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Revise Surgery Posters of Common Surgical Topics Compiled & Edited By Dhiren Nehra Nikhil Rao Jibran Qureshi

Dhiren Nehra, FRCS MPhil Consultant General & Upper Gastrointestinal Surgeon Epsom & St Helier University Hospitals NHS Trust Nikhil Rao, MBBS MRCS FHEA MSc Clinical Teaching Fellow in Surgery Epsom & St Helier University Hospitals NHS Trust Jibran S Qureshi Final Year Medical Student, St George’s University, London

Contributions The posters in this book were all designed by students from St George’s University of London (SGUL) medical school. It is thanks to their hard work and diligence that this book is possible. It is hoped that this will serve as a useful revision tool for medical students before examinations and well as a quick reference during clinical training.

Contents General Surgery

Contributing Authors

• Abdominal Wall & General Topics –Abdominal Trauma…………………………………………………………………………………..Guy Bower –Acute Abdomen………………………………………………………………………………………Nahida Khan, Charlotte Doyle –Incisional Hernias……………………………………………………………………………...........Crystal D’Cruz, Leah Priest –Herniae – Inguinoscrotal and femoral……………………………………………………........... –Stomas………………..............................................................................................................Yvonne Apendi, Bhuri Mulchandani, Pavandeep Singh Sandhu –Nutrition……………………………………………………………………………………………….Genevieve Shouls, Lauren Standing

• Upper Gastro Intestinal –OGDs……………………………………………………………………………………………………Namrata Gandhi, Aimal Khan, Laura Hayes –Barrett’s Disease……………………………………………………………………………............Victoria Chamorrow, Frances Bailey –Upper GI Bleed………………………………………………………………………………............Niroshan Neminathan, Thomas Isbister, Oniaza Syed –Hiatus Hernia………………………………………………………………………………………….Jennifer Nowers, Tariq Tabiner –Gastric Cancer………………………………………………………………………………………..William Farkas, Robert Cann, Anne Elias –Gallstones……………………………………………………………………………………………..Dean Chatterjee, Jennifer Rickard, Charlie Mitchell –Saint’s Triad…………………………………………………………………………………………..Josephine Cassell, Hemali Chauhan, Andrew Howe, Lee Hudson –Surgical Jaundice……………………………………………………………………………...........Ben Blackman –Acute Pancreatitis……………………………………………………………................................Shaun Davey, Fatima Neves Ferreira, Nimalan Sanmugalingam –Pancreatic Cancer……………………………………………………………………………………Rabiya Aseem –Pancreatic Pseudocysts…………………………………………………………………………….Gregory Landon, Lynn Wong

• Lower Gastro Intestinal –Acute Appendicitis………………………………………………………………………….............Pavandeep Singh Sandhu –Appropriate colonoscopy…………………………………………………………………............Laura Corbett, Ian Alberts –Colorectal Cancer……………………………………………………………………………………Luise Brown, Aled Daniels, Daniel Griffin, Joseph Tait –Non Malignant Causes of Large Bowel Obstruction…………………………………………..Anna Clark, Eleanor Dodson –Small Bowel Obstruction………………………………………………………………….............Hannah Newham –Rectal Bleeding……………………………………………………………………………………… –Diverticular Disease…………………………………………………………………………………Lucy Ashken, Alice Brooks, Hannah Harris –Fistula in ano…………………………………………………………………….............................Oliver Bendall, Sindy Lee

Contents General Surgery

Contributing Authors

• Breast & Endocrine –Benign Breast Disease………………………………………………………………………………Nida Pasha –Breast Cancer (Triple Assessment)…………………………………………..............................Rajiv Atchuthanaikabahu –Thyroid……………………………………………………………………………............................

• Vascular –Acute Ischaemia of the Lower Limb……………………………………………………………...Vanessa Jonga –Chronic Vascular Disease of the Lower Limb…………………………………………………. –Venous Disorders of the lower Limb…………………………………………..........................Sophia Broderick –Varicose Veins………………………………………………………………………………………..

Urology • • • • • • •

Acute Cystitis & Pyelonephritis……………….........................................................................Staci Boston Bladder Outflow Obstruction / BPH…………………………………………………………………Vanessa Jonga Renal & Ureteric Calculi……………………………………………………………………………….Myriam Guessom, Grethe Goss Nielsen, Davina Cavallaro Common Conditions of the Scrotum……………………………………………………………….Rhiannon Chapman, Kate Kendrick Renal Cell Carcinoma………………………………………………………………………………….Timothy Cooper Transitional Cell Carcinoma………………………………………………………………………….Neelam Parmar, Jibran Qureshi Prostate Cancer…………………………….................................................................................Hannah Bowles


Abdominal Wall & General Topics

Abdominal Trauma Guy Bower, 4th Medical Student (2012) Epsom & St Helier University Hospitals NHS Trust Definition

Clinical Presentation


Any injury to the walls or contents of the abdominal cavity caused by blunt or penetrating trauma.

