PANCREAS 15 16 17 18 19 20 21 22 23

Acute Cholecystitis Gall Stones Murphy’s Sign Boas Sign Mucocele of Gall Bladder Cholecystectomy Obstructive Jaundice Courvoisier’s Law Acute Pancreatitis

139 147 155 156 157 159 167 179 183

PERITONIUM 24 25

Acute Peritonitis Subphrenic spaces

195 209

SMALL INTESTINE 26 27 28 29 30 31 32 33

Small Gut Obstruction Paralytic Ileus Acute Intussusception Acute Appendicitis Appendicular abscess Right Iliac Pain Carcinoid Tumor and Syndrome Appendicectomy

215 227 231 237 247 251 259 263

LARGE INTESTINE 34 35 36 37 38 39 40 41 42 43 44

Blood Supply and lymphatic Drainage of Large gut Sigmoid Volvulus Ulcerative colitis Bleeding Per Rectum Colorectal Carcinoma Anal Fissure Pilonidal Sinus Anorectal abscess Fistula in ano Haemorrhoids Index

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273 279 285 291 297 311 317 323 327 339 349 xii

Gastrointestinal Problems

SURGERY - GASTRO-INTESTINAL PROBLEMS

EMBRYOLOGY

OBJECTIVES ! ! ! !

To understand development and anatomy of gastrointestinal tract. To understand the congenital abnormalities of gastrointestinal tract. To be able to diagnose problems of gastrointestinal tract. To be able to manage gastrointestinal problems.

SURGERY - GASTRO-INTESTINAL PROBLEMS

EMBRYOLOGY

GIT - 01

GASTRO-INTESTINAL TRACT EMBRYOLOGY Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Irfan Ahmad Mughal, M.Phil, Ph.D.

The gastrointestinal system develops from the primordial gut which forms during the fourth week of gestation from the part of the yolk sac that is incorporated into the embryo. The endoderm of the primordial gut gives rise to the epithelial lining of most of the digestive tract and biliary passages together with the parenchyma of its glands, including the liver and pancreas. 01.01

Heart

Pharynx Aorta Esophageal region

Stomodeum

Gastric and duodenal regions

Septum transversum

Celiac trunk Yolk stalk and vitelline artery

Primordium of liver

Allantois Superior mesenteric artery

Proctodeum

Inferior mesenteric artery

Cloacal membrane Cloaca

Hindgut

Development of gastro-intestinal tract (fourth week of gestation) 01.02

Posterior abdominal wall

Pancreas Spleen

Liver

Duodenum

The epithelium at the cranial and caudal extremities of the digestive tract is derived from the ectoderm of the stomodeum and proctodeum, respectively. The muscular and connective tissue components of the digestive tract are derived from the splanchnic mesenchyme surrounding the primordial gut. FOREGUT All of the foregut derivatives except pharynx, respiratory tract and most of oesophagus are supplied by foregut artery the celiac trunk. The foregut gives rise to the pharynx, lower respiratory system, esophagus, stomach duodenum (proximal to the opening of the bile duct), liver, pancreas, and biliary apparatus. The oesophagus develops from part of foregut just caudal to pharynx. The trachea gets separated from oesophagus in the initial period by tracheo-oesophageal septum. Esophagus is short initially but elongates rapidly afterwards and reaches its final length by 7th week of gestation. Its common developmental anomalies are; Esophageal Atresia It is lack of canalization of esophagus (blockage of esophagus). Its incidence is 1 in 3000 - 4500 births. It is associated with tracheoesophageal fistula in more than 85% of cases. 33% of these infants deliver prematurely. It occurs due to deviation of tracheoesophageal septum in posterior direction leading to incomplete separation of esophagus from laryngotracheal tube. It may also occur due to failure of recanalization during 8th week of gestation.

Stomach Right gastro-omental artery

Greater omentum

Development of foregut derivatives

SURGERY - GASTRO-INTESTINAL PROBLEMS

EMBRYOLOGY

Esophageal Stenosis ! It is commonly seen in distal 1/3 and is usually due to incomplete recanalization of esophagus during the 8th week of gestation. It may result from failure of esophageal blood vessels to develop in the affected area resulting in atrophy of anoxic segment. Short Esophagus It is seen due to failure to elongate sufficiently and is associated with Hiatus hernia. !

! Duodenal Stenosis It is partial occlusion of duodenal lumen. It occurs due to incomplete recanalization. It is usually seen in 3rd and 4th part of duodenum. 01.03 Dilated duodenum

Stomach

DEVELOPMENT OF STOMACH Distal part of foregut is initially a simple tubular structure. Around the middle of forth week, a slight dilatation indicates site of stomach primordium. This dilatation is fusiform initially than within next two weeks, the dorsal border enlarges faster than its ventral border leading to demarcations of greater curvature of stomach. The stomach rotates at 90째 in clockwise direction. A common developmental anomaly is congenital hypertrophic pyloric stenosis. DEVELOPMENT OF DUODENUM It develops from distal part of forgut and proximal part of midgut and adjacent splanchnic mesenchyme during early 4th week of gestation. The junction of forgut and midgut is part of duodenum just distal to the origin of bile duct. The duodenum comes to lie reteroperitoneally after gastric rotation. The duodenum is supplied by both celiac and superior mesenteric vessels. The duodenal lumen becomes smaller and obliterates during 5th and 6th week of gestation. Normally, the duodenum gets recanalized by the end of embryonic period. Its common developmental anomalies are; ! Doudenal Atresia It is complete occlusion of duodenal lumen. The blockage is commonly near the junction of bile and pancreatic ducts. Ocassionaly it may be seen in the third part of duodenum. Polyhydramnios is usually associated as atresic duodenum fails to absorb swallowed amniotic fluid.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Duodenal stenosis

Developmental anomalies (duodenal stenosis) 01.04 Dilated duodenum

Duodenal atresia

Duodenum (decreased in size)

Developmental anomalies (duodenal atresia)

DEVELOPMENT OF SPLEEN It develops from mesenchymal mass present between layers of dorsal mesogastrium. It is a vascular lymphatic organ. It begins to develop during 5th week of gestation. It is lobulated in fetus but lobules disappears before birth. It assumes its natural adult position after rotation of the stomach. DEVELOPMENT OF BILIARY APPARATUS Liver, gall bladder and biliary apparatus arise as a ventral outgrowth from caudal part of foregut early in 4th week of gestation. Hepatic diverticulum and ventral bud of pancreas develop from embryonic endoderm. Hepatic

EMBRYOLOGY

diverticulum extends into septum transversum. It enlarges and divides into two parts and grows into future liver, gall bladder, cystic duct and biliary tree. Following developmental anomalies are seen; ! ! ! ! !

Variations of hepatic duct, bile duct & cystic duct Extra hepatic biliary atresia Accessory pancreatic tissue Annular pancreas Accessory spleen

MIDGUT The midgut gives rise to the duodenum (distal to bile duct), jejunum, ileum, cecum, appendix, ascending colon, and the right two-thirds of the transverse colon. The midgut forms a U-shaped intestinal loop that herniates into the umbilical cord during the sixth week because there is no room for it in the abdomen. While in the umbilical cord, the midgut loop rotates counter clockwise through 90 degrees. During the tenth week, the intestines return to the abdomen, rotating a further 180 degrees during this process. DEVELOPMENT OF CECUM AND APPENDIX The cecal swelling occurs in midgut during 6th week of gestation. The appendix appears as a small diverticulum from this swelling. In about 64% cases, the appendix lies retrocecally. Anomalies of midgut are; ! Congenital omphalocele It is seen in one in 5000 births. It is due to failure of repositioning of the herniated midgut. ! Umbilical hernia This anomaly is seen when peritoneal contents herniate through imperfectly closed umbilicus. It occurs usually during 10th week of gestation. ! Gastroschisis It is relatively uncommon anomaly. It results from a defect lateral to the median plane of the anterior abdominal wall without involving the umbilical cord. ! !

Non rotation of midgut Reversed rotation

SURGERY - GASTRO-INTESTINAL PROBLEMS

! ! ! ! ! ! !

Sub hepatic cecum Ileal diverticulum and appendix Internal hernia Midgut volvulus Stenosis and intestinal atresia Omphaloenteric fistula Mobile cecum

HINDGUT The hindgut gives rise to the left one-third of the transverse colon, the descending colon, sigmoid colon, the rectum, and the superior part of the anal canal. The inferior part of the anal canal develops from the proctodeum. The caudal part of the hindgut-the cloaca, is divided by the urorectal septum into the urogenital sinus and rectum. The urogenital sinus mainly gives rise to the urinary bladder and urethra. By the 7th week, the urorectal septum has fused with the cloacal membrane, dividing it into anal membrane and ventral urogenital membrane. The area of fusion of the urorectal septum with the cloacal membrane is perineal body. Anal membrane usually ruptures at the end of the 8th week. DEVELOPMENT OF ANAL CANAL The superior 2/3 of adult anal canal (2.5 cms) is derived from the hindgut. The inferior 1/3 of adult anal canal (1.3 cms) is developed from proctodeum. The endodermal and proctodial junction is indicated by irregular pectinate (white) line. The superior 2/3 of anal canal is supplied by superior rectal vessels - branches of inferior mesenteric vessels. Its developmental anomalies are; Congenital megacolon (Hirschsprungâ&#x20AC;&#x2122;s disease) It is seen in 1 in 5000 births. There is absence of ganglionic cells in a variable length of bowel. It is most common cause (33%) of neonatal large gut obstruction. !

! Imperforate anus It occurs in 1 in 5000 births. It is more common in males. It can be seen at lower or higher end in relation to puborectalis muscle.

EMBRYOLOGY

! Anal agenesis It can be present with or without fistula. The anal canal may end blindly or at an ectopic site or as an ano-perineal fistula. More than 90% of lower anomalies are associated with external fistula.

Anal Stenosis It is narrowing of the anal canal. !

! ! !

Membranous atresia of anus Anorectal agenesis Rectal atresia

REFERENCES 1. Moore & Persaud. The developing human Clinically oriented embryology. 2.

Langman's Medical Embryology.

SURGERY - GASTRO-INTESTINAL PROBLEMS

ANATOMY OF GASTROINTESTINAL TRACT

GIT - 02

GASTRO-INTESTINAL TRACT ANATOMY Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Irfan Ahmad Mughal M.Phil., Ph.D. Gastrointestinal tract is by definition primarily concerned with the intake, digestion and absorption of nutrients. Essentially, the gastrointestinal tract is an epithelium lined muscular tube extending from mouth to anus. 02.01

02.02

Epigastric region or epigastrium

Umbilical region

Hypogastric region or hypogastrium

Gastro intestinal tract (gross anatomy) ABDOMINAL QUADRANTS Abdominal regions

02.04 Median plane Transumbilical plane

Midclavicular planes

Anterior superior iliac spine

RUQ

02.03

LUQ Subcostal plane

Inguinal ligament

RLQ

LLQ Iliac crest Transtubercular plane

Iliac tubercle Anterior superior iliac spine

Abdominal quadrants Key to figure 2.02, 2.03 & 2.04 RH

Right hypochondriac

Right lumbar

RUQ Right upper quadrant

Right inguinal

LUQ Left upper quadrant

Left hypochondriac

RLQ Right lower quadrant

Left lumbar

LLQ Left lower quadrant

Pubic symphysis

Left inguinal

SURGERY - GASTRO-INTESTINAL PROBLEMS

Abdominal reference plane

ANATOMY OF GASTROINTESTINAL TRACT

ESOPHAGUS The esophagus is a 25cm long muscular tube with an average diameter of 2 cm that extends from the pharynx to the stomach. It starts in the median plane at the inferior border of the cricoid cartilage and ends by the entering into the stomach at cardiac end. The function of the esophagus is to convey food from the pharynx to the stomach. Oesophagus normally has four constrictions; Circo-pharangeal It is the first constriction approximately 15 cm from the incisor teeth and caused by the crico-pharyngeus muscle. It is known clinically as the upper esophageal sphincter. Aortic It is the second constriction approximately 22.5 cm from the incisor teeth seen at the crossing of arch of the aorta. 02.05

DILATATIONS Oesophagus has normally two dilated parts. These dilatations are clinically important when passing instruments through the esophagus and into the stomach. The short abdominal part of the esophagus extends from the diaphragm to the cardial (cardiac) orifice of the stomach; Superior The first dilated part of oesophagus is seen between cricophrangeal & broncho-aortic constriction. Inferior The second dilated part is seen between broncho-aortic & diaphragmatic constriction. Esophagus follows the curve of the vertebral column as it descends through the neck and mediastinum. It passes through the elliptical esophageal hiatus in the muscular right crus of the diaphragm, just to the left of the median plane at the level of T-10 vertebra. It terminates by entering the stomach at the cardiac orifice of the stomach to the left of the midline at the level of the 7th left costal cartilage and T11 vertebra. It is encircled by the esophageal nerve plexus distally. It is retroperitoneal but is covered anteriorly and laterally by peritoneum. The esophagus has internal circular and external longitudinal layers of muscle. The external layer comprises of skeletal muscle in its superior third. The inferior third is composed of smooth muscle, and the middle third is made up of both types of muscle.

Esophagus (gross anatomy) Bronchial It is the third constriction approximately 27.5 cm from the incisor teeth seen at the crossing of left main bronchus. Diaphragmatic It passes through diaphragm which is approximately 40 cm from the incisor teeth. It is clinically known as the lower esophageal sphincter.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Vascular Supply and Lymphatic Drainage The arterial supply of the abdominal part of the esophagus is from the left inferior gastric artery, a branch of the celiac trunk, and the left inferior phrenic artery. The venous drainage is to the portal venous system through the left gastric vein and into the systemic venous system through esophageal veins entering the azygos vein. The lymphatic drainage of the abdominal part of the esophagus is into the left gastric lymph nodes; efferent lymphatic vessels from these nodes drain mainly to celiac

ANATOMY OF GASTROINTESTINAL TRACT

lymph nodes. The innervation is from the vagal trunks (becoming anterior and posterior gastric nerves), the thoracic sympathetic trunks, the greater and lesser splanchnic nerves and the esophageal nerve plexus around the left gastric and inferior phrenic arteries.

most marked toward the pyloric part and along the greater curvature. 02.06

STOMACH It is the expanded part of the digestive tract between the esophagus and small intestine. It is capable of considerable expansion and can hold 2 â&#x20AC;&#x201C; 3 liters of food. A newborn infant's stomach (approximately the size of the lemon) can hold upto 30 ml of milk. PARTS OF STOMACH The stomach has four parts (cardia, fundus, body and pyloric part) and two curvatures (greater and lesser). Cardia is the part surrounding the cardial orifice. Fundus is the dilated superior part that is related to the left dome of the diaphragm and is limited inferiorly by the horizontal plane of the cardial orifice. The superior part of the fundus usually reaches the level of the left 5th intercostal space. Body lies between the fundus and the pyloric antrum. Pyloric part is the funnel-shaped region of the stomach; its wide part, the pyloric antrum, leads into the pyloric canal - its narrow part. Its wall is thicker because it contains more circular smooth muscle. The middle layer of the muscularis externa is greatly thickened to form the pyloric sphincter. The pylorus is normally in tonic contraction; it is closed except when emptying. Lesser curvature forms the shorter concave border of the stomach: the angular incisure (notch) is the sharp indentation approximately two-thirds of the distance along the lesser curvature. Greater curvature forms the longer convex border of the stomach.

INTERIOR OF THE STOMACH The smooth surface of the gastric mucosa is reddishbrown during life, except in the pyloric part where it is pink. When contracted, the gastric mucosa is thrown into longitudinal ridges â&#x20AC;&#x201C; gastric folds, or rugae; they are

SURGERY - GASTRO-INTESTINAL PROBLEMS

Stomach (gross anatomy) RELATIONS OF THE STOMACH The stomach is covered by peritoneum, except where blood vessels run along its curvatures and in a small area posterior to the cardiac orifice. The two layers of the lesser omentum extend around the stomach and leave its greater curvature as the greater omentum. ! Anteriorly, the stomach is related to the diaphragm, the left lobe of liver, and the anterior abdominal wall. ! Posteriorly, it is related to the lesser sac and pancreas. Its posterior surface forms most of the anterior wall of the lesser sac. The bed of the stomach on which the stomach rests in the supine position is formed by the structures forming the posterior wall of the omental bursa. From superior to inferior, the stomach bed is formed by the: ! Left dome of the diaphragm ! Spleen ! Left kidney and suprarenal gland ! Splenic artery ! Pancreas ! Transverse mesocolon and colon. VASCULAR SUPPLY OF STOMACH The stomach has rich arterial supply. The gastric arteries arise from the celiac trunk and its branches.

ANATOMY OF GASTROINTESTINAL TRACT

VENOUS DRAINAGE The gastric veins parallel the arteries in position and course. The left and right gastric veins drain into the portal vein and the short gastric veins and left gastroomental vein drain into the splenic vein which joins the superior mesenteric vein (SMV) to from the portal vein. The right gastro-omental vein empties in superior mesenteric vein (SMV). A prepyloric vein ascends over the pylorus to the right gastric vein. Because this vein is obvious in living persons, surgeons use it for identifying the pylorus.

02.07

Interior of stomach (endoscopic view) LEFT GASTRIC ARTERY It arises directly from the celiac trunk and runs in the lesser omentum to the cardia and then turns abruptly to course along the lesser curvature of the stomach and anastomose with the right gastric artery. RIGHT GASTRIC ARTERY It arises from the hepatic artery and runs to the left along the lesser curvature to anastomose with the left gastric artery. RIGHT GASTRO â&#x20AC;&#x201C; OMENTAL ARTERY (GASTROEPIPLOIC ARTERY) It arises as one of two terminal branches of the gastroduodenal artery, runs to the left along the greater curvature, and anastomoses with the left gastro-omental artery. LEFT GASTRO â&#x20AC;&#x201C; OMENTAL ARTERY It arises from the splenic artery and courses along the greater curvature to anastomose with the right gastroomental artery SHORT GASTRIC ARTERIES (FOUR TO FIVE) These arise from the distal end of the splenic artery or its splenic branches and pass to the fundus of the stomach.

SURGERY - GASTRO-INTESTINAL PROBLEMS

LYMPHATIC DRAINAGE OF THE STOMACH The gastric lymphatic vessels accompany the arteries along the greater and lesser curvatures of the stomach. These drain lymph from its anterior and posterior surfaces toward its curvatures, where the gastric and gastro-omental lymph nodes are located. The efferent vessels from these nodes accompany the large arteries to the celiac lymph nodes. The following is a summary of the lymphatic drainage of the stomach; ! Lymph from the superior two-third of the stomach drains along right and left gastric vessels to the gastric nodes; lymph from the fundus and superior part of the body of the stomach also drains along the short gastric arteries and left gastro-omental vessels to the pancreatico-splenic nodes. ! Lymph from the right two-third of the inferior third of the stomach drains along the right gastroomental vessels to the pyloric nodes. ! Lymph from the left one-third of the greater curvature drains along the short gastric and splenic vessels to the pancreatico-duodenal nodes. NERVES OF STOMACH The parasympathetic nerve supply of the stomach is from the anterior and posterior vagal trunks and their branches, which enter the abdomen through the esophageal hiatus. The anterior vagal trunk lies on the anterior surface of the esophagus and runs towards the lesser curvature of the stomach, where it gives off hepatic and duodenal branches that leave the stomach in

ANATOMY OF GASTROINTESTINAL TRACT

the hepatoduodenal ligament. The rest of the anterior vagal trunks continue along the lesser curvature, giving rise to anterior gastric branches. The larger posterior vagal trunk enters the abdomen on the posterior surface of the esophagus and passes toward the lesser curvature of the stomach. The posterior vagal trunk supplies branches to the anterior and posterior surface of the stomach. It gives off a celiac branch that runs to the celiac plexus and then continues along the lesser curvature, giving rise to posterior gastric branches. The sympathetic nerve supply of the stomach is from T6 through T9 segments of the spinal cord passes to the celiac plexus through the greater splanchnic nerve and is distributed through the plexuses around the gastric and gastro-omental arteries. SMALL INTESTINE Small intestine consists of the duodenum, jejunum, and ileum. It extends from the pylorus to the ileocecal junction. DUODENUM The duodenum is the first and shortest part of the small intestine – is also the widest and most fixed part. It pursues a C-shaped course around the head of the pancreas. It begins at the pylorus on the right side and ends at the duodenojejunal junction on the left side. The junction occurs approximately at the level of the L2 vertebra, 2 to 3 cm to the left of the midline. The junction usually takes the form of an acute angle, the duodenojejunal flexure. Most of the duodenum is fixed by peritoneum to structures on the posterior abdominal wall and is considered partially retroperitoneal. It has four parts; FIRST PART OF DUODENUM It is superior and short (approximately 5 cm). It lies anterolateral to the body of L-1 vertebra. The first 2 cm of the superior (first) part of the duodenum has a mesentery and is mobile.

SURGERY - GASTRO-INTESTINAL PROBLEMS

02.08

Duodenum (gross anatomy) The distal 3 cm of the (superior) first part and the other three parts of the duodenum have no mesentery and are immobile because they are retroperitoneal. Superior (first) part of the duodenum ascends from the pylorus and is overlapped by the liver and gallbladder. Peritoneum covers its anterior aspect but it is bare of peritoneum posteriorly, except for the ampulla – the first 2 cm that joins the pylorus. The proximal part has the hepatoduodenal ligament (part of the lesser omentum) attached superiorly and the greater omentum attached inferiorly. Posterior to the superior part are the portal vein, bile duct, gastroduodenal artery, and inferior vena cava (IVC). SECOND PART OF DUODENUM It is longer (about 7 – 10 cm) and descends along the right sides of L-1 through L-3 vertebrae. Descending (second) part of the duodenum runs inferiorly curving around the head of the pancreas. Initially it lies to the right and parallel to the inferior vena cava (IVC). The bile and pancreatic ducts enter its posteromedial wall. These ducts usually unite to form the hepatopancreatic ampulla, which opens on the summit of an eminence located

ANATOMY OF GASTROINTESTINAL TRACT

posteromedially in the descending duodenum – the major duodenal papilla. The descending part of the duodenum is entirely retroperitoneal. The anterior surface of its proximal and distal thirds is intimately covered with peritoneum. However, the peritoneum reflects from its middle third to form the double-layered mesentery of the transverse colon, the transverse mesocolon.

superior mesenteric artery (SMA) and vein and the root of the mesentery of the jejunum and ileum. Superior to it is the head of the pancreas and its uncinate process. The anterior surface of the horizontal part is covered with peritoneum, except where it is crossed by the superior mesenteric vessels and the root of the mesentery. Posteriorly it is separated from the vertebral column by the right psoas major, inferior vena cava (IVC), aorta and the right testicular or ovarian vessels.

02.09

Interior of duodenum (endoscopic view) 02.10

FOURTH PART OF DUODENUM It is short (5 cm) and begins at the left of L-3 vertebra and rises superiorly as far as the superior border of L-2 vertebra. Ascending (fourth) part of the duodenum runs superiorly and along the left side of the aorta to reach the inferior border of the body of the pancreas. Here it curves anteriorly to join the jejunum at the duodenojejunal junction that takes the form of an acute angle – the duodenojejunal flexure – which is supported by the attachment of a suspensory muscle of the duodenum (ligament of Treitz). This muscle is composed of a slip of skeletal muscle from the diaphragm and a fibromuscular band of smooth muscle from the third and fourth parts of the duodenum. Contraction of this muscle widens the angle of the flexure, facilitating movement of the intestinal contents. The suspensory muscle passes posterior to the pancreas and splenic vein and anterior to the left renal vein.

Interior of duodenum (adenocarcinoma)

VASCULAR SUPPLY The duodenal arteries arise from the celiac trunk and the superior mesenteric artery (SMA). The celiac trunk, via the gastroduodenal artery and its branch-the superior pancreaticoduodenal artery supplies the duodenum proximal to the entry of the bile duct into the descending (second) part of the duodenum.

THIRD PART OF DUODENUM It is 6 to 8 cm long and crosses L-3 vertebra. Inferior or horizontal (third) part of the duodenum runs transversely to the left, passing over the inferior vena cava (IVC), aorta and L3 vertebra. It is crossed by the

The superior mesenteric artery (SMA), through its branch-the inferior pancreaticoduodenal artery supplies the duodenum distal to the entry of the bile duct. The anastomosis of the superior and inferior pancreaticoduodenal arteries, which occurs approximately at the

SURGERY - GASTRO-INTESTINAL PROBLEMS

ANATOMY OF GASTROINTESTINAL TRACT

level of entry of the bile duct or at the junction of the descending and horizontal parts of the duodenum is an anastomosis between the celiac and superior mesenteric arteries.

NERVE SUPPLY The nerves of the duodenum are derived from the vagus and sympathetic nerves through the celiac and superior mesenteric plexuses on the pancreaticoduodenal arteries.

02.11

Celiac artery and its branches An important transition in the blood supply of the digestive tract occurs; ! Proximally (extending from the abdominal part of the esophagus), the blood is supplied by the celiac trunk. ! Distally (extending to the left colic flexure), the blood is supplied by the mesenteric artery.

JEJUNUM AND ILEUM The jejunum begins at the duodenojejunal flexure and the ileum ends at the ileocecal junction. Together, the jejunum and ileum are 6 to 7 meters long, the jejunum constitutes approximately two-fifths and the ileum approximately three-fifths. Most of the jejunum lies in the left upper quadrant, whereas most of the ileum lies in the right lower quadrant. The terminal ileum usually lies in the pelvis from which it ascends, ending in the medial aspect of the cecum. 02.12

The basis of this transition in blood supply is embryological. The duodenal veins follow the arteries and drain into the portal vein-some directly and others indirectly through the superior mesenteric and splenic veins. LYMPHATIC DRAINAGE The lymphatic vessels of the duodenum follow the arteries. The anterior lymphatic vessels of the duodenum drain into the pancreaticoduodenal lymph nodes located along the superior and inferior pancreaticoduodenal arteries, and into the pyloric lymph nodes that lie along the gastroduodenum artery. The posterior lymphatic vessels pass posterior to the head of the pancreas and drain into the superior mesenteric lymph nodes. Efferent lymphatic vessels from the duodenal lymph nodes drain into the celiac lymph nodes.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Small intestine (gross anatomy)

The mesentery attaches the jejunum and ileum to the posterior abdominal wall. The root of the mesentery (approximately 15 cm long) is directed obliquely, inferiorly, and to the right. It extends from the duodenojejunal junction on the left side of the L2 vertebra to the ileocolic junction and the right sacroiliac joint. The average breadth of the mesentery from its root to the intestinal border is 20 cm. The root of the mesentery crosses (successively) the: 13

ANATOMY OF GASTROINTESTINAL TRACT

lacteals â&#x20AC;&#x201C; in the intestinal villi (projections of the mucous membrane 0.15 - 1.5 mm in length) empty their milk like fluid into the lymphatic plexuses in the walls of jejunum and ileum. The lymphatic vessels pass between the layers of the mesentery; the mesenteric lymph nodes are located; ! Close to the intestinal wall. ! Among the arterial arcades. ! Along the proximal part of the SMA.

02.13

Superior mesenteric artery ! ! ! ! ! !

Ascending and horizontal parts of the duodenum Abdominal aorta Inferior vena cava (IVC) Right ureter Right psoas major Right testicular or ovarian vessels.

Efferent lymphatic vessels from the mesenteric lymph nodes drain to the superior mesenteric lymph nodes. Lymphatic vessels from the terminal ileum follow the ileal branch of the ileocolic artery to the ileocolic lymph nodes. 02.14

The superior mesenteric vessels, lymph nodes, a variable amount of fat, and autonomic nerves are present between the two layers of the mesentery. VASCULAR SUPPLY Superior Mesenteric Artery (SMA) It supplies the jejunum, ileum and large gut upto proximal 2/3 of transverse colon. It usually arises from the abdominal aorta at the level of the L-1 vertebra, approximately 1 cm inferior to the celiac trunk, and runs between the layers of the mesentery, sending 15 to 18 branches to the jejunum and ileum. The arteries unite to form loops or arches (arterial arcades) that give rise to straight arteries (the vasa recta).

Superior mesenteric artery and its branches

VENOUS DRAINAGE The superior mesenteric vein (SMV) drains the jejunum and ileum. It lies anterior and to the right of the SMA in the mesentery. The superior mesenteric vein (SMV) ends posterior to the neck of pancreas where it unites with the splenic vein to form the portal vein.

NERVES OF JEJUNUM & ILEUM The superior mesenteric artery (SMA) and its branches are surrounded by a perivascular nerve plexus through which the nerves are conducted to the parts of the intestine supplied by this artery. The sympathetic fibers in the nerves to the jejunum and ileum originate in the T5 through T9 segments of the spinal cord and reach the celiac plexus through the sympathetic trunks and greater and lesser splanchnic nerves. The parasympathetic fibers in the nerves to the jejunum and ileum are derived from the posterior vagal trunk.

LYMPHATIC DRAINAGE The specialized lymphatic vessels that absorb fat â&#x20AC;&#x201C;

In general, sympathetic stimulation reduces motility of intestine and secretion and acts as vasoconstrictor,

SURGERY - GASTRO-INTESTINAL PROBLEMS

ANATOMY OF GASTROINTESTINAL TRACT

reducing or stopping digestion and making blood available for fleeing or fighting. Parasympathetic stimulation increases motility of the intestine and secretion, restoring digestive activity. LARGE INTESTINE The large intestine consists of the cecum; the appendix; the ascending, transverse, descending and sigmoid colon, rectum and anal canal. The large intestine can be distinguished from the small intestine by; ! Teniae coli - which are three thickened bands of muscle. ! Haustrations - which are sacculations of the c o l o n between the teniae coli. ! Omental appendices - which are small fatty projections of the omentum. ! The internal diameter of large intestine is much larger than small intestine. 02.15

Large gut (gross anatomy) The three teniae coli comprise most of the longitudinal muscle of the large intestine; except in the rectum. The teniae are shorter than the intestine. The colon has the typical sacculated shape formed by the haustra. There are no teniae in the appendix or rectum; they begin at the base of the appendix and run through the large intestine to the rectosigmoid junction.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Ascending colon

02.16

Omental appendices

Ileocecal junction

Caecum Tip of appendix

Appendix

Cecum and Appendix (gross anatomy)

CAECUM Caecum is the first part of the large intestine and is continuous with the ascending colon - is a blind intestinal pouch (approximately 7.5cm in both length and breadth) in the right lower quadrant where it lies in the iliac fossa inferior to the junction of the terminal ileum. The caecum, usually lies within 2.5cm of the inguinal ligament, is almost entirely enveloped by peritoneum and is reasonably mobile. It has no mesentery. The terminal ileum enters the caecum obliquely and partly invaginates into it. VERMIFORM APPENDIX The vermiform appendix is a blind intestinal diverticulum about 6-10 cm in length. It arises from the posteromedial aspect of the cecum inferior to the ileocecal junction. The wormlike appendix has a short triangular mesentery, the mesoappendix, which is derived from the posterior sides of the mesentery of the terminal ileum. The mesoappendix attaches to the cecum and proximal part of the appendix. The position of the appendix is variable, but is usually retrocecal. VASCULAR SUPPLY The cecum is supplied by the ileocolic artery, the terminal branch of the superior mesenteric artery (SMA). The appendix is supplied by the appendicular artery, a branch of the ileocolic artery. A tributary of the superior

ANATOMY OF GASTROINTESTINAL TRACT

mesenteric vein (SMV) - the ileocolic vein, drains blood from the cecum and appendix. The lymphatic vessels from the cecum and appendix pass to lymph nodes in the mesoappendix and to the ileocolic lymph nodes that lie along the ileocolic artery. Efferent lymphatic vessels pass to the superior mesenteric lymph nodes.

cavity from the cecum to the right lobe of the liver, where it turns to the left at the right colic flexure (hepatic flexure). The ascending colon is narrower than the cecum and lies retroperitoneally along the right side of the posterior abdominal wall. The ascending colon is covered by peritoneum anteriorly and on its sides. The ascending colon is separated from the anterolateral abdominal wall by the greater omentum.

02.17

Arterial supply of colon NERVE SUPPLY The nerve supply to the cecum and appendix derives from the sympathetic and parasympathetic nerves from the superior mesenteric plexus. The sympathetic nerve fibers originate in the lower thoracic part of the spinal cord, and the parasympathetic nerve fibers are derived from the vagus nerves. Afferent nerves fibers from the appendix accompany the sympathetic nerves to the T10 segment of the spinal cord. COLON The colon is described in four parts; ascending, transverse, descending, and sigmoid. The colon lies first to the right of the small intestine, then successively superior and anterior to it, to the left of it, and eventually inferior to it. ASCENDING COLON Ascending colon is the second part of the large intestine. It passes superiorly on the right side of the abdominal

SURGERY - GASTRO-INTESTINAL PROBLEMS

VASCULAR AND LYMPHATIC SUPPLY The arterial supply to the ascending colon and right colic flexure is from branches of the superior mesenteric artery (SMA) the ileocolic and right colic arteries. The right branch of the middle colic artery usually anastomoses with the right colic artery. Tributaries of the SMV - the ileocolic and right colic veins, drain blood from the ascending colon. The lymphatic vessels pass first to the epicolic and paracolic lymph nodes, next to the ileocolic and intermediate right colic lymph nodes, and from them to the superior mesenteric lymph nodes. The nerves to the ascending colon are derived from the superior mesenteric nerve plexus. TRANSVERSE COLON It is approximately 45 cm long. It is the largest and most mobile part of the large intestine. It crosses the abdomen from the right colic flexure to the left colic flexure, where it bends inferiorly to become the descending colon. The left colic flexure (splenic flexure) usually more superior, more acute, and less mobile than the right colic flexure. It lies anterior to the inferior part of the left kidney and attaches to the diaphragm through the phrenicocolic ligament. The transverse mesocolon loops down, often inferior to the level of the iliac crests, and is adherent to or fused with the posterior wall of the omental bursa. The root of the transverse mesocolon lies along the inferior border of the pancreas and is continuous with the parietal peritoneum posteriorly. Being freely moveable, the transverse colon is variable in position. It usually hangs to the level of the umbilicus.

ANATOMY OF GASTROINTESTINAL TRACT

VASCULAR, LYMPHATIC AND NERVE SUPPLY The arterial supply of the transverse colon is mainly from the middle colic artery - a branch of the superior mesenteric artery (SMA). It is also supplied by the right and left colic arteries. Venous drainage of the transverse colon is through the superior mesenteric veins (SMV). The lymphatic drainage of the transverse colon is to the middle colic lymph nodes, which in turn drains to the superior mesenteric lymph nodes. The nerves of the transverse colon arise from the superior mesenteric nerve plexus and follow the right and middle colic arteries.

the sigmoid colon; these disappear when the sigmoid mesentery terminates. The teniae coli also disappear as the longitudinal muscle in the wall of the colon broadens to form a complete layer in the rectum.

DESCENDING COLON Descending colon passes retroperitoneally from the left colic flexure into the left iliac fossa, where it is continuous with the sigmoid colon. Peritoneum covers the colon anteriorly and laterally and binds it to the posterior abdominal wall. The descending colon, especially in the iliac fossa, has a short mesentery in approximately 33% of people; It is usually not long enough to cause volvulus of the colon. As it descends, the colon passes anterior to the lateral border of the left kidney. The descending colon has a paracolic gutter on its lateral aspect. SIGMOID COLON Sigmoid colon is characterized by its S-shaped loop of variable length (approximately 40 cm). It links the descending colon and the rectum. The sigmoid colon extends from the iliac fossa to the third sacral segment where it joins the rectum. The termination of the teniae coli, approximately 15 cm from the anus, indicates the rectosigmoid junction. It has a long mesentery and is mobile especially in its middle part. The root of the sigmoid mesocolon has an inver ted V-shaped attachment, extending first medially and superiorly along the external iliac vessels and then medially and inferiorly from the bifurcation of the common iliac vessels to the anterior aspect of the sacrum. The left ureter and the division of the left common iliac ar tery lie retroperitoneally, posterior to the apex of the root of the sigmoid mesocolon. The omental appendices are long in

SURGERY - GASTRO-INTESTINAL PROBLEMS

VASCULAR SUPPLY The arterial supply of the descending and sigmoid colon is from the left colic and superior sigmoid arteries branches of the inferior mesenteric artery. The sigmoid arteries descend obliquely to the left where these divide into ascending and descending branches. The most superior branch of the superior sigmoid artery anastomoses with the descending branch of the left colic artery, thereby forming a part of the marginal artery of the colon. The inferior mesenteric vein (IMV) drains blood from the descending colon and sigmoid colon, flowing into the splenic vein and then the portal vein on its way to the liver. 02.18

Venous supply of colon LYMPHATIC SUPPLY The lymphatic vessels from the descending colon and sigmoid colon pass to the epicolic and paracolic nodes and then through the intermediate colic lymph nodes along the left colic artery. Lymph from these nodes passes to the inferior mesenteric lymph nodes that lie around the inferior mesenteric artery. Lymph from the left colic flexure may also drain to the superior mesenteric lymph nodes. 17

ANATOMY OF GASTROINTESTINAL TRACT

NERVE SUPPLY The sympathetic nerve supply of the descending and sigmoid colon is from the lumbar part of the sympathetic trunk and the superior hypogastric plexus through the plexuses on the inferior mesenteric artery and its branches. The parasympathetic nerve supply is from the pelvic splanchnic nerves.

circular muscle layer of the rectal wall. The dilated terminal part of the rectum, lying directly above and supported by the pelvic diaphragm (levator ani) and anococcygeal ligament, is the ampulla of the rectum. The ampulla receives and holds an accumulating fecal mass until it is expelled during defecation. The ability of the ampulla to relax to accommodate the initial and subsequent arrivals of fecal material is another essential element of maintaining fecal continence.

RECTUM AND ANAL CANAL The rectum is the fixed terminal part of the large intestine. It is continuous with the sigmoid colon at the level of S-3 vertebra. The junction is at the lower end of the mesentery of the sigmoid colon. The rectum is continuous inferiorly with the anal canal. RECTUM The rectum is the part of the alimentary tract continuous proximally with the sigmoid colon and distally with the anal canal. The rectosigmoid junction lies anterior to the S-3 vertebra . The teniae of the sigmoid colon spread out to form a continuous outer longitudinal layer of smooth muscle, and the fatty omental appendices are discontinued. The rectum follows the curve of the sacrum and coccyx, forming the sacral flexure of the rectum. The rectum ends anteroinferior to the tip of the coccyx by turning sharply posteroinferiorly - the anorectal flexure as it perforates the pelvic diaphragm (levator-ani) to become the anal canal. The anorectal flexure is an important mechanism for fecal continence, being maintained during the resting state by the tonus of the puborectalis muscle and by its active contraction during peristaltic contractions if defecation is not occurring. With the flexures of the rectosigmoid junction superiorly and the anorectal junction inferiorly, the rectum has an S-shape when viewed laterally. When viewed anteriorly, the rectum demonstrates three sharp lateral flexures (superior, intermediate, and inferior) because of the presence of three internal infoldings (transverse rectal folds) of the mucous and submucous coats overlying thickened parts of the

SURGERY - GASTRO-INTESTINAL PROBLEMS

02.19

Rectum with its arterial supply Peritoneum covers the anterior and lateral surfaces of superior third of the rectum, only the anterior surface of the middle third, and no surface of the inferior third because it is subperitoneal. In males the peritoneum reflects from the rectum to the posterior wall of the bladder, where it forms the floor of the rectovesical pouch. In females, the peritoneum reflects from the rectum to the posterior fornix of the vagina, where it forms the floor of the rectouterine pouch (cul-de-sac). In both sexes, lateral reflections of peritoneum from the superior one-third of the rectum forms pararectal fossae, which permit the rectum to distend as it fills with feces. The rectum rests posteriorly on the inferior three sacral vertebrae and the coccyx, anococcygeal ligament, median sacral vessels, and inferior ends of the sympathetic trunks and sacral plexuses. In males the

ANATOMY OF GASTROINTESTINAL TRACT

rectum is related anteriorly to the fundus of the urinary bladder, terminal parts of the ureters, ductus deferens, seminal vesicles, and prostate. The rectovesical septum lies between the fundus of the bladder and the ampulla of the rectum and is closely associated with the seminal vesicles and prostate. In females the rectum is related anteriorly to the vagina and is separated from its posterior fornix and the cervix by the rectouterine pouch. Inferior to this pouch, the weak rectovaginal septum separates the superior half of the posterior wall of the vagina from the rectum.

from there to the inferior mesenteric and lumbar lymph nodes. Lymphatic vessels from the inferior half of the rectum ascend with the middle rectal arteries and drain into the internal iliac lymph nodes.

ARTERIAL SUPPLY OF THE RECTUM The superior rectal artery- the continuation of the inferior mesenteric artery supplies the proximal part of the rectum. The two middle rectal arteries usually arising from the inferior vesical arteries supply the middle and inferior parts of the rectum, and the inferior rectal arteries arising from the internal pudendal arteries supply the anorectal junction and anal canal. Blood from the rectum drains through the superior, middle, and inferior rectal veins. Anastomoses occur between the portal and systemic veins in the wall of the anal canal. Because the superior rectal vein drains into the portal veins system and middle and inferior rectal veins drain into the systemic system, these anastomoses are an important area of portocaval anastomosis. The submucosal rectal venous plexus surrounds the rectum and communicates with the vesical venous plexus in males and the uterovaginal venous plexus in females. The rectal venous plexus consists of two parts - the internal rectal venous plexus just deep to the mucosa of the anorectal junction and the subcutaneous external rectal venous plexus external to the muscular wall of the rectum.

NERVE SUPPLY The nerve supply to the rectum is from the sympathetic and parasympathetic systems. The rectum derives its sympathetic supply from the lumbar part of the sympathetic trunk and the superior hypogastric plexus through plexuses on the branches of the inferior mesenteric artery. The parasympathetic supply derives from the pelvic splanchnic nerves. Fibers pass from these nerves to the left and right inferior hypogastric plexuses to supply the rectum. Visceral afferent or sensory fibers also join these plexuses and reach the spinal cord through the pelvic splanchnic nerves. ANAL CANAL It is the last part of the gastro intestinal tract. It starts at the end of the rectum and it opens to the exterior at external anal opening. The anal orifice separates the perianal skin from the mucosa of anal canal. The mucosa is pink and perianal skin is pigmented and demarcation is very clear. Anoractal ring is at 05 cm from the anal orifice. Lower rectal fold is visible at about 08cm from the anal orifice. The superior rectum fold is about 10-12cms from the anal orifice. REFERENCES 1. Clinically oriented Anatomy by Keith L. Moore. 2.

John Skandalakis et al. Surgical anatomy and technique. Colon and anoractal. Second edition, Springer; 1999. P 516-529.

Lymphatic vessels from the superior half of the rectum ascend along the superior rectal vessels to pararectal lymph nodes. They then pass to lymph nodes in the inferior part of the mesentery of the sigmoid colon and

SURGERY - GASTRO-INTESTINAL PROBLEMS

Esophagus

SURGERY - GASTRO-INTESTINAL PROBLEMS

STOMACH

OBJECTIVES ! ! ! ! ! ! !

To understand development, anatomy and physiology of esophagus. To understand the congenital abnormalities of esophagus. To be able to diagnose esophageal problems. To be able to manage esophageal problems. To be able to prepare the patient for esophageal surgery. To be able to look after the patient after esophageal surgery. To be able to prevent, diagnose and treat complications.

SURGERY - GASTRO-INTESTINAL PROBLEMS

DYSPHAGIA

GIT - 03

DYSPHAGIA Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS Dysphagia is difficulty in swallowing. It may be experienced after swallowing the solids or liquids. It must be clearly differentiated from odynophagia which is painful swallowing1.

ODYNOPHAGIA Painful lesions interfere with the various stages of swallowing and thus cause painful swallowing. Painful tongue fails to push the food backwards during oral phase of swallowing. Painful lesions of the mouth, oropharynx, upper respiratory tract, pharynx, tongue and the retro-pharyngeal abscess may also lead to 1 painful swallowing .

ETIOLOGY Causes of dysphagia are mainly divided in two; pharyngeal and esophageal. PHARYNGEAL DYSPHAGIA Neurological deficit associated with cerebro vascular accidents, head injuries and cranial nerve neuropathies results in inco-ordination of swallowing. It happens due to some abnormality of the swallowing reflex in the following conditions ; ! Pharyngitis ! Peritonsilar abscess ! Pharyngeal pouch ! Bulbar paralysis / Pseudobulbar Palsy ! Myasthenia gravis ! Acute anterior poliomyelitis ! Plummer Vinson syndrome ! Systemic Sclerosis

ESOPHAGEAL DYSPHAGIA Difficulty in swallowing could be due to physical obstruction of esophagus which may be ; ! Congenital ! Acquired CONGENITAL CAUSES Atresia Stenosis Short esophagus and congenital hiatus hernia Dysphagia lusoria (due to compression by a vessel)

! ! ! !

INTRALUMINAL CAUSES Foreign bodies Gastric carcinoma blocking the esophageal opening into the stomach

! !

INTRINSIC CAUSES Stricture (benign, malignant or post-irradiation) Carcinoma esophagus Achalasia cardia Plummer Vinson syndrome Spasm (generalized) Diffuse esophageal spasm Esophageal ring or web

! ! ! ! ! ! !

EXTRINSIC CAUSES Thyroid swellings (retrosternal) Pharyngeal pouches Aortic aneurysm Mediastinal swelling (Neoplasms,abscess,enlarged lymph glands) ! Hiatus hernia ! ! ! !

SURGERY - GASTRO-INTESTINAL PROBLEMS FIRST EDITION

DYSPHAGIA

RARE CAUSES Hysteria Anorexia Nervosa Drug Induced Syphilitic degeneration of the medullary centers

! ! ! !

EVALUATION OF DYSPHAGIA HISTORY & CLINICAL EXAMINATION Dysphagia is only a symptom. The diagnosis of the cause of dysphagia should be made. History of precise description of dysphagia, its duration, its site and its time after ingestion of food must be noted. Pattern of dysphagia, intermittent or progressive should be noted. A variety of associated symptoms may help to narrow the differential diagnosis. History of general behavior of the patient, anxiety and psychosomatic problems should be found out. History of vomiting, regurgitation and upper respiratory tract (URT) infection is noted. Weight loss and loss of appetite indicate towards malignant disease. ASSOCIATED SYMPTOMS

Cough Early in Swallowing Late in Swallowing Weight loss In elderly With regurgitation Halitosis (foul smelling breath)

Neuromuscular Dysphagia Obstructive Dysphagia

URINE EXAMINATION It is a simple nonspecific investigation. It helps to assess the general condition of the patient. BLOOD EXAMINATION Haemoglobin estimation Leukocyte count Sedimentation rate Urea and electrolytes Protein level These tests are also nonspecific but help to assess the general condition of the patient. RADIOLOGICAL EXAMINATION X-RAY CHEST It is a very helpful investigation. It picks up the abnormalities due to effects of esophageal obstruction, regurgitation and aspiration such as pneumonitis and helps in diagnosis. ESOPHAGOGRAM (BARIUM SWALLOW) Barium study is often the first step in evaluating patients with dysphagia especially if an obstructive lesion is suspected. Double contrast studies provide better visualization of esophageal mucosa. 03.01

03.02

03.03

Carcinoma Achalasia Zenkerâ&#x20AC;&#x2122;s Diverticulum

General examination of the patient showing weight loss, anaemia, koilonychia, enlarged lymph glands and enlarged thyroid is helpful in reaching satisfactory diagnosis. Systematic examination is of minimum yield.

INVESTIGATIONS Investigations are most useful to diagnose the cause of dysphagia in most of the cases.

Barium Swallow ENDOSCOPIC SONOGRAPHY (EUS) It is another improvement in the diagnosis of esophageal and upper gastro-intestinal malignancies. EUS is used for accurate assessment of the extent of intramural involvement and enlargement of adjacent lymph nodes.

SURGERY - GASTRO-INTESTINAL PROBLEMS FIRST EDITION

DYSPHAGIA

DIAGNOSIS OF DYSPHAGIA Dysphagia

Difficulty in initiating Swallowing Cough, Choking

Food Sticks after Swallowing

Oropharyngeal Dysphagia

Esophageal Dysphagia

Solid + Liquid

Solid food only

Mechanical obstruction

Progressive

Neuromuscular Disorder

Intermittent

Progressive Chronic heartburn

Age > 50 years

Chronic heartburn

Peptic stricture

Intermittent

Malignancy

Lower esophageal ring

Respiratory Symptoms

Scleroderma

SURGERY - GASTRO-INTESTINAL PROBLEMS FIRST EDITION

Achalasia

Chest pain

Diffuse esophageal pain

DYSPHAGIA

This procedure confirms the diagnosis by histopathological examination of the tissue from the diseased part.

03.04

DIFFERENTIAL DIAGNOSIS Different causes of dysphagia have to be differentiated from each other. These are ;

Endoscopic sonography (EUS)

It is helpful to assess the ; ! Depth of tumour infiltration in the wall. ! Lymph node involvement. ! Spread to adjacent organs2.

ACHALASIA CARDIA This is the functional obstruction of the lower end of the esophagus. The exact cause is unknown. It could be possible that some derangement of the lower esophageal sphincter is present. 03.06

03.07

It is more than 80-87% accurate in esophageal and gastric cancers staging as compared to CT scan which has (43-47%) accuracy to pick up early tumours. ESOPHAGEAL MANOMETERY Manometery assesses the motor function of the esophagus and is indicated if no abnormality is identified by barium study or endoscopy. ESOPHAGOSCOPY This is visualizing the esophagus directly through the esophagoscope. Most of the diseases causing dysphagia are diagnosed by direct visualization. Endoscopy is used to obtain tissue biopsy and brush cytology. It is also used for therapeutic dilation of stricture and placement of stent.

X-ray chest showing Air/fluid interface and dilated esophagus

There could be following basic possible abnormalities ; Lack of peristalsis (Aperistalsis) Dis-organized peristalsis (dysperistalsis) Partial or incomplete relaxation of the lower esophageal sphincter (Failure of relaxation) ! Increased basal tone of lower esophageal sphincter. ! ! !

03.05

There is primary failure of cardiac sphincter to relax. There is progressive dilatation of the esophagus proximal to the lower esophageal sphincter. The esophagus becomes dilated and tortuous. It has got a narrow neck. It may become too big to be called as sigmoid esophagus. The ganglions of myenteric plexus are defective. There is BIOPSY

Esophagoscopy

SURGERY - GASTRO-INTESTINAL PROBLEMS FIRST EDITION

DYSPHAGIA

retention esophagitis and presence of foul smelling liquid in the dilated esophagus. Its wall may be thicker, thinner or of normal thickness. It may be present in any age group and any sex but is common in females of 40 years age. The main symptoms are as following; ! Dysphagia ! Chest pain ! Regurgitation

The symptoms get worse by emotional stress and cold liquids. Its onset is gradual and dysphagia is progressive. The breath is foul smelling. There is foetid flatulence and patient loses weight. There is regurgitation few hours after the meal and not the vomiting. There is retro-sternal discomfort. There are features of aspiration pneumonia. Toxic rheumatoid arthritis is common in these patients. It is a pre-malignant condition and 2-7% of the patients develop carcinoma.

DIAGNOSIS Esophagoscopy confirms the diagnosis. Barium swallow (esophagogram) also helps in the confirmation of diagnosis with the following features ; ! Smooth and pencil shaped narrowing of lower end of the esophagus. ! Dilated and tortuous lower end of the oesophagus ! No gas bubble in the stomach ! Incoordinated peristalsis

03.08

03.09

Barium swallow

TREATMENT The treatment is done is two stages ! Initial treatment ! Definitive treatment

Achalasia cardia

SURGERY - GASTRO-INTESTINAL PROBLEMS

INITIAL TREATMENT The initial treatment is conservative. Aspiration of the stagnant fluid from the esophagus is done. Pulmonary complications such as aspiration pneumonia are treated with antibiotics and chest physiotherapy. Anaemia and malnutrition are treated. 27

DYSPHAGIA

DEFINITIVE TREATMENT There are following options for definitive treatment ; ! Medical Treatment ! Endoscopic Pneumatic dilation ! Botolinum Toxin Injection ! Surgical Myotomy MEDICAL TREATMENT Oral long-acting nitrates and calcium channel blockers are used. They act by lowering the lower esophageal sphincter pressure. SURGICAL TREATMENT Heller's operation (esphago-cardio-myotomy) is the definitive treatment. The constricting fibers of the cardiac sphincter of the stomach are incised extra-mucosally. Laparoscopic esophagocardiomyotomy is more popular now-a-days. It is minimally invasive and simple to do. KELLY PATERSON (PLUMMER VINSON) SYNDROME

Dysphagia

Blood picture shows iron deficiency anaemia and low serum iron level. Anaemia is treated by iron replacement and blood transfusions. All the symptoms disappear after iron replacement4. It is treated by hydro-dilatation of the stricture through esphagoscope. The dilatation is done with Guntzig catheter of small diameter and narrow end. It is done with 3 stepwise progressive but slow filling of the balloon . Patient's general condition is improved by balanced food or parenteral feeding. CONGENITAL ATRESIA OF ESOPHAGUS It is a congenital problem. The neonate presents within twenty four hours of birth with the history of regurgitation of food and saliva. Attacks of coughing and cyanosis are also seen after feeding. The fetus with esophageal atresia is unable to swallow amniotic fluid. The mother presents with polyhydramnios. Mother of one third of these fetuses may present with premature labour. The most common associated congenital anomaly is imperforate anus. It is diagnosed from history and by introducing a soft rubber catheter into the esophagus. The obstruction is usually felt at about 10 cm from the lips.

Glossitis

Anemia

It is a premalignant condition. It is commonly seen in middle aged women. The patient suffers from anaemia. There is history of progressive difficulty of swallowing. It may present with dysphagia, odynophagia, glossitis and features of hypochromic anaemia. Clinical examination reveals ; ! Smooth tongue ! Pallor. ! Koilonychia. ! Swollen tongue. ! Enlarged spleen.

SURGERY - GASTRO-INTESTINAL PROBLEMS

The contrast medium (Lipoidal or gastrographin) can be introduced and x-rays are taken which confirm the diagnosis. The contrast medium should be aspirated as soon as the x-rays are taken. Aspiration causes severe chest complications and delays the definitive procedure. Absence of air from the stomach on chest x-ray film excludes fistula between trachea and distal esophagus. Definitive treatment is excision of atresic segment and end to end anastomosis of the two ends (Proximal and distal) of esophagus. If the fistula is present, its closure is also done.

DYSPHAGIA

If patient has chest complications, gastrostomy should be done, upper esophageal contents are sucked regularly. Antibiotics are given and definitive surgery is performed when the infant is fit. FOREIGN BODIES Different sorts of foreign bodies have been ingested accidentally or deliberately by the patients. History is usually available. X-ray examination and barium swallow help in the diagnosis. Esophagoscopy helps in the diagnosis and in the removal of the foreign body.

STRICTURES OF ESOPHAGUS The stricture is segmental fibrosis of the oesophagus. It could be benign or malignant. The benign stricture is segmental fibrosis of the esophagus. It may follow acute esophagitis followed by chronic intramural esophagitis and subsequent fibrosis. 90% of benign strictures occur due to reflux esophagitis. Less common causes are ; ! Post operative (anastomotic) ! Corrosive ingestion ! Nasogastric tube trauma

03.10

03.11

Foreign body esophagus SURGERY - GASTRO-INTESTINAL PROBLEMS

Strictures of esophagus 29

DYSPHAGIA ! !

! ! ! !

Foreign body impaction Moniliasis Post radiotherapy Viral infection Congenital Miscellaneous such as Crohn's disease and Plummer Vinson syndrome etc.

03.12

History of ingestion of corrosives and ingestion of foreign bodies may give clues about benign stricture. Post caustic ingestion esophagitis is treated with high doses of steroids, nasogastric intubation and antibiotics. Early endoscopy and dilatation is done if stricturation is 5 occurring. Parental nutrition is given to these patients . History of peptic ulceration or hiatus hernia is suggestive of peptic stricture (inflammatory) of the esophagus. History of severe loss of weight, weakness and mass in the epigastrium is suggestive of carcinoma. Treatment is of the cause of the stricture and dilatation of stricture through the esophagoscope. In case of failure to dilate the stricture, excision of the stricture and anastomosis of the oesophagus to stomach or jejunum is performed. CARCINOMA OF THE ESOPHAGUS It is the malignant lesion of the esophagus leading to dysphagia. It should be diagnosed as early as possible. Its staging should be performed and appropriate treatment is carried out. General condition of the patient is improved by naso-gastric or parenteral feeding. Surgery or radiotherapy helps in the treatment. HYSTERIA The patient is usually young female. There is history of other hysterical manifestations. There is no significant weight loss or vomiting. SURGERY - GASTRO-INTESTINAL PROBLEMS

Carcinoma of esophagus Diagnosis is easy on history and examination. Conservative treatment helps to relieve the symptoms. Sedatives should be used. Psychiatric help is required in these cases.

DYSPHAGIA

ANXIETY, ANOREXIA NERVOSA These are also common causes of dysphagia. The patients are usually young females but no age or sex is immune to this problem. History and examination are suggestive of the diagnosis which is relatively easy. Conservative treatment achieves satisfactory results. Tranquilizers and sedatives are used. It is always appropriate to ask for psychiatric help in such cases.

REFERENCES 1. Peter J Morris. Ronald A Malt. The Esophagus. Oxford text book of surgery. Oxford university press London. 1994. p: 866-907. 2. Grim H. Soehendra N. Hamper K. Mass R. Contribution of endosonography to preoperative staging in esophageal and stomach cancer. Chirurg [JC:d5u] 1989 Oct. 60(10) : 1684-9. 3. Bohutora J. Pokorny M. Sram F. Dilatation of stenosis of the oral part of esophagus in the kellypaterson syndrome (Plummer-vinson). Ceskoslovenska. Radiologie. [JC:cx6] 1990 Jan. 44(1) : 26-31. 4. Dantas R O. Villanov a MG. Esopha geal motility impair ment in plummer-vinson syndrome cor rection by iron treatment. Digestive diseases and sciences. [JC:ead]1993 May. 38(5) : 968-71. 5. Suarez cortina L. Olivares de Miguel F. Camarero salces C. et al. Caustic esophagitis in children. Anales espanoles De pediaria. [JC:49n] 1992 Mar. 205-7.

SURGERY - GASTRO-INTESTINAL PROBLEMS

SUMMARY Dysphagia Odynophagia Etiology Diagnosis Investigations Esophagography Esophagoscopy Endoscopic sonography Esophageal manometery Biopsy Achalasia cardia Plummer Vinson syndrome Congenital atresia Foreign bodies Stricture of esophagus Carcinoma of esophagus Differential diagnosis Hysteria Anxiety Anorexia Nervosa POSSIBLE QUESTIONS 1. What is dysphagia? 2. How do you investigate it? 3. Discuss differential diagnosis?

? 31

CARCINOMA ESOPHAGUS

GIT - 04

CARCINOMA ESOPHAGUS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS

The carcinoma of the esophagus is the malignant tumour 1,2,3 of the esophagus . It is common, aggressive tumour which is increasing in frequency. 1

INCIDENCE AND EPIDEMIOLOGY ! It is seen in 5-10 percent of all malignancies. ! It is seen in 10 % of all gastro-intestinal malignancies. ! Its incidence is rising. ! It is the fifth most common malignant tumour in developed world23. ! It is less common than carcinoma of bronchus, stomach, colon, prostate and pancreas. ! It is common between fifty to seventy years age group. ! It is common in males . ! Nearly 28 % of the patients are females. ! Male to female ratio varies between 2:1 to 20:1 in different studies. ! It is four times more common in colored people as compared to white races. ! Black to white ratio is 4:1. ! It is 25 times more common in alcoholics. ! It is 6-7 times more common in smokers. ! 10-20 new patients of carcinoma of esophagus are seen per 100,000 per year in France and U.K. ! It is more common in Japan, China, Scotland, Russia and Scandinavian countries. ! It is 20-30 times more common in China than Europe and is seen commonly in younger males. ! Squamous cell carcinoma is the most common type (80-90%). ! Adenocarcinoma is seen in 5-10 % of the cases . SURGERY - GASTRO-INTESTINAL PROBLEMS

! ! ! !

The incidence of adenocarcinoma is rising and squamous cell carcinoma is decreasing. Anaplastic carcinoma is seen in 5-10% of the cases. The tumour is usually diagnosed quite late. Only 40% of the patients with carcinoma of esophagus report within three months of the onset of symptoms. The prognosis is very poor and depends upon stage of the disease. Overall 5 years survival is less than 5%. It causes 20% of all cancer deaths.

Its incidence is higher in patients who suffer from following conditions2,3 ; ! ! ! ! ! !

Esophagitis (Barrett's esophagus) Achalasia cardia Strictures of esophagus Plummer-Vinson syndrome Diverticula Webs

Barrett's esophagus is the replacement of esophageal squamous epithelium by columnar-lined mucosa and it carries an increased risk of malignancy4. ETIOLOGY The exact cause of carcinoma of the esophagus is not known. Environmental and dietry factors are blamed for causing this disease. Following conditions are carcinogenic. CARCINOGENESIS IN FOOD Eating salted, pickled or smoked food. Hot and spicy food intake, amount of fat ingested and total calories influence its occurrence. 33

CARCINOMA ESOPHAGUS

different sites of oesophagus is as given below ; ! Upper 1/3 20% ! Middle 1/3 50% ! Lower 1/3 30%

04.01

04.02 Upper 1/3

17 %

Middle 1/3

50 %

Lower 1/3

33 %

Barrettâ&#x20AC;&#x2122;s Esophagus showing velvety appearance on esophagoscopy

INGESTION OF EXOGENOUS CARCINOGENS Ingestion of exogenous carcinogens and promoting factors such as nitrosamine and tannins etc increase the risk of carcinoma of esophagus. INFECTION WITH HUMAN PAPILLOMA VIRUS It is also associated with increased risk of carcinoma esophagus. ABSENCE OF PROTECTIVE SUBSTANCES Absence of protective substances in fruits, green vegetables (vit A, B2, C and E) and trace elements such as Iron, Zinc. Selenium etc may lead to increased risk of esophageal carcinoma. ASSOCIATED CONDITIONS Plummer-Vinson syndrome, achalasia cardia and chronic strictures of the esophagus are commonly associated with esophageal cancer. PATHOGENESIS The carcinoma of esophagus is mainly squamous cell carcinoma, but lesions of lower end may be adenocarcinoma in nature. Frequency of carcinoma of esophagus may be of columnar cell type. These may possibly be an extension of carcinoma of stomach. The frequency of malignancy at

SURGERY - GASTRO-INTESTINAL PROBLEMS

Frequency of carcinoma of esophagus

50% of the squamous carcinomas are present in the middle part of the esophagus and one third at the lower end of the esophagus. Previous view that the tumour is present at the points of constriction of the esophagus has not been proved by any investigation. 1,2

PATHOLOGY MACROSCOPIC FEATURES Following types are seen : SMALL EARLY LESION The carcinoma of esophagus begins as in-situ lesion. Early lesions appear as small gray white plaque like thickened lesions. These lesions appear as thickening of mucosa and submucosa. These extend with the time and encircle whole of the esophageal lumen.

CARCINOMA ESOPHAGUS

The prognosis after surgery is very good. 5 years survival is achieved in 85% of patients if treated at this stage. CONSTRICTIVE LESIONS (STENOSING OR SCIRRHOUS OR FLAT LESIONS) These lesions tend to spread within the wall of the esophagus causing thickening, rigidity and narrowing of the lumen.

patients with long standing reflux. Majority of these lesions are seen to arise from lower esophagus. Its prognosis is poor. Its spread is similar to squamous cell carcinoma. 04.03

FUNGATING LESIONS CAULIFLOWER TYPE (60%) The lesion protrudes into the esophageal lumen and blocks it. It is the most common type of carcinoma of esophagus. It is seen in 60% of the cases. ULCERATING LESION EXCAVATING LESION (25%) The lesion is similar to epithelioma. It is seen in 25% of the cases. The lesion presents with everted and raised margins. It erodes deeper into esophageal wall, respiratory passages, mediastinum, aorta and pericardium. MICROSCOPIC APPEARANCE Histologically 80-90% of the lesions are squamous cell carcinoma and rest of these are adenocarcinomas. Rarely sarcomas are also seen. Leiomyosarcoma is the most common type of sarcoma. Mixed tumours may also be seen. Some tumours have large pleomorphic anaplastic cells. Some are "oat cell" type tumours having small uniform cells with deeply chromatic nuclei (APUDOMAS) The carcinomas are seen from well differentiated to anaplastic types. Most of the carcinomas have spread beyond the esophageal wall at the time of diagnosis. Adenocarcinoma arises from barrett's epithelium in

SURGERY - GASTRO-INTESTINAL PROBLEMS

80-90% Squamous cell Carcinoma

Microscopic appearance

The cyto-pathologic changes of adenocarcinoma of 5

esophagus are ; Loss of orientation and nuclear crowding. High nuclear / cytoplasmic ratio. Prominent nucleoli. Nuclear and cytoplasmic molding. Hyperchromatic nucleus. Coarse chromatic clumps. Multilayered tissue fragments. SPREAD The tumour spreads ; Directly (Trans-mucosal) Through lymphatics Through blood vessels

DIRECT SPREAD It occurs both in transverse and longitudinal directions. It may involve the muscle wall of the esophagus,

CARCINOMA ESOPHAGUS

pulmonary tree, mediastinum, aorta and pericardium and may lead to fatal outcome. LYMPHATIC SPREAD The rich lymphatic network in the submucosa promotes extensive longitudinal and circumferential spread. It occurs both by embolization and permeation of the tumour cells. The spread occurs to supra-clavicular, para esophageal, tracheo-bronchial and subdiaphragmatic lymph nodes. The spread of tumour from upper one third of the esophagus is to the cervical lymph glands. The spread from middle one third of the esophagus is to the paratracheal, tracheo-bronchial and mediastinal group of lymph glands. The spread from the lower one third of the esophagus is to the gastric glands, coeliac and subdiaphragmatic glands. SPREAD THROUGH BLOOD VESSELS The blood borne spread of carcinomas of esophagus 04.04 Upper 1/3

To cervical lymph glands

Middle 1/3

To tracheo broncheal lymph glands

Lower 1/3

To coeliac and Gastric lymph glands

occurs commonly to liver and lungs. STAGING 2,3 T.N.M STAGING (T) PRIMARY TUMOUR Tx Primary tumour cannot be assessed To No evidence of primary tumour Tis Carcinoma in situ T1 Tumour involves only mucosa T2 The tumour invades muscularis mucosae T3 The tumour invades the peri-oesophageal tissue T4 The tumour invades adjacent structures (N) REGIONAL LYMPH NODES Nx Regional lymph node can not be assessed. N0 No regional lymph node metastasis present. N1 Regional lymph node metastasis present. N2 Juxta regional lymph node involvement. (M) DISTANT METASTASIS Mx Distant metastasis can not be assessed. M0 No distant metastasis. M1 Distant metastasis present. STAGE - I The tumour is limited to the lamina propria or submucosa only. STAGE -II The tumour is limited to the esophagus. Lymph glands may be involved (regional mobile nodes) but are resectable. STAGE - III The tumour is more than 10 cm in length. It extends to the adjacent lymph glands. The tumour or the lymph glands or both are inoperable. (inoperable local extension).

Lymphatic spread of carcinoma of esophagus

SURGERY - GASTRO-INTESTINAL PROBLEMS

CARCINOMA ESOPHAGUS

Management of Carcinoma esophagus

Staging

Unresectable disease

Resectable disease

Resection probable

Resection improbable

Risk assessment

Chemoradiation

Palliation

Good risk

Poor risk

Good response

Endoscopic methods Selected patients with radiotherapy + chemotherapy

Radical resection

Poor response

Palliation Study protocol neoadjuvant/adjuvant radiotherapy + chemotherapy

SURGERY - GASTRO-INTESTINAL PROBLEMS

Definitive Chemoradiation

CARCINOMA ESOPHAGUS

STAGE - IV All the features of stage three. Perforation or fistula formation. Presence of distant metastasis. DIAGNOSIS AND CLINICAL FEATURES The carcinoma of the esophagus presents in the 50-70 years age group men. History is very much suggestive of the diagnosis. Local examination has very little to offer in the diagnosis. General examination of the patient is also suggestive of the diagnosis such as severe weight loss, anorexia and cervical lymph-adenopathy may be due to carcinoma of the esophagus. The usual presenting features are: WEIGHT LOSS These patients progressively lose weight. They are unable to eat enough food and also lose weight because of malignancy. General nutritional state should be assessed and monitored by serial measurements of skin fold thickness and triceps girth on regular basis. DYSPHAGIA It is difficulty in swallowing which is not severe in the beginning and may be noticed only to solid foods. It gets worse progressively and then is noticed to fluids also. When the esophageal obstruction becomes complete, necrosis and swallowing of the tumour may make the dysphagia better occasionally.

Some of these secretions are aspirated into the tracheobronchial passages and some come out of mouth. It is commonly known as pseudo-vomiting. RETEROSTERNAL DISCOMFORT It is a fairly common symptom. The usual cause is esophagitis due to esophageal obstruction and collection of food material and salivary secretions proximal to the obstruction. This may be severe in case of certain complications of carcinoma esophagus such as perforation, pericarditis and pleural effusion. INVESTIGATIONS Following investigations are helpful in the assessment of general condition of the patient and confirmation of the diagnosis : URINE EXAMINATION It is a simple investigation for the general assessment of the patient. BLOOD EXAMINATION ! Haemoglobin estimation ! Total leucocyte count ! Differential leucocyte count ! Sedimentation rate ! Urea and electrolytes ! Serum iron level ! Serum transferrin level ! Serum protein (Albumin) level

ODYNOPHAGIA It is a late presentation of carcinoma of esophagus. Painful tongue fails to push the food backwards during oral phase of swallowing.

ULTRASOUND SCAN It is performed to check up the diaphragmatic movements which may be absent in phrenic nerve paralysis due to tumour. It also picks up the secondaries in the liver.

REGURGITATION The swallowed secretions which fail to enter the stomach due to esophageal obstruction, trickle out of esophagus.

C.T. SCAN The main value of CT scan in staging of esophegeal cancer lies in its ability to detect distant disease such as that of liver, lungs, bones and kidney. These may be

SURGERY - GASTRO-INTESTINAL PROBLEMS

CARCINOMA ESOPHAGUS 12

useful in staging the tumour in advanced carcinoma . Both of these imaging investigations are more expensive and unsatisfactory in diagnosis of early esophageal carcinoma (lesions smaller than 5cms) and spread into the mediastinum. These investigations are helpful in advanced carcinoma of esophagus. These have nearly same accuracy in predicting the resectability of the 13 tumours in patients with carcinoma of esophagus . ENDOSCOPIC ULTRASONOGRAPHY(EUS) It is endoscopic ultrasonography. The ultrasound probe is attached to the endoscope. It helps to assess the tumour and detects depth of tumour penetration and its extension into para-esophageal tissue and regional nodal involvement. Endoscopic ultrasonography (EUS) is helpful in the diagnosis of very early and subepithelial lesions. It is the most superior investigation to assess transmural 6 invasion . The accuracy of EUS for tumour and nodal staging averages 85% and 75%. It is superior to CT in 7 detection of the metastasis to regional lymph nodes . It can be used to perform FNAC of regional nodes. It has its 8 own limitations as it cannot pick up distant metastasis . It is not helpful in non-traversable malignant stricture. RADIOLOGY X-RAY CHEST It helps to show lung parenchymal involvement and features of aspiration pneumonia. BARIUM SWALLOW (ESOPHAGOGRAPHY) Single or double contrast films may be exposed. It shows typical malignant features which are mucosal irregularity and shouldering, narrowing of the lumen and proximal dilation of the esophagus. ESOPHAGOSCOPY Esophagoscopy shows the lesions in upper, middle and lower third of the oesophagus. Dye endoscopy using lugols solution is very important because it allows detection and evaluation of the extent of esophageal mucosal cancer. The lesions show as unstained areas9.

SURGERY - GASTRO-INTESTINAL PROBLEMS

04.05

Esophagogram (carcinoma of esophagus) BRONCHOSCOPY Bronchoscopy is performed to exclude involvement of trachea and bronchial tree in all types of carcinoma of upper and middle third of esophagus. LUGOLS TEST The lugols staining pattern helps in the detection of earlier lesion of carcinoma esophagus, carcinoma in situ and intra epithelial extension which are otherwise difficult to detect. These can be easily detected by Lugol staining. This method is useful to detect severe dysplasia and 11 extension of tumour . The usefulness of the staining pattern with Lugol's solution to diagnose the esophageal lesions such as squamous cell carcinoma and severe dysplasia has been proved by many studies. The precise

CARCINOMA ESOPHAGUS

delineation of the proximal resection line during surgery of esophageal carcinoma with unexpected wide extension is detectable11. Four grades of Lugols test are seen ; ! Grade I Normal greenish ! Grade II Brown staining ! Grade III Less intense staining ! Grade IV Unstained PET (POSITRON EMISSION TOMOGRAPHY ) PET scan does not provide information of esophageal wall and thus has no value in tumour staging. It is useful in detecting locoregional nodes and distant metastasis. LAPAROSCOPY AND THORACOSCOPY It is used to pick up intra abdominal extension of the disease process. It is much better than other 12,14 investigations . Thoracoscopy identifies positive nodes. Metastatic disease is missed by CT scan in 50% of patients. TREATMENT Management of carcinoma esophagus comprises of; ! Pre-operative initial therapy ! Definitive therapy PRE-OPERATIVE THERAPY

All patients should be optimally prepared before under taking major esophageal surgery.

DEFINITIVE THERAPY Multiple modalities of treatment are available for treatment as ; ! Surgery ! Radiotherapy ! Chemotherapy ! A combination of all these modalities is used to treat patients of different stages of disease process. SURGERY It is gold standard for the treatment of carcinoma esophagus. Resection of esophageal malignancy with intent to cure is based on concept that if all neoplastic tissue can be removed a worth while period of survival and possible cure might be achieved. Following principles are adopted for surgical treatment; To achieve resection (Complete macroscopic and microscopic clearance). ! Proximal extent of resection should be 10 cm above the macroscopic tumour and 5cm distal to it11. ! The principal aim of lymph-adenoectomy should be to minimize staging error and reduce loco regional risks of recurrence. !