Initial clinical examination may be inaccurate (4) but repeated assessment of the whole patient (not just the abdomen) is a crucial for assessing haemodynamic status and peritonism. •Signs of abdominal trauma: Bruising / abrasions Lacerations / penetrating wounds Abdominal fullness / doughy consistency Rectal bleeding (always perform rectal examination) Frank haematuria (suggests urinary tract injury) •Signs of hypovolemia Pallor / cold peripheries / increased capillary refill Tachycardia Hypovolemia Oligouria / anuria Loss of consciousness •Signs of peritonitis Percussion – dullness / tenderness Palpation – involuntary guarding / rebound tenderness Auscultation – absent bowel sounds if ileus •Signs of sepsis Pyrexia / tachypnea


Aetiology Abdominal trauma is best categorised by mechanism of injury: blunt trauma or penetrating trauma. •Blunt trauma: most commonly caused by motor vehicle accidents, car-pedestrian collisions, assault and falls from height. Alcohol is involved in 1/3 or RTAs causing trauma (1). •Penetrating trauma: stab wounds and gunshot wounds are the most common cause of penetrating abdominal trauma (1). Industrial accidents are an important cause. Gunshot wounds cause unpredictable patterns of injury (2).

Pathophysiology Abdominal trauma can be lethal. Many injuries are occult and develop over time (3), Main risks to life are intra-abdominal haemorrhage, peritonitis and sepsis. Haemorrhagic shock may follow rupture of the large vessels in the abdomen or of the highly vascularised organs – spleen, liver and kidneys. The abdomen can hold a large amount of blood without becoming visibly distended (2) and patients may quickly exsanguinate if intra-abdominal bleeding is not controlled. Acidosis and coagulopathy may develop in haemorrhagic shock. Intra-abdominal haemorrhage is not confined to cases of penetrating trauma. Compression of abdominal viscera against bony structures may cause rupture. In high-speed collisions, sheering forces generated between non-fixed organs their fixed supporting structures can rupture liver and spleen (2). Restraining devices (e.g. lap-belts) may also generate sheering forces and rupture organs. Peritonitis may develop following the introduction of organisms by penetrating injury, or from the leaking of blood or gastrointestinal excretions into the peritoneal space. Generalised peritonitis may cause hypovolaemic shock following loss of fluid in the inflammatory exudate. The systemic inflammatory response syndrome and electrolyte imbalances may develop, complicating the clinical picture. Sepsis may develop after initial treatment, complicating recovery. Abscess formation is later complication. Patients with penetrating wounds or rupture of gastrointestinal organs are the most at risk of developing infection.

Diagram: Managing Abdominal Trauma

G&S / FBC / U+E / Glucose / β-HCG / ABG / Amylase •Urine Urine output (β-HCG, if blood test not available) •Imaging Radiograph trauma series – C-spine, CXR, AXR & pelvis Ultrasound (FAST) – if haemodynamically unstable CT scan – if haemodynamically stable •Procedural / Surgical: Direct Peritoneal Lavage (DPL) – if FAST inconclusive / unavailable Emergency laparotomy – indicated if shocked despite resuscitation, signs of peritonitis, or abdominal bleed as detected by FAST / DPL

Management There are three stages to management; resuscitation, investigation, treatment. •Resuscitation begins with clearance of the airway and C-spine. Breath sounds are checked and oxygen administered. Heart rate and blood pressure are monitored closely. The patient is cannulated, bloods drawn and fluids started. Neurological status is assessed by the GCS. The patient should be exposed and completely examined for signs of traumatic injury. A urinary catheter is inserted to monitor urine output. Penetrating wounds are explored to see which structures are damaged and whether the peritoneum is punctured (2). •Investigation of intra-abdominal haemorrhage is a priority. Haemodynamically stable patients are sent to CT for detailed imaging of the abdomen. Haemodynamically unstable patients are assessed for intra-abdominal bleeding. This is done with bedside ultrasound scan (FAST). DPL is rarely performed as FAST is less invasive and easily repeatable. However, DPL is a sensitive test for haemoperitoneum (2) and is a useful adjunctive investigation in this setting (1). It involves aspirating intra-peritoneal fluid and analysing it for blood or bile. Lower rib or pelvic fractures are further indications for FAST or DPL (2). •Treatment is guided by the pattern and severity of injury as documented by CT. Haemodynamically stable patients may undergo regular observation (2),(4). Serial examinations of the abdomen and vital signs are crucial as CT may miss injuries (2). New tachycardia and hypotension suggest occult haemorrhage. Tachypnea and pyrexia suggest sepsis or abscess formation. New onset peritonitism is an indication for emergency surgery (4). •Laparotomy provides definitive treatment for most intra-abdominal injury and is done following CT whenever possible. Interventional radiography plays a role in the treatment of solid organ injuries (e.g. embolisation of splenic arteries in highgrade splenic rupture) (4). Emergency laparotomy is indicated for patients unsuitable for CT due to haemodynamic instability, with clinical signs of peritonitis, or with intra-abdominal bleeding as detected by FAST or DPL.

The Acute Abdomen – The Body As A House (I)

Nahida Khan & Charlotte Doyle, 4th Year Medical Students (2010) Epsom & St Helier University Hospitals NHS Trust Concept of Acute Abdomen as a House The acute abdomen can be visualised as a house. The 6 anatomical regions of the stomach relate to each part of the house in order to identify possible disease processes. Attic: Nasopharynx and Thorax Upper Floor: Upper Quadrant Ground Floor: Lower Quadrant Basement: Suprapubic Region Oil Tank: Blood Vessels Electrical Supply: Nerves Attic Myocardial Infarction (MI)— heart tissue death commonly due to atherosclerosis. Symptoms: central squeezing chest pain radiating to left arm, dyspnoea, nausea, vomiting, palpitations, sweating, anxiety. Pancreatitis— autodigestion of pancreas. Presents with pain &vomiting. Associated with raised amylase levels. Lower lobe pneumonia— especially at right base, gives rise to abdominal pain prevents deep inspiration. Associated with increased respiratory rate. Perforated Oesophagus— Due to GORD, oesophageal cancer, and Mallory-Weiss syndrome. Symptoms: burning chest pain, and pain with breathing. Upper Floor Acute Cholecystitis—gall bladder inflammation due to stones. Symptoms: constant severe pain referred to right shoulder, fever, nausea, vomiting, and Murphy’s sign positive. Peptic Ulcer Disease— mucosal erosions of an area of the GI tract. Can be stomach (gastric ulcer) and duodenum (duodenal ulcer). Symptoms: pain relating to mealtimes; gastric ulcers exacerbated by it and duodenal ulcers relieved, dyspepsia, bloating, nausea, vomiting, hematemesis, appetite & weight loss, melena. Hepatitis— liver inflammation cause by hepatrophic viruses. Present with nausea, vomiting, myalgia, fatigue/malaise, pain in RUQ, change in sense smell or taste, coryza, photophobia, headache. Cholangitis— complication obstructive jaundice. Charcot’s triad—jaundice, abdominal pain and rigors or fever. Untreated can result in shock, renal failure or death. Pyelonephritis— infection within renal pelvis. Acute onset unilateral or bilateral loin pain, with fever, malaise, vomiting and occasionally diarrhoea. May be lower urinary tract symptoms i.e. frequency, dysuria, haematuria or hesitancy. Splenic Injury—the spleen is the most vascular organ of the body therefore injury to it is life threatening. Symptoms: pain, restlessness, anxiety, mild pallor, and with increasing blood loss into the abdominal cavity, abdominal distension and overt shock. Splenic Infarction—refers to occlusion of the splenic vascular supply leading to tissue death. Symptoms: left upper abdominal pain, pleuritic chest pain, left shoulder pain, fever and chills, nausea and vomiting. Oil Tank Abdominal Aortic Aneurysm (AAA)—dilation of aorta >150%. Symptoms: intermittent/continuous abdominal pain radiating to back and groin, collapse, shock. Ischaemic bowel— impaired blood perfusion to the intestine, bacterial translocation and systemic inflammatory response. Symptoms: Poorly localized moderate to severe colicky or constant pain. With physical findings out of proportion to degree of pain.

Ground Floor Appendicitis—inflammation of appendix. Symptoms: pain starting periumbilically before localising to RIF, appetite loss, +/- fever, vomiting, constipation/diarrhoea. Signs: guarding, rebound & percussion tenderness & Rovsing’s sign +ve. Mesenteric adenitis—swollen mesenteric lymph nodes causing pain & pyrexia. Difficult to distinguish from appendicitis, however temperature is usually higher and pain is less well localised. Meckel's Diverticulitis—complication arising from congenital outpouching of small intestine. Symptoms: pain pattern similar to appendicitis, but can be with a history of rectal bleeding. Ectopic—fertilised ovum in tissue outside uterus. Symptoms: pain, tubal and vaginal bleeding. Ovarian cyst— pain is caused by rupture, rapid growth, bleeding into the cyst or torsion of the cyst. Uteric colic (renal colic)—serve acute onset pain in loin to groin, associated with haematuria. Pain can radiate to testis, scrotum, labia or anterior thigh. Usually nausea and vomiting. Often urinary symptoms. Perforated caecum— may be due to carcinoma, obstruction or diverticulum. May see gas under diaphragm in erect X-ray. Can cause faecal peritonitis. Psoas abscess— tender swelling below inguinal ligament. Usually apyrexial. Can be confused with femoral hernia or enlarged inguinal lymph nodes. Incarcerated hernia— irreducible hernia. Signs and symptoms of bowel obstruction may occur. Crohn’s Disease—is a chronic inflammatory disease of the GI tract, favouring the terminal ileum and proximal colon. Symptoms: diarrhoea mixed with mucus, pus or blood, tenesmus, pain, eight loss, appetite loss, tiredness, anaemia, mouth ulcers, anal fissures and skin tags. Ulcerative colitis—chronic inflammatory disease of colon. Symptoms: bloody diarrhoea, colicky abdo pain, tenesmus. Abdo tenderness with distension may be a sign of toxic megacolon which can be fatal. Diverticulitis—inflammation of bowel outpouching. Symptoms: pain and tenderness in left iliac fossa, fever, local signs of peritonitis, and raised white count. Pelvic Inflammatory Disease (PID)—infection which includes vagina, cervix, uterus, and uterine tubes. Symptoms: lower abdo and back pain and tenderness, fever, heavy and painful periods, occasional vaginal discharge and dyspareunia. Basement UTI—infection of urinary tract. Presents with frequency, dysuria, haematuria, urgency, foul smell, incontinence, suprapubic or loin pain, rigors, pyrexia, nausea & vomiting, acute confusional state. Electrical Supply Tabetic crisis— complication of tabes dorsalis (degeneration of nerve cells that carry sensory information to the brain). Presents with severe abdominal pain and vomiting Preherpetic pain– due to herpes Zoster infection. Pain is associated with burning, itching and hypersensitivity, usually in dermatomal arrangement.