SELECTION OF PATIENTS Radical surgery should be recommended for patients with localized tumours who are sufficiently fit to tolerate the procedure. Mucosal disease is treated by minimally invasive methods.

TREATMENT OF PRE-EXISTING CONDITIONS

Pharmacological treatment of angina, hypertension, asthma and COPD is optimized. Pre-operative chest physiotherapy may be beneficial. Hematological and biochemical abnormalities should be corrected to appropriate levels. NUTRITIONAL STATUS Patients at their ideal body weight may do better after surgery. Nutritionally patients should be improved to prevent risk of complications.

SURGERY - GASTRO-INTESTINAL PROBLEMS

CHOICE OF OPERATION

STAGE

CHOICE OF PROCEDURE

Mucosal Disease

PDT (Photodynamic Therapy) EMR (Endoscopic Mucosal Resection)

T1 T2

Esophagectomy

T3 N1

Esophagectomy +Chemotherapy + Radiotherapy

The choice of surgery depends upon the site and stage 40

CARCINOMA ESOPHAGUS

of tumor. Following table explains the choice of surgery depending upon stage of disease. ! Tumour of Cervical esophagus These are diagnosed late in majority of the cases. However if resectable at presentation, the choice of surgery is pharyngo laryngo esophagectomy (PLE ). ! Tumour of Intrathoracic esophagus Upper thoracic esophagus tumours are removed obtaining a sufficient proximal resection margin which helps to achieve an anastomosis placed in the neck. This is best carried out with Three phase esophagectomy or Mc keown approach. ! Tumours of Abdominal esophagus Abdominal esophageal or gastric cardiac cancers are best treated by Abdomino-thoracic approach.

LYMPHADENECTOMY The principal aim of lymphadenectomy is to minimize staging error, reduce loco regional risks of recurrence. Three fields (Abdomen, thorax, and neck) drain lymph from esophagus. Generally two field dissection embracing thoracic and abdominal group of lymph nodes are removed. CHOICE OF CONDUIT AND ROUTE After removal of esophagus, commonest conduit is the stomach. Colon interposition is the next most suitable Conduit when the stomach is not available. Pre vertebral route for resection is preferred. CHEMOTHERAPY NEO-ADJUVANT CHEMOTHERAPY Pre-operative chemotherapy for all patients with operable esophageal cancer other than those with 15 unequivocally T1 is recommended .

SURGERY - GASTRO-INTESTINAL PROBLEMS

PALLIATIVE CHEMOTHERAPY Palliative chemotherapy is used along with radiotherapy in advanced non-operable tumours. This has not been very successful in this disease. It can be used in T3 and T4 15 tumours before surgery . RADIOTHERAPY The squamous cell carcinoma of the esophagus is radiosensitive tumour. Adenocarcinoma of the esophagus is not radio-sensitive and has poor prognosis after radiotherapy. Radiotherapy has only slight effect on the prognosis of inoperable carcinoma of esophagus17. 5000-6000 rads have been used. Smaller doses have also been used preoperatively. Radiotherapy has its own problems such as radiation pneumonitis and stricture formation. Five years survival rate is poor (6% only). T3 and T4 tumours above the level of tracheal bifurcation are best treated by radiotherapy and chemotherapy pre15 operatively . The treatment of unresectable carcinoma of the esophagus patients can be done with external beam radiotherapy (EBRT) 55Gy18. Intra-cavity radiotherapy (brachytherapy) is also a useful method of radio therapy for carcinoma of esophagus. LASER COAGULATION In advanced carcinoma of esophagus, complete resection is not feasible, Nd-YAG laser is used for photo-coagulation. It is helpful in only mucosal tumours. Other types of small probes are also available which can produce photo-coagulation of few millimeter deeper tissue. These are helpful in more advanced disease as a palliative procedure19. Endoscopic palliation and laser therapy has almost 100% technical success rate. The laser therapy requires several sessions and relapses of obstruction are

CARCINOMA ESOPHAGUS

frequent but laser therapy is safe and carries minimum risk of complication. It can be combined with endoscopic intubation which offers definitive palliation but runs the risk of causing perforation in about 5% cases20. A combination of endoscopic laser therapy (ELT) and insertion of wallstents is a good alternate therapy for palliation of 21 esophageal carcinoma . It produces good palliation in over 60% of cases. It needs to be repeated every 4-6 weeks. INTUBATION/ STENTING 04.06

Intubation and bypass of the constricting lesion of the esophagus can be performed in poor risk patients for palliation and some patients as an initial treatment for building up the patients for definitive surgery. Various tubes for intubation are available such as ; ! Mousseou barbin tube ! Celestin tube ! Atkinson tube ! Self expanding stents (wall stents) All these tubes are used to bypass the tumour and maintain the gastrointestinal continuity from upper part of esophagus to stomach. Endoscopic or radiological

SURGERY - GASTRO-INTESTINAL PROBLEMS

placement of tubes is communally practiced. These are less traumatic and do not require surgical procedure. Anaesthesia is not always required. These are used to build up the general health of the patient. Mousseou Barbin and Celestin tubes are not any more used. Atkins tube is most commonly used for stenting in palliation of terminal patients. The placement of tubes requires dilatation of malignant stricture. It runs the risk of perforation. Tubes can get displaced. The tube may get blocked due to in growth or 23 over growth of tumours . PHOTO DYNAMIC THERAPY (PDT) It is an alternative to major surgery. A photo sensitizing agent is injected and then activated by exposing the tumour to light, usually through a low power laser endoscopically. The agent absorbs energy from light and produces high energy oxygen molecules and destroys the tumour cells. It can be performed under sedation and as 24 an outdoor procedure . MISCELLANEOUS Various Chinese herbal medicine have been successfully used in the treatment of carcinoma of esophagus. Menis pernum dehuricum (Herb) has shown prominent stromal lymphoid-cell infiltration and cancer cell degeneration in patients with carcinoma esophagus. This anti tumour action seems to be due to activation of an immunological rejection mechanism22. PROGNOSIS

Resectable tumours

5 year survival 10%-25%

Stage-I Carcinoma

80%-94%

Stage-III Carcinoma

10%-14%

Description

CARCINOMA ESOPHAGUS

Out come of the treatment with various modalities is shown with 5 years survival rate ; Description Surgery alone Radiotherapy alone Radiotherapy & surgery Radiotherapy (EBRT) and brachytherapy

5 year survival 0% 2% 18% 11%

The prognosis of carcinoma of oesophagus is poor as shown below ; Description

Outcome

Operable tumours

50%

Patients dead within one year

70%

Survival rate in five years

5% - 10%

REFERENCES 1. James M. Crawford. Esophagus. Robins pathological basis of disease. 5th ed. Ramzi S Cotran. Stanley L. Robins. Vinay Kumar. WB Saunder s. London. 1994 P. 755-766. 2. A C u s c h i e r i . D i s e a s e s o f e s o p h a g u s. Essential surgical practice. 3rd Edtion. A cuschieri. GR Giles. AR Moossa. Butter wor th-Heinemann.1996 P:1088-1099. 3. Camer on Wright. Henning A Gaisser t. Francesco Puma. Douglas Mathisen. Benign and malignant tumours. Oxford text book of surgery. Peter J. Morries. Ronald A Malt. Oxford University Press London. 1994 P: 893904. 4. Wang HH. Doria Mir. Puropit Duch S et al. Bar r ett's esopha gus, the c ytolo g y of dysplasia in comparison to benign and malignant lesiions. Acta. cytologica. [JC: Oli]

SURGERY - GASTRO-INTESTINAL PROBLEMS

1992 Jan-Feb. 36 (1) : 60-4. 5. Shinbai MS. Erozen YS. The cytopathological diagnosis of esophageal adenocarcinoma. Acta cytologica. [JC:oli]1991 Mar-Apr. 35(2) :18994. 6. Maillet P. Baulieux J. Valette PJ. Souquet JC. Contribution of enodsonography in the ev aluation of cancer of the esophagus. Annales De Gastroenterologic ETD Hepatologie.[JC:55a]1990 May. 26(3) : 123-7. 7. Vilgrain V. Momprint D. Palazzol et al staging of esophageal carcinoma: comparison of results with endoscopic sonography and CT Ajr. Amercican journal of roentgenology: [JC:3ae]1990 Aug. 155(2) : 277-81. 8. Maillet P. Baulieux J. Valette PJ. Souquet JC. Contributiion of endo-sonography in the evaluation of cancer of the esophagus. Annales De Gastro entrologic. ETD Hepatologic. [JC:55a] 1990 May. 26(3) : 123-7. 9. Misumi A. Harada K. Murakami A et al. Early diagnosis of esophageal cancer. Analysis of 11 cases of esophageal mucosal cancer. Annals of surgery [JC:675]1989 Dec. 210(6) : 732-9, 10. Lay field LJ. Reichman A. Weinstein WM. Endoscopically directed fine needle aspiration biopsy of gastric and esophageal lesions. Acta cytologica. [JC:Oli]1992 Jan, Feb. 36(1) : 69-74. 11. Mori M. Adachi Y. Mxtsushina T. Matsuda H. Kuwano H. Lugols staining pattern and histology of esophageal lesins. American journal of gastroenterology [JC:zhe]1993 May. 8 8 ( 6 ) : 701-5.

CARCINOMA ESOPHAGUS

12. Lozac HP. Le Cocquen D. Senecail B. Morin JF. Value of x-ray and C.T scan in evaluating the operability of esophageal cancer. Results of a prospective study. Annales De chirurgie. [JC:5oe]1989. 43(6) : 443-6. 13. Takashima S. Takeuchi N. Shiozaki H. et al. Carcinoma of esophagus. CT & MR imaging in detemining resectability Ajr American journal of Roentgenology. [JC:3ae]1991 Feb. 156(2) : 297-302. 14. M e a r z L L . D e v e r n ey C W. L o p e z R R . M c Connell DB. Role of C.T scans in the staging of esophageal and proximal gastric m a l i g n a n c i e s . American Journal of surgery. [JC:3z4]1993 May. 165(5) : 558-60. 15. Allum W.H GUT 2002; 50(Supp IV): 16. Siewert JR. Holscher AH. Current strategy in s u r ge r y fo r e s o p h a ge a l c a n c e r. A n n a l i Italiani Di Chirurgia. [JC:5CO]1992 Jan-Feb. 63(1) : 13-8, 17. K e l l o k u m p u L e h t i n e e n P. H u o v i r e n R . Nukkanen V Sir vova. Esophageal passage after radiotherapy of inoperable esophageal carcinoma. A r eterospective study of 106 cases. Acta oncolgica [JC:aon] 29(2) : 175-8, 1990.

modalities for esophageal carcinoma: clinical review. Acta chirurgica scaudinavica. [JC:Oka]1990 Jan. 156(1) : 95-8. 20. Buset M. Cremer M. Endoscopic palliation of malignant dysphagia. Acta gastroenterologica Belgic. [JC:ony]1992 MayJun. 55(3) : 264-70. 21. Lindberg CG. Cwikiel W. I vamcew K et al. Laser therapy and imser tion of wallstents for palliative treatment of esophageal carcinoma. Acta Radiologica [JC:ata]1991 Sep. 32(5) : 345-8. 22. Xian MS. Hayashi K. Lu JP Awai M. Efficacy of traditional chinese herbs on squamous cell carcinoma of the esophagus: histopathological analysis of 240 cases. Acts media okayoma. [JC:12m]1989 Dec. 43(6) : 345-5. 23. Cowling M G. Stenting in the esophagus. Hosp Med 2000; 61:33-66. 24. NICE. Photo-dynamic therapy for early esophageal cancer: guidance: December 2006.

18. Petrovich Z. Langholz B. Formenti S. Luxton G. Astraham M. Management of carcinoma of esophagus. The role of radiotherapy. American jour nal of clinical oncology [JC:3ez]1991 Feb. 14(1) : 80-6. 19. Ahmed ME. Gustans Bon S. Current palliative

SURGERY - GASTRO-INTESTINAL PROBLEMS

CARCINOMA ESOPHAGUS

SUMMARY CARCINOMA OF THE OESOPHAGUS Incidence & Epidemiology Etiology Pathology Small early lesions Constrictive lesions Fungating lesions Ulcerating lesions Spread Staging Clinical features Weight loss Dysphagia Odynophagia Regurgitation Retrosternal dyscomfort Investigations Urine examination Blood examination X-ray chest Barium swallow (Oesophagography) Endoscopic ultrasonography (EUS) Oesophagoscopy Bronchoscopy Lugolâ&#x20AC;&#x2122;s test Ultrasound scan CT Scan Positron Emission Tomography (PET) Laparoscopy and Thoracoscopy Treatment Pre-operative therapy Treatment of pre-existing conditions Treatment of nutritional status Definitive treatment Surgery Radiotherapy Chemotharapy Combination of all Laser coagulation Intubation / Stenting Photo dynamic therapy (PDT) Prognosis

SURGERY - GASTRO-INTESTINAL PROBLEMS

POSSIBLE QUESTIONS 1. 2. 3.

Discuss stages of carcinoma oesophagus? Discuss preparation for oesophageal surgery? Discuss post operative care of oesophageal surgery?

Stomach

SURGERY - GASTRO-INTESTINAL PROBLEMS

STOMACH

OBJECTIVES ! ! ! ! ! ! ! !

To understand development, anatomy and physiology of stomach. To understand the congenital abnormalities of stomach. To be able to diagnose the diseases of stomach. To be able to manage gastric problems. To be able to prepare the patient for gastric surgery. To be able to look after the patient after gastric surgery. To be able to follow up patients on treatment for gastric diseases. To be able to prevent, diagnose and treat gastric complications.

SURGERY - GASTRO-INTESTINAL PROBLEMS

ANATOMY OF STOMACH

GIT-05

STOMACH Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Irfan Mughal, M.Phil, Ph.D. The stomach is a dilated part of the foregut lying between esophagus and duodenum. It is endodermal in origin. It is a muscular bag which is fixed at both ends although pylorus is relatively mobile. It is "J" shaped but the shape varies at different times depending upon the food intake. Its size also varies in different people and at various times according to the amount of contents present in it. It has two orifices (openings) : CARDIAC ORIFICE The cardiac orifice is the proximal opening. It is present at esophago-gastric junction. It remains closed normally. It opens up to accept the food and salivary secretions from the esophagus. It prevents the retrograde flow of gastric contents into the esophagus. In patients with portal hypertension the varicose vessels are present near the cardiac orifice in the lower end of esophagus. The area of esophagus near cardiac orifice is inflammed and ulcerated in different stages of esophagitis. PYLORIC ORIFICE It is the distal orifice of the stomach. It remains closed normally. It opens to allow the gastric contents to pass into the first part of duodenum for onward movement. Its intermittent opening allows controlled gastric emptying. It fails to open normally and empty the stomach in infants suffering from hypertrophic pyloric stenosis . The pyloric sphincter which is not normally visible anatomically becomes hypertrophic and is clinically palpable and visible to naked eye. It prevents retrograde flow of intestinal contents into the stomach normally. The stomach has two surfaces :

SURGERY - GASTRO-INTESTINAL PROBLEMS

ANTERIOR SURFACE Anterior surface of the stomach is present in the greater sac of peritoneal cavity. The ulcer of anterior wall perforates into the peritoneal cavity and leads to peritonitis. POSTERIOR SURFACE Posterior surface of stomach is present in the lesser sac. The ulcers on the posterior wall usually penetrate into pancreas. The haemetemesis may occur from bleeding of posterior wall ulcers. CURVATURES The stomach has two curvatures : GREATER CURVATURE It is large and is convex curvature. It is the initial dorsal border which rotates and becomes inferior border and greater curvature. LESSER CURVATURE Lesser curvature is smaller and concave upwards. It is present superiorly. The new growths of this area are commonly malignant. GREATER (PERITONEAL) SAC Greater sac or peritoneal cavity is the site of generalized peritonitis due to perforation of stomach. LESSER (POSTERIOR) SAC The lesser sac is the posterior sac and is the site for pseudocyst or abscess formation. The stomach consists of fundus, body, antrum and pylorus. The fundus is the part of stomach present under the left dome of

ANATOMY OF STOMACH

diaphragm above the level of the cardiac orifice. The body is rest of the part upto incisura angularis which is a notch at lower part of lesser curvature. Antrum is next to the body upto pylorus which is thicker than rest of the stomach and forms the pyloric canal which is normally closed and opens only to allow the passage of food. The stomach is related to the abdominal wall with greater omentum anteriorly and lesser omentum posteriorly. 05.01

esophagus

Arterial supply of stomach

05.02

Coeliac axis Common hepatic artery

Left gastric artery

Gastro duodenal artery

STOMACH Left gastrolepiploic

fundus Pylorus Right Superior mesenteric artery gastro-epiploic

Body Antrum The fundus and upper part of the body are fairly constant in shape and size lying under the left dome of diaphragm and left costal margin. Lower part of the body and antrum are variable in size and shape. Normally the greater curvature of the stomach lies just below the umbilicus in standing position. RELATIONS Upper part of the stomach is covered by left lobe of liver. The lower end of greater curvature lies in contact with the transverse colon. The posterior wall of the stomach lies in contact with the spleen. The pylorus is enclosed between the peritoneum of both the lesser and greater omentum. It lies over the head of the pancreas. ARTERIAL SUPPLY LEFT GASTRIC ARTERY It enters from the upper border of pancreas across left crus of diaphragm. It is a branch of coeliac axis. It runs towards the cardiac end beside the peritoneum and then along the lesser curvature to anastomose with the right gastric artery. It lies under pancreatico-gastric fold and gives esophageal branch. SURGERY - GASTRO-INTESTINAL PROBLEMS

Short gastric

RIGHT GASTRIC ARTERY It is a branch of the common hepatic artery and supplies lesser curvature from right side. It anastomoses with the left gastric artery. GASTRO DUODENAL ARTERY It is the largest branch of hepatic artery. It branches into superior pancreatico-duodenal and right gastro epiploic artery which supply along the greater curvature of the stomach. LEFT GASTRO EPIPLOIC ARTERY It is the largest branch of splenic artery and it supplies along the greater curvature of the stomach. VASA BREVIA (SHORT GASTRIC ARTERIES) These are direct branches of splenic artery and supply along the greater curvature of the stomach. These are the vessels which may get injured while doing splenectomy. These should be carefully ligated. VENOUS DRAINAGE Right and left gastric veins drain directly into the portal vein. Left gastro-epiploic and short gastric veins drain 50

ANATOMY OF STOMACH

into the splenic vein. Right gastro epiploic veins drain into the superior mesenteric vein. All these veins run along their corresponding arteries. 05.03

Portal vein

Splenic

quarters of the stomach is drained to appropriate groups of glands. The lymph from lesser curvature drains to the left through left gastric lymphatics and eventually drains into celiac group of lymph glands along the aorta. These lymphatics also drain the lower part of the esophagus. The lymph from lesser curvature also drains to right side through lymphatics along the right gastric artery which drains into hepatic group of lymph glands. These are drained to coeliac lymph glands via lymphatics running along the hepatic artery.

Right gastric

Left gastroepiploic Right gastro-epiploic

Superior mesenteric

Venous drainage of stomach LYMPHATIC DRAINAGE 05.04 Right gastric lymph glands

Glands in gastrosplenic omentum

Right gastro-epiploic lymph glands

Left gastric lymph glands

Left-gastro-epiploic lymph glands

Lymphatic Drainage of Stomach Scattered lymph glands lie along the lesser and greater curvatures. The stomach drains its lymph through the lymphatics which run along the arteries. The lymph from the four SURGERY - GASTRO-INTESTINAL PROBLEMS

The lymph from the fundus and upper part of the greater omentum is drained into glands present in the gastrosplenic omentum. The lymphatic drainage from here onwards is through the lymphatics running along left gastro-epiploic artery and drain into splenic glands and then on to celiac lymph glands. The lymph from the lower end of the greater curvature is drained through the lymphatics running along right gastro-epiploic artery to the glands along hepatic artery and then on to the celiac lymph glands. The pylorus is drained by the lymphatics draining both lesser and greater curvatures. The lymphatic drainage from here onwards is through the lymphatics running along left gastro-epiploic artery and drain into splenic glands and then on to celiac lymph glands. The lymph from the lower end of the greater curvature is drained through the lymphatics running along right gastro-epiploic artery to the glands along hepatic artery and then on to the celiac lymph glands. The pylorus is drained by the lymphatics draining both lesser and greater curvatures.

ANATOMY OF STOMACH

NERVE SUPPLY VAGUS NERVE (PARA SYMPATHETIC) It is motor, secretomotor and sensory to the stomach. It supplies through its two branches ; Anterior nerve of Latarjet Posterior nerve of Latarjet

SYMPATHETIC SUPPLY Sympathetic supply is from the coeliac plexus and nerve fibers run along the blood vessels. INTRINSIC INNERVATION The stomach is also innervated with intrinsic innervation through Auerbach's plexus and Meissner's plexus. It can be independent of outside control.

REFERENCES 1.

RMH McMin. T he abdomen. Last's Anatomy regional and applied eight edition. ELBS. Churchil Livingstone London. 1990. p: 295-339.

SURGERY - GASTRO-INTESTINAL PROBLEMS

SUMMARY Orifices of stomach Surfaces of stomach Curvatures of stomach Relations of stomach Arterial supply Venous drainage Lymphatic drainage Nerve supply

POSSIBLE QUESTIONS

1. Discuss the relations of stomach 2. Discuss vascular supply of stomach 3. Discuss lymphatic drainage of stomach

HYPERTROPHIC PYLORIC STENOSIS

GIT - 06

HYPERTROPHIC PYLORIC STENOSIS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS It is the complete or partial obstruction of pylorus due to hypertrophy of circular muscles of the pylorus leading to obstruction to the onward flow of gastric contents (gastric outflow obstruction). It is a disease of the infants. The pylorus is hypertrophic causing obstruction to the normal flow of gastric contents. The congenital preformed muscular hypertrophy has not been seen in infants who later develop pyloric stenosis. It shows that pyloric hypertrophy is not congenital but develops in the 1 neonatal period . The inflammation or mucosal or submucosal edema of the pylorus makes the obstruction even worse.

INCIDENCE AND EPIDEMIOLOGY ! ! ! ! ! ! ! ! ! ! ! ! !

It is seen in 2-5 /1000 births in males. It is seen in 01 /1000 births in females. Overall incidence is 3-4/1000. Monozygotic twins show a high rate of concordance of the condition. It is more common in twins. It is common in first born male. It is less common in negroes and Asians. These cases are more often seen during the winter months. It is more common in Caucasians. 7% of affected patient's children also have this problem. If mother had this problem, 80% of her offsprings are likely to suffer from congenital pyloric stenosis. It is common in families and in 50% cases, the mother has suffered from this disease in infancy. It is more common in certain families with greater

SURGERY - GASTRO-INTESTINAL PROBLEMS

! !

frequency. Brothers are affected in 10% of cases. Sisters are affected in 2% of cases3.

ETIOLOGY It is of unknown etiology but following views have been postulated ;

! ! !

Maternal gastrin may be the causative factor. Absence of ganglion cells from hypertrophic area. Failure of pylorus to relax.

All these views do not explain the disease adequately but primary failure of pylorus to relax (like achalasia) is more near the truth. Increased stress causing a hormonal effect during pregnancy or postnatally may cause hypertrophic pyloric stenosis2. Immunocyto-chemical studies show a reduced number of nerve fibers containing vaso-active intestinal peptide. The pyloric ganglia are normall2.

PATHOLOGY The pylorus is hypertrophic, thick and firm. It is about 2-3 cm in diameter. The size varies with age of the infant and duration of the illness. The enlargement of size is entirely due to hypertrophy and spasm of the muscular layers. Hypertrophy of the musculature increases distally and it is maximum where circular muscles are involved. The hypertrophy is only present in pylorus and stops abruptly. The duodenum is normal. Macroscopically olive shaped tumour upto 2.5 cm 53

HYPERTROPHIC PYLORIC STENOSIS

diameter is seen blending with the musculature of the antrum. The tumour bulges into the duodenum and stomach is dilated due to outflow obstruction. There is 2 lengthening of pyloric canal . The patients with hypertrophic pyloric stenosis present with various biochemical disturbances at different stages of the disease process. In early presentations, metabolic alkalosis and normal potassium levels are seen. In late presentations (more than 3 wks) metabolic alkalosis and low potassium levels 4 are seen .

severe cases the patient presents as acute renal failure. VISIBLE PERISTALSIS Soon after feed, if baby is examined, peristaltic waves are visible passing from left to right in the upper abdomen. This is usually followed by vomiting. The examination should be conducted in day light and after adequate exposure. The peristalsis can be started by stroke on abdomen as well in these patients. 06.01

CLINICAL FEATURES The infant usually presents between 3-9 weeks of age (Peak age incidence is around seven weeks of age) with following complaints : VOMITING Projectile vomiting in this age group is the characteristic feature of the disease. The vomitus contains mucous and gastric contents. Blood flakes may be present and bile is usually not present. The baby becomes very hungry after vomiting.

Distended abdomen and visible peristalsis

06.02

CONSTIPATION It is a common feature. The stool is small and dry and its frequency is less. It is similar to that of a rabbit. LOSS OF WEIGHT These infants continue loosing weight and after a while look cachexic in case adequate treatment has not been done. DEHYDRATION It is a very common feature in all patients with this disease. The fontanelle are depressed. Skin turgor is lost and eyes are sunken. DECREASED URINARY OUTPUT Only small amount of concentrated urine is passed and in

SURGERY - GASTRO-INTESTINAL PROBLEMS

Distended abdomen and visible peristalsis PALPABLE LUMP There is a palpable lump in the epigastrium. This is in fact hypertrophic pylorus. The size varies with the duration of symptoms. The longer the duration, the bigger the swelling. The lump becomes more obvious after feeding.

HYPERTROPHIC PYLORIC STENOSIS

HYPERTROPHIC PYLORIC STENOSIS MANAGEMENT PLAN History suggestive of Pyloric Stenosis

Examination palpable pyloric mass visible peristalsis

Ultrasound Abdomen confirming the diagnosis

Lab Investigations Acid base abnormalities (pH less than 7.45, Chloride less than 98 Base excess more than +3)

Admit for resuscitation and correction of fluid and electrolyte balance

Medical Treatment (less likely to be successful)

Surgical Treatment Ramstedtâ&#x20AC;&#x2122;s operation or Laparoscopic pyloro myotomy

Start oral feeding 8-10 hours after surgery

Follow up

SURGERY - GASTRO-INTESTINAL PROBLEMS

HYPERTROPHIC PYLORIC STENOSIS

LETHARGY The child becomes lethargic and hypotonic. HAEMATEMESIS Occasionally infants suffering from hypertrophic pyloric stenosis present with haematemesis following reflux esophagitis. Endoscopy helps in finding the site and cause of bleeding5.

It is non invasive and confirmatory of the diagnosis. Ultrasound scan of abdomen is an accurate, reliable and rapid screening method to differentiate the causes of severe vomiting in infancy6. It shows distended abdomen with an abrupt stoppage of the gastric distension. A soft tissue mass is also seen at the pyloric area. Pyloric length and muscle thickness is also good predictor of infantile hypertrophic pyloric stenosis. 06.04

DIAGNOSIS & INVESTIGATIONS History and examination are usually suggestive of the diagnosis. Feeling the hypertrophic pylorus and test feeding are diagnostic features. URINE EXAMINATION It is very simple investigation to assess the general condition of the patient. In patients with hypertrophic pyloric stenosis, the urine is concentrated and of small quantity.

Ultrasound scan Pyloric stenosis

BLOOD COMPLETE EXAMINATION There is deficiency of fluids and electrolytes particularly sodium, potassium and chloride levels are low. Compensatory metabolic changes show intracellular acidosis and an extra cellular alkalosis.

06.05

ULTRASOUND SCAN 06.03

Ultrasound scan soon after feeding (Pyloric stenosis)

SURGERY - GASTRO-INTESTINAL PROBLEMS

Ultrasound scan Pyloric stenosis

HYPERTROPHIC PYLORIC STENOSIS

Pyloric thickness of 4 mm or greater and length of 17 mm or greater in neonates or 3 mm thickness in infants of less than 30 days age is diagnostic of hypertrophic 7 pyloric stenosis (HPS) . Serial sonographic examinations show the evolving hypertrophic stenosis8.

06.07

PLAIN X-RAY ABDOMEN (ERECT) It shows single gastric gas bubble. 06.06

Barium Meal x-ray (pyloric stenosis)

DIFFERENTIAL DIAGNOSIS This condition is to be differentiated from all other conditions causing infantile vomiting. Following conditions are commonly associated with infantile vomiting ;

! ! ! ! Plain x-ray abdomen single gas bubble (pyloric stenosis) BARIUM MEAL OR GASTROGRAPHIN MEAL The diagnosis is clinical and sonographic. Contrast medium studies are helpful in patients where these investigations have been found to be inconclusive. The contrast medium is given orally and x-ray pictures are exposed. These also confirm the diagnosis and show ; ! String sign of stenosis ! Shoulders of the hypertrophic pylorus The gastric and pyloric lumen is shown due to presence of radio-opaque dye in the lumen.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Duodenal atresia Fibrous stenosis Milk idiosyncrasy High intestinal obstruction (Volvulus neonatorum and intussusception) Intracranial haemorrhage

TREATMENT These children should be managed under close collaboration and co-operation of surgeon and pediatricians. It decreases the morbidity and mortality9. Intravenous fluids and electrolytes such as quarter to half strength glucose saline is given in required amounts. Nasogastric aspiration of the gastric contents is performed. As soon as the patient's hydration is satisfactory, electrolytes are corrected and acid base balance is corrected. Definitive treatment is carried out

HYPERTROPHIC PYLORIC STENOSIS

which is surgery. MEDICAL TREATMENT It is not satisfactory and should not be offered. SURGICAL TREATMENT (RAMSTEDT'S OPERATION) (PYLOROMYOTOMY) The neonate is resuscitated. Fluid and electrolyte balance is corrected to normal. Laparotomy is performed. The pylorus is recognized and definitive surgery is performed. The hypertrophic muscle layer is incised completely leaving the gastric and pyloric mucosa intact. 06.08

PROGNOSIS The outcome is normally 100% survival.

REFERENCES 1. Rollins MD. Shields MD. Qiinn RJ. Woldrige MA. Pyloric stenosis. Congenital or acquired. Archives of Diseases of Childhood. [JC:6xg]1989, Jan. 64(1): 138-9. 2. D Mervyn Griffiths. Disorders in gastrointestinal tract in children. Oxford text book of surgery. Peter J Morris. Ronald A Malt. Oxford university press London. 1994. p: 2034-2043. 3. Charles V Mann. RCG Russell. Norman S. Williams. Bailey and Love's short practice of surgery. 22nd edition ELBS. London. 1995. p: 673-678. 4. Nmada PT. Alterations in serum electrolytes in congenital hypertrophic pyloric stenosis. A study in Nigerian children. Annals of tropical paediatrics [JC:6ba]1992. 12(2) : 169-72.

Ramstedtâ&#x20AC;&#x2122;s Operation LAPAROSCOPIC EXTRA MUCOSAL PYLOROMYOTOMY Laparoscopic extra mucosal pyloromyotomy is a new surgical approach. It is minimally invasive and relatively less traumatic for the infants. Certain precautions against 10 complications of pneumoperitoneum should be taken . FOLLOW UP There is no rush to start oral feeding so early. It may be started next day when the patient has settled. Patient can be kept on intravenous fluids and electrolytes till then. Intravenous fluids are stopped when the infant starts taking normal feed.

SURGERY - GASTRO-INTESTINAL PROBLEMS

5. Takeuchi S. Tamate S. Nakahira M. et al. Oesophagitis in infants with hypertrophic pyloric stenosis. A source of haematemesis. Journal of paediatric surgery. [ JC:jmj]1993 Jan. 28(1) : 59-62. 6. Rallins MD. Shields MD. Quinn RJ. Worldridge MA. Value of ultrasound in differentiating causes of persistent vomiting is infants. Gut [JC:fvt]1991 Jun. 32(6) : 612-4. 7. Lamki N. Athey PA. Round ME. Hypertrophic pyloric stenosis in the neonate. Diagnostic criteria. Canadian Association of Radiologist's Journal [JC:caj]1993 Feb. 44(1) : 21-4.

HYPERTROPHIC PYLORIC STENOSIS

8. Tam PK. Chan J. Increasing incidence of hyper trophic pyloric stenosis. Archives of diseases in Childhood. [JC:6xg]1991 Apr. 66(4): 530-1.

SUMMARY Introduction Incidence Etiology Pathology Clinical Features Investigations Differential diagnosis Management Plan Treatment

9. Jahangir M. Osbor ne MJ. Jayatung AP. Infantile hyper trophic pyloric stenosis: where it should be treated. Annals of the Royal College of surgeons of England. [JC:5vv]1993 Jan. 75(1) : 34-6, discussion 36-7. 10. Alain JL. Grousseau D. Terrier G. Extramucosal pylorotomy by laparoscopy. Journal of paediatric surgery. [JC:jmj]1991, Oct. 26(10) : 1191-2.

POSSIBLE QUESTIONS

1. 2. 3.

SURGERY - GASTRO-INTESTINAL PROBLEMS

What is hypertrophic pyloric stenosis? How is it diagnosed? Give management of pyloric stenosis?

DUODENAL ULCER COMPLICATIONS

GIT-07

COMPLICATIONS OF PEPTIC ULCER Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS The complications of chronic duodenal ulcer may present as acute surgical emergencies or as non emergency abdominal problems requiring surgical intervention.

07.01

The acute surgical emergencies require active resuscitation and early treatment which is surgical intervention in most of the patients. The non emergency problem also requires surgical intervention in most of the patients after pre-operative investigations and preparation of the patient for elective 1,2 surgery. These complications are ; ! Perforation ! Bleeding (haematemesis, melaena) ! Residual abscess formation ! Pyloric stenosis ! Gastric deformities (hour glass deformity, tea pot deformity) ! Penetration into other viscera (such as pancreas) ! Internal fistula formation

Perforated peptic ulcer 07.02

Perforated peptic ulcer

PERFORATED PEPTIC ULCER It is the perforation of peptic ulcer into the peritoneal cavity leading to chemical peritonitis initially which changes into generalized bacterial peritonitis unless it is treated adequately and quickly3. The peptic ulcers of the first part of duodenum perforate commonly. ! It is twenty times common in males ! It occurs commonly between forty to sixty years of age. ! It is much more common in smokers ! The patients are usually nervous and may be having psychiatric problems.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Most of the ulcers which perforate are present on the anterior wall of the duodenum. ! Prolonged history of peptic ulcer is available in most of the patients. History of ingestion of some ulcerogenic drug (analgesics & steroids) may be associated with perforation of peptic ulcer. !

CLINICAL PRESENTATION The patients have previous history of acid peptic disease. The patients are usually smokers. History of drug intake,

DUODENAL ULCER COMPLICATIONS

burns and major trauma may be available in larger percentage in patients with perforation of acute ulcer . The patients usually present with following features; PAIN ABDOMEN The patients have long standing pain in the upper abdomen which suddenly gets worse and is felt in the epigastrium. The pain is severe and excruciating. The pain gets worse on movements, on eating or drinking anything. The pain is continuous. GENERAL CONDITION The patient looks ill and in severe pain. The patient tries to lie still to avoid discomfort and pain. The patient keeps breathing movements shallow to avoid pain. Conscious level and general hydration is normal in early stages. Later on the patient may be disoriented, semiconscious or even unconscious. 07.03

02 All this loss of effective fluid and electrolytes leads to severe fluid and electrolyte imbalance. BOARD LIKE RIGIDITY The abdominal wall muscles go into spasm as soon as the perforation occurs and peritonitis occurs. All the muscles are rigid due to sustained spasm. This is a typical feature of intra peritoneal gastro-intestinal perforation in the initial stages. At later stages, the spasm is relieved due to paralysis of muscles and board-like rigidity disappears and abdominal distension is seen. TENDER AND SILENT ABDOMEN The abdomen is tender all over on palpation, maximum tenderness is felt in the epigastrium. The bowel sounds are not audible on auscultation. Occasionally the tinkling sounds are listened due to presence of air and stagnant fluid in the bowel loops. These are listened at a later stage. DEHYDRATION These patients may present late, then the patient may be dehydrated with sunken eyes and hippocratic face. The dehydration is partially due to fluid and electrolytes loss in vomiting and partly due to fluid loss from circulation into the peritoneal cavity. It results in dehydration and 1 electrolyte imbalance . ABDOMINAL DISTENSION The abdomen is distended due to collection of fluid in the peritoneal cavity initially. As the time passes, the paralytic ileus sets in and gaseous distension also occurs leading to gross abdominal distension.

Patient with perforated peptic ulcer NAUSEA AND VOMITING The patient usually feels nauseated. Vomiting also occurs but large quantity of gastro-duodenal secretions leak into the peritoneal cavity than being vomited out.

SURGERY - GASTRO-INTESTINAL PROBLEMS

SHOCK OR SHOCK LIKE CONDITION The patient may go into shock initially reversible but later on it may become irreversible. The patient is pale and has ashen gray colour. The eyes are sunken. The skin is cold and clammy. The patient has cold sweating. The patient is confused. Compensatory tachycardia may be present. The blood pressure may be normal initially but drops later on and patient suffers from hypotension.

DUODENAL ULCER COMPLICATIONS

JAUNDICE Jaundice is seen in these patients at late stage due to peritonitis and cholangitis. It is usually light.

07.05

INVESTIGATIONS URINE EXAMINATION The urine is usually concentrated and less in quantity due to loss of fluid and electrolytes. It should be tested for presence of sugar and proteins. BLOOD EXAMINATION Haemoglobin concentration Total leucocyte count Differential leucocyte count Sedimentation rate Urea and electrolyte estimation Serum amylase level Serum protein level Serum calcium level RADIOLOGICAL EXAMINATION Erect x-ray chest shows air under the right dome of the diaphragm (pneumoperitoneum). It is seen few hours (about 4-6 hours) after the perforation. It may not be present in all patients with perforation.

Tension Pneumoperitoneum 07.06

Pneumoperitoneum ULTRASOUND SCANNING It is a useful investigation which has become commonly available. It helps in the diagnosis of generalized peritonitis. The free fluid is seen in the peritoneal cavity.

07.04

07.07

Pneumoperitoneum SURGERY - GASTRO-INTESTINAL PROBLEMS

Pneumoperitoneum (ultrasound scan) 63

DUODENAL ULCER COMPLICATIONS

C.T SCAN It is extremely useful investigation to diagnose perforated duodenal ulcer. It is less often used as clinical examination and other simple investigations confirm the diagnosis.

DEFINITIVE TREATMENT It is surgery followed by medical treatment. SURGICAL TREATMENT Laparotomy Peritoneal Lavage Repair of the perforation with omental patch Laparoscopic repair of Perforated ulcer

! ! ! !

07.08

In all cases post operative medical treatment would be necessary. The gastric perforation may be associated with malignancy in about 10% of cases. Wide excision of ulcer should be done followed by closure of the defect.

CT Scan showing pneumoperitoneum It helps in difficult cases where ambiguities are present in defining the etiology of peritonitis. It modifies the 4 treatment strategies and helps in accurate diagnosis .

TREATMENT It is carried out in two steps ; Resuscitation Definitive treatment

! !

RESUSCITATION ! Nasogastric aspiration is started immediately. ! Intravenous fluids and electrolytes are infused rapidly. ! Parenteral analgesia is given after the confirmation of the diagnosis. ! As soon as the general condition of the patient is improved, blood pressure and pulse are normal or near normal and urinary output is satisfactory, the definitive treatment is carried out. ! Antibiotics are required if there has been delay in the treatment. If surgery is done within first 4-6 hours, antibiotics may not be required.

SURGERY - GASTRO-INTESTINAL PROBLEMS

NON-OPERATIVE MANAGEMENT OF PERFORATED ULCER ! Non-operative management of selected patients with perforated peptic ulcer is both safe and efficatious. It has following components; ! Resuscitation ! Administration of fluids ! Parenteral antibiotics ! Parenteral acid reducing drugs (PPI, H2 blockers) ! Active monitoring The non operative management can be shifted to surgical treatment in case of clinical deterioration on emergency basis. MEDICAL TREATMENT Acid reducing drugs ! Proton pump inhibitors (omeprazole). ! H2 receptor antagonists are started (injection cimetidine 200 mg intravenously 8 hourly). ! Cimetidine tablet 200 mg thrice daily or 400 mg once every night. ! Ranitidine (Zantac) tablet twice daily. Gastric Mucosal Protection agents Sucralfates

DUODENAL ULCER COMPLICATIONS

Helicobacter Pylori Eradication Therapy This significantly reduces the relapse of duodenal ulcer, therefore, H. Pylori eradication therapy should be prescribed for all patients with perforated duodenal ulcer after repair.

HAEMORRHAGE (HAEMATEMESIS AND MELAENA) This is another common complication of chronic peptic ulcer. Commonly it starts from the ulcers present on the posterior aspect of the duodenum. Nearly 20,000 patients suffer from haematemesis every year in U.K. No such data is available locally. Nearly 10% of the patients having haematemesis meet a fatal end. The bleeding from chronic peptic ulcer is more common in the older group of patients as they have associated atherosclerosis of the vessels. There is significant increase in the risks in older patients having haematemesis. Commonly involved vessels are splenic or gastroduodenal arteries which get eroded by the ulcer.

ETIOLOGY COMMON CAUSES ! Duodenal ulcer 65% ! Gastric ulcer ! Esophageal varices ! Non steroidal anti-inflammatory drug induced bleeding ! Mallory Weiss syndrome ! Esophagitis ! Carcinoma stomach RARE CAUSES Stress ulceration Chemotherapy Angiodysplasia Aorto enteric fistula Duodenal diverticulae Hereditary haemorrhagic diseases

! ! ! ! ! !

SURGERY - GASTRO-INTESTINAL PROBLEMS

DIAGNOSIS PRESENTATION These patients usually present with small bleeding episodes (warning haemorrhage ) which are followed by severe gastric or duodenal bleeding. Sometimes patient may even present with major haemorrhage to start with. All these patients have previous history of peptic ulcer. There may be history of ingestion of the analgesics or steroids. Patient presents with haematemesis (vomiting blood) and later on with melaena (black tarry stools). Mortality is double in patients having both haematemesis and melaena. Mortality is four times higher in patients who rebleed. 25% of the patients need surgical intervention during the episode of bleeding. Mortality is nearly 8% after surgery. It can be reduced to 5%. Mortality is approximately 18% after medical treatment. Recurrence rate is about 20% after medical treat-ment. The recurrence rate after surgery is between 4-5%. The vast majority (67%) of the patients with haematemesis and melaena bleed from the duodenum or stomach ulcer. Bleeding from esophageal varices and por tal hypertension is the other important cause. The site of bleeding must be diagnosed for adequate treatment. ENDOSCOPY The endoscopy may not be always helpful in cases of severe and sudden bleeding for technical reasons. It can be repeated after gastric suction and wash out (lavage). Once the esophageal variceal bleeding is excluded through endoscopy. LAPAROTOMY Laparotomy should be undertaken for diagnosis and definitive treatment when noninvasive investigations fail to achieve correct diagnosis. A wide gastrostomy in the pyloric area usually helps in the satisfactory diagnosis and treatment.

DUODENAL ULCER COMPLICATIONS

TREATMENT The speed of treatment is most important in the management of haematemesis and melaena.The aims of treatment are ; ! To stop bleeding. ! To replace the lost blood and electrolytes. ! To prevent recurrence. ASSESSMENT OF THE PATIENT Following features are to be noticed ; ! Amount of blood loss ! Duration of blood loss ! Site of blood loss RESUSCITATION Nasogastric aspiration of the gastric contents (blood clots, food and secretions) should be performed. If the clots are not evacuated, these stimulate further bleeding. Intravenous blood transfusion is given and the lost amount of the blood is replaced. Lost amount of fluids and electrolytes is also replaced. Injection morphine 15 mg intravenously (adults) is given to relieve the anxiety of the patient. Injection cimetidine 200 mg or Ranitidine 100 mg is given intravenously three to four times daily. CONSERVATIVE TREATMENT Most of the patients are resuscitated and no more bleeding is seen. These patients can be offered conservative treatment which includes resuscitation and ! Intragastric cooling ! Intragastric milk drip ! H2 receptor antagonists for adequate period ! Bland diet in small quantities and at frequent intervals. ! Ulcerogenic drugs should be completely stopped. ! Proton pump inhibitors such as omeprazole are given. ! Sucralfates are given.

SURGERY - GASTRO-INTESTINAL PROBLEMS

An adequate therapeutic course of H2 receptor antagonists (H2RAs) over 2-3 months heals almost 90% of peptic ulcers. The symptoms are relieved within 2-3 days. Omeprazole which is a proton pump inhibitor, heals the resistant ulcers. The ulcer recurrence is a problem at the discontinuation of medication. If maintenance therapy is continued, the recurrence rate is minimum. The relapse rate after (H2RAs) is about 16%-26%. It is commonly seen in smokers and patients with pre-pyloric ulcers and with high gastric secretory capacity. Sucralfates appear to be better as maintenance therapy. Bismuth is associated with low recurrence rate. Eradication of Helicobacter pylori with antibiotics (Triple drug therapy) Bismuth, metronidazole and amoxycilline or clarithromycin for 4 weeks helps in healing of the ulcers and almost no recurrence. SURGICAL TREATMENT In certain cases the conservative measures fail and surgery becomes inevitable to save the life of the patient. Indications for surgical treatment are ; ! Continuous and heavy loss of blood ! Recurrent bleeding ! Failure to resuscitate conservatively ! Shortage of blood available for transfusion (Rare blood groups) ! Chronic nature of the ulcer disease Laparotomy is performed and following procedures can be carried out depending upon condition of the patient, cause of bleeding and choice of the surgeon; ! Ligation of the bleeding vessel. ! Excision of the ulcer, ligation of bleeding vessel, repair and anastomosis of the duodenum. ! Partial gastrectomy

PYLORIC STENOSIS This is a late complication of chronic peptic ulcer. This is usually due to fibrosis as a result of cicatrization (scar formation) near the ulcer area.

DUODENAL ULCER COMPLICATIONS

BLOOD EXAMINATION Haemoglobin percentage estimation Total leucocyte count Differential leucocyte count Sedimentation rate Urea and electrolytes

07.09

RADIOLOGICAL EXAMINATION Barium meals (gastrogram) confirms the diagnosis

Pyloric stenosis (endoscopic view) It is more common in females but may also be seen in males. The onset is slow. The patient presents with history of pain and fullness in the epigastrium becoming worse progressively. The patient looses weight and vomits after every meal. The vomitus is large and foul smelling. Examination reveals enlarged and distended stomach, visible peristalsis and positive succussion splash. 07.10

ULTRASOUND SCANNING The stomach is seen full of fluid collection even four to six hours after fluid intake. ENDOSCOPY Gastroscopy confirms the diagnosis.

TREATMENT Nasogastric aspiration and emptying the stomach with gastric tube is performed. Fluids and electrolytes of the patient are brought to normal by accurate replacement. Anaemia is corrected. Hypoproteinemia is corrected. Patient's general condition is improved by high caloric fluid diet or parenteral feeding. As soon as the patient is fit for surgery, definitive treatment is carried out. ENDOSCOPIC BALLOON DILATATION The ulcers causing pyloric stenosis are treated medically. The balloon catheter (diameter 1.5-1.8 cm) in size is passed through the fibroscope. The dilatation of the stenosis is performed under vision. The outcome is good and has low complication rate6.

Pyloric Stenosis (ultrasound scan showing fluid filled stomach) INVESTIGATIONS URINE EXAMINATION It is a simple investigation for the general assessment of the patient.

SURGERY - GASTRO-INTESTINAL PROBLEMS

SURGERY Following surgical procedures may help the ulcer patient ; ! Vagotomy and gastro-jejunostomy ! Vagotomy and pyloroplasty ! Partial gastrectomy ! Gastro-jejunostomy

DUODENAL ULCER COMPLICATIONS

The last procedure (Gastro jejunostomy) is carried out in old and weak patients. It relieves the symptoms but does not cure the disease.

REFERENCES 1.

A Cuschieri. GR Giles. AR Moossa. Essential surgical practice. third edition. Butterwor th Heinemann London.1995.P 1100-1137.

John P Walch. Claude E. Walch. Peptic ulcer, stomach and duodenum. Oxford text book of surgery Peter Morris and Ronald A Malt. Oxford university press Oxford. 1994. p: 911-929.

Muhammad Shuja Tahir. Acute peritonitis: Timely and active mangement can improve the outcome. The Professional Vol: 03 No. 03. 1996 Jul-Sep. p 171-182.

C. Marshal, P. Ramaswamy Evaluation of a protocol for non-operative management of perforated peptic ulcer. BJS 1999 86 (131134).

SUMMARY Acute emergencies Non acute problems Perforated duodenal ulcer Haemetemesis & melaena Pyloric stenosis

POSSIBLE QUESTIONS

Taourel P. Baron MP. Pradel J et al. Acute abdomen of unknown origin: impact of CT on diagnosis and management. Gastrointestinal radiology. [JC:fgz]1992. 17(4) : 287-91.

Malangoni MA. Pathogenesis and treatment of intraabdominal infection. Surgery, Gynaecology and Obstetrics. [JC:vbd]1990. 191 supp: 31-4.

Schmudderich W. Harloff M. Riemamn JF. Through-the-scope balloon dilatation of benign pyloric stenosis. Endoscopy. [JC:ehp]1989 Jan. 21(1) : 7-10.

Ashita C. Bose, Vikrankate, H. Pylor eradication prevents reoccurrence after simple closure of perforated deodonal ulcer. Journal of Gastroentrology and hepatology 22 (2007) (345-348).

SURGERY - GASTRO-INTESTINAL PROBLEMS

1. 2. 3.

Discuss treatment of perforated duodenal ulcer? How do you diagnose pyloric stenosis? Discuss management of Haemetemesis & melaena?

HAEMATEMESIS AND MELAENA

GIT - 08

HAEMATEMESIS AND MELAENA Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS HAEMATEMESIS Haematemesis means vomiting of fresh blood. Coffee ground vomiting is vomiting of black colored blood due to conversion of haemoglobin to met - haemoglobin by acid in the stomach. MELAENA Melaena is passage of altered blood (black and tarry) in the stools. It is caused by oxidation of haemoglobin in small intestine. Melaena may persist for several days after upper gastro-intestinal bleeding without further rebleeding. Both of these are manifestations of upper gastrointestinal bleeding. If the patient of haematemesis requires more than five pints of blood transfusion during resuscitation, it is called massive haematemesis. Two third of haematemesis patients bleed from gastric or duodenal ulcer. The other major source of bleeding is esophageal varices.

MANAGEMENT The objectives of management of a patient with haematemesis and melaena are ; ! Resuscitation and immediate treatment of the patient. ! Assessment of the severity of bleeding. ! Diagnosis of the cause of bleeding. ! Definitive treatment. Resuscitation of the patient is started before any history is taken or examination is conducted or any investigation is asked. As soon as the patient is reasonably fit for providing information about disease process and undergoing clinical examination, these procedures are started. SURGERY - GASTRO-INTESTINAL PROBLEMS

Most of the time, necessary information is obtained from the patient or attendants during resuscitation. The examination and re-examination is also conducted during resuscitation whenever possible. It helps to diagnose the cause of haematemesis and to assess the condition of the patient and to monitor the effects of resuscitation. It further helps to formulate new strategies for further management of the patient. Standard ABCDE resuscitation plan is followed:

RESUSCITATION The active resuscitative measures are used ; A. AIR WAY The airway is usually clear. Sometimes in old patients, semicomatose or comatose patients, the vomited blood from the upper gastro-intestinal tract may enter into the tracheobronchial passages . The blood from the oral and tracheo-bronchial passages should be mechanically removed or sucked with the help of an electric sucker. The airway should be maintained and breathing of patient should be assessed and maintained. B. BREATHING Breathing problems are uncommon in these patients until the terminal stage and irreversible shock. C. CIRCULATORY VOLUME Loss of blood occurs from upper gastro-intestinal tract. The lost amount of blood is replaced with blood or other intravenous fluids to keep the circulatory volume as normal as possible. Regular and careful monitoring of the circulatory volume is done by measurement of pulse and blood pressure record, skin perfusion and by calculating urinary output. 69

HAEMATEMESIS AND MELAENA

Fresh blood should be transfused in these patients. Fresh frozen plasma and platelet concentrates should be transfused1. The transfusion should be started as soon as the patient is received. The blood should be replaced as quickly as possible. Pulse, blood pressure and central venous pressure are good guides for the adequate blood replacement and monitoring the patient. Acid base balance should also be maintained as these patients develop metabolic acidosis which gets worse by repeated blood transfusions. Sodium bicarbonate should be given intravenously slowly to treat the metabolic acidosis. D. DISABILITY The patients with haematemesis and melaena may show features of encephalopathy. The bowel should be cleared of the retained blood as early as possible. Lactulose (Duphalac) enemas or oral intake or both help in the improvement of the symptoms of encephalopathy. E. EXPOSURE Proper exposure is most important for accurate and complete examination. The patient should be completely exposed after adequate resuscitation for re-examination. STRUCTURED EXAMINATION It is advisable to perform structured examination so that nothing is missed and it should be ticked on the examination check list. Continuous monitoring and repeated examinations are very important for correct assessment in these patients.

ASSESSMENT OF PATIENT Following information is collected immediately; ! Drug history (anticoagulant therapy, NSAIDs, Iron therapy & cyclo-oxigenase inhibitors) ! History of abdominal surgery (stomach and aorta) Chronic liver disease Following information is very essential for the assessment of the general condition of the patient; ! Amount of blood loss

SURGERY - GASTRO-INTESTINAL PROBLEMS

! ! ! !

Speed of blood loss Duration of blood loss Site of blood loss Cause of blood loss

AMOUNT OF BLOOD LOSS This is usually estimated by indirect means as it is not always possible to obtain exact figures. This information is extremely important as lost amount of the blood has to be replaced accurately and with adequate speed. History of amount of blood loss could be misleading as patient may not have vomited so much blood but bleeding might have been severe. It is the problem when haemorrhage is concealed and patient has not reported for medical help. When the haematemesis and melaena both are present, the blood loss is severe and prognosis is poor. Another factor which is difficult to ascertain, is the condition of the patient prior to the bleeding. The old patients, anaemic, malnourished and patients with other associated diseases have a very poor outcome. Examination of the patient is more helpful as the pulse, blood pressure, central venous pressure and general condition of the patient gives a fair idea about the amount of blood loss. SPEED OF BLOOD LOSS Sudden loss of blood causes more dramatic effects than the slow loss of blood. Usually there are few warning bleeds before the actual episode of extensive bleeding. Sudden loss of larger quantities of blood leads to shock and even death of the patient unless the lost amount of blood is replaced quickly. SITE OF BLOOD LOSS Site of bleeding should be known for the proper management and planning of conservative or surgical treatment of the control of bleeding. History may be helpful in suggesting the site of bleeding

HAEMATEMESIS AND MELAENA

MANAGEMENT OF UPPER G.I HAEMORRHAGE Diagnosis of Upper G.I Haemorrhage

Resuscitation

Upper G.I Endoscopy

Lesion Seen

Active Bleeding

No Lesion Seen

No Active Bleed

Endoscopic Therapy

Haemostasis Achieved

Repeat Endoscopy & Reassess after 24 hrs

Minor Bleed

Angiography

Conservative Management

Continued Bleed / Rebleed

No Lesion Seen

Repeat Endoscopic Therapy

Continued Bleed / Rebleed

Surgery

SURGERY - GASTRO-INTESTINAL PROBLEMS

Major Bleed

Lesion Identified

Radiographic Treatment

Haemostatis

HAEMATEMESIS AND MELAENA

as previous history of dyspepsia indicates bleeding peptic ulcer and history of excessive vomiting suggests bleeding due to Mallory-Weiss syndrome. History of hepatitis or jaundice in the past may suggest bleeding from the esophageal varices.

bleeding. There is very little change in the haemoglobin level in the early period, but at later stages serial haemoglobin estimations indicate the amount of blood loss and are reasonable guide for replacement of blood. It also helps in monitoring the condition of the patient.

CAUSE OF BLOOD LOSS Once the patient is properly resuscitated, the cause of the bleeding is found out. Adequate history and complete examination are very important to differentiate between various causes of haematemesis and melaena.

Total leucocyte count Usually, it is not altered and may be normal in early stages. Later on it may be raised due to associated infections. Differential leucocyte count It is normal and unaltered in most of the cases.

CAUSES OF UPPER GI BLEEDING ! ! ! ! ! ! !

Esophageal varices Duodenal & Gastric ulcers Gastric erosions Mallory Weiss syndrome Esophagitis Upper GI carcinoma Anastomotic ulcers

(05% - 10%) (35% - 50%) (08% - 15%) (10% - 15%) (05% - 15%) (05% - 10%)

Rare causes of bleeding (05% - 10%) are; ! Duodenal tumours ! Pancreatic tumours ! Haemophilia ! Clotting disorders ! Hereditary telangiectasias ! Arterial aneurysm ! Aorto-enteric fistula ! Von Willebrand's disease ! Pseudo-xanthoma elasticum

INVESTIGATIONS Following investigations are performed for the assessment and management of the patient ; Urine Examination It is a simple investigation for the general assessment of the patient. Haematocrit / Haemoglobin Estimation Haematocrit is a good indicator in early phases of

SURGERY - GASTRO-INTESTINAL PROBLEMS

Erythrocyte Sedimentation rate It is within normal range in initial stages and may be slightly raised in later stages. Liver function tests These are altered when bleeding is due to cirrhosis or other liver diseases. These give information about the function of the liver and help in planning the treatment of patients bleeding from esophageal varices. One should always remember that patients with known liver disease may bleed from peptic ulcer many times. Patient should be investigated for the presence of virus for hepatitis-B, C and for HIV infection. Urea And Electrolytes Level Estimation of serum urea and serum electrolytes is helpful in the assessment of fluid and electrolyte balance and in treating it properly. Serum Protein Level Serum proteins are in lower concentration in patients with poor liver function. These are also low in malnourished patients. ESOPHAGO-GASTRO-DUODENOSCOPY It should be performed in a patient presenting with upper G.I hemorrhage. In general, presentation with hematemesis &

HAEMATEMESIS AND MELAENA

melaena indicates a more severe blood loss than melaena alone. Upper G.I endoscopy has got following objectives; ! To establish cause of bleeding ! To find out site of bleeding ! To obtain prognostic information ! To administer endoscopic therapy

system is used for risk assessment. A total score of less than 3 is associated with favorable prognosis. Score >8 is associated with a high risk of death. Rockall Scoring System Variable Age

Endoscopy is usually performed under sedation with a benzodiazepine and local anaesthetic gargles (4% xyloaine solution) to anasthetise upper G.I tract. Supplemental oxygen with blood pressure monitoring and pulse oximetry should be done. General anaesthesia is required in order to protect the airway in severely compromised patients or because the patient is already on ventilator. This is helpful not only to confirm the diagnosis but also to evacuate the gastric clots.

The endoscopy should be performed after taking necessary precautions as the patient may aspirate blood during emergency endoscopy. It is an important cause of post-endoscopy hypoxia2. The high risk patients and high risk ulcers should be selected at the earliest stage. These should be treated early. MESENTERIC ANGIOGRAPHY If the condition of the patient allows mesenteric angiography, is helpful and essential to plan therapeutic embolisation. RADIOLOGICAL EXAMINATION Barium swallow (Esophagogram) Barium meals (Gastrogram) Both these investigations help in the diagnosis of the site of bleeding and cause of bleeding. Most of the lesions are picked up by contrast medium studies.

RISK ASSESSMENT It is essential to categorize patients at the time of admission into high or low risk of death. Rockall scoring

SURGERY - GASTRO-INTESTINAL PROBLEMS

Score 0 <60

Shock

Co-morbility

Diagnosis Major Stigmata of recent hemorrhage (SRH)

60 - 79

>80

Tuchycardia Hypotention No shock (systolic BP>100) (systolic BP>100) (systolic BP<100) pulse>100) pulse>100) Pulse <100) Cardiac falinne Ishenic heart discase any major co-morbidity

Nil Major Mallory weiss kar, no lesion and no SRH

All other diagnosis

None or dark spot

Renal faline liver jaline disseminated malignancy

Malignancy of upper GI Blood in upper GI tract adherpil clot, vineble spunting vessel

TREATMENT ! ! ! ! !

Resuscitation (immediate) Medical treatment Endoscopic treatment Surgical treatment Radiological embolisation

The resuscitation of the patient is started as early as possible. Sometimes it is started even before the history or examination is performed. This happens in patients who are in shock and are bleeding profusely. Standard ABCDE plan of resuscitation is followed. IMMEDIATE TREATMENT NASOGASTRIC ASPIRATION & GASTRIC LAVAGE Aspiration of the blood from stomach should be carried out through a wide bore nasogastric tube. All the clots should be aspirated. This helps in the assessment of blood loss and removal of the clots. SEDATION Injection morphine 15 mg intravenously helps in sedating the patient when patient is very anxious due to severe blood loss. These should be used very carefully in patients with compromised liver functions. 73

HAEMATEMESIS AND MELAENA

GASTRIC COOLING (GASTRIC LAVAGE) After aspirating the clots, stomach wash is performed with ice cold water through the nasogastric tube. This procedure is repeated few times and helps in controlling the bleeding to some extent. MEDICAL MANAGEMENT Three classes of drug therapy have been used to treat upper GI bleeding. ACID SUPPRESING DRUGS Their use is based on observation that the stability of a blood clot is reduced in acidic environment, thus a pH>6 6 is essential in this respect . PROTON PUMP INHIBITORS Following successful endoscopic therapy high dose PPI are recommended; SOMATOSTATIN High dose IV somatostatin suppresses acid secretion and reduces splanchnic blood flow and is an attractive hemostatic agent1. ANTIFIBRINOLYTIC DRUGS Tranexamic acid therapy, while not reducing open rebleeding, does appear to reduce the need for surgical intervention and tends to reduce mortality in ulcer bleeding patients.

MECHANICAL CLIPS Mechanical clips can be applied to bleeding points. These are particularly useful for actively bleeding vessels. ENDOSCOPIC SCLEROSING THERAPY Endoscopic sclerotherapy can be used in the bleeding tears after Mallory Weiss syndrome. It is helpful in terminating the bleeding3. These are injected into the bleeding esophageal varices through the esophagoscope. There is temporary relief of bleeding but recurrence is quite common. APPLICATION OF HEAT Thermal haemostasis is achieved using either heater probe or multipolar coagulation. TELANGIECTASIA These lesions are best managed by heater probe or argon plasma coagulation. SENGSTAKEN TUBE Balloon tamponade is used to control the bleeding from esophageal varices as a temporary measure. It may be used in association with sclerotherapy. UNCONTROLLED UPPER G.I HAEMORRHAGE If the above mentioned measures fail to control bleeding then the mainstay of treatment lies with;

Endoscopic therapies can be classified as those based on injection, application of heat or mechanical clips5.

THERAPEUTIC EMBOLISATION Bleeding vessel (e.g, gastroduodenal artery) is embolised using endovascular sponges and coils. Such treatment needs expertise and specialised setup.

INJECTION Injection of 1:10000 adrenaline solution in normal saline is injected in all quadrants around bleeding point. This is successful in 95% of patients and re-bleeding occurs in 15-20% after injection1, 2.

LASER THERAPY ND-YAG Laser photo co-agulation is superior than Argon Laser. The bleeding is successfully terminated in 75% of these patients. The complications after laser treatment are minimum4.

MALLORY WEISS TEAR Usually bleeding stops spontaneously. Injection therapy may be required occasionally.

SURGICAL TREATMENT Any patient who gets attack of haematemesis and melaena during adequate medical treatment and

ENDOSCOPIC TREATMENT

SURGERY - GASTRO-INTESTINAL PROBLEMS

HAEMATEMESIS AND MELAENA

requires four to five pints of blood for resuscitation, should be treated surgically. Following procedures can be performed after laparotomy ;

! ! ! ! ! ! !

Ligation of bleeding points. Excision of ulcer and control of bleeding. Control of bleeding and vagotomy and pyloroplasty. Control of bleeding and selective vagotomy. Partial or sub total gastrectomy for gastric bleeding. Various operations for control of bleeding from esophageal varices. Shunt operations in patients with por tal hypertension.

SURGERY It is the final line of defense in cases where all measures to stop bleeding have failed. The bleeding vessel is ligated under vision. ESOPHAGEAL VARICES Such patients are usually managed in specialised liver units. There are following methods of treatment; MEDICAL TREATMENT Splancnic vasoconstrictor drugs e.g, Vasopressin, Octreotide. ! B-blockers produce similar effects of reducing portal blood flow.

REFERENCES 1. Imperiale TF, Brigisson S. Somatostain & octresilde compared with H2 antagonists and placebo in the management of acute nonvariceal bleeding Ann. Intern Med 1997; 127:1062-71. 2. Chung SSC, Ieung JWC, Steele RJC Endoscopic injection of adrenaline for actively bleeding ulcers; a randomized control trial. BMJ 1986; 298: 1631-3. 3. Chung IK, Han HC Comparison of heamostatic efficacy of endoscopic hemoclip method with hypertonic saline epinephrine injection. Endoscopy 1999; 49: 13-18. 4. Konigsrrainer A. Sandbichler P. Aignerf et al Endoscopic sclerotherapy of bleeding mallory. Weiss mucosal tear. Wiener Klinische wochens chrift. [JC:xop] 1989 Nov 10. 101(21): 734-5. 5. Lipper B. Simon D. Cerrone F. Pulmonary aspiration during emergency endoscopy in patients with upper gastrointestinal haemorrhage. Critical care medicine. [JC:dtf]. 1991 Mar. 19(3): 330-3.

6. Barer, Ogilive A. Cimetidine and tranexemic acid in the treatment of acute upper GI bleeding. NEJM 1983; 308: 1571-5.

BALLOON TAMPONADE Minnesota or sengstaken tube may used for this purpose. ENDOSCOPIC MANAGEMENT It involves ! Injection sclerotherapy ! Band ligation ENDOVASCULAR TREATMENT It includes transjugular intrahepatic portosystemic shunting.

SURGERY - GASTRO-INTESTINAL PROBLEMS

HAEMATEMESIS AND MELAENA

SUMMARY Haemetemesis Melaena Recussitation Management Plan Assessment of patient Amount of blood loss Speed of blood loss Site of blood loss Cause of blood loss Investigations Risk assessment Rockall scoring system Treatment POSSIBLE QUESTIONS 1. What is haemetemisis? 2. What is melaena? 3. Discuss their management?

SURGERY - GASTRO-INTESTINAL PROBLEMS

? 76

CARCINOMA OF STOMACH

GIT - 09

CARCINOMA STOMACH Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS 09.01

Fundus

! !

Cardia

Lesser Curvature

Body (Corpus)

Pylorus Antrum

Greater Curvature

SITES OF CARCINOMA STOMACH Pylorus 50% Lesser curvature 25% Cardiac end 10%

Stomach - diagrammatic view Carcinoma of the stomach is the malignant tumour of the stomach. Most commonly it is adenocarcinoma1. It is the second most common cause of cancer related deaths in the world. It is a difficult disease to cure mainly because patients present with advanced disease. Few decades ago this used to be the most common abdominal malignancy. Now its incidence has fallen progressively but reasons for this decline are obscure. INCIDENCE AND EPIDEMIOLOGY It represents 3% of all cancer deaths. Incidence of carcinoma of stomach has decreased upto 25% as compared to its incidence fifty years ago. ! Its incidence is about 11% by the age of 75 years. It is common in 40-70 years age group but it may be present at any age even in infants. ! Its incidence is low in central Africa. ! This malignancy is more common in Asia, Japan and South America. ! It is twice or even three times more common in males than females. ! !

SURGERY - GASTRO-INTESTINAL PROBLEMS

It is four times more common in the relatives of the patients with gastric carcinoma than in the normal population. It is common in lower socio-economic group. It is more common in people with blood group"A", smokers and spirit drinkers. It is more commonly present in the antral and prepyloric region as given in the table below;

! ! ! ! ! !

2%-8% gastric malignancies are lymphomas. Proximally placed carcinomas have worse prognosis. 7-8 per 100,000 population die of carcinoma of stomach. It causes nearly 52% of cancer deaths in males and 38% cancer deaths in females. Fifty percent of all the deaths in Japan are due to carcinoma of the stomach. Nearly 50,000 people die of carcinoma of stomach every year in United Kingdom.

ETIOLOGY No exact etiological factor is known. Genetic, hereditary, racial and environmental factors are associated with the appearance of carcinoma of the stomach. HELICOBACTER PYLORI Helicobacter positive patients have 2-5 fold increased risk for gastric carcinoma. Helicobacter pylori infestation is associated in nearly 81% of gastric cancer patients but is common in younger age group6. 77

CARCINOMA OF STOMACH

GENETIC FACTORS Familial clustering of carcinoma of the stomach is very famous as Napoleon, his father, his grand father, brother, three sisters died of carcinoma of stomach. About 4% of the patients have positive family history. It is 1-2 times more common in people with blood group “A” (relative risk is 1.2) than “O” group. ENVIRONMENTAL AND DIETRY FACTORS It is probably more common in people consuming low quality diet poor in milk, animal proteins and vitamins but rich in starch. Heavily salted, pickled and smoked fish are associated with increased risk. Higher intake of 2 vegetables and fruits leads to lower risk . Role of nitrosamines is carcinogenic on gastric mucosa. Food preservatives converting into nitrosamines also increase the risk of carcinoma of stomach. Iodine excess is associated with the development of gastric carcinoma3. Neat spirit, cigarette smoking and elevated levels of zinc and lead in water, talc and asbestos in atmosphere all are high risk associations. Workers of metal industry, painters, printers, fishermen, and clay workers all are at a higher risk of having carcinoma stomach. RADIATION EXPOSURE Atomic bomb survivors have had increased risk of gastric cancer. Other population exposed to radiation has higher risk as well . SUPPRESSION OF ACID SECRETION Sustained suppression of gastric acid secretion is an increased source of concern. It is because of association of gastric malignancy with achlorhydria and pernicious anaemia. There is change in gastric flora, level of 4 carcinogens and changes in hormonal milieu . Following premalignant conditions are associated with carcinoma of stomach ; ! Gastric polyps. ! Pernicious anaemia.

SURGERY - GASTRO-INTESTINAL PROBLEMS

! ! ! ! !

Chronic gastric ulcer (this is doubtful). Atrophic gastritis or gastric atrophy. Intestinal metaplasia or dysplasia. Hyperplastic secretory gastropathy. Achlorhydria.

ATROPHIC GASTRITIS AND INTESTINAL METAPLASIA Patients with Hypogammaglobulinemia and pernicious anaemia have associated chronic atrophic gastritis. These run a higher risk of gastric carcinoma. It is probably the first step towards progression of gastric cancer5. Atrophic gastritis is a commonly associated condition with gastric carcinoma. The intestinal type of gastric carcinoma is the most common associated type in males over 40 years of age. Achlorhydria results from atrophic gastritis and 75% of patients with gastric carcinoma are achlorhydric. Intestinal metaplasia of gastric mucosa is commonly associated with gastric carcinoma. It may be a second step in progression of gastric carcinoma. GASTRIC ULCERS The development of gastric cancer at the edge of benign ulcer is rare. Location of benign ulcers is different (52%70% occur on lesser curvature). 70% of early gastric cancers may heal as part of life cycle of gastric ulcer. GASTRIC POLYPS These are rare. 0.5% of autopsy shows its presence. Most of these are hyperplastic polyps. These don't have strong association with gastric carcinoma. Adenomatous polyps are truly pre-malignant. These are larger (greater than 2 cms). These may be villous or tubulo-villous in shape. PREVIOUS GASTRIC SURGERY There is some increased risk of development of gastric cancer due to post-operative achlorhydria or bile reflux or atrophic gastritis.

CARCINOMA OF STOMACH

HYPERPLASTIC GASTROPATHY The gastric mucosa is hyperplastic and rich in proteins and mucous but poor in acid. It is associated with increased risk of gastric carcinoma. GEOGRAPHIC FACTORS Risk of carcinoma stomach declines on migration from high risk area to low risk area only after second generation. PATHOLOGY 09.02

Carcinoma of stomach Common type of gastric carcinoma is adenocarcinoma. The tumour is usually multicentric and smaller lesions join each other to make bigger tumour. Most of the time tumours arise from areas of intestinal metaplasia1. Two common cell types of carcinoma stomach have been described as ; ! Intestinal (metaplastic ) ! Gastric It shows different biological behaviour such as ; ! Large primary tumour with no distant metastasis but local spread to lymph glands and viscera is present. (most common) !

Small primary tumour but large metastatic spread.

Two dimensional spread is present. (linitis plastica or leather bottle stomach)

SURGERY - GASTRO-INTESTINAL PROBLEMS

It spreads to esophagus, duodenum and jejunum through submucosa. It has only 0% 5 years survival rate. Carcinoma of the stomach has been described and classified according to various parameters such as; ! Macroscopic appearance ! Extent of invasion ! Microscopic appearance ! Anatomical sites ! Biological behavior MACROSCOPIC PICTURE The macroscopic appearance of tumour correlates with prognosis but microscopic picture does not. The gastric carcinoma could be ; SUPERFICIAL SPREADING CARCINOMA OR EARLY GASTRIC CARCINOMA (E G C) Early gastric carcinoma presents in 10-35% cases. It presents as following types ; Type I (Protruding type) Type II (Superficial type) & Elevated & Flat & Depressed Type III (Excavated) Early phase of gastric tumour in which carcinoma invasion is limited to mucosa and submucosa irrespective of the regional lymph node involvement4. All gastric carcinomas arise as in-situ lesions confined to the mucosa only. 50% of these lesions are multifocal and present near each other. The lesions grow on all sides and involve submucosa. It is called early gastric carcinoma at this stage only. It is a flat area of mucosal thickening and induration. It may be missed on inspection but is easily palpable. It may sometimes present as polypoid or protruding lesion. It may also present as ulcerated , depressed or excavated lesion.

CARCINOMA OF STOMACH

All these lesions may be larger or multicentric but all can be moved over muscularis mucosae as this type doesn't penetrate outside submucosa. It may spread to the local lymph glands in 5% cases. It may take nearly eight years for the tumour to become invasive. Five year survival rate in this type after surgery is 65-95%. FUNGATING CARCINOMA (30%) It appears as large intraluminal mass protruding several centimeters above the gastric wall. It infiltrates on all sides and occasionally may become polypoidal in appearance. ULCERATIVE INFILTRATING CARCINOMA (30%) The ulceration may be shallow or deep in this type. The edges of the ulcer are raised and indurated which slope towards the haemorrhagic base. It has shaggy and necrotic base. The ulcer margins are beaded, irregular and heaped up. The malignant ulceration can be easily differentiated from chronic peptic ulcer because those have clean base and perpendicular regular margin. The surrounding gastric wall is infiltrated and thickened in this type of carcinoma of stomach. There could be lateral spread of the tumour. DIFFUSELY INFILTRATIVE CARCINOMA (10%) This type, when manifested, gives rise to leather bottle stomach or linitis plastica. The thickening and induration is produced by combination of widely permeating carcinoma and scirrhous stromal reaction. The overlying mucosa is thick and edematous. It may involve whole of the gastric wall without protruding any mass into the gastric lumen. The rugal gastric folds are totally absent. Cut surface of the tumour shows greyish white infiltrating tissue prominent in the submucosa. UNDIFFERENTIATED CARCINOMA OR ANAPLASTIC CARCINOMA The tumour is too invasive and un-differentiated.

SURGERY - GASTRO-INTESTINAL PROBLEMS

MICROSCOPIC PICTURE Carcinoma stomach may be represented by complete range of differentiation such as ; ! Tubulo-papillary type of adenocarcinoma ! Muco-cellular or signet-ring cell type ! Solid cell anaplastic lesions. Tumour usually comprises of columnar cells but cuboidal and squamous cells may be present. All stages overlap each other at different parts of the tumour. Following features are also seen ; ! Atypia in the adjacent glands. ! More infiltrative pattern of carcinoma and tendency to desmoplasia and destruction of muscularis mucosa. ! Demonstration of intracellular mucin in scattered tumour cells. Histologically carcinoma can be graded into following types ; ! Papillary adenocarcinoma ! Tubular adenocarcinoma ! Well differentiated ! Moderately differentiated ! Poorly differentiated adenocarcinoma ! Signet-ring cell carcinoma SPREAD OF GASTRIC CARCINOMA The gastric carcinoma spreads by following routes; INTRAMURAL SPREAD This is when tumour spreads directly through the gastric wall. It spreads as small gray white sub-serosal nodule formation. The spread occurs laterally through whole of the stomach and sometimes even through duodenum. The duodenal invasion is sub-serosal and mucosa is spared. LYMPHATIC SPREAD This occurs through the lymphatics. The common modes of spread are ;

CARCINOMA OF STOMACH

Permeation Embolization Regional lymph node involvement is 80-90%. Regional and distant lymph nodes are involved in the spread such as ; ! !

VIRCHOW'S NODES These are enlarged left supraclavicular nodes, (Troisier's sign). TRANSCOELOMIC SPREAD It is the spread due to gravity when gastric carcinoma spreads to pelvic organs. It is seen in 20-40% cases. Involvement of ovaries is seen in 10% cases and is known as Krukenberg's tumours. TNM STAGING OF GASTRIC CARCINOMA

Tx T1 T2 T3 T4

Nx N0 N1 N2

Mx M0 M1

T Degree of involvement not known. Tumour confined to mucosa. Involving all layers to serosa. Penetrating serosa with or without direct invasion of adjacent tissues or organs. Diffuse infiltration of gastric wall. N Lymph node status unknown. No nodal involvement. Peri-gastric lymph nodes adjacent to tumour involvement. Metastasis to nodes on both antral or regional areas. M Metastatic status unknown No metastasis. Distant lymph node or organs involvement.

SURGERY - GASTRO-INTESTINAL PROBLEMS

STAGING FOR GASTRIC CARCINOMA STAGE 1a Tumour confined to gastric mucosa only (T1, N0, M0). STAGE 1b Tumour extending to but not through serosa (T2,N0,M0). STAGE 1c Tumour extending through serosa with or without local invasion (T3, No,Mo). STAGE II

Diffuse involvement of gastric wall (T4,No,Mo) or gastric wall involvement with perigastric lymph node involvement (T1-4,N1, M0).

STAGE III

Any degree of gastric wall involvement with peri-gastric lymph node involvement on both curvatures and distant from tumour (T1-4, N2, M0).

STAGE IV Distant metastasis (T1-4, N1-2,M1). CLINICAL FEATURES 25% Gastric cancer patients present with localized disease. ! 31% present with regional disease. ! 32% present with distant metastatic disease. ! Early disease has no associated symptoms. !

GASTRIC DISTENSION It is noticed with dyspepsia and inability or difficulty to take normal meals. This problem is mainly due to presence of the tumour (space occupying lesion) in the stomach and obliteration of gastric cavity. Post prandial fullness may be a common symptom. Unexplained or new dyspepsia in patients above forty years of age must always be investigated properly. PAIN IN THE EPIGASTRIUM Peptic ulcer like pain may be due to carcinoma of stomach. Many times it responds to antipeptic ulcer treatment but only temporarily and symptoms recur very quickly.

CARCINOMA OF STOMACH

INDIGESTION, NAUSEA, VOMITING It is a symptom which may be present in patients with early disease . HAEMATEMESIS AND MAELENA These features may be seen in patients with early and even advanced disease. MASS IN THE EPIGASTRIUM There is a mass present in the epigastrium but this is usually a late symptom and mostly the tumour has become inoperable when it is palpable. GENERAL SYMPTOMS ! Anorexia ! Anaemia ! Weakness ! Loss of weight ! Tiredness ! Offensive smell through mouth ! Symptoms due to metastasis in lungs, liver, common bile duct, oesophagus, pylorus, ovaries (Krukenberg's tumour). ! Phlebothrombosis of superficial veins of legs (Trousseau's sign). ! Enlarged left supra clavicular lymph glands (Troisier's sign). Following features may also be seen in patients with gastric carcinoma ! Palpable enlarged stomach with succession splash. ! Hepatomegaly ! Peri umbilical metastasis (Sister Mary Joseph Nodule) Irish node (Anterior axillary) Blumer shelf (Shelf like tumour of the anterior rectal wall) ! Para neoplastic syndromes such as; Dermatomyositis

SURGERY - GASTRO-INTESTINAL PROBLEMS

Acanthosis Nigricans Circinate erythema Microangiopathic hemolytic anaemia. INVESTIGATIONS Objectives of investigation are; ! To diagnose the disease at earliest possible stage. ! To confirm the diagnosis histologically. ! To assess the nutritional deficiency of the patient. Following investigation are carried out; URINE EXAMINATION This is a simple investigation which helps to assess the general condition of the patient. BLOOD EXAMINATION Haemoglobin percentage. (Anaemia is present in nearly half of the cases) Total leucocyte count Differential leucocyte Erythocycyte sedimentation rate is raised in nearly 70% of patients. LIVER FUNCTION TESTS Liver function test are done and hepatitis virus status is assessed. (HCV) (Hepatitis-C virus) (HBV) (Hepatitis-B virus) Carcino embryonic antigen (CEA) is increased in 45%50% of cases. Cancer antigen (CA) 19-9 is elevated in about 20% cases. STOOL EXAMINATION Occult blood is present in nearly 80% cases. ULTRASOUND SCANNING It helps in differentiating from other lesions present in the epigastrium such as pseudocyst of the pancreas, hydatid cyst and liver abscess etc.

CARCINOMA OF STOMACH

CT SCAN/M.R.I SCAN It helps to assess the regional and distant metastasis. Its 13 contribution to assess local disease is limited . It picks up the potential areas of spread. (enlarged lymph glands and liver spread). RADIOLOGICAL EXAMINATION Chest x-ray is done to evaluate metastatic lesions.

be taken. Brushing of the tumour can be done and gastric aspirate can be sent for exfoliative cytology. Use of endoscopy as first line diagnostic modality in patients with gastrointestinal complaints in the detection of early gastric carcinoma (EGC) has significantly increased the yield4. 65% of malignant stomach ulcers are diagnosed correctlyendoscopically7.

09.03

09.04

Barium meals x-ray (carcinoma of stomach)

Gastroscopy (carcinoma stomach)

BARIUM MEALS/DOUBLE CONTRAST STUDY These are contrast medium x-rays of the stomach. Single or double contrast pictures can be taken. ! 90% of pyloric growths can be detected. ! 75% of cardiac growths can be detected in this way. ! Its average accuracy rate is 67%7. ! 60% of neoplasms of body of stomach can be detected. ! Small lesions and flat growths may be missed but double contrast medium has improved the efficacy.

ENDOSCOPIC SONOGRAPHY It is a valuable test to evaluate the upper gastrointestinal tract. It helps to improve the prognosis of gastric carcinoma by diagnosing it at an earlier stage. It is used to assess the horizontal extent of cancerous invasion below the mucosal layer9,10. It is performed with a specially designed endoscope with fixed transducer for 10 endoluminal ultrasonography . Its correct prediction rate is about 84%11.

The most common reason of delay in the diagnosis of gastric carcinomas by doctors is due to negative barium meal8.

EXFOLIATIVE CYTOLOGY Gastric lavage after brushing of the tumour helps to achieve maximum positive results. Its accuracy rate is 73%7.

GASTROSCOPY This is an excellent investigation. It has 95% diagnostic accuracy and tumour can actually be seen and biopsy can

BIOPSY Multiple ulcer edge biopsies are taken. All gastric ulcers are biopsied. Endoscopic biopsy is confirmatory of the diagnosis. Its accuracy rate is 80%7. Cytology and biopsy

SURGERY - GASTRO-INTESTINAL PROBLEMS

CARCINOMA OF STOMACH

in combination yield about 95% correct diagnosis in case of malignant gastric ulcers. If repeated again, the pickup 7 rate is about 100% . These are complementary to each 12 other . TREATMENT Treatment of carcinoma stomach is; ! Symptomatic ! Definitive SYMPTOMATIC Nutritional support is given to correct the deficiency. Symptomatic treatment is done for control of pain, control of nausea, vomiting, Constipation, depression and mouth care.

cancers of distal 2/3 of stomach. ! Distal pancreas in only removed if direct invasion with tumour is seen. ! Removal of spleen has an adverse effect on prognosis. ! Excision of spleen and its Hilar nodes are performed in patients with tumours of proximal stomach, greater curvature and posterior wall of stomach close to splenic hilum. Other surgical procedure may be used as per surgeonâ&#x20AC;&#x2122;s choice are; RADICAL TOTAL GASTERECTOMY 09.05

DEFINITIVE TREATMENT Surgery is the treatment of choice 50% cases are inoperable at the time of diagnosis. The only hope is early diagnosis and curative resection.Its indicators are; ! Early diagnosis ! Resectability Peri operative mortality is 2%. MEDICAL TREATMENT No curative medical treatment is available. SURGICAL TREATMENT Excision of the stomach with its growth is performed but prognosis is poor. Distal (antral ) tumours are treated with subtotal gasterectomy and proximal tumours require total gasterectomy. Limited gastric resections are performed for palliation or in elderly patients. Patients with early disease and curable cancer undergo; ! Excision of primary gastric lesion ! Excision of quantum and N1 and N2 lymph glands. ! D2 lymph-adenectomy (distant lymphnodes) Distal pancreas and spleen are not removed in

Tumour

Carcinoma of stomach Following parts are removed ; !Whole of the stomach !Lymph nodes. !Gastrocolic mesocolon !Spleen 09.06

Oesophago-jejunostomy

Total Gastrectomy and oesophago-jejunostomy

SURGERY - GASTRO-INTESTINAL PROBLEMS

CARCINOMA OF STOMACH

RADICAL UPPER PARTIAL GASTRECTOMY When upper part of the stomach is resected and anastomosed with esophagus or is closed as a stump and esophago-jejunostomy is performed.

When lower part of stomach is resected and gastrojejunostomy is performed. 09.10

09.07

Anastomosis

Stomach

Upper partial gastrectomy Lower partial gastrectomy and gastro-duodenal anastomosis

09.08

Anastomosis

Upper partial gastrectomy and oesophagogastric anastomosis

PALLIATIVE OPERATIONS These are the operations to relieve the symptoms when the malignancy is widespread and inoperable. ! Palliative gastro jejunostomy ! Exclusion operations. ! Introduction of any one of the tubes for cardiac end growths. 09.11

RADICAL LOWER PARTIAL GASTRECTOMY 09.09

Tumour

Tumour Area to be resected

Lower partial gastrectomy

SURGERY - GASTRO-INTESTINAL PROBLEMS

Palliative surgery for gastric carcinoma

CARCINOMA OF STOMACH

! ! ! ! ! ! ! ! ! ! !

09.12

Paliative gastro-jejunostomy RADIOTHERAPY It is not very helpful. Results of surgery and radiotherapy are almost similar as far as the prognosis is concerned. CHEMOTHERAPY It is not very useful in the treatment of carcinoma of stomach. There is small survival advantage with adjuvant chemotherapy. Operative chemo-radiation improves survival in short term. 5-FU (flouro-uracil) is the most effective chemo therapeutic agent. When combined with epirubicin and cisplastin it is most effective combination. There is no role of second line chemotherapy in the treatment of carcinoma stomach.

Immuno deficiency syndroms Symptoms due to gasterectomy Gastro oesophageal junction obstruction Small bowel obstruction Cholecystitis Pancreatitis Bleeding in stomach from oesophageal varices Anastomotic failure (bleeding and or leakage) Intra hepatic and extra hepatic Jaundice Thrombo embolism Aftermath of starvation or cachexia of tumour origin Direct surgical mortality rate is less than 2%

PROGNOSTIC FEATURES Following factors influence survival in resectable gastric tumours. ! Depth of cancer invasion through gastric wall ! Gross appearance of tumour ! Size (Staging) ! Location of tumour ! Regional lymph node involvement ! Linitis plastica (5% of primary gastric carcinoma) (Entire stomach is extensively infiltrated with tumour) has very poor prognosis. ! Positive margins after resection are associated with very poor prognosis14. OUT COME

COMPLICATIONS The gastric carcinoma presents with following complications; ! Pathological peritoneal effusion ! Pathological pleural effusion ! Gastric out let obstruction ! Dumping Syndromes (early and late) ! Vit B-12 deficiency ! Reflux oesophagitis ! Bone disorders such as osteoporosis

SURGERY - GASTRO-INTESTINAL PROBLEMS

5 years survival rate for curative surgical resection for gastric carcinoma is a follows; ! ! !

Stage-I Stage-II Stage-III

60%-95% 30%-50% 10%-25%

REFERENCES 1. Cotran. Kumar. Robbins. Robbins pathologic basis of disease. 5th ed. W.B. Saunders Company London. P: 767-783. 1994.

CARCINOMA OF STOMACH

Weiburger JH. Carcinogenesis in our food and cancer prevention. Advances in experimental medicine and biology [JC : 21u] 289:137-51, 1991. Venturi S. Venturi A. Cimini D. Anduini C. Venturi M. Guidi A. A new hypothesis. Iodine and gastric cancer. European journal of cancer prevention [JC : bnn] 2(1): 17-23, 1993, Jan. Longo WE. Zucker KA. Zdon MJ. Modlin IU. Detection of early gastric cancer in an aggressive endoscopy unit. American surgeon [JC : 43e] 55(2): 100-4, 1989 Feb.

Brinton LA. Gridley G. Hrubec Z et al British journal of cancer [JC: av4] 59(5): 810-3, 1989 May.

Jaskiewicz K. Lowwreus HD. Chronic atrophic gastritis in population at risk for gastric carcinoma. Anticancer research. [JC : 591] 11(2) : 835-9, 1991 Mar Apr.

Newbold KM. Thompson H. Dykes PW. The effect of routine endoscopy on the detection rate of T1 gastric cancer (early gastric cancer). in Birminglan. Endoscopy [JC : ehp] 21(2): 56-9, 1989 Mar.

Zilling TL. Walther BS. Ahren B. Delay in diagnosis of gastric cancer: a prospective study evaluating doctors and patients delay and its influence on five year survival. Anticancer research [JC : 591] 11(2A): 411-6, 1990 Mar-Apr.

Maruta S. Tsukanok Y. Niva Y. Goto H. et al endoscopic ultrasonography for assessing the horizontal extent of invasive gastric carcinoma

SURGERY - GASTRO-INTESTINAL PROBLEMS

American Journal of Gastroenterology [JC : 3he] 88 (4) : 555-9, 1993 Apr. 10.

Nicholson DA. Shorvon PJ. Review article; Endoscopic ultrasound of the stomach. British journal of radiology [JC : b28] 66(786) : 487-92, 1993 Jun.

11.

Rosch T. Lorenz R. Zenker K. et al. Local staging and assessment of resectability in carcinoma of the oesophagus, stomach and duodenum by endoscopic ultrasonography. Gastrointestinal endoscopy. [JC : fh8] 38(4): 460-7, 1992 Jul, Aug.

12.

Moreno-Otero R. Marron C. Cantero J. Pajares JM. Martmez Raposo A. Endoscopic biopsy and cytology in the diagnosis of malignant gastric ulcers. Diagnostic cytopathology. [JC : eah] 5(4): 366-70, 1989.

13.

Hakim NS. Sarr NG. Van Hearden JA. Does endoscopy really help the surgeon evaluate gastric cancer. Canadian journal of surgery. [JC:cri] 32(3): 175-7, 1989 May.

14.

Elwyn C Cabebe. Vivek K Mebta. Michael C pemy. Gastric cancer emedicine 2007 Jul 23rd.

CARCINOMA OF STOMACH

SUMMARY Carcinoma stomach Incidence Etiology Pathology Spread of tumor Staging Clinical features Investigations Treatment Prognostic features Outcome Follow up

POSSIBLE QUESTIONS 1. 2. 3.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Discuss pathology of carcinoma Stomach? How do you stage carcinoma stomach? What are the prognostic features of carcinoma stomach?

Spleen

SURGERY - GASTRO-INTESTINAL PROBLEMS

SPLENIC TRUAMA

OBJECTIVES ! ! ! ! ! ! !

To understand development, anatomy and physiology of spleen. To understand various diseases of spleen. To understand splenic injuries, their effects and clinical presentations. To assess the injury status (grading) of splenic trauma. To be able to prepare the patient for splenic surgery. To be able to look after the patients after splenic surgery. To be able to prevent, diagnose and treat complications.

SURGERY - GASTRO-INTESTINAL PROBLEMS

SPLENIC TRUAMA

GIT - 10

SPLENIC TRAUMA Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS Rupture of the spleen is an acute surgical emergency. If it is not diagnosed, assessed and managed correctly, the patient may lose his life. It is common in patients with left lower chest injuries. It is common in patients with diseased and enlarged spleen. It is common in males. It is common in younger age group1,2. Children are more susceptible to splenic trauma because spleen is exposed below rib cage and ribs are less ossified. Blunt trauma is responsible for about 90% and penetrating trauma for remaining 10% of splenic injury.

ETIOLOGY Blunt Trauma Road transport accidents Assaults, kicks and sports injuries Crush injuries

! ! !

CLINICAL FEATURES INJURY There is always history of injury. Most of the time the injury is severe and high rate of suspicion is already present. Sometimes the injury may be trivial and injury to spleen may not even be suspected. Injury to left lower chest and fractures of 8th, 9th& 10th ribs are associated with some degree of splenic trauma in about 20% of the patients1,2. PAIN The pain is experienced following injury. Typically the pain is felt in the left hypochondrium and lower chest and other sites of injury. The pain is continuous and gets worse on movements. It is seen in 20% cases of lower left rib fractures.

Penetrating Trauma War injuries Stab injuries Missile injuries

NAUSEA AND VOMITING This is often present in patients with rupture of the spleen and hemoperitoneum.

Operative (Iatrogenic) Trauma The splenic injury occurs following various operations of 3 stomach, aorta, left kidney and colonoscopy . Its incidence has not fallen even after decrease in gastric 2,3 surgery. Careful surgery may decrease the incidence .

SHOCK If the amount of blood loss has been severe or the patient has reported late, patient may be suffering from haemorrhagic shock due to loss of blood intraperitoneally (concealed haemorrhage). These patients may present in different ways as ;

! ! !

Spontaneous Rupture Spontaneous rupture seen in cases of enlarged spleen is usually due to ; ! Infectious mononucleosis ! Leukemia ! Malaria ! Typhoid ! Necrotizing Pancreatitis SURGERY - GASTRO-INTESTINAL PROBLEMS

ACUTE HEMORRHAGIC SHOCK The shock may be so severe that the patient dies before any medical help or resuscitation. TRANSIENTLY COMPENSATED SHOCK Shock may not be severe or the patient may be young and healthy and might get compensated and may suffer from shock again. 91

SPLENIC TRUAMA

DELAYED CASE The patient may recover from initial shock and may not even show any physical sign of rupture of the spleen. This happens in cases of splenic haematoma which does not bleed immediately. ABDOMINAL TENDERNESS AND RIGIDITY This is commonly seen in the patients with rupture of the spleen and hemoperitoneum. This is due to peritonitis.

GRAY TURNER'S SIGN It is positive in patients wiht haemoperitoneum after 24 hours of injury. There is bruising of the lumbar area starting from loin towards the umbilicus. It is because of extravasation of blood into the subcutaneous tissue of that area. 10.02

ABDOMINAL DISTENSION This is also a common feature in these patients. In earlier period, it is due to increasing hemoperitoneum which makes the haemorrhagic shock worse. In later stages, it is due to paralytic ileus following the hemoperitoneum. SHIFTING DULLNESS (BALANCE'S SIGN) Both flanks are dull on percussion due to pressure of blood and peritoneal fluid in the peritoneal cavity. But the dullness shifts from right side on movement while it is present on the left hypochondrium all the time even after moving to the opposite side. CULLEN'S SIGN It is commonly known as abdominal black eye. There is bruising around the umbilicus without any local injury. It is due to extravasation of blood into the subcutaneous tissue around the umbilicus. It is positive in patients with haemoperitoneum after 24 hours of the injury.

Gray Tuner’s Sign KEHR'S SIGN 10.03

10.01

Cullen’s Sign

SURGERY - GASTRO-INTESTINAL PROBLEMS

Kehr’s sign

SPLENIC TRUAMA

The tenderness is present in the left upper abdomen in patients with blunt injury. The pain is also felt at the tip of the left shoulder even when the shoulder has not been injured at all. This is referred pain due to the irritation of left side of the diaphragm due to haemo-peritoneum present there. It is called positive Kehr's sign.

10.04

In suspected cases of hemoperitoneum, if the foot end of the patient's bed is elevated, the patient feels pain at the tip of left shoulder. (Kehr's sign positive)

DIFFERENTIAL DIAGNOSIS It is to be differentiated from other causes of acute abdominal emergencies and concealed haemorrhage such as ; ! Left haemothorax ! Left renal injury Injuries to other intraperitoneal structures such as; Stomach. colon, liver and pancreas. Retroperitoneal injuries

! !

INVESTIGATIONS URINE EXAMINATION Macroscopic and microscopic examination of urine, offers useful information to exclude or include renal injury. Patients with gross or microscopic haematuria and shock may have renal and extra renal abdominal injuries. BLOOD EXAMINATION ! Haemoglobin percentage ! Total leucocyte count ! Differential leucocyte count ! Erythrocyte sedimentation rate ! Urea and electrolytes ! Amylase level ! Calcium level FOCUSED ASSESSMENT SONOGRAPHY IN TRAUMA (FAST) This is a very helpful investigation in suspected cases of ruptured spleen. It is non-invasive and can be performed on the bedside of the patient even if the patient is severely ill. It clearly shows the size and site of rupture of 4 the spleen .

SURGERY - GASTRO-INTESTINAL PROBLEMS

Focused assessment sonography in trauma (FAST)

It also shows the peritoneal fluid if present. It can be very effectively used to monitor the cases of splenic haematoma by serial examinations and measurements of the changes in the size of the splenic haematoma4,5,6. Repeated ultrasound examination during monitoring of the splenic trauma is very helpful. The lesions, not visible on initial examination become visible during subsequent examinations. Ultrasound examination is not accurate enough to predict need for laparotomy. Its diagnostic accuracy varies between 60%-90% depending upon type of the injured organ4,5,6. ABDOMINAL CT SCAN CT scan remains gold standard diagnostic tool for splenic injury. CT scan is an excellent investigation which helps in the diagnosis and grading of splenic trauma. It also helps in the monitoring of the patients treated non-operatively. CT scan has a 100% accuracy in the determination of type and the extent of injury. It is the most sensitive 7,8 diagnostic method for splenic trauma . Most of the splenic injuries are diagnosed with noninvasive methods of investigations confidently. Some of these are minor and don't bleed so much. These can be regularly assessed and monitored with the help of ultrasound scan and CT or MRI scan.

SPLENIC TRUAMA

DIAGNOSTIC PERITONEAL LAVAGE (DPL) The diagnostic peritoneal lavage (DPL) is still used by many surgeons but it is becoming less popular. Diagnostic peritoneal lavage is very accurate in the immediate diagnosis of blunt abdominal trauma. It is still an investigation of choice at many centres6,7,8.

10.05

As the imaging scans are available freely, the peritoneal lavage is progressively being abandoned in favour of ultrasound scan5. Grade II splenic injury (parenchymal laceration 3cm and haematoma <5cm in diameter) free fluid in the peritoneal cavity.

SPLENIC INJURY SCALE Assessment of splenic injury is performed with injury scoring system.

10.06

SPLENIC INJURY SCALE GRADE

Repeat CT scan 48hrs after admission, showing resolving post traumatic changes.

RADIOLOGICAL EXAMINATION X-RAY CHEST It may show fractured lower ribs on the left side X-RAY ABDOMEN Erect and supine views are exposed. X-ray of the abdomen shows following features in the cases of rupture of the spleen. ! Increased splenic shadow. ! Obliteration of the psoas shadow on left side. ! Indentation of the gastric gas shadow ! Raised left hemidiaphragm. ! Sentinel loops of bowel in left hypochondrium.

SURGERY - GASTRO-INTESTINAL PROBLEMS

INJURY

DESCRIPTION

Haematoma Subcapsular, <10% surface area Laceration Capsular tear, <1cm parenchymal depth

Haematoma Subcapsular, 10-50% surface area Intraparenchymal, <5cm diameter Laceration 1-3cm parenchymal depth not involving a parenchymal vessel

III

Haematoma Subcapsular, >50% surface area or expanding Ruptured subcapsular or parenchymal haematoma Intraparencymal haematoma >5cm Laceration >3cm parenchymal depth or involving trabecular vessels

Laceration

Laceration of segmental or hilar vessels producing major devascularization (>25% of spleen)

Laceration Vascular

Completely shattered spleen Hilar vascular injury which devascularized spleen

Advance one grade for multiple injuries to same organ up to Grade III

MANAGEMENT There are following steps in management of splenic trauma; ! Resuscitation ! Assessment of Splenic and Associated Injury ! Definitive Treatment RESUSCITATION The active resuscitative measures are used according to the standard ATLS protocol;

SPLENIC TRUAMA

MANAGEMENT OF SPLENIC TRAUMA SPLENIC INJURY

RESUSCITATION

ASSESSMENT

GADE IV+V INJURY

GADE I-III INJURY

HAEMODYNAMICALLY STABLE

HAEMODYNAMICALLY UNSTABLE

HAEMODYNAMICALLY STABLE

REBLEED

URGENT SPLENECTOMY

NON-OPERATIVE MANAGEMENT (NOM)

RECOVERED

SURGERY - GASTRO-INTESTINAL PROBLEMS

SPLENIC TRUAMA

A. AIR WAY Adequate airway should be secured and maintained. The debris and blood from the oral and tracheo-bronchial passages should be mechanically removed or sucked with the help of an electric sucker. B. BREATHING Breathing problems are seen due to decreased respiratory drive and unstable chest wall. It can be managed with assisted ventilation. The common causes of ineffective ventilation after clear and patent airway are; ! Malposition of endotracheal tube ! Haemothorax ! Pneumothorax C. CIRCULATORY VOLUME Loss of blood may also occur from associated injuries. It should be controlled and stopped as quickly as possible. Bleeding from superficial wounds can be controlled by compression dressing, ligation or stitching of the wound. Internal bleeding requires surgery and control. The lost amount of blood is replaced with blood or other intravenous fluids to keep the circulatory volume as normal as possible. D. DISABILITY The patients with associated brain trauma have various degree of neurological disability. Glasgow coma score should be accurately documented mentioning clearly whether the patient is paralysed or intubated endotracheally. E. EXPOSURE Proper exposure is most important for accurate and complete examination. The patient should be completely exposed after adequate resuscitation for re-examination. It is advisable to perform structured examination so that nothing is missed and it should be ticked on the examination check list. Associated injuries should be documented and treated according to the priority. Continuous monitoring and repeated examination is very important in these patients.

SURGERY - GASTRO-INTESTINAL PROBLEMS

ASSESSMENT OF SPLENIC & ASSOCIATED INJURY The splenic injury must be graded to assess the condition of the patient and to monitor the outcome of the patient. It can be done by using organ injury scaling for the spleen. Following points are kept in mind while deciding about the mode of treatment to be followed. Sub-capsular splenic haematoma is neither a predictor for delayed splenic rupture nor by itself an indication for operative management in the hemo-dynamically stable patient. Degree of parenchymal injury based on CT morphology, specifically hilar involvement signifies the need for laparotomy and splenectomy. Splenorrhaphy has a reduced role in splenic trauma as most of injuries treated surgically are severe9. Splenic injury may not always be an isolated injury. As multiple organs may be involved in the trauma. Injury severity score (ISS) should be performed to plan the management and anticipate the outcome. All major organ injuries are assessed according to the scale. Three highest scores are squared and added. Scores between 25-40 are usually associated with 50% mortality depending upon the age10,11. DEFINITIVE TREATMENT The traditional treatment of splenic injury has been revised in recent years. The splenic salvage is preferred considering the physiologic importance of the spleen. The non-operative management of splenic trauma has been very successful. The definitive treatment for splenic trauma is planned according to ; ! ! !

Trauma score Number of pints of blood transfusion required 11,13 Degree of haemodynamic stability .

SPLENIC TRUAMA

There are following options ; Non operative management Splenic salvage Fibrin glue injection Splenic surgery.

! ! ! !

NON-OPERATIVE MANAGEMENT Non-operative management of blunt splenic trauma is now well recognized. It is comprised of following components; ! Identification of suitable candidate ! Continuous Monitoring and serial assessment ! Splenic artery embolization Following precaution should always be taken in cases of non-operative treatment of splenic trauma; ! The patient should be hospitalized. ! Lost blood should be replaced. ! Antibiotics should be given parenterally. ! Analgesics should be given parenterally. ! Patient should be kept nil by mouth and on parenteral fluid and electrolyte therapy till suitable resuscitation. IDENTIFICATION OF SUITABLE CANDIDATE Maximum efforts are done to preserve the spleen. Injury severity score is done to assess the outcome. Non operative management is preferred in early splenic injuries. It has increased the splenic salvage without increasing morbidity or mortality 7,11,12. Following is recommended criteria for NOM in Splenic Trauma; ! Diagnosis of splenic Injury Grade I-III ! Haemodynamically stable patient ! No diffuse peritoneal signs ! Glasgow coma scale >8 or evidence of no significant head injury ! No other major sources of ongoing blood loss MONITORING AND SERIAL ASSESSMENT It requires a formulated protocol ; ! Rigorous monitoring and resuscitation in the early post trauma period. ! Availability of team ready to under take

SURGERY - GASTRO-INTESTINAL PROBLEMS

! ! ! ! ! ! !

surgery at urgent notice. Monitor hourly vital signs Maintain urine output> 30ml/hr Strict bed rest Nil by mouth and intravenous access Serial haematocrit and haemoglobin 4 hourly for 24-48 h Serial imaging of spleen Antibiotic therapy as a part of conservative therapy11,12.

Minor lacerations of the spleen can be successfully treated by nonoperative treatment for splenic trauma11,13,14,15. SPLENIC ARTERY EMBOLIZATION Embolization of the main splenic artery is an acceptable practice to achieve haemostasis quickly. The role of angiography and embolization in the NOM of patients is still unclear. At present, this technique can only largely be referenced based on young adults. Furthermore, angioembolization as an adjunct to NOM of splenic injury significantly reduced the need for secondary 16 splenectomy (2.7%) . Parameters predicting successful outcome of nonoperative treatment of splenic trauma are ; ! Localized trauma to left flank or abdomen ! Haemodynamic stability ! Blood transfusion requirement less than four pints. ! Rapid return of gastrointestinal functions. ! Age less than 60 years ! Early resolution of splenic defect on CT scanning13,14. The nonoperative management should be abandoned when ; ! The splenic defect star ts expanding on CT scanning or sonography. ! When blood loss is more than four pints. The delayed laparotomy does not increase morbidity or mortality.

SPLENIC TRUAMA

SPLENIC REPAIR (SALVAGE) SPLENORRHAPHY It is a method which has been used more often during last decade. The injured spleen has been repaired or a larger piece of spleen has been salvaged in patients wherever 14,17 possible. These days it is less often required . The splenic salvage is very important to prevent syndrome of overwhelming post splenectomy infection (OPSI). All methods of splenic salvage should be tried except in multiorgan injuries and hemodynamically 17 unstable patients . Splenorrhaphy is performed whenever possible. It is a useful method of treatment4. Splenorrhaphy achieves good results in grade I, II and III splenic injuries. If rebleeding occurs, Laparotomy and splenectomy can be 13 performed at a reoperation . It should be used in 3 properly selected adult patients . It can be safely 14 performed in 65-75% of splenic injuries . FIBRIN GLUE INJECTION Fibrin glue is made with highly concentrated human fibrinogen and clotting factors. It is used to stop the bleeding from injured spleen and may help in its salvage. Fibrin glue can be applied topically in splenic trauma. It is an effective haemostatic agent. It is even more effective when injected intraparenchymally. It is very useful adjunct 18 to surgery in abdominal trauma . SURGERY Early laparotomy should be performed in patients who have higher grade (III, IV and V) of splenic trauma and are hemodynamically unstable. Reinfusion of autologous blood may be done or homologous blood may be transfused. Spleen or a large remnant of spleen may be salvaged if possible11.

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REFERENCES 1. Tariq Mufti. Khalid Khan. Sajjad Ahmad. O p e r a t i v e m a n a ge m e n t o f s p l e n i c trauma. The Professional. Vol 03, No.2. 1996. P: 121-124. 2. SR Shackford. Chest injuries. Essential surgical practice. A Cushieri. GR Giles. AR Moosa 2nd ed. Butter-worth Heinmann international edition London. 1988. p: 280290. 3.

Coon WW. Iatrogenic splenic injur y American journal of surgery. [JC:3z4] 1990 Jun. 159(6): 585-8.

Feliciano DV. Spont Patrinely V. Burch JM. et al. Splenorrhaphy. The alternative. Annals of surgery [JC:67s]1990 May. 211(5): 569-80 discussion 580-2.

Siniluoto TM. Paivansalo MJ. Lanning FP et al. Ultrasonography in traumatic splenic r uptur e. Clinical r adiology. [JC:diu] 1992 Dec. 46(6): 391-6.

Roche BG. Bugmann P. Le Coultre C. Blunt injuries to liver, spleen, kidney and pancreas in paediatric patients. European journal of paediatric surgery. [JC: azo] 1992 Jun. 2(3):154-6.

Do HM. Cronan JJ. CT appearance of splenic injuries managed nonoperatively Ajr. American journal of roentgenology. [JC:3ae] 1991 Oct. 157(4): 757-60.

Frame SB. Browder IW. Lang CK. McSwain NEJR. Computed tomography ver sus diagnostic peritoneal lavage; usefulness in immediate diagnosis of blunt abdominal trauma annals of emergency medicine. [JC:4z7] 1989 May. 18(5): 513-6.

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10.

11.

12.

13.

14.

15.

Black JJ. Sinow RM. Wilson SE. Williams RA. Subca psular haemotoma as a predictor of delayed splenic rupture. American surgeon. [JC:43e]1992 Dec. 58(12):732-5. Nigel R. Webster. Management of the acutely injured and seriously ill patient. Essential surgical practice 3rd ed. A Cuschieri. GR Giles. AR Moosa. Butterworth LONDON 1995.

16.

Edmund Leung, Ling wong and John Taylor Non-operative management for blunt splenic trauma in children. Surgical practice (2007) 11, 29-35 ( C ) 2007.

17.

Lucas CE. Splenic trauma. Choice of management. Annals of surgery. [JC:67s] 1991 Feb. 213(2): 98-112.

18.

Hauser CJ. Haemostasis of solid viscus trauma by intraparanchymal injection of fibrin glue Archives of suregry [JC:8ia] 1989 Mar.124(3) : 291-3.

Williams MD. Young DH. Schiller WR. Trend toward nonoperative management of splenic injuries. American journal fo srugery. [JC:3z4]1990 Dec. 160 (6): 588-92: discussion 592-3. Oller B. Armengol M. Comps I. Rodriguez N. Montero A. Nonoperative management of splenic injuries. American journal surgery [JC:43e]1991 Jul. 57(7) 409-13. Longo WE. Baker CC. McMillen MA et al. Nonoper ative management of adult blunt splenic trauma. Criteria for successful outcome. Annals of surgery. [JC:67S]1989 Nov. 210 (5): 626-9. Pachter HL. Spencer FC. Hofstetter SR et al Experience with selective operative and nonoperative treatment of splenic injr uies in 193 patients. Annals of surgery. [JC:67S] 1990 May. 211 (5): 583-9: discussion 589-91.

SUMMARY Splenic trauma Etiology Clinical features Investigations Management Follow up

POSSIBLE QUESTIONS 1. 2. 3.

What are the causes of splenic Injury? How do you diagnose and grade splenic injury? Outline its management?

Witte CL. Esser MJ. Rappaport WD. Updating the management of salvageable splenic injury. Annals of surgery. [JC:67s]1992 Mar. 215 (3):261- 5.

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SPLENECTOMY

GIT - 11

SPLENECTOMY Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS Splenectomy is the excision of spleen. Its indications are becoming less and less as splenic conservation is preferred if possible and safe. The splenic conservation is preferred because of its significant role in the development and maintenance of immune response.

INDICATIONS FOR SPLENECTOMY RUPTURE OF SPLEEN ! Immediate rupture. ! Delayed rupture. ! Iatrogenic rupture. HYPERSPLENISM ! Primary a. Idiopathic thrombocytopenic purpura b. Haemolytic anaemia I. Hereditary spherocytosis ii. Autoimmune haemolytic anaemia iii. Thalassemia iv. Sickle Cell Disease c. Parasitic infestations i. Leishmaniasis ii. Chronic malaria d. Portal hypertension MECHANICAL ! Massive splenomegaly ! Mobile or wandering spleen NEOPLASIA ! Myeloid metaplasia ! Lymphoma (Hodgkins, non Hodgkins) ! Reticulosarcoma. ! Leukaemia (chronic lymphocytic, chronic granulocytic & Hairy cell) SURGERY - GASTRO-INTESTINAL PROBLEMS

! !

Primary sarcomas Secondary tumours

FACILITATIVE INDICATIONS ! During pancreatectomy. ! During total gastrectomy. ! For the treatment of splenic aneurysms, splenic cysts, splenic Torsion IMMUNO-SUPPRESSIVE Prior to renal transplantation. Portal hypertension. The splenectomy used to be performed when the obstruction was confined to splenic vein in patients with massive splenomegaly and healthy liver. Now-a-days splenectomy is not performed and spleen is conserved. Other surgical procedures such as spleno-renal shunt are preferred. ! !

MISCELLANEOUS ! Tuberculosis ! Abscess

MANAGEMENT RESUSCITATION Resuscitation of the patient is performed in traumatic rupture of the spleen. Adequate intravenous blood transfusion after cross matching should be done to compensate the lost amount of blood. For elective cases of splenectomy, blood should be arranged for use during and after the operation. 101

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All other necessary investigations should be performed before laparotomy so that any other associated pathology is not missed. Ultrasound scan should be performed to diagnose gall stones in haemolytic anaemia patients so that it can be dealt with during the same operation. VACCINATION Vaccination against streptococcus pneumonia, Hemophilus Influenzae type III and Neisseria meningitides should be given to the patients undergoing splenectomy to prevent future infection. This should be given 14 days pre-operatively in elective cases and as soon as possible in cases of emergency. Splenectomy, if possible should be deferred in children because of high risk of infection following this operation. Splenorraphy should be performed.

POSITION Supine position with pillow or sand bag under the left lower chest. The necessary precautions against deep venous-thrombosis should be taken. Pillows can be put under the heels to avoid pressure over calf muscles. Pneumatic bags around calf muscles can also be used to avoid D.V.T during surgery. INCISIONS Different incisions can be used depending upon the size of the patient and choice of the surgeon such as ; !

! !

ANTIBIOTICS Penicillin or other appropriate antibiotics must be given to these patients pre-operatively.

! !

Midline. Extending from xiphi sternum to the umbilicus. It can be extended downwards if required. Left paramedian of about the same length (most preferred incision) Left subcostal (muscle cutting) Left transverse subcostal (muscle cutting) Left thoraco abdominal for massive spleen. 11.01

THROMBOPROPHYLAXIS Necessary precautions against deep vein thrombosis should be taken in this operation as platelets rise after operation and may lead to DVT. ANAESTHESIA ! General endotracheal intubation relaxant anaesthesia is preferred for adequate surgery. ! Local anaesthesia can be used in very rare situations. ! Spinal anaesthesia should preferably be avoided in these patients.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Black : Red: Blue: Green:

Upper mid-line incision Left transverse incision Left paramedian incision Left sub-costal incision

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11.02

11.04

Skin Preparation for Splenectomy (a)

Left Paramedian Incision (b)

11.03

11.05 Superiopr polar a. Short gastric a.

Splenic a.

Left gastroepiploic a. Inferior polar a.

Exposure of Spleen ( c )

SURGERY - GASTRO-INTESTINAL PROBLEMS

Diagrammatic View (d)

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and massive spleens. ELECTIVE SPLENECTOMY LAPAROTOMY When peritoneal cavity is opened and proper laparotomy is performed (liver, gall bladder and other viscera are seen for any abnormalities).

11.06

A search for accessory spleen should be made (it is present in 12% of patients). It lies near the actual spleen. It may be more than one in number. It may be present any where in peritoneal cavity. 11.08

Laparotomy and Exposure PROCEDURE When elective operation is performed for intact and mobile spleen following procedure is adopted. 11.07

Ligation of Short Gastric Vessels MOBILIZATION OF SPLEEN Once the whole situation is assessed, spleen is mobilized. It is done by holding the spleen and pulling it medially, thus stretching the lieno renal ligament. At this stage, the assistant retracts the left costal margin with a deep retractor. Diagrammatic View Slightly different steps are required for ruptured spleen

SURGERY - GASTRO-INTESTINAL PROBLEMS

The stretched lieno renal ligament and splenocolic ligament is breached near the splenic hilum gently by long Mayo's scissors and then incised along its whole length without injuring the vessels.

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between ligatures as it contains blood vessels. Ligature should be applied with care on the gastric side to avoid involvement of the gastric wall.

11.09

11.11

Isolation of Splenic Artery 11.10

Excision of Spleen HILAR DISSECTION Once the spleen is mobilized, splenic vessels are ligated separately and splenic artery is doubly ligated. All these vessels are ligated as near as possible to the splenic hilum to protect the tail of the pancreas from injury. The vessels are divided from splenic side leaving the long pedical to avoid slipping of ligature. Few vasa brevia in gastro splenic ligament may still be holding the spleen. These are ligated and divided.

Ligation of Splenic Artery Then lateral leaf of ligament is brushed more laterally and spleen is pulled gently towards the wound. At this stage, the mobilization is prevented by gastrosplenic ligament at the superior splenic pole. It should be divided

SURGERY - GASTRO-INTESTINAL PROBLEMS

SPLENIC EXCISION Spleen is removed and splenic bed is cleaned with packs. Bleeding from small vessels is stopped by diathermy coagulation or ligation. SEARCH FOR ACCESORY SPLEEN This should be conducted in elective splenectomy. They are present in approximately 12 to 20% of patients. The splenic hilum, gastro splenic ligament, gastro colic

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Fluid intake out put charts are maintained and monitored regularly.

Chest and limb physiotherapy is regularly performed during early post operative period.

SPLENECTOMY FOR RUPTURED SPLEEN It is easier than elective splenectomy. The spleen is usually already mobilized due to its rupture and injury to ligaments of spleen.

Splenectomy is almost always followed by leukocytosis and thrombocytosis which start soon after the operation and reach its peak between seven to fourteen days.

However following precautions should be taken before undertaking this operation. Patient should have a dependable intravenous line and plenty of cross matched blood available. The patient should be reasonably well resuscitated.

Anticoagulants are not required as precautionary measure as there is no rise in the incidence of deep venous thrombosis, or pulmonary embolism after splenectomy.

ligament, greater omentum, mesentry and presacral space are potential sites. Hemostasis is checked and rechecked after few minutes. Drain is left in the left subphrenic area and the wound is closed in layers.

The incision should be longer than for the usual operation. On opening up of the peritoneal cavity, one should suck out the liquid blood and then check the liver for any gross injury. If the liver is not injured and the splenic area is full of clots, one should hold the spleen with one hand. Try to hold the spleen from the hilum with the other hand3. One should remove as many clots as possible very gently. Wet and warm packs should be used to keep the field as less haemorrhagic as possible. The splenic area should be made as clean as possible and anatomical structures should be clearly visible. As lieno renal ligament will be already torn due to injury. The torn spleen will be mobile. The splenic vessels should be ligated near the hilum separately and rest of the operation is completed as previously described. POST OPERATIVE MANAGEMENT ! Nasogastric aspiration should be continued for 45 days to avoid paralytic ileus and acute gastric dilatation. !

Intravenous fluids and electrolytes are given for the first 48-72 hours or till the paralytic ileus is relieved and bowel movements have started.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Low dose aspirin may be used to avoid platelet stickiness and thrombotic disorders.

Penicillin should be given for long periods to avoid sepsis.

COMPLICATIONS ANAESTHETIC All complications of anaesthesia can be seen SURGICAL ! Per operative ! Post operative PER OPERATIVE Haemorrhage (Primary) Injury to the stomach Injury to the pancreas Injury to any other organ accidentally

! ! ! !

POST OPERATIVE ! Paralytic ileus. ! Deep venous thrombosis. The incidence is not higher than other operations. ! Pulmonary embolism. 1 ! Chest infection . 1 ! Wound infection . ! Acute gastric dilatation. ! Sub phrenic abscess.

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! ! !

! !

Pancreatic fistula. Post-splenectomy leukocytosis. White blood cell count is a useful indicator of acute infection in postoperative period2. Increased incidence of infection due to depression of immunological capability. Sepsis syndrome1.

REFERENCES

SUMMARY Splenectomy Indications Pre-operative management Post-operative management Complications

1. Tariq Mufti. Khalid Khan. Sajjad Ahmad. Operative management of splenic trauma. The Professional. 1996 Apr- Jun. 3(2): 121-124. 2. Horowitz J. Leonard D. Smith J. Brotman S. Postsplenectomy leukocytosis. Physiologic or an indicator of infection. American surgeon [JC : 43e] 1992 Jul. 58(7): 387-90. 3. Rappaport WD. Rocrder V. Raid technique for splenectomy injury. Birtish journal of accident surgery. [JC : gon] 1989 May. 20(3): 157-8.

SURGERY - GASTRO-INTESTINAL PROBLEMS

POSSIBLE QUESTIONS 1. 2. 3.

Enumerate indications of splenectomy? What is pre-operative preparation? Enlist post-operative complications?

107

Liver

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109

STOMACH

OBJECTIVES ! ! ! ! !

To understand pathology of hepatic abscess. To understand management of liver abscess. To evaluate infective liver diseases. To be able to evaluate liver trauma. To understand steps of management of liver trauma.

SURGERY - GASTRO-INTESTINAL PROBLEMS

LIVER ABSCESS

GIT - 12

LIVER ABSCESS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS Liver abscess is the collection of purulent material in the liver parenchyma. It is common in tropical areas. The liver abscess can be ; ! ! ! !

Bacterial or pyogenic. Parasitic. Fungal. Mixed.

These include; Bacterial endocarditis Pneumonia Osteomyelitis Urinary tract infection Intravenous drug abuse The cause remains unknown in 15-35% of patients.

! ! ! ! ! !

12.01

Bacterial or Pyogenic liver abscess may be ! Acute ! Chronic

ACUTE PYOGENIC LIVER ABSCESS The pyogenic abscess is more common in temperate climates. Both lobes may be involved but most of the 1 abscesses are present in the right lobe of the liver . Acute pyogenic abscess is usually present at multiple sites. Sometimes these may coalesce to form a single larger abscess. It is commonly associated with biliary or abdominal disease. It is seen in old and malnourished patients. The usual causative organisms are E.coli, Staphylococci, Streptococci and Anaerobic organisms. It follows septicaemia due to following diseases in 45% to 75% of cases ; ! Biliary disease (cholangitis, acute cholecystitis). ! Portal vein pyelophlebitis. ! Hepatic arterial infection. ! Diverticulitis. ! Pancreatitis ! Appendicitis ! Post traumatic (Infected haematoma). ! Direct extension after gall bladder, colonic, gastric or duodenal perforation. ! Miscellaneous. 10% to20% abscesses in liver are due to haematogenous spread from non-gastrointestinal sources. SURGERY - GASTRO-INTESTINAL PROBLEMS

Multiple liver abscesses CHRONIC IDIOPATHIC PYOGENIC LIVER ABSCESS This is usually single and seen in elderly females without any obvious cause. Onset is usually insidious or even silent. It has very high mortality rate (approx' 30% even 1 after adequate treatment) . LIVER ABSCESS DUE TO ACTINOMYCOSIS It usually arises by transport of organisms through portal system or may result from trans-diaphragmatic spread. The abscess burrows and extends widely through the liver and produces multiple sinuses leading to honeycomb appearance of spaces lined by granulation tissue which contains sulfur granules. The organisms can be identified very easily by microscopic examination. 111

LIVER ABSCESS

AMOEBIC LIVER ABSCESS It is caused by Entamoeba histolytica which may present in trophozoite or cyst form. Liver abscess is the most common extra intestinal presentation of infection with Entamoeba histolytica. â&#x20AC;&#x153;It is not the disease but neglect of the remedy which generally destroys life." This saying of Samuel Johnson holds true for this disease affecting all the human spheres of the world2.

The cyst wall is digested by the gastric juice. Amoebic liver abscess is one of the terminal events of amoebic liver disease. It is a complication of amoebic dysentery. 83% of abscesses are seen in right lobe of liver.

INCIDENCE AND EPIDEMIOLOGY ! ! ! !

12.02

! ! !

Amoebic liver abscesses Amoebic liver disease is one of the widely distributed diseases of the tropics leading to severe complications. Amoebic liver abscess is more common in warmer areas. Amoebiasis is the condition of harbouring the parasite, Entamoeba histolytica with or without clinical 9 manifestations . Hepatic amoebiasis is usually secondary to intestinal amoebiasis. The causative agent of hepatic amoebiasis, Entamoeba histolytica is a protozoa belonging to class Rhizopoda, order Amoeba and genus 2 Entamoeba . The vegetative form of Entamoeba histolytica (E.H) is trophozoite form, producing abscess usually in the right lobe of liver. The abscess is commonly single and large but multiple small abscesses may also be seen3. It kills host cells on contact. It is actively phagocytic and may contain red cells and other debris. Host inflammatory response is usually poor. It is very motile in fresh state.

SURGERY - GASTRO-INTESTINAL PROBLEMS

It is more common in younger age group (28-48 years). Male to female ratio is 10:1. It is more common in developing countries. It is most common type of liver abscess in the sub continent. It is solitary in 70% cases. More than one abscess is seen in 30% cases. The most common primary site is colon, caecum or ascending colon followed by sigmoid colon, rectum and appendix. Liver is the most common extra-intestinal site. Lungs and brain are next common extra intestinal sites. Superimposed infection is also seen with E.Coli, Staphylococci and Streptococci in 50% cases.

MODE OF TRANSMISSION Mode of transmission of this disease is feco-oral. Food or drinks contaminated with faeces containing cysts of E.H are ingested. After changing to trophozoite form, E.H infects intestine and liver. Vector transmission is possible commonly through houseflies and cockroaches4. High risk groups are mentally retarded immuno-deficient or 2 malnourished persons .

PATHOLOGY AND PATHOGENESIS The parasite reaches the intestine and infiltrates the colon. It passes from focal lesions in the colonic wall into a radicle of the inferior mesenteric vein. It enters the liver via portal vein. It harbours in the superior and posterior part of the right lobe of the liver. Entamoeba causes liquefactive necrosis in the liver which is proportional to the; ! Size of the colony ! Resistance of the host

112

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Extent of secondary infection The abscess is solitary in 70% of the cases and multiple abscesses are present in 30% cases. The pus is pasty, chocolate colored anchovy sauce like and consists of broken down liver cells, leucocytes and red blood cells. The pus may be greenish due to the presence of the bile. The pus also contains Staphylococci, Streptococci E.coli and Entamoeba. It may burst into the right lung, the peritoneal cavity, the right pleural cavity or rarely any other hollow viscus. Exceptionally, it points out subcutaneously. Sometimes erosion into the lung and expectoration may lead to natural cure. Multiple Amoebic abscesses have very poor prognosis. !

CLINICAL PRESENTATION Commonly the patient with liver abscess (both pyogenic & amoebic) present with; ! Pain in right Hypochondrium ! Fever with/without rigors ! Anorexia ! weight loss ! Right shoulder pain(due to diapragmatic irritation)

! !

Immobilization Test19 Precipitin test10 20

Biochemical tests such as; ! Intradermal test13 ! Passive cutaneous anaphylaxis test13 ULTRASOUND SCAN It is very helpful and a non invasive investigation. It is useful in the diagnosis and follow up of progress of the liver abscess. The abscess can be easily diagnosed, It shows fluid filled lesion in the liver. The lesion may be oval or round in shape. It shows hypoechogenic pattern. The abscess is usually located near the capsule of the liver. Its size can be measured and the site of the abscess becomes obvious. It can be aspirated under ultrasound control16,31. The lesion contains fluid and changes are not specific for amoebic liver abscess21,22. 12.03

On examination these patients are usually pale, weak and lethargic. Associated cholangitis may present with mild jaundice. Other signs of liver abscess include; ! Tender Hepatomegaly ! Reduced air entry in the lower lung zones due to either effusion or consolidation BLOOD EXAMINATION It reveals anaemia, leukocytosis (upto 35,000 per cubic mm of blood2) with eosinophilia and raised sedimentation rate. There is raised concentration of c-reactive protein. 15 Liver function tests may or may not be normal . All the following tests have become history and are no more used since the development of ultrasonography. Serological tests such as; 11 Goldman test 18 Compliment fixation test Indirect haemagglutination test10

! ! !

SURGERY - GASTRO-INTESTINAL PROBLEMS

Liver abscess (sonography) COMPUTED TOMOGRAPHY It offers convenient means for evaluating the development and resolution of the abscess23. Computerized tomography is a very specific investigation to diagnose the site and size of the abscess. It further helps to find out the relationship of the abscess to other important intrahepatic and extra-hepatic structures. It is used as a second line investigation after ultrasonography in complex liver abscesses.

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diaphragm. These radiographs may show a high right dome of diaphragm for right lobe abscess and a crescent 8 deformity of liver for left lobe abscess .

12.04

12.06

Liver abscess (CT scan) 12.05

Liver abscess with gas forming organisms showing gas shadow in upper part of the abscess under right dome of diaphragm

Liver abscess (CT scan) RADIO-ISOTOPE LIVER SCAN It is very rarely performed since the development of ultrasonography and CT scan. These are history and no more used; !

Radio-isotope liver scan shows abscess cavity as well and can help to reach the proper diagnosis.

Scinti-scanning and hepatic photo scan shows a filling defect in the lesion. It was first done by using iodine (I131) labelled Rose Bengal as trace element13.

RADIOLOGICAL FINDINGS X-RAY CHEST This may show consolidation, collapse or even pleural effusion of the right lung. The screening of the chest shows diminished movements of right dome of the

SURGERY - GASTRO-INTESTINAL PROBLEMS

SIGMOIDOSCOPY It may reveal characteristic ulcers and help in the diagnosis of amoebic colitis which may be the actual cause of amoebic liver abscess. ASPIRATION Indications for aspiration include large size and failure of chemotherapy. Exploratory percutaneous puncture is done to confirm diagnosis, assisted by ultrasound or x11 ray . The absolute diagnosis is made by aspiration of the pus of typical chocolate color. TREATMENT (PREVENTIVE) Amoebic dysentery should be treated and liver abscess should not be allowed to form. Amoebic infestation should be prevented by strict cleaning of the eatables and treatment of drinking water. Only uncontaminated fresh fruit, vegetables and water should be used.

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LIVER ABSCESS

PERSONAL PROPHYLAXIS Personal sanitation, use of the boiled water, protection of contamination of food, and safe disposal of the human excreta are crucial factors for prevention25. Restricted use of raw vegetables, that can be disinfected with aqueous solution of 10% acetic acid or vinegar. COMMUNITY LEVEL PROPHYLAXIS Safe water supply by applying iodination should be made 27 possible in high risk areas . Health education about the effects of the disease should be provided to the people. Human excreta should not be used as fertilizers. CURATIVE ! Medical ! Surgical MEDICAL Drugs acting on trophozoites and cysts are ; Metronidazole 750 mg three times a day for 5-10 days is the treatment of choice. I/V preparations are also available 500 mg i/v infusion 8 hourly in adults and 5 mg / kg body weight in children, orally or i/v infusion. Side effects are nausea vomiting, metallic taste, dizziness and discoloration of skin. Burning micturition, neuropathy and epileptic fits on long term therapy may also occur17. 2

Tinidazole 2 gm daily, single dose for three days . Dehydro-emetine, in injectable form can be used. Chloroquine phosphate 300 mg base 12 hourly for two days, followed by 150 mg 12 hourly for 14 days28,29. Iodoquinol with Dehydro emetine for resistant 17 cases and combination is the best . COMBINATION THERAPY Diloxanide furate 250 mg and Metronidazole 200

SURGERY - GASTRO-INTESTINAL PROBLEMS

mg (Entamizole) two tablets three times a day for five days is the treatment of choice30. ! Antibiotics for superimposed infection are also used. SURGICAL (ASPIRATION) Aspiration of the abscess is mandatory. Repeated aspirations may be required for patients with failure of medical therapy. Percutaneous aspiration of the abscess is performed under ultrasound control with percision. DRAINAGE UNDER ULTRASOUND CONTROL / LAPAROSCOPIC DRAINAGE These are preferred methods for the abscesses which lie close to the liver surface. Wide bore drain is left in place after ultrasound guided aspiration or laparoscopically assisted drainage of the abscess. LAPAROTOMY, INCISION AND DRAINAGE At times it is not possible to aspirate the abscess completely because of the thickness of pus or presence of loculi or for technical reasons such as unapproachable site of the abscess. It is reserved in rare cases of secondary infection of abscess cavity8. RESOLUTION The liver abscess may lead to automatic resolution in the beginning if the host resistance is good. Spread of abscess may occur by bursting of the abscess. The abscess may burst into ; ! Right lung ! Peritoneal cavity ! Right pleural cavity ! Pericardium ! Rarely a hollow viscus COMPLICATIONS Following complications are seen with the amoebic liver abscess ; ! Empyema thoracic ! Lung abscess ! Subphrenic abscess

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LIVER ABSCESS

! ! ! ! ! !

Interloop abscess Pelvic abscess. Pericarditis. Bronchopleural fistula. Brain abscess. Renal abscess and pyonephrosis.

Sargeaunt PG. Jackson. Simmee A. Biochemical homogenity of E.H. Isolates especially those from liver abscess. Lancet 1982. P: 1386.

10.

Edward KM. Marieta V. Davi TJ. Medical parasitology. 6th Ed W.B. Saunders. 1986. P: 116-117.

11.

Richear Knight. Parasitic disease in man. 6th edition. ELBS. Company. 1982. 29-32.

12.

Adam. Macload. Invasive amoebiasis. Amoebic liver abscess and its complications. Med 1977. 56: 325-334.

13.

KD Chatterji. A Text Book of Parasitology. 2nd Edition. New Dehli. 1984. P: 15-20.

14.

WHO. Technical Rep. Series. 1963. P:421.

REFERENCES 1.

A Cuschieri. GR Giles. AR Moosa. Essential surgical practice. Third edition. Butterworth Heinermann London. 1995. P: 1139-1174.

Usman Ghani. Khawaja M. Fayyaz. Ammar Ahmad. Amoebic liver disease. The Professional 1996 Jul-Sep. Vol: 3 No. 03 P: 183-191.

Beaver PC. Jung RC. Clinical parasitology. 9th Edition. Lea & Febiger, Phaladelphia. 1984. P: 105-114.

JE Park. A text book of social and preventive medicine. 13th Ed. M/S Banarsidas Bhanot, Jabalpur, India. 1993. P: 163-164.

15.

Marsden PD. Parasitic disease of liver lippencott company, Phaladelphia. 1975. P:1078-1088.

Bull. WHO. 1985. 63(3): 417-426.

16.

Chuah SK. Change Cluieks. Sheen IS. et al. The prognostic factors of severe amoebic liver abscess. A retrospective study of 125 cases. American journal of tropical medicine and Hygiene. 1992 Apr. [JC:3zq] 46(4): 398402.

Maltz G. Knauer CM. Amoebic liver abscess. A 15 years experience. American journal of Gastro enterology. 1991 Jun. [JC:3he] 86(6): 704-10.

17.

Sodeman WA. Beaver PC. A study of therapuetic effects of some of amoebicidal drugs. Am. Jr. Med. 1952. 12:440-446.

Imperato PJ. Conclusions about amoebiasis. Bull NY. Acad. 1980. Med. 57: 240-242.

18.

Knight. An in vitro model for measuring of cytopathic effects of E.H. Jour. of Parasitol. 1977. 63: 388-389.

Sheila Sherlock. Diseases of liver and biliary system. 7th Ed. Blackwell Scientific Publications. 1984. P:455-460.

19.

Je witz. Melnick. Aldelber g. Medical Microbiology, 13thEd. Appleton and Lang:

SURGERY - GASTRO-INTESTINAL PROBLEMS

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20.

1995. P: 327-328. Ravdin JI. Entamoeba hystolytica, from adherance to enteropathy Jour. of infectious diseases. 1989. 159:420.

21.

Griffen J. Jenning C. Owens A. Hepatic amoebic abscess communicating with biliary tree. 1983. Br. J. Rad. 56.

22.

Sepulvida B. Progress in amoebiasis. Scand. Jr of gastroentrology supp. 1982. 77:153164. Mertin. Kirks. Amoebic liver abscess in children the role of diagnostic imaging. Am. Jr. Roentgonal. 1984. 143: 1325-1329.

31.

Nidyaya P. Bibic A. Babic Z. et al. Amoebic liver abscess ultrasonographic characteristics and results of different therapeuitic approaches. Acta medica Iugoslarica. 1991. [JC:10s] 45(1): 15-21,

SUMMARY

23.

24.

Mann CV. Russell CG. Willium NS. Bailey & Love's Short practice of surgery 22 ed. 1995. ELBS. 707-708.

25.

Rajagopalens. Shifffman MA. A guide to sanitary measures for control of enteric diseases. Geneva 1974.

26.

W.H.O. Tech. Rep. Series. 1964.

27.

Khan FH. Visscher. A simple effective method of iodination. West. Jr. Med. 1975. 112: 450-453.

28.

Sodeman WA. Doerner A. Gorden EM. Chloroquine in hepatic amoebiasis. Annual inter Med. 1951. 35:337-341.

29.

Conan NJ. Treatment of hepatic amoebiasis with chloroquine. Bull. N.Y. Acad Med. 1949. 24: 545-546.

30.

Sainani GS. Despande JM. Ind. Practioner. 1979. 32:565.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Liver abscess Acute pyogenic Chronic Amoebic Clinical features Investigations Treatment Complications

POSSIBLE QUESTIONS 1. 2. 3. 4.

What is liver abscess? What are the different types of liver abscess? How will you diagnose liver abscess? What is the treatment of different types of liver abscess?

117

HYDATID CYST

GIT - 13

HYDATID CYST OF LIVER Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS Hydatid cyst is caused by the larval stage of parasite echinococcus granulosus. Rare species of echinococcus are E. multilocularis, E. oligaettas and E. Vogeli. Echinococcus granulosus possibly originated in wolf-deer life in the Northern hemisphere. Now it is present in dogs, sheep and other domestic animals as well. The disease is common in sheep rearing areas. The adult tape worm parasitizes the small gut of dogs. When the dog defecates, proglottids containing eggs contaminates the grass and vegetables. These eggs may be ingested by the sheep through grazing contaminated grass / fodder etc. These develop into larval stage (cyst) within liver and other viscera. The cysts grow in size. The cycle is completed when dog eats the infected sheep.

INCIDENCE Liver is the site of hydatid cyst in 70% of cases . Lung hydatid cyst is next common3. It is more common in Mediterranean, south America, the pacific and temperate zones rearing sheep, pigs and dogs, etc. Greece, Australia, Newzealand, Argentine and Iceland. It is more common in southern Punjab, Baluchistan and 1,2 upper Sindh in Pakistan . LIFE CYCLE AND PATHOGENESIS 13.01

Human beings are incidental intermediate Hosts. Echinococcus granulosus is a few mm long tape worm. It requires two mammalian hosts for its life cycle. It is hermaphrodite. Its life cycle involves sheep and dog as definite hosts.

Ingestion of cyst (in organs) by definitive host (dog) 13.02

Adult tape worm has a series of hooks and suckers at its anterior end and it parasitizes in the jejunum of its definitive host. Each definitive host has thousands of worms in the intestine. The terminal segment of the worm contains upto 1500 eggs. It is passed in the faeces. These eggs are ingested by sheep while grazing on the contaminated area. Human beings become incidental intermediate hosts by ingestion of eggs. SURGERY - GASTRO-INTESTINAL PROBLEMS

Ingestion of eggs from faeces by intermediate host (sheep) 119

HYDATID CYST

13.03

Scolex attaches to intestine Adult in small intestine

Protoscolex from cyst

Ingestion of cysts (in organs)

Definitive Host (dogs & other canidae)

Intermediate Host (sheep, goats, swine, etc.)

Ingestion of eggs (in feces)

Embryonated egg in feces

= infective Stage Hydated cyst in liver, lungs, etc.

= Diagnostic Stage

Oncosphere hatches; penetrates intestinal wall

Life cycle of Echinococcus Granulosis 13.04

13.05

Hydatid cyst SURGERY - GASTRO-INTESTINAL PROBLEMS

Hydatid cyst excised 120

HYDATID CYST

The egg hatches with the digestion of its envelop and oncosphere enters portal circulation or lymphatics. Liver is the most favorite organ. Other organs may also be involved. 70% oncosphere reach the liver and develop into metacystode. Metacystode is cystic and has two layers ; Inner germinal layer Germinal layer is cellular. It is very thin (22-25 Âľm) and it gives rise to brood capsules with scolices. It secretes specific hydatid fluid and forms outer layer.

Outer laminated layer Laminated layer is gelatinous acellular layer 1 mm thick. It is white and elastic.

ENDOCYST Germinal layer and laminated layers form endocyst which can be separated easily from ectocyst. ECTOCYST Host responds with its inflammatory layer formation called ectocyst. The embryo induces active cellular reaction consisting of macrocytes (macrophages), giant cells and eosinophils around the parasite. Many parasites are destroyed by this phagocytic activity. Some escape to develop into hydatid cysts. PERICYST The cellular reaction disappears and new fibrous reaction follows which forms a layer around the growing embryo. This layer is called pericyst. The pericyst may become sclerosed or calcified and parasite within may die or degenerate.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Asexual reproduction occurs in the germinal layer and protoscolices are formed which are released into the cystic fluid to form hydatid sand. Daughter cysts may form in larger cysts. HYDATID FLUID It is colorless or pale yellow. Its specific gravity is 1.005-1.010. Its pH is 6.7 It contains ; ! Sodium chloride ! Sodium sulphate ! Sodium phosphate ! Sodium and calcium salts of succinic acid. It is antigenic It is toxic It contains hydatid sand which consists of liberated brood capsules, free scolices and loose hooklets. The daughter cysts develop inside the mother cyst and arise from germinal layer or from brood capsule. Even grand daughter cysts may develop. The brood capsules develop from germinal layer. It is spherical at first then it becomes vacuolated and transformed into a vesicle. The scolices 5-20 or more develop within these brood capsules.A fully developed scolex represents future head of adult worm with suckers and a circle of hooklets invaginated inside the scolex.

CLINICAL FEATURES ASYMPTOMATIC The patient may be diagnosed accidently and may not have any complaints. ABDOMINAL PAIN The patient may present with upper abdominal

121

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discomfort. Usually the pain is not severe. It is continuous and nagging. It is the most common clinical symptom of this disease.

present with shoulder pain, productive cough and blood stained sputum containing hydatid membranes.

INVESTIGATIONS ABDOMINAL MASS The patient may present with a mass in the upper abdomen, right hypochondrium or anywhere in the abdomen. The mass may be painless or tender. It is the most common sign of this disease. JAUNDICE The patient may present with variable degree of jaundice depending upon the extent of pressure over the biliary passages. It is a relatively less common feature. ASCITES The patient may present with abdominal swelling which is fluid filled. Fluid thrill may be clinically palpable. FEVER AND RIGORS The patient may present with chills and spiking temperature due to secondary infection in the cyst. These may be associated with the tender abdominal mass. ANAPHYLACTIC REACTION Abdominal pain and anaphylactic reaction may be the presenting feature of rupture of hydatid cyst into the peritoneal cavity. BILIARY COLIC It is a rare feature and follows rupture of the hydatid cyst into the biliary passages. It may be associated with jaundice and vomiting hydatid membranes in the vomitus.

URINE EXAMINATION It is a simple investigation for the general assessment of the patient. BLOOD EXAMINATION Hb% TLC DLC ESR Liver function tests. RADIOLOGICAL ! X-ray chest ! X-ray abdomen These show hepatomegaly with raised right dome of diaphragm. Calcified cysts may be seen in 20-40% of patients. ULTRASOUND SCAN It is a noninvasive and very economical investigation. It is easily available. Its specificity and sensitivity to diagnose hydatid cyst is 98%. It can be used to follow up the patient and to monitor the outcome of the treatment. It has high accuracy in detecting the type, size, number and location of the hydatid cyst. It also shows whether these are live (Type I, IR and II) or dead (Type III). Presence of hydatid cyst in peritoneal cavity can also be 7 detected with sonography .

COUGH AND HAEMOPTYSIS Rupture of the hydatid cyst into the thoracic cavity may

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122

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13.06

Ultrasound showing hepatic hydatid cyst CT SCAN 13.07

It is a very sensitive but expensive investigation. It can show daughter cyst within the hydatid cyst. It can show the extent of disease and determine relationship between cyst and adjacent structures. It has been found more sensitive than ultrasonography and conventional radiography in demonstrating the small size (less than 1cm) hydatid cysts. MRI SCAN It is another sensitive but expensive investigation. It is more effective than CT scan in detecting the complications of hydatid cysts. IMMUNOLOGICAL TESTS Immuno electrophoretic test (IEP) Complement fixation test (CFT) Casoni skin test (intradermal test) Indirect haemagglutination test (IHA) Enzyme linked Immunosorbent assay (ELI)

TREATMENT CT scan showing hydatid cyst of liver

! ! !

Medical Percutaneous aspiration & scolicidal injection Surgery

MEDICAL TREATMENT The role of medical treatment should be restricted to unfit and inoperable patients only.

13.08

Mebendazole and albendazole are two drugs specifically used for hydatid cyst but their penetration into the cyst wall is doubtful. The cysts may regress in size but scolices are not killed. These drugs decrease the recurrence rate.

CT scan showing hydatid cyst of liver

SURGERY - GASTRO-INTESTINAL PROBLEMS

Albendazole is more effective and safe. It shows its cysticidial activity within first 2-3 months. It may be used 4,5 as an alternative to surgery 123

HYDATID CYST

PRAZIQUANTEL1,2,3,4 It is an effective scolicidal agent but its effect is more on protoscolices than germinal membrane. Its use should be restricted to prophylaxis against implantation at surgery. It can be used with albendazole. PERCUTANEOUS ASPIRATION AND INJECTION OF SCOLICIDAL DRUGS This procedure remained unpopular because of risk of hydatidosis of the abdominal cavity due to leakage of aspirate. Recently it has gained some acceptance with some modifications. The aspiration and hypertonic saline injection has been tried to avoid spillage and spread of disease. Aspiration of hepatic hydatid cyst and alcoholic 6 injection (95% sterile alcohol ) has been found quite satisfactory in non-invasive treatment of hydatid cyst. SCOLICIDAL AGENTS Injection of scolicidal agents is given into the hydatid cyst to kill scolices in order to prevent recurrence. Various scolicidal agents have been used. ! 20% sodium chloride. ! 10% H2O2 (Hydrogen peroxide). ! 2% formaldehyde. These are minimally helpful and there is larger risk of their accidental entry into the biliary passages and resulting in more damage to those. SURGERY Various procedures have been used depending upon the presentation of disease and condition of the patient. ! Laparotomy and removal of the parasitic elements and management of the residual cavity (marsupialization or closure of the cavity with or without omental packing.

Laparoscopic aspiration of the cyst.

SURGERY - GASTRO-INTESTINAL PROBLEMS

! ! !

Partial hepatectomy with hydatid cysts Wedge resection of liver part containing hydatid cyst. Cystopericystectomy.

LAPAROTOMY AND REMOVAL OF PARASITIC ELEMENTS The cyst may be removed. The marsupialization of large cysts may be done when it is infected and omentoplasty may be done. Marsupialization and external drainage is associated with higher incidence of sepsis and bile leakage. It should be avoided. The residual cavity may be managed by following methods ; ! Capsulorraphy ! Open drainage ! Closed tube drainage ! Capitonnage ! Introflexion ! Omentoplasty LAPAROSCOPIC ASPIRATION Laparoscopy is performed and the cyst is aspirated through the laparoscopic aspiration needle. It is filled with scolicidal solutions. It is reaspirated, refilled and reaspirated. It is a minimally invasive procedure. It is helpful in selected cases. CYSTOPERICYSTECTOMY It is excision of the hydatid cyst by blunt dissection between ectocyst and normal liver. The cyst should not be punctured. It should be completely excised. Fibrous ectocyst may be removed to avoid subsequent biliary leakage. HEPATIC RESECTION It is performed when the cyst is present on one side and

124

HYDATID CYST

partial hepatectomy is technically possible. It is excision of the part of liver containing hydatid cyst. It has minimum complications.

hydatid disease. Australasian radiology. [JC:9iu] 1989 Nov. 33(4) : 373-5.