The Acute Abdomen – The Body As A House (II)

Nahida Khan & Charlotte Doyle

Epsom & St Helier University Hospitals NHS Trust

RIGHT SIDE Acute cholecystitis Duodenal ulcer Hepatitis Cholangitis Pylonephritis

MI Pancreatitis Perforated oesophagus Lower lobe pneumonia Tonsillitis in children

Attic Tabetic crisis Compression of spinal nerve roots Preherpetic pain

AAA Haemorrhage Ischaemic bowel

Upper Floor Electricity Supply

Oil Tank

RIGHT SIDE Appendicitis Mesenteric adenitis Perforated peptic ulcer Meckel’s diverticulitis Ectopic pregnancy Ovarian cyst PID Uteric colic Incarcerated hernia Perforated caecum Psoas abscess

Ground Floor


UTI & retention Gynaecological cause

Investigations LEFT SIDE Gastric ulcer Splenic infarct or injury Pancreatitis Pylonephritis LEFT SIDE Diverticulitis Uteric colic Ectopic pregnancy Ovarian cyst PID Incarcerated hernia Perforated colon Crohn’s disease Ulcerative colitis

Serology -Routine Hb, FBC, U&E’s, LFT’s, Serum Amylase -Blood Culture, ABG -Inflammatory markers -CRP, ESR, PL viscosity -Tumour markers - CEA, Ca19-9, Ca 125 Body Fluids -Pregnancy test -Urine/stool / sputum / pus/ discharge culture and sensitivity Radiology -Plain X-ray Abdo/ Chest -USG -Barium swallow/ meal/ enema/ small bowel meal -Contrast enhanced Spiral CT -MRI/ MRCP - ERCP Endoscopy -OGD -Flexible Sigmoidoscopy -Colonoscopy -Endoluminal USG -Diagnostic laproscopy

Incisional Hernias Crystal D’Cruz & Leah Priest, 3rd Year Medical Students Epsom & St Helier University Hospitals NHS Trust Background Information A hernia can be described as “an abnormal protrusion of an organ or other contents of a body compartment through the wall which normally contains them.”1 An incisional hernia is due to a disruption of the deeper layers of a wound following abdominal surgery. This is usually in the early postoperative period, but can present years after the initial operation. The abdominal contents are retained only by the skin sutures and increased pressures can force them to bulge as a hernia. Incisional hernias are created following a breakdown of muscle closure after previous surgery in 11-20% of cases.2 Incisional hernias require no investigations, and a diagnosis can be made on clinical history and examination alone. As shown in figure 1. Modern methods of mass closure or early recognition and re-suture of deep dehiscence may prevent herniation later.

Patient Presentation and Clinical Features The patient will present with an abdominal mass which may or may not be reducible. The clinical history will include previous abdominal surgery. The mass may be tender to touch or may cause discomfort. On inspection a mass is normally seen although when the patient is lying down it may disappear. On palpation the mass may be reducible and tender. The weakness in the abdominal wall may also be felt surrounding the mass. On auscultation, bowel sound may be heard over the mass.



Follow up studies have shown that primary incisional hernias occur in 11% to 20 % of patients who undergo laparoscopy. These incisional hernias can lead to serious morbidities such as incarceration (in 6% to 15% of cases), and strangulation (in 2%). The strangulated bowel may become ischaemic if left and not dealt with promptly. Ischaemic bowel can then lead to perforation or necrosis.4

Incisional hernias are most commonly repaired using a mesh, seen in figure 2. Occasionally suture repair is performed. However, a trial done 1990s suggests that hernia repair using a mesh is superior to suture repair.4 The mesh reinforces the abdominal wall. The mesh is commonly a lightweight and partially absorbable mesh. This allows a strong repair, as well as allowing the abdominal wall to move naturally. The mesh can be placed in the five positions shown in figure 3. The hernia is reduced into it’s correct position. The mesh is then sutured or stapled into place preventing further abdominal wall weakness and recurrence.