SUMMARY

REFERENCES 1.

Rathore AH. Manzoor I. Hydatid cyst of spleen. Pak J. Surg. 1986. 1: 206.

Malik MR. Incidence of hydatid cyst in rural district of Pakistan (Dera Ghazi Khan). Unpublished report presented at Alumni meeting at Nishtar Medical College Multan Pakistan, 1982.

Fanto S. Baptist S. Daliana M. Large Echinococcal cyst of the liver with right hepatic lobectomy. Journal of abdominal surgery. 1984. 8:57-63.

Nahmias J. Goldsmith R. Sobelman M. et al. 3-7 years follow up after albendazole treatment of 68 patients with cystic echinococcus. Ann. Trop-Med-parasital.1994. 88(3): 295-304.

De-Rosa F. Stamatakis JD. Stringer MD. et al. Treatment of echinococcus granulosus by hydatid disease with albendazole. Ann tropmed-parasited. 1990. 84(5): 467-72.

Filice C. Pirola F. Bruntti E. et al. A new therapeutic approach for hydatid liver cysts. Aspiration and alcohol injection under sonographic guidance. Gastroentrology. 1990. 98 (5PM): 1366-8. Jain AK. Gupta NC. Gupta PD. Saba Sonographic appearance of hepatic

SURGERY - GASTRO-INTESTINAL PROBLEMS

Hydatid cyst of liver Incidence Lifecycle Clinical features Investigations Treatment

POSSIBLE QUESTIONS 1. 2. 3.

What is hydatid cyst? What is its lifecycle? Give outline of its management.

? 125

LIVER INJURIES

GIT - 14

LIVER TRAUMA Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS

14.01

! ! ! ! ! Grade - 5 liver injury Liver is the largest solid intra abdominal organ. It is most likely to get injured in any kind of abdominal trauma. The effects of liver injury on haemodynamic stability of the patient are very significant. Early and correct assessment helps in the proper management and achievement of better outcome of the treatment. Liver injuries are seen as a part of blunt abdominal trauma, penetrating abdominal trauma, right lower chest injuries as a consequence of road transport accidents, civil terrorism and war injuries.

INCIDENCE AND EPIDEMIOLOGY ! ! ! !

Commonly associated with other injuries in 80% cases. Incidence is getting more common. It is seen following road transport accidents. Mostly blunt injuries are secondary to high speed automobile injuries. It may follow blunt trauma. 60% of blunt trauma leads to these injuries.

SURGERY - GASTRO-INTESTINAL PROBLEMS

! ! ! ! ! ! !

85% of liver injuries are not bleeding at the time of laparotomy. 5-8% of all liver injuries require segmental lobectomy. It is common in old age than in children. 25% injuries are combined thoracic and abdominal trauma. 10% of rib fractures of right lower chest are associated with liver injury. 10% of traumatic deaths are due to failure to diagnose occult abdominal injury during civil life. Overall mortality of liver injuries is about 10% 70%-90% liver injuries are minor in nature. Complex hepatic injuries account for 10-30% of all injuries. Mortality rate of complex hepatic trauma is about 50%. Penetrating trauma is also increasing. 37% of penetrating injuries are liver injuries. Combined thoracic and abdominal injuries are 25% of all penetrating injuries. Bursting type of injuries cause more damage.

ETIOLOGY PENETRATING INJURIES ! Stab wounds 20% ! Gun shot wound 80% BLUNT INJURIES Crush injury Blast injury Seat belt injury

! ! !

IATROGENIC INJURIES Biopsy

127

LIVER INJURIES

! ! ! ! ! !

Laparascopic procedures. Percutaneous transhepatic cholangiography Endoscopic Cardiac massage Peritoneal dialysis Paracentesis

PATHOLOGY The pathological changes are seen depending upon ; Site of injury. ! Size of injury. ! Subcapsular tears. ! Non bleeding lacerations. ! Large fractures. ! Lobar destruction. ! Vascular injuries of liver. ! Acceleration and deceleration injuries. ! Blast trauma. ! Associated injuries. ! Organs involved in injury. ! Duration of injury before treatment. ! General condition of the patient. ! Age of the patient. !

CLINICAL FEATURES HISTORY OF INJURY The time of injury and mechanism of injury should be noted. Site of injury is suggestive of injury to liver or other organs. Blunt abdominal trauma is likely to injure the solid organs. Injury to right upper abdomen and lower chest is commonly associated with injuries to liver. If lower right chest injury is present and right lower ribs are fractured, the chances of liver injury are more. Injuries to the right chest are associated with injuries to the liver because of the anatomical site of the liver. The outcome is poor when multiple organs are involved in the trauma. Many times patients with blunt injury of abdomen present with right hypochondrial mass. It may be abdominal wall

SURGERY - GASTRO-INTESTINAL PROBLEMS

haematoma or liver haematoma. Liver injuries may be isolated. Most of the time these occur in association with injuries to other abdominal viscera as a part of multiorgan trauma. Bony fractures may also be associated with liver injuries. Head injuries may be associated with the liver injuries. The prognosis is poor. There are a number of diagnostic difficulties which are encountered with head injuries. PAIN ABDOMEN The patient complains of continuous pain in the right hypochondrium. The pain may be of variable intensity. The pain gets better on resting. The pain may be referred to the right shoulder. NAUSEA AND VOMITING The patient with the liver injury may present with nausea and vomiting due to haemoperitoneum. It may be present due to paralytic ileus or peritonitis in the later stages. TENDERNESS & REBOUND TENDERNESS The right hypochondrial tenderness is felt on palpation of the area. The tenderness may be of severe degree or palpable on deep palpation. Rebound tenderness may also be present. GUARDING AND RIGIDITY These features may be present even in the minor injuries. SHOCK Palor, low blood pressure, cold skin, ashen gray color, thready and fast pulse, cold sweats are the common features of shock. It may be due to large amount of intraperitoneal concealed haemorrhage. FEATURES OF PERITONITIS Following features are associated with paralytic ileus or bacterial peritonitis in patients with liver injuries ; Silent abdomen ! Distension ! Fluid thrill !

128

LIVER INJURIES

Shifting dullness CULLEN'S SIGN !

It is positive in patients with haemoperitoneum after 24 hours of injury. There is bruising of the lumbar area starting from loin towards the umbilicus. It is because of extravasation of blood into the subcutaneous tissue of that area1.

14.02

INVESTIGATIONS

Cullen’s Sign It is commonly known as abdominal black eye. There is bruising around the umbilicus without any local injury. It is due to extravasation of blood into the subcutaneous tissue around the umbilicus. It is positive in patients with 1 haemoperitoneum after 24 hours of the injury . GRAY TURNER'S SIGN

URINE EXAMINATION ! Macroscopic ! Microscopic ! Biochemical ! Microbiological The urine examination is a simple investigation. It helps to pick up associated renal injuries. It also helps to assess the patient in general. BLOOD EXAMINATION Haemoglobin level is performed immediately and serial haemoglobin level estimations are performed at least twice daily. Progressive decrease is an indication of expanding haematoma. Total leukocyte level Differential leukocyte count Sedimentation rate

14.03

LIVER FUNCTION TESTS Bilirubin level Prothrombin time SGOT SGPT Alkaline phosphatase level Amylase level X-RAY ABDOMEN Erect and supine films are exposed to see the Psoas shadow obliteration, gas shadow under the diaphragm 2 (pneumoperitoneum), sentinal loops over the area .

Gray Turner’s Sign

SURGERY - GASTRO-INTESTINAL PROBLEMS

X-RAY CHEST It is performed to see the haemopneumothorax,

129

LIVER INJURIES

diaphragmatic hernia and rib fractures if present. FAST (FOCUSED ASSESSMENT SONOGRAPHY IN TRAUMA) 14.04

6,7

type of the injured organ . Sonography performed by emergency surgeons achieves 81.5% sensitivity and 99.7% specificity. It seems as if it will replace CT in future as a first line investigation in the management of blunt injury of abdomen. Ultrasonography has almost replaced diagnostic peritoneal lavage (DPL) as a diagnostic study of first choice in blunt injury of abdomen8.

Focused assessment sonography in trauma (FAST) It is a simple and easily available investigation with high degree of sensitivity and specificity. It is used to see the hemoperitoneum, to see hematoma and the solid organ architecture. It is reliable in detecting intra-abdominal solid organ injuries and retroperitoneal injuries. This is a very helpful investigation in suspected cases of ruptured liver. It is non invasive and can be performed on the bedside of the patient even if the patient is severely ill. It clearly shows the size and site of rupture of the liver. It also shows the peritoneal fluid if present. It can be very effectively used to monitor the cases of hepatic haematoma by serial examinations and measurements of the changes in the size of the hepatic haematoma. It is a 3,4,5,6,7 versatile and cost affective investigation . Repeated ultrasound examination during monitoring of the hepatic trauma is very helpful. The lesions, not visible on initial examination become visible during subsequent examination. Ultrasound examination is accurate enough to predict need for laparotomy in 76.9% cases. Its diagnostic accuracy varies between 60%-90% depending upon

SURGERY - GASTRO-INTESTINAL PROBLEMS

CT SCAN MRI SCAN CT scan is an excellent investigation which helps in the diagnosis and grading of liver trauma. It also helps in the 8,9 monitoring of the patients treated non-operatively . CT scan can demonstrate the haemostasis and healing of injured liver. It can pick up the enteric, diaphragmatic and retroperitoneal injuries as well. It can quantitate haemoperitoneum10. CT scan has a 100% accuracy in the determination of type and the extent of injury. It is the most sensitive diagnostic method for liver trauma. Most of the liver injuries are diagnosed with non-invasive methods of investigations confidently. Some of these are minor and don't bleed so much. These can be regularly assessed and monitored with the help of ultrasound scan, CT or MRI scan. It is the single greatest contributing factor allowing the non-operative management of hepatic injuries. PERITONEAL TAP, FOUR QUADRANT PERITONEAL ASPIRATIONS DIAGNOSTIC PERITONEAL LAVAGE (DPL) These are different methods of detecting the hemoperitoneum. The first two are less often used nowa-days as these are invasive and do not confirm the diagnosis.

130

LIVER INJURIES

14.05

14.08

Liver Injury - grade 1 (CT scan)

Liver-laceration (Liver trauma)

14.06

14.09

Liver Injury - grade 2 (CT scan)

Grade 2 intra-parenchymal liver injury (CT scan)

14.07

14.10

Liver trauma - grade 3 (ultrasound scan)

SURGERY - GASTRO-INTESTINAL PROBLEMS

Liver trauma - grade 3

131

LIVER INJURIES

The peritoneal lavage is progressively being abandoned in favour of ultrasound scan as the imaging scans are available freely. The role of DPL has diminished due to development of sonography and CT scanning. Its accuracy rate is 98% in detecting haemoperitoneum. It has following drawbacks ; ! It lacks specificity as to which organ system has injured. ! It is too sensitive in detecting minute quantities of blood which may lead to non-therapeutic laparotomies. ! It is inaccurate in detecting retroperitoneal and diaphragmatic injuries10,17. Diagnostic peritoneal lavage is very accurate in the immediate diagnosis of blunt abdominal trauma. it is still an investigation of choice at many centres but it is getting less popular8.

TREATMENT The objectives of the treatment are ; Resuscitation Diagnosis Assessment of the injury and patient. Definitive treatment. Standard ABCDE plan is followed as the liver injury is associated with other injuries as well.

! ! ! !

RESUSCITATION The active resuscitative measures are used according to the standard trauma management plan such as ; A. AIR WAY Adequate airway should be secured. The debris and blood from the oral and tracheo-bronchial passages should be mechanically removed or sucked with the help of an electric sucker. The airway should be maintained and breathing of patient should be assessed and maintained. Endotracheal intubation or tracheostomy will ensure clear airway. SURGERY - GASTRO-INTESTINAL PROBLEMS

Assisted ventilatory support should be offered if required. B. BREATHING Breathing problems are seen due to decreased respiratory drive and unstable chest wall. It can be managed with assisted ventilation. The common causes of ineffective ventilation after clear and patent airway are; ! Malposition of endotracheal tube ! Haemothorax ! Pneumothorax These can be properly managed after correct diagnosis. C. CIRCULATION Circulatory support must be started as soon as the patient is received. The blood should be replaced as quickly as possible. Pulse, blood pressure and central venous pressure are good guides for the adequate blood replacement and monitoring the patient. Loss of blood may also occur from associated injuries. It should be controlled and stopped as quickly as possible. Bleeding from superficial wounds can be controlled by compression dressing, ligation or stitching of the wound. Internal bleeding requires surgery and control. The lost amount of blood is replaced with blood or other intravenous fluids to keep the circulatory volume as normal as possible. The hypothermia during the pre-treatment period may lead to catastrophic effects on outcome of treatment. The hypothermia may exacerbate operation room blood loss independent of degree of physiologic or anatomic injury. Trauma scores and presence of shock correlates with the development of intra-operative hypothermia. Hypothermic patients with similar injury severity score have greater blood loss. Its prevention and correction during resuscitation is most important in reducing the 11 blood loss . Simple procedures such as covering the patient with

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blankets, infusing warm fluids or blood and irrigating peritoneal cavity with warm saline helps to improve the 10 general condition . Regular and careful monitoring of the circulatory volume is done by measurement of pulse and blood pressure record, skin perfusion and calculating urinary output. Fresh blood should be transfused in these patients. Fresh frozen plasma and platelet concentrates should be transfused as well. Acid base balance should also be maintained as these patients develop metabolic acidosis which gets worse by repeated blood transfusions. Sodium bicarbonate should be given intravenously slowly to treat the metabolic acidosis. D. DISABILITY The patients with associated brain trauma have various degree of neurological disability. Glasgow coma score should be accurately documented mentioning clearly whether the patient is paralysed or intubated endotracheally. E. EXPOSURE Proper exposure is most important for accurate and complete examination. The patient should be completely exposed after adequate resuscitation for re-examination. STRUCTURED EXAMINATION It is advisable to perform structured examination so that nothing is missed and it should be marked on the examination check list.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Associated injuries should be documented and treated according to the priority. Regular and careful monitoring of the circulatory volume is done by measurement of pulse and blood pressure record, skin perfusion and by calculating urinary output. ASSESSMENT OF INJURY AND PATIENT INJURY SEVERITY SCORE12 Major organ system injury

Score

Minor

Moderate

Severe but not life threatening

Life threatening but survival probable

Survival not probable

Fatal CVS and neurosurgical injuries

Multiorgan trauma is assessed using injury severity score(ISS). Liver injury may not always be an isolated injury. As multiple organ may be involved in the trauma. Injury severity score (ISS) should be performed to plan the management and anticipate the outcome. All major organ injuries are assessed according to the scale. Three highest scores are squared and added. Scores between 25-40 are usually associated with 50% mortality depending upon the age12. 13

LIVER INJURY SCALE The general assessment of the patient with multiple injuries is performed by meticulous clinical examination and injury severity scoring. It helps to assess the overall condition of the patient and to predict the outcome of the treatment.

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The isolated liver injury is assessed by liver injury scale. It helps in uniform audit of various treatment modalities and prediction of the outcome of the treatment.

14.12

LIVER INJURY SCALE Grade

Injury Description

AIS-90

Hematoma

Subcapsular,<10% surface area

Laceration

Capsular tear, <1 cm parenchymal depth

Hematoma

Subcapsular, 10%-50% surface area: Intraparenchymal <10 cm in diameter

Laceration

Capsular tear, 1-3 cm parenchymal depth, <10 cm in length

Hematoma

Subcapsular, >50% surface area or expanding : Ruptured subcapsular or parenchymal hematoma : Intraparenchymal hematoma >10 cm or expanding

Laceration

>3 cm parenchymal depth

Laceration

Parenchymal disruption involving 25%75% of hepatic lobe or 1-3 couinaud's segments within single lobe

Laceration

Parenchymal disruption involving >75% of hepatic lobe or >3 couinaud's segments within a single lobe

Vascular

Juxtahepatic venous injuries i.e. retrohepatic vena cava / central major hepatic veins

Vascular

Hepatic avulsion

* Advance one grade for multiple injuries up to grade III.

Grade - 3 liver injury DEFINITIVE TREATMENT The outcome of treatment has improved during recent years. The mortality rate of liver injuries of grade III & IV has been brought to nearly under 10% during the last decade. It has been helped by following factors ; ! Influence of CT scanning on the non-operative treatment of adult blunt hepatic trauma. ! Pringle maneuver (portal triad occlusion). ! Topical hypothermia isolated to liver only. ! Hepatorrhaphy with intrahepatic haemostasis. ! Perihepatic packing and planned re-exploration as a part of damage control. The surgery is terminated under circumstances of haemodynamic instability and coagulopathy. ! Management of juxtahepatic venous injuries with or without intracaval shunts.

14.11

After initial successful resuscitation, decision is made to choose the mode of treatment. Patients who remain hemodynamically unstable after 4 pints of blood transfusion or fluid (after excluding the blood loss and replacement for associated injuries) require urgent surgical intervention.

Grade - 1 liver injury

SURGERY - GASTRO-INTESTINAL PROBLEMS

Following modalities of treatment are commonly used for complex hepatic injuries ; ! Non-operative management

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! !

Fibrin glue Operative management

NON OPERATIVE MANAGEMENT CRITERIA The patients are selected for non operative management according to the following criteria ; ! Haemodynamic stability ! CT scan delineation of the injury ! Lack of associated enteric and retroperitoneal injuries ! Absence of peritoneal signs. Limited number of hepatic related transfusions ! during resuscitation and observation period. The treatment for suspected liver injuries used to be immediate laparotomy in patients who had positive peritoneal signs and who were haemodynamically unstable. The patients who used to be haemodynamically stable, diagnostic peritoneal lavage (DPL) was done and surgery was performed if it was positive. Trauma grading was not done. A very significant observation was noted that majority of patients 67% with blunt abdominal trauma and liver injuries were not actually bleeding actively when laparotomy was done. The non operative management of liver trauma was restricted to only grade I -III during last decade. Now-adays grade IV-V are also being managed non-operatively under CT control (repeated CT monitoring). Following problems may be faced while undertaking nonoperative management of blunt hepatic trauma. These should be kept in mind and should be avoided ; ASSOCIATED INTRA-ABDOMINAL INJURIES 14 Its incidence is about 5% with isolated hepatic injuries . Repeated clinical assessment of patient and CT imaging helps to pick up the initially missed injuries. The management can be altered accordingly.

SURGERY - GASTRO-INTESTINAL PROBLEMS

HAEMORRHAGE It is usually diagnosed on clinical examination. The only differentiation is to be made whether it is hepatic related or from other injuries. Haemodynamic instability is indicative of ongoing haemorrhage and it warrants early surgical intervention. Failure to embolize the bleeding vessel is also an indication for early surgical intervention. Following errors should be avoided; !

The bleeding should not be attributed to nonhepatic related causes without CT scan verification.

Excessive hepatic-related-blood transfusions should not be preferred to surgical intervention.

The pooling of contrast material noted during initial scanning should not be under estimated even when patient is haemodynamically stable and grade of liver trauma is II or less.

BILE COLLECTION AND ABSCESSES Intrahepatic and perihepatic collection of bile (Bilomas) occurs in about 0.5%-20% cases15. FOLLOW UP AFTER NON-OPERATIVE MANAGEMENT Patient is advised to refrain from vigorous activities to avoid possibility of haemorrhage for 3-6 months. Liver injuries usually take 3-4 times in healing and restoration of normal architecture. The bursting strength of healing liver is near normal or better within three weeks of injury. Successful non-operative management of the liver injuries after blunt abdominal trauma has been carried out in about 50%-82% cases during recent years10. FIBRIN GLUE INJECTION Fibrin glue is made with highly concentrated human fibrinogen and clotting factors. It is used to stop the

135

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bleeding from injured liver and may help in its salvage. Fibrin glue can be applied topically in hepatic trauma. It is an effective haemostatic agent. It is even more effective when injected intraparenchymally. It is very useful adjunct 16 to surgery in abdominal trauma . Following precautions should always be taken in cases of non-operative treatment of hepatic trauma; ! The patient should be hospitalized. ! Lost blood should be replaced. ! Antibiotics should be given parenterally. ! Analgesics should be given parenterally.

to have adequate exposure. Intra operative resuscitation is carried out. Complex hepatic injuries grade III and IV are managed by following orderly steps ; ! Portal triad occlusion (Pringle maneuver) ! Finger fracture of hepatic parenchyma (hepatotomy) to expose hepatic vessels and ducts for repair or ligation. ! Debridement of non-viable hepatic tissue. ! Insertion of viable omental pedicle into injury site (omentoplasty). ! Closed suction drainage for grade III and IV hepatic injuries10. 14.14

Patient should be kept nil by mouth and on parenteral fluid and electrolyte therapy till suitable resuscitation. OPERATIVE MANAGEMENT OF COMPLEX HEPATIC INJURIES 14.13

Grade - 5 liver injury PORTAL TRIAD OCCLUSION (Pringle maneuver) It is performed with atraumatic vascular clamp and it can keep the bleeding under control during surgery. It may be required in nearly 72% of complex hepatic injury patients. Grade 4 liver injury from a right thoracoabdominal gunshot wound Following surgical procedures are carried out ; Laparotomy and hepatorrhaphy. Partial hepatectomy or segmental resection. Omental pack or omentoplasty. Perihepatic packing

! ! ! !

A long midline incision is used to open the abdomen and

SURGERY - GASTRO-INTESTINAL PROBLEMS

The occlusion of hepatic vessels may cause hepatic Ischaemia. The liver can tolerate normothermic ischaemia for 90 minutes. The occlusion should be kept 10 for lesser period . HEPATORRHAPHY It is a suitable procedure for grade III to V complex hepatic injuries. The vessels and ducts are repaired under vision. It can be performed after pringle maneuver.

136

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Absorbable meshwrapping of burst hepatic injuries containing viable parenchymal fragments is done. VIABLE OMENTAL PACK Once the bleeding has been controlled, intrahepatic and perihepatic sepsis is most common complication. It can be avoided by doing adequate debridement and omentoplasty and drainage10. PERIHEPATIC PACKING It may be required in 4-5% of all cases undergoing operative management. Its indications are ; ! Onset of intra-operative coagulopathy. ! Failure of other maneuvers to control bleeding. ! Presence of bilobar injuries. DRAINAGE Closed drainage should be used for grade III to V injuries and lesser grade injuries may be left undrained. It will keep the sepsis rate to minimum.

63. 3.

Akgur FM. Tanyel FC. Akhan O. et al. The place of ultrasonographic examination in the initial evaluation of children sustaining blunt abdominal tr auma. Journal of Pediatric surgery. [JC:jmj] 1993 Jan. 28(1): 78-81.

Rozycki GS. Ochsner MG. Jaffin JH. Champian HR. Prospective evaluation of surgeons use of ultrasound in the evaluation trauma patients. Journal of trauma. [JC:kaf]1993 Apr. 34(4): 516-26: discussion 526-7.

Luke FI. Lemire A. St-Vil D. et al. Blunt abdominal tr auma in children. The pr actical value of ultr asonogr aphy. Journal of trauma. [JC:kaf]1993 May. 34(5): 607-10: discussion. 610-1.

Kimwa A. Otsuka T. Emergency centre ultrasonography in the evaluation of haemoperitoneum: A prospective study. Journal of trauma. [JC:kaf] 1991 Jan.31(1).

Roche BG. Bugmann P. Le Coultre C. Blunt injuries to liver, spleen, kidney and pancreas in paediatric patients. European journal of paediatric surgery. [JC: azo] 1992 Jun. 2(3):154-6.

Kearning PA Jr. Vahey T. Burney RE. Glazer G. Computed tomography and diagnostic peritoneal lavage in blunt abdominal trauma. Their combined role. Archives of surgery [JC:8ia]1989 Mar. 124(3): 344-7.

Frame SB. Browder IW. Lang CK. McSwain NEJR. Computed tomography ver sus

COMPLICATIONS ! ! ! ! ! ! ! !

Pulmonary complications Coagulopathies Hypoglycemia Jaundice Biliary fistulas Haemobilia Sub diaphragmatic Abscesses. Disseminated intravascular coagulopathy.

(Most important factor is hypothermia and inadequate blood component replacement).

REFERENCES 1.

Shuja Tahir. Mahnaz Roohi. Zahid Yasin Hashmi. Surgery Clinical Examination System. 3rd Edition. Uro-Obs (Pvt) Ltd. Faisalabad, Pakistan. 1992. P: 115-116.

Shuja Tahir. Mahnaz Roohi. Muhammad Saeed. Surgery Investigations. Uro-Obs (Pvt) Ltd. Faisalabad, Pakistan. 1995. P:61-

SURGERY - GASTRO-INTESTINAL PROBLEMS

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diagnostic peritoneal lavage; usefulness in immediate diagnosis of blunt abdominal trauma. annals of emergency medicine. [JC:4z7] 1989 May.18(5): 513-6. 10.

11.

17.

H Leon Pachter. David V. Feliciano. Complex hepatic injuries. Surgical clinics of North America. Aug 1996. p 763-782, Vol 76 No. 4. Bernakei AF. Levision MA. Bender JS. The effects of hypothermia and injury severity on blood loss during trauma laparotomy. Journal of trauma. [JC:kaf]1992 Dec. 33(6): 835-9.

12.

Nigel R. Webster. Management of the acutely injured and seriously ill patient. Essential surgical practice 3rd ed. A Cuschieri. GR Giles. AR Moosa. Butterworth LONDON 1995.

13.

Earnest E Moore. Thomas H Coghill. Mark A Malangoni et al. Organ injury scaling. Surgical clinics of North America Vol: 75 No.12 1995 Apr. p: 293-303.

14.

Buckman RF. Piano G. Durham CM. et al. Major bowel and diaphragmatic injuries associated with blunt spleen or liver rupture. J. Trauma. 28:1317, 1988.

15.

Croce MA. Fabian TC. Menke PG. et al. Non-operative management of blunt hepatic trauma is the treatment of choice for haemodynamically stable patients. Results of a prospective trial. Annals of surgery. 221-744, 1995.

16.

Hauser CJ. Haemostasis of solid viscus trauma by intraparanchymal injection of

SURGERY - GASTRO-INTESTINAL PROBLEMS

fibrin glue. Archives of suregry [JC:8ia] 1989 Mar. 124(3) : 291-3. Visvanathan R. Low HC. Blunt abdominal trauma-injury assessment in relation to early surgery. Journal of the Royal College of Surgeons of Edinburgh. [JC:jvc]1993 Feb. 38(1):19-22.

SUMMARY Liver injury Incidence Etiology Pathology Clinical features Investigations Treatment Complications

POSSIBLE QUESTIONS 1. 2. 3. 4.

Discuss diagnosis of liver injury? How do you grade liver injuries? What is the non-operative management of liver trauma? What are the different surgical options to deal with hepatic trauma?

138

GallBladder

SURGERY - GASTRO-INTESTINAL PROBLEMS

139

ACUTE CHOLECYSTITIS

OBJECTIVES ! ! ! ! ! !

To understand development, its variations, anatomy and physiology of gall bladder. To be able to understand basis of various investigations used for the diagnosis of gall bladder diseases. To be able to prepare the patient for surgery. To be able to plan the type of gall bladder surgery. To be able to look after the patient after surgery. To be able to prevent and treat post surgical complications.

SURGERY - GASTRO-INTESTINAL PROBLEMS

140

ACUTE CHOLECYSTITIS

GIT - 15

ACUTE CHOLECYSTITIS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS attack and continue throughout the illness. The vomiting makes the pain even worse. It is usually because of pylorospasm.

15.01

PYREXIA It is almost always present. Sometimes 38 degrees centigrade or even higher degrees are associated with rigors. This happens specially in fulminating cases. Inflamed gall bladder seen with naked eye Acute cholecystitis is the acute inflammation of the gall bladder and it presents as an emergency with upper abdominal pain, fever and vomiting. The onset of the symptoms may be sudden or gradual.

CLINICAL FEATURES PAIN It is severe, agonizing and of sudden onset lasting for more than 12hrs. It is located in the right hypochondrium and radiates to the back in between the shoulder blades. The pain may be felt in the epigastrium. It may be continuous and progressive with the progress in the disease process. The pain may be colicky in nature and it may be worse in post-prandial period in obstructive cholecystitis.

JAUNDICE It may be present due to inflammation of the biliary passages. Cholangitis is associated in 20-25% of the patients. Obstructive jaundice may also be associated with acute cholecystitis. Bile duct stones are present in 23% of the patients with acute cholecystitis. ABDOMINAL DISTENSION Mild abdominal distension is seen in severe cases of acute cholecystitis. TENDERNESS AND RIGIDITY It is present in the right hypochondrium. MURPHY'S SIGN 15.02

Acute cholecystitis is obstructive in nature in 95% of cases due to impaction of stone in the Hartmann's pouch 1 or cystic duct . The pain may occur during night always at 2 about same time . NAUSEA AND VOMITING These symptoms are present earlier during the

SURGERY - GASTRO-INTESTINAL PROBLEMS

Murphyâ&#x20AC;&#x2122;s Sign 141

ACUTE CHOLECYSTITIS

It is inspiratory arrest during gross palpation of the right subcostal region due to pain. It is positive in acute cholecystitis3. BOAS' SIGN It is the presence of area of hyperaesthesia below the tip of right scapula and opposite T11, T12 and L1 vertebrae in the posterior axillary line3. 15.03

! ! !

the type of jaundice Screening for Hepatitis B & C Clotting profile is advisable in cases of jaundice Urea and electrolytes: may be disturbed due to vomiting and dehydration.

ULTRASOUND SCAN Th diagnosis is usually confirmed by ultrasonography. The diagnostic characteristics are ; ! Thick walled (>3mm) gall bladder ! Distended gall bladder with/without stones in cases of acalculous cholecystitis ! Pericholecystic fluid ! Murphyâ&#x20AC;&#x2122;s sign elicited by ultrasound probe.

15.04

Boas Sign (red area represents area of hyperaesthesia)

MASS UPPER ABDOMEN A tender palpable mass of variable size is present in the right hypochondrium and subcostal area. It is present in 25% of the patients. It indicates following complications of acute cholecystitis ; ! Mass formation due to omental adhesions along inflammed gall bladder. ! Empyema of gall bladder. ! Perforation and local abscess formation. ! Carcinoma gall bladder associated with acute inflammation. BLOOD EXAMINATION Haemoglobin estimation Total leucocyte count (leucocytosis) Differential leucocyte count (polymorphs are Increased) ! Sedimentation rate (raised) ! Liver function tests done to rule out associated Hepatic pathology and in case of Jaundice to define

Acute cholecystitis with gallstone

15.05

! ! !

SURGERY - GASTRO-INTESTINAL PROBLEMS

Inflammed gallbladder with pericholecystic fluid (white arrow)

142

ACUTE CHOLECYSTITIS

Acute Cholecystitis

Hospital admission Supportive care Antibiotics

Determine Surgical risk

Low risk (ASA I,II)

Clinical Improvement

Delayed Cholecystecomy after 6 weeks

Early Cholecystectomy with in 24 hours

Clinical deterioration

Emergency Cholecystectomy

High risk (ASA III-V)

Clinical Improvement

Clinical deterioration

Discharge

Percutaneous Cholecystostomy

Delayed Cholecystectomy

SURGERY - GASTRO-INTESTINAL PROBLEMS

143

ACUTE CHOLECYSTITIS

RADIOLOGICAL EXAMINATION X-ray of the chest and abdomen (plain). These help in the diagnosis of radio opaque gall stones and chest lesions (pneumonia and pleural effusion). Oral cholecystogram is not performed during acute attack of cholecystitis. In fact this investigation is no more performed for any indication.

CT SCAN CT scan is extremely helpful in the diagnosis of acute cholecystitis. It is available at most of the places. 15.08

ULTRASOUND SCAN It is the best investigation during acute cho-lecystitis as it helps to confirm the diagnosis immediately and it is not invasive at all. 15.06

CT Scan showing inflamed gall bladder

DIFFERENTIAL DIAGNOSIS

Ultrasound scan showing inflamed gall bladder

15.07

This condition is to be differentiated from all causes of acute abdomen and certain chest lesions such as ; ! Acute appendicitis. (specially high and retrocaecal) ! Perforated duodenal ulcer ! Acute pancreatitis. ! Acute pyelonephritis on right side. ! Acute coronary thrombosis (Inferior wall ischemia) ! Right basal pneumonia.

TREATMENT Acute cholecystitis is a surgical emergency and requires treatment which is initially conservative and followed by definitive surgical treatment.

Ultrasound scan showing inflamed gall bladder

SURGERY - GASTRO-INTESTINAL PROBLEMS

CONSERVATIVE Most patients respond to conservative treatment. More than 90 % of patients get satisfactory relief from acute attack of cholecystitis with the following conservative

144

ACUTE CHOLECYSTITIS

regimen : ! Nil by mouth and NG aspiration ! Fluid and Electrolyte replacement ! Parenteral Analgesia ! Parenteral Antibiotic

15.09

NIL BY MOUTH AND NG ASPIRATION Rest to the gall bladder and biliary passages is provided by stopping oral intake. It is further offered to upper gastrointestinal track by nasogastric aspiration. Inflammed gall bladder seen at laparotomy FLUIDS AND ELECTROLYTES Fluids and electrolytes are given intravenously or in less severe cases, oral fluids may be permitted.

15.10

PARENTERAL ANALGESICS: Parenteral analgesia is given to make the patients pain free. NSAIDS in mild and moderate cases. Narcotic analgesia is recommended in severe pain. ANTIBIOTICS Quinolones, penicillins and appropriate antibiotics (cepha-losporins) to cover gram negative gut organism, are used parenterally or orally. Diabetics are prone to gangrenous cholecystitis. Anaerobic cover should be provided to them (e.g. metronidazole). SURGICAL Conservative management is followed by definitive surgical removal of gall bladder. It can be either laparoscopic or open depending upon the choice of surgeon and facilities available. The timing of surgery is of crucial importance. EARLY CHOLECYSTECTOMY This is removal of gall bladder within 24 to 48 hours of acute episode. It is the preferred timing for surgery in patients who have responded to conservative measures.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Inflammed gall bladder with stone DELAYED CHOLECYSTECTOMY Six to twelve week after the relief of acute episode, delayed cholecystectomy is performed. URGENT CHOLECYSTECTOMY This is an emergency procedure indicated in following conditions; ! Failed response to conservative measures ! Generalized peritonitis ! Diabetic patients Cholecystectomy can be performed through open surgery or laparoscopic surgery depending upon expertise available. If signs of peritonitis develop or the patient fails to get relief after conservative management. Cholecystectomy is considered as early as possible.

145

ACUTE CHOLECYSTITIS

COMPLICATIONS ! ! ! ! ! !

Empyema of the gall bladder. Gangrene of the gall bladder. Gas gangrene. Local abscess formation. Perforation and peritonitis. Internal fistula formation. Chronic cholecystitis.

REFERENCES

SUMMARY Acute cholecystitis Clinical features Investigations Differential diagnosis Treatment Complications Follow up

1. A Cuschieri. GR Giles. AR Moossa. Essential surgical practice third edition. Butterworth Heineman. 1995. p:1175-1237. 2. Tranerso LW. Clinical manifestation and impact of gall stone disease. American journal of surgery. [JC:3z4]1993 Apr. 165(4): 405-9. 3. Shuja Tahir. Mahnaaz Roohi. Zahid Yasin Hashmi. Surgery clinical examination system third edition. URO-OBS (Pvt) LTD. 1992 Dec. p: 131-133.

POSSIBLE QUESTIONS 1. 2. 3.

Discuss diagnosis of acute Cholecystitis? Discuss treatment options for acute cholecystitis? Discuss complications of acute Cholecystitis?

4. Runbens DJ. Hepatobiliary imaging and its pitfalls. Radiol clin north am 2004; 42:257-278. 5. Cameron IC, Chadwicke management of acute chole cystitis in U.k hospitals: time for a change. postgrad med J2004;80:292-294.

SURGERY - GASTRO-INTESTINAL PROBLEMS

146

GALL STONES

GIT - 16

GALL STONES Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS Cholelithiasis is the presence of stones in the biliary tree. Almost all of these stones are formed in the gall bladder but occasionally these may form in the bile ducts or liver1.

INCIDENCE AND EPIDEMIOLOGY Fat, fertile, flatulent and females of forty or fifty is no more the exact description of gall stone sufferers. Both sexes and any age can have gall stones. Gall stones are rare during first two decades but their frequency in early 2 age group is higher than formally supposed . 5 million patients are present in UK with gall stones. 25 million patients are present in USA with gall stones. 10-20 % adult population have gall stones. It is seen in 4% people between 30-40 years of age. It is seen in 27% people between 60-70 years of age. First degree relative of gall stone sufferers have double the incidence. The incidence is increased with intake of refined carbohydrates and low fibre diet. Crohn's disease, ileal resection and jejuno-ileal bypass increase the incidence four times. The incidence of gall stones increases with age in patients suffering from Thalassemia1. It is more common in women who take contraceptive pills. 20 % of gall stones are present in the bile ducts. Female to male ratio is 3:2. 3

Gall stones are rare in Africa (less than 1%). Gall stones are sometimes associated with diverticulosis and hiatus hernia. This triad of symptoms is called "Saint's Triad". 10% of the gall stones contain enough calcium to be radio-opaque on x-ray exposure. 5%-38% (average 18.5%) of dead bodies of people above 50 years of age revealed gall stones on autopsy.

ETIOLOGY Exact cause of the gall stone formation is unknown. A single factor for gall stone formation has never been recognized. Multiple factors are responsible for its occurrence. RISK FACTORS FOR CHOLELITHIASIS Female sex. Obesity. Age. Genetic and ethnic factors. Diet (refined, fibre depleted, high animal fat). Diabetes mellitus. Ileal disease and resection. Haemolytic states. Infections of biliary tract. Parasitic infestations. Cirrhosis. Cystic fibrosis.

! ! ! ! ! ! ! ! ! ! ! !

Its incidence is doubled in patients with aortic aneurysm . These are more common in white population than in dark races. SURGERY - GASTRO-INTESTINAL PROBLEMS

Obesity is a well recognized risk factor for gall stones4. Risk of gall stone disease increases with age, educational status and subscapular skin fold thickness in males. Risk 147

GALL STONES

of gall stone disease increase with age, body mass index, diabetes mellitus, impaired glucose tolerance and oral contraceptives in females. Parity does not influence the risk of cholelithiasis5.

bilirubinate with the polymerization of the pigment in the gall bladder with deposition of inorganic salts, calcium carbonate and phosphate results in black pigment gall stone formation.

PATHOGENESIS OF GALL STONE

GALL BLADDER HYPOMOTILITY Hypomotility of the gall bladder does not influence the pigment stone formation but is almost always associated with the formation of cholesterol gall stones. It is caused by surgery, burns, TPN, pregnancy and oral contraceptives.

FORMATION Gall stones form as a result of following derangements ; ! Increased cholesterol to bile acid ratio ! Accelerated nucleation. ! Gall bladder hypomotility. ! Accumulation of mucin gel.

HMGCoAR

HMGCoAR 7-a-OHase

7-a-OHase

16.01

INCREASED CHOLESTEROL TO BILE ACID RATIO Increased biliary secretion of cholesterol happens due to obesity high caloric and cholesterol rich diet and drugs (Clofibrate). Increased synthesis of cholesterol due to high activity of HMG-CoA reductase, and decreased synthesis of bile acids because of reduced activity of 7alpha hydrolase. Less common is bile salt hyposecretion from impaired synthesis in constitutional disorders and cirrhosis and uncompensated interruption of the enterohepatic circulation in ileal dysfunction syndrome. ACCELERATED NUCLEATION Gall stones are formed due to nucleation of cholesterol monohydrate crystals. This is accelerated due to excess of pronucleating factors or deficiency of antinucleating factors. Nucleation and the precipitation of the calcium hydrogen

SURGERY - GASTRO-INTESTINAL PROBLEMS

Normal cholesterol Cholesterol Normal bile acids Bile acids Normal lecithin Normal lecithin

Cholesterol Bile acids Normal lecithin

Supersaturation

Promotes nuclueation Mucous glycoproteins Heat labile proteins

Inhibits nucleation Apolipoprotein Lecithin vesicles

Nucleation

Microstone

Gallstone

Formation of Gall stones FORMATION OF PIGMENT STONES Supersaturation of the bile with calcium hydrogen

148

GALL STONES

PATHOGENESIS OF FORMATION OF GALLSTONES

Increased Cholesterol

Decreased Bile acids

Obesity Cholesterol Rich Diet Enzyme Defects Drugs (clofibrate) Oral Contraceptive

Cirrhosis Ileal dysfunction Constitutional disorders

Disturbed Ratio of Cholesterol/Bile acids

Lithogenic bile

Formation of Gall Stones

Nucleation Mucus glycoprotein Apolipoprotein Lecithin vesicles

SURGERY - GASTRO-INTESTINAL PROBLEMS

Gall Bladder Hypomotility Burns TPN Pregnancy Oral contraceptives

149

GALL STONES

bilirubinate (Acid calcium salt of un-conjugated bilirubin bilirubinate) is essential for pigment gall stone formation. There is hypersecretion of bilirubin conjugates in haemolytic disorders. Bile salt deficiency causes incomplete solubilization of unconjugated bilirubin and impaired binding of calcium.

These stones are formed in patients when the bile becomes supersaturated with cholesterol and the ratio of cholesterol to bile acids becomes 25:1. 16.02

Stasis and anaerobic bacterial infection is responsible for brown pigment gall stone formation. There is precipitation of unpolymerized calcium hydrogen bilirubinate. There is also deposition of calcium salts of saturated fatty acids and free bile acids due to 6

bacterial enzymatic hydrolysis of biliary lipid .

TYPES OF GALL STONES Cholesterol and bile pigments are two principal constituents of gall stones. Other salts are calcium carbonate, phosphate and palpitate. Mostly stones are mixed pure stones are rare. Following three main types of gall stones are seen;

! ! !

16.03

Cholesterol and mixed stones Black pigment stones Brown pigment stones

Majority of the stones are composed of more than one component. CHOLESTEROL AND MIXED STONES These are the most common stones. 75% of all gall stones in the West are cholesterol stones.

The critical level for precipitation of cholesterol is 13:1.

These are about 6 % of the total gall stones in our part of the world.

This happens due to either increase in cholesterol concentration or decrease in the bile salts or lecithin concentration.

SURGERY - GASTRO-INTESTINAL PROBLEMS

150

GALL STONES

The liver seems to be responsible for cholesterol gall stones and not the gall bladder. These are usually solitary, oval or round, about 1-5 cm or larger in size. These may be multiple and medium sized. If solitary, these are of large size7. These are present in the gall bladder and are preceded by presence of biliary sludge. These also contain bile pigments, calcium carbonate and calcium palmitate in variable quantities. These are usually not associated with infected bile. BLACK PIGMENT STONES These form in the gall bladder. These are 25% of the gall stones in western countries. These are seen in higher percentage in Asian countries. These are composed of bilirubin polymers and some amount of cholesterol. 16.04

carbonate or calcium bilirubinate. These are black or dark green in colour. These are multiple. These are small and of irregular size. These may be present in patients with or without obvious haemolytic 7 states . BROWN PIGMENT STONES These are formed in the bile ducts. These are associated with infection. 98% of these stones contain bacteria within them. These are composed of calcium bilirubinate, calcium palmitate and small amounts of cholesterol in a matrix of organic material7.

CLINICAL FEATURES SILENT GALL STONES The gall stones may be present without giving rise to any symptom. These are found out accidentally while investigating the patient for some other problem. 50% of these patients, if left alone start having symptoms within two years. FLATULENT DYSPEPSIA There is the feeling of fullness, belching and heart burn. 70% of patients get relief of their symptoms after cholecystectomy. Temporary relief is also seen after fat restriction. BILIARY COLIC The patient suffers from severe excruciating pain in the upper part of the abdomen which radiates to the back in between the shoulder blades. The pain occurs in attacks and is usually noticed after fatty meals.

These are faceted by friction against each other. These stones are found to be laminated. It has on section layers of cholesterol alternating with layers of calcium

SURGERY - GASTRO-INTESTINAL PROBLEMS

JAUNDICE Patient may have obstructive jaundice due to the presence of stone in the common bile duct causing obstruction. This is present in about 18% of patients. Slight jaundice may be present due to infection of the biliary passages (cholengitis).

151

GALL STONES

MURPHY'S SIGN The patient is asked to take a deep breath while palpating over the right upper quadrant of the abdomen, there is a catch in the breath just before the extreme of inspiration.

Cystic duct

Hepatic duct

Gallbladder

This is due to pain produced by the inflamed gall bladder touching the parietal peritoneum.

16.07

Liver

Gallstones Gallbladder

Common bile duct

16.05 Pancreatic duct Duodenum

COMPLICATIONS The gall stones produce following complications if these are not treated adequately and in time ; COMPLICATION RELATED TO GALL BLADDER

Murphyâ&#x20AC;&#x2122;s Sign

! Acute cholecystitis.

Chronic cholecystitis. ! Mucocele of the gall bladder. ! Empyema of the gall bladder. !

BOAS SIGN There is an area of hyperaesthesia opposite T11,T12 and L1 vertebral bodies about 3 cms lateral to spine and inferior to ribs below the tip of the scapula posteriorly on the right side. This is due to acute inflammation of the gall bladder.

Gangrene of the gall bladder.

Perforation of the gall bladder.

Carcinoma of the gall bladder

COMPLICATIONS RELATED TO BILIARY TRACT ! Cholangitis. ! Obstructive jaundice. ! Liver failure. ! Acute or recurrent pancreatitis. ! Mirrizi Syndrome.

16.06

COMPLICATIONS RELATED TO INTESTINAL

Boas Sign SURGERY - GASTRO-INTESTINAL PROBLEMS

TRACT ! Biliary peritonitis.

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GALL STONES

! Penetration into other viscera and internal fistula

Carey MC. Pathogenesis of gall stones. American journal of surgery. [JC:3z4] 1993 Apr. 165(4) 410-9.

A Cuschieri. GR Giles. AR Moossa. Essential surgical practice third edition. Butterworth Heinemann London. 1995. p: 1175-1237.

Heinrich D. Meier J. Wehrli H. Buhler H. Upper gastrointestinal haemor rhage preceding development of Bouverets' syndrome. American journal of gastroenterology. [JC:3he] 88(5): 77780, 1993 May. severe obesity. American Journal of clinical nutrition. [JC:3ey] 1992 Mar. 55(3): 652-8.

formation. ! Gall stones ileus. ! Bouveret's syndrome.

BOUVERET'S SYNDROME Gastric outlet obstruction by a gall stone is a very uncommon clinical entity. It is called Bouveret's syndrome. Upper gastrointestinal bleeding may occur in these patients due to erosion of the cystic artery8.

REFERENCES 1.

Gold farb A. Grisaru D. Gimmn Z. High incidence of cholelithiasis in older patient with homozygous beta Thalassemia. Acta haematologica. [JC:088] 1990. 83(3): 120-2.

Ljimg R. Ivarsson S. Nilsson P. et al. Cholelithiasis during first year of life. Case reports and literature review. Acta Paediatrica. [JC:bgc] 1992 Jan. 81(1): 69-72.

Schuster JJ. Raptopoulos V. Baker SP. Increased prevalance of cholelithiasis in patients with abdominal aor tic aneurysm. Sonographic evaluation. (Ajr). American jour nal of Roentgenology. [JC:3ae] 1989 Mar. 152 (3): 50911.

Stamfer MJ. Maclure KM. Colditz GA. et al. Risk of symptomatic gall stones in women with severe obesity. American Journal of clinical nutrition. [JC:3ey] 1992 Mar. 55(3): 652-8. Maurer KR. Everhart JE. Knowler WC. Risk factors for gall stone disease in the Hispanic populations of the united states. American journal of Epidemiology. [JC:3h3] 1990 May. 131(5): 83644.

SURGERY - GASTRO-INTESTINAL PROBLEMS

SUMMARY Gall stones Incidence Etiology Risk factors Pathogenesis Types of stones Clinical features Complications POSSIBLE QUESTIONS 1. 2. 3.

What are the risk factors for cholelithiasis? How will you diagnose cholelithiasis? What are the different complications of cholelithiasis?

153

MURPHY'S SIGN

GIT - 17

MURPHY’S SIGN Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) MURPHY’S SIGN This sign is named after famous surgeon John Benjamin Murphy from Chicago, United States of America. This sign is also called Naunyn’s Sign after the name of Bernard Naunyn Professor of Medicine Strausburg who described it thirteen years before Murphy. METHOD The patient is examined in supine (lying) position. The patient is asked to take a deep breath, while doing gentle palpation of the right hypochondrium. There is catch in the breath (inspiratory arrest) just before the inspiration. It is due to contact of the inflammed gall bladder with the abdominal peritoneum during deep inspiration which causes reflex catching of the breath due to pain. Deep breath is painful and difficult in acutely inflammed gall bladder many times even without palpation. It is murphy’s 1,2 positive sign .

The patient holds his/her breath during ultrasound examination due to pain caused by pressure of the ultrasound probe. However, other features of gall stone disease become obvious on sonographic examination. 17.02

Murphy’s Sign (sonographic)

REFERENCES 1. Shuja Tahir. Mahnaaz Roohi. Zahid Yasin Hashmi. Surgery clinical examination system third edition. URO-OBS (Pvt). 1992 Dec. P:131-33.

17.01

2. Julian Britton. Kenneth I. Bickerstaff. Adrian savage. Benign diseases of biliary tract. Peter J Morris. Ronald A Malt. Oxford Textbook of surgery. Oxford University Press.1994. P:1223-1224.

Murphy’s Sign

3. Shuja Tahir. Mahnaaz Roohi. Surgery clinical & sonographic examination system. (Unpublished) June 2009.

SONOGRAPHIC MURPHY'S SIGNS3 Nowadays ultrasound probe is also used to elicit murphy’s sign in similar fashion as in clinical examination. SURGERY - GASTRO-INTESTINAL PROBLEMS

155

BOAS SIGN

01 GIT - 18

BOAS SIGN Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) BOAS SIGN It is another clinical test to diagnose gall bladder disease.

18.01

It is positive when an area of hyperaesthesia is felt on the 11right chest just below the tip of right scapula opposite T 12 and L1 vertebrae about 3 cms lateral to the spine. It presents due to posterior radiation of the pain from 1,2,3 inflammed gall bladder .

REFERENCES

Boas Sign (red area represents area of hyperaesthesia)

1. Shuja Tahir. Mahnaaz Roohi. Zahid Yasin Hashmi. Surgery clinical examination system third edition. URO-OBS (Pvt). 1992 Dec. P:131-33. 2. Julian Britton. Kenneth I. Bickerstaff. Adrian savage. Benign diseases of biliary tract. Peter J Morris. Ronald A Malt. Oxford Textbook of surgery. Oxford University Press.1994. P:1223-1224. 3. Shuja Tahir. Mahnaaz Roohi. Surgery clinical & sonographic examination system. (Unpublished) June 2009.

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156

MUCOCELE OF GALL BLADDER

GIT - 19

MUCOCELE OF GALL BLADDER Shuja Tahir, FRCS (Edin), FCPS Pak (Hon)

MUCOCELE OF GALL BLADDER Mucocele or hydrops of gall bladder is an over distended gall bladder filled with mucoid or clear and watery content. This over distension is usually non inflammatory. About 3% of diseased gall bladders are mucoceles.

CAUSES ! ! ! ! ! ! !

Impacted stone in the gall bladder neck or cystic duct. Spontaneously resolved acute cholecystitis. Tumour and polyps or malignancy of gall bladder Extrinsic compression of neck or cystic duct by lymph node, inflammatory fibrosis or adjacent malignancies of liver, duodenum or colon. Prolonged total parenteral nutrition or ceftriaxone therapy. Congenital narrowing of cystic duct Parasites such as Ascaris causing cystic duct obstruction.

PATHOGENESIS Mucocele develops as a result of outlet obstruction of the gall bladder caused by impacted stone at neck of the gall bladder or cystic duct. The already present bile is absorbed. Bile pigments are also absorbed and the gall bladder is distended with the mucous secreted by the gall bladder epithelium. Long standing gallbladder out flow obstruction leads to over distension occasionally even up to 1.5 litres. Bile and bile pigment is reabsorbed gradually. Secretion from gall bladder mucosa results in clear and mucoid content. The gall bladder wall may be of normal thickness or atrophic SURGERY - GASTRO-INTESTINAL PROBLEMS

and even transparent. Thickening of wall may be seen in recurrent cholecystitis patients.

COMPLICATIONS Empyema of Gall Bladder The contents of gall bladder are usually sterile in mucocele. Any bacterial contamination results in empyema of gall bladder. Gangrene and Perforation of Gall Bladder Gross over distension may result in gangrene or perforation of gall bladder with pericholecystic collection or even peritonitis. Peri-cholecystic collection It results from inflamation and perforation of mucocele of gall bladder.

CLINICAL FEATURES The patients suffering from this disease present with a palpable mass in right hypochondrium. Sometimes the mass is too big to occupy whole of the right half of the abdomen. Usually it is not tender and is not associated with jaundice. Right hypocondrial pain, tenderness, fever and chills suggest infection and acute cholecystitis or empyma of gall bladder. Jaundice may be present due to co existing CBD stone or extrinsic compression (Mirizziâ&#x20AC;&#x2122;s Syndrome). EXAMINATION FINDINGS Gall bladder is easily palpable on examination. Some times it may be grossly enlarged and in fact reaches into the pelvis. 157

GALL STONES

HISTOLOGICAL FEATURES Microscopic examination reveals a flattened mucosa lined with low columnar or cuboidal cells. Increased intra luminal pressure results in rokitansky aschoff sinuses.

19.02

DIAGNOSTIC CRITERIA ! A large palpable mass in right hypochondrium. ! Ultrasound shows over distended gall bladder and an impacted stone. Aspirate from gall bladder is clear, watery and mucoid ! No inflammatory signs are seen

Mucocele of Gall Bladder (ultrasound scan)

INVESTIGATIONS ! ! !

Ultrasound scan CT scan MRI scan

19.03

ULTRASOUND SCAN It is the first line investigation for suspected patients of mucocele of gall bladder. The gall bladder shows as a hypoechoic globular mass in the right hypocondrium lying with the liver. It is seen even after intake of full fatty meals. The stone or obstruction is also seen in the cystic duct3. 19.01

Mucocele of Gall Bladder (operative finding)

REFERENCES 1. Shuja Tahir. Mahnaaz Roohi. Zahid Yasin Hashmi. Surgery clinical examination system third edition. URO-OBS (Pvt).1992 Dec. P:131-33. 2. Julian Britton. Kenneth I. Bickerstaff. Adrian savage. Benign diseases of biliary tract. Peter J Mor ris. Ronald A Malt. Oxford Textbook of surgery. Oxford University Press. 1994. P:1223-1224.

Mucocele of Gall Bladder (ultrasound scan)

TREATMENT ! !

Cholecystectomy (Open) Laparoscopic cholecystectomy

SURGERY - GASTRO-INTESTINAL PROBLEMS

3. Shuja Tahir. Mahnaaz Roohi. Surgery clinical & sonographic examination system. (Unpublished) June 2009.

158

CHOLECYSTECTOMY

GIT - 20

CHOLECYSTECTOMY Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS It is an operation for excision of the gall bladder. It can be performed in the following ways; ! Conventional (open) cholecystectomy. ! Laparoscopic cholecystectomy. It is a combined endoscopic operative technique for the excision of the gall bladder. ! Laparoscopic laser cholecystectomy. It is similar to percutaneous laparoscopic choleystectomy except that the laser is used and electric cautery is not used. It is safe and a rewarding procedure for both the patient and the surgeon. ! Transvaginal endoscopic cholecystectomy. 1

INDICATIONS ! ! ! ! ! ! ! ! ! ! !

Acute cholecystitis. It may be treated conservatively at first unless perforation has occurred. Cholelithiasis. Mucocele of the gall bladder. Torsion of the gall bladder. Empyema of the gall bladder. Asymptomatic gall bladder disease. Internal biliary fistula. Chronic cholecystitis. Gall bladder injury in accidents or during operations. If gall bladder is perforated or injured, it should be removed. Carcinoma of the gall bladder. If it is operable. Gall bladder polyps.

PRE-OPERATIVE PREPARATION Obese patients are advised to lose weight if possible. SURGERY - GASTRO-INTESTINAL PROBLEMS

Diagnosis is differentiated from peptic ulcer, diverticulosis and hiatus hernia. Pulmonary and prostatic diseases are treated as far as possible. Arrangements for operative cholangiography are made if it is indicated. ANAESTHESIA General

OPEN CHOLECYSTECTOMY POSITION Supine position with head end raised about 15 degrees for easy access to the gall bladder. Skin is prepared with appropriate antiseptic solution (pyodine solution) at least 1/2-1 hour before surgery and just before surgery. Sterile sheets are used to cover all of the body except the operation site and adhesive drapes are stuck on the operation site. INCISIONS ! Long right paramediam (from costal margin upto 3 cms below the umbilicus). ! Kockers right subcostal (about 15-20 cm long and 5 cm below and parallel to right costal margin). ! Right transverse subcostal (about 15-20 cm long about 5 cm below the xiphisternum and in hairline). PROCEDURE A long right paramedian incision starts from the costal margin upto 3 cm below the umbilicus and on the right side of midline about 2 cm from the linea alba.

159

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20.03

Long Right Paramedian incision 20.02

Right transverse subcostal incision The triangular area is exposed which is bounded by liver, common hepatic duct, cystic duct and gall bladder. This is called calotâ&#x20AC;&#x2122;s triangle. The peritoneal covering over cystic duct, artery and common bile duct is separated from the structure. Cystic artery is cleared, ligated and divided between ligatures. Cystic duct is cleared and common bile duct is recognized. The cystic duct is ligated and divided between ligatures. 20.04

Anterior rectus sheath is cut in the line of incision after cutting the fascia. Haemostasis is secured. Rectus muscle is retracted laterally and the epigastric vessels are ligated. All the viscera are covered with warm and wet towels. The assistant retracts the peritoneal viscera gently under a moist towel to expose the cystic duct and common bile duct area. The other assistant retracts the liver from the surgeonâ&#x20AC;&#x2122;s side.

Right sub-costal incision 20.05

The surgeon palpates cystic duct and then the gall bladder. The gall bladder is held from its fundus with sponge holding forceps and is pulled gently upwards, thus stretching the cystic duct at its entry into the common bile duct. Open cholecystectomy SURGERY - GASTRO-INTESTINAL PROBLEMS

160

CHOLECYSTECTOMY

Operative cholangiography is performed at this stage of operation if indicated. The gall bladder is separated from its bed and removed. Haemostasis is secured. The gall bladder bed area and common bile duct are re-inspected. A drain is inserted in subhepatic area through a separate stab incision. All the swabs are removed from peritoneal cavity and counted loudly at least twice. The swab count is doubly checked by the surgeon and assistant independently. Posterior rectus sheath and peritoneum are closed together with absorbable suture. Anterior rectus sheath is repaired with non absorbable sutures. Skin is closed with non absorbable sutures or metal staples. OPERATIVE CHOLANGIOGRAPHY A cannula is passed through the cystic duct into common bile duct and operative cholangiography is performed whenever indicated. It is perfor med before cholecystectomy. After looking at the operative cholangiogram, if it is satisfactory, the cystic duct part towards common bile duct is ligated as near to the common bile duct as possible and cystic duct is divided after ligation. Rest of cholecystectomy is performed as described above.

LAPAROSCOPIC CHOLECYSTECTOMY / LASER CHOLECYSTECTOMY The patient is anesthetized and prepared for surgery.

POSITION The patient is fixed to the operation table with the help of straps and is kept in supine. Skin preparation is performed in the similar manner2,3. STEP- 1:CREATION OF PNEUMO PERITONEUM A work space, generally provided by a preumoperitoneum is essential to operate. This is established by maintaining intra-abdominal pressure between 12-15 mm of Hg. CLOSED METHOD (SAFE METHOD) Carbon Dioxide is insufflated into peritoneal cavity through a veress needle which is subsequently replaced with a laparoscopic port (10mm). OPEN METHOD In this technique a laparoscopic port is inserted under direct vision. Only after ensuring definitive and safe peritoneal entry, pneumoperitoneum is established. STEP-2: PORT PLACEMENT AND EXPOSURE Four ports are placed in routine after positioning patient in reverse trendelenbergâ&#x20AC;&#x2122;s position while rotating the operation table to the left by 150. This causes the colon and duodenum to fall away from liver edge. 10mm port is inserted just above the umbilicus and is used as optical port. Two small accessory ports are placed under direct vision. First 5mm is placed in right anterior axillary line between 12th rib and iliac crest. This port is used for retraction of

20.06 20.07

Open cholecystectomy SURGERY - GASTRO-INTESTINAL PROBLEMS

Laparoscopic cholecystectomy 161

CHOLECYSTECTOMY

gall bladder. Second 5mm port is inserted in right sub costal area in mid clavicular line. A 10mm epigastric port is usually inserted 5cm below xiphoid process. These last two mentioned ports are used for operating by surgeon. STEP-3: RETRACTION OF GALL BLADDER The fundus of gall bladder is then pushed in lateral and cephaloid direction. This maneuver exposes the entire gall bladder, cystic duct and porta hepatis.

fibrous bands and lymphatics. A lymph node is usually a land mark for cystic artery. Cystic artery is similarly exposed and skeletonised. It is critical that no structure is divided until the cystic duct and cystic artery are un equivocally identified. 20.10

20.08

Laparoscopic cholecystectomy (dissection of calot's triangle)

Laparoscopic cholecystectomy STEP-4: REMOVAL OF ADHESIONS Most patients have adhesions between gall bladder and the omentum, hepatic flexure and/or duodenum. These are usually avascular and may be lysed bluntly by grasping them with dissecting forceps at their site of attachment to gall bladder and gently stripping them down.

STEP-6: CLIP LIGATION OF CYSTIC ARTERY AND CYSTIC DUCT Clip ligation of cystic duct and artery is performed under vision, and cut between clips. 20.11

20.09

Laparoscopic cholecystectomy (clipping of cystic duct) STEP-7: DISSECTION OF GALL BLADDER The gall bladder is dissected off the liver bed while maintaining traction on the fundus of gall bladder, with the help of electro-cautery. Laparoscopic cholecystectomy (Retraction) STEP-5: DISSECTION IN CALOTâ&#x20AC;&#x2122;S TRIANGLE The dissection is started from gall bladder downwards. Anterior and posterior peritoneal leaves are stripped off gently. Cystic duct is gradually exposed by stripping SURGERY - GASTRO-INTESTINAL PROBLEMS

STEP-8: RETRIEVAL OF GALL BLADDER After securing hemostasis and suction of free fluid, gall bladder is retrieved through umbilical port with "BERT" bag (bag for endoscopic retrieval of tissue). A tube drain is left through the portal under vision in the subhepatic space and all fluid is sucked out. 162

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have undergone laparoscopic cholecystectomy. It presents with deterioration of vital signs and ECG changes during monitoring. Cardiac arrest may occur during surgery. Thus leading to death of the patient. It should be diagnosed as early as possible. The procedure should be stopped and patient should be ventilated with hyperbaric oxygen and symptomatic treatmentmay be given5.

20.12

Laparoscopic cholecystectomy (gall bladder dissection) 20.13

Laparoscopic cholecystectomy (Retrieval) STEP-9: CLOSURE The fascia of umbilical incision is closed with one / two large absorbable sutures. For other ports only skin is closed. The drain is fixed. All cannulae are removed and stab wounds are stitched with the silk. POST OPERATIVE CARE Nasogastric suction and intravenous fluids are infused over next 24 hours.

HYPOXEMIA AND HYPERCARBIA The patients who undergo laparoscopic surgery may show respiratory depression, decrease in minute ventilation, tidal volume and superimposed ventilation perfusion mismatch. It occurs after intravenous sedation and leads to hypoxemia hypercarbia and acidosis8. The patient should be monitored very carefully during anesthesia. (OPERATIVE) HAEMORRHAGE Primary haemorrhage can occur either from cystic artery, hepatic bed or vessels supplying the common bile duct. The bleeding area is packed. Blind application of the forceps should never be tried. After five minutes, the pack is removed and bleeding vessel is ligated under vision. The vessels are cut after proper application of clips and cauterization during laparoscopic cholecystectomy to avoid operative haemorrhage. The bleeding points are diathermized under vision and field is cleared after washing with normal saline and suction. The laparoscopic operation may be converted to open operation in case of uncontrolled bleeding. INJURY TO THE COMMON BILE DUCT It is prevented by being very careful. All the structures are recognized before any ligation or excision is started. If injury has occurred it should be recognized, repaired and drained.

COMPLICATIONS

Disruption of the biliary tree and extravasation of bile and /or biloma formation after percutaneous laparoscopic cholecystectomy is reported7. It should be recognized early. Conversion to open operation and repair of common bile duct with T-tube drainage is carried out if it is 4 diagnosed during surgery .

(ANAESTHETIC ) CARBON DIOXIDE EMBOLISM This rare but dreadful complication is seen in patients who

INJURY TO THE LIVER It should best be prevented, if it has occurred,

Patient is mobilized as soon as possible. Chest physiotherapy is started as early as possible. Drains are removed as soon as these stop draining. Sutures are removed on the 7th day.

SURGERY - GASTRO-INTESTINAL PROBLEMS

163

CHOLECYSTECTOMY

haemostasis should be secured and it should be repaired if required. 20.14

SUBCUTANEOUS EMPHYSEMA Subcutaneous emphysema and hypercarbia occur in patients during laparoscopic cholecystectomy. It is a rare 9 complication . It is treated symptomatically. INCISIONAL HERNIA It is a late complication of open operation which can occur in patients with low haemoglobin and mal-nourishment states. It may also occur in patients whose wounds get infected or who suffer from chronic cough or asthmatic states.

Laparoscopic cholecystectomy (post operative) POST OPERATIVE CHEST COMPLICATIONS Infection, collapse and consolidation may occur. These are treated symptomatically. Chest physiotherapy is very helpful in these patients. SUBHEPATIC COLLECTION OF BLOOD OR PUS It presents with pyrexia and upper abdominal pain which is not related to the wound. It is aspirated or drained. BILE PERITONITIS If the cystic duct ligature slips or an accessory bile duct has been cut and left unnoticed, this complication is seen. Treatment is laparotomy, peritoneal toilet and ligation of the cystic duct. JAUNDICE If serious error has occurred as bile duct may have been ligated or stone has been left in common bile duct, the jaundice appears. Treatment is laparotomy, removal of the suture and repair of the common bile duct or removal of the stone as the case may be. Bile duct stenosis may occur after laparoscopic cholecystectomy when electric cautery has been used near the common bile duct. It presents with post operative jaundice. It should preferably be prevented but if it occurs surgical repair is performed7. SURGERY - GASTRO-INTESTINAL PROBLEMS

It may also occur in laparoscopic cholecystectomy if the larger cannula (10 mm or larger) wound is not properly repaired. The peritoneum and abdominal muscles are 6 repaired before the skin is closed .

REFERENCES 1.

Fraser GM. Pilpel D.Hollis S.Kosecoff J. The agreed indication and contraindication for cholecystectomy. Quality Assur ance in Health care. [JC:a6w] 1993 Mar: 5(1): 81-5.

Donohue. JH. Grant CS. Farnell MB. Van heeren JA. Laparoscopic cholecystectomy. Operative technique. Mayo clinic Proceedings [JC:LLY] 1992 May: 67(5):441-8.

Stair JM. Delloach JM Jr. Wood ward LA. Ludwing F.R. Laparoscopic laser cholecystectomy: Results of 100 successful operations. Journal of Arkansas medical society. [JC:hev] 1991 Jul: 88 (2) : 83-5.

Duncon D. Carbon dioxide embolism during laparoscopy. journal [JC:o2p] 1992 Mar: 60(2): 139-44.

Brady EE 3d. Harkleroad LE. Pierson WP. Alter ations in oxygen satur ation and ventilation after intravenous sedation for Peritoneoscopy. Archives of internal medicine [JC:7fs] 1989 May: 149(5) 1029-32.

Walker AT. Shapiro AW. Brooks DC. Braver JM. 164

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Tumeh SS. Bile duct disruption and biloma after lapar oscopic c holecystectomy. Imaging evaluation. Ajr American Jour nal of Roentgenology [JC:3ae] 1992 Apr: 158 (4) 785-9. 7.

Park Yh.Ospanian Z. Obstructive jaundice after laparoscopic cholecystectomy with Electrocautery. American surgeon [JC:43 e] 1992 May: 58(5) :321-3.

Kent TB Bd. Subcutaneous emphysema and hypercarbia following laparoseopic Choloecystectomy. Archives of surgery [JC:8ia] 1991 Sep: 126(9) 1154-6, .

Kadar N. Reich H. Liucy. Manko GF. Gunpelsm R. Incisional hernia after major laparoscopic procedures. American journal of obstetrics and gynaecology. [ JC:3xi] 1993 May: 168 (5): 1493-5.

SUMMARY Cholecystectomy Open Preparation Anaesthesia Position Incisions Laparoscopic Position Ports Procedure Post operative care Complications POSSIBLE QUESTIONS 1. 2.

SURGERY - GASTRO-INTESTINAL PROBLEMS

What is cholecystectomy? What are the advantages and complications of laparoscopic Cholecystectomy? Enlist different steps of laparoscopic and open Cholecystectomy.

165

Obstructive Jaundice

SURGERY - GASTRO-INTESTINAL PROBLEMS

167

OBSTRUCTIVE JAUNDICE

OBJECTIVES ! ! ! ! ! ! !

To be able to diagnose patients with jaundice. To be able to diagnose causes and type of jaundice. To be able to assess the hepato-renal functions. To be able to plan mode of treatment. To be able to prepare patients for surgical treatment if required. To be able to look after the patient during and after surgical treatment for jaundice. To be able to prevent and treat complications of jaundice and its treatment.

SURGERY - GASTRO-INTESTINAL PROBLEMS

168

OBSTRUCTIVE JAUNDICE

GIT - 21

OBSTRUCTIVE JAUNDICE Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS Jaundice is the yellow discoloration of the skin and mucous membranes due to increased serum bilirubin level caused by the obstruction to the normal out flow of the bile. (normal serum bilirubin level is 17 Âľmol / litre or 0.2- 0.8 mg / 100 mls). It is also called as surgical jaundice.

liver cells. This combination is acted upon by the glucuronyl transferase (enzyme present in the hepatocytes) and bilirubin glucuronide is formed which is excreted into the biliary passages. This is called conjugated bilirubin (direct reacting bilirubin). It is water soluble.

Obstruction of any type caused by any reason such as stone, stricture, tumor, secondary deposits, pressure from outside, ligation or injury anywhere in the biliary passages leads to obstruction to the flow of the bile.

The bile is produced in the liver and is transported via intrahepatic biliary canaliculi to the right and left hepatic ducts. These ducts join together to form the common hepatic duct which carries bile to the gall bladder through the cystic duct and to the duodenum through the common bile duct.

Liver

21.01

Spleen Red-cell breakdown

Bilirubin and globin Glucoronyl transferase

Bilirubin glucuronide

The bile is stored in the gall bladder where it is concentrated and evacuated mainly under the effect of the fatty meals. Jaundice or hyperbilirubinemia occurs due to following reasons ; ! Pre-hepatic (Haemolytic) ! Hepatic (Hepato-cellular) ! Post Hepatic (Obstructive or surgical)

Bile duct

Some reabsorbed Urobilinogen

Bilirubin glucuronide

Urobilinogen

Urobilin

Urobiiln in faeces Kidney

Bilirubin Metabolism

PHYSIOLOGICAL BASIS OF JAUNDICE Bilirubin is a breakdown product of haemoglobin. Free bilirubin combines with plasma albumin which is carried to the liver through its circulation. This is also called unconjugated bilirubin. It is water insoluble. (indirect reacting bilirubin). The albumin separates from bilirubin in the liver and circulates in the plasma while bilirubin enters the cells (hepatocytes). Bilirubin combines with the cytoplasmic proteins in the SURGERY - GASTRO-INTESTINAL PROBLEMS

PRE-HEPATIC JAUNDICE It occurs due to excessive breakdown of red blood cells and excessive production of bilir ubin. The production of bilirubin is much rapid than its excretion leading to increased serum levels and clinical appearance of jaundice. It is also called prehepatic jaundice. Mainly indirect bilirubin is raised in this type of jaundice. HEPATIC JAUNDICE (Hepato-cellular) It occurs due to ; ! Defective uptake of bilirubin by the liver cells. ! Defective conjugation by hepatocytes (absent enzyme). ! Defective secretion of conjugated bilirubin to the 169

OBSTRUCTIVE JAUNDICE

biliary passages. OBSTRUCTIVE OR SURGICAL JAUNDICE It occurs due to the obstruction to the outflow of bile. It may present due to obstruction in the lumen of the biliary duct or in the wall of the duct or by pressure from outside the duct.

MIRIZZI'S SYNDROME Mirizzi's syndrome is the condition presenting with obstructive jaundice due to pressure of an impacted gall stone in the cystic duct (hartmanâ&#x20AC;&#x2122;s pouch) and inflammation, resulting edema and extrinsic compression of the common bile duct or common hepatic duct. It is an 3 uncommon complication of cholelithiasis .

WITHIN LUMEN ! Gall Stones ! Parasites

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INTRINSIC CAUSES ! Congenital atresia ! Strictures ! Cholangitis ! Cholangioma EXTRINSIC CAUSES Pancreatitis Tumour of head of Pancreas Tumour of ampula of vater

! ! !