Risk Factors • Surgical: - Laparotomy - Caesarean sections - Sub-costal incisions - Poor surgical technique • Anything which increases intra-abdominal pressure post operatively: - Coughing: people with respiratory condition which may cause them to cough frequently - Sneezing: people with allergies who may sneeze a lot - Overweight or obese - Exercise - Heavy lifting

Prognosis Originally, after primary repair, recurrent herniation was reported to occur in 30% to 50% of cases5,6. However, recent prosthetic materials used for repair has lowered this recurrence rate to between 0% and 10%6.

• Anything that reduces wound adhesion or healing: - Diabetes - Wound infection - Malnutrition - Old age - Immunosuppressed patients

Figure 3. A cross-sectional representation of the anterior abdominal wall demonstrates the sites to place a mesh7.

Figure 1. Photograph showing the clinical appearance of an incisional hernia, noting the scar from recent surgery3.

Figure 2. A photograph demonstrating mesh repair of an incisional hernia in the anterior abdominal wall.

Abdominal Stomas Yvonne Apendi, Bhuri Mulchandani, Pavandeep Singh Sandhu, 4 th Year Medical Students (2011) Epsom & St Helier University Hospitals NHS Trust 2. Colostomy (Loop)


A stoma is a surgically created opening in the abdominal wall, fashioned to divert the flow of faeces or urine.


Indications for a stoma 1.

No physical distal bowel present (e.g. after surgical resection of the rectum and anus).

2. Dysfunctional bowel (e.g. incontinence). 3. To de-function or rest the bowel (e.g. a distal fistula in Crohn’s disease, or a distal surgical anastomosis); 4. When a primary anastomosis would be unsafe to perform (e.g. In acute diverticulitis with peritonitis). 5. To divert the urinary tract (e.g. Urostomy for bladder cancer,or a neuropathic bladder).

Fig 3: Stoma site is above the waistline

Fig 4. Two stomal openings

A loop of colon is brought to the surface. The bowel wall is partially cut to produce two openings— an afferent limb which leads to the functioning part of the colon (through which stool and gas pass out) and an efferent limb to the non-functioning part of the colon. It is usually temporary.

•Ischaemia •Necrosis •Sepsis •Bleeding •Ileus •Retaction

Fig 7: Skin excoriation

Late •Skin excoriations •Prolapse •Parasternal hernia •Stenosis •Fistula •Infection/ Dermatitis

Fig 8: Stoma prolapse

3. End ileostomy Fig 9: stoma retraction

Types 1. Colostomy (End) Fig 5: Ileostomy in right iliac fossa

Fig 6: An everted spout stoma protects the skin from the irritating ileal fluid

When the entire colon, rectum, and anus are removed (panproctocolectomy), an end ileostomy is employed. This occurs most commonly in severe ulcerative colitis, familial polyposis or hereditary non-polyposis colorectal cancer). Fig 1: End colostomy situated in left iliac fossa

Fig 2: The stoma is flush with the skin

A permanent end colostomy is formed following resection of the rectum and anus (abdominoperineal excision of rectum) to manage carcinoma of the rectum or anus, diverticular disease, and faecal incontinence unresponsive to medical management. A temporary end colostomy is formed following a Hartman’s procedure. A second operation is needed to reconnect the two ends of the bowel.

Fig 9: stoma retraction

Fig 10: Parastomal hernia

Stoma nurse The stoma nurse forms an integral part of the multidisciplinary team caring for a patient with a stoma. Prior to the operation, they find a suitable site for the stoma. Post- operatively, they address early complications and provide information and support for any physical and psychological problems.

4. Urostomy (ileal conduit) After the bladder has been resected, an ileal conduit is formed by anastomosing part of the ileum to the ureters and creating an end ileostomy from which urine from the kidneys drains constantly. Stoma bags The base is a sheet of adhesive that is applied to the skin around the stoma to which the bag clips.

Skin care Skin complications are reduced by ensuring that: •The bag fits snugly around the stoma, sticks well to the skin and doesn’t leak. •The bag is changed when it is a third way full. •The stoma is measured regularly to ensure that the correct bag size is used. •The skin surrounding the stoma is gently cleaned with warm water and mild soap and then patted dry each time the bag is changed. •Soap and creams are avoided unless recommended by the stoma nurse.