ERCP showing dilatation of CBD & common duct stones 21.03

Obstruction in the hepatic ducts and common bile duct leads to progressive rise of serum bilirubin level and appearance of the jaundice while obstruction of the few intrahepatic biliary canaliculi doesn't cause clinically obvious jaundice. Generalized multiple obstructions of the intrahepatic canaliculi such as sclerosing cholangitis also lead to obstructive jaundice. BILIARY CALCULI (CHOLEDOCHOLITHIASIS) It is the most common cause of obstructive jaundice. Usually one or few of the smaller and multiple gall stones slip into the common bile duct through the cystic duct and cause obstruction to the flow of bile. It leads to obstructive or surgical jaundice. The jaundice caused by calculi is usually intermittent as the stones allow passage of accumulated bile intermittently by changing their position.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Obstructed distal bile duct (MRI)

NEOPLASTIC LESIONS Primary or secondary tumors of biliary passages and of viscera lying nearby may cause obstructive jaundice. The fungating growth may obstruct the lumen from inside or pressure of the tumor outside the biliary tree may obstruct lumen from outside leading to obstructive jaundice. Tumors of the gall bladder may lead to obstructive jaundice due to extrinsic common bile duct compression. It is very uncommon entity4.

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Obstructive Jaundice Ultrasonography Dilated bile ducts

Non-dilated bile ducts

Gall Stones Present

Parenchymal liver disease or Ductal disease

Not Present (MRCP/Liver Biopsy)

MRCP CT Scan

Stone in CBD Stone Disease

ERCP Endoscopic sphincteropapillotomy Percutaneous transhepatic cholangiography Surgery

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Mass Lesion

Staging of Tumour Endoscopic sonography / Laparoscopy

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STRICTURES Strictures of the biliary passages may be; ! Multiple. ! Single. These could also be ; Inflammatory. Neoplastic. Iatrogenic

! ! !

BISMUTH CLASSIFICATION FOR STRICTURES

Type I

Low common bile duct; stump >2cm

Type II

Middle common hepatic duct; stump> 2cm

Type III

Hilar- confluence of right and left duct intact

Type IV

Right and left ducts separated

Type V

Involvement of the intra hepatic ducts.

BILIARY ATRESIA It is a progressive sclerosis of the extra hepatic biliary tree that occurs within the first three months of life. It is one of the most common causes of neonatal cholestasis. It accounts for 50%-60% of the children who undergo liver transplantation. It is seen in 1 in 8000 to 1 in 15000 live births5. MULTIPLE STRICTURES It could be the manifestation of sclerosing cholangitis which is a non malignant condition of the biliary passages leading to multiple stricture formation in the intrahepatic and extrahepatic biliary passages. Sometime cholangiocarcinoma also presents as multiple strictures of the intrahepatic passages leading to jaundice. SINGLE STRICTURE It is usually present either in the common hepatic duct or common bile duct. The single stricture, when present in intrahepatic biliary canaliculi or in one of the hepatic ducts does not cause jaundice. INFLAMMATORY STRICTURE It is very rare and occurs secondary to collection of the

SURGERY - GASTRO-INTESTINAL PROBLEMS

bile or pus around the biliary passages. These strictures also present secondary to infestations with Ascaris Lumbricoids and Liver fluke. Both these worms lead to fibrous stricture and multiple stone formation in the biliary tree. NEOPLASTIC STRICTURES These are the strictures due to primary or secondary malignancies. Carcinoma of the head of pancreas and peri-ampulary carcinoma also obstruct the lumen of the lower end of the common bile duct leading to the obstructive jaundice. Bile duct neuromas also cause surgical jaundice. Biliary obstruction due to bile duct neuroma typically occurs after previous cholecystectomy. IATROGENIC STRICTURES These are the strictures which occur accidentally during surgery of the biliary tree. If the ligature is applied after pulling the cystic duct during cholecystectomy, the lumen of the common bile duct is also partially ligated and stricture develops. Injury to common bile duct and its improper repair may result in stricture due to cicatrization and fibrosis. Stricture formation is more common after exploration of the common bile duct and after emergency operation on the biliary tree. Stricture of common bile duct may also follow use of electrocautery in close vicinity of common bile duct during laparoscopic cholecystectomy6.

FEATURES OF OBSTRUCTIVE JAUNDICE The symptoms and signs are very important and useful in the diagnosis of jaundice and its nature. ! Yellowish discoloration. ! Dark colored urine (due to presence of water soluble bilirubin). ! Clay colored stools (due to lack of stercobilin). ! Itching (due to irritation by the crystals of bilirubin which is excreted in sweat).

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! ! !

Yellowish discoloration of sclera, mucous membranes and skin. Scratch marks on skin (due to itching) Shiny nails (due to itching the nails become shiny when patient scratches skin).

BLOOD EXAMINATION Haemoglobin estimation. Total leucocyte count. Differential leucocyte count. Sedimentation rate.

! ! ! !

LIVER FUNCTION TESTS ! Bilirubin level is raised (direct more than indirect) ! Enzyme assays help to assess damage to liver parenchyma ! Alkaline phosphatase level is raised. ! Prothrombin time needs correction if disturbed. ! Serum proteins help to assess overall liverâ&#x20AC;&#x2122;s synthetic capacity.

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Diagnosis of Jaundice

Looking at the sclera for jaundice ABDOMINAL EXAMINATION ! liver may get enlarged due to biliary congestion/ metastatic spread. ! Palpable gall bladder (indicates malignant obstruction)

Test

Pre-hepatic

Urine

Urobilinogen

Hepatic Urobilinogen

Serum bilirubin

Unconjugated bilirubin

ALT (SGPT) AST (SGOCT) ALP

Normal

Conjugated and uncojugated Raised

Blood glucose

Normal

Normal or moderately raised Low if level failure

Reticulocyte count Haptoglobins Prothrombin time

Raised in haemolysis

Normal

Low due to haemolysis Normal

Normal Prolonged due to poor synthetic function

Ultrasound

Normal

May be abnormal liver texture, e.g. Cirrhosis

Normal

Obstructive No urobilinogen. Bilirubin present Conjugated bilirubin

Normal or moderately raised Raised Sometimes raised if pancreatic tumour Normal Normal Prolonged due to vitamin K malabsorption; corrects with vitamin K Dilated bile ducts

PALPABLE MASS Mass may be palpable in epigastrium in case of carcinoma head of pancreas causing biliary obstruction. ! Ascites (Signifying peritoneal metastasis or cirrhosis)

TUMOR MARKERS ! Serum Carcino Embryonic Antigen (CEA) ! Mild CA 19-9 elevation during jaundice or cholangitis 8 is not necessarily indicative of cholangio carcinoma .

Both of these features are very reliable and have sensitivity of 92% and specificity of 86%7.

IMAGING Intrahepatic problems leading to obstructive jaundice are best picked up by ultrasound, CT and MRI scan5. All three types of scanning are complementary to each other.

INVESTIGATIONS These are performed to confirm the diagnosis and plan the management. URINE EXAMINATION Urine contains bilirubin but no urobilinogen in obstructive jaundice.

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ULTRASONOGRAPHY9 It is used as first line investigation for obstructive jaundice. The ultrasonographic examination shows; ! Size of bile ducts ! Defines the level of obstruction ! Identifies the cause (in some cases) ! Gives other information related to the disease

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(e.g. hepatic metastases, gall stones and hepatic parenchymal changes)

the lower parts of biliary passages. It is an excellent investigation for lower bile duct obstruction.

Ultrasound scan is very helpful as one can see the site of obstruction and cause of obstruction. It is non invasive investigation. It has almost replaced other invasive investigations. It can be performed in severely jaundiced and ill patients at bed side. CT SCAN (SPIRAL) When jaundice is due to malignancy, CT scan is best investigation to diagnose9. It is an excellent investigation to pickup the site of obstruction and cause of obstruction to the biliary passages. It may not be available at every hospital and is expensive. Thin-cut spiral CT scan predicts resectability in about 70%-80% of patients with carcinoma of the head of pancreas. The ability of dual phase CT scan to identify vascular involvement has 9,10 eliminated the need for angiography .

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Stones

(E.R.C.P.) Endoscopic retrograde, cholangio-pancreaticography

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MRCP(MAGNETIC RESONANCE CHOLECYSTO PANCREATICO GRAPHY)

It is an expensive investigation. It may not be available at every center. It offers excellent soft tissue definition. It can image in all planes without moving the patient. It avoids radiation exposure. It is non invasive and does not carry any biological hazard. Proximal bile duct stricture can be imaged well with MRCP. MRS (magnetic resource spectrometry) probably will be 10 best of liver function tests in future . ENDOSCOPIC ULTRASONOGRAPHY (EUS) It is the use of ultrasonography through endoscope. It is useful in the diagnosis of bile duct and proximal pancreatic pathology. Recent advancement is use of intra ductal ultrasonography (IDUS) in which the ultrasound probe is introduced into bile duct or pancreatic duct while 2 performing ERCP .

It is invasive but it is one of the most accurate and essential investigations for obstructive jaundice. It is most helpful when the obstruction is benign and extra hepatic. It has an advantage of being therapeutically 9,10 useful as well .

E.R.C.P (E.R.C.P) Endoscopic retrograde, cholangiopancreaticography helps in finding out the obstruction specially in

PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY (PTC) Chiba needle is used under x-ray control and dye is

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E.R.C.P. showing stones in CBD

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OBSTRUCTIVE JAUNDICE

injected into the biliary canaliculi and x-ray pictures are taken. This shows the site of obstruction and dilatation of the biliary passages. This is an excellent investigation as it shows proximal biliary passages very clearly. 21.07

MANAGEMENT OBJECTIVES OF MANAGEMENT ! To understand pathophysiology of jaundice. ! To establish the cause of jaundice. ! To identify the patients with obstructive / surgical jaundice requiring relief of cholestasis. ! To plan appropriate surgical procedure (treatment of cause of obstruction) ! To understand the principles of management during peri operative period (before, during and after 2 surgery) .

TREATMENT

(PTC) Cholengiography It is extremely helpful as it drains the cholestasis and offers not only diagnostic but therapeutic help as well. It is not used as a first line investigation because of its invasive nature. It cannot be used to insert stents through proximal inoperable cholangio carcinoma. It can lead to intra peritoneal bleeding and leakage of bile into the peritoneal cavity. It may cause cholengitis as well. The patient must be admitted and kept under observation for at least 24 hours after the procedure. LAPAROSCOPY It is performed when biliary or pancreatic cancer is suspected. It provides most sensitive and reliable means of assessing, staging and judging the operability of biliary and pancreatic cancers, especially when combined with endoscopic ultrasonography. It also helps to palliate 9,10 the patients .

DIFFERENTIAL DIAGNOSIS Different causes of obstructive jaundice are to be differentiated from each other. History, examination and above mentioned investigations help to differentiate between all types of obstructive jaundice.

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The aim of treatment is to restore flow of bile into gastrointestinal tract and correct any metabolic or other complications due to biliary obstruction. Treatment of obstructive jaundice has two main components as given below; ! Conservative ! Definitive CONSERVATIVE It is used to prepare the patient for surgery as the definitive treatment for obstructive jaundice is surgical. FLUID AND ELECTROLYTES Fluids and electrolytes are given intravenously in calculated amount. URINE OUTPUT MONITORING Urethral catheter is passed to collect urine from the bladder and to monitor hourly urinary out put. It has to be kept > 30ml/ Hour to prevent hepatorenal syndrome. CORRECTION OF COAGULATION DEFECTS Vitamin K has to be given intravenously as there is deficiency of this vitamin due to lack of absorption of fat soluble vitamins leading to bleeding disorders. (Prolonged PT). Fresh frozen plasma is infused if Vitamin K injection fails to bring down the prothrombin time to normal limits.

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removed. Laparoscopic cholecystectomy and exploration of the common bile duct and removal of stones is done.

PREVENTION OF INFECTION The obstruction in the biliary tract leads to cholangitis and severe infections and septicaemia. If the patient is pyrexial, appropriate antibiotic is started prophylactically which will cover gram negative bacteria. 2nd/ 3rd generation Cephalosporin and quinolones are commonly used.

Per-operative cholangiography is performed to ensure complete removal of the stones. T-tube drainage of the bile duct is performed.

PREVENTION OF HEPATO-RENAL SYNDROME Jaundiced patients are likely to suffer from renal failure (hepato-renal syndrome). Loop diuretics or Mannitol 500 ml is given intravenously within 15-30 minutes just before the operation or during operation to clear the nephrons by causing diuresis to prevent renal failure.

MALIGNANT OBSTRUCTION OF BILE DUCT Different options of resection depending upon stage and site of tumor are available. Surgery is aimed at reestablishing reliable, long term conduit for bile flow from biliary to the gastrointestinal tract. Options for operative repair may include;

NUTRITION Basic caloric requirement of patient should be met. Enteral route is the preferred route. Large amount of glucose (carbohydrate) are required to replenish the glycogen content of the liver. (Rule out diabetes mellitus before giving glucose).

! ! ! ! !

SURGICAL TREATMENT This is the definite treatment of obstructive jaundice and it varies with the cause of obstruction and condition of the patient. Surgery is performed in physically fit patients to minimize morbidity. Surgical resection is performed in patients with operable disease in fit patients. Various surgical options are available depending upon the cause and site of obstruction. GALL STONES AND BILE DUCT STONES The principle of treatment is; ! Removal of stones from CBD ! Removal of gall bladder Following combination of procedures is performed for treatment of obstructive jaundice due to stone disease. ! ERCP and Laparoscopic cholecystectomy is performed. Stones from the bile duct are removed. ! Open cholecystectomy and exploration of the common bile duct is performed and stones are

SURGERY - GASTRO-INTESTINAL PROBLEMS

Roux-en-Y hepaticojejunostomy Choledochojejunostomy Choledochoduodenostomy End-to-end repair (controversial) Mucosal grafting

Whipples resection is performed for operable carcinomas in case of carcinoma head of pancreas and tumors of ampulla. Previously its operative mortality used to be almost 22%. Now with the improvements in anesthesia and critical care, the mortality is reduced to about 10%. PALLIATIVE PROCEDURES These are performed when definitive and potentially curative resections are not possible. Palliation is provided by interventional endoscopy, radiology or open surgery11,12. Following criteria is used to evaluate irresectable disease; CRITERIA FOR IRRSECTABILITY Extra hepatic metastasis. Extra hepatic organ invasion. Peripheral hepatic metastasis remote from primary tumor. ! Major vascular involvement. OBJECTIVES OF PALLIATION ! Relief of jaundice and pruritus. ! Prevention of recurrent cholangitis.

! ! !

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OBSTRUCTIVE JAUNDICE

Prevention of post cholestatic hepatic failure.

If the stricture is due to inoperable malignancy and bypass is not possible, intubation of the bile duct with appropriate stent is performed to have adequate bile flow to the duodenum. ENDOSCOPIC STENTING It is use of stents to bypass the obstruction of bile flow. It reduces the hospital stay and is associated with lower procedure related morbidity and mortality. It is safe and effective in palliation of major symptoms associated with inoperable pancreatic carcinoma and cholangio carcinoma. Plastic, polyethylene or self expanding metal stents (SEMS) are used in various sizes depending upon the size of lesion. The plastic stents occlude early and metal stents remain patent for longer period and are most cost effective in patients who survive for 3-6 months8. Complications of stenting are; ! ! ! ! ! !

Pancreatitis Cholangitis Perforation Stent Migration Stent Occlusion Stent Fracture

stricture. Higher doses of radiation can be achieved at local level. It helps to relieve the obstruction by downsizing the tumor. PHOTO DYNAMIC THERAPY (PDT) It involves the intravenous administration of a photo sensitizer that preferentially accumulates in neoplastic tissue. Activation of the photo sensitizer is achieved by endoscopically applying laser light directly which results in the formation of free oxygen radicals in the tumor cells leading to ischemic necrosis10. HIGH INTENSITY INTRA-DUCTAL ULTRASOUND (HIUS) Localized ablation of tumor cells by high intensity ultrasound has been found to be effective in experimental models as clinically in men with prostatic cancer. It is performed by passing an ultrasound probe over a guide wire into the bile duct during ERCP. Several treatments are applied throughout the length of stricture and stent is inserted after wards. It can be used as neo adjuvant therapy prior to performing potentially curative resection10.

REFERENCES 1. Muhammad Shuja Tahir. Mahnaaz Roohi. Clinical examination system 5th edition Uro-Obs (Pvt) Ltd Faisalabad. 2005 Jan. P: 30-33. 10

These are recognized & treated on urgent basis . ERCP and stenting of proximal bile duct stricture adds little to diagnosis and management of the non infected operable patient. CHEMO-RADIATION Chemotherapy only offers marginal benefit. Radiotherapy helps in some tumors. INTRA LUMINAL BRACHYTHERAPY (ILBT) It is offered for the palliation of irresectable cholangio carcinoma. It gives mixed results. It can be performed endoscopically or percutaneously. Iridium-192 seeds implanted on a catheter are placed directly across the

SURGERY - GASTRO-INTESTINAL PROBLEMS

2. Sir Alfred Cuscheri, Lynn E Bell, Ronald M, Harden. E Anne Hespeth. Sharon J.Johnson, Jennifer M Laid low. Sarah M Morrison, LorraiveJ Rebertson, Robert JC steele. Alastair M Thopson, Iain MC Macintyre, Robert C Smith, Jaundice module 4. The RCSE SELECT programme Royal College of surgeons of Endinburgh UK. 3. Rust KR. Clamcy TV. Warren G et al. Mirizzis syndrome: A contraindication to coelioscopic cholecystectomy Journal of laparoendoscopic surgery. [JC:0g3] 1991 Jun. 1(1) 133-7.

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4. Simmouus IC. Miller C. Pesigan AM. Lewin KJ. Cystadenoma of the gall bladder. American journal of gastroenterology. [JC:3he]1989. 84(11): 142730. 5. Ronald J. Sokol. Etiopatho genesis of Biliary Atresia Semin liver dis 21(4).2001. 6. Park YH. Oskanian Z. Obstructive jaundice after laparoscopic cholecystectomy with electro cautery American surgeon. [JC:43e] 1992 May. 58(5). 3213. 7. Pascnan PA. Pikkarainen P. Alhaver E. at al. The value of clinical assessment in the diagnosis of icterus & cholestasis. Journal of gastroenterology. [JC:aqi] 1992 Jul-Aug. 24(6): 313-9. 8. Joshua Hyman; Sharon P Wilczynski; Roderich E Schwarz. Extra hepatic bile duct stricture and elevated CA 19-9: malignant or Benign? South Med J 96(1): 89-92, 2003. 9. Pasanen PA. Partonon KP. Plkkaraianen PH et al. A comparison of ultrasound CT and ERCP in the differential diagnosis of benign and malignant jaundice and cholestasis. European journal of surgery. [JC:a21]1993 Jan 159(1): 23-9.

SUMMARY Obstructive Jaundice Physiological basis of jaundice Pre-hepatic Hepatic Post-hepatic Biliary stones Neoplastic lesions Strictures Atresia Diagnosis Clinical features Investigations Treatment

POSSIBLE QUESTIONS 1. 2. 3.

What is obstructive Jaundice? Discuss diagnosis of obstructive jaundice? Discuss management of obstructive Jaundice?

10. Emad M. Abu-Hamda; Todd H. Baron. Endoscopic management of cholangiocarcinoma. Sem in liver Dis 24(2): 165-175, 2004. 11. Ananya Das. Michael V. Sivak. Endoscopic palliation for inoperable pancreatic cancer. Cancer control 7(5):452-457, 2000. 12. Boris W. Kuvshinoff; Mark P. Bryer. Treatment of resectable and locally advanced pancreatic cancer. Cancer control 7(5): 428-436. 2000.

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COURVOISIER’S LAW

GIT - 22

COURVOISIER’S LAW Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) This converse of Courvoisier’s law is not true; the cause of jaundice in a patient with a non-palpable gallbladder is not necessarily gallstones as 50% of dilated gallbladders are impalpable.

22.01

Following situations give false observations of this law;

Jaundice seen on sclera

A stone impacted in the Hartmann’s Pouch leading to formation of mucocele of gall bladder. Another stone present in the common bile duct leading to the obstructive Jaundice.

Mucocele of the gall bladder and infective hepatitis present at the same time in the same patient.

Carcinoma of the gall bladder present with a stone impacted in common bile duct causing mass and jaundice in the same patient at the same time.

Ludwig Courvoisier was Professor of Surgery at Basle Switzerland. He described this law. “If in a jaundiced patient, the gall bladder is palpably enlarged it is probably not a case of stone impacted in the common bile duct because in that case previous attacks of cholecystitis have already made the gall bladder fibrotic and non distendable” This law helps in diagnosing the cause of jaundice in severely jaundiced patients. Although there may be some false positive findings yet it helps in the diagnosis most of the time.

REFERENCES 1.

Charles V MANN. RCG Russell. Norman S Williams. The gall bladder and bile ducts. Bailey & Love’s Short Practice of Surgery. 22nd Ed. 1995. P: 744-45.

Courvoisier’s law states that in the presence of jaundice, an enlarged gallbladder is unlikely to be due to gallstones; rather carcinoma of the pancreas or the lower biliary obstruction is more likely. This may be explained by the observation that the gallbladder with stone is usually chronically fibrosed and so, incapable of enlargement. SURGERY - GASTRO-INTESTINAL PROBLEMS

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Pancreas

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ACUTE PANCREATITIS

OBJECTIVES ! ! ! ! ! !

To understand development, anatomy and physiology of pancreas. To be able to diagnose the diseases of pancreas. To be able to plan various modes of management for pancreatic problems. To be able to prepare the patient for surgical management of pancreatic problems. To be able to look after post - operative patients following pancreatic surgery. To be able to manage the complications following pancreatic problems or their treatment.

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GIT - 23

ACUTE PANCREATITIS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS - Faisal Bilal Lodhi, FCPS 23.01

! ! ! !

Acutely inflamed pancreas Acute pancreatitis is the acute inflammation of the pancreas. It is followed by bacterial invasion and peritonitis. It is almost always associated with acinar cell injury and autodigestion. It is still not clear what triggers the sequence of pathological changes. Normal recovery never occurs.

INCIDENCE AND EPIDEMIOLOGY ! ! ! ! ! ! ! ! !

! !

It is more common in western society. It is present in 5 per 100,000 population. It occurs once in 500-600 hospital admissions. It is commonly seen in middle aged and obese patients. Common age group is between 50-60 years. It is slightly more common in females than males. Male to female ratio in patients with biliary disease is 1:3. It is common in alcoholics. The incidence in alcoholics is rising. Male to female ratio in alcoholics is 6:1. Strong family history is also associated with this disease. Familial etiology is commonly seen in children

SURGERY - GASTRO-INTESTINAL PROBLEMS

suffering from this problem. 5% of the patients with gall stones develop this disease. 30% - 60% patients suffering from pancreatitis have gall stones. Its mortality rate is 20%. 30% of deaths in patients of pancreatitis are due to respiratory insufficiency.

ETIOLOGY CAUSES OF PANCREATITIS Alcohol Billiary stone disease Hyperlipidemia Hypercalcemia Hereditary Trauma External Surgical ERCP Ischemia Hypoperfusion Atheroembolic Vasculitis Pancreatic duct obstruction Neoplasms Pancreatic division Ampullary & duodenal lesions Infections Venom Drugs Idiopathic 183

ACUTE PANCREATITIS

The etiology of acute pancreatitis is a complex subject because different factors have been implicated as cause of this disease. Two main factors, billiary stone disease and alcoholism account for 80-90% of the cases.

INFECTIONS Mumps, coxsackievirus and mycoplasma pneumoniae are believed to be causative organisms of acute pancreatitis.

BILIARY STONE DISEASE Choledocholithiasis represents most common form of associated biliary abnormality. Bile duct stones get stuck at sphincter of oddi and block pancreatic duct. This leads to elevated intraductal pressure causing rupture of small ductules and leakage of pancreatic juice into parenchyma leading to acute inflammation.

TRAUMATIC Trauma is possibly an etiological factor in only 01% of the cases. It is seen after injuries to pancreas and spleen. It is also seen after endoscopic retrograde cholangio pancreaticography. (ERCP)

ALCOHOL Alcohol is a common cause of acute pancreatitis. Ethanol causes spasm of sphincter of oddi leading to elevated intraductal pressure and consequently inflammation. Ethanol also acts as a toxin to pancreatic acinar cells where it can cause inflammation. TUMOURS About 1-2% patients with acute pancreatitis have pancreatic carcinoma. Pancreatitis possibly results from blockage of secreted juice and as a consequence of pent up secretions. IATROGENIC PANCREATITIS Acute pancreatitis is associated with number of surgical procedures such as pancreatic biopsy, bile duct exploration, distal gastrectomy and splenectomy. ERCP results in pancreatitis in 2-10% cases. Pancreatitis is also reported with cardiopulmonary by pass and cardiac transplantation. DRUGS Certain drugs are known to cause pancreatitis such as thiazide diruretics, Frusamide, estrogens, azothioprine, Methyldopa, sulphonamides, tetraycline, nitrofurantoin, valproic acid and steroids.

SURGERY - GASTRO-INTESTINAL PROBLEMS

RARE CAUSES Mumps, carcinoma, hyperparathyroidism are less common causative factors of this disease. Acute ischaemia caused by thrombo-embolic phenomenon may lead to acute pancreatitis.

PATHOGENESIS ACINAR CELL INJURY Acinar cell injury seems to be the root cause of all the changes occurring in acute pancreatitis. The viruses, endotoxins, toxic chemicals, ischaemia and trauma may lead to the injury to the acinar cells of the pancreas. This leads to activation and release of the enzymes which cause autodigestion of the tissues and acute inflammation of the pancreas. HYPERSECRETION, PARTIAL OBSTRUCTION AND REFLUX This view proposes that rupture of pancreatic ducts occurs due to pancreatic secretions in the presence of partial obstruction of the pancreatic ducts. This leads to leakage of enzymes from smaller ducts due to raised intraductal pressure. It leads to acute attack of pancreatitis. Total obstruction of the ducts leads to the suppression of pancreatic activity and not pancreatitis. Associated biliary and duodenal reflux is also very essential for the occurrence of acute pancreatitis.

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ACUTE PANCREATITIS

HYPERLIPIDEMIA Its mechanism of action is not clear.

! !

The exogenous part of pancreas produces nearly 22 enzymes such as; ! Proteases (approx' 15) ! Amylase (approx' 06) ! Lipase ! Phospholipase ! Elastase These are produced as proenzymes which are activated on release. Proteases, trypsin, chymotryspin and elastase produce broth which is rich in enzymes. Lipase and phospholipase-A cause fat necrosis and release free fatty acids. All these lead to local damage and systemic effects. The basic abnormalities are ;

! ! ! !

Proteolytic destruction of the pancreatic substance. Necrosis of the blood vessels resulting in subsequent haemorrhage. Fat necrosis by lipolytic enzymes. Inflammatory reaction.

The extent and predominance of these changes varies from patient to patient. There may be only interstitial edema or areas of frank necrosis in endocrine and exocrine parts of the gland. The affected cells show glossy and cloudy appearance and then granular coagulative necrosis. Haemorrhage and extravasation of varying degrees is also seen.

CHARACTERISTIC CHANGES ! Focal areas of fat necrosis occurring in the stromal, peri-pancreatic fat and fat deposits throughout the abdominal cavity. ! Leucocytic reaction is present between the areas of haemorrhage and necrosis of both fat and protein elements

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! !

Secondary bacterial invasion is common after 3-4 days which modifies the whole picture. Acute necrotizing damage resolves slowly in the patients who survive but occasionally liquified areas are walled off by fibrous tissue thus forming pseudocyst. The parenchyma shows areas of gray white proteolytic destruction, haemorrhage and chalky white areas of fat necrosis and calcium deposition. The peritoneal cavity is filled with serous fluid full of fat globules (similar to chicken broth).

WEEK 1

WEEK 2

Inflammatory Phlegmon

Necrosis

Non-Operative Management

WEEK 3

WEEK 4

Infected Necrosis

ABSCESS OR PSEUDOCYST

Operative management

CLINICAL FEATURES ABDOMINAL PAIN Almost 90% of cases present with sudden attack of acute abdominal pain which is mainly in the epigastrium and

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ACUTE PANCREATITIS

is seen only in 10% cases and it may be partly due to circulating kinins. It may also be due to severe septicaemia.

23.02

RARE FEATURES Cyanosis is less common than believed. Jaundice, ascites, paralytic ileus, haematemesis, discoloration of the skin may be present in loins (Gray Turner's sign) or it may be present around umbilicus (Cullen's signs)1. Retinopathy 2 and visual disturbances can also be seen . Cullen sign Cullen's sign, periumbilical ecchymosis is most often seen with haemorrhagic pancreatitis, splenic rupture and other causes of haemoperitoneum. It resolves within 14 days of its presentation1.

23.03

DIAGNOSIS Diagnosis is made on clinical grounds by proper history and examination. It may not be easy and other tests required to confirm the diagnosis are; Gray Turner sign radiating through to the back. 5-8% of patients have no pain at all. VOMITING AND RETCHING Repeated and noisy retching is characteristic feature. It may be associated with vomiting. RIGIDITY (ABDOMINAL) This develops slowly as the disease progresses and may become generalized (peritonitis).

URINE EXAMINATION It is a very simple and economical investigation. It is very valuable. Glycosuria may be present even in non diabetics. Urinary amylase excretion in 24 hours specially when interpreted with the serum amylase level is a useful guide. BLOOD EXAMINATION ! Heamoglobin ! Total leucocyte count ! Differential leucocyte count ! Sedimation Rate (ESR)

TENDERNESS It is more marked in the epigastrium, left hypochondrium and left renal area.

C-REACTIVE PROTEIN If above 150mg/l is strong predictor of severe disease.

SHOCK Peripheral vascular collapse and severe shock like state

ARTERIAL BLOOD GASES These are mandatory to evaluate Pa O2 which is a predictor of severity of disease process.

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ACUTE PANCREATITIS

PANCREATIC ENZYMES Serum Amylase Serum lipase

LIVER FUNCTION TESTS Serum bilirubin level is slightly raised. Rest of the liver function tests also show abnormal values.

SERUM AMYLASE LEVEL This is confirmatory if in excess of 1000 somogyi units / 100 mls of blood within 24 hours of onset of symptoms of acute pancreatitis. Elevation of amylase is as sensitive as that of lipase, pancreatic isoamylase, immuno reactive trypsin or elastase after 24 hours of onset of symptoms. Amylase is the least sensitive of the enzyme estimation tests.

TRYPSIN ACTIVATED PEPTIDE (TAP) TAP is elevated in the urine of patients within 12 hours of onset of symptoms. It has sensitivity and specificity of 96% and 95% respectively.

! !

RENAL FUNCTION TESTS Serum urea level is raised. Creatinine clearance also indicates defective renal function.

Amylase determination is non specific. Serum amylase rises within 2-12 hours of the onset of acute pancreatitis and returns to normal in 3-4 days. Raised serum amylase level for more than a week is indicative of development of a complication in a case of acute pancreatitis. 5% of the patients with this disease do not have elevation of serum amylase.

ELECTROCARDIOGRAM E.C.G. may show abnormalities and should be carefully interpreted. The changes are similar to cardiac ischaemia such as S-T elevation & T wave inversion.

SERUM LIPASE ESTIMATION Lipase assays are fast, reliable, practical and more specific and almost as sensitive and no more expensive3. It has sensitivity of 95% and specificity variable from 5595%.

ULTRASOUND EXAMINATION It is the first line investigation for the diagnosis of acute pancreatitis. It is economical, simple, easily available and very useful investigation. It can differentiate it from other causes of acute abdomen. Findings noted may include swollen pancreas, gall stones and ascites. Acute pancreatitis is most accurately predicted.

AMYLASE CREATININE CLEARANCE RATIO (A.C.C.R) Following formula is used to calculate its ratio ; urinary amylase 100 x -------------------urinary creatinine

23.03

serum creatinine x ------------------serum amylase

The value of more than 5 is practically diagnostic. SERUM CALCIUM LEVEL Serum calcium undergoes delayed fall due to saponification in the peritoneal cavity.

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Ultrasound scan (acute pancreatitis) RADIOLOGICAL EXAMINATION X-ray of the abdomen shows fluid levels and gas shadow

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ACUTE PANCREATITIS

at left upper abdomen (sentinel loop). It may also show calcification in biliary and pancreatic areas. X-ray chest is advised especially in patients with respiratory distress. CT GRADING OF SEVERITY DESCRIPTION A Normal Pancreas

CT GRADE 0

B Edematous Pancreas

C (B) plus mild extra pancreatic changes

D Severe extra pancreatic changes including single fluid collection

E Multiple fluid collections GRADE

None < 1/3 > 1/3 > Half

0 2 4 6

FNAC CT guided fine needle aspiration of the para-pancreatic fluid collection has been frequently used as a diagnostic tool for pancreatic abscess and necrosis. It is safe and a reliable method of diagnosis of pancreatic infection4.

DIFFERENTIAL DIAGNOSIS 4

NECROSIS

DIAGNOSTIC LAPAROSCOPY/ LAPAROTOMY If there is any doubt in the diagnosis, exploratory laparotomy is performed to confirm the diagnosis. Laparotomy may increase the morbidity slightly but it decreases the mortality due to uncertain diagnosis and inadequate treatment.

Acute pancreatitis has to be differentiated from other conditions causing acute abdominal emergencies such as; !

CT / MRI SCANNING Acute pancreatitis is most accurately predicted with CT. CT is useful in diagnosing the presence of and estimating the extent of pancreatic necrosis3. 23.04

Swollen pancreas

CT scan (acute pancreatitis)

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! ! ! ! ! !

Acute cholecystitis. Perforated peptic ulcer. Mesenteric thrombosis or infarction. Strangulated intestinal obstruction. Ruptured aortic aneurysm. Acute appendicitis. Acute coronary Occlusion.

COMPLICATIONS SYSTEMIC ! Systemic inflammatory Response syndrome (SIRS). ! Respiratory Faliure. ! Renal Faliure ! Multiple organ dysfunction and failure (MODF) LOCAL Pancreatic and peri-pancreatic necrosis ! Infected pancreatic necrosis ! Pancreatic abscess ! Pseudocyst ! Infected pseudocyst ! Chronic pancreatitis ! Hypocalcaemia !

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LOCAL COMPLICATIONS OF ACUTE PANCREATITIS

23.05

Necrosis

Mild acute pancreatitis

23.06

23.07

Recurrence of severe acute pancreatitis with extra and intra pancreatic necrosis

Necrosis

Severe acute pancreatitis predominantly with Mild acute pancreatitis extra-pancreatic necrosis

23.09

Development of chronic pancreatitis

23.10

Pseudocyst

Development of extra-pancreatitc psudocyst

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23.08

End stage chronic pancreatitis

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! ! !

Colonic stricture. Visceral pseudoaneurysm Venous thrombosis

IMRIE SCORE

MANAGEMENT Management of pancreatitis comprises of following steps; VOLUME RESUSCITATION Fluid and electrolytes replacement optimal fluid and electrolytes are infused to achieve urine output of 0.5 ml/kg body wt/Hour. GASTRIC DECOMPRESSION AND NUTRITION Naso-gastric decompression is performed to decrease stimulation of pancreatic secretion. Nutrition is provided via naso-jejunal route if possible. Parenteral nutrition is the less preferred route for nutrition. OXYGEN SUPPLEMENTATION Continuous supplemental oxygen is administered to achieve 95% arterial saturation.

ANTIBIOTICS The role of prophylactic antibiotics is controversial. However, recently Cephalosporins have been used for prophylaxis with encouraging results. GLUCAGON It is thought to be helpful as it suppresses the pancreatic secretion and also increases celiac blood flow which tends to maintain pancreatic microcirculation (its value is doubtful). APROTININ (TRASYLOL) This is proteolytic enzyme inhibitor thus helps by inhibiting proteolytic enzyme in acute pancreatitis. (its

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>60 mmHg <60 mmHg

<8 mg/dl

>180 mg/dl

>600 u/l

>45 mg/dl

Urea

1 severe disease

>15000

If score >=3 ANALGESIA Adequate analgesia is provided through parenteral route. Opiates are drugs of choice.

<3.2g/dl

If score <3

unlikely severe disease

FEATURE THAT MAY PREDICT A SEVERE ATTACK Initial ASSESSMENT ! Clinical impression of severity ! Body mass index >30 ! Pleural effusion on chest radiograph ! APACHE II score > 8 24 HOUR AFTER ADMISSION ! Apache II score >8 ! IMRIE score >3 ! CR Proteins > 150 mg/dl ! Persistent multiorgan failure

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value is doubtful). It definitely decreases the mortality in old patients. MONITORING Continuos monitoring of blood pressure, pulse, temperature and urinary output is performed. ESTIMATION OF SEVERITY OF DISEASE This is essential part of management and predicts outcome and helps in decision of the management of disease process. Various scoring systems are used to predict the severity. Commonly used is IMRIE scoring and APACHE II. SURGERY Indications of surgery are following; ! Irreversible clinical deterioration despite supportive care for at least 2 weeks from onset of symptoms. ! Extensive > 50% pancreatic necrosis is on CT scan. ! Biliary obstruction / ascending cholangitis and gall stone disease. OBJECTIVES OF SURGERY To evacuate necrotic and infected material To drain toxic products of the process To prevent accumulation of these products To avoid injury to adjacent visceral and vascular structures. ! To decompress biliary system ! To prevent future attacks

! ! ! !

TYPE OF SURGERY Laparotomy and pancreatic necrosectomy and abdominal drainage. ! Laparoscopic necrosectomy ! CT-guided /US guided drainage ! ERCP to decompress biliary system ! Cholecystectomy is performed in patients with gall stones to prevent future episodes.

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Survival can not be expected in patients with infected pancreatic necrosis without adequate surgical debridement. Ongoing sepsis and the multi-organ failure syndrome (ARDS, renal and hepatic failure) are frequently associated with the terminal phase of necrotizing pancreatitis6.

PROGNOSIS RANSON SCORING ON ADMISSION age > 55 WCC > 16000 / ul RBS > 200 mg/dl LDH > 350 iu/l AST > 250 iu/l

INITIAL 48 HOURS hematocrit decrease > 10% BUN > 5 mg/dl calcium < 8 mg/dl arterial PO2 < 60 mmhg Base deficit > 4meq/l Fluid loss > 6 l

SCORE 0-2 3-4 5-6 >6

MORTALITY 0% 15 % 50 % 70 - 90 %

Ransonâ&#x20AC;&#x2122;s scoring helps to assess early prognostic signs of acute pancreatitis. This can be predicted by following markers. It is poor if; ! Patient is older than 60 years. ! White cell count is more than 15000/cmm. ! Arterial pO2 is less than 60 mm of Hg. (Arterial oxygen pressure) ! Serum calcium level is less than 2.0 mmol/L. ! Serum albumin is less than 32 G/L. ! Serum glucose is more than 10 mmol/L. ! Urea is more than 16 mmol/L. ! Methemalbumin is present in the blood. E.C.G. shows ischaemic changes. ! Serum LDH is more than 350 mmol/L. ! SGOT more than 250 SF units / dL11. ! Base deficit is more than 4 meq/L. 191

ACUTE PANCREATITIS

Estimated fluid sequestration is more than 6 Litres.

Description

Mortality

More than 7 of above signs present

90%-100%

5-7 signs present

50%

Less than 5 signs present

15-20%

9. Moshe shein Sheins common sense emergency Abdominal surgery 2nd edition 2004 page 151161.

SUMMARY

REFERENCES 1. Chung MA. Qung C. Szilagyi A. Cullen's sign. It does not always mean haemorrhagic pancreatitis. American journal of gastroenterology. [JC:87] 1992 Aug(8) 1026-8 . 2. Semlacher EA. Chan Yan C. Acute pancreatitis presenting with visual disturbances. American journal of gastroenterology. [JC:3he] 1993 May. 88(5): 756-9. 3. Agarwal N. Pitchumonics. Swaparasal AV. Evaluating tests for acute pancreatitis. American journal of gastroenterology. [JC:3he] 1990 Apr. 85(4): 358-66. 4. Stiles GM. Berne TV. Thomven VD et al. Fine needle aspiration of pancreatic fluid collection. American surgeon. [JC:43c] 1990 Dec. 56(12): 764-8. 5. Puolakkainen PA. Early assessment of acute pancreatitis. A comparitive study of computed tomography and laboratory tests. Acta chirurgica scandinavica. [JC:oka] 1989. 155(1) : 25-30. 6. Bradley EL. 3rd ed. Olson RA. Current management of pancreatic abscess. Advances in surgery. [JC:2pj] 1991. 24: 361-88.

Acute pancreatitis Incidence Etiology Pathogenesis Clinical features Investigations Differential diagnosis Complications Management Early Definitive IMRIE scoring Predictive factors Treatment options

POSSIBLE QUESTIONS 1. 2. 3.

What is acute pancreatitis? How will you resuscitate a patient with acute pancreatitis? What are the different complications of acute pancreatitis?

7. Schwartzis principles of surgery eight edition 2005 page 1229-1235 Chapter 32. 8. UK guidelines of management of acute pancreatitis Gut 2005; 54 (Suppl 111).

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192

Peritoneum

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ACUTE PERITONITIS

OBJECTIVES ! ! ! ! ! ! !

To understand anatomy of peritoneum. To understand peritoneal compartments. To understand the diagnosis of clinical presentations of peritoneal problems. To prepare patients with peritoneal problem for surgical management. To be able to plan immediate and definite management of peritoneal problems. To be able to look after patients with peritoneal problems during and after surgery. To be able to prevent and treat complications of peritoneal problems and their treatment.

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GIT-24

ACUTE PERITONITIS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Peritoneum is unicellular lining of peritoneal cavity. It is formed by mesothelial cells. Its area is about 2m2 These cells secrete 100 ml of serous fluid providing lubrication of both visceral and parietal layers. It is a closed cavity except at fimbrial ends of fallopian tubes in females. Acute peritonitis is the sudden generalized inflammation of the peritoneal cavity. It is caused by the bacterial, fungal or chemical invasion of peritoneum. Patients with diffuse and generalized peritonitis show an overall mortality of about 20% probably due to;

! ! !

Breakdown of local defense mechanisms. Out spread of bacteria and toxins. Septic shock syndrome.

Peritonitis is of following types; A PRIMARY (SPONTANEOUS) B SECONDARY C TERTIARY Tertiary peritonitis or recurrent peritonitis occurs after operation or secondary bacterial peritonitis. It is persistence of intra abdominal infection after initial treatment of secondary peritonitis1,2. The major risk factors are; Malnutrition A high Acute Physiology and Chronic Health Evaluation score (APACHE). ! Presence of organisms resistant to antibiotics. ! Organs system failure. These patients always have fever & leukocytosis even in the absence of other features. ! !

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Its management should include appropriate physiologic support, administration of antimicrobial therapy, operation or surgical intervention for control of source of contamination and unburdening of bacterial load. The mortality of tertiary peritonitis is greater due to antibiotic resistant bacteria, bacteremia and septicaemia. Early diagnosis and effective intervention is critical in achievement of successful results2.

PRIMARY PERITONITIS SPONTANEOUS BACTERIAL PERITONITIS (SBP) SBP is defined as an infection of the ascitic fluid in the absence of any obvious intra abdominal (perforation) sources3,4. It is a common and often fatal complication occurring in cirrhotic patients with ascites. Its presentation is fever, abdominal pain and distension. Its signs include presence of ascites and rebound tenderness. Ascitic culture is found positive for E Coli, Streptococci and klebsiella. Diagnosis is made on presence of more than 1000 polymorphs/cmm in ascitic fluid4. It occurs without any obvious source of contamination. It is relatively uncommon. Usual causative organisms are E. Coli (50-60 %) and pneumococci. It is possibly 5 hematogenous in origin . Klebsiella and haemolytic Streptococci have also been obtained from the ascitic fluid during the recent years. 195

ACUTE PERITONITIS

It is usually seen in children suffering from nephrotic syndrome or after splenectomy. It is seen in adults suffering from cirrhosis of liver. 10% of patients with ascites develop this condition. This type of peritonitis is also seen in chronic renal failure patients who are on Continuous Ambulatory Peritoneal Dialysis (CAPD).

the peritoneal cavity due to suppurative bacteria. It is also called secondary bacterial peritonitis. Secondary peritonitis has an intra abdominal focus of 1 infection which initiates the infection (peritonitis) . Acute peritoneal infection results from; Gastro-Intestinal perforation. Anastomotic dehiscence. Infected pancreatic necrosis.

The symptoms of peritonitis are not typical in these patients and could cause diagnostic problems as abdominal cavity is already filled with ascites or dialysis fluid which gets infected. Strong suspicion should be made due to unexplained pyrexia, anorexia, rigors, confusion and deteriorating general condition6.

! ! !

Microscopic examination of the intra peritoneal fluid usually confirms diagnosis. Immediate and early treatment should be started. It is also common in patients with Chronic active hepatitis, AIDS, Wilson's disease, Rheumatoid arthritis, Pancreatitis, SLE (systemic lupus erythematosus) and patients with cardiac failure. It is common in patients with ascites of low protein content. It is highly morbid and often a fatal complication of cirrhosis 7 and ascites . The mortality is approximately 5-10% perepisode.

All types of chemical and biliary peritonitis also change into suppurative peritonitis after few hours if not treated or treated inadequately. Its mortality rate ranges between 20-60%. Severe sepsis complicates the course of nearly 11% of all patients with peritonitis.

SECONDARY PERITONITIS Secondary peritonitis has following types according to the causative factors; ! Chemical peritonitis. (Aseptic) ! Biliary peritonitis. ! Suppurative peritonitis. ! Meconium peritonitis. ! Granulomatous peritonitis. (Tuberculous) ! Interventional ! Traumatic ! Drug-induced ! Foreign body ! Carcinomatosis

SUPPURATIVE PERITONITIS This is the actual type of generalized peritonitis. It follows bacterial invasion. It is the generalized inflammation of

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It also follows perforation of inflamed appendix, typhoid ulcer and inflamed colonic diverticulum.

Risk factor analysis identifies patient at greatest risk for severe sepsis. These patients have severe organ dysfunction. These patients require aggressive surgical intervention and more effective antimicrobial agents8. Risk factors for severe sepsis ; ! Old age (68 years Âą19). ! Female sex. ! Pre existing illness. ! Pre-morbid organ dysfunction. ! Appendicular perforation. ! Mesenteric infarction.

CHEMICAL PERITONITIS This is the type of generalized peritonitis which follows irritation by extravasated secretions such as urine, blood or meconium. It follows perforation of duodenal ulcer and leakage of acid gastric juice and gastric contents into the peritoneal cavity. Perforation of the duodenal ulcer is a common cause of peritonitis. Few hours after perforation, the

196

ACUTE PERITONITIS

bacteria (intestinal commensal) invade the peritoneal cavity and change the chemical peritonitis into bacterial peritonitis. Another type of chemical peritonitis is seen with intra peritoneal rupture of the urinary bladder leading to urinary peritonitis. This also changes into suppurative peritonitis after few hours unless treated adequately.

BILIARY PERITONITIS This is the type which follows biliary leakage into the peritoneal cavity. It is the most common type of sterile peritonitis. Next common peritonitis is due to pancreatitis. It is also a sort of chemical peritonitis which changes into suppurative peritonitis later on. This usually follows injuries and perforation of the biliary passages or gall 5 bladder. This is a less common type of peritonitis .

ME CONIUM PERITONITIS It is non bacterial type of peritonitis. It occurs during intrauterine life of the fetus and is due to fetal gut perforation. It leads to adhesive peritonitis, intense fibrosis and calcification. It may get secondarily infected. Pseudocyst or meconium ascites may be present. It can present in three different types ; ! Generalized. ! Localized. ! Cystic. It is diagnosed antenatally by ultrasonography. The ultrasonic findings in meconum peritonitis vary and may be as follows ; ! Intra abdominal mass in fields ! Dilated bowel loops in fetal abdomen ! Intra abdominal cyst formation in fetus ! Fetal ascites. ! Intra abdominal calcification in fetus. ! Polyhydramnios. During neonatal period pneumo peritoneum may be seen on plain x-ray abdomen or chest. The neonate may

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present with small gut obstruction. Post natal ultrasound finding "opaque index" of small gut 9,10 reveals multiple stenosis . B19 parvo virus seems to be responsible for nonlethal fetopathies11.

GRANULOMATOUS PERITONITIS It is presence of chronic granulomata within the peritoneal cavity in association with peritonitis. It is the result of infection due to ; ! Tuberculosis. ! Fungi such as candida albicans. ! Non specific.

TUBERCULOUS PERITONITIS Tuberculosis is caused by mycobacterium tuberculosis (human variety). There is usually an intra peritoneal focus (Intestine, mesenteric lymph-gland, fallopian tubes) occasionally haematogenous spread is also possible when the tuberculous focus is outside abdominal cavity. Its incidence is rising. Females are affected twice as commonly as males. It presents with abdominal ascites or adhesion formation. It could present as following varieties ; ! Ascitic form. ! Encysted form. ! Fibrous form. ! Purulent form. Clinically patients present insidiously with generalized weakness, anorexia, loss of weight, fever, cough & vague abdominal pain. The abdomen is distended and features of intestinal obstruction are present. The blood examination shows lowered Haemoglobin level, leukocystosis with lymphocytic predominance. Sedimentation rate is raised. The ascitic fluid also shows raised lymphocytes. Its culture may show positive results in less than 50% cases.

197

ACUTE PERITONITIS

The peritoneal cavity is studded with tuberculous nodules. It is very easily diagnosed even by naked eye appearance. The intestinal loops are adherent with each other. The diagnosis is confirmed by histo-pathological examination.

FUNGAL PERITONITIS It is a very rare type of peritonitis. It is also called mycotic peritonitis. It follows bowel perforation and peritoneal invasion by the fungi. Fungemia and candida sepsis may also be seen. It has very poor prognosis (mortality rate is about 75%). It is seen in severely ill patients having several risk factors promoting fungal disease. Antimycotic treatment should be initiated with other appropriate measures12.

SCLEROSING PERITONITIS CHRONIC NON BACTERIAL PERITONITIS GRANULOMATOUS PERITONITIS It may also occur classically. It is characterized by dense adhesions. The loops of gut are matted together and can not be separated without damage. It is also seen in patients of CAPD (Continuous Ambulatory Peritoneal Dialysis). Tuberculosis and carcinomatosis are other causes of chronic granulomatous peritonitis. The patients present with subacute or acute-on-chronic intestinal obstruction. Treatment has been very unsatisfactory. Intra and extra peritoneal bowel fistula formation is quite common. It also occurs due to introduction of foreign body into the peritoneal cavity such as talc. The starch is usually introduced from surgical gloves during surgery. The reaction is minimal and localized. It is usually asymptomatic but due to adhesions and internal herniation, intestinal obstruction may occur. Endometriosis may also produce sterile peritonitis. Ruptured ovarian or follicular cysts or ruptured dermoid cysts may also lead to severe

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granulomatous peritonitis . A second operation is sometimes required to confirm the diagnosis. Peritoneal biopsy or ascitic fluid cytology confirms the diagnosis. It can be safely treated by using non steroid anti inflammatory analgesia or even steroids in some 13 patients .

INTERVENTIONAL PERITONITIS (IATROGENIC) Endoscopic examination (gastroscopic or colono-scopic) may lead to perforation of abdominal esophagus or colonic diverticulum. It leads to bacterial peritonitis. Other intervention such as laparoscopy, percutaneous liver biopsy, drainage of abscess. E R C P and stenting, CT guided abdominal biopsy, CAPD (continuous ambulatory peritoneal dialysis). Bladder biopsy or resection of tumor leading to intra peritoneal perforation and peritonitis.

TRAUMATIC PERITONITIS Abdominal trauma both blunt and penetrating leads to exogenous or endogenous bacterial contamination by direct entry, perforation or ischaemic necrosis and bacterial invasion.

DRUG INDUCED PERITONITIS Warfarin sodium used for anticoagulation after DVT or coronary embolization may lead to retro-peritoneal haematoma formation. The leakage of haematoma may lead to peritonitis.

PATHOPHYSIOLOGY The patho-physiological events in peritonitis are as below; ! Irritation of peritoneal membrane due to contamination. (chemicals or bacterial). ! Loss of gray and glistening quality of peritoneum within 2-4 hours of contamination.

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ACUTE PERITONITIS

! ! ! ! ! !

Peritoneum becomes dull and lustreless. Small collections of serous or turbid fluid are seen. Occasionally this exudate becomes creamy and obviously suppurative. Sometimes it may become thick plastic or even inspissated. Its volume varies from patient to patient. It may be localized in some cases leading to intra peritoneal collection. Inflammatory process is usually typical.

The gut mucosal integrity is impaired in these patients. The phagocytic activity of Kupffer cells is depressed. The intestinal bacteria reach peripheral blood and infect the peritoneal cavity. The humoral immunity is impaired due to low levels of complement (C3), opsonin and fibronectin. Local trauma or bacterial contamination is responsible for acute phase inflammatory reaction which involves the release of certain cytokines such as: ! TNF alpha (Tumour necrosis factor alpha). ! Interleukin-1 (IL-1). ! Interleukin-6 (IL-6). Its role is most significant in acute phase reaction and its 9 level indicates the probable outcome of peritonitis . Its 14 level remains high in patients who are likely to die . The serum levels of endotoxin binding proteins such as transferrin, alpha 2 macro globulin and Gc-globulin allow an early prediction of forth-coming organ failure15. Severity of the disease depends upon many factors: AGE OF THE PATIENT The disease is severe and spreads quickly in extremes of age. The omentum is smaller in children and is unable to localize the infection which spreads quickly. It is aging, low resistance, atherosclerosis and associated

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illness in old patients which leads to lack of adequate control and early spread of infection. CO-MORBID FACTORS (ASSOCIATED ILLNESSES) The outcome of peritonitis is worse in patients suffering from various illnesses. The outcome is poor when peritonitis is faecal in nature. It is worse in patients suffering from malignancy, cirrhosis, diabetes mellitus, renal failure and in patients on steroid and anticancer therapy. CAUSE OF PERITONITIS If duodenal, urinary bladder or gall bladder perforations are dealt within few hours of peritonitis, the patients have better outcome, as they are still in the stage of chemical peritonitis. Faecal contamination or typhoid perforation are the bad forms of peritonitis and have very poor prognosis due to severity of invasion and decreased body resistance. SITE OF PERFORATION Gastric, duodenal, biliary or urinary bladder perforations do not cause severe form of peritonitis initially. Distal colonic perforations are bad for patients as these cause severe peritoneal contamination and severe generalized peritonitis. DURATION OF PERFORATION Longer the duration, worse is the prognosis. Prolonged contamination leads to severe form of infection, lowering of body resistance and failure of immune response. All the complications and septic shock syndrome progresses and may lead to a stage of irreversibility and death of the patient. BACTERIOLOGY Most of the known organisms have been found to cause peritonitis at various occasions. Most commonly seen organisms are given below ; ! E- Coli.

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ACUTE PERITONITIS

! ! ! ! ! ! ! !

Streptococci. Staphylococcus aureus. Enterococci. Gram negative Bacilli. Clostridium perfringens. Gonococcus. Chlamydia. Pneumococci.

The invading organisms cause generalized peritonitis once these are free in the peritoneal cavity by following ways. ! Direct spread. ! Local extension. 16 ! Blood vascular spread . DIRECT SPREAD Perforation of the gastro-intestinal-tract causes peritonitis directly by peritoneal contamination. It is seen in following conditions ; ! ! ! ! ! ! !

Perforated duodenal ulcer or gastric ulcer. Perforated typhoid ulcer. Perforated diverticulitis. Penetrating intra-peritoneal wounds. Blunt trauma leading to visceral injuries (peritoneal). Intra peritoneal rupture of amoebic liver abscess17. Post operative conditions, such as ; > Leakage from intestinal anastomoses. > Vaginal operations. > (Tubal ligation and D & C). > Rupture or perforation of uterus.

LOCAL EXTENSION The infection spreads directly from inflammatory intraperitoneal conditions such as ; ! ! ! !

Appendicitis Cholecystitis Pancreatitis Diverticulitis

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! ! ! ! !

Salpingitis Strangulation and gangrene of the loops of bowel Strangulated hernias Mesenteric artery thrombosis Ischaemic gangrene of the midgut part of the bowel

HEMATOGENOUS SPREAD This usually follows severe septicaemias. The intensity of the peritonitis depends upon the severity and the virulence of organisms, resistance of the patient and duration of peritoneal contamination. FACTORS LIMITING PERITONITIS There are many natural factors which limit the spread of peritonitis. The nature has provided means to localize and control the spread of infection. There are multiple factors which localize the infective process. Once these natural barriers fail, the infection spreads and unless treated adequately and quickly, may lead to disastrous results. These factors are ; ANATOMICAL FACTORS COMPARTMENTS OF PERITONEAL CAVITY The peritoneal compartments are functional divisions of the peritoneal cavity such as subphrenic spaces, paracolic spaces, subhepatic space and pelvic cavity. These help in limiting the spread of intra-peritoneal infection by localizing the infected cavity from the general peritoneal cavity. OMENTUM Greater omentum is commonly known as abdominal policeman. It tries to cover the intestinal perforation, infective foci and any gangrenous tissue present in the peritoneal cavity immediately. It limits the infective process by covering and localizing the diseased tissue from other parts of peritoneal cavity. SENTINEL LOOPS OF BOWEL The loops of bowel aggregate around the infective area. These try to limit the infective process and help omentum to localize the infective process. 200

ACUTE PERITONITIS

PATHOLOGICAL FEATURES PARALYTIC ILEUS The intestinal peristalsis stops and the movements of gastrointestinal tract stop. It helps minimize the spread of intraperitoneal infection. ADHESIONS The adhesions are formed in the peritoneal cavity. These separate the infected areas from healthy intra-peritoneal tissue. These segregate the intra-peritoneal compartments from the general peritoneal cavity and limit the infection. EXUDATION The intra-peritoneal exudation occurs in response to peritonitis as a normal inflammatory response. It dilutes the toxins and kills the bacteria. It limits the infection depending upon the general condition of the patients and virulence of the micro-organisms. FACTORS SPREADING PERITONITIS There are many factors which lead to the spread of disease. These are described below : DIFFUSION OF THE PERITONITIS The peritonitis becomes generalized and infection spreads very quickly when the body defenses are weak or inadequate. The etiological organisms are more virulent. There is failure of natural barriers of localization. Medical help is late or inadequate. Following factors also lead to spread and diffusion of the peritonitis. These are ; ! Increased peristalsis. ! Ingestion of food. ! Small size omentum. ! Laxatives. ! Enemas. ! Virulent organisms. ! Associated diseases (malignancy, renal failure, hepatic failure, Immune deficiency states such as AIDS).

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! !

Patients after tissue grafting. Patients on steroids and anticancer drugs.

CLINICAL FEATURES Clinical features of the causative condition are usually noted before peritonitis actually develops. Following general features are also noted when acute generalized peritonitis sets in: PAIN The patients complain of sudden excruciating pain at the site of perforation which spreads in whole of the abdomen. It is worse in the area of perforation, gangrene or infection. The pain may be severe or moderate but is continuous and gets worse on movements. The pain is severe at the time of perforation or leakage of intestinal contents but gets less severe due to exudation into the peritoneal cavity at later stages. Pain is experienced even with the respiratory movements thus leading to shallow respiration and subnormal oxygenation. FEVER Fever is almost always present. It may not be present in the earlier hours of peritonitis but is present all the time later on. Hypothermia is one of the terminal events. VOMITING This is another common feature of generalized peritonitis. It causes severe pain with every effort. It is present due to toxaemia and paralytic ileus. TENDERNESS Tenderness is present all over the abdomen and it is worse over the causative viscera. The tenderness is worse in the epigastrium in perforated duodenal ulcer, it is worse in right iliac fossa in perforated appendicitis. Rebound tenderness is almost always present in these cases.

201

ACUTE PERITONITIS

Rectal examination should always be performed in these cases. It is tender and the tenderness is severe when the cause of peritonitis lies in the pelvis (pelvic appendicitis, perforated uterus, twisted ovarian cyst, strangulated pelvic hernias etc). GUARDING, RIGIDITY (BOARD-LIKE) These are also the features of generalized peritonitis. The localized guarding is present in the very early period. In fact it is felt before the peritonitis has become generalized. Board like rigidity (total abdominal guarding) is present when the inflammation has become generalized. It is due to reflex spasm of abdominal musculature. At this stage abdominal wall cease to move with respiration. At late stages, when the muscles lose their ability for contraction, the board like rigidity disappears but other symptoms of peritonitis become more evident. PARALYTIC ILEUS, SILENT ABDOMEN All the patients with generalized peritonitis have absent bowel sounds on auscultation. This is due to the paralysis of the intestine and due to absence of peristalsis. It manifests as paralytic ileus. It is partly due to bacterial toxins which disrupt the intestinal motility. DISTENSION OF THE ABDOMEN The abdominal distension is another feature of peritonitis. It increases with the duration of peritonitis and paralytic ileus. The distended loops of bowel filled with fluid and gas give rise to tinkling sounds on auscultation due to passive movements of fluid (to and fro movements) within the distended and paralyzed bowel loops. FLUID AND ELECTROLYTE DISTURBANCES Progressive distension of intestine with fluid and gas occurs in generalized peritonitis. Vomiting leads to loss of fluids and electrolytes. The sequestration of fluid and electrolytes in the dilated loops of intestine and

SURGERY - GASTRO-INTESTINAL PROBLEMS

peritoneal cavity results in hypovolemia, dehydration and electrolyte imbalance5. HIPPOCRATIC FACE The patient has typical blank, drawn and anxious look with sunken eyes, dehydration and lethargy. JAUNDICE It is a fairly common feature which is seen in patients suffering from peritonitis. It may occur due to reactive toxic hepatitis or hemolysis consequent to septicaemia and endotoxemia. DISSEMINATED INTRAVASCULAR COAGULOPATHY The presentation of bleeding which is difficult to control is seen in patients suffering from peritonitis. It is seen as one of the terminal features of peritonitis due to endotoxaemia. It requires quick and active management. TACHYCARDIA, SHOCK AND GENERAL SYMPTOMS Tachycardia is associated with pyrexia and is aggravated by abdominal distension and diaphragmatic splinting. Tachypnoea, rapid and shallow respiration are features of the generalized peritonitis. As the peritonitis progresses, shock like condition is developed unless adequate treatment is given in time. TERMINAL EVENTS As the condition worsens, confusion, delirium and irritability is noted. Cold clammy skin and hypotension is seen. Coma occurs as a terminal event and death may occur in hopeless cases. Hypothermia is a poor prognostic sign and indicates advanced irreversible septic shock syndrome. The prognosis is very poor in patients with septicaemia. Generalized peritonitis may lead to more than fifty percent deaths inspite of adequate treatment

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INVESTIGATIONS The diagnosis of peritonitis is mainly based on history and clinical features. Following laboratory investigations are used to assess the clinical state of the patient and diagnose the peritonitis with confirmation. LABORATORY INVESTIGATIONS ! Urine C.E. ! Blood C.E. ! Blood Sugar. ! Urea and electrolytes estimation. ! Serum Amylase and Liver Function Tests. ! Blood grouping and cross matching. URINE EXAMINATION Oliguria and anuria may be present. Hourly urinary measurement is essential in such states. Urine is concentrated on naked eye appearance. No special microscopic feature is seen. BLOOD EXAMINATION Rising haematocrit due to dehydration is often seen.

RADIOLOGICAL INVESTIGATIONS X-RAY CHEST In the early stages, it is normal. Pneumo peritoneum may be seen under the right dome of diaphragm in many patients. In late stages when septic shock syndrome has become irreversible and ARDS or shock lung syndrome has also set in. The x-ray chest shows typical features of this condition involving major part of the lung fields. Occasionally pleural effusion may be present with peritonitis and it may be seen on x-ray chest. X-RAY ABDOMEN (ERECT AND SUPINE VIEWS)

This x-ray shows free gas under the right dome of diaphragm and dilated small gut loops. Free fluid in the peritoneal cavity is also seen (ground glass appearance). The dilated loops of bowel are present in the area where focus of infection is present. These are called sentinel loops.

Polymorpho-leukocytosis of varying degree is always seen. Some times in severe uncontrolled sepsis polymorpho-leukopenia may be seen. It is a very poor prognostic feature.

24.01

Blood urea is raised due to dehydration. Hyper-glycaemia may be noted in diabetics and patients with pancreatic problems. Electrolytes disturbances are frequently seen due to dehydration, vomiting and sequestration of fluid and electrolytes in the dilated loops of bowel and peritoneal cavity. Commonly hyponatremia and hypochloremia is seen. Serum amylase is raised in pancreatitis. Liver function tests show raised bilirubin level and raised level of transaminases.

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Pneumoperitonium 203

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ULTRASOUND SCAN It is one of the most valuable investigation available for the diagnosis of generalized peritonitis, even localized peritonitis in all age groups. It is much superior to the clinical impression of the surgeon in detecting cause of peritonitis18. It is diagnostic even antenataly for meconium peritonitis. The ultrasonic features vary for different types of peritonitis. General and common features to all types of peritonitis are; ! ! ! !

Presence of free fluid in the peritoneal cavity. Absence of bowel movements. Presence of dilated loops of bowel. To and fro movements of the sequestered fluid in the dilated loops of bowel.

COMPUTED TOMOGRAPHY It is valuable in detection of many intra-peritoneal inflammatory conditions. A dilated thickened appendix is suggestive of appendicitis. Caecal distension and circumferential thickness of caecal wall is seen in inflammatory involvement of caecum. Similar features are 19 seen in the inflammatory bowel diseases . MAGNETIC RESONANCE IMAGING It is a special investigation to find out the exact pathology. It is expensive and may not be available at all centers. It can be used selectively and is extremely helpful. DIAGNOSTIC PARACENTESIS It is a potent diagnostic tool and helps to diagnose peritonitis rapidly. Chemical analysis, cell count, differential count and cytology of the fluid helps in the diagnosis20. DIAGNOSTIC PERITONEAL LAVAGE (DPL) This slightly invasive investigation is used to confirm the diagnosis of acute peritonitis. The peritoneal cavity is punctured with a cannula and 100 mls of normal saline are infused and then allowed to drain out. This lavage fluid is examined microscopically for the white cell and red cell count. White cell count in the lavage fluid greater than 13 200 cells/mm3 is suggestive of peritonitis .

SURGERY - GASTRO-INTESTINAL PROBLEMS

LAPAROSCOPY MINI LAPAROSCOPY It is a very helpful investigation in doubtful cases for diagnostic purposes and even for therapeutic purpose. It brings down the morbidity in patients suffering from 21 peritonitis . Small size laparoscope is available which can be used under local anaesthesia and intravenous sedation. Nitrous oxide is used for insufflation of the peritoneal cavity. The examination of the peritoneal cavity is direct and diagnostic.

TREATMENT It is immediate resuscitation and preparation for surgery. As soon as the generalized peritonitis is diagnosed, treatment should start. Time is the most important factor affecting the prognosis. NIL ORALLY, NASOGASTRIC ASPIRATION The patient is asked to stop all sorts of oral intake as soon as the condition is clinically diagnosed. Nasogastric aspiration is started. This helps in the decompression of the upper gastro intestinal tract. It stops vomiting. It also minimizes leakage from the gastro intestinal tract and decreases the intensity of the peritonitis and shock syndrome. INTRAVENOUS FLUIDS AND ELECTROLYTES The patients lose lot of fluids into the dilated loops of gastro intestinal tract. The fluid losses are made worse at first by vomiting and then by nasogastric aspiration. All this fluid has to be replaced parenterally. Normal saline (0.9%), 5% dextrose solution and colloid solutions should be infused in correctly estimated amount. Electrolytes should be constantly checked and replaced. Acid base balance should also be maintained. Metabolic acidosis is treated by adequate treatment of the septic shock and adequate replacement of fluids.

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Blood transfusion should be given in patients with hemoperitoneum or low haemoglobin states. It should be transfused with care. Haemo filtration is most helpful in patients with disseminated suppurative peritonitis for the treatment of ARDS. It reduces the amount of extravascular fluid in the lungs. It increases right to left pulmonary shunt. It eliminates the mediators causing higher permeability of 22 pulmonary vessels . MONITORING The vital signs should be monitored regularly and carefully such as ; ! Pulse rate. ! Respiratory rate. ! Blood pressure. ! Central venous pressure. URINARY OUTPUT ESTIMATION The patient should be catheterized and hourly urinary output should be monitored. An hourly output of about 40-50 ml is fairly satisfactory. The catheter keeps the bladder decompressed in severely ill patient and keeps the patient comfortable. It also helps in precise and timed measurements of urinary output. ANALGESICS The pain should be relieved by using the parenteral analgesics. It has been a common practice not to use the analgesics before the diagnosis has been made with reasonable certainty as it can mask the symptoms and may lead to wrong diagnosis. In fact, the analgesics help to achieve patient cooperation, correct assessment and diagnosis. Adequate analgesia is very essential part of the treatment of peritonitis and it should not be withheld. SEDATION Sedation helps to keep the patient calm and less irritable. It helps in correct diagnosis and management.

SURGERY - GASTRO-INTESTINAL PROBLEMS

ANTIBIOTICS Intravenous peri-operative prophylaxis should be given 30-60 minutes before surgical incision. Antibiotic prophylaxis should be of short duration to decrease toxicity, antimicrobial resistance and excess cost23. Correctly selected antibiotics are started immediately parenterally. A combination of antibiotics should be started to cover all possible organisms before the culture and sensitivity reports are available. Bacteroides and gram negative organisms are the common causative organisms. Other anaerobes are also involved in causing the peritonitis. Metronidazole and aminoglycosides should be used parenterally. Antibiotics against gram-positive organisms are also given. STEROIDS Bolus and single dose of steroids may be used to improve the septicaemic shock. It is essential to use only a single dose of steroids in septicaemic shock. Repeated doses of steroids are harmful rather than helpful. DEFINITIVE TREATMENT As soon as the patient is resuscitated and is well hydrated, definitive treatment is carried out which is as follows : LAPAROTOMY Thorough laparotomy is performed to find out the cause of peritonitis. Treatment of the cause of peritonitis is performed such as resection and anastomoses or repair of the perforation. Excision of the infected focus such as appendicectomy, cholecystectomy or any other appropriate procedure is performed. PERITONEAL TOILET It is cleaning of the peritoneal cavity of all the foreign contents, dead and degenerate tissue, pus and blood clots. Whole of the abdomen is cleaned. All intraperitoneal compartments are cleaned individually to avoid post operative intra-peritoneal abscess formation. Extensive intra-operative lavage reduces the reoperation rate and achieves low mortality rate in patients

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with defined peritonitis. But many studies show that it does not influence the outcome following laparotomies 24,25 for peritonitis .

! !

Instillation of antibiotics in the peritoneal cavity is not helpful at all. It only causes production of resistant strains of organisms and may increase the risk of postoperative intraperitoneal adhesion formation.

! !

DRAINAGE Multiple drains in various compartments of the peritoneal cavity are also used to achieve complete and continuous drainage of pus from peritoneal and pelvic cavity during post operative period. ABDOMINAL WALL CLOSURE It should be closed with tension sutures (through and through) over a sterile gauze and skin wound is left open. Secondary suturing is performed 5-6 days later after the control of infection. The method allows free drainage of pus. ZIP CLOSURE Marlex mesh with zip fastener is sutured to the wound edges. The zip is opened under I/V sedation and peritoneal cavity is inspected frequently during early post operative period. It is supposed to reduce the sepsis rate significantly3. DEBRIDEMENT Radical peritoneal debridement has recently been advocated to achieve good results. It is meticulous removal of inflammatory fibrous membrane, excision of small abscesses and infected parts of the omentum. It leads to greater blood loss and results of this procedure are still awaited5. COMPLICATIONS ! Bacteremia, septicaemia. ! Adult respiratory distress syndrome (ARDS). ! Septic shock syndrome.

SURGERY - GASTRO-INTESTINAL PROBLEMS

! ! !

Recurrent uncontrolled intra abdominal sepsis. Residual intraperitoneal abscess such as subphrenic, subhepatic, pelvic, paracolic and inter loop abscesses. Portal pyemia, Pyelophlebitis and liver abscess. Wound infection, impaired wound healing and limb 26 ischaemia . Synergistic gangrene. Intra peritoneal incisional hernia. Adhesions and recurrent intestinal obstruction.

MINIMALLY INVASIVE SURGERY Laparoscopic toilet of peritoneal cavity and simultaneous endoscopic stenting of biliary leak may help to treat biliary peritonitis. It can be used to repair perforated peptic ulcer as well27,28.

REFERENCES 1. W. Conard Likes; E Patchen dellinger. Peritonitis and intra abdominal abscess. ACP medicine 2004. 2. Malagoni MA. Evaluation and management of tertiary peritonitis. Am Surg. 66:2, 157-61. 2000 Feb. 3. Robin stein P, Morales M, Pandiani A, Bagattin JC. Spontaneous bacterial peritonitis in hepatic cirrhosis with ascites; incidence, bacteriology and mortality in urology. 4

Lobkha P. Chunlertrith K. Spontaneous bacterial peritonitis, causes and antibiotic usage in srinagarind hospital.

5. A. cuschieri. Peritonitis: Essential surgical practice 3rd edition: A Cuschieri. G.R Giles. AR Moossa. Butterworth Heinemann. 1412-1421, 1995. 6. Gribkin JC. Cox CJ. Spontaneous Bacterial peritonitis in a healthy adult male. Australian and New Zealand journal of surgery. [JC:9ic] 1980 Sep. 60(9): 723.

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7. Murray L. Lee VT. Primary peritonitis. An unusual operative diagnosis. American surgeon [JC:43c]. 1989 Dec.55(12):710-3.

pathophysiology Infection. [JC:go 8]1991 Nov-Dec. 19(6): 447-52.

Danjel A Anaya. Avery B. Risk factors for severe sepsis Natheus in secondary peritonitis. Surg infect 4(4): 355-362, 2003.

17. Sarda AK. Bal S. Sharma AK. Kapur MM. Intraperitoneal Rupture of amoebic liver abscess British journal of surgery. [JC:634]1989 Feb. 76(2): 202-3.

9. Soong JH. Hsieh CC. Chiu TH. et al. Meconium peritonitis antenatal diagnosis by ultrasound chang Keng I H Chang Gung medical journal. [JC:chg] 1992 Sep. 15(3):155-60.

18 Chen SC, Lin FY, H Sieh YS, Chen WJ, Accuracy of ultrasonography in the diagnosis of peritonitis compared with clinical impression of surgeon. Arch surg. 2000 Feb. 135:2, 170-3-4.

10. Yang CJ. Hung DS. Meconium peritonitis with enterobacter aeragenes infection; a case report. Chung Hug iH sueb Tsa chih- Chinese medical journal. [JC:chq]1989 Jan. 43(1):71-4.