Nutrition in Surgical Patients Genevieve Shouls and Lauren Standing, 4th Year Medical Students (2011) Epsom & St Helier University Hospitals NHS Trust Assessing Nutritional Need

Types of nutritional support

Gastrostomy/ jejunostomy tube

MUST Scoring

Increased intake of normal diet


Prescribed supplements e.g. Fortisip

Long term enteral feeding

Nasogastric/ nasojejunal tubes

•Neurological – stoke, dementia, MS

Gastrostomy /jejunostomy tube (PEG/PEJ)

•Head and neck cancers

Parenteral (TPN)

•Bowel – cancer, strictures, Crohns,

Prescribed supplements Indications High calorie/protein drinks for undernourished patients. Can be used pre-op for nutritional optimisation or post-op For patients that can tolerate oral intake Method Prescribed on drug chart. Patients are encouraged to take.

Nasogastric/ jejunal Tube

•Acutely ill patients •Patients with short life expectancy •Patients with severe coughing Method Usually OP with sedation + GI endoscopy Complications •Perforation •Peritonitis •Gastro-colic fistula

Inability to meet oral requirements e.g. Anorexia, dementia

•Internal leakage

NG = If food must bypass mouth and oesophagus

•Site infection

NJ = When food must bypass mouth, oesophagus, stomach, duodenum •Post major upper GI/ pancreatico-biliary surgery •Pancreatitis Contraindications •Base of skull fractures/ severe facial fractures •Oesophageal varices •GORD Method Patients need to be maximised nutritionally pre-operatively

Insert with patient upright in clear nostril

•Causes of malnutrition

Check in stomach by CXR before feeding!!!

•Increased catabolism = sepsis, surgery

Bolus/Intermittent/continuous feed

•Increased losses = liver disease, enteropathy


•Decreased intake = vomiting, dysphagia

•Nose bleeds

•Decreased absorption = fistulae, short bowel, IBD

•Throat irritation

•Other = trauma, chemotherapy, radiotherapy


•Poor nutrition results in post operative morbidity and mortality due to poor wound healing and decreased resistance to infection.


Short-medium term

•Oesophageal stricture/ cancer

Involve dietician if needed.

MDT Meeting needed!!!!!!


•Unsafe swallow e.g. CVA, Parkinson’s, MND

Start nutritional support for high risk patients with an appropriate method.

•Burns patients

•Discomfort •Oesophageal perforation

Total Parenteral Nutrition Indications Inadequate intake via enteral routes •Intestinal obstruction •Intestinal perforation •Short bowel (anatomical/ functional) •High output small bowel fistula/stoma •Prolonged ileus Method Peripheral or central lines Line ideally in lower 1/3 of IVC On the shelf/ custom made mixtures Complications •Infections •Thrombosis •Electrolyte disturbance •Hepatic dysfunction – fatty liver, bile stasis •Hyperglycaemia •Re-feeding syndrome

Upper GastroIntestinal Surgery

When to use OGD’s Namrata Gandhi, Aimal Khan and Laura Hayes, 4th Year Medical Students (2010) Epsom & St Helier University Hospitals NHS Trust Diagnostic Indications •Dyspepsia (>55 y.o) •Dyspepsia + alarm symptom* •Gastric Biopsy (? cancer) •Duodenal Biopsy (? cancer) •Unintentional weight loss •Symptoms of Upper GI Bleed e.g. Haematemesis •Dysphagia •Iron deficiency anaemia •Persistent vomiting •Epigastric mass •Suspicious barium meal (RED = alarm symptoms)

Therapeutic Indications •Treatment of bleeding lesions •Variceal banding and sclerotherapy •Stricture dilatation •Palliation (e.g. stent insertion and laser therapy)




Complications •Transient sore throat •Amnesia following sedation •Perforation < 0.1% •Cardio-respiratory arrest < 0.1%


Oesophageal diverticulum

Banded varices

Gastric Cancer

Gastric Ulcer


* Note: NICE guidelines state: Routine OGD’s in patients <55yrs are NOT indicated for dyspepsia without alarm symptoms A 1 month study at St Helier’s showed ~57% of OGD’s were inappropriate according to NICE guidelines. Acknowledgements: Mr D. Nehra

Barrett’s Oesophagus Frances Bailey and Victoria Chamorro, 4 th Year Medical Students(2011) Epsom & St Helier University Hospitals NHS Trust


Clinical Features:

In gastro-oesophageal reflux disease incompetence of the Patients present with features of GORD: lower oesophageal sphincter (LOS) leads to retrograde flow of •Heartburn – burning, retro sternal discomfort which is related to gastric contents and acid into the oesophagus. Prolonged eating, lying down, stooping , straining and it is relieved by antacids exposure leads to benign oesophageal strictures, oesophagitis •Belching and histological changes of the mucosa, known as Barrett's •Acid brash – acid or bile regurgitation oesophagus. This gives a predisposition to oesophageal •Waterbrash – excessive salivation cancers. •Odynophagia – painful swallowing due to oesophagitis This means that Barrett’s and GORD are inextricably linked. •Nocturnal asthma – cough and wheeze with small inhalation of The management of GORD aims to prevent progression to gastric contents Barrett’s by medical therapy or treat surgically depending on the extent of histological change.

Investigations: History: Mr Norman Barrett, a thoracic surgeon, first described his namesake in 1950. It was later found that the metaplastic changes are caused by the disorder GORD in 1953.

Epidemiology: Now it is thought to affect 2% of all adults in the United Kingdom, mainly in men, smokers and patients with a history of more than 10 years of GORD.

•Upper GI Contrast Radiography – not diagnostic: assesses for mass lesion or stricture, GORD and hiatal hernia. •Upper GI endoscopy and biopsy – diagnostic test: showing violaceous epithelium proximal to the gastro-oesophageal junction, the Z line (boundary between the oesophageal and gastric epithelium) migrated upwards. Areas of ulceration and nodularity are biopsied.

Histology: Barrett’s oesophagus is defined as:


Areas of mucous secreting columnar epithelium in



A) Normal oesophagus showing columnar epithelium B) Barrett’s oesophagus showing areas of metaplasia

Management: Patients Without High-grade Dysplasia: First Line: -Proton Pump Inhibitor –controls symptoms, doesn’t affect prognosis. -Endoscopic Surveillance –every 2 years to check dysplasia -Endoscopic Radiofrequency Ablation – removes Barrett’s in 70% of patients, followed by endoscopy at 3 months with possible further ablation. There is no recorded risk reduction for adenocarcinoma. Second Line: -Anti-reflux Surgery e.g. Nissen Fundoplication– reduces acid exposure and development of dysplasia. -Endoscopic Radiofrequency Ablation.

The normal squamous epithelium of the distal oesophagus is replaced the oesophagus proximal to the gastro-oesophageal by columnar gastric epithelium. This is called metaplasia where one junction. This is termed metaplasia. cell type is replaced by another. It is a protective measure against the Patients with High-grade Dysplasia: refluxing acid. The columnar cells progress proximally, so that the This epithelium is then at a high risk of developing dysplasia and -Oesophagectomy – 20-40% of patients will also have earlysquamous-columnar junction migrates upwards. invasive adenocarcinoma.

Risk Factors: •Smoking. •Alcohol. •Obesity. •Large meals. •Hiatus Hernia.

•Pregnancy. •Surgery for achalasia. •Drugs – tricyclic anti-depressents, anticholiner-gics, nitrates. •Systemic sclerosis. •Helicobacter pylori.




A) Metaplasia showing columnar epithelium with goblet cells. B) Metaplasia with low-grade dysplasia with irregular cells and nuclei. C) Metaplasia with high-grade dysplasia with intramucosal carcinoma .

stage adenocarcinoma. -Endoscopic Radiofrequency Ablation – eliminates dysplasia and reduces the risk of oesophageal carcinoma. -Endoscopic Mucosal Resection – removes nodular or a small section of Barrett’s oesophagus for pathology. A preoperative endoscopic ultrasound is needed to ensure the submucosa is not involved.

Upper Gastrointestinal Bleed Niroshan Neminathan, Thomas Isbister, Oniaza Syed, 4 th Year Medical Students(2011) Epsom & St Helier University Hospitals NHS Trust

Definition An upper gastrointestinal bleed if one from a from a source between the pharynx and the ligament of Treitz (which connects the fourth portion of the duodenum to the diaphragm near the splenic flexure) Bleeding can be microscopic, where the amount of blood is so small that it can only be detected by laboratory testing or macroscopic where hypovolaemia and shock may develop.

8. Dizziness 9. Postural Syncope

Management Initial Management – RESUSCITATION High Risk

Risk Factors Increasing age Low socio-economic class Alcohol abuse Chronic renal failure Liver disease Coagulopathy Iatrogenic: NSAIDs, SSRIs, anticoagulant therapy (Heparin, Warfarin)

Above: Oesophageal varices Below: endoscopy showing large gastric ulcer

Epidemiology UGIB is the most common emergency managed by gastroenterologists, with approximately 25 000 inpatient admissions in the UK per year. 1 Upper GI bleeding occurs largely among people in older age groups, incidence is greatest in males. 2-4

Aetiology 1.Peptic ulcer (duodenal > gastric) 2.Gastric erosions/gastritis 3.Mallory-Weiss tear 4.Gastro-oesophageal varices (5% of acute bleeds) 5.Duodenitis 6.Oesophagitis 7.Tumours (gastric > oesophageal) 8.Gastric antral vascular ectasia 9.Dieulafoy lesion 10.Hereditary haemorrhagic telangiectsasia

Clinical Features 1.Haematemesis (vomiting of fresh blood)/ Coffee ground vomit (partially digested blood) 2.Melaena (black tarry stools due to blood being altered by passage through the gut) 3.Unaltered red blood PR- If bleeding massive and very brisk (usually accompanied with shock) 4.Collapse 5.Weakness 6.Sweating 7.Palpitations