19 Horton KM; Cort FM; Fishman EK. CT evaluation of the colon: inflammatory disease. Radiographics, 20:2, 399-418, 2000,00.

11. Bloom MC. Rolland M. Bernard JD. et al. Maternofetal infection by parvovirus associated with meconium peritonitis. Archives francares De pediatric. [JC:7Iq]1990 Jun. Jul.(47)(6): 437-9. 12. Kujath P. Kochendonfer P. et al. Fungal peritonitis chirurg. [JC:d5u]1990 Dec. 61(12): 900-5. 13. Justo E. Clofent J. Lao F. et al. Starch-induced granulomatous peritonitis. Angles de medicine Interna. [JC:a5e] 1991 Apr. 8(4) 185-7. 14. Riche FC, Challey BP, Panis YH et al. Inflammatory cytokine response in patients with septic shock secondary to generallized peritonitis. Crit care Med, 28:2; 433-7, 2000 Feb. 15. Berer D. Kullerer WR. Berger HG. Are the serum levels of endotoxin binding protein reliable predictors of complications in the course of peritonitis. European jour nal of clinical investigation.[JC:en3] 1990 Feb. 20(1):66-71. 16. Halzheimer RJ. Muhrer KH. etal. Intraabdominal infection: Classification, mortality scoring and

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20. Hoefs JC. Diagnostic paracentesis. A potent clinical tool. Gastroenterology. [JC: fh3]1990 Jan. 98(1): 230-6. 21. Hil AB. Meakins JL. Clinics in Geriatric medicine. [JC:c1n] 1992 Nov. 8(4): 869-87, 22. Ender LA. Lobakov AI. Vatazin AV. machulina NIU. Haemofiltration in the adult respiratory distress syndrome in patients with diffuse suppurative peritonitis. Anestaziologia I eamimatologiia. [JC:4st]1991 Sep-Oct. (5): 12-5. 23 Osman DR. Antimicrobuial prophylaxis in adults. Myo clin proc, 2000 Jan. 75:1, 98-109.

24 Seiler CA, Bruager L, Forssmann U et al. Conservative surgical treatment of diffuse peritonitis. Surgery. 2000 Feb. 127:2, 178-84. 25. Schein M. Gecelter G. Freinkel W et al. Peritoneal lavage in abdominal sepsis. A controlled clinical study. Archives of surgery. [JC:8ia] Sep 1990. 125(9):1132-5

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SUMMARY

26. Varty K. Cambell WB. Peritonitis causing acute limb ischaemia. European journal of vascular surgery. [JC:eus]1992 Sep. 6(S): 572-3.

Acute peritonitis Incidence Etiology Pathogenesis Clinical features Investigations Types Complications Management

27 Griffen M, Ochoa J, Bolulanger BR. A minimally invasive approach to bile peritonitis after blunt liver injury. Am Surg. 2000 March. 66:3; 309-12. 28 Robertson GS, Wemyss Holden SA, Madder GJ, Laparoscopic repair of perforated peptic ulcers. The role of laparoscopy in generalized peritonitis. Ann R coll Surg Engl: 2000 Jan. 82: 1, 6-10.

POSSIBLE QUESTIONS 1. 2. 3.

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What is acute peritonitis? What are the different types of peritonitis? Outline the different investigations and steps of management of acute peritonitis.

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GIT - 25

SUBPHRENIC SPACES Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS 25.01 Ri

c ati gm ce hra spa ap

iap

d eft

ag m sp atic ac e

Liver

Stomach

Inferior and posterior boundary Right lobe of the liver. Anterior layer of the coronary ligament of the liver. Right triangular ligament of the liver. Medial Boundary Falciform ligament.

rea

Lateral boundary Diaphragm.

Spleen Kidney Kidney

RIGHT SUB HEPATIC, RIGHT POSTERIOR INTRA-PERITONEAL SPACE, RIGHT RUTHERFORD MORRISON'S KIDNEY POUCH This is a transverse space formed by :

Subphrenic spaces (anatomy) The subphrenic or subdiaphragmatic spaces are potential spaces formed by the coverings of the peritoneum on the abdominal viscera. Normally these spaces contain only few milliliters of peritoneal fluid and communicate freely with the peritoneal cavity. These spaces become important anatomically when there is collection of fluid, blood or pus in the peritoneal cavity, because these get enlarged and distended. These spaces get localized and non communicating to the rest of the peritoneal cavity due to adhesion formation. There are four intra-peritoneal and three extraperitoneal spaces in the sub diaphragmatic region. RIGHT SUB DIAPHRAGMATIC OR RIGHT ANTERIOR INTRA-PERITONEAL SPACE This space is formed by : Anterior and superior boundary Diaphragm. SURGERY - GASTRO-INTESTINAL PROBLEMS

Superior boundary Right lobe of the liver. Lateral boundary Right lobe of the liver. Diaphragm. Medial boundary Foramen of winslow. Duodenum. Anterior boundary Liver. Gall bladder. Posterior boundary Upper part of the right kidney. Diaphragm. 209

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Inferior boundary Transverse colon. Hepatic flexure. RIGHT EXTRA-PERITONEAL SPACE This is right perinephric space. LEFT SUBDIAPHRAGMATIC, LEFT ANTERIOR INTRA-PERITONEAL SPACE It has following boundaries : Anterior and superior boundary Diaphragm. Posterior boundary Left triangular ligament. Left lobe of the liver. Gastro-hepatic omentum. Anterior surface of the stomach. Lateral Boundary Spleen. Gastro-splenic omentum. Diaphragm. Medial Boundary Falciform ligament. LEFT POSTERIOR INTRA-PERITONEAL SPACE OR LESSER SAC It lies between the posterior wall of the stomach and peritoneum of the posterior abdominal wall. LEFT EXTRA PERITONEAL SPACE It is the left perinephric space. MIDLINE EXTRAPERITONEAL SPACE This is the space between the bare area of liver and the diaphragm.

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SUBPHRENIC ABSCESS Subphrenic abscess (collection of pus) is an abscess which forms below the diaphragm and above the transverse colon. It follows intra peritoneal infection. Subphrenic abscess is usually secondary to; ! Peritonitis; local or general ! Perforated peptic ulcer ! Perforated typhoid ulcer ! Appendicitis ! Pelvic inflammatory disease ! Trauma causing perforation of intra peritoneal hollow viscous. ! Contamination following laparotomy ! Stab wound ! Ruptured liver abscess. The usual course of events is determination of general condition of patient between 14th day and 21st day after laparotomy with a low, slowly increasing swinging fever, sweating and tachycardia and leukocytosis. The patient becomes anorexic, wasted and cachectic. There may be no sign of visible infection. Digital rectal examination is also normal. The pus may be present under the diaphragm in one or more of these spaces. Right subphrenic abscess is seen in 60% cases. Left subphrenic abscess is seen in 25% cases. The abscess is bilateral in occurrence in 15% cases. It requires good nursing care to look after these patients and satisfy their attendents1. The minor cause of subphrenic abscess is hepato-biliary in nature2.

DIAGNOSIS Lab Investigations Imaging studies - Ultrasound scan - CT scan - MRI scan - Radiological investigations

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ULTRASOUND SCAN It is the first line investigation of choice and helps to diagnose immediately. It is non-invasive, easily available and economical. It also helps to drain the abscess under ultrasound guidance.

25.04

Ultrasonography is correct in 60% of cases. Right subdiaphragmatic abscess is seen in 60%-90% of cases. Mean abscess volume is about 500 mls2. Ultrasound scan can differentiate the difficult cases of 3 subphrenic abscesses . 25.02

Subphrenic abscess (CT scan)

Subphrenic abscess (Ultrasound scan)

RADIOLOGICAL INVESTIGATIONS 2 Radiological diagnosis is correct in about 61% of cases . It is an investigation which is not performed these days. Radiological screening is performed where ultrasound and CT scan facilities are not available. Movements of diaphragm are checked. Failure or restriction of these movements indicate subphrenic collection. X-ray chest shows raised diaphragm and associated pleural effusion.

CT SCAN / MRI SCAN

DIFFERENTIAL DIAGNOSIS

These are very helpful investigations in different cases for the diagnosis of intra-peritoneal subphrenic collections.

Subphrenic abscess is to be differentiated from following conditions which present very closely and may cause diagnostic problem; ! Liver abscess ! Empyema thoracis ! Pulmonary collapse

25.03

TREATMENT

Subphrenic abscess (CT scan) SURGERY - GASTRO-INTESTINAL PROBLEMS

ULTRASOUND GUIDED DRAINAGE Percutaneous catheter drainage is a safe, effective and definitive method of treatment for intra-abdominal abscess. It may be used as first line treatment and open exploration should only be tried, if it is unsuccessful. It can be performed with the help of ultrasound or CT

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localization4,5. Anastomotic bowel leakage is a common cause of post-operative subphrenic abscess. Percutaneous catheter drainage is a satisfactory and less 6 invasive method of treatment . SURGICAL DRAINAGE It is surgical as soon as the patient is fit for surgery. Drainage of the abscess is performed through a wide incision. Subcostal incision on the side of the abscess offers satisfactory exposure for proper drainage2. Full cover of antibiotics is given for adequate period. General condition is improved. Blood transfusion is given if so required.

REFERENCES 1.

Bachermann S. Galloway SC. Nursing care of a patient with subphrenic abscess. Canadian critical care nursing journal.[JC: cgn]Sep-Oct. 6(3): 10-5, 1989.

Haluk GI. Ismail K. Salim D. I-event B. Hnkar K. Subdiaphragmatic abscesses: myths and realities. a report of sixty two cases. International surgery [JC:gup] 1991 Apr-Jun. 76(2)" 84-6.

Vijay aragliavan SB. Fat Ped VS anterior subphrenic abscess a new real time sign. journal of clinical ultrasound. [JC : htv]1989 Nov-Dec. 17(9): 635-5

Stylianos S. Martin EC. Starker PM et al. Percutaneous drainage of intra-abdominal collection. Journal of trauma [JC : kaf] 1989 May. 29(5): 584-8.

Treutner KH. Truong S. Klose K. et al. Intra abdominal abscess-Percutaneous catheter drainage versus operative treatment. Klinische wochen schrift. [JC : kwh]1989 May. 67(9).

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486-90. 6.

Takeda J. Hashimoto K. Tanakat et al. Postoperative subphrenic abscess following gastrectomy for gastric cancer. Kurume medical journal [JC: kxh]1990. 37(3): 165-70.

X-ray chest downloaded from www.pediatriatics.org@pakistan. Sep. 5th, 2008.

SUMMARY Subphrenic spaces Anatomy of subphrenic spaces Subphrenic abscess Investigations Differential diagnosis Treatment POSSIBLE QUESTIONS 1. 2. 3.

What are the different subphrenic spaces? What are the different causes of subphrenic abscess? What investigations will you advise in a patient with suspected subphrenic collection? What are the different treatment options in a case of subphrenic abscess?

? 212

Small Intestine

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213

SMALL GUT OBSTRUCTION

OBJECTIVES ! ! ! ! ! ! ! !

To understand the development, anatomy and physiology of small & large gut. To understand the congenital abnormalities of small & large intestine. To be able to diagnose large & small intestinal problems. To be able to manage diseases of small & large intestine. To be able to prepare these patients for surgery. To be able to look after the patients after intestinal surgery. To be able to follow up the patients on treatment for intestinal diseases. To be able to present, diagnose & treat complications following intestinal diseases or their treatment.

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GIT - 26

SMALL GUT OBSTRUCTION Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS Small gut obstruction is the obstruction to the onward flow of contents in the duodenum, jejunum and ileum. It is the blockage that completely stops or seriously impairs the passage of intestinal contents. The obstruction may occur anywhere along the small intestine and it may be complete or partial. Approximately 20% of patients admitted with acute abdomen are due to intestinal obstruction1. Small gut obstruction is responsible for more than 80% of these cases. Commonly it is the name given to ileal or jejunal obstruction. Duodenal obstruction is not included in small gut obstruction for description. Duodenal obstruction mimics pyloric obstruction. It is rare and is seen in neonates due to congenital problems (duodenal atresia). Its clinical presentation and biochemical changes are similar to gastric outlet obstruction and not similar to intestinal obstruction. Small gut obstruction is associated with rapid accumulation of gas (due to swallowed air) and fluid (intestinal fluid excretion2) in small gut proximal to obstruction. Peristalsis causes intestinal distension near the obstruction at first and then gradual accumulation of gas and fluid in proximal parts of intestine. Initially there is hyperperistalsis proximal to the obstruction, later on peristalsis declines to total lack of peristalsis.

SURGERY - GASTRO-INTESTINAL PROBLEMS

The intestinal mucosa becomes edematous and inflammed. Bacterial overgrowth and stagnation changes the intestinal fluid to feculent and smelly. If the obstruction is not treated timely and appropriately the intestine may perforate leading to infection of peritoneal cavity (Peritonitis) The small gut obstruction could be ; ! Dynamic (mechanical). ! Adynamic (paralytic ileus). DYNAMIC (MECHANICAL) It occurs due to mechanical occlusion of the bowel lumen. ADYNAMIC (PARALYTIC ILEUS) The adynamic obstruction is due to paralysis of the small gut (paralytic ileus) without any organic obstruction.

MANAGEMENT The small gut obstruction presents as an acute surgical emergency and may require urgent surgical treatment. Objectives of management of the acute small gut obstruction are; ! Resuscitation. ! Diagnosis. ! Definitive Treatment. RESUSCITATION As soon as the patient presents with acute intestinal obstruction, resuscitation is started.

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NIL ORALLY The patient is advised not to take anything orally. It is essential as anything taken orally makes the obstruction worse. NASOGASTRIC ASPIRATION The gastro intestinal tract not only contains food taken orally but also secretes large quantities of its juices which are full of enzymes and electrolytes. Their quantity is increased in the small gut proximal to the obstruction making obstruction even worse. The nasogastric tube is passed immediately and all the contents are aspirated. It helps to decompress the obstructed small intestine. All the swallowed air, sequestrated secretions and food material which is stagnant and decomposed is aspirated to minimize toxemia and bowel distension. It helps in the relief of symptoms and estimation of amount of fluid and electrolytes to be replaced. It minimizes septicemia and toxemia. The edema of the intestine is relieved and obstruction may be relieved completely in many cases but surgery may be required in other patients. FLUIDS AND ELECTROLYTES Intravenous cannula of appropriate size is passed and fluids and electrolytes are infused. The amount of fluids and electrolytes is calculated according to the losses and duration of obstruction. The patients have usually lost lot of fluids and electrolytes due to vomiting or sequestration of large amount of fluid into the lumen, intestinal wall and peritoneum. More fluid and electrolytes are lost through nasogastric aspiration. Adequate replacement of fluid & electrolytes is mandatory. It is done over a short period. The patient is monitored carefully by measurements of ; 1. Pulse rate. 2. Respiratory rate. 3. Blood pressure. 4. Central venous pressure. 5. Urinary output.

SURGERY - GASTRO-INTESTINAL PROBLEMS

ANALGESICS Intravenous analgesics are given to relieve the severe and unbearable pain. Oral analgesics are lost through vomiting or stagnation in small gut. These fail to get absorbed into circulation and do not provide analgesic effect. Morphine 15 mg, pethidine or any other suitable analgesic injection can be used. These injections can be repeated if required during investigations and prior to definitive treatment. Injection of non steroidal anti inflammatory drugs can also be used to relieve the pain and minimize edema at the site of obstruction. Injectable antispasmodics are also used to relieve the colic. BLOOD TRANSFUSION It may be required if the cause of obstruction is intussusception or strangulated loop of small gut as in these cases there is loss of blood in the intestine. URINARY OUTPUT The urinary output is a simple but excellent guide for assessment of correct fluid and electrolyte replacement. Initially hourly urinary output is monitored. Sixty mls of urine per hour is a satisfactory indication of fluid replacement. The electrolytes are checked by testing the blood biochemically.

DIAGNOSIS The objectives of diagnosis are to find out ; ! Cause of obstruction ! Type of obstruction ! Site of obstruction ! Duration of obstruction Clinical, radiographic and sonographic findings are most valuable tools in the differential diagnosis of intestinal obstruction. Repeated observations are necessary for correct diagnosis, assessment and management3.

ETIOLOGY There are three main causes of mechanical small bowel

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SMALL GUT OBSTRUCTION MANAGEMENT

Resuscitation Nil Orally

Diagnosis Biochemical Tests

N.G Suction X ray Abdomen I/V Fluids and electrolytes

U.S

Analgesia

C.T

Blood Transfusion Monitoring urinary out put

Definitive Treatment

Treatment of Cause / Surgery

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obstruction ; 1. Intraluminal (Foreign bodies, bezoars and food bolus) 2. Intramural (tumours, crohn's disease, tuberculosis) 3. Extraluminal ( Adhesions, hernias, volvulus) INTRALUMINAL These are usually uncommon. Any food material passed through pylorus can pas through normal small bowel. The obstruction can occur due to compromised small bowel lumen. Possible factors are; ! Bezoars ! parasites such as Ascaris ! Gall Stones(Cholecystsoenteric fistula) ! Indigestible food material ! Inspissated meconium may result in obstruction of distal ileum in patients of cystic fibrosis. INTRA MURAL CASES Neonatal atresia and stricture Thickening of small bowel with Luminal compromise (Crohn's disease) ! Tuberculosis ! Strictures following medication and irradiation. ! Post traumatic intramural haematoma ! Lipomatosis, Leiomyomas, carcinoid tumors and lymphoma or rarely adenocarcinoma. ! Secondary tumours from gastric, colonic, ovarian or malignant melanomas ! Intussusception.

! !

It may be caused by polypoid tumours or submcosal lesion. Intussusception in children younger than two years of age due to meckel's diverticulum, polyps and Henoch-Schonlein purpura.

EXTRA LUMINAL CAUSES These are the most common. ! Adhesion due to previous surgery, peritonitis. Adhesive bowels between bowel loops.

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! ! !

Congenital intra peritoneal bands. Congenital mal-rotation leading to torsion or volvulus Hernias (Both external and internal) occasionally the obstruction may be caused by more than one cause.

Small gut obstruction in neonates and infants is caused by some congenital defect, meconium or twist in the loop (volvulus) or intussusception telescoping of a segment into another. Adhesions are cause of obstruction in more than 50% adult patients. Abdominal and internal hernias are the 2nd most common cause. CLOSED LOOP OBSTRUCTION the closed loop obstruction of small bowel is rare. It is most commonly encountered in colon from an obstructing mural lesion in the presence of intact ileocecal valve. It leads to rapid intra luminal pressure in the closed loop and impairment of its vascular supply leading to avascular necrosis of caecum and perforation (Pistol 2 shot-perforation) . The intestinal obstruction is diagnosed on history and clinical examination. It is important to diagnose the site of obstruction and most probable cause of obstruction. One should find out the duration of obstruction and assess the biochemical abnormalities.

CLINICAL FEATURES The acute small gut obstruction presents with the following features; PAIN Pain is the presenting feature of small gut obstruction. Severe colicky abdominal pain is experienced which is sudden in onset. The pain appears and then disappears to reappear after few minutes and this cycle of pain and relief of pain continues. The colic is experienced more

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around the umbilicus although it spreads all over the abdomen. VOMITING Vomiting is severe and recurrent. The higher the obstruction in the small gut, more is the vomiting. In jejunal or upper ileal obstruction, the vomiting is practically experienced with every attack of pain and patient gets dehydrated very quickly. During the early stage of obstruction, the vomitus contains gastro intestinal secretions and food particles. Then it gets bile stained. During later stage of obstruction, it becomes faeculent. DISTENSION AND CONSTIPATION These are also features of intestinal obstruction but may be either minimally present or even absent in small gut obstruction. This is because patient gets too ill much before these features could appear. DEHYDRATION & ELECTROLYTE IMBALANCE

This is always present in small gut obstruction due to excessive vomiting. The patients have usually lost lot of fluid and electrolytes. The patient has hyponatremia, hypochloremia and hypokalemia. VISIBLE PERISTALSIS This may be seen in fully established small gut obstruction. It is more obvious in thin patients. BOWEL SOUNDS Exaggerated bowel sounds (borborygmi) are audible. It is a typical feature of acute small gut obstruction.

! ! ! ! ! ! !

Rapid and weak pulse Cold and clammy extremities Low blood pressure (Hypotension) Ashen grey colour of skin Blank look Cold sweating Sunken eyes

As soon as the history and examination is completed, following investigations are arranged:

INVESTIGATIONS URINE EXAMINATION Quantity of urine measured on hourly basis. Complete physical, biochemical and microbiological examination is conducted. BLOOD EXAMINATION Haemoglobin estimation. Leucocyte count. Sedimentation rate. Urea and electrolytes estimation. ULTRASOUND SCAN Ultrasonography is an excellent investigation for the diagnosis of small gut obstruction. It is definitely helpful to differentiate between similar conditions (acute abdominal emergencies) by showing peritoneal fluid collection, distended loops of bowel or other intraperitoneal pathologies. 26.01

HERNIAL SITES, ABDOMINAL SCARS Hernial sites may show obstructed or even strangulated hernias many times which could be the cause of small gut obstruction. Abdominal scar may be present suggesting previous operation and adhesion formation causing small gut obstruction. GENERAL FEATURES The abnormal vital signs suggesting shock like condition always follow, if patient is not managed adequately. These are ;

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Ultrasound is quite useful in diagnosing gall stone ileus. ! It shows the dilated bowel loops. ! To and fro movements of fluid in isolated intestinal segments, air in the gall bladder and an ectopic gall stone while the plain x-ray of abdomen demonstrates only features of small gut 2 obstruction . ! Lack of peristalsis in later stages.

26.03

26.02

CT Scan of Small Gut Obstruction RADIOLOGICAL EXAMINATION Plain x-ray abdomen (Erect and Supine view). Radiography is inconclusive in the diagnosis of roundworms as cause of obstruction.

Ultrasonography of Small Gut Obstruction Roundworms causing small gut obstruction can be diagnosed ultrasonologically by visualization of the alimentary canal and individual body segments alongwith 4 its movements .

Ultrasonography and CT scan are helpful in the diagnosis of closed loop intestinal obstruction showing typical features such as ; ! Isolated conglomerate of dilated fluid filled bowel loops. ! Fixation of "U" shaped distended loops. ! Thickened bowel wall. 5 ! Extra luminal fluid . CT SCAN This investigation is less often used as other simpler investigations are equally helpful in the diagnosis. Occasionally, it gives excellent diagnosis when other investigations have failed. Oral and I/v contrast enhanced CT has been shown to accurately define the level of obstruction and identify a strangulated bowel segment.

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These views are helpful to some extent in the diagnosis and planning of surgery. The presence of fluid levels in the erect view confirms the diagnosis. The distended loops of small intestine show the level of gut obstruction. In the erect film air fluid levels are visible in the small gut. It is usually present in the center of abdomen. It confirms the diagnosis of intestinal obstruction. The site of obstruction can be looked by observing the abrupt 26.04

Distended loops of Small Gut (Small Gut Obstruction)

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absence of distension of the loops of small gut. The caecum is undistended in small gut obstruction. Barium meal study should never be performed in patients with small gut obstruction. It may lead to deterioration of condition by making the obstruction worse or it may even lead to perforation of over distended gut and cause generalized peritonitis. 26.05

Plain abdominal x ray showing multiple air fluid levels (Small Gut Obstruction) 26.06

Once the patient is resuscitated and diagnosis is confirmed, the definitive treatment is carried out which is surgical. Hypertonic saline enema helps to relieve the intestinal obstruction caused by roundworms and surgery may not be required at all4.

NON-OPERATIVE TREATMENT Non-operative management of small bowel obstruction is reported to be successful in 62-85% of patients treated by this approach. Non-operative management has following components; ! Fluid & electrolytes replacement ! Decompression of bowel ! Gastrograffin challenge If contrast is within colonic lumen within 8 hours 93% patients would settle without surgery. Contra Indications to non operative management; ! Suspected ischemia ! Large bowel obstruction ! Closed-loop obstruction ! Strangulated hernia ! Perforation SIGNS FOR OPERATIVE MANAGEMENT Tachycardia Leukocytosis Continuous abdominal pain Peritonitis

! ! ! !

SURGICAL TREATMENT Choice of surgical treatment depends on the cause of the small gut obstruction. Distended loops of Small Gut (Small Gut Obstruction)

TREATMENT The objectives of the treatment of acute intestinal obstruction are ; ! Rapid fluid and electrolyte replacement. ! Intestinal decompression and relief of obstruction. ! Surgical correction of the obstruction.

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OBSTRUCTED OR STRANGULATED EXTERNAL HERNIA When small intestinal obstruction is due to obstructed or strangulated hernia, treatment of these conditions is performed surgically. If the part of bowel is gangrenous and not viable, resection and anastomoses should be performed.

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26.07

Dilated loops of bowel (small gut obstruction) 26.08

use the nasogastric aspiration for decompression of the gastro intestinal tract. Abdomen is closed with tension sutures as it is likely to stay distended for few days postoperatively. LAPAROSCOPY Laparoscopy can be used successfully in the diagnosis and treatment in selected patients of acute small gut obstruction. Pneumoperitoneum should be done carefully in order to avoid perforation of distended gut. Adhesolysis and excision of obstructing bands can be done. The post-operative recovery is quick6.

COMPLICATIONS Following complications can occur with small gut obstruction if treatment is delayed; ! ! ! ! !

Gangrenous bowel loop (Strangulated small gut obstruction) INTRAPERITONEAL PATHOLOGY When no external hernia is the cause of small gut obstruction, it is preferable to perform laparotomy through right lower paramedian incision and exploration of the peritoneal cavity is performed. The cause of the obstruction is identified, treated and reconstruction of gastro-intestinal anatomy is performed. Following procedures can be performed ; ! Resection and anastomoses. ! Removal of the bands or adhesions. ! Untwisting of the volvulus. ! Peritoneal toilet is performed if required.

Per-operative Intestinal decompression is not performed as the intestines distend soon after operation and leak through the hole made for decompression. It is best to

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Prolonged ileus Septicaemia and septic shock syndrome Intestinal perforation Generalized peritonitis Gangrene or strangulation of the bowel.

REFERENCES 1. Byme JJ. Intestinal obstruction, its serious nature and various pitfalls. Postgraduate medicine. [JC:pfk]1990 May. 87(6): 217-20. 2. Cho-KC. Hoffman-Iretin JC. Alterman DD. Closed-loop obstruction of the small bowel CT and sonographic appearance. Journal of computer assisted tomography. [JC:hvt]1989.13(2): 256-8.

3. Davies RJ. Sandrasagra FA. Joseph AE. Case report: Ultrasound in the diagnosis of gall stone ileus. Clinical radiology. [JC:diu] 43(4): 282-4, 1991 Apr. 4. Malde HM. Chadha D. Roundworm obstruction. Sonographic diagnosis. Abdominal imaging. [JC:but] 1993.18(3): 274-6.

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5. Keating J. Hill A. Schroeder D. Whittle D. Laparoscopy in the diagnosis and treatment of acute small bowel obstruction. Journal of laparoscopic surgery. [JC:a93] 1992 Oct. 2(s): 239-44. 6. Ali Nawaz Khan, Sumaira Mac Donald. Small bowel th obstruction, 2004 May 10 Medicine Specialities radiology ,Gastrointestinal.

SUMMARY Small gut obstruction Introduction Types of Obstruction Initial Management Diagnosis Closed Loop Obstruction Clinical Features Investigations Definitive Treatment Complications POSSIBLE QUESTIONS 1. 2. 3.

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How would you resuscitate a patient with Small Gut Obstruction? What are causes of Small Gut Obstruction? Discuss Definitive Treatment of Small Gut Obstruction?

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PARALYTIC ILEUS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS

! ! !

27.01

! ! ! ! !

Result of abdominal surgery. Reflex inhibition of intestinal motility. Metabolic abnormalities. (Hypokalemia, Hypothyroidism). Intraperitoneal sepsis. Mesenteric vascular disease. Drugs such as tricyclic antidepressant agents. Steroid withdrawal. Pancreatitis 28.02

Paralytic ileus Paralytic ileus is adynamic intestinal obstruction in which paralysis of the intestine occurs leading to absence of peristaltic propulsion of the intestinal contents. It is also called psuedo obstruction. It is one of the major causes 5 of gut obstruction in infants and children . Paralytic ileus may lead to complications causing jaundice and electrolyte imbalance. It is associated with destruction of bowel wall in newborn infants (Necrotizing entero-colitis). It may lead to septicemia and even death of the infant.

ETIOLOGY Paralytic ileus could occur due to ; ! Uncoordinated activity of the intestine. (Heavy metal poisoning, porphyria and uremia). ! Vascular occlusion of the intestinal vessels. It leads to anoxia and ischaemia leading to the inability of normal function.

The loss of peristaltic activity may result from5 ; ! Spinal cord Injury. SURGERY - GASTRO-INTESTINAL PROBLEMS

Distended loops of small gut (Paralytic ileus)

PATHOLOGY 12% of infants with acute diarrhoeal disease develop full picture of paralytic ileus. It may be due to use of 2 antimotility drugs. Hypokalemia may contribute to ileus . The adynamic ileus could be ; ! Physiological ! Pathological 227

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PATHOPHYSIOLOGY Adynamic ileus is very common feature after every abdominal or pelvic operation. The rate of recovery is different in different patients and variable in different parts of the intestinal tract. Gastric motility returns within forty eight hours.Small intestinal motility returns within twenty four hours. Large gut motility returns within three to five days. If the ileus doesn't disappear in time and motility of the intestinal tract is delayed, it becomes pathological. This usually occurs when there is inflammation of the peritoneal cavity or there is some foreign body in the peritoneal cavity (swab, instrument), retroperitoneal pathologic conditions of the spine or thoracic lesions (fracture ribs, basal pneumonia) or due to systemic causes such as septicaemia, hyponatremia or hypokalemia.

LAB INVESTIGATIONS Complete blood examination (CBC) Urine complete examination Blood urea Blood sugar Serum electrolyte (K+ - Na+, Ca++)

! ! ! ! !

ULTRASOUND SCAN Ultrasound scan is an easily available investigation which is very useful in the diagnosis of paralytic ileus. It shows distended loops of bowel. It also shows to and fro movements of the fluid present in the bowel lumen. 28.03

It presents with distension of the abdomen, absent bowel sounds, vomiting and constipation and abdominal pain. Other features are dehydration and features of impending or actual shock.

CLINICAL FEATURES SYMPTOMS Abdominal distention (Gaseous) Abdominal pain (Cramping) Vomiting Failure to pass flatus or stool Diarrhea Breath odor

Distended loops of bowel (Paralytic ileus) C.T SCAN It shows distended loops of small gut and lack of peristaltic movements. 28.04

SIGNS Silent abdomen or Absent bowel sounds Adynamic ileus involves both small and large intestine. It is characterized by abdominal distension and absent bowel sounds. Distended loops of bowel (Paralytic ileus) CT Scan

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PLAIN X-RAY OF THE ABDOMEN It is extremely useful investigation. It helps in the diagnosis of paralytic ileus. It shows distended loops of bowel with air fluid levels. It also helps to find out the level of obstruction if present.

Nasogastric aspiration should be continued for 10-14 days. Operation is necessary after that3. NIL ORALLY All the patients who are at risk to develop paralytic ileus should not be allowed oral fluids or food.

28.05

All patients with abdominal, pelvic and retroperitoneal operations should be kept nil orally for 3-4 days or till bowel has started working (normal bowel sounds, passage of flatus). NASO-GASTRIC ASPIRATION A nasogastric tube is passed and gastro intestinal secretions are aspirated. This helps to decompress the intestine and promote early motility. FLUIDS AND ELECTROLYTES When the patient is not taking anything orally, fluids and electrolytes should be infused intravenously. Distended loops of bowel (Paralytic ileus) X-ray abdomen

OBJECTIVES OF TREATMENT To decompress the intestine To correct the electrolytes and fluid balance to treat the cause of paralytic ileus

! !

TREATMENT One should always try to differentiate between the dynamic and adynamic intestinal obstruction before starting the treatment.

Potassium should be given very carefully as sudden increase in its serum level may lead to cardiac toxicity and death of the patient. Daily requirement of 0.6-0.8 m. moles per kg body weight. Pre-mixed intravenous fluids containing potassium should be infused. The potassium and other electrolytes must be monitored by regular biochemical assessment of the electrolytes. Sudden withdrawal of steroids in patients suffering from ulcerative colitis leads to acute ileus. It is relieved within four hours of intravenous 4 injection of hydrocortisone .

CONSERVATIVE (INITIAL TREATMENT) The treatment for adynamic ileus is conservative. The cause of persistent ileus must be found out. Most of the patients would get relieved on conservative management. In case of prolonged ileus with some pathology, surgery may be required after preparation and resuscitation.

DEFINITIVE TREATMENT The cause of the paralytic ileus is treated such as infection is treated with total cover of all possible microorganisms and source of infection should be treated properly. Hypokalemia or anaemia or hypoproteinemia is treated.

Ischaemic bowel as a cause of paralytic ileus is very unlikely in patients with early post-operative obstruction.

If there is any leaking intestinal anastomosis or abscess formation, these should be treated surgically. If any swab

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or instrument is left accidentally in the peritoneal cavity, exploration should be performed and these should be removed.

COMPLICATIONS ! ! !

Infection Gangrene of the bowel Intestinal perforation

REFERENCES 1. A Cuschieri. GR Giles AR. Moossa. Essential surgical practice. Third edition. Butterworth Heinmann London. 1995. p 1408-35. 2. Murtaza A. Khan SR. Butt KS. Finkel Y. Asperia A. Paralytic ileus as serious complication in acute diarrhoeal disease among infants in developing countries. Acta paediatrica Scandinavica. [JC:11v] 1989 Sep. 78(5) : 701-5.

SUMMARY Paralytic ileus Etiology Pathogenesis Clinical features Investigations Treatment Complications POSSIBLE QUESTIONS 1. 2. 3.

What is paralytic ileus? What are its causes? What are the different treatment Options?

3. Pickleman J. Lec RM. The management of patients with surpected early postoperative small bowel obstruction. Annals of surgery. [JC:67s]1989 Aug. 210(2) : 216-9. 4. Stelzner M. Phullips JD. Fonkalsrud EW. Acute ileus from steroid withdraw simulating intestinal obstruction after surgery for ulcerative colitis. Archives of surgery. [JC:8ia] 1990 Jul.125(7) : 914-7. 5. A.D.A.M Editorial team paralytic ileus. Adam health illustrated encyclopedia 04-12-2007.

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GIT - 27

PARALYTIC ILEUS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS

! ! !

27.01

! ! ! ! !

The loss of peristaltic activity may result from5 ; ! Spinal cord Injury. SURGERY - GASTRO-INTESTINAL PROBLEMS

Distended loops of small gut (Paralytic ileus)

PARALYTIC ILEUS

LAB INVESTIGATIONS Complete blood examination (CBC) Urine complete examination Blood urea Blood sugar Serum electrolyte (K+ - Na+, Ca++)

! ! ! ! !

It presents with distension of the abdomen, absent bowel sounds, vomiting and constipation and abdominal pain. Other features are dehydration and features of impending or actual shock.

CLINICAL FEATURES SYMPTOMS Abdominal distention (Gaseous) Abdominal pain (Cramping) Vomiting Failure to pass flatus or stool Diarrhea Breath odor

Distended loops of bowel (Paralytic ileus) C.T SCAN It shows distended loops of small gut and lack of peristaltic movements. 28.04

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28.05

OBJECTIVES OF TREATMENT To decompress the intestine To correct the electrolytes and fluid balance to treat the cause of paralytic ileus

! !

TREATMENT One should always try to differentiate between the dynamic and adynamic intestinal obstruction before starting the treatment.

Ischaemic bowel as a cause of paralytic ileus is very unlikely in patients with early post-operative obstruction.

If there is any leaking intestinal anastomosis or abscess formation, these should be treated surgically. If any swab

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or instrument is left accidentally in the peritoneal cavity, exploration should be performed and these should be removed.

COMPLICATIONS ! ! !

Infection Gangrene of the bowel Intestinal perforation

SUMMARY Paralytic ileus Etiology Pathogenesis Clinical features Investigations Treatment Complications POSSIBLE QUESTIONS 1. 2. 3.

What is paralytic ileus? What are its causes? What are the different treatment Options?

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GIT-28

ACUTE INTUSSUSCEPTION Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS Acute intussusception is the sudden invagination of a part of intestine into adjacent part of the intestine (telescoping of a segment of intestine into an adjacent segment).

INCIDENCE & EPIDEMIOLOGY ! ! ! ! !

It is a common cause of acute intestinal obstruction in an infant. It occurs in infants of 8-12 months of age. Peak age incidence is at 4 months. Usual victim is a male infant. It may occur in adults as well. The peak seasons are spring and summer.

ETIOLOGY 70-95% are idiopathic (No lead point). It is suspected that hyperplasia of lymphoid patches in the terminal ileum may be the lead point. 1 ! It may be seen after viral infection of intestine . ! There is always a conceptive lesion such as polyp or lipoma or any other neoplastic lesion. ! !

CLINICAL FEATURES Intussusception is most often diagnosed in wellnourished 7-10 months old infants. It may be seen in older children as well. Older children usually have less than average weight. Majority of intussusception is idiopathic3. The diagnosis may be very difficult sometimes due to vague symptoms. Commonly the infant presents with following features :

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PAIN The infant develops severe colicky pain in the abdomen suddenly. The pain may be intermittent in the beginning. The infant behaves normally in between the attacks of pain. After about twenty four hours, the pain becomes constant and severe. VOMITING This occurs in between the attacks of severe pain and relief of pain usually occurs after vomiting. The vomiting is also intermittent in the early period of this disease. When more than twenty four hours have passed, the vomiting becomes a constant feature and the infant loses lot of fluid and electrolytes. RED CURRENT JELLY STOOLS Blood stained mucous is passed per rectum with the progress of the disease. This is a typical feature of intussusception in the infants. DIGITAL RECTAL EXAMINATION Rectal examination shows blood on the examining finger. Sometimes even mass is palpable on rectal examination. Occasionally intussusception is prolapsed per rectum. GENERAL FEATURES Lethargy, anorexia, dehydration, sunken eyes and shock like condition results, if the infant is not treated adequately and in time. ABDOMINAL EXAMINATION There is generalized tenderness and rigidity. When the infant is sedated and asleep, a lump may be palpable in

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the right upper quadrant or epigastrium and nothing is palpable in right iliac fossa. Usually abdominal distension is not present.

Then the Foley’s catheter is pulled back till the balloon hitches snugly in the rectum and the buttocks are taped together to maintain anal seal.

INVESTIGATIONS

Ultrasound with high resolution is used to image the intussusception. Sedation in the form of Injection Diazepam 0.05 mg / Kg is given slow intravenously to calm the patient.

! Lab investigation = Urine examination = Blood examination ! Ultrasound scanning ! Radiological examination

TREATMENT RESUSCITATION NIL ORALLY / NASOGASTRIC ASPIRATION The infant should not be given any thing orally. This will help in the relief of pain and vomiting. FLUID AND ELECTROLYTES The fluid and electrolyte balance should be maintained by intravenous infusion of the fluid and electrolytes. Quarter strength normal saline is usually used in the infants and amount of fluid is calculated according to the weight of the infant. BLOOD TRANSFUSION This may be necessary specially in the patients with history of intussusception for more than twenty four hours as these are likely to have developed gangrene of the tissue involved in intussusception. The amount of the blood is also calculated according to the weight of infant and amount of other infusions given. DEFINITIVE TREATMENT CONSERVATIVE / HYDROSTATIC ENEMA Hydrostatic pressure produced by barium enema can be used to reduce the intussusception but the results vary between 49%-81%3. With the patient lying in left lateral position a 16–18 Fr Foley’s catheter is introduced into the rectum till its Ypiece and the balloon is inflated with 20–30 ml of saline.

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The enema is performed by holding the container with normal saline about 100–150 cm above the patient and letting the fluid flow down by gravity into rectum through an intravenous infusion set. No pump is used and no pressure monitors are connected to this enema circuit. A maximum of three attempts are made; each attempt is approximately 15–20 minutes in duration, between two attempts 6–8 hours gap is given. Patients are looked for the features of peritonitis or shock. Successful reduction is defined as disappearance of the intussusception and free reflux of saline into the terminal ileum. If barium solution has been used to reduce the intussusception, reduction is accepted as satisfactory when it has completely occurred and barium is seen in proximal small gut loops as well. Patients with successful hydrostatic reduction are kept under observation for 24 hours and gradually advanced on diet thereafter as their symptoms are improved. Review ultrasound study is performed prior to discharge usually on the 4th–5th day. The patients are followed up at 1 and 6 months after discharge. The perforation of the bowel may occur during attempt at hydrostatic reduction of intussusception. It occurs through areas of localized ischaemic infarction on the 5 basis of direct pressure by intussusception . Recurrence rate varies between 8-12% after barium and gas enema reduction.

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PNEUMATIC ENEMA (GAS ENEMA) All patients with intussusception should have a gas enema. However it should not be attempted if perforation 2 or peritonitis is present . Therapeutic pneumatic enemas are better, simpler, cleaner and faster for the reduction of intussusception in 4 children. The success rate is about 79% . The air pressure is continuously monitored and kept between 80-110 mm of Hg in infants and children. SURGICAL TREATMENT Surgery is still the reliable method of treatment and following procedures are carried out depending upon the circumstances. Laparotomy and ; ! Reduction of intussusception. ! Reduction of intussusception and fixation of the gut. ! Resection of the gangrenous part of intussusception and anastomosis of the healthy gut. Recurrence is very rare after surgery. POST OPERATIVE CARE Intravenous fluids and electrolytes and blood transfusion is continued for few days post-operatively till the paralytic ileus disappears. Oral fluids and milk is started gradually.

REFERENCES 1. A Cuschieri. GR Giles. AR Moossa. Essential surgical practice. Third edition. Butterworth Heinmann London. p 1408-35, 1995. 2. Katz M. Phelan E. Carlin JB. Beacley SW. Gas enema for reduction of intussusception relationship between clinical signs and symptoms and outcome. Ajr-American Journal of Roentgenology. [JC:3ae] 160(2): 363-6, 1993 Feb. 3. Luks FI. Yazbeck S. Pereault G. Desjardins JG. Changes in the presentation of intussusception. American journal of Emergency Medicine. [JC:aa2] 10(6): 574-6, 1992 Nov. 4. Mevor F. Cortina H. Marco A. Olagve R. Effectiveness of pneumatic reduction of ileocolic intussusception in children. Gastrointestinal radiology. [JC:fgz] 17(4): 339 43, 1992. 5. Reijnen JA. Mravunac M. Festen C. Intussusception complicated by bowel perforation during hydrostatic reduction. Zeitschoft fur kinderchirurgre. [JC:yf2] 45(4): 219-21, 1990 Aug.

SUMMARY Antibiotics should be used in infected and gangrenous cases. POST OPERATIVE COMPLICATIONS Prolonged ileum Fever Wound infection Pneumonitis Urinary tract infection Enterostomy stenosis Wound dehiscence Sub hepatic abscess

! ! ! ! ! ! ! !

SURGERY - GASTRO-INTESTINAL PROBLEMS

Acute intussusception Incidence Etiology Clinical features Investigations Treatment POSSIBLE QUESTIONS 1. 2. 3.

What is acute intussusception? How it is diagnosed? Discuss management options?

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Appendix

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OBJECTIVES ! ! ! ! ! ! ! !

To be able to understand anatomy of appendix. To be able to diagnose diseases of appendix (acute appendicitis). To be able to understand basis of investigations for the diagnosis of appendix related problems. To be able to understand the clinical presentation of various appendiceal problems. To be able to plan mode of management to treat appendix related problems. To be able to prepare these patients for surgery. To be able to look after these patients during and after surgery. To be able to prevent, diagnose and treat complications associated with problems related to appendix or their surgery.

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GIT-29

ACUTE APPENDICITIS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon)

Acute appendicitis is the acute inflammation of the vermiform appendix.

INCIDENCE AND EPIDEMIOLOGY ! ! ! ! ! ! ! ! ! ! !

! ! !

It is the most common acute abdominal emergency. It is rare before the age of 2 years. The peak age incidence is between 20-30 years of age. No age group is an absolute exemption. It is seen in 1.5-1.9 per 1000 population. There is an estimated 7% incidence of appendicitis. It is more common in males. Male to female ratio is 1.5:1. The incidence of perforation at the time of surgery is 15%-20%. The incidence of perforation is high in infants, young children and elderly. It results in considerable morbidity. The children with symptoms of appendicitis for more than 48 hours may have a perforation rate upto 98%1. Overall wound infection after appendicectomy is 10%-12%. The wound infection in perforated group is 35%-75%. The mortality rate in patients above 60 years of age is 6%-14%.

ETIOLOGY Obstruction to the lumen of appendix is considered to be the basic problem predisposing pathologic

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changes. It may be in the form of a faecolith, tumour or collection of worms. Sharp angulation, fibrous bands and lymphoid hyperplasia may be the other factors causing intraluminal obstruction. Acute appendicitis may be due to viral infections which lead to lymphoid hyperplasia and mucosal ulceration.

PATHOPHYSIOLOGY This intraluminal obstruction initiates the chain of pathologic changes. The mucinous secretions produced in the appendix cannot be drained because of lumenal obstruction. The collection of secretions raises the intraluminal pressure. It leads to vascular stagnation and a process of strangulation is initiated. The ischaemic injury to the appendix is produced and it promotes bacterial invasion and acute infection. The disease progresses rapidly and thrombosis of appendicular vessels occurs. It leads to gangrene and perforation which results in localized or generalized peritonitis. The appendix is found to be perforated in 16% patients at the time of surgery. The frequency of perforation is low in first 36 hours of onset of symptoms (less than 20%) but increases by 5% every 12 hours onwards. Significant factors for perforation of inflamed appendix are; ! Total time since onset of infection ! Age above 65 years

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! !

Fever Tachycardia17.

PATHOLOGY (MACROSCOPIC FEATURES) The appendix is enlarged and swollen. It is reddish in colour but may be bluish or black in colour if the gangrenous process has started. There is purulent material on the appendicular serosa. The omentum is usually stuck to the appendix. The mesoappendix is edematous, thick and it bleeds and ruptures easily on touch. Later on there is increased fibrous reaction along the walls of appendix showing multiple adhesions. The inflammation usually stops short of caecum. MICROSCOPIC PICTURE The cut-section of appendix shows increased leukocytic infiltration in the mucosa, submucosa and muscularis mucosae. The pus cells are also present and there is fibro purulant reaction over the serosa. There are multiple small abscesses present in the wall of the appendix and suppurative necrosis of the mucosa. The diagnosis is confirmed by polymorphonuclear-leukocytic infiltration of the muscularis mucosae.

CLINICAL FEATURES

unwell and doesn't show any interest in food. This is more common in children. Anorexia may be partly due to bacteremia and partly because of nausea and vomiting. NAUSEA AND VOMITING The nausea and vomiting may also be the feature of presentation. Every effort of vomiting makes the pain worse. The nausea and vomiting may be severe in cases where the appendix has perforated. FEVER Low grade fever is usually present. It is continuous in most of the cases of acute appendicitis. If the fever is high grade and progressive, it may be an indication of appendicular abscess formation. FREQUENCY OF MICTURITION Occasionally the patient complains of frequency of micturition and other features of bladder irritability. This is more common in cases of pelvic appendicitis. ACUTE RETENTION It may be associated with acute appendicitis. It is the presenting symptom in elderly patients more commonly but in young and children it may also be seen2. GENERAL FEATURES Patient looks unwell and usually avoids movements. In severe cases even the breathing movements, retching and straining of any kind makes the pain severe.

PAIN The pain is continuous and usually starts in the epigastrium which increases in intensity and localizes into the right iliac fossa later on. The pain becomes worse on coughing, sneezing, laughing and on movements. Occasionally the pain can also be colicky in nature. The pain gets better to some degree on lying still.

RIGHT QUADRANT TENDERNESS The right lower quadrant of the abdomen is tender on palpation. In severe cases, even respiratory movements may be painful.

ANOREXIA This is possibly one of the most common and earliest features of acute appendicitis. The patient feels

SHERREN'S TRIANGLE An area of hyperaesthesia is present in the right lower quadrant of the abdomen. It is bounded by

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anterior superior iliac spine, right pubic tubercle and umbilicus. It is present in acute appendicitis.

is felt due to contact of inflammed appendix with parietal peritoneum3. 29.03

29.01

SHERRENâ&#x20AC;&#x2122;S TRIANGLE:

MACBURNY'S SIGN When the maximum tenderness is present at MacBurney's point on palpation with the tip of index finger, MacBurny's sign is positive3. 29.02

REBOUND TENDERNESS (BLUMBERG'S SIGN) Deep palpation of abdomen is performed in a patient of suspected appendicitis. The palpating hand is suddenly removed after deep palpation. The positive rebound tenderness test is positive if pain is felt on removal of the pressure. It is helpful in diagnosing early inflammatory intraperitoneal lesions. The pain

SURGERY - GASTRO-INTESTINAL PROBLEMS

ROVSING'S SIGN Rovsing's sign is positive if pain is felt in the right iliac fossa while palpation is performed in left iliac fossa. It is due to contact of inflammed appendix with parietal peritoneum3. 29.04

PINCH AN INCH TEST19 This is test is reverse of rebound tenderness. The skin over McBurneyâ&#x20AC;&#x2122;s point is grasped and elevated above from the peritoneum. Then suddenly it is allowed to recoil back briskly against the peritoneum. If patient complains of increased pain, the test is positive. 239

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29.04

PSOAS TEST The patient is asked to lie on the side and right hip joint is hyperextended. It elongates the Psoas muscle. Severe pain is experienced in positive test. It occurs due to contact of inflammed appendix with Psoas muscle. Psoas test may be positive in acute appendicitis3. 29.04

29.04

PERCUSSION Percussion is tender in the right iliac fossa. AUSCULTATION Bowel sounds are absent only in cases of perforated appendix with generalized peritonitis. DIGITAL RECTAL EXAMINATION It is tender in the acute appendicitis specially when the appendix lies in the pelvis or is perforated. Rectal examination is unpleasant to majority of the patients and it doesn't give any further diagnostic information4,5. Other tests like sonography are more sensitive and specific.

DIAGNOSIS History, examination and investigations help in the diagnosis. The appendicitis may be very easily diagnosed if it presents with typical features. OBTURATOR TEST The flexed right hip joint is internally rotated. It elongates the obturator internus muscle. The painful response indicates positive test. Obturator test may be positive in acute appendicitis if the inflammed appendix lies in contact with obturator internus muscle3. SURGERY - GASTRO-INTESTINAL PROBLEMS

Its diagnosis is really difficult and test of the diagnostic skills in atypical cases. Special diagnostic problems are faced in pregnant women and old age patients. History of menstrual period is extremely important for an accurate diagnosis. Acute appendicitis is the most common non 240

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gynaecological surgical emergency occurring during pregnancy. Symptoms, signs and investigation are unhelpful in the confirmation of diagnosis. These patients should be treated on doubt6. The diagnosis of acute appendicitis may have 10%30% false positive results. Repeated examinations may be required to achieve accurate diagnosis.

INVESTIGATIONS URINE EXAMINATION It is a simple investigation. It must be performed in all patients with suspected appendicitis. It is an essential investigation to exclude keto-acidosis which mimics acute appendicitis. It helps to exclude other similar conditions. BLOOD EXAMINATION

! ! ! ! !

Haemoglobin percentage. Total leucocyte count more than 10,000/mm3. Differential leucocyte count more than 75%. Sedimentation rate is raised. Urea and electrolytes.

TRIPLE TEST

C-reactive proteins (CRP), total white blood cells count, total and differential leukocyte counts are performed and interpreted in combination. This triple test combination has a predictive value of negative result at 100%. It indicates that if the test is negative, acute appendicitis is unlikely. It can cut the rate of negative appendicectomies8. RADIOLOGICAL EXAMINATION X-RAY ABDOMEN

It helps to find out any radio-opaque shadow in the right lower abdomen indicating faecolith or ureteric stone. It may show the presence of sentinel loops in the right iliac fossa indicating presence of an SURGERY - GASTRO-INTESTINAL PROBLEMS

inflammatory lesion. It is not specific in the diagnosis of acute appendicitis. ULTRASOUND SCAN

It helps to diagnose many conditions which mimic acute appendicitis. Ultrasonography is an investigation with 96% sensitivity and 94% specificity and accuracy rate of 95% in the diagnosis of acute appendicitis10. Graded compression sonography is a valuable procedure in detecting acute appendicitis in pregnant women. Self localization for sonography improves the pick up rate11,12. CT SCAN

It can reliably distinguish phlegmonous inflammation from a liquified abscess. It can delineate the full extent of such inflammatory mass. Overall accuracy of CT Scan detection ranges between 93% - 98%. It saves of cost of treatment of appendicitis patients significantly. It can differentiate even between uncommon mimics of appendicitis18. Percutaneous drainage under CT control is safe, effective and carries low morbidity13. LAPAROSCOPY

It is a minimally invasive method of diagnosing and treating the acute appendicitis. It has an advantage that if the diagnosis is found incorrect on laparoscopy, the appendicectomy can be avoided and actual disease can be treated. It can be performed under general anaesthesia. It must be used regardless of age and sex in patients who have atypical picture and offer diagnostic problems15. ISOTOPE SCAN TC-99 (HMPAO)

TC-99 Hexamethyl propleneamine oxide (HMPAO) labeled white blood cell scan is performed half hour

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after the injection and is repeated after 2 hours and 4 hours. A positive study shows increased isotope uptake in right lower quadrant. It has a sensitivity of 81% and specificity of 100% and overall accuracy of 89%. It is useful and non invasive for the diagnosis of appendicitis9. FINE CATHETER PERITONEAL CYTOLOGY

This investigation is no more used because better, more specific and less invasive investigations are available these days. ALVARADO SCORING

Scoring is done to assess the status of appendicitis before planning its treatment. Various features are allotted scores. Combination of these scores helps to assess the disease status and decide the appropriate treatment. SCORING ITEM SYMPTOMS Migrating RIF pain Anorexia Nausea/vomiting SIGNS Tenderness RIF Rebound tenderness RIF elevated temperature LABORATORY TESTS Leukocytosis Shift of neutrophils to left Total score DIAGNOSIS Unlikely appendicitis Possible appendicitis Probable Acute Appendicitis (needs surgery) Definite Acute Appendicitis (needs surgery)

SCORE 1 1 1 2 1 1 2 1 10 SCORE (01 - 04) (05 - 06)

DIFFERENTIAL DIAGNOSIS

The pain in the right iliac fossa has to be differentiated from following conditions causing similar features ; 1. Mesenteric lymph adenitis. 2. Mittelschmerz (ovulation pain). 3. Ruptured or twisted ovarian cyst. 4. Dysmenorrhoea. 5. Meckel's diverticulitis. 6. Right ectopic pregnancy. 7. Acute cholecystitis. 8. Right ureteric colic. 9. Salpingitis. 10. Cystitis. 11. Severe constipation. UNCOMMON MIMICS 18

! ! ! ! ! ! ! ! ! ! ! ! ! ! !

Mucocele of appendix Mesenteric vein thrombosis Ovarian dermoid Necrotic uterine Lieomyoma Ovarian torsion Endometriosis Ectopic pregnancy Typhilitis Sigmoid diverticulitis Intussusception Psuedo-membranous colitis Perforated peptic ulcer Perforated gall bladder Pancreatitis

TREATMENT As soon as the diagnosis is made and decision for treatment is finalized, the preparation for surgery is started as below:

(07 - 08)

PREPARATION FOR SURGERY Consent:

(09 - 10)

Informed consent is obtained for surgery in writing

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from adults. Parents are requested to sign the consent in case of children patients. Nil Orally:

As soon as the diagnosis is even suspected, patient is advised to stop taking anything orally. It gives rest to upper gastro intestinal tract and keeps the patient prepared for emergency. NASOGASTRIC ASPIRATION

Nasogastric aspiration is not required under normal circumstances in acute appendicitis, but nasogastric tube should be passed and upper gastro intestinal tract is aspirated in cases of perforated appendix or appendicular mass.

Skin Preparation:

Skin (over the right quarter of the abdomen) is painted with antiseptic solutions (pyodine solution) 30 minutes to one hour before the planned surgery. Shaving is also done at the same time (soon before surgery). PATIENT PREPARATION The patient is advised to hand over all his/her valuables to his/her attendant/relatives or staff nurse before shifting to operation theatre. The patient wears the operation theatre clothes after removing his/her clothes. The operation theatre clothes are special and can be removed easily when required and can be easily changed for adequate exposure during surgery.

FLUIDS AND ELECTROLYTES

OPERATION THEATRE ARRANGEMENT

The patient requires 4-6 hours fasting before anesthesia and surgery. Intravenous fluids are given during this period, during surgery and during early post-operative period.

Operation room is booked for surgery after the patient is resuscitated and is ready for operation. The anesthetist, anesthesia staff and operation staff is informed in time to be ready for assisting in surgical procedure.

The appropriate fluids should be star ted immediately after the diagnosis is made. A calculated amount of electrolytes and fluids is given intravenously. ANALGESIA

The pain should be relieved after the diagnosis has been made with reasonable certainty. If the analgesia is administered before the diagnosis, the symptoms may be masked and inaccurate treatment may be offered. ANTIBIOTICS

The commonly invading organisms are both aerobic and anaerobic organisms such as E.coli and Bacteroides. The antibiotics should be used to cover both these organisms. These should start soon after the diagnosis is confirmed.

SURGERY - GASTRO-INTESTINAL PROBLEMS

DEFINITIVE TREATMENT It is always surgical. Appendicectomy is the treatment of acute appendicitis and it should be performed as soon as the patient is resuscitated adequately. Open or laparoscopic appendicectomy can be performed. Patient is shifted to the operation room. Anesthesia is given. Right lower half of the abdomen is prepared with appropriate antiseptic solution (pyodine). The definitive treatment (appendicectomy) is performed. When patient has recovered from anesthesia, preparation for shifting to the recovery room is made.

243

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POST OPERATIVE CARE

diagnosis is confirmed in only 30% - 50% of cases.

The patient is shifted from the operation theatre to the recovery room for early post operative care. Blood pressure, pulse, temperature, and respiration is monitored for some time till the patient is fully conscious. The patient is shifted to the ward as soon as fit enough to be looked after in the ward. Standard post operative care is carried out such as nil by mouth for 4 - 6 hours. Intravenous fluids, antibiotics and analgesics as per requirement of the patient. The wound care is performed till healing has completely occurred and patient is ready to be discharged home.

Common clinical symptoms are anorexia, vomiting and right lower quadrant pain. Increased uterine contractions also observed. Appendix is displaced upwards during later weeks of gestation and can produce right upper quadrant pain and tenderness even involving entire right side. Rectal pain and vaginal tenderness especially in the first trimester may be evident. Laboratory investigations are unhelpful as leukocytosis is common in normal pregnancy. Graded compression all around has shown to be highly sensitive and specific. Clinical evaluation is the final answer to this complex situation.

MANAGEMENT COMPLICATIONS If the appropriate treatment has not been given to the patient suffering from acute appendicitis, following complications may be observed : EARLY COMPLICATIONS Appendicular mass. Perforation of the appendix and peritonitis. Appendicular abscess. Paracolic abscess. Pelvic abscess. Subphrenic abscess. Septicaemia.

! ! ! ! ! ! !

LATE COMPLICATIONS ! Intestinal obstruction. ! Faecal fistula. ACUTE APPENDICITIS IN PREGNANCY Incidence of appendicitis in pregnancy is 0.05-0.07%1 approximately in 1500. The incidence rate is highest in 2nd 2 trimester ranging 27% - 60% . Perforation rate for pregnant patients have been reported as high as 55% of cases as compared with 4% - 12% of general population. Diagnosis of appendicitis is a dilemma for even experienced clinician during pregnancy. Pathological

SURGERY - GASTRO-INTESTINAL PROBLEMS

Early surgical intervention with less than 24 hrs delay has shown to be vital in minimizing maternal and fetal morbidity and mortality. Open or laparoscopic appendicectomy can be performed during first trimester. Incision for appendicectomy can be altered as per requirement as appendix relocates upwards with the progress in gestation. COMPLICATIONS OF APPENDICITIS IN PREGNANCY ! Risk of perforation in pregnancy ! Pre-term labour ! Fetal loss (un-ruptured appendicitis has risk of fetal loss 1.5% - 09% and perforated appendix carries risk of fetal loss upto 36%) ! Maternal mortality has been reported from none to 02%

REFERENCES 1. Rappaport WD. Peterson M. Stauton C. Factors responsible for the high perforation rate seen in early childhood appendicitis. American surgeon. [JC:43e] 55(10): 602-5,1989 Oct.

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2. Parrish GA. Wright GD. Falk JL. Acute urinary retention an unusual presentation of appendiceal abscess. Annals of emergency medicine. [JC:4z7] 22(5); 851-60 1993 May.

11. Lin HK. Bae SH. Seo GS. Diagnosis of acute appendicitis in pregnant women: value of sonography. Ajr. American Journal of Roentgenology [JC: 3ae] 159(3): 539-42, 1992 sep.

3. Shuja Tahir. Mahnaaz Roohi. Surgery clinical examination system. Uro-Obs (pvt) ltd. Faisalabad Pakistan p:67-84, 2005.

12. Chesbraugh RM. Burkhard TK. Balsara ZN. Goff WB. Davis DJ. Self localization in US of appendicitis: an addition to graded compression. Radiology [JC:qsh] 187(2) : 349-51, 1993 May.

4. Dixon JM. Elton RA. Rainey JB. Macleod DA. Rectal examination in patients with pain in the right lower quadrant of abdomen. BMJ [JC:bmj] 302(6773): 386-8, 1991 Feb. 5. Dunning PG. Goldman MD. The incidence and value of rectal examination in children with suspected appendicitis. Annals of Royal College of Surgeons of England. [JC:5vv] 73(4) :233-4,1991 Jul. 6. MCGee TM. Acute appendicitis in pregnancy. Australain and New Zealand journal of obstetrics and gynaecology. [JC:9io] 29(4): 378-85, 1989 Nov. 7. Christian F. Christian GP. A simple scoring system to reduce the negative appendicectomy rate. Annals of Royal College of Surgeons of England. [JC:5vv] 74(4): 281-5, 1992 Jul. 8. Dulkalm S. Baqi P. Bud M. Laboratory aid in the diagnosis of acute appendicitis. A blinded prospective trial concerning diagnostic value of leukocyte count, neutrophil differential count and Creactive protein. Diseases of the colon and rectum. [JC:eab] 32(10): 855-9, 1989 Oct. 9. Foley CR. Latiner RG. Rimkus DS. Detection of acute appendicitis by technetium 99 HMPAO scanning. American surgeon. [JC:43e] 58(12): 761-5, 1992 Dec. 10. Larson JM. Peirce JC. Ellunger DM. Parish GH et al. The validity and utility of sonography in the diagnosis of appendicitis in the community setting. Afr. American Journal of Roentgenology [JC:3ae] 153(4): 687-91, 1989 Oct.

SURGERY - GASTRO-INTESTINAL PROBLEMS

13. Shapiro MP. Gale ME, Gerzof SG. CT of appendicitis diagnosis and treatment. Radiologic clinics of North America. [JC: qq1] 27(4): 753-62, 1989, Jul. 14. Baigrie RJ. Scott-coombes D. Saidan Z. et al. The selective use of fine catheter peritoneal cytology and laparoscopy reduces the unnecessary appendicectomy rate. British journal of clinical practice. [JC:avk] 46(3) : 173-6, 1992 Autumn. 15. Kuster GG. Gilroy SB. The role of laparoscopy in the diagnosis of acute appendicitis. American surgeon [JC:43e] 58(10):627-9, 1992 Oct. 16. Donglas S. Katz; lily Belfi; Shibhan R.l Weston. CT of suspected appendicitis in adults: current status. App Radiol. 2005; 34 (7): 8-16. 17. Bickell NA; Aufses AH; Rojas M. Bodian C. How time affects the risk of rupture in appendicitis. J. Am. Coll Surg. 2006; 202; 401-406. 18. Jinxing Yu; Ann S Fulcher; Mary Ann Turner; Robert A Halvorson. Helical CT evaluation of acute right lower quadrant pain; uncommon mimics of appendicitis. Am J Roentgenol. 2005; 184 (4): 1143-1149. 19. LTc. Bruce D Adams; Capt. Devin Rickett; Capt. Philip A Albaneze et.al. Pinch an Inch test for appendicitis. South Med. J. Dec. 2005; 98(12): 1207-1209. 1. MOURAD J, ELLIOT JP, ERICKSON L, LISBOAL Appendicitis in pregnancy: new information that contradicts long held clinical beliefs. AM J OBS Cifne 2000; 182:1027-9. 2. TRACEY M, FLETCHER HS. Appendicitis in pregnancy.

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Am Surg 200; 66:555-9: discussion 559-60. 3. TAMIR R, BONGARD FJ, KLEIN SR. Acute appendicitis in the pregnant patients. AMJ Sung 1990; 160:571-6. 4. MUSSLEMAN RC. Nunndee JD Ware DB. Appendicitis during pregnancy. Clin Excell Nurse Pract 1998; 2 : 338-42.

POSSIBLE QUESTIONS 1. How would you diagnose appendicitis? 2. How will you prepare a patient for appendicectomy? 3. How will you look after a patient after appendicectomy?

SURGERY - GASTRO-INTESTINAL PROBLEMS

SUMMARY Acute appendicitis Incidence and epidimiology Etiology Pathophysiology Pathology Clinical features Investigations Scoring Differential diagnosis Treatment Preparation for surgery Operation theater arrangements Complications Acute appendicitis in pregnancy Complications of appendicitis in pregnancy

246

APPENDICULAR ABSCESS

GIT - 30

APPENDICULAR ABSCESS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS Appendicular abscess is the localized collection of pus in the peri-appendicular area (right iliac fossa) following appendicitis and its perforation. An inflammatory mass occurs either as phlegmon or abscess in 2% to 6% patients with appendicitis.

105

103

CLINICAL FEATURES History of pain in right iliac fossa and mass formation over few days is always present. Rarely it may present without prolonged history which may happen in deep and retrocaecal appendicitis. The common presenting features are : PAIN Pain is usually present in the right iliac fossa. It is not very severe to start with. It is continuous and gets worse gradually. The pain becomes throbbing and unbearable as the abscess formation occurs. MASS RIGHT ILIAC FOSSA There is mass formation in the right iliac fossa which is tender to touch. Over lying skin is usually normal. The local temperature may or may not be raised. The mass may increase in size and become more painful than before. FEVER Fever is present in association with other symptoms. It is continuous and is not responsive to antibiotics. It has a typical pattern showing progressive rise in the peak of temperature. (Swinging temperature) 1,2,3 In fact the appendicular abscess is diagnosed with reasonable certainty when the patient with appendicular mass starts running high grade temperature regularly.

SURGERY - GASTRO-INTESTINAL PROBLEMS

101

TENDERNESS The mass in the right iliac fossa becomes tender not only to touch but to respiratory movements as well. On examination even gentle palpation is very painful. PARALYTIC ILEUS Mostly these patients are already diagnosed cases of appendicular mass and are on conservative treatment when they develop paralytic ileus. Patients may present with paralytic ileus which may be due to appendicular abscess. ASSOCIATED SYMPTOMS Patient may present with difficulty in micturition, frequency of micturition, acute retention of urine and haematuria. The symptoms are due to presence of abscess and inflammatory mass near right lower ureter and bladder.

247

APPENDICULAR ABSCESS

INVESTIGATIONS URINE EXAMINATION It is a simple investigation which helps to exclude the renal causes of urological symptoms in patients with appendicular abscess. BLOOD EXAMINATION Haemoglobin percentage is decreased. Leukocyte count is raised. Polymorphonucleo-leukocytosis is present. Sedimentation rate is raised. RADIOLOGICAL EXAMINATION PLAIN X-RAY OF THE ABDOMEN It may show loops of distended small gut around the abscess area (sentinel loops). ULTRASOUND SCAN The differentiation between appendicular mass and abscess is easily done with the ultrasound scan. The abdominal ultrasound scan shows a solid mass in the right iliac fossa as hypo epoic area (fluid collection). The amount of fluid collection varies with the amount of pus present. The shadow of adherent and distended loops of bowel is also seen. Percutaneous drainage under ultrasound guidance is minimally invasive. CT SCAN It can reliably distinguish phlegmonous inflammation from a liquified abscess. It can delineate the full extent of such inflammatory mass. Percutaneous drainage under CT control is safe, effective and carries low morbidity4.

TREATMENT The treatment of appendicular abscess has following components; • • • • •

Ultrasound guided drainage of abscess Emergency surgery Laparoscopic drainage Expectant treatment Delayed surgery

SURGERY - GASTRO-INTESTINAL PROBLEMS

ULTRASOUND GUIDED PERCUTANEOUS DRAINAGE When the appendicular abscess is diagnosed by sonography. It can be aspirated with the help of a wide bore needle under ultrasound control. It is simple, safe and effective. It may be repeated if the abscess collects. In fact, the drainage is a better option than the aspiration. EMERGENCY (IMMEDIATE) SURGERY It is required when abscess fails to resolve or recurs. It is also required when the general condition of patient deteriorates inspite of conservative management. Incision and drainage of the abscess is performed. The appendix, its debris or inflammatory mass is also removed if safely possible at the same operation, otherwise, it is left for later stage to be removed as elective operation. LAPAROSCOPIC DRAINAGE 30.01

Appendicular abscess (laprascopic view) It is less traumatic and less invasive procedure but it should better be avoided as the risk of spread of infection into the peritoneal cavity is too high. EXPECTANT TREATMENT If the patient is haemodynamically stable, the patient is observed and treated symptomatically and conservatively. It is safe and effective alternative to immediate surgery. It is monitored with ultrasound and CT scan5. Initial expectant treatment has following components.

248

APPENDICULAR ABSCESS

APPENDICULAR MASS LEADING TO ABSCESS FORMATION

Parenteral antibiotics Fluid replacement Nill Orally

Serial Ultrasounds

Abscess formation No abcess

Mass Resolves

Delayed surgery (Appendicectomy) Age >40 years Barium enema Colonoscopy

SURGERY - GASTRO-INTESTINAL PROBLEMS

Percutaneous drainage

Persistent Recurrent abcess

Open drainage Surgery

249

APPENDICULAR ABSCESS

FLUID AND ELECTROLYTES The patients are given fluids intravenously. These are given according to the daily requirements of the patient. Serum electrolytes are estimated and any deficit should be corrected. NIL ORALLY The patients with appendicular abscess are not given any thing orally. Nasogastric aspiration is required in some cases to help in relieving the paralytic ileus, vomiting and abdominal discomfort. PARENTERAL ANTIBIOTICS Appropriate antibiotics are started as soon as the condition is diagnosed. Triple regimen of antibiotics is usually used. It is a combination of drugs against gram negative, gram positive and anaerobic organisms. Commonly used drugs are amino glycosides, ampicillin and metronidazole. There are two forms of surgery for treatment of appendicular abscess as following; DELAYED SURGERY Interval appendicectomy is performed about six to eight weeks afterwards. This is performed to prevent recurrent attacks and will provide definitive diagnosis. Recently there is growing evidence against routinely performing interval appendicectomy as the risk of recent attack is only 14% and most of it occurs in first three months.

COMPLICATIONS Following complications may be seen in patients with appendicular abscess ; ! Peritonitis. ! Pelvic abscess. ! Subphrenic abscess. ! Paralytic ileus. ! Adhesion formation. ! Intestinal obstruction. ! Septicaemia.

SURGERY - GASTRO-INTESTINAL PROBLEMS

REFERENCES 1.

Okoji GD. Caveron BH. Appendicitis presenting with dysuria in a 2 years old: Ultrasound aided diagnosis. Annals of tropical paediatrics. [JC:6ab]1991.: 38990.

2. Parrish GA. Wright GD. Falk JL. Acute urinary retention an unusual presentation of appendiceal abscess. Annals of emergency medicine. [JC:4z7] 1993 May. 22(5); 851-60. 3. Monu JU. Akumabor PN. Appendiceal abscess unusual cause of acute urinary retention. International journal of urology and nephrology. [JC:gug] 1990. 22(5) : 429-32. 4. Shapiro MP. Gale ME. Gerzof SG. CT of appendicitis diagnosis and treatment. Radiologic clinics of North America. [JC: qq1]1989, Jul. 27(4): 753-62. 5. Haffmann J. Rolff M. Lomborg V. Franzmam M. Ultraconservative management of appen-diceal abscess. Journal of the Royal College of Surgeons of Edinburgh. [JC:jvc]1991 Feb. 36(1): 18-20. 6. A Tekin, tic kurtoglu. Routine interval appendectomy is unnecessary after conservative treatment of appendicle mass colorectal disease, April 2007. 10,465-468.

SUMMARY Appendicular abscess Clinical features Investigations Treatment

POSSIBLE QUESTIONS 1. 2. 3.

What is an appendicular abscess? How it is diagnosed? Discuss treatment options?

250

RIGHT ILIAC FOSSA PAIN

GIT - 31

RIGHT ILIAC FOSSA PAIN Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS 31.01

Acute appendicitis 31.02

Accurate diagnosis is essential for adequate management. The common conditions causing pain in the right iliac fossa and frequency of micturition in a 17 years old girl are ; ! Acute appendicitis. ! Appendicular mass. ! Appendicular abscess. ! Dysmenorrhoea. ! Right ureteric colic. ! Vesical stone. ! Urinary tract infection. ! Abortion. ! Ectopic pregnancy. ! Salpingitis. ! Twisted or ruptured ovarian cyst. ! Ovulation pain or mittelschmerz. ! Endometriosis. ! Hysteric neurosis. ! Ileo-caecal tuberculosis. All these conditions must be kept in mind while taking the history and conducting the examination. 31.03

IVU (Right Ureteric stone) SURGERY - GASTRO-INTESTINAL PROBLEMS

Hemorrhages in right ovarian cyst 251

RIGHT ILIAC FOSSA PAIN

The right iliac fossa pain is common in other conditions mimicking acute appendicitis. Accuracy of diagnosis can 1 be improved by proceeding slowly but methodically . These can be excluded or included in the possible list of provisional diagnosis. The management of a seventeen years old girl with right iliac fossa pain and frequency of micturition is planned after correct diagnosis. The plan of management is carried out in following steps ; ! History ! Examination ! Investigations. ! Emergency treatment. ! Definitive treatment. HISTORY Complete history is extremely important for correct diagnosis and adequate treatment. History of injury or surgery should be noted. History of fever, nausea and vomiting must be asked. The menstrual history should not be omitted. Psychiatric history should also be noted. The patient should be asked probing questions regarding pain and frequency of micturition such as: PAIN When did the pain start? How and where did it start? Where is the pain now? What is it like? What makes it worse? What makes it better? Does it radiate? Where to? Relationship of the pain with food intake, micturition, movements, breathing, exercise and menstruation should be noted. FREQUENCY OF MICTURITION Exact nature of frequency such as how many times per hour? Amount of urine passed every time. Whether it is painful or not? Whether haematuria or pyuria is present? History of nocturia must be asked.

SURGERY - GASTRO-INTESTINAL PROBLEMS

EXAMINATION Complete examination, both general physical examination and systemic examination must be performed. GENERAL EXAMINATION Vital signs should be noted and repeated observations are noted regularly. The examination may be repeated if it is not conclusive initially. Sometimes analgesia or anaesthesia may be required for accurate examination. The examination must be performed methodically and completely. ABDOMINAL EXAMINATION INSPECTION It should be performed in the presence of a nurse or female attendant in good light and privacy. Adequate exposure should be achieved. The examination should be performed from foot end, head end and sides. The patient should be asked to cough while inspecting. All the abnormalities should be noted. PALPATION The abdomen should be palpated at first gently. Deep palpation should be performed methodically. Tenderness and rebound tenderness should be tested. All the tests required for diagnosing intra-abdominal lesions should be performed. PERCUSSION Percussion helps to find out tender areas and intraabdominal lesions. AUSCULTATION Auscultation offers valuable information about intraabdominal pathologies. Absent bowel sounds are a clear indication of generalized peritonitis. DIGITAL RECTAL EXAMINATION Rectal examination has always been an unpleasant experience by the patient. It has remained a very valuable clinical observation.

252

RIGHT ILIAC FOSSA PAIN

Although recent studies show no added advantage of this examination in diagnosing acute appendicitis yet it is helpful in clinically diagnosing pelvic and abdominal pathologies2,3. VAGINAL EXAMINATION It must be performed in case a gynaecological problem is suspected such as abortion or ectopic pregnancy.

INVESTIGATIONS No single investigation is able to confirm diagnosis. Following investigations are helpful in confirming the diagnosis. URINE EXAMINATION It is a simple, economical and easily available investigation. It provides very valuable information in confirming the diagnosis. Haematuria indicates urinary tract calculi and infection, pyuria indicates urinary tract infection. ketone bodies and low pH indicates ketoacidosis and uncontrolled diabetes mellitus. BLOOD EXAMINATION Haemoglobin percentage is suggestive of loss of blood. It also helps to monitor the general condition of the patient and the disease process. Total leukocyte count is a very valuable observation. It helps to suspect or exclude inflammatory lesions. It can be used as an individual test or in combination with other tests when the diagnostic efficacy is increased.

Liver function tests are usually unaltered. Amylase level is helpful in excluding other causes of abdominal pain. TRIPLE TEST It is combination of three tests ; ! Leukocyte count. ! Neutrophil differential count. ! C-reactive protein. The test can predict a negative value of 100%. If these tests are simultaneously negative, it is unlikely that 4 patient is suffering from acute appendicitis . RADIOLOGICAL EXAMINATION X-RAY ABDOMEN PLAIN The plain x-ray of abdomen is not a specific investigation. It is very valuable as it may show a radio-opaque shadow in 10% cases in the right iliac fossa (faecolith). It may show a radio-opaque shadow in the area of right lower ureter (ureteric stone). It may show the presence of sentinel loops of gut in the right iliac fossa indicating the site of an inflammatory lesion. ULTRASOUND SCAN Abdominal and pelvic ultrasound scan is extremely helpful. It should be performed on full bladder. It can confirm the diagnosis of ectopic pregnancy, missed or inevitable abortion, twisted or ruptured ovarian cyst, cholecystitis and other similar conditions. 31.04

Differential leukocyte count is suggestive of the type of inflammatory lesion such as acute or chronic. Sedimentation rate is a non specific test. It helps in monitoring the disease process, its progress or deterioration. Urea and electrolytes estimation helps in the assessment of general condition of the patient. Ultrasound scan (Acute appendicitis)

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RIGHT ILIAC FOSSA PAIN

calculated according to the weight of the patient and the state of hydration of the patient.

31.05

ANALGESIA Analgesia should never be given before the complete history is noted and examination is conducted. Once the clinical diagnosis is made, only then the analgesia should be given in adequate amount to relieve the pain. Analgesia before diagnosis masks the symptoms and makes the diagnosis not only difficult but inaccurate. Ultrasound scan (Acute appendicitis) It is very valuable in achieving correct diagnosis in seventeen year old girls with right iliac fossa pain. The ultrasonography has a sensitivity of 96% and specificity of 94% and accuracy of 95%5. LAPAROSCOPY It can be performed under anaesthesia to establish the site of pain if no obvious pathology is found with less invasive investigations. It should be performed in all cases presenting with atypical picture of appendicitis regardless of age and sex6. MISCELLANEOUS INVESTIGATIONS Specialized investigations such as urography and barium studies may be sometimes required to confirm the diagnosis. EMERGENCY TREATMENT The treatment depends upon the provisional diagnosis. NIL ORALLY The patient should be advised not to take anything orally. It will help to give rest to gastrointestinal tract. It will keep the patient prepared for emergency surgery if required. INTRAVENOUS FLUIDS Intravenous cannula should be passed and fluids and electrolytes should be infused. The fluids should be

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ANTIBIOTICS Appropriate antibiotics should be given if inflammatory lesion is suspected. DEFINITIVE TREATMENT It is the treatment of the cause according to the diagnosis.

REFERENCES 1. Blalock JB Jr. Improving diagnostic accuracy in appendicitis. Alabama medicine. [JC:3aj] 1989 Oct. 59(4) :13-7. 2. Dixon JM. Elton RA. Rainey JB. Macleod DA. Rectal examination in patients with pain in the right lower quadrant of abdomen. BMJ. [JC:bmj] 1991 Feb. 302(6773): 386-8. 3. Dunning PG. Goldman MD. The incidence and value of rectal examination in children with suspected appendicitis. Annals of Royal College of Surgeons of England. [JC:5vv]1991 Jul. 73(4) :233-4. 4. Dueholm S. Baqi P. Bud M. Laboratory aid in the diagnosis of acute appendicitis. A blinded, prospective trial concerning diagnostic value of leukocyte count. neutrophil differential count and C-reactive proteins.

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5. Larson JM. Peirce JC. Ellinger DM. et al. The validity and utility of sonography in the diagnosis of appendicitis in the community setting. Ajr. American Journal of Roentgenology. [JC:3ae] 1989 Oct. 153 (4) : 687-91. 6. Kuster GG. Gilroy SB. The role of laparoscopy in the diagnosis of acute appendicitis. American surgeon. [JC:43e]1992 Oct. 58(10) : 627-9.

POSSIBLE QUESTIONS 1. 2. 3.

What are the causes of pain right iliac fossa? How it is diagnosed? What is its treatment?

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SUMMARY Right iliac fossa pain in 17 years old girl Acute appendicitis. Appendicular mass Appendicular abscess Dysmenorrhoea Right ureteric colic Vesical stone Urinary tract infection Abortion Ectopic pregnancy Salpingitis Twisted or ruptured ovarian cyst Ovulation pain or mittelschmerz Endometriosis Hysteric neurosis Ileo-caecal tuberculosis Clinical Examination Investigations Treatment

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Carcinoid Tumor & Syndrome

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257

CARCINOID TUMOR

GIT - 32

CARCINOID TUMOR & SYNDROME Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS The term carcinoid was first employed by Obernodfer in 1907 to describe a group of tumours of GIT that had a relatively indolent course. Carcinoid tumour is the most common endocrine tumour of the intestine. It is also called argentaffinoma because it arises from argentaffin cells of Kultschitzaky.

INCIDENCE & EPIDEMIOLOGY !

! ! ! ! ! ! ! ! !

The most common site for carcinoid in the body is the vermiform appendix (about 60%) then ileum and large intestine. It is 10 times more common than any other appendicular tumour. It is seen once in every 400 appendicectomies. 85% of these tumours are located in the intestine. It has been found in stomach and some type of bronchial adenoma as well. Rarely it is present in ovary and testis and it may be of teratomatous origin. It is more common in between 16-60 years. Only 4% of these tumors show metastasis. The carcinoid tumors arise from foregut, midgut and hindgut. Foregut carcinoid are mainly from stomach. Midgut carcinoids arise from distal duodenum, jejunum, ileum, appendix, ascending and right transverse colon. Hindgut carcinoids arise mainly from rectum.

PATHOLOGY MACROSCOPIC PICTURE It has a characteristic yellow colour and tends to stimulate schirrhous reaction and thus leads to stricture formation around the bowel. SURGERY - GASTRO-INTESTINAL PROBLEMS

MICROSCOPIC PICTURE The small, round, darkly staining cells are arranged in solid clumps or cylinders. Acinar differentiation is unusual. If the cells are fixed freshly in formalin, special granules can be demonstrated in silver stains. The tumor is locally invasive and may metastasize to the local lymph glands and liver. Despite multiple metastasis, the patient may survive for many years in comparatively good health. 32.01

Carcinoid tumor WHO classification describes three grades of gastrointestinal neuroendocrine tumour. WELL DIFFERENTIATED ENDOCRINE TUMOUR (CARCINOID) An epithelial tumour showing mild or no atypia and restricted to mucosa or submucosa. WELL DIFFERENTIATED ENDOCRINE CARCINOMA (MALIGNANT CARCINOID) A malignant epithelial tumour showing moderate atypia which invades deeply beyond muscularis or shows metastasis to regional lymph nodes or liver. 259

CARCINOID TUMOR

POORLY DIFFERENTIATED ENDOCRINE CARCINOMA (SMALL CELL CARCINOMA) A malignant epithelial tumour composed of highly atypical, often with necrosis and prominent angioinvasion and/or perineural invasion.

SOMATOSTATION RECEPTOR SCINTIGRAPHY A radiation measuring device detects the radioactive material highlighting the tumor.

CLINICAL FEATURES

BIOPSY It is gold standard and provides definitive diagnosis. Large carcinoid tumours can cause obstruction.

The presentation depends upon the site of carcinoid tumor. Gastric carcinoids are usually silent, when symptomatic may present with epigastric pain or bleeding. Midgut carcinoids are asymptomatic and may be found accidently.

PET SCAN (POSITRON EMISSION TOMOGRAPHY SCAN) This is useful to detect malignant cells and metastases in different parts of body.

Carcinoids of appendix may cause obstructive appendicitis. Carcinoids of small gut remain silent for a long time and may present with intermittent pain, irritable bowel syndrome or features of obstruction. The hindgut carcinoids present with bleeding per rectum or a palpable mass.

CURATIVE SURGERY The carcinoid tumours should be excised surgically or endoscopically. The surgical treatment may not help the patients with carcinoid syndrome due to extensive metastasis.

RISK FACTORS Sex (More common in women) MEN Type-I syndrome Smoking Atrophic gastritis (Pernicious anemia)

! ! ! !

DIAGNOSIS Following investigations are specific for carcinoid tumour diagnosis. URINARY 5-HIAA LEVELS Patients with carcinoid tumours may show excess levels of a chemical called 5 hydroxy indole acetic acid (5-HIAA) in their urine. GI ENDOSCOPY It is performed to examine GIT for lesions and biopsy. CT SCAN It is performed to confirm the diagnosis. It helps to locate tumour and determine its spread.

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TREATMENT

PALLIATIVE TREATMENT Debulking surgery may help to relieve the symptoms for sometime. ! Hepatic artery embolization, liver transplant and various pharmacologic agents have been used to treat this syndrome. ! Octreotide slows the growth rate of carcinoid tumour ! Radio frequency ablation uses heat energy to ablate malignant cells ! Chemotherapy is useful in metastatic disease !

COMPLICATIONS CARCINOID SYNDROME It occurs in less than 10% cases of carcinoid tumour. It occurs when venous drainage from carcinoid tumour gains access to systemic circulation and vasoactive secretory substances escape hepatic degradation. It happens when ; ! Wide spread hepatic metastases is present. ! Venous blood from extensive retroperitoneal

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metastases drains into paravertebral veins. Primary carcinoid is not of gastro-intestinal in origin. Carcinoid syndrome develops in 1% of all cases and 20% of cases with metastasis,

SUMMARY Carcinoid tumor and syndrome Incidence Pathology Clinical features Risk factors Investigations Treatment Complications

It presents with paroxysmal facial flushing, diarrhoea, bronchospasm with dyspnoea and sometimes organic heart disease (usually pulmonary stenosis or tricuspid regurgitation). Flushing, sweating, wheezing, diarrhoea, abdominal pain, cardiac valvular fibrosis, pallegra and dermatosis. The tumour produces large amounts of the 5hydroxytryptamine (5HT) which is excreted in urine as 5hydroxyindole-acetic-acid (5-HIAA). Adrenaline (catecholamine) triggers the attack of carcinoid syndrome and probably actual mediator is bradykinin. Alcohol can also induce the attack. PEPTIC ULCER Carcinoids of the stomach and bronchus may also secrete histamine, thus causing peptic ulceration.

POSSIBLE QUESTIONS 1. 2. 3. 4.

What is carcinoid tumor? What is carcinoid syndrome? Enlist essential investigations to diagnose carcinoid tumor? Give treatment options?

VALVULAR HEART PROBLEMS The cardiac valvular lesions are probably due to subendothelial fibrosis produced by the kinins and possibly by "5HT" . INTESTINAL OBSTRUCTION Large carcinoid tumour in the gut can cause intestinal obstruction.

REFERENCES 1. Hails T. Debas. Susan L. Orloff. Carcinoid tumours and the carcinoid syndrome. Text book of surgery. Sabiston.14th edition. W.B. Saunders London. 1991. p: 869-72.

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APPENDICECTOMY

01 GIT - 33

APPENDICECTOMY Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS

APPENDICECTOMY It is surgical excision of vermiform appendix. Its most common indication is acute appendicitis. It may be performed in conventional way or through laparoscope. Once the diagnosis has been made, the patient is prepared for operation as soon as possible as it is a surgical emergency. PRE-OPERATIVE PREPARATION Confirmation of the diagnosis to maximum certainty is done. The diagnosis of appendicitis is mainly clinical. Investigations help to ascertain a most probable diagnosis. NIL ORALLY The patient is asked to stop all oral intake immediately. It is done as a preparation for general anaesthesia. It also helps to delay the complications of appendicitis. INTRAVENOUS FLUIDS & ELECTROLYTES A suitable size intravenous cannula is passed and intravenous fluids are given. It helps to improve the hydration of the patient, corrects the electrolytes and offers a route for intravenous drug administration. ANTIBIOTICS Appropriate antibiotics are also given for the control of infection. ANALGESIA The analgesia is not given till the diagnosis is confirmed and operation is planned. It is withheld initially to avoid masking of symptoms and to reach correct diagnosis in time. Then intravenous analgesia is given to relieve the pain.

SURGERY - GASTRO-INTESTINAL PROBLEMS

INVESTIGATIONS Necessary investigations are performed. Ultrasound scan is performed before the specimen of urine is taken, so that it can be done on full bladder. CONSENT FOR OPERATION The operation should be explained in simple language to the adult patient and to the guardian of a child. The consent must be written and signed for anaesthesia and surgery. PREPARATION OF THE SITE OF OPERATION The operation site (Abdomen) is shaved in case hair are present. It is washed and cleaned with soap and water. The abdomen is painted with antiseptic solution (pyodine). The patient is asked to wear operation theatre gown and remove his clothes. The patient is asked to pass urine and empty the bladder before shifting to the operation theatre. The identification band (name band) is fixed to the arm of the patient. If the patient is wearing any valuable ornaments like jewellery or watch, these are removed and handed over to the relatives of the patient. Dentures, glasses, contact lens are also removed and either handed over to the relatives of the patient or kept in safe custody before the patient is shifted to operation theatre. PREMEDICATION (SEDATION) Patient is given appropriate premedication as advised by the anaesthetist.

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ANAESTHESIA General Spinal Epidural

! ! !

33.01

The peritoneum is picked up by tissue forceps carefully, so that no intraperitoneal structure is picked up by the tissue forceps. If there is any collection of pus or fluid in the peritoneal cavity, a peritoneal pus swab is taken and sent for culture and sensitivity and all the fluid is sucked out. The appendix is lifted out of the wound with the help of index finger. If it is not found so easily, ascending colon or caecum are recognized and pulled out of the wound gently, tinea coli are followed till their convergence at the base of appendix.

Exposed and painted area ready for surgery POSITION AND PREPARATION Patient lies on the operation table in supine position. The patient is prepared with skin disinfectant and is draped (toweled) leaving right lower quadrant of the abdomen exposed. INCISIONS Grid iron incision ! Lanz (skin crease) incision ! ! Right lower paramedian incision 33.02

Now the caecum and appendix are delivered out of the wound. The appendix is held by two non crushing forceps (Babcock's forceps). Meso-appendix is clamped, ligated and divided, till whole of the appendix is devascularised and cleared of its mesentry. The base of the appendix is clamped with an artery forceps. The crushed part of base of appendix is ligated with absorbable suture and appendix is cut. The purse-string sutures are used at about one centimeter from the base of the appendix. The stump is inverted and purse-string sutures are tightened and ligated thus burying the appendicular stump. Haemostasis is secured and checked. Packs used during surgery are counted and checked doubly at least twice loudly before the peritoneum is closed. The peritoneum is closed with absorbable sutures. Muscles are also approximated with absorbable sutures. Skin is closed with non absorbable sutures or any method of sugeonâ&#x20AC;&#x2122;s choice.

Black : Grid iron incision Red: Lanz (skin crease) incision Blue: Right lower paramedian incision

PROCEDURE Grid iron incision is given at McBurney's point at right

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33.03

33.06

Grid Iron incision (external oblique muscle splitted in line of its fibers)

33.04

Identification of appendix before excision

33.07

Grid Iron incision (internal oblique muscle and transverses splitted in line of their fibers)

33.05

Grid Iron incision (abdominal wall muscles separated bluntly to expose peritoneum)

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Identification of appendix before excision

33.08

Ligation of appendicular vessels 265

APPENDICECTOMY

33.09

33.12

LAPPROSCOPIC APPENDICECTOMY This mode of appendicectomy is a safe procedure. It can provide less morbidity in experienced hands. Indications and preparation is the same as for open surgery.

Base of appendix ready for ligation

33.10

Operation time is longer with laparoscopic procedure than with traditional appendicectomy. It has no added advantage over traditional method2. Skin wound closed after completion of operation

Preparation for excision of appendix over a swab

33.13 5mm

33.11

Burying the appendicular stump with a purstring suture

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instrument PREPARATION port camera port Preparation is same as for open appendicectomy, including stopping of all oral intake, appropriate peri10mm instrument port operative antibiotics and analgesia. Operative site (Abdomen) is washed and cleaned with soap and water. Antiseptic preparation is performed as for open surgery prior to operating.

POSITION The position is supine. Surgeon and camera-assistant are on the left side of the patient. For coaxial alignment the surgeon stands near left shoulder and monitor is

266

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placed near right hip facing towards surgeon for better vision during surgery. OPERATIVE TECHNIQUE Pneumo-peritoneum is created in usual fashion through infra umbilical site. 10 mm port is inserted and this is used as optical port for camera.

CONTROL OF MESO APPENDIX 33.15

Two 10 mm ports are used (umbilical and left lower quadrant port). One 5 mm right upper quadrant port is used (can be moved below bikini line in females). Transvaginal port may be used in patients who want 33.14

Upward Traction

33.16

Visualization of the Appendix VersaPort 12-5

VersaPort 10-5 Endo Babock Clamp VersaPort 5

Endo Grasp Instrument

scarless surgery for appendicitis. STEPS OF OPERATIONS EXPLORATION OF PERITONEAL CAVITY Abdominal cavity is examined for conformation of diagnosis and to look for any collection of pus or other pathology. EXPOSURE OF APPENDIX & MESOAPPENDIX After exploration, the appendix is identified and released with blunt and sharp dissection. The appendix is grasped from its tip with a 05 mm atraumatic grasper via the right upper quadrant trocar, it is held in upward position. CREATION OF MESENTERIC WINDOW Lower left quadrant grasper is used to create a mesenteric window behind the base of appendix. A Dolphin nose grasper is used to create a mesenteric window as close as possible to the base of appendix.

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Upward Traction

Endo Dissect Instrument

33.17

Mesenleric Window

Meso appendix is controlled with endo clips, intra corporeal suturing or application of serial endo GIA stapler. LIGATION AND RESECTION OF APPENDIX The next step of procedure involves ligation and re-

267

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Intravenous fluids and electrolytes are infused till paralytic ileus is relieved.

Endo Grasp Instrument

33.18

Adequate analgesia is required for pain relief. Continuous parenteral analgesia is best as it offers continuous pain relief. Antibiotics may be required depending upon the extent of spread of infection.

Mesenteric Window Multifire Endo GIA" 30 Stapler

section of appendix near the base avoiding any fecal contamination.

Endo Grasp Instrument

33.19

Messappendix

Messappendix Erula Gia 30 Stapler

upon the type of anaesthesia given.

33.20

COMPLICATIONS The appendicectomy is a relatively safe, easy and simple procedure. It may have serious complications in case proper care is not taken. The commonly seen complications are ; ANAESTHETIC COMPLICATIONS These are due to various types of anaesthesia. The complications of general anaesthesia are respiratory embarrassment and cyanosis. OPERATIVE COMPLICATIONS Many times the appendix is hidden in the adhesions and it may be difficult to find out as this operation is usually performed by trainee and less experienced surgeons and many times through a small exposure. The incision is enlarged and operation is conducted carefully to avoid surgical complications. Common post-operative complications are; ! Infection ! Haemorrhage ! Portal pyemia ! Septicaemia ! Deep venous thrombosis ! Urinary retention ! Post operative chest complications ! Pulmonary embolism ! Prolonged paralytic ileus ! Evisceration or burst abdomen ! Pelvic abscess LATE COMPLICATIONS ! Faecal fistula.

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268

APPENDICECTOMY

! ! !

Intestinal obstruction due to adhesions. Incisional hernia. Right inguinal hernia.

COMPLICATIONS OF LAPROSCOPIC APPENDICECTOMY ! Vascular /visceral injury ! Wound infection ! Trocar site hernia ! Incomplete appendicectomy ! Intra-abdominal abcess

REFERENCES 1. Schirmer BD. Schmieg Rejr Dix J Edge SB, Hanks JB. Laparoscopic versus traditional appendicectomy for suspected appendicitis. American Journal of Surgery [JC.324] 165 (6):670-5, 1993 Jun. 2. Schorden DM. Lathrop JC. Llyoid X LR et al. Laparoscopic appendicectomy for acute appendicitis. Is then really any benefit? American Surgeon [JC 8430] 59(8): 541-7: Discussion 5478, 1993 Aug. 3. RM Kirk. General Surgical Operation; 5th edition 2006; chapter 8-9, 107-118.

SUMMARY Appendicectomy Pre-operative preparation Preparation of site of operation Incisions Procedure Laparoscopic appendicectomy Position Procedure Complications POSSIBLE QUESTIONS 1. 2. 3.

Discuss preparation for Appendicectomy? Discuss post-operative care after appendicectomy? Discuss complications of Appendicectomy?

4. M J Zinner, Stanely W Ashley. Maingot's abdominal operations. 11th edition, 1997. Chapter 21: 589593.

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269

Large Intestine

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271

SMALL GUT OBSTRUCTION

OBJECTIVES ! ! ! ! ! ! ! !

To understand anatomy and physiology of large gut, rectum and anal canal. To be able to understand diseases of large gut, rectum and anal canal. To be able to diagnose diseases related to rectum and anal canal. To be able to plan various modes of management of problems related to rectum and anal canal. To be able to prepare the patients for rectal or anal canal surgery. To be able to look after the patient with Ano rectal problems during & after surgery. To be able to screen & follow patients with problems related to rectum & anal canal. To be able to prevent, diagnose & treat complications related to problems of rectum and anal canal.

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BLOOD SUPPLY AND LYMPHATIC DRAINAGE OF LARGE GUT

01 GIT - 34

BLOOD SUPPLY & LYMPHATIC DRAINAGE Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Irfan Mughal, M.Phil, Ph.D. The large gut includes caecum, ascending colon, transverse colon, descending colon, sigmoid colon and rectum. All these viscerae are supplied by midgut and hind gut vessels. which are ;

! !

Superior mesenteric artery. Inferior mesenteric artery.

branches supply the medial aspect and long branches supply the lateral and antimesenteric side of colon. These also supply epiploic appendages. It arises from the superior mesenteric artery and runs towards ileo-caecal junction. It anastomosis with right colic artery and supplies caecum and ascending colon through the anterior and posterior caecal arteries.

34.01

RIGHT COLIC ARTERY It is a branch of superior mesenteric artery and runs towards the ascending colon to anastomose with the colic branches of ileo-colic and middle colic arteries to supply the ascending colon.

The midgut vessels supply uptil right two third of the transverse colon. The hindgut vessels supply distal to the left one third of transverse colon, descending colon, sigmoid colon, rectum and part of anal canal.

SUPERIOR MESENTERIC ARTERY ILEO-COLIC ARTERY Caecum and ascending colon receive blood from ileocolic and right colic arteries. These form arcades from which vasa recta arise to enter into medial aspect of colon by dividing into short and long branches. Short SURGERY - GASTRO-INTESTINAL PROBLEMS

MIDDLE COLIC ARTERY It is the superior most branch of superior mesenteric artery and it runs towards hepatic flexure to divide into right and left branches which run along the mesenteric border of the colon. These anastomose with the colic branches of right and left colic arteries and supply the distal parts of midgut. It supplies the most of the transverse colon.

INFERIOR MESENTERIC ARTERY It is the main arterial supply of the hind gut. It arises from aorta just before bifurcation opposite 3rd lumbar vertebra2. It supplies from splenic flexure upto rectum. It supplies the distal part of large gut through its branches. UPPER LEFT COLIC ARTERY It is the upper most branch of inferior mesenteric artery. It supplies the splenic flexure and upper part of the descending colon. It also supplies left part of transverse colon. It supplies the area of colon via its 273

BLOOD SUPPLY AND LYMPHATIC DRAINAGE OF LARGE GUT

upper and lower branches which anastomose with left branch of middle colic artery. LOWER LEFT COLIC ARTERY These may be two or three branches leaving the inferior mesenteric artery. These supply the lower part of the descending colon and iliac colon. SIGMOID ARTERIES These are three four branches arising from inferior mesenteric artery. These supply the pelvic colon. MARGINAL ARTERIES All these vessels anastomose with each other along the concave border of the large gut thus forming a separate channel running along whole of the concavity of the colon. It is named as marginal artery. Its smaller branches sink into the colon and supply it. The rectum is supplied by superior and middle rectal arteries. SUPERIOR RECTAL ARTERY It is a direct branch of inferior mesenteric artery. It divides into right and left branches. Its right branch further subdivides into anterior and posterior branches and supplies the rectum. VENOUS DRAINAGE All superior mesenteric ar tery branches are accompanied by the veins. All these veins drain into superior mesenteric vein which drains into the portal vein.

LYMPHATIC DRAINAGE CAECUM AND ASCENDING COLON These drain from the lymphoid follicles of the gut wall into the epicolic lymph glands lying along the ileo-colic artery and right colic artery. The lymph is drained from here to superior mesenteric group of pre-aortic lymph glands. TRANSVERSE COLON The lymph from the midgut part of transverse colon is drained into epicolic glands which are drained into paracolic glands of transverse colon. Main drainage is to the superior mesenteric group of lymph glands of pre-aortic group glands. SPLENIC FLEXURE, DESCENDING AND PELVIC COLON The lymph is drained into the epicolic glands which drain into the pericolic glands lying along the branches of inferior mesenteric artery. These lymphatics drain into the inferior mesenteric group of pre-aortic lymph glands.

REFERENCES 1. RMH MCMINN. Lasts Anatomy regional applied eight edition. ELBS. Churchill Livingstone London1990. p: 327-330, 2. Joln.E.Skandalakis; Panajiotisn Skandalakis; Lee Jolmskandalakis. Colon and Ano rectum. Surgical Anatomy and technique second edition. Atlanta USA. 1999. 457-480

All arterial branches of the inferior mesenteric artery are also accompanied by their veins which drain into inferior mesenteric vein which joins the splenic vein to drain into the portal vein.

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BLOOD SUPPLY AND LYMPHATIC DRAINAGE OF LARGE GUT

SUMMARY Blood supply of large gut Arterial supply Venus drainage Lymphatic drainage

POSSIBLE QUESTIONS 1. 2. 3.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Discuss arterial supply of ascending colon? Discuss venous drainage of large gut? Discuss lymphatic drainage of large gut?

275

SIGMOID VOLVULUS

GIT-35

SIGMOID VOLVULUS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Volvulus is a loop of bowel which has twisted on itself causing compression of its blood supply. Abnormal twisting of gut leads to following; ! Bowel obstruction ! Bowel Ischaemia ! Necrosis of Bowel ! Acidosis and death The sigmoid volvulus is the abnormal axial rotation of a 1 portion of the sigmoid colon . It has been described many centuries ago by Egyptians, Romans and Greek.

! ! ! ! ! ! !

PATHOPHYSIOLOGY !

INCIDENCE AND EPIDEMIOLOGY ! ! ! ! ! ! ! ! !

It is extremely rare in neonates2. It is 20 times more common in patients above 60 years of age. The rotation usually occurs in counter-clockwise direction. More common in patients with chronic constipation. It is more common in East European countries, Africa, India, Pakistan and Scandinavian countries. It causes 54% cases of gut obstructions in Ethopia. Sigmoid volvulus is the site of 75% of the large gut volvulus. It may present with cecal-volvulus (synchronous 3 volvulus) . It is uncommon in English speaking countries only 1-3% of all bowel obstructions are due to this case

ETIOLOGY Sigmoid volvulus is caused by ; ! Bands or adhesions. (Post operative or due to peri

SURGERY - GASTRO-INTESTINAL PROBLEMS

diverticulitis) Over loaded pelvic colon. Long pelvic mesocolon. Narrow attachment of pelvic mesocolon. Redundant sigmoid loop. Chronic constipation. Neuropsychiatric disorders. Pregnancy.

! !

It is caused by the acquired redundancy of sigmoid colon due to use of high fibre diet over a prolonged period. It is associated with chronic constipation relieved by laxatives and enamas. Neuropsychiatric disorders such as parkinsons disease, Alzheimers disease, multiple sclerosis, traumatic paralysis, schizophrenia, psuedobulbar palsy and senility.

This abnormal rotation causes occlusion of bowel lumen at the end of turn initially resulting in acute obstruction. Then the vascular supply is compromised leading to strangulation.

CLINICAL FEATURES Sigmoid volvulus is an acute abdominal emergency. It presents with the following features : PAIN ABDOMEN Abdominal pain is severe, colicky, cramping and sudden in onset. It is present in the lower abdomen.

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DISTENSION OF ABDOMEN Abdominal distension is the most prominent feature. It is progressive and it becomes severe within few hours. OBSTIPATION (ABSOLUTE CONSTIPATION) Inability to pass feces and flatus is a typical feature of the sigmoid volvulus. Occasionally large amount of gas is passed per anus suddenly; and it is due to untwisting of the volvulus. VOMITING AND DEHYDRATION These occur late when whole of the intestine is involved in obstruction. The vomiting causes severe dehydration. CHRONIC SECRETORY DIARRHOEA The sigmoid volvulus may present as chronic secretory diarrhoea and hypokalemia. It happens in cases of intermittent sigmoid volvulus4. RESPIRATORY EMBARRASSMENT This is present due to severe abdominal distension and elevation or tenting of the diaphragm, due to large amount of gas present proximal to the twist (obstruction).

as intermittent volvulus in old patients presenting with subacute abdominal distension and/ or chronic secretory diarrhoea and hypokalemia specially in patients with 4,5 redundant sigmoid colon .

DIAGNOSIS History and physical examination suggest diagnosis. Following investigations help to confirm the diagnosis and assess the general condition of the patient

INVESTIGATIONS BLOOD EXAMINATION Haemoglobin estimation. Leucocyte count. Sedimentation rate. Urea and electrolyte estimation. RADIOLOGICAL EXAMINATION PLAIN X-RAY OF THE ABDOMEN The plain abdominal x-ray is diagnostic of the condition and rarely any other investigation is required. It shows distended single loop present in the left half of the abdomen from pelvis to diaphragm forming "omega loop sign". Two air fluid levels are seen within the sigmoid loop. 35.01

EMPTINESS OF LEFT ILIAC FOSSA There is palpable emptiness of left iliac fossa distal to the twist. The positive predictive value has been almost 100%5. GENERAL FEATURES Rapid and thready pulse, hypotension, cold and clammy extremities, sweating and constant lower abdominal pain. Development of generalized abdominal pain, tenderness, fever and features of hypovolaemia suggest strangulation of the twisted loop. The patient develops shock which becomes irreversible if left untreated and death may occur. Sigmoid volvulus may not always be acute. It may present

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Volvulus of Sigmoid Colon

278

SIGMOID VOLVULUS

SIGMOID VOLVOLUS MANAGEMENT

NON-COMPELLING SIGNS

DECOMPRESSED

NO-DETORSION

ELECTIVE MANAGEMENT

COMPELLING SIGNS

URGENT LAPAROTOMY

VIABLE BOWEL

GANGRENOUS BOWEL

RESECTION

PRIMARY ANASTOMOSIS

COLOSTOMY

NON RESECTIONAL OPTIONS PRIMARY ANASTOMOSIS

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GASTROGRAFFIN ENEMA Enema with water-soluble gastrographin can be used to 6 diagnose sigmoid volvulus in emergency . CT SCAN It is very important and helpful investigation. It is available at most of the centers now7. 35.02

FLUID AND ELECTROLYTES These should be replaced intravenously and correctly. The amount of fluids should be calculated by maintaining intake and output chart. It is monitored by the urinary output. ANALGESIA Intravenous analgesics are used to relieve the pain. Strong analgesics such as morphine, pethidine and temgesic are helpful to relieve the pain. URINE OUTPUT The urine output is a simple but excellent guide for the assessment of correct fluid and electrolyte replacement. Initially hourly urinary output is monitored. 30 - 60mls/hr of urine in an adult indicate satisfactory fluid replacement. The electrolytes are checked by testing the blood.

Sigmoid Volvulus (CT Scan)

TREATMENT The objectives of treatment are ; ! Resuscitation ! Definitive treatment RESUSCITATION NIL-ORALLY All the patients who are suspected of suffering from sigmoid volvulus should not be allowed any fluids or food orally. It will help to keep the obstruction less severe and delay the vomiting and dehydration. NASOGASTRIC ASPIRATION Nasogastric tube is passed and gastro intestinal contents are aspirated. This helps in decompression of the upper gastro intestinal tract.

SURGERY - GASTRO-INTESTINAL PROBLEMS

TREATMENT OF SHOCK The patient usually goes into septic shock when volvulus leads to strangulation of the loop of bowel. Appropriate antibiotic therapy especially against gram negative and anaerobes should be started. Blood transfusion will be required in such cases. Pulse rate, blood pressure and central venous pressure are monitored during the treatment of shock and replacement of fluids. MANAGEMENT OF SIGMOID VOLVULUS8 Principles of treatment of sigmoid volvulus are following ! Relief of obstruction ! Prevention of recurrent attacks NON OPERATIVE METHODS Sigmoidoscopy Decompression of volvulus Insertion of rectal Tube.

! ! !

If torsion is within 15cm of anal verge rigid sigmoidoscope can be used otherwise flexible sigmoidoscope in used to decompress colon which will lead

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to detorsion. A Rectal tube should be placed in situ for 2448hrs. GASTROGRAFFIN ENEMA It may result in detorsion of the volvulus in about 5% of patients1. OPERATIVE METHODS In acute sigmoid volvulus. Following are indications for emergency surgery ;

! !

Failed decompression Fever and leucocytosis persisting after decompression suggesting peritonitis.

2. De Caluwe D, Kelleberj, Corbaly MT. Neonatal sigmoid volvulus: A complication of anal stenosis. J Pediater Surg; 2001 July. 36 (7): 1679. 3. Smith SD. Goiladay ES. Waqner C. Serbert JJ. Sigmoid volvulus in childhood. Southern medical journal. [JC:uvk]1990 Jul. 83(7): 778-81. 4. Almog Y. Dramitzki - Elhabl M. Lax E. Zimerman J. Glaser B. Sigmoid volvulus presenting as chronic secretary diarrhoea, responsive to octreotide. American jour nal of g astr oenter olo g y. [JC:3he]1992 Jan. 87 (1): 148-50. 5. Raneen Thiran V. Emptiness of the left iliac fossa: A new clinical of sigmoid volvulus PMID sign 11009578.

SURGICAL OPTIONS ! Laparotomy, resection of non viable bowel, colostomy and mucus fistula. ! Laparotomy resection of non viable bowel and Hartman procedure. ! Primary anastomoses can be performed but not advisable on unprepared large bowel.

6. Chin LW, Lin MT, Wang HP, Chion HM, Chen WJ. Rapid diagnosis of sigmoid volvulus with water soluble urographin in emergency service. 2001 Nov. 18: Am J Med.

Elective surgery for decompressed bowel is mainly of two varieties resectional and non resectional.

7. Tubiana JM. Imaging in acute abdominal syndromes. 2000 Oct.11: Rev Prat; 51 (15): 1648-53.

RESECTION AND ANASTOMOSIS Redundant sigmoid colon is resected and primary anastomosis is performed. Sometimes in case of mega colon subtotal colectomy is advised.

8. Te Madiba & SR Thomson. The management of sigmoid volvolus. J.R. College.Surg. Edinb, April 2000 45, 74-80.

Laparoscopic assisted sigmoidectomy is performed since 9 advent of laparoscopy .

9. Walsh S, Lee J, Stokes M. Sigmoid volvulus after laparascopic cholecystectomy. 40 surg Enclosc; 2001 Feb.15(2): 218c.

MESOSIGMOIDOPLASTY Plication of mesocolon is performed to reduce redundant mesocolon. ! Per cutaneous endoscopic colopexy. !

REFERENCES 1. Anthony L. Zubembo. Kerl A. Zuder. Vovulus of the colon. Text book of surgery. Sabiston. 14th ed. WB Saunders London. 1991. p: 940-944. SURGERY - GASTRO-INTESTINAL PROBLEMS

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SUMMARY Sigmoid volvulus Incidence and epidemiology Etiology Pathophysiology Clinical features Diagnosis Treatment

POSSIBLE QUESTIONS 1. 2. 3. 4.

SURGERY - GASTRO-INTESTINAL PROBLEMS

What do you understand from sigmoid volvulus? How would you diagnose it? What are the non-operative treatment options for sigmoid volvulus? Enlist different operative procedures for sigmoid volvulus?

282

ULCERATIVE COLITIS

GIT - 36

ULCERATIVE COLITIS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS It is an inflammatory condition of the colon of unknown cause that affects any age group. The peak incidence rd th occurs in 3 and 4 decade. EPIDEMIOLOGY There are 10-15 new cases/100,000 a year in UK.

MULTI-FACTORIAL ETIOLOGY Diet

Stress

Drugs

Genetic Tendency

Infections

Allergens

The male to female ratio is equal and most patients are between ages of 20 and 40.

ALTERED IMMUNITY

The patient suffering from ulcerative colitis are found worldwide.

ULCERATIVE COLITIS Etiology of ulcerative colitis

It is common in USA, UK and northern Europe. It is especially common in people of Jewish descent. Ulcerative colitis is rare in Eastern Europe, Asia and South America.

ETIOLOGY The etiology of ulcerative colitis is unclear and multiple factors have been held responsible for this disease. Following hypothesis are considered;

Defective mucosal metabolism of butyrates There is reduction in ability of colonic mucosa to utilize butyrate as an energy source and reduction in carboxy peptidase activity which is required to degrade bacteria. Genetic factors First degree relatives are 15 times more at risk to develop ulcerative colitis. It is associated with HLA B-27.

PATHOLOGY

Mucosal immunological reaction About 50% of patients with ulcerative colitis have anticolon antibodies detectable in the serum.

Ulcerative colitis starts in rectum and spreads proximally and may involve variable extent of proximal colon. The percentage of involvement of colon is as given below;

Weakened mucosal barrier There is reduction in production of mucin and it may represent loss of important mucosal protective mechanism.

Percentage of involvement of colonic areas

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Rectosigmoiditis Left sided colitis Total colitis

60% 25% 15% 283

ULCERATIVE COLITIS

Macroscopic appearance The colon is always affected in continuity, disease is marked by erythema, loss of normal vascular pattern, petechial hemorrhages and bleeding. Mucosal ulceration with adjacent areas of regenerating mucosa which appear polypoid (pseudopolyps). Microscopic appearance It predominantly affects mucosa & superficial sub mucosa. It is a chronic nonspecific inflammatory process characterized by crypt abscess and presence of chronic inflammatory cells such as lymphocytes, plasma cells, eosinophills and Mast cells. Specific features are reduction in number of goblet cells and crypts of Lieberk端hn. These changes become severe and precancerous with time and develop into dysplasia and carcinoma in-situ.

! ! !

Rectal bleeding Rectal pain Tenesmus (Painful urge to move bowel)

PROCTOSIGMOIDITIS AND LEFT COLITIS This involves inflamation of the rectum, sigmoid colon and descending colon. It produces symptoms as above and; ! Abdominal pain and cramps ! Weight loss PANCOLITIS This is inflamation of entire colon. Symptoms of pan colitis include; ! Bloody diarrhoea ! Fatigue and fever ! Night sweats

CLINICAL FEATURES

36.01

Ulcerative colitis has variable course and not proportional to extent of bowel involvement. Following are common presentations; ! Recurrent attacks ! Acute presentation ! Complications at presentation Ulcerative colitis has following symptoms; Rectal Bleeding Diarrhea Abdominal pain Feeling of being unwell

! ! ! !

Ulcerative Colitis Disease severity

Variability of symptoms reflects differences in the extent of disease.

Mild attack

< 4 bowel motions / day non systemic signs

ULCERATIVE PROCTITIS It is referred to inflamation that is limited to rectum. It can produce symptoms as;

Moderate attacks

4-6 bowel motions/ day no systemic sign

Severe attack

Colonic symptoms systemic sign.

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INVESTIGATIONS ! Complete blood picture ! CRP (C-reactive protein) ! Endoscopic examination ! Radiological examination ! Radio isotope scan

36.02

COLONIC ENDOSCOPY AND BIOPSY It is gold standard investigation. Diagnosis is confirmed by mucosal biopsy. Total colonoscopy is advised occasionally to determine extent of disease. Muliple ulcers on the cecum (colonoscopy) 36.05 36.03

Muliple ulcers on sigmoid colon (colonoscopy) Muliple ulcers on ascending colon (colonoscopy)

36.06

36.04

Muliple ulcers on transverse colon (colonoscopy)

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Ulcerative colitis (barium enema)

285

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BARIUM ENEMA It should not be performed during acute attack. It is not very useful in chronic longstanding disease. It has following features; ! Loss of haustration. ! Pseudopolyps ! Narrow contracted colon Stool Culture This is performed to detect evidence of infective colitis which can be bacterial or parasitic infection. RADIO ISOTOPE LEUCOCYTE SCAN It is non-invase method to detect extent of disease. It is carried out by injection of radio isotope labeled leucocytes.

MANAGEMENT Three modes of treatment are commonly used; ! Medical ! Surgical ! Surveillance The mainstay of management of ulcerative colitis is medical however failure of medical management indicates surgical treatment. Cancer surveillance is also part of management as it helps in early detection of disease and its adequate management. Medical Management The medical management is not curative and has following objectives. ! To induce remission ! Maintain remission ! Minimize side effects of treatment ! Improve quality of life Medication treating ulcerative colitis include ; 5-ASA compounds Systemic Steroids

! !

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! !

Topical Steroids Immunomodulators

5-Amino salicylic acid derivatives (5ASA) These act locally, aid systemically and are mainly used to maintain remission. Following agents are commonly used; ! Sulfa salazine (Azulfidine) ! Mesalamine (Pentasa, Rowasa, Asacol) ! Olsalazine (Dipentum) ! Balsalazide (Colazy) 5-Aminosalicyllic acid is chemically similar to aspirin. It can be effective in treating ulcerative colitis if the drug can be delivered directly on to inflamed colonic mucosal lining. It is given in form of retention enema. It is as effective as an oral agent 5-ASA is modified chemically to escape absorption by the stomach and upper intestine when given as enema. Steroids These are usually given to induce remission. Steroids are used rectally, orally and parenterally. Following preparations are used; ! Hydrocortisone ! Prednisolone Immunomodulators These decrease tissue inflamation by reducing population of immune cells and by interfering with the production of proteins that promote immune activation and inflamation. Immunomodulators include; ! Azathioprine ! 6-mercepturine ! Cyclosporine ! Methotrexate These are indicated when ulcerative colitis is not responding to steroids and patients have undesirable side effects of steroid therapy. Antidiarrhoeal therapy Loperamide is commonly used to reduce number of bowel motions.

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ULCERATIVE COLITIS MANAGEMENT

Mild Attack

Distal disease Steroid enema Oral Mesalazine

Moderate Attack

Severe Attack

Proximal disease Oral prednisolone Oral mesalazine

Oral Steroid Oral mesalazine

Parenteral steroid Supportive treatment

Failure to improve or complications

improves

Surgical treatment

Oral mesalazine

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287

ULCERATIVE COLITIS

SURGICAL TREATMENT The principle of surgery in ulcerative colitis is removal of whole colonic and rectal mucosa. The indications of surgery are; ! Severe fulminating disease ! Failure to respond to medical treatment. ! Steroid dependent disease ! Massive hemorrhage ! Toxic megacolon ! Colorectal carcinoma The choice of procedure depends upon clinical situation and general condition of the patient. Following options are available; ! ! ! !

Colectomy and Ileostomy. Colectomy and Ileorectal anastomosis Proctocolectomy and permanent ileostomy. Restorative proctocolectomy.

COMPLICATIONS Anemia Blood loss from inflamed intestines can lead to anemia and may require treatment with iron supplements or even blood transfusion. Toxic Megacolon Inflammatory process involves all layers of colon in this condition. It is characterized by; • Fever • Severe Abdominal pain and distention • Dehydration and malnutrition • Colon Diameter 6cm on x-ray abdomen.

Massive hemorrhage It rarely occurs but requires hemodynamic support and surgical intervention Colorectal Carcinoma It is a recognized complication of chronic ulcerative colitis the risk of colorectal carcinoma begins to rise after 8 to 10 years of disease. The current estimates of incidence of colorectal carcinoma associated with ulcerative colitis is as below;

Years 10

% Risk of malignancy

7.6%

10.8%

2.5%

Extra-intestinal disease Complications of ulcerative colitis can involve other parts of the body as well. 10% of patients can develop inflamation of joints. Extra intestinal complications of ulcerative colitis are; ! Arthrits ! Sacro-ileitis ! Erythema nodosum ! Pyoderma gangrenosum ! Aphthous ulcer ! Irits ! Episcleritis ! Sclerosing cholangitis REFERENCES 1. Dattimer C R, Wilson NM; Key topic in general surgery. 2nd Edition; 2002, P-311-313.

It is treated with surgery. Perforation Toxic mega colon can lead to perforation of colon. It presents with peritonitis and sepsis. It requires urgent surgery after resuscitation.

SURGERY - GASTRO-INTESTINAL PROBLEMS

2. Cuscheri A, Steele R J C; Essential surgical practice. 4th Edition; 2002, S-14.5, P-600-602. 3. Bailey & Loves; Short practice of surgery. 25th Edition; 2008, Part 11, Section 65, P-1150-1175.

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SUMMARY Ulcerative Colitis Epidemiology Etiology Pathology Clinical features Investigations Management Complications POSSIBLE QUESTIONS 1. 2. 3.

SURGERY - GASTRO-INTESTINAL PROBLEMS

What is ulcerative colitis? How is it diagnosed? What is its treatment?

289

ULCERATIVE COLITIS

SURGERY - GASTRO-INTESTINAL PROBLEMS

289

BLEEDING PER RECTUM

GIT-37

BLEEDING PER RECTUM Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS Passage of blood through the rectum is called bleeding per rectum. The bleeding may not be necessarily from the rectum itself. The bleeding from the anal canal, which doesn't even pass through the rectum is also considered under the same subject with bleeding per rectum. Bleeding per rectum could be ; ! Fresh bleeding ! Passage of altered blood ! Melaena

NEOPLASTIC Benign rectal polyps and carcinoma of rectum also present with bleeding per rectum.

Fresh bleeding is usually from the lower part of the large gut such as rectosigmoid junction, rectum and anal canal. Passage of altered blood is usually seen in cases of bleeding from upper colon, ileo caecal region or ileum. Melaena is usually due to the bleeding from upper gastro-intestinal-tract such as esophagus, stomach and duodenum.

MISCELLANEOUS ! The bleeding hemorrhoids are one of the most common cause of bleeding per rectum. ! Fissure in ano may present with bleeding per rectum. ! Very rarely endometriosis may present in women with bleeding per rectum. ! Intussusception of small intestine and appendix may 2 present as pain abdomen and bleeding per rectum . ! Aorto-enteric Fistulae Severe rectal bleeding may occur from aorto-enteric fistula. Usually the history of aortic surgery is available. It should be suspected regardless of age and sex1.

ETIOLOGY

DIAGNOSIS

TRAUMATIC Accidents and medico legal injuries of the anal canal and rectum may lead to bleeding per rectum. Introduction of pointed and hard objects into the rectum leads to injury of the rectum and causes bleeding per rectum.

It is essential to find out the following information ; Cause of bleeding per rectum. Site of bleeding. Amount of loss of blood. Duration of bleeding.

! ! ! !

Road side accidents, crush injuries of pelvis, gun shot injuries and penetrating injuries due to stabs can cause injury of sigmoid colon, rectum and anal canal. It may present with bleeding per rectum and other symptoms of peritonitis.

It is also important to assess the general condition of the patient to plan the mode of treatment. This can be achieved by proper and complete history, examination and investigations.

INFLAMMATORY Inflammatory diseases of bowel may lead to bleeding per rectum such as typhoid fever, ulcerative colitis, Crohn's colitis and amoebic colitis.

HISTORY Age, sex and socio-geographical background of the patient is noted. Amount of blood loss and type of blood loss is also noted. Presence of mucous with blood or history of colicky pain is found out.

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BLEEDING PER RECTUM

History of similar problem in the family or history of malignancy in the family may be available. History of altered bowel habits, ascites, anorexia, malaise, weight loss and cachexia may be present. PHYSICAL EXAMINATION General examination should be performed to find out pallor, jaundice, weight loss, dehydration, lymph adenopathy and koilonychia. Left supra clavicular lymph glands (Virchow's nodes) may be enlarged in cases of malignancy.

37.01

Abdominal examination should be performed to feel any palpable mass. The liver and spleen should also be palpated and the consistency and size of these organs should be noted. DIGITAL RECTAL EXAMINATION Rectal examination is most important as approximately 75% of the lesions are within the reach of examining finger. The patient should be informed about procedure. Gentle technique, plenty of lubricant, a relaxed supportive atmosphere and gradual inward pressure of the finger helps to achieve maximum information3. Fissure in ano and hemorrhoids can be seen on the inspection of the anal canal opening.

Ulcerative colitis (endoscopic view)

PROCTOSCOPY Proctoscopy is helpful in looking at the lower rectal lesions and anal canal lesions. It should not be tried in painful anal conditions without proper anaesthesia. It is a simple procedure and can be performed in the out patients. Correct positioning of the patient is of utmost 4 importance for successful examination . SIGMOIDOSCOPY Rigid sigmoidoscope lubricated with xylocaine gel can be used very easily without any analgesia or preparation. It is quite safe and very useful procedure. Approximately thirty centimeters of distal gut can be examined. Biopsy can also be taken if indicated.

SURGERY - GASTRO-INTESTINAL PROBLEMS

37.02

Ulcerative colitis (endoscopic view)

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BLEEDING PER RECTUM

37.03

37.06

Rectal polyp causing bleeding per rectum

Rectal Polyp (endoscopic view) 37.07

37.04

Rectal polyp causing bleeding per rectum

Carcinoma rectum causing rectal bleeding

37.05

37.08

Rectal adenoma (endoscopic view)

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Carcinoma rectum causing rectal bleeding

293

BLEEDING PER RECTUM

ULTRASONOGRAPHY Transrectal ultrasonography and endoscopic ultrasonography are used to pick up early colonic lesions. It is very useful in the diagnosis of early sub-epithelial lesions. 37.09

URINE EXAMINATION It is a simple investigation. It must be performed in all patients. It helps in the general assessment of the patients. BLOOD EXAMINATION ! Haemoglobin estimation ! Leucocyte count ! Sedimentation rate ! Urea and electrolytes estimation ! Liver function tests RADIOLOGICAL EXAMINATION PLAIN X-RAY OF ABDOMEN ! Erect view ! Supine view

Rectal Polyp (Transrectal ultrasonography) 37.10

BARIUM ENEMA Barium sulfate is introduced into the large gut through enema tube and x-ray pictures are taken. 37.11

Endoscopic ultrasonography ENDOSCOPIC EXAMINATION Colonoscopic examination is performed with a fiberoptic flexible colonoscope. Biopsy of the lesion should also be taken and sent for histopathological examination.

INVESTIGATIONS Following investigations are also carried out to assess the general condition of patient ;

SURGERY - GASTRO-INTESTINAL PROBLEMS

Ulcerative colitis (Barium enema) The barium is pushed upto terminal ileum. Whole of the large gut and ileocecal junction can be seen with this xray. The lesions are seen as negative shadows. Loss of haustrations is seen in ulcerative colitis.

294

BLEEDING PER RECTUM

DOUBLE CONTRAST BARIUM ENEMA Air is also insufflated with the barium through enema tube. The pictures thus taken are better than with ordinary barium enema. Smaller lesions also become visible with this procedure. 37.12

McIntosh JC. Mroczek EC. Baldwin C. Mestre J. Intussusception of the appendix in a patient with cystic fibrosis. Journal of pediatric gastroenterology nutrition. [JC:j16]1990 Nov. 11(4): 542-4.

Farver KC. Church JM. Open sesame: tips for traversing the anal. Diseases of the colon and rectum. [JC:eab]1992 Nov. 25(1) 1092-3.

Fraser A. Office proctology and sigmoidoscopy Australian family physician. [JC:9ec]1990 May. 19(5): 661-3.

Matter SE. Campbell DR. Significance of distal polyps detected with flexible sigmoidoscopy in a symptomatic patient. Archives of internal medicine. [JC:7fs] 1992 Sep.152(9): 1776-80.

Rex DK. Lehman GA. Hawes RH. Oconnor KW. Smith JJ. Performing screening sigmoidoscopy using colonoscopes. Experience in 500subjects. Gastrointestinal endoscopy. [JC:fh8] 1990 Sep-Oct. 36(5):486-8.

Ulcerative colitis (Double contrast barium enema) TREATMENT Immediate The patient is resuscitated. Lost amount of blood is replaced with blood transfusions till the haemoglobin level becomes normal and patient is haemodynamically stable.

SUMMARY Bleeding per rectum Etiology Investigations Treatment

DEFINITIVE TREATMENT It is treatment of cause of bleeding per rectum.

REFERENCES 1.

Billingham GT. Bessen HA. Aorto-enteric fistula in a 21 years old. Journal of Emergency medicine. [JC:ibo]1991 Sep-Oct. 9(5):343-5.

SURGERY - GASTRO-INTESTINAL PROBLEMS

POSSIBLE QUESTIONS 1. 2. 3.

Discuss benign causes of bleeding per rectum? Discuss malignant causes of bleeding per rectum? Discuss endoscopy for bleeding per Rectum?

295

COLORECTAL CARCINOMA

GIT-38

COLORECTAL CARCINOMA Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS

ETIOLOGY

38.01

Different factors have been blamed for the causation of carcinoma of the colon. Such as ;

! ! ! ! ! ! Carcinoma colon Carcinoma of the colon is the most common malignancy of the colon.

INCIDENCE & EPIDEMIOLOGY ! ! ! ! ! ! ! ! !

98% of all malignancies of the large gut are carcinomas. It is the number two killer in the cancer deaths (Number one killer is bronchogenic carcinoma). Higher incidence is seen in USA and European countries than in Japan. It is common in 60 to 80 years age group. It is three to four times common in the children of the patients suffering from this malignancy. 25% of the cases appear as an emergency with intestinal obstruction or peritonitis. Male and female ratio is 3:2. Carcinoma of ascending colon is more common in females. 75% of the colonic malignancies are seen in left colon and most of these are present in the distal colon.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Genetic factors. Dietary factors. Pre-malignant lesions. Neoplastic polyps. Familial polyposis coli. Ulcerative colitis.

GENETIC FACTORS It is seen that children and grand children of the patients with colonic carcinoma suffer from this malignancy three to four times more than ordinary people. Now the evidence is available that genetic factors and geographic factors are less responsible for the causation of colonic carcinoma. DIETARY FACTORS These are thought to be much more responsible for the colonic carcinoma. The effects of diet are explained as ;

! ! ! !

Ingestion of carcinogens. Variation of the fiber content in diet. Amount and type of lipid and protein in diet. Diet related changes in the intestinal flora.

Oral carcinogens like cycasin and many others such as (4Amino biphenyl, 1-2 dimethyl-hydrazine) have been found to produce colonic carcinoma. The transit time of the food and especially of the undigested food is more in the colon than in small gut giving the carcinogenic substances more time to affect the colonic tissue. This could be one of the reasons for higher incidence of colonic carcinoma than small gut malignancies.

297

COLORECTAL CARCINOMA

High fiber diet and large quantities of indigestible food are consumed in Africa and Asia. These areas show low incidence of polyps, diverticulosis and colonic carcinoma. The population in USA and European countries consumes refined foods having very little roughage or fiber showing high incidence of polyps, carcinoma and diverticulosis. It may be possible that high fiber diet alters the intestinal flora, thus protecting the colon from malignancy. An interesting correlation has been found between the level of animal fat and protein in the diet and colonic cancer. Higher the animal fat, higher the incidence of carcinoma. High fat diet also changes the intestinal flora thus making the colon prone to carcinoma PRE MALIGNANT LESIONS Neoplastic polyps, Gardener's syndrome and ulcerative colitis are known premalignant conditions leading to colonic carcinoma. NEOPLASTIC POLYPS Adenomatous polyps are potentially malignant specially when these are larger than 2 cm in diameter. Villous papillomas have higher incidence of malignancy than adenomatous polyps. FAMILIAL POLYPOSIS COLI These show higher incidence of colonic carcinoma. The polyps are not present at birth but appear later on and malignant change doesn't occur before twenty years of age. The patients with family history of polyps should have sigmoidoscopy and barium enemas regularly. ULCERATIVE COLITIS The patients with ulcerative colitis run a definite risk of malignancy. These are usually diagnosed early due to routine follow up with sigmoidoscopy and biopsy.

PATHOPHYSIOLOGY The vast majority of colorectal cancers are adenocarcinomas, which arise from preexisting adenomatous polyps that develop in the normal colonic

SURGERY - GASTRO-INTESTINAL PROBLEMS

mucosa. This adenoma-carcinoma sequence is a wellcharacterized clinical and histopathologic series of events with which discrete molecular genetic alterations have been associated. Another predisposing condition is hereditary nonpolyposis colon cancer, in which affected individuals inherit a mutation in one of several genes involved in DNA mismatch repair, including MSH2, MLH1, and PMS2. ras gene mutations have been detected in the stool of patients with colorectal cancer and may in the future be useful in early diagnosis.

PATHOLOGY The colonic carcinoma starts as carcinoma in situ and follows two patterns depending upon the site of lesion ;

! !

Carcinoma of left colon. Carcinoma of right colon.

COLONIC SUBMUCOSAL TUMOURS The colonic submucosal tumours are classified on the basis of radiological findings into five types ;

! ! ! ! !

Wide based sessile lesion with gradually sloping margin and smooth surface. Wide based sessile lesion more polypoid with smooth surface. Wide base sessile lesion with lobulated surface. Pedunculated lesion with smooth or granular surface. Diffusely stenotic or aneurysmal lesions.

CARCINOMAS OF LEFT COLON These are usually annular (circular) and lead to early intestinal obstruction. These appear as small polypoid mass or flat button like plaque. These grow and infiltrate circumferentially. It takes one to two years to involve whole of the lumen. Deeper infiltration is seen late. Ulceration occurs showing heaped up margins. Pericolic spread is seen to the fat and lymph glands. Pericolic abscess may be seen or even peritonitis may occur.

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COLORECTAL CARCINOMA

Metastasis occurs late to liver, lungs and bones.

38.04

38.02

Carcinoma colon (ulcerating) Carcinoma colon !

CARCINOMAS OF RIGHT COLON These are usually cauliflower type, polypoidal or fungating in nature. The intestinal obstruction is late feature in these carcinomas. It appears as irregular mass which grows and becomes large and cauliflower type. It fills the lumen of the intestine. These lesions extend through the wall to the mesentry, lymph nodes and distant sites. Very rarely these can be annular type as well. Multiple lesions are seen in cases of ulcerative colitis, Crohn's disease and polyposis coli. MACROSCOPIC APPEARANCE All of the colonic carcinomas present macroscopically in the following ways ;

38.03

Carcinoma colon (fungating)

SURGERY - GASTRO-INTESTINAL PROBLEMS

! ! !

Fungating or cauliflower type. Ulcerating type. Polypoid or villous type. Colloid or mucinous tumours.

MICROSCOPIC APPEARANCE The colonic carcinoma is mostly columnar cell tumour. 95% of these tumours are adenocarcinomas. Many of these lesions produce mucin extracellularly. The tumour could vary in differentiation. Anaplastic lesions show irregularly placed cords of cells without any suggestion of the gland formation. Malignant cells show pleomorphism, hyperchromatism, large vesicular nuclei of various sizes, shapes and positions. Sometimes metaplasia to squamous epithelium is also seen in distal colonic tumours and these are called adeno-acanthomas. Another variant is undifferentiated small cell carcinoma which may be of endocrine origin. SPREAD The colonic carcinoma spreads by ; ! Direct extension. ! Lymphatic spread. ! Vascular spread. ! Gravitational spread. ! Spread during operations.

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DIRECT SPREAD The tumour takes long time to grow to the size large enough to cause symptoms. The tumours of caecum remain unrecognized for quite a while and are usually inoperable by the time these are diagnosed. Many times the tumour penetrates the adjacent viscera (urinary bladder and female pelvic organs) and sometimes even extends towards the abdominal wall leading to fistula formation. INTRAMURAL SPREAD Intramural spread is quite common and it spreads more longitudinally than outwards. LYMPHATIC SPREAD It spreads to local lymph glands such as epicolic lymph glands and then to the paracolic glands along the branches of superior and inferior mesenteric vessels.

Operative manipulations also spread the tumour through all routes of spread. STAGING Normal Intestinal Tissue (Cross section of digestive tract)

Epithelium Connective tissue Thin muscle layer Submucosa

Mucosa

Thick muscle layers Subserosa Serosa

The layers of the Colon wall

From paracolic glands, the tumour spreads to pre-aortic groups of lymph glands (superior and inferior mesenteric groups of glands). VASCULAR SPREAD It is through the veins to the liver. The secondary deposits reach the liver early. This is seen even before the symptoms of local disease have become evident. GRAVITATIONAL SPREAD It shows characteristic example of transcoelomic spread in the form of the deposits over the ovaries (Krukenberg's tumour). OPERATIVE SPREAD The tumour spreads and infiltrates the layers of the abdominal wounds during operation if it is not done very carefully.

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Colorectal carcinoma (TNM staging) TNM STAGING Tx: No description of the tumor's extent is possible because of incomplete information. Tis: The cancer is in the earliest stage. It involves only the mucosa. It has not grown beyond the muscularis mucosa (inner muscle layer). T1: The cancer has grown through the muscularis mucosa

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and extends into the submucosa. T2: The cancer has grown through the submucosa and extends into the muscularis propria (outer muscle layer).

M1: Distant spread is present. DUKE'S CLASSIFICATION

T3: The cancer has grown through the muscularis propria and into the subserosa but not to any neighboring organs or tissues. T4: The cancer has grown through the wall of the colon or rectum and into nearby tissues or organs. N categories for colorectal cancer N categories indicate whether or not the cancer has spread to nearby lymph nodes and, if so, how many lymph nodes are involved. Nx: No description of lymph node involvement is possible because of incomplete information. N0: No lymph node involvement is found. N1: Cancer cells found in 1 to 3 nearby lymph nodes. N2: Cancer cells found in 4 or more nearby lymph nodes. M categories for colorectal cancer M categories indicate whether or not the cancer has spread to distant organs, such as the liver, lungs, or distant lymph nodes. Mx: No description of distant spread is possible because of incomplete information. M0: No distant spread is seen.

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Colorectal carcinoma (Duke's classification) Dukes stage A Carcinoma in situ limited to mucosa or submucosa (T1, N0, M0) Dukes stage B Cancer that extends into the muscularis (B1), into or through the serosa (B2) Dukes stage C Cancer that extends to regional lymph nodes (T1-4, N1, M0) Dukes stage D (Modified classification) Cancer that has metastasized to distant sites (T1-4, N1-3, M1)

CLINICAL FEATURES The clinical features of colonic carcinoma depend upon the size, site and extent of the spread of the tumour. Many cases remain asymptomatic for quite some time and are diagnosed incidently while the patient is being investigated for some other problems. PAIN It is usually intestinal colic and is due to obstruction. If the pain is constant and progressive, it is probably due to

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extra mural spread. Colicky pain is common in constricting or stenosing lesions. ALTERED BOWEL HABITS/CHANGE IN BOWEL HABITS The symptoms are alarming especially if these occur in patients above 40 years of age. The patients complain of increasing constipation followed by diarrhoea. This is due to partial intestinal obstruction and intake of purgatives to relieve it. PALPABLE LUMP The lump in the abdomen may be palpable anywhere throughout the course of large intestine. Usually it is freely mobile but when it spreads it may be fixed to the abdominal wall. Many times it is the bunched up faecal matter which is palpable proximal to obstructing lesion. DISTENSION It is present due to intestinal obstruction. It may be painful and is relieved by passage of flatus and faeces. TENESMUS Fungating growths of the lower colon may cause a painful sensation and an urge for evacuation of stools. BLEEDING PER RECTUM This is more common in lesions of distal colon especially at rectosigmoid junction or sigmoid colon. SPURIOUS DIARRHOEA It is seen in rectal malignancy. There is passage of loose feces with mucous and blood especially early in the morning. GENERAL SYMPTOMS General symptoms due to colonic carcinoma may be the presenting features such as pallor, malaise, fatigue, anorexia and sometimes continuous pyrexia. The pallor or anaemia is more marked in patients with growths of caecum.

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Cachexia, jaundice, hepatomegaly and ascites are the late features of the carcinoma colon (features of terminal malignancy). Occasionally patient may present with bladder symptoms such as frequency of micturition, dysuria and pneumaturia. These may be due to colo-vesical fistula.

DIFFERENTIAL DIAGNOSIS ! ! ! ! ! ! ! !

Crohn's Disease Diverticulitis Diverticulosis Inflammatory Bowel Disease Kaposi Sarcoma Peritonitis and Abdominal Sepsis Ulcerative Colitis Angiodysplasia

Differential diagnosis in patients who present with lower GI bleeding includes colorectal cancer, inflammatory bowel disease (ulcerative colitis or Crohn's disease), diverticular disease, foreign bodies, polyps, metastatic disease, intestinal lymphomas, or Kaposi sarcoma involving the gut.

DIAGNOSIS History should be taken and recorded carefully. Examination should be performed completely. Abdominal and rectal examination should be performed meticulously. Following investigations are performed to confirm the diagnosis and assess the general condition of the patient. INVESTIGATIONS URINE EXAMINATION It is a simple but very valuable investigation to assess the general condition of the patient and to find out the involvement of bladder by colonic malignancy.

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BLOOD EXAMINATION Haemoglobin estimation. Leucocyte count. Sedimentation rate. Urea and electrolytes. CARCINOEMBRYONIC ANTIGEN (CEA) Preoperative carcinoembryonic antigen (CEA) level can be helpful in the clinical management of colorectal cancer. CEA is much less likely to be elevated in poorly differentiated colon or rectal carcinomas. Elevated CEA level preoperatively can be monitored for evidence of recurrence. ! CEA may be elevated for reasons other than colon cancer, such as pancreatic or hepatobiliary disease, and elevation does not always reflect cancer or disease recurrence; ! CEA level may be helpful to monitor the response . ! The real value of monitoring CEA after initial resection is in early identification of patients who may benefit from additional surgery with curative intent.

It is used to stage rectal cancer by assessing the depth of invasion through bowel wall layers and / or involvement 1 of lymph nodes . CT/MRI SCAN Abdominal/pelvic CT scan can be useful in diagnosis of colon cancer that has metastasized to lymph nodes and liver. Multiple metastases in the liver renders colon cancer incurable by surgery and chemotherapy. Metastatic colon cancer does not, however, preclude surgery as an option for palliation, e.g, in cases with bleeding or obstruction. 5-year tumor-free survival rate of 34% and 10-year survival rate of 21% in such patients can be achieved. 38.06

CANCER ANTIGEN 19-9 Tumor markers, such as cancer antigen 19-9 (CA 19-9) may also be helpful, if initially elevated. ENDOSCOPIC ULTRASONOGRAPHY (EUS)

Carcinoma colon - MRI

38.05

38.07

Carcinoma colon (EUS)

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Carcinoma colon - CT Scan

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Chest CT scan can be helpful to identify lung metastases. Prognosis is poor in patients with liver and lung metastases.

BARIUM ENEMA It helps to show most of the colonic lesions. 38.09

CT scan also is very helpful in the follow-up of patients with resected, as well as metastatic disease. It can diagnose recurrent disease and can document response to chemotherapy. PET imaging (FDG-PET) may be useful for staging colorectal cancer and may be very useful in detecting recurrent disease. PET/CT and contrast-enhanced CT (ceCT) provide similar information regarding hepatic metastases of colorectal cancer, whereas PET/CT is superior to ceCT for the detection of recurrent intrahepatic tumors after hepatectomy, extrahepatic metastases, and local recurrence at the site of the initial colorectal surgery. RADIOLOGICAL EXAMINATION CHEST RADIOGRAPHY It is part of the routine evaluation and staging workup. It may reveal metastatic spread to the lungs.

Carcinoma colon (barium enema)

DOUBLE CONTRAST BARIUM ENEMA 38.10

PLAIN X-RAY ABDOMEN 1. Erect view. 2. Supine view. It helps to pick up the features of intestinal obstruction. 38.08

Apple Core appearance in Carcinoma colon

Air fluid levels (Plain x-ray abdomen)

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Double-contrast barium enema is used for screening of colorectal cancer. It can aid in establishing the diagnosis of colon cancer. It is a better investigation as the pre-

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sence of air and barium shows even smaller mucosal lesions of colon quite clearly. It has limitations and can miss lesions in the region of the ileocecal valve or the distal rectum or in patients with severe diverticulosis. It is valuable in the diagnosis of colon cancer, comparing favorably with colonoscopy. The primary reason for missed radiologic diagnosis is failure to observe important lesions visible on the radiographs. Correct diagnosis can be made in 90.9% of cases with barium enema.

Endoscopic examination of whole of the colon is performed through a fiberoptic flexible colonoscope. It is a good investigation but can be performed by skilled endoscopist only. It is more accurate than other investigations such as mesenteric angiography. It can be used not only for diagnostic but for therapeutic purposes as well. Laser therapy (photocavitation) can be per6 formed through colonoscopy . Colonoscopy allows examination of the entire colon, and can be used to obtain a biopsy of suggestive lesions or to remove polyps.

FLEXIBLE SIGMOIDOSCOPY It is an excellent endoscopic examination. A 60- cm fiberoptic flexible sigmoidoscope is used. It has almost replaced colonoscopy as it picks up most of the lesions and use of endoscopes longer than 60 cms gives very 2,3 little additional information . It covers nearly 75 % of the colonic lesions. The advantage is that biopsy and even excision of the pedunculated lump can be performed through the sigmoidoscope. The lesions of lower colon which are not shown on barium enema can be seen through the sigmoidoscope. It is a screening tool that can detect polyps or cancers as far as 60 cm from the anus. If polyps are found in the distal colon, others may be present in the proximal colon and can be detected by colonoscopy.

38.12

Sigmoidoscopy 38.13

COLONOSCOPY 38.11

Colonoscopic procedure

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Colonoscopy

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It can be performed safely in older individuals as well. The decision to perform colonoscopy is considered to see proximal lesions of clinical interest, life expectancy of the patient, costs, and risks associated with the procedure. Periodic colonoscopy may be the most effective and costeffective screening method. It is also effective method of surveillance in patients who have undergone colonoscopic polypectomy than double-contrast barium enema. 37.14

electrolytes. High caloric and low or no residue diet is given to these patients.

DEFINITIVE TREATMENT Surgery is the definitive treatment used for colonic carcinoma. Bowel preparation is required before surgery. BOWEL PREPARATION Bowel may be prepared by mechanical methods (enema), chemical methods (antibiotics, laxatives) or a combination of the two. Enemas are given to clear the bowel. In cases of intestinal obstruction, many times colostomy will be required to clear the proximal obstructed large intestine.

Carcinoma colon (AP resection)

Different medicine can be used for the preparation of intestine before definitive surgery is undertaken. Following drugs are commonly used for this purpose ; ! Neomycin sulfate 1 gram 6 hourly for two days. ! Flagyl 400 mg 8 hourly for five days. ! Sulphathiazole 2 grams 6 hourly for five days. ! Gentamycin 80 mg intramuscular 8 hourly for five days.

EXFOLIATIVE CYTOLOGY The bowel preparation is done and the fluid obtained after the bowel wash out is centrifuged and the sediment is seen for the malignant cells. It is a very time consuming and less fruitful investigation4. It has a sensitivity of 73% 5 and specificity of 100% .

Several other preparations are used for bowel cleansing (eg, polyethylene glycol 3350 [GoLYTELY, NuLYTELY], magnesium citrate [Citroma], senna [X-Prep]) in preparing patients for surgery or gastrointestinal procedures such as endoscopy, colonoscopy, and barium x-ray studies.

TREATMENT

Bowel cleansing preparations may be used with various dietary preparations (eg, clear liquid diet 1-2 days before surgery or procedure) and are convenient to administer on an outpatient basis.

GENERAL PREPARATION Anaemia is corrected. Blood transfusion or packed cell transfusion may be required in severely anaemic patients. Fluid and electrolyte balance is corrected and maintained by oral intake or intravenous infusion of the fluids and

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SURGICAL TREATMENT OPEN OPERATION Exploration through laparotomy is performed. Liver is

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Sites of Carcinoma Colon with Resection and Anastomosis Plan

Carcinoma ascending colon Limited right hemicolectomy with ileocolic anastomosis

Carcinoma descending colon Limited left hemicolectomy with colo-colic anastomosis

Carcinoma transverse colon Transverse colectomy with colo-coilc anastomosis

Carcinoma sigmoid colon Sigmoid colectomy with colo-colic anastomosis

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seen and palpated thoroughly for the presence of secondary deposits. Mesenteric and pre-aortic lymph glands are seen and palpated for their size, consistency and involvement. The abdomen is explored to determine whether the tumor is resectable. Resection of the colonic carcinoma is performed followed by anastomoses of the healthy intestine to keep the bowel continuity. Right hemicolectomy, transverse colectomy, left hemicolectomy and pelvic colectomy may be performed for the lesions present at different anatomical sites. The classic surgical procedure for rectal cancer is anterior resection that involves a "no touch" isolation technique. A resection margin of 10 cm of grossly normal bowel on both sides of the tumor along with associated lymph nodes is recommended. Total colonic resection is performed for patients with familial polyposis and multiple colonic polyps. The role of lymphatic mapping (LM) and sentinel lymphadenectomy (SL) is undergoing investigations, although preliminary results appear conflicting. However, identification of micrometastatic nodal disease results in upstaging of disease in 5-50% of patients. LAPAROSCOPIC COLON RESECTION The technology exists to use laparoscopic techniques to achieve colon resection with favorable results on 5 years of follow-up. OTHER OPTIONS Partial hepatectomy for colorectal cancer metastases limited to the liver is a therapeutic option for the patients with recurrent colorectal cancer that appears to be confined to the liver. Predictors of a better outcome include; ! A single metastasis ! Longer disease-free interval from resection of the primary tumor to presentation with metastasis, ! CEA level less than 200 ng/mL.

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! ! !

Tumors less than 5 cm in diameter Unilobar disease Negative margins after resection

Early detection of recurrent colorectal cancer includes imaging by CT or MRI. PET scanning appears to be more accurate than CT and has become increasingly used to identify recurrent disease, but it can miss small foci of the disease. CEA levels also may be useful to detect recurrence, although false-positives and false-negatives occur. Other therapeutic options for liver metastases include; ! !

Cryoablation (a technique currently performed during abdominal surgery) Hepatic arterial infusion (HAI) of chemotherapeutic agents such as FUDR

Chemotherapy helps in converting the unresectable tumor into resectable disease. ENDOSCOPIC LASER THERAPY The primary role of ND:YAG laser is to relieve the obstruction and control haemorrhage associated with non resectable malignant colonic neoplasms. It is a safe and acceptable alternative to permanent colostomy with its morbidity and mortality7. MEDICAL CARE (CHEMOTHERAPY) Important advances have been made regarding the firstline standard therapy of metastatic colorectal cancer. Combination of 5-FU, leucovorin (LV), and irinotecan (CPT11) is used. Significantly improved response rates are seen with the addition of oxaliplatin to the 5-FU/leucovorin regimen. Anti-VEGF therapy with bevacizumab (Avastin) increases survival in these patients. Colorectal cancer is the first cancer type to be shown to respond to antiangiogenic therapy.

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Standard therapy for metastatic colon cancer is CPT11 plus 5-FU/leucovorin, also known as the Saltz regimen. Each of the agents in the Saltz regimen is administered by IV injection weekly for 4 weeks every 6 weeks. Diarrhea is the most commonly encountered adverse effect with this regimen. Other adverse effects include mucositis, neutropenia, hair loss, and skin hypersensitivity reactions. Intraarterial floxuridine (FUDR) is used for colon cancer with liver metastasis. Systemic chemotherapy with a standard regimen following resection of the primary colon cancer and lymph nodes such as 5-FU/leucovorin/CPT11 or intrahepatic (intraarterial) chemotherapy with FUDR is used. The major adverse effect of intraarterial FUDR is sclerosing cholangitis, which may be quite severe and may necessitate discontinuation of therapy.

RADIOTHERAPY It is not very helpful in the treatment of colonic carcinoma.

endoscopy. [JC:fh8] 1990 Sep-Oct. 36(5):486-8. 4.

Rozen P. Taki M. Darwon E. Kaufman L. Exfoliative colonic cytology. A simplified method of collection and initial results. Acta cytologica. [JC:oli]1990 Sep-Oct. 34(5): 627-31.

Bardawil RG. D'Ambrosis FG. Hajdu SI. Colonic cytology. A retrospective study with histopathologic correlation. Acta cystologica [JC:Oli] 1990 Sep-Oct. 34(5): 620-6. Van Gossum A. Bourgeois F. Gay F. Lieveus P. Adler M. Gremer M. Operative colonoscopic endoscopy. Acta Gastroenterologica Belgica. [JC:ony] 1992 May-Jun.55(3) : 314-26.

Eckhauser ML. Mansour EG. Endoscopic lasertherapy for obstructing and / or bleeding colorectal carcinoma. American surgeon. [JC:43e] 1992 Jun.58(6): 358-63.

REFERENCES 1.

Roubein LD. David C. Dubrow R. Fauntuch J. et al Endoscopic ultrasonography in staging rectal cancer. American journal of Gastroenterology. [JC:3he]1990 Oct. 85 (10): 1391-4.

Matter SE. Campbell DR. Significance of distal polyps detected with flexible sigmoidoscopy in a symptomatic patient. Archives of internal medicine. [JC:7fs] 1992 Sep. 152(9): 1776-80.

Rex DK. Lehman GA. Hawes RH. O connor KW. Smith JJ. Perfor ming screening sigmoidoscopy using colonoscopes. Experience in 500 subjects. Gastrointestinal

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SUMMARY Carcinoma colon Incidence Etiology Genetic factors Dietary factors Pre malignant lesions Neoplastic polyps Familial polyps Ulcerative colitis Pathology Staging Clinical features Investigations POSSIBLE QUESTIONS 1. 2. 3. 4.

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What is carcinoma colon? Enumerate pre cancerous conditions of colon. Enlist different diagnostic modalities for colorectal carcinoma. How do you stage colorectal carcinoma? What are different surgical options for rectal carcinoma?

? 310

Rectum & Anal Canal

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311

ANAL FISSURE

OBJECTIVES ! ! !

To understand the development, anatomy & physiology of rectum & anal canal. To be able to understand the congenital anomalies related to rectum & anal canal. To be able to understand basis of investigations for disease related to rectum of anal canal.

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GIT-39

ANAL FISSURE Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS Anal fissure is a tear of the muco-cutaneous part of the anal canal. It is present along the long axis of the anal canal. The anal fissure is slightly more common in the females. It is usually present in the young age group. It is a condition which results in morbidity and constant agony. Most of the time the anal fissure is present in the midline posteriorly. Occasionally it is present in the midline anteriorly. Other sites show fissures very rarely. 39.01

canal also causes the fissure-in-ano formation. Anal fissure can also occur after trauma but these are usually acute and heal early. Anal fissure can be secondary to ulcerative colitis, Crohn's disease, pruritus, tuberculosis, syphilis and leukaemia. Maximal basal pressure and maximum contraction pressures of the anal fissure patients are significantly raised as compared to normal (87Âą39) mm of Hg (Control 71 Âą 25 mm of Hg) on anal manometric studies3.

PATHOLOGY Anal fissure can be ; ! Acute ! Chronic Anal fissure can also be ; Specific (due to Crohn's disease, ulcerative colitis, tuberculosis, syphilis, leukaemia and pruritus).

! Acute anal fissure

ETIOLOGY Exact cause is not known why the fissure lies in the midline posteriorly. It is possible that rectum and anal canal are unsupported posteriorly and when the patient strains during defecation, a tear appears in the midline posteriorly. The anterior tears are more common in women specially the multiparous women. It may be due to lack of support to the anterior wall of the anal canal due to weak or damaged pelvic floor muscles. Constipation is always a predisposing factor in the causation of the anal fissure. Tight anal sphincter and anal stenosis following haemorrhoidectomy or after any procedure on anal

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Non specific

ACUTE ANAL FISSURE Acute anal fissure is a suddenly appearing tear in the anal canal. It is deep and painful. It heals early or changes into a chronic fissure. CHRONIC ANAL FISSURE Chronic anal fissure is a tear with inflamed and indurated margins. It is present over a longer period. The granulation tissue formation occurs at the base and a skin tag is present at its distal margin. The skin tag is called sentinel pile. The ulcer is elliptical with its long axis along the long axis of the anal canal. The anal sphincter is usually tightly closed. It is a very painful condition. The patients suffering from this problem learn to remain

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constipated out of fear of the pain following defecation. Specific chronic fissures are less painful.

Occasionally more bleeding may occur but it is rarely very severe. DISCHARGE Slight degree of serous discharge may be present.

39.02

IRRITABILITY The patients with fissure in ano are irritable and anxious.

DIAGNOSIS History is very suggestive of the disease. Clinical examination is confirmatory of the diagnosis. Inspection of the perineum should be performed at first . Chronic anal fissure 39.03

The fissure is clearly visible or the anal sphincter is very tightly closed over the fissure. The sentinel pile may also be present guarding the fissure. Digital examination should never be performed without proper anaesthesia. Once the anal fissure is treated surgically, the tissue should be sent for histological examination to find out the cause of fissure.

TREATMENT

Chronic anal fissure

CLINICAL FEATURES PAIN There is severe and agonizing pain at the beginning of the defecation . The pain is so severe that patients reflexly try to stop defecation and get constipated. The thought of pain also depresses the urge to defecate reflexly and the patient gets constipated more and more. The reflex spasm of the anal sphincter and severe constipation make the anal fissure even more painful. BLEEDING Usually a line of blood is seen on the hard stool.

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CONSERVATIVE High fiber diet rich in indigestible fiber should be used such as vegetables, fruits and whole wheat. This will help in proper evacuation of the faeces and healing of the ulcer. LAXATIVES Mild laxatives, such as liquid paraffin, creamaffin, agarol, celevac and duphalac should be used to keep the bowels working. These should be given in doses enough to keep the stools soft but never watery as excessive purgation and loose stools make the condition even worse. LOCAL ANAESTHETIC CREAMS Creams having local anaesthetic agents can be used to achieve symptomatic relief. These are very helpful but have only temporary effect. Solcoderm topical applications have been found to be simple safe, cost

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effective and without systemic side effects1. GLYCERAL TRINITRATE (GTN) PASTE This paste is applied to increase the local blood supply. It leads to healing of the ulcer. It has 90% success rate when applied for 4-8 weeks. The main disadvantage is severe headache which occurs because of dilatation of cerebral vessels but headache can be treated with use of oral aspirin. ANAL DILATATION Anal dilators can be used in anal fissures of lesser duration, mild degree and those associated with less fibrosis. These should be used after the local anaesthetic has anaesthetized the area. The smallest size anal dilator is lubricated and introduced gently into the anal canal. The large size dilators are gradually introduced into the anal canal. The dilator is kept in the anal canal for at least half an hour. The anal dilatation is continued for two to three weeks and it is performed twice or three times daily. SURGERY LORDS' PROCEDURE (MAXIMUM ANAL DILATION) It is the maximum anal dilatation. It is performed under general or spinal anaesthesia. It helps to stretch the anal sphincter and break it at many places. It helps in the healing of anal fissure. It should be performed gently and over a period of 3-5 minutes. It may be used as first line treatment of the anal fissure. It gives satisfactory pain relief2.

LATERAL SUBCUTANEOUS SPHINCTEROTOMY It is the operation to cut the internal anal sphincter at the lateral aspects (3'0 or 9'0 Clock position). It is the most favourable operation for this problem at present. The fissure may also be excised. The wound heals nicely and chances of infection are few. Its results are effective and it gives significantly less post operative 2,5 discomfort . The complications associated with other surgical procedures are more than lateral sphincterectomy. ANOPLASTY When the anal fissure is associated with stenotic anal opening, a longitudinal incision is given across the stenotic area to open the anal canal wide. It is stitched transversely to make the anal opening wider. It is a very simple operation and achieves very satisfactory results4.

REFERENCES 1. C h e n J . M i c h o w i t z M . B a w n i k J B . Solcoder m as alter native conser v ative treatment for acute anal fissure: A c o n t r o l l e d c l i n i c a l s t u d y. A m e r i c a n surgeon. [JC:43e]Nov. 58(11): 705-9. 2. Giebel GD. Horch R. Treatment of anal fissure: A comparison of three different for ms of ther apy. Nippon Geka Hokan A r c h i v e F u r. J a p a n i s c h e c h i r u r g i e . [JC:70c]1989 Jan I. 58(1): 126-33.

This procedure has been abandoned by most of the surgeons because of its complications such as partial fecal or wind incontinence.

3. Lin JK. Liang CL. HsuH. Wang FM. Anal manometric studies in haemorrhoids and anal fissures. Chung Hu a i Hsueh Tsa Chih Chinese Medical Journal. [JC:chg]1989 Apr. 43(4): 249-54.

FISSURECTOMY AND DORSAL SPHINCTEROTOMY It is excision of the ulcer or fissure and cutting of the anal sphincter posteriorly. It helps in the healing of the wound and fissure. This operation is minimally used these days.

4. Case B. Chronic anal fissure: A new method of treatment by anoplasty. Diseases of colon and rectum [JC:eab] 1991 Feb. 34(2): 198-9. 5. Kartbeck JB. Langevin JM. Khoo RE. Haive JA. Chronic fissure-in-ano. A randomized study

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comparing open and subcutaneous lateral internal sphincterotony. Disease of colon and rectum. [JC:eab]1992 Sep. 35(9): 835-7.

SUMMARY Anal fissure Etiology Pathology Clinical features Diagnosis Treatment

POSSIBLE QUESTIONS 1. 2. 3.

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What is an anal fissure? What are its causes? What is its treatment?

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GIT - 40

PILONIDAL SINUS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon)

fistulae is unclear.

40.01

A Pilonidal Fistula-in-ano is extremely uncommon and a rare complication of pilonidal sinus. It was originally thought to be of congenital origin but is now widely regarded as acquired and this theory is based on the formation of a sinus by penetration of the skin by hair . 4

Pilonidal sinus may also present as a tiny pit in the natal cleft which was joined by a track to an opening near the anus. But there was no communication to the anal canal.

Pilonidal abscess

Pilonidal sinus is a blind-end tract lined with granulation tissue commonly containing hair. Pilonidal sinus originates from Latin word “pilus” for hair, “nidus” for nest, and “sinus” for connections to skin, meaning nest of hair connected to skin. Pilonidal sinuses are situated in the natal cleft overlying the sacral and coccygeal areas. It leads to a cystic cavity lined with epithelial tissue enclosed by the adjacent tissue having a nest of hairs. It may discharge pus off and on. It is also called jeep seat disease in USA as it is seen in jeep traveling soldiers. The sinus track goes vertically down into buttocks (in the natal cleft). It is generally regarded as an acquired disorder although the pits through which hairs enter the subcutaneous tissue may be congenital with usually dead hair in it. The most common site is in the postnatal region. Pilonidal sinus may be found in the axilla, the groin, the interdigital web and on the feet and occiput . Very rarely the Pilonidal sinus may communicate with the anal canal forming a Pilonidal fistula in ano. The causation of these 1

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40.02

Pilonidal fistula-in-ano

ETIOLOGY Exact cause is not clear. It may develop from a main congenital on hereditory abnormality in the skin of the natal cleft (it runs in certain families). It may be that hair grow into the skin rather than outwards. It may develop as dimples in the skin between the buttocks. These may develop from damaged hair follicles due to local pressure of friction and growing hair from the 317

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natal cleft may get pushed into the dimples. The irritating hair lead to inflammation and infection which persists and drains out when pus increases in amount. It leads to sinus formation. Usual sufferers are young adults or even teenagers. It is rare in children and people over 40 years of age. It is more common in fat and hairy men than women. Certain factors increase the risk; ! Sedentary occupation (sitting a lot) 44% ! Obesity 50% ! Previous persistent irritation or injuries 34% ! Family history 38% ! Drivers 40.03

compared to adjacent area. FEVER It is noticed during acute infected episode when the abscess has formed and pus has not yet discharged. DISCHARGING SINUSES The swelling in the natal cleft starts discharging pus as the abscess grows. The swelling decreases in the size as the pus is discharged. Sometimes hair may be seen coming out of the sinuses. The swelling also becomes painless or less painful after the discharge of pus. All of the above symptoms persist for a long period till treatment is given. These symptoms become acute from time to time when the infection flares up. The symptoms become less painful in between the episodes of infection but never disappear completely without treatment.

INVESTIGATIONS

Pilonidal abscess

CLINICAL FEATURES Pilonidal sinus presents in three forms; ! Acute abscess ! Chronic discharging sinus ! Unhealed midline wound These presentations are as follows; SWELLING A swelling is felt at natal cleft. It may not be painful initially but becomes gradually painful as it gets infected.

Lab investigations Urine examination Blood examination Imaging It is less often required as the diagnosis is confirmed by clinical examination. ! ! !

MRI Scan 40.04

PAIN The natal cleft becomes painful gradually. The pain is usually continuous and increasing in nature. The area is tender to touch and when condition becomes worse, is painful even without touch. REDNESS The area at the natal cleft becomes red as the infection progresses and it has increased temperature as

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Pilonidal sinus (MRI Scan postro-anterior view)

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It is extremely useful investigation in the assessment of complex and recurrent pilonidal sinus. It is a non-invasive investigation. It is less easily available and only present at few centers. It helps to clarify the anatomy of sinuses for adequate excision and clearance of sinus and fistula tracks. It is required to achieve complete removal of diseased tissue. 40.05

PHENOL INJECTION It is not a very satisfactory treatment option as it does not offer permanent cure and has high recurrence rate and recurrent episodes of infection. Local phenol injection into the sinuses may help to close the sinus. It is less often used treatment option as its use is risky and hazardous to the adjacent tissue. SURGICAL TREATMENT There are two phases of surgery for pilonidal sinus ! Emergency surgery ! Definitive surgery Variety of options are available: ! Incision and drainage ! Excision and healing by 2nd degree ! Excision and primary closure ! Excision and reconstructive flap techniques 40.06

Pilonidal sinus (MRI Scan lateral view)

TREATMENT Objectives ! To relieve the symptoms and cure the disease ! To be acceptable to the patient in terms of discomfort. ! To be able to resume work and social activities as early as possible. CONSERVATIVE It may be helpful in the patients who are not in acute phase or in patients who have already undergone surgery and need follow up management to avoid recurrence. Following measures are taken; ! Meticulous depilation (hair removal) ! Improved local hygiene ! Appropriate antibiotics ! Adequate analgesia ! Regular local shaving

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Excision and (left open) healing by second degree 10% Incision and Drainage 15%

Excision and Primary Closure 39%

Excision and Reconstruction flap techniques 36%

Average percentage of surgical options used INCISION AND DRAINAGE (15%) It is the treatment of choice in acute phase of pilonidal abscess or sinus and in recurrent and complex cases. It is performed when acute abscess is present. It is the simplest method of treatment. Short anaesthesia is

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required and complete drainage of pus and removal of hair is done. It has higher recurrence rate as the etiological factors still persist. WIDE EXCISION AND LEAVING THE WOUND OPEN (HEALING BY SECOND DEGREE) 10% It is the conventional method of treatment for pilonidal sinus during acute phase disease. In fact, this method is used for all types of pilonidal sinuses.

healing. It heals within seven to ten days. It achieves early recovery and return to normal social and working activities. The recurrence rate is higher than with wide excision and second degree healing. It is because the etiological factors are still persistent. 40.08

All the diseased tissue is excised leaving only healthy skin and underlying tissue behind. The wound is gently packed with sterilized gauze packs. The wound is allowed to heal with second degree healing. It takes nearly six to twelve weeks to heal. The healing occurs with granular tissue formation. Patient may have to stay away from work and social activities during this period. The recurrence rate is minimum with this method of treatment. Pilonidal sinus (post operative view)

40.07

40.09

Pilonidal sinus (pre operative view)

WIDE EXCISION WITH PRIMARY CLOSURE 39% It is the surgical option used for chronic phase disease or when the acute infection has settled after incision and drainage. The advantage of wide excision with primary closure is less time required for primary and early

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Pilonidal sinus (healing phase)

EXCISION AND RECONSTRUCTION FLAPS Two methods are commonly used;

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Karydakis technique Bascom’s technique Wide excision is performed. A variety of reconstruction flap techniques are used. It is a better option which helps in achieving early healing and minimum recurrence. ! !

Z-plasty and rotation flaps (rhomboid flap) are commonly used. These help in getting rid of deep natal cleft (the cause of pilonidal sinus formation). Primary closure leads to early return to work and social activities. KARYDAKIS TECHNIQUE It is a technique of asymmetric natal cleft wound closure. Eccentric elliptical incision is given. Mobilization of flap from median side of wound is done. All sinus tracts are excised completely to sacral periosteum. Mobilized flap is sutured to sacro-coccygeal fascia and wound is closed. BASCOM’S TECHNIQUE The incision is given away from the midline. The midline pits are excised with minimal tissue. Abscess cavity is drained laterally from the midline. A fibrous and fatty flap is lifted from post-sacral fascia. This flap is sutured to the bridge of skin between midline pits. Midline wound is closed. Lateral wound is left for drainage.

REFERENCES 1. Michael R.B.Keighley, Norman S.Williams. Pilonidal Sinus (chap 18), Surgery of The Anus, Rectum and Colon ,vol 1, pg 467-68. 2. Guiseppe Accarpio, Mario Doris Davini, Armando Fazio, Osama H.Senussi, Alla Yakubovich. Pilonidal sinus with an Anal Canal

4. Millar DM. Etiology of Post-anal pilonidal sinus. Proc.R.Soc.Med. 1970; 63:1263-4. 5. Lord PH. Unusual Case of Pilonidal Sinus. Proc.R.Soc.Med. 1970;62:967-8. 6. S.Vallance. Pilonidal fistulas mimmicking fistulas-in-ano. Br.J.Surg. Vol.69(1982) 161162. 7. Weston SD, Schlachter IS. Pilonidal cyst of the anal canal: Case report. Diseases of the Colon and Rectum 1963;6: 138-41. 8. Wilson E, Failes DG, Killingback M. Pilonidal sinuses of the anal canal: report of a case. Diseases of the Colon and Rectum 971;14:46870. 9. Walsh TH, Mann CV. Pilonidal sinuses of the anal canal. Br J Surg. 1983;70:23-4. 10. Karydakis GE. Easy and successful treatment of pilonidal sinus after removal of its etiological process. ATTST N2J. Surg 1992: (62) 385-389. 11. Mosquera DA, Quayle JB, Bascom’s operation for pilonidal sinus. JR Soc. Med. 1995: (88) 4546.

Fistula. Diseases of the Colon and Rectum 1998; 31: 965-67. 3. Hodges RM. Pilonidal Sinus. Boston Med Surg.J. 1880;103:485-6.

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SUMMARY Definition Etiology Clinical Features Investigations Treatment Conservative Surgical Incision and drainage Wide excision and lay open Wide excision and primary closure Wide excision and reconstruction flaps

POSSIBLE QUESTIONS 1.

What is the pilonidal sinus?

2. How it is caused?

3. What are the treatment options?

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GIT - 41

ANORECTAL ABSCESS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS Perianal or anoractal abscess is a localized collection of pus near the anus close under the skin, or deeper adjacent to the rectum. Perianal abscess is a common condition. It is more common in patients with Inflammatory Bowel Disease (in particular Crohn's disease), Diabetes Mellitus and AIDS. Anorectal abscess leads to fistula in-ano formation on discharge to skin or after surgical drainage. It is a very painful condition. Its exact incidence is unknown. A fistula-in-ano complicates 30-50% of perianal abscesses. 41.01

thrombosed pile. It is present in the area of subcutaneous part of external sphincter. It is seen in patients of all ages. It is diagnosed easily clinically. It can be treated effectively by incision and drainage. ISCHIORECTAL ABSCESS (2ND MOST COMMON) It is the next common abscess in occurence than perianal abscess. It is seen in 30% of patients. The infection of this area occurs due to lateral extension through external anal sphincter. The infection may spread through lymphatic or haematogenous route. The ischiorectal space filled with fat is vulnerable to infection because of its poor blood supply. The speed of abscess formation is very quick. The ischiorectal space is connected posteriorly with the opposite side. The abscess can extend to the other side if not treated in time. It may lead to horse shoe abscess formation. It presents with severe constitutional symptoms such as high fever and throbbing pain. It is seen more commonly in men than women.

Perianal abscess Anoractal abscess could be; ! Perianal ! Ischiorectal ! Submucous ! Pelvi-rectal

It is treated surgically through cruciate incision and whole of abscess is drained. If it is associated with internal opening into the anorectum, the treatment of fistula-inano is performed. SUBMUCOUS ABSCESS

PERIANAL ABSCESS (MOST COMMON) It is one of the most common sites for abscess formation in this region. It is present in 60% of the patients. It occurs following suppuration of an anal gland or

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It is a less common type of abscess of this area. It is seen in only 5% of patients. It may occur following an injection for the treatment of haemorrhoids. It is easily diagnosed clinically and can easily be treated by incision and drainage of pus. 323

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PELVI-RECTAL ABSCESS

INVESTIGATIONS

It is collection of pus between pelvic peritoneum and levator ani muscle. It is practically a pelvic abscess. It follows appendicitis, salpingitis, Crohn's disease, diverticulitis and perameteritis. It may follow over enthusiastic use of probes to follow the fistula track as well.

No general investigations are required for the diagnosis of the above condition. A Full blood count and blood sugar level can be used to screen for an inflammatory disorder or diabetes. 41.02

ETIOLOGY Perianal abscess occurs as a result of a blocked anal gland that subsequently becomes infected. These are more common in patients with Diabetes Mellitus, Crohn's disease, and patients who are immuno compromised for any reason.

CLINICAL FEATURES ! ! ! ! ! ! !

Painful swelling in perianal area Inability to sit on chair Difficulty in micturition Acute retention of urine Fever (swinging pyrexia) Rigors Painful defecation

CLINICAL COURSE Anorectal abscess is such a painful condition that patient almost always rushes for early treatment. If left alone, the pus is likely to discharge to the skin. It leads to formation of fistula-in-ano in many cases (30-50%). The fistula does not heal spontaneously. Surgical treatment is always required and is successful. Neglected fistulas can result in repeated abscesses and multiple openings. Abscess that is deeper, involving the upper portion of the anal sphincters (further away from the anus) is more complex and requires specialist treatment to avoid the complication of faecal incontinence if the internal sphincter is damaged.

Perianal abscess (MRI scan)

TREATMENT MEDICAL TREATMENT It is not useful as no antibiotic can reach the perianal abscess and control the infection. SURGICAL TREATMENT It is the only method for effective treatment of ano-rectal abscesses. It can be drained under general anesthesia. Surgery is undertaken immediately when the patient is fit and ready for anesthesia. One should not wait for abscess to become fluctuating because then it is too late. It should be drained and left open when it is still indurated. A cruciate incision is given for continuous and uninterrupted drainage. There is little role for antibiotics unless the patient is systemically unwell. ULTRASOUND GUIDED DRAINAGE It is a less invasive method of drainage of perianal abscess. It has not become a standard practice yet. Its efficacy and problems are still not clearly known.

REFERENCES 1. Cotran, Kumar, Collins 6th edition. Robbins Pathologic Basis of Disease. WB Saunders Company.

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1999.

SUMMARY

2. MEDLINE Plus Perianal abscess Etiology Clinical features Clinical course Investigations Treatment

3. Norman S. Williams. The anus and anal canal. Bailey and Love's short practice of surgery. 25th edition. Arnold publishers London. 2008. 1263-1265.

POSSIBLE QUESTIONS 1. 2. 3.

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What is peri-anal abscess? How is it caused? What is its treatment?

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GIT - 42

FISTULA-IN-ANO Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS

FREQUENCY

42.01

! ! ! ! ! Fistula-in-ano Fistula-in-ano is a disease with a very long history which dates back to antiquity. Fistula-in-ano is a hollow tract lined with granulation tissue connecting a primary opening inside the anal canal to a secondary opening in the perianal skin. Secondary tracts may be multiple and communicate through the same primary opening. A fistula in ano is a tunnel like (pipe like) track developed in the peri-anal region, usually having one or more external openings around the anus leading to an internal opening in the mucosa of the anal canal or the rectum. Anal fistula, a rare condition, is a chronically inflamed, abnormal tunnel between the anal canal and the outer skin of the anus. Fistula-in-ano remains a perplexing problem even after 25 centuries. Fistula in ano is an old problem, involving the anorectal region. It is notorious for its chronicity, recurrences and frequent acute exacerbations. Hippocrates described the use of seton to cure fistula in ano. The first surgical lay open of fistula in ano was performed in 13th century.

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The prevalence rate is 8.6 cases per 100,000 population. The prevalence in men is 12.3 cases per 100,000 population. In women, it is 5.6 cases per 100,000 population. Male-to-female ratio is 1.8:1. Mean age of patients is 38.3 years.

ETIOLOGY An anal fistula usually results from an infection that occurs in the tissue lining the anal canal. The infection may be caused by spread of bacteria that normally exist in the rectum. Occasionally, it may occur as a result of ; ! Healed sore in the rectal area ! Ulcerative colitis, a disease associated with ongoing breakdown of tissues that causes ulcers in the lining of the colon ! Diverticulitis inflammation of the wall of the large intestine ! Crohn's disease a chronic inflammation of the small intestine ! Tuberculosis ! Gonorrhea ! Cancer of the large intestine Fistula-in-ano is nearly always caused by a previous anorectal abscess. Anal canal glands situated at the dentate line afford a path for infecting organisms to reach the intramuscular spaces. Other fistulae develop secondary to trauma, Crohn's disease, anal fissures, carcinoma, radiation therapy, actinomycoses, tuberculosis, and chlamydial infections.

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PATHOPHYSIOLOGY Infection begins in the anal gland and progresses into the muscular wall of the anal sphincters to cause an anorectal abscess. Occasionally, a granulation tissue lined tract is left behind in the perianal skin following surgical or spontaneous drainage causing recurrent symptoms. Formation of a fistula tract following anorectal abscess occurs in 7-40% of cases.

CLINICAL HISTORY Patients often provide a reliable history of previous pain, swelling, and spontaneous or planned surgical drainage of an anorectal abscess. It often drains watery pus, which can irritate the outer tissues causing itching and discomfort.

! ! ! ! !

Diverticulitis Previous radiation therapy for prostate or rectal cancer Tuberculosis Steroid therapy HIV infection

If a patient of fistula-in-ano has got following symptoms in addition. He/she should be thoroughly investigated for possible malignancy; ! Abdominal pain ! Weight loss ! Change in bowel habits 42.02

Signs and symptoms (in order of prevalence)

! ! ! ! ! ! !

Perianal discharge Pain Swelling Bleeding Diarrhea Skin excoriation

Fistula-in-ano

External opening

Following information is obtained preoperatively to achieve better outcome. ! Decreased tone observed during preoperative evaluation If decreased, surgical division of any portion of the sphincter mechanism should be avoided. ! History of previous fistulotomy ! History of obstetrical trauma ! High transsphincteric or suprasphincteric fistula (if known) ! Very elderly patients

A patient of fistula in ano often suffers from a recurrent, small or large boil/boils/abscess surrounding the anus, accompanied with pain, discomfort & pus/blood discharge. The symptoms subside when the boil / abscess bursts spontaneously causing some more discharge for a couple of days. The boil / abscess "heals up" temporarily but almost always reappears after some time. Itching, discharge of watery pus, irritation of tissue around the anus, discomfort & pain these are the main symptoms of the fistula in ano. A complex fistula is suggested if history includes;

Inflammatory bowel disease

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PHYSICAL EXAMINATION Physical examination findings remain the mainstay of diagnosis. The examiner should observe the entire perineum, looking for an external opening that appears

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as an open sinus or elevation of granulation tissue. Spontaneous discharge via the external opening may be apparent or expressible upon digital rectal examination.

42.02 Levator ani m.

DIGITAL RECTAL EXAMINATION Digital rectal examination may reveal a fibrous tract or cord beneath the skin. It also helps delineate any further acute inflammation that is not yet drained. Lateral or posterior induration suggests deep post-anal or ischiorectal extension. The examiner should determine the relationship between the anorectal ring and the position of the tract before the patient is relaxed by anesthesia. The sphincter tone and voluntary squeeze pressures should be assessed before any surgical intervention to delineate whether preoperative manometry is indicated. Anoscopy is usually required to identify the internal opening.

Puborectalis m. Denate line Internal sphincter muscle

Deep

}

Superficial

External sphincter muscle

Subcutaneous

Anal verge

Anatomy of anal canal 42.03 Levator Ani Muscle

Peritoneum

Supralevator Space

DIFFERENTIAL DIAGNOSIS The following conditions have similar presentation but do not communicate with the anal canal; ! Hidradenitis suppurativa ! Infected inclusion cysts ! Pilonidal disease ! Bartholin gland abscess in females

Ischiorectal space

Intersphincteric Space

Transverse Septum of Ischiorectal Fossa

Anatomy of anal canal Posterior 42.04

RELEVANT ANATOMY A thorough understanding of the pelvic floor and sphincter anatomy is a prerequisite for clearly understanding the classification system for fistulous disease. The external sphincter muscle is a striated muscle under voluntary control by three components. These are submucosal, superficial, and deep muscle. Its deep segment is continuous with the puborectalis muscle and forms the anorectal ring, which is palpable upon digital examination. The internal sphincter muscle is a smooth muscle under autonomic control and is an extension of the circular muscle of the rectum.

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Goodsall’s rule GOODSALL’S RULE The Goodsall’s rule can help to anticipate the anatomy of fistula-in-ano in simple cases. The rule states that fistulae with an external opening anterior to a plane passing

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transversely through the center of the anus will follow a straight radial course to the dentate line. Fistulae with their openings posterior to this line will follow a curved course to the posterior midline. Exceptions to this rule are external openings more than 3 cm from the anal verge. These almost always originate as a primary or secondary tract from the posterior midline, consistent with a previous horseshoe abscess.

! ! !

These account for about 25% of all fistulae. Common course - Low via internal and external sphincters into the ischiorectal fossa and then to the perineum Other possible tracts - High tract with perineal opening; high blind tract 42.06

PARKS CLASSIFICATION SYSTEM The Parks classification system defines 4 types of fistulain-ano that result from cryptoglandular infections. INTERSPHINCTERIC Intersphincteric fistulae are confined to the intersphincteric space and internal sphincter. They result from perianal abscesses. ! These account for about 70% of all fistulae. ! Common course - Via internal sphincter to the intersphincteric space and then to the perineum

High transsphincteric Fistulotomy (divided muscle is dotted) 42.07

42.05

Transsphincteric fistula Intersphincteric fistula

! !

Seventy percent of all anal fistulae Other possible tracts - No perineal opening; high blind tract; high tract to lower rectum or pelvis.

TRANSSPHINCTERIC Transsphincteric fistulae are the result of ischiorectal abscesses, with extension of the tract through the external sphincter.

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SUPRASPHINCTERIC ! Suprasphincteric fistulae are the result of supralevator abscesses. They pass through the levator ani muscle, over the top of the puborectalis muscle, and into the intersphincteric space. ! These account for about 5% of all fistulae. ! Common course - Via intersphincteric space superiorly to above puborectalis muscle into ischiorectal fossa and then to perineum

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Other possible tracts - High blind tract (ie, palpable through rectal wall above dentate line) 42.08

Suprasphincteric fistula EXTRASPHINCTERIC Extrasphincteric fistulae bypass the anal canal and sphincter mechanism, passing through the ischiorectal fossa and levator ani muscle, and open high in the rectum. ! These account for about only 1% of all fistulae.

Common course - From perianal skin through levator ani muscles to the rectal wall completely outside sphincter mechanism 42.09

Pelvic Abscess

CLASSIFICATION OF FISTULA -IN-ANO ! !

Subcutaneous

Complex, recurrent (high transsphincteric, suprasphincteric and extrasphincteric, multiple tracts, recurrent)

Second stage

Submuscular (intersphincteric, low transsphincteric)

Unlike the current procedural terminology coding, the Parks classification system does not include the subcutaneous fistula. These fistulae are not of cryptoglandular origin but are usually caused by unhealed anal fissures following anorectal procedures such as hemorrhoidectomy or sphincterotomy.

INVESTIGATIONS Lab Studies No specific laboratory studies are required; the normal preoperative studies are performed based on age and comorbidities. IMAGING STUDIES These are not performed for routine fistula evaluation. They can be helpful when the primary opening is difficult to identify or in the case of recurrent or multiple fistulae to identify secondary tracts or missed primary openings. FISTULOGRAPHY

This involves injection of contrast via the internal opening, which is followed by anteroposterior, lateral, and oblique x-ray images to outline the course of the fistula tract.

! !

The accuracy rate is 16-48%.

! Extrasphincteric fistula SURGERY - GASTRO-INTESTINAL PROBLEMS

The procedure is well tolerated but requires the ability to visualize the internal opening. Except in the case of recurrent disease, fistulography may be only slightly more useful than a

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careful examination under anesthesia. BARIUM ENEMA/SMALL BOWEL SERIES This is useful for patients with multiple fistulae or recurrent disease to help rule out inflammatory bowel disease. ENDOANAL/ENDORECTAL ULTRASOUND

These studies involve passage of a 7- or 10-MHz transducer into anal canal to help define muscular anatomy differentiating intersphincteric from transsphincteric lesions.

A standard water-filled balloon transducer can help evaluate the rectal wall for any suprasphincteric extension.

Studies show that the addition of hydrogen peroxide via the external opening can help outline the fistula tract course. This may be useful to help delineate missed internal openings.

These studies are reported to be 50% better than physical examination alone to help find an internal opening that is difficult to localize.

This modality has not been used widely for routine clinical fistula evaluation.

MRI SCAN Findings show 80-90% concordance with operative findings when observing a primary tract course and secondary extensions. MRI is becoming the study of choice when evaluating complex fistulae. It has been shown to achieve lower recurrence rates by providing information on otherwise unknown extensions. 42.11

Fistula-in-ano MRI Scan

42.10

42.12

Endo-anal ultrasonography

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Fistula-in-ano MRI Scan 332

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CT SCAN It is not as satisfactory investigation in showing the anatomy of fistula in ano as MRI scan. ! CT scan is more helpful in the setting of perirectal inflammatory disease than in the setting of small fistulae because it is better for delineating fluid pockets that require drainage than for small fistulae. ! CT scan requires administration of oral and rectal contrast. ! Muscular anatomy is not delineated well. PROCTOSIGMOIDOSCOPY

Rigid sigmoidoscopy can be performed at the initial evaluation to help rule out any associated disease process in the rectum.

COLONOSCOPY

Colonic evaluation is performed only if indicated.

ANAL MANOMETRY Pressure evaluation of the sphincter mechanism is helpful in certain patients.

EXAMINATION UNDER ANESTHESIA Examination of the perineum, digital rectal examination, and anoscopy are performed after the appropriate anesthesia is administered. This examination is necessary before surgical intervention, especially if outpatient evaluation causes discomfort or has not helped delineate the course of the fistulous process. Several techniques have been described to help locate the course of the fistula and, more importantly, identify the internal opening. Inject hydrogen peroxide, milk, or dilute methylene blue is given into the external opening and its excretion is seen at the dentate line. It has been experienced by surgeons that methylene blue often obscures the field more than it helps identify the opening.

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Traction (pulling or pushing) on the external opening may also cause a dimpling or protrusion of the involved crypt. Insertion of a blunt-tipped probe via the external opening may help outline the direction of the tract. If it approaches the dentate line within a few millimeters, a direct extension is likely to be present. Care should be taken not to use excessive force as it can create false passages.

TREATMENT Little has changed in the understanding of the disease process over years. Parks refined the classification system that is still in widespread use. Over the last 30 years, many surgeons have presented new techniques and in an effort to minimize recurrence rates and incontinence complications. Therapeutic intervention is indicated for symptomatic patients. Symptoms usually involve recurrent episodes of anorectal sepsis. An abscess develops easily if the external opening on the perianal skin seals itself. MEDICAL THERAPY No definitive medical therapy is available, long-term antibiotic prophylaxis and anti-inflammatory drugs may have a role in prevention of recurrent fistulae in patients with Crohn's disease. SURGICAL THERAPY Surgery should not be performed for definitive repair of the fistula in the setting of anorectal abscess (ie, unless the fistula is superficial and the tract is obvious). Simple incision and drainage of the abscess is sufficient in acute phase. Only 7-40% of patients are likely to develop fistula. FISTULOTOMY/FISTULECTOMY The laying-open technique (fistulotomy) is useful for 8595% of primar y fistulae (ie, submucosal, intersphincteric, low transsphincteric).

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A probe is passed into the tract through the external and internal openings.

The overlying skin, subcutaneous tissue, and internal sphincter muscle are divided with a knife or electrocautery, thereby opening the entire fibrous tract.

At low levels in the anus, the internal sphincter and subcutaneous external sphincter can be divided at right angle to the underlying fibers without affecting continence.

It is not the case if the fistulotomy is performed anteriorly in female patients.

If the fistula tract courses higher into the sphincter mechanism, seton placement should be performed.

CURETTAGE

Curettage is performed to remove granulation tissue in the tract base.

FISTULECTOMY

Complete fistulectomy creates larger wounds that take longer to heal and offers no recurrence advantage over fistulotomy.

Opening the wound out on the perianal skin for 12 cm adjacent to the external opening with local excision of skin promotes internal healing before external closure.

! ! ! !

Some advocate marsupialization of the edges to improve healing time.

Anterior fistulae in female patients Poor preoperative sphincter pressures Patients with Crohn's disease or patients who are immunosuppressed

Seton has two purposes beyond giving a visual identification of the amount of sphincter muscle involved. These are;

! ! !

To drain and promote fibrosis To cut through the fistula. Setons can be made from large silk suture, silastic vessel markers, or rubber bands that are threaded through the fistula tract.

SINGLE-STAGE SETON (CUTTING) The seton is passed through the fistula tract around the deep external sphincter after opening the skin, subcutaneous tissue, internal sphincter muscle, and subcutaneous external sphincter muscle.

The seton is tightened down and secured with a separate silk tie.

With time, fibrosis occurs above the seton as it gradually cuts through the sphincter muscles and essentially exteriorizes the tract.

The seton is tightened on subsequent visits until it is pulled through over 6-8 weeks.

A cutting seton can also be used without associated fistulotomy.

MARSUPIALIZATION

Recurrent fistulae after previous fistulotomy

BIOPSY

TWO-STAGE SETON (DRAINING/FIBROSING)

Biopsy is performed on any firm, suspected tissue.

The seton is passed around the deep portion of the external sphincter after opening the skin, subcutaneous tissue, internal sphincter muscle, and subcutaneous external sphincter muscle.

Unlike the cutting seton, the seton is left loose to drain the intersphincteric space and to promote fibrosis in the deep sphincter muscle.

Once the superficial wound is healed completely (2-

SETON PLACEMENT A seton can be placed alone, combined with fistulotomy, or in a staged fashion. This technique is useful in patients with the following conditions:

Complex fistulae (ie, high transsphincteric, suprasphincteric, extrasphincteric) or multiple fistulae

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3 mo later), the seton-bound sphincter muscle is divided.

Identifying the internal opening to prevent recurrence is imperative.

Once wound healing is complete, the seton is removed without division of the remaining encircled deep external sphincter muscle. It achieves eradication of the fistula tract in about 60-78% of cases.

A local anesthetic block at the end of the procedure provides postoperative analgesia.

MUCOSAL ADVANCEMENT FLAP

POSTOPERATIVE DETAILS Most patients can be treated in an ambulatory setting with discharge instructions and close follow-up care. Follow-up

Mucosal advancement flap is reserved for use in patients with chronic high fistula but is indicated for the same disease process as seton use.

Advantages include a 1-stage procedure with no additional sphincter damage.

A disadvantage is poor success in patients with Crohn's disease or acute infection.

This procedure involves total fistulectomy, with removal of the primary and secondary tracts and complete excision of the internal opening.

! !

A rectal mucomuscular flap with a wide proximal base (2 times the apex width) is raised.

COMPLICATIONS

The internal muscle defect is closed with an absorbable suture, and the flap is sewn down over the internal opening so that its suture line does not overlap the muscular repair.

PREOPERATIVE DETAILS Rectal irrigation with enemas should be performed on the morning of the operation.

Sitz baths, analgesics, and stool bulking agents (eg, bran, psyllium products) are used in follow-up care. Frequent office visits within the first few weeks help ensure proper healing and wound care. Importantly, ensure that the internal wound does not close prematurely, causing a recurrent fistula. Digital examination findings can help distinguish early fibrosis. Wound healing usually occurs within 6 weeks.

EARLY POSTOPERATIVE

! ! ! !

Urinary retention Bleeding Fecal impaction Thrombosed hemorrhoids

DELAYED POSTOPERATIVE

Anesthesia can be general, local with intravenous sedation, or a regional block.

Recurrence

! !

Preoperative antibiotics are given.

Incontinence (stool)

Prone jackknife position with buttocks apart is the most advantageous position.

INTRAOPERATIVE DETAILS

The patient is examined under anesthesia to confirm the extent of the fistula.

SURGERY - GASTRO-INTESTINAL PROBLEMS

ANAL STENOSIS The healing process causes fibrosis of the anal canal. Bulk laxatives for stool help prevent narrowing. DELAYED WOUND HEALING Complete healing occurs by 12 weeks unless an underlying disease process is present (ie, recurrence,

335

FISTULA-IN-ANO

Crohn's disease).

Buchanan GN, Bartram CI, Phillips RK. Efficacy of fibrin sealant in the management of complex anal fistula: a prospective trial. Dis Colon Rectum. Sep 2003;46(9):1167-74. [Medline].

Buchanan GN, Halligan S, Williams AB, Cohen CR, Tarroni D, Phillips RK, et al. Magnetic resonance imaging for primary fistula in ano. Br J Surg. Jul 2003;90(7):877-81. [Medline].

Cosman BC. All's Well That Ends Well: Shakespeare's treatment of anal fistula. Dis Colon Rectum. Jul 1998;41(7):914-24. [Medline].

Hancock BD. ABC of colorectal diseases. Anal fissur es and fistulas. BMJ. A pr 4 1992;304(6831):904-7. [Medline].

10.

Ho YH, Tan M, Leong AF, Seow-Choen F. Marsupialization of fistulotomy wounds improves healing: a randomized controlled trial. Br J Surg. Jan 1998;85(1):105-7. [Medline].

OUTCOME AND PROGNOSIS Description

% Recurrence

% Incontinence

Fistulotomy

0 - 18

3-7

Seton use

0 - 17

Mucosal advancement flap

1 - 10

REFERENCES 1.

Champagne BJ, O'Connor LM, Ferguson M, Orangio GR, Schertzer ME, Armstrong DN. Efficacy of anal fistula plug in closure of cryptoglandular fistulas: long-term follow-up. Dis Colon Rectum. Dec 2006;49(12):1817-21. [Medline].

Johnson EK, Gaw JU, Armstrong DN. Efficacy of anal fistula plug vs. fibrin glue in closure of anorectal fistulas. Dis Colon Rectum. Mar 2006;49(3):371-6. [Medline].

11.

H채m채l채inen KP, Sainio AP. Incidence of fistulas after drainage of acute anorectal abscesses. Dis Colon Rectum. Nov 1998;41(11):1357-61; discussion 1361-2. [Medline].

American Society of Colon and Rectal Surgeons. Practice parameters for treatment of fistula-in-ano-supporting documentation. The Standards Practice Task Force. Dis Colon Rectum. Dec 1996;39(12):1363-72. [Medline].

12.

Loungnarath R, Dietz DW, Mutch MG, Birnbaum EH, Kodner IJ, Fleshman JW. Fibrin glue treatment of complex anal fistulas has low success rate. Dis Colon Rectum. Apr 2004;47(4):432-6. [Medline].

13.

McCourtney JS, Finlay IG. Setons in the surgical management of fistula in ano. Br J Surg. Apr 1995;82(4):448-52. [Medline].

14.

Parks AG, Gordon PH, Hardcastle JD. A classification of fistula-in-ano. Br J Surg. Jan 1976;63(1):1-12. [Medline].

15.

Present DH, Rutgeerts P, Targan S, Hanauer SB, Mayer L, van Hogezand RA, et al. Infliximab for the treatment of fistulas in patients with Crohn's disease. N Engl J Med. May 6

Beckingham IJ, Spencer JA, Ward J, Dyke GW, Adams C, Ambrose NS. Prospective evaluation of dynamic contrast enhanced magnetic resonance imaging in the evaluation of fistula in ano. Br J Surg. Oct 1996;83(10):1396-8. [Medline]. Belliveau P. Anal fistula. Current Therapy in Colon and Rectal Surgery. Philadelphia: BC Decker; 1990:22-7.

SURGERY - GASTRO-INTESTINAL PROBLEMS

336

FISTULA-IN-ANO

1999;340(18):1398-405. [Medline]. 16.

Ratto C, Gentile E, Merico M, Spinazzola C, Mangini G, Sofo L, et al. How can the assessment of fistula-inano be improved? Dis Colon Rectum. Oct 2000;43(10):1375-82. [Medline].

17.

Rosen L. Anorectal abscess-fistulae. Surg Clin Nor th Am. Dec 1994;74(6):1293-308. [Medline].

18.

Ross ST. Fistula in ano. Surg Clin North Am. Dec 1988;68(6):1417-26. [Medline].

19.

Sainio P. Fistula-in-ano in a defined population. Incidence and epidemiological aspects. Ann Chir Gynaecol. 1984;73(4):219-24. [Medline].

20.

Sangwan YP, Rosen L, Riether RD, Stasik JJ, Sheets JA, Khubchandani IT. Is simple fistula-inano simple? Dis Colon Rectum. Sep 1994;37(9):885-9. [Medline].

21.

Seow-Choen F, Nicholls RJ. Anal fistula. Br J Surg. Mar 1992;79(3):197-205. [Medline].

22.

Topstad DR, Panaccione R, Heine JA, Johnson DR, MacLean AR, Buie WD. Combined seton placement, infliximab infusion, and maintenance immunosuppressives improve healing rate in fistulizing anorectal Crohn's disease: a single center experience. Dis Colon Rectum. May 2003;46(5):577-83. [Medline].

23.

Weisman RI, Orsay CP, Pearl RK, Abcarian H. The role of fistulography in fistula-in-ano. Report of five cases. Dis Colon Rectum. Feb 1991;34(2):181-4. [Medline].

SURGERY - GASTRO-INTESTINAL PROBLEMS

SUMMARY Fistula in ano Frequency Etiology Pathogenesis Clinical features Differential diagnosis Parkâ&#x20AC;&#x2122;s classification Investigations Treatment Complications Outcome and prognosis Future and controversies

POSSIBLE QUESTIONS 1. 2. 3.

What is a fistula in ano? Discuss its types? Discuss its treatment?

? 337

FISTULA-IN-ANO

SURGERY - GASTRO-INTESTINAL PROBLEMS

338

HAEMORRHOIDS

01 GIT-43

HAEMORRHOIDS Shuja Tahir, FRCS (Edin), FCPS Pak (Hon) Awais Shuja, MRCS Haemorrhoids (internal piles) are the varicosities of the tributaries of the haemorrhoidal veins and the downward displacement of the anal mucosa and submucosa (anal cushions). Frequently the perianal skin is also redundant and filled by varicose veins of the external haemorrhoidal plexus (external piles).

43.01

ETIOLOGY ! ! ! ! !

Hereditary weakness of the vessels. Downward displacement of the anal cushions. Absence of venous valves. Constipation. Raised ano-rectal pressure.

HEREDITARY It has been seen that haemorrhoids run in the families. Although it is quite common yet the exact reason is unknown. It may be hereditary weakness of the venous musculature. These patients may have associated varicose veins of the lower limbs as well. DISPLACEMENT OF THE ANAL CUSHIONS The anal lining buldges as three main pads when the haemorrhoidal veins are filled. These are divided by three vertical folds or columns of Morgagni. These are called anal cushions. These are present at 3'O clock, 7'O clock and 11'O clock areas (lithotomy position). The anal cushions are the part of anal canal in which the submucosa is thickened and is more vascular like cavernous tissue. These are three masses of tissue and are present above and below the dentate line. These cushions are supported by the smooth muscles of submucosa against shearing and extruding forces of defecation. SURGERY - GASTRO-INTESTINAL PROBLEMS

Haemorrhoids seen above and below the dentate line Anatomical studies of the haemorrhoids show that there is downward displacement of the anal cushions due to straining during defecation which further leads to downward prolongation of the anal mucosa and development of haemorrhoids. ABSENCE OF VENOUS VALVES The veins of portal system don't have valves which leads to increased venous pressure in the rectal vessels during straining. This leads to dilatation of the anal plexus of the veins and development of haemorrhoids. OBSTRUCTION OF THE VENOUS RETURN This also leads to haemorrhoids formation. This is due to increased venous pressure and consequent dilatation of the veins of the anal plexus of veins. This may occur in cases of rectal carcinoma. CONSTIPATION Constipation has got definite correlation with the formation of haemorrhoids. Chronic constipation and straining damage the anal cushions and lead to downward displacement of mucosa and submucosa. 339

HAEMORRHOIDS

RAISED ANO-RECTAL PRESSURE Maximal basal pressure and the maximal contraction pressure of the haemorrhoid patients are significantly raised as compared to the controls. (85Âą28 mm of Hg) (control 71Âą25 mm of Hg1. PATHOLOGY The internal haemorrhoids are formed due to the dilatation of the venous tributaries accompanying the terminal divisions of the superior rectal artery. These are present at 3'0 clock, 7'0 clock and 11'0 clock positions when examined in the lithotomy position. There may be some smaller dilatations of venous plexus present in between these primary haemorrhoids. These smaller varicose venous collections may be called accessory or daughter haemorrhoids. Occasionally haemorrhoids are associated with carcinoma of rectum and very rarely portal hypertension. these are called secondary haemorrhoids. Each haemorrhoid can be divided into following parts ; ! Pedicle. ! Internal haemorrhoid. ! External haemorrhoid.

These haemorrhoids are present in the anal canal. These don't prolapse but may bleed. SECOND DEGREE HAEMORRHOIDS These may prolapse on straining but get reduced on their own and stay reduced till next strain. These may or may not bleed. 43.03

Second degree haemorrhoids THIRD DEGREE HAEMORRHOIDS These haemorrhoids prolapse and don't reduce on their own. These have to be manually reduced. These may or may not bleed.

The haemorrhoids have been classified according to their size into the following degrees :

43.04

FIRST DEGREE HAEMORRHOIDS 43.02

First degree haemorrhoids SURGERY - GASTRO-INTESTINAL PROBLEMS

Third degree haemorrhoids 340

HAEMORRHOIDS

CLINICAL FEATURES

43.05

BLEEDING Fresh bleeding in drops is the most common presenting feature. The bleeding may be slight or severe. It presents for few days to few weeks and stops spontaneously but presents again after a variable time. The frequency of bleeding episodes is increased with time. Occasionally spontaneous cure is also experienced. The episodes of bleeding may have seasonal variation.

Third degree haemorrhoids FOURTH DEGREE HAEMORRHOIDS (INTERNO EXTERNAL) These are the haemorrhoids which have both internal and external component of the varicosities. These are usually associated with perianal soiling, pruritis and mucous discharge. 43.06

PROLAPSE Feeling of something coming out of rectum is usually present. Second or third degree and prolapsed piles may present at later stages. It gets worse when the piles are thrombosed. PAIN Haemorrhoids are usually associated with discomfort. In the presence of thrombosed or prolapsed and infected piles, the pain may be present. These are painful in the presence of fissure-in-ano. DISCHARGE Mucous discharge may be the only presenting feature. It is commoner in prolapsed piles and interno external piles.

Fourth degree haemorrhoids 43.07

ITCHING It is very uncomfortable symptom. It is common with prolapsed piles. PALLOR Anaemia is seen in patients with long standing history of bleeding piles. It is iron deficiency anaemia due to chronic loss of blood.

DIAGNOSIS

Fourth degree haemorrhoids SURGERY - GASTRO-INTESTINAL PROBLEMS

HISTORY The above mentioned clinical features are suggestive of the diagnosis. Constipation, lethargy and weakness may also be present. In older patients, history of liver disease and altered bowel habits must be asked. In females

341

HAEMORRHOIDS

pregnancy should be ruled out. EXAMINATION Complete examination is very important. Presence of a mass in the abdomen or pelvis may suggest the cause of bleeding per rectum. Presence of ascites and palpable liver may also suggest a different pathology. DIGITAL RECTAL EXAMINATION This is the most important examination which should never be missed. The haemorrhoids can not be diagnosed on rectal examination unless these are thrombosed but other associated pathology such as carcinoma rectum is diagnosed. PROCTOSCOPY / SIGMOIDOSCOPY Both of these examinations should be carried out. Proctoscopy shows exact site, nature and degree of piles. Sigmoidoscopy helps to see above the piles upto recto-sigmoid junction.

INVESTIGATIONS BLOOD EXAMINATION Haemoglobin level. Leukocyte count. Erythrocyte sedimentation rate. Liver function tests. Urea and electrolytes.

! ! ! ! !

TREATMENT Following methods are used for the treatment of different degrees of piles; CONSERVATIVE TREATMENT HIGH FIBRE DIET High fibre diet is very good to treat the constipation. Vegetables, fruits and whole bran are used. LAXATIVES Mild laxatives like liquid paraffin, celevac, lactulose (duphalac), agarol and cremaffin can be used to keep the bowels working regularly. These should not be used

SURGERY - GASTRO-INTESTINAL PROBLEMS

excessively as watery stools make the symptoms even worse. MEDICATION Certain drugs are used to treat heamorroids medically such as daflon tablets. LOCAL CREAMS Different creams for local application can be used (droxaryl, lignocaine etc) in cases of pain and itching. These are only of temporary help or of no help at all. INJECTION SCLEROTHERAPY 5% Phenol in almond or arachis oil can be used for injection into the pedicle of the piles. 1-2 mls are injected in each pile. The injections can be repeated at fortnightly intervals. It may cause ulceration, prolapse or oil granuloma formation. It is injected in submucosa of pedicle of haemorrhoids. BAND LIGATION Barron's banding apparatus is used to push the tight elastic bands on the pedicles of the haemorrhoids. This can be performed without anaesthesia or under some 2 sedation . INFRA-RED PHOTOCOAGULATION THERAPY It is performed with a simple instrument. The improved photo-coagulation probe is used through the proctoscope No anaesthesia is required. The rate of complications is minimum. It can be used in patients with first and second degree haemorrhoids3. HEATER PROBE COAGULATION THERAPY It is similar to infrared coagulation for the treatment of early degrees of haemorrhoids. ULTROID D C CURRENT THERAPY It is another method of treating the first and second degree haemorrhoids4.

342

HAEMORRHOIDS

LASER THERAPY ND-YAG. Laser phototherapy for internal haemorrhoids can be combined with CO2 laser for external piles. It is a good alternative to conventional treatment but laser hazards should be avoided. Hospitalization period is reduced markedly (24-48 hrs)5. CRYO HAEMORRHOID THERAPY It is treatment of the haemorrhoids by freezing. Cryosurgery apparatus is used to freeze the piles. The haemorrhoids are frozen and necrosis due to freezing is caused to the dilated veins and redundant mucosa overlying these veins. The cryoprobe is applied to the piles individually which freezes them upto temperatures minus 75 degrees centigrade. It is a good method for treating the piles. Patient doesn't require anaesthesia and no pain is felt during the procedure. It is a very effective measure for treatment of 2,6 early haemorrhoids .

OPEN HEAMORROIDECTOMY The haemorrhoids are dissected from the external splincter upto their pedicle above dentate line. Pedicle is transfixed and haemorrhoid is excised. Each heamorhoid is dealt separately making sure that there is intact skin bridge between dissected heamorrhoids to avoid future anal stenosis. Homoeostasis is secured. CLOSED HEAMORROIDECTOMY Dissection, transfixation and excision of haemorrhoids is done as in open technique. The unclosed defect is closed to cover the raw area using absorbable suture. STAPLED HEAMORROIDECTOMY Circular stapling device as shown in figure is used to excise the redundant mucosa and submucosa containing pedicle of the haemorrhoids above dentate line. Fine staples approximate the defect simultaneously. This method is gaining popularity these days as its associated with less operative morbidity. 43.08

SURGICAL TREATMENT LIGATION OF THE PILES It has much less morbidity than the conventional hemorrhoidectomy. It is much less painful post operatively. If facilities for the band ligation are not available or the patient is nervous and uncooperative, ligation of the piles is performed under anaesthesia. HEMORRHOIDECTOMY This is the conventional operation which means excision of all the haemorrhoids. It is performed under anaesthesia. Different types of haemorrhoidectomy operations are; ! Open heamorrhoidectomy (Milligan Morgan) ! Closed heamorrhoidectomy ! Stapled heamorrhoidectomy The choice of treatment is different for different degrees of piles and it is given below ;

SURGERY - GASTRO-INTESTINAL PROBLEMS

Internal Haemorrhoids

Stapling gun

Circular stapling of haemorrhoids FIRST DEGREE HAEMORRHOIDS Conservative treatment If it fails or is unsatisfactory, one of the following treatment is used ; ! Injection sclerotherapy. ! Cryo - haemorrhoid therapy. ! Combination of above methods.

343

HAEMORRHOIDS

SECOND DEGREE HAEMORRHOIDS Conservative treatment. If it fails ; ! Injection sclerotherapy. ! Banding ! Ligation of piles. ! Stapled heamorrhoidectomy !

THIRD DEGREE PILES Haemorroidectomy (Open, closed, stapled)

COMPLICATIONS ANAEMIA Chronic loss of blood may lead to iron deficiency anaemia. THROMBOSIS Thrombosis may occur and piles may become painful. PROLAPSE The piles may prolapse when these are edematous.

POST OPERATIVE COMPLICATIONS URINARY RETENTION It is the common complication following haemorrhoidectomy. Use of longer lasting anaesthetic agent and preoperative intravenous fluids more than 1000 mls increase the incidence of retention8. HAEMORRHAGE The haemorrhage can be primary, reactionary or secondary. Primary haemorrhage should be controlled by ligation of the bleeding vessels during surgery. Reactionary haemorrhage is controlled reoperation and ligation/control of bleeding vessels. Secondary haemorrhage is controlled with appropriate antibiotics. The lost amount of blood should be transfused.

REFERENCES 1.

Lin JK. Liang CL. HsuH. Wang FM. manometric studies in haemorrhoids anal fissures. Chung Hu a i Hsueh Tsa Chinese Medical Journal. [JC:chg]1989 43(4): 249-54.

Rudd WW. Ligation and cryosurgery of all haemor rhoids. An office procedur e. International Surgery. [JC:gup]1989 Jul-Sep. 74(3) 148-51.

Morris DL. A Randomized comparison of infra-red-coagulations with bipolar diathermy for the out patient treatment of haemorrhoids. Diseases of Colon and Rectum. [JC:eab] 1990 Jan 33(1): 32-4.

Zinberg SS. Stern DH. Furman DS. Wittbs JM. A personal experience in comparing thr ee non-oper ati ve tec hniques for treating internal haemorrhoids. American Jour nal of Gastroenterology. [JC:3he] 1989 May. 84(5):488-92.

STRANGULATION It can occur in the prolapsed piles. These may get infected and are very painful. ULCERATION It commonly occurs in the prolapsed piles. GANGRENE It commonly occurs in strangulated piles. FIBROSIS This complication may occur in long standing haemorrhoids. INFECTION It is common in prolapsed and strangulated piles. PORTAL VEIN THROMBOSIS It is seen in infected haemorrhoids. It is a serious complication. It may lead to septic shock like syndrome.

SURGERY - GASTRO-INTESTINAL PROBLEMS

Anal and Chih Apr.

344

HAEMORRHOIDS

Wang TY. Chang-Chien CR. Chen JS. Lai CR. Ta n g R P. T h e r o l e o f l a s e r s i n haemorrhoidectomy. Diseases of the Colon and Rectum. [JC:eab] 1991 Jan.34(1): 78-82.

Tanak S. Cr yosur gical tr eatment of haemor rhoids in Japan. Inter national Surgery. [JC:gup]Jul- Sep. 74(3): 146-7, 1987.

MacDonald A. Smith A. McNeil AD. Finlay IG. Manual dilatation of Anus. British Journal of Surgery [JC:D34]1992 Dec. 79(12): 1381-2.

Petros JG. Brodley TM. Factors influencing urinary retention in patients undergoing surgery for benign ano-rectal diseases. American Journal of Surgery. [JC:3z4] 1990 Apr. 159(4): 374-6.

SUMMARY Haemorrhoids Etiology Pathology Degrees Clinical features Investigations Treatment Complications POSSIBLE QUESTIONS 1. 2. 3.

4. 5.

SURGERY - GASTRO-INTESTINAL PROBLEMS

What are haemorrhoids? What are different degrees of haemorrhoids? What are different non-operative measures in management of haemorrhoids? What is stapled heamorrhoidectomy? Enlist important complications following heamorrhoidectomy?

345

INDEX

SURGERY - GASTRO-INTESTINAL PROBLEMS

347

INDEX

A 6 Anal Agenesis 6 Anal Stenosis 7 Anatomy of gstrointestinal tract 16 Ascending Colon 18,19 Anal Canal 26 Achalasia Cardia 31 Anxiety 31 Anorexia Nervosa 78 Atrophic Gastritis 80 Anaplastic Gastric Carcinoma 109 Acute Pyogenic Liver Abscess 110 Amoebic Liver Abscess 141 Acute Cholecystitis 183 Acute Pancreatitis 187 Amylase Creatinin Clearance Ratio (ACCR) 193 Acute peritonitis 231 Acute intussusception 237 Acute appendicitis 238 Anorexia 242 Alvarado scoring 244 Acute appendicitis in pregnancy 249,251 Appendicular Abscess 263 Appendicectomy 313 Anal fissure 315 Anoplasty 323 Anorectal abscess 339 Anal cushions

B Baruim Swallow Bronchoscopy Barium Meals Boas’s Sign Bouveret’s Syndrome Bile Peritonitis

24,39 39 83 142,152, 156 153 162,195

SURGERY - GASTRO-INTESTINAL PROBLEMS

Biliary Calculi Bismith classification Biliary atresia Blumberg’s sign Blood supply of large gut Bleeding per rectum Barium screening Bowel preparation Bascom’s technique Band ligation

170 172 172 239 271 289 285,292,302 304 321 342

C Congenital Omphamocele Congenital megacolon Cecum Colon Congenital esophageal atresia Carcinoma Esophagus Cardiac orifice Carcinoma Stomach Complication of Ca stomach Cull en’s sign Complication of Splencetomy Complications of liver Trauma Complications of cholecystitis Cholithiasis Complications of gall stones Cholecystectomy Complications of cholecystectomy Courvoiser’s law Causes of pancreatitis Complications of pancreatitis Chemical Peritonitis Co-morbid factors Complications of appendicitis Complication of ulcerative colitis Colorectal carcinoma Colonic submucosal tumours

5 5 15 16 28 30,33 49 77 86 92,127,184 105 135 145 145 152 157 160 179 183 188 194 197 244 288 295 296 349

INDEX

Carcinoma left Colon Carcinoma right Colon Carcino Embryonic Antigen Colonoscopy Crohn's disease Classification of fistula in Ano Cryohaemorrhoid therapy Complications of haemorrhoidectomy

296 297 300 303,333 317 331 343 344

D 05 Development of caecum and appendix 05 Anal canal 11 Duodenum 17 Descending Colon 23 Dysphagia 25 Diagnosis of Dysphagia 94 DPL 173 Diagnosis of Jaundice 196 Drug Induced Peritonitis 202 Disseminated Intravascular Coagulopathy 240,290,318 Digital rectal examination Dukeâ&#x20AC;&#x2122;s classification of Colorectal Carcinoma 299 Diverticulitis 317 Degrees of Haemorrhoids 340

E 7, 21 Esophagus 24,83,172,301 Endoscopic Sonography 26,39 Esophagoscopy 67 Endoscopic balloon dilatation 75 Esophageal varices 79 Early gastric carcinoma 83,303 Exfoliative cytology 118 Echinococus (life cycle granulosis) 119 Ectocyst 119 Endocyst

SURGERY - GASTRO-INTESTINAL PROBLEMS

174 305 331 332

ERCP Endoscopic laser therapy Extrasphincteric fistula Endo anal or endo rectal sonography

F Focused Assessment sonography trauma FAST Fibrin glue injection Fungal peritonitis Familial Polyposis coli Flexible sigmoidoscopy Fistula in Ano Fistulography Fistulectomy

93,128 98 196 290,302 298 305 327 331 334

G Gartroschisis Gastric cooling Helico Bacter Pylori Gastric polyps Gastric ulcers Gastroscopy Gray turner sign Gall stone Pathogenesis of gall stone formation Grading of pancreatitis Granulomatous Peritonitis Gas Enema Gastro graphin enema Goodsallâ&#x20AC;&#x2122;s rule

5 74 77 78 78 83 92,127,184 147 149 188 197 233 280 329

350

INDEX

H Hindgut Heller's operation Hysteria Hemorrhage (Haemetemisis) Hyperplastic gastropathy Hydatid cyst of liver Hydatid fluid Hepatorrhaphy Hepatic Jaundice Hippocratic face Haemorrhoids

K 5 28 30 64,69,81 79 117 119 134 167 202 339

I Imperforate anus Ileum Indications of splenectomy Injury severity score Injury to CBD Incisional hernia Imrie scoring Interventional peritonitis Isotope Scan Inferior mesenteric artery Ileo-colic artery Ischio rectal abscess Inter sphincteric fistula Injection sclerotherapy Infra red photo coagulation

05 13 100 131 162 162 188 198 241 271 271 323 330 342 342

J Jejunum Jaundice

13 162

SURGERY - GASTRO-INTESTINAL PROBLEMS

Kelly Peterson syndrome Kehr’s sign Karydakis technique

28 92 321

L Large gut Laparoscopy Laser coagulation Liver abscess Liver injuries Liver injury score Laparoscopic cholecystectomy Liver function test Lesser Sac Lord’s procedure Laparoscopic appendicectomy Laser therapy Ligation of piles

15 40,173,258 41 109 125 131 159 173 208 315 365 342 343

M 5 Midgut 6 Membranons atresia of anus 37 Management of Ca oesophagus 35 Management of Pyloric Stenosis 69,81 Melaena 73 Mesenteric angiography 95 Management of splenic trauma 141,151,155 Murphy’s sign 157 Mucocele of gall bladder 170 Mirizzi’s syrdrome 171 Management of obstructive Jaundice

351

INDEX

MRCP Meconeum Peritonitis Mcburneyâ&#x20AC;&#x2122;s Sign Middle Cotic artery M.R.I Scan for fistula

174 197 239 271 332

N Non operative Management (NOM) Neoplastic polyps

133 289,296

O Odynphagia Open cholecystectomy Operative cholangiography Obstructive Jaundice Operative management of Pancreatitis Obturator test Open appendicectomy Obstipation

23 157 159 169 190 240 263 278

P Plummer vinson syndrome PET PDT Pyloric orifice Pyloric Stenosis Peptic ulcer Perforated peptic ulcer Pericyst Portal triad occlusions

28 40 42,175 49 53,66 61 61 119 134

SURGERY - GASTRO-INTESTINAL PROBLEMS

151 Pigment stones 167 Pre hepatic jaundice 173 Per cutaneous Transheptic cholangography 188 Predictors of pancreatitis severity 189 Prognosis of Pancreatitis 193 Primary peritonitis 215,225,249 Paralytic Ileus 239 Pinch an inch test 240 Psoas test 251 Pain Right iliac fossa 290,323,338 Procto sigmoidoscopy 284 Pancolitis 284 Procto sigmoditis 317 Pilonidal sinus 323 Perianal abscess 324 Pelvi rectal abscess 329 Parks classification

R Rectal atresia Rectum Radiotherapy Ramstedtâ&#x20AC;&#x2122;s operation Rockall scoring system Risk factors for gall stones Ransons Scoring of pancreatitis Red current jelly stools Rovsings sign Rebound tenderness Right colic artery

6 18 41 58 73 147 189 231 239 239 271

S Stomach Small intestine Superior mesenteric astery Superior Mesenteric vein

9,47,49 11 14 14

352

INDEX

Sigmoid colon Stricture esophagus Staging of cancer esophagus Stenting Spread of ca stomach Staging of ca stomach Splenic trauma Splenic injury scale Splenic salvage Splenic artery embolization Splenectomy Subcutaneoms emphysema Strictures of biliary tree Spontaneous bacterial peritonitis (S.B.P) Secondary Peritonitis Suppurative peritonitis Sclerosing peritonitis Subphrenic spaces Subhepatic space Subphrenic abscess Small intestinal obstruction Management Strangulated gut Sherren's triangle Superior mesenteric artery Superior rectal artery Sigmoid volvulus Sigmoid volvulus management Sigmoidoscopy Staging of carcinoma colon (TNM) Submucous abscess Supra sphincteric fistula Seton placement Stapling for haemorrhoids

17 29 36 42 80 81 91 94 97 97 100 162 170 193 194 194 196 207 207 208 215 217 219 238 271 272 277 279,280 285,290 298 323 330 334 343

Traumatic peritonitis Tenesmus Trans sphincteric fistula

198 300 330

U Upper G.I Bleed management Ulcerative colitis Ulcerative colitis management

71 283,296,317 286

V Vermiform appendix Virchows nodes

15 81

T Transverse colon Thoracoscopy Tuberculous peritonitis

16 40 197

SURGERY - GASTRO-INTESTINAL PROBLEMS

353

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