Low Risk

Restore blood volume (blood/blood Oral fluids substitutes) Monitor for signs of re-bleeding Admit to high dependency ward Oral PPI (i.e. Omeprazole 40mg BD) (monitoring of BP, CVP and pulse rate) IV Omeprazole 40mg BD (if active bleeding noted 80mg STAT dose to be given followed by an infusion 8mg/hr for 72hrs)

Rockall Score Identifies patients at risk of adverse outcome following acute upper GI bleed (rebleed or death). A score <3 carries good prognosis and a score >8 carries high risk of mortality. Variable Age

Score 0 <60

Score 1 60-79

Score 2 >80

Score 3 -



HR >100

SBP <100



Nil major


IHD/CCF/major morbidity

Renal failure/liver failure


Mallory Weiss tear

All other diagnoses

GI malignancy


Endoscopic Findings



Blood, adherent clot, spurting vessel

Investigations Blood tests FBC (esp. Check Hb and platelets, may initially be within normal limits) Clotting Studies (esp. Prothrombin time) U&Es (Elevated blood urea suggests severe bleeding) LFTs (Liver disease is a significant risk factor) Crossmatch (2 units will suffice unless severe bleeding; 6 units of blood in the case of oesophageal varices) Imaging Endoscopy (gold-standard; can be used to establish the aetiology, review the severity of the UGIB and in some cases treat it)

Second Phase – Medical Management: Correct clotting (IV vit. K; FFP; platelets [if ↓50x10 9/L], including discontinuation of anti-platelet therapy (ie. Aspirin) Antibiotic prophylaxis (Co-amoxiclav 1.2g IV TDS, or Ciprofloxacin 400mg IV BD if penicillin allergy) Prevent encephalopathy if indicated – Give oral lactulose 15-20ms tds. Avoid benzodiazepines & cautionary use of opiates. Check Blood glucose regularly. Pharmacological – Give vasoconstrictor drugs (such as Terlipressin 2mg IV every 4-6 hrs for up to 5 days) Endoscopic – Band ligation is the treatment of choice. Start sucralfate 1g qds after banding. In patients unsuitable for band ligation, beta-blocker, nitrate or adrenaline/cyanoacrylate injection therapies can be used. Radiological – embolisation coil therapy can also be used to stem the bleeding. Failure to control active bleeding: Endoscopic – Balloon Tamponade- Insert Sengstaken Blakemore tube, then progress to Surgical – Transjugular intrahepatic portosystemic stent shunt (TIPPS)



Mortality is around 3% in 20s to 15% in seventh decade of life. Mortality increases with risk factors & need for surgery; varices carry a mortality in excess of 30%.

Hiatus Hernia Jennifer Nowers & Tariq Tabiner, 4th Year Medical Students (2010) Epsom & St Helier University Hospitals NHS Trust Definition:



A hiatus hernia is a protrusion of the upper part of the stomach into the thorax through a tear or weakness in the diaphragm.

Hiatus hernia has often been known as “the great mimic” due to it’s varied presentations. Although it is most often asymptomatic the common presentations include:

Asymptomatic = no treatment


•Reflux symptoms

There are two major types of hiatus hernia

•Epigastric/chest pain •Shortness of breath (effect on diaphragm) •Palpitations (vagus nerve irritation) •Dysphagia

1) Conservative: • Raise head of bed • Avoid raised intra-abdominal pressure • Treat risk factors (weight loss/smoking cessation)

Investigations: •Barium meal or CT + Contrast •Best method •Endoscopy •Good for assessing damage due to reflux •Oesophageal manometry •Rarely used due to low sensitivity.



•Gastro-oesophageal junction and stomach herniate through the diaphragm • Accounts for 90% of hiatus hernias

•Only the stomach herniates through the diaphragm •Accounts for 10% of hiatus hernias


2) Medical (of reflux): • Proton pump inhibitors • H2 receptor antagonists 3) Surgical: • Laparoscopic Nissen fundoplication

Other types of hiatus hernia include “mixed” and “total”

Risk factors: •Increased intra-abdominal pressure •Family history •Smoking •Stress •Muscle atrophy with aging

Stomach contraction reinforces the LOG, therefore decreasing reflux.

Complications include: •Gas bloat syndrome •Inability to vomit •Dysphagia

Gastric Cancer William Farkas, Robert Cann, Anne Elias , 4th Year Medical Students (2011) Epsom & St Helier University Hospitals NHS Trust


• 2nd most common cancer globally, 2/3 of cases are in developing world (1) • Common in China, Japan and parts of South America, less common in UK and USA. UK has 12-13 deaths per 100,000 of population (2) • In West proximal tumours > than those in body or antrum (2) • Men > women, incidence rises after 50 years of age (2)

Aetiology and Risk Factors

•Helicobacter Pylori may be cause of 60-70% of cases (2) •Diets rich in salt, complex carbohydrates and nitrates increase risk of adenocarcinoma. Fresh fruit and vegetables are protective (3) •No clear genetic abnormality, but cancer risk rises 2-3x in 1st degree relatives of patients (2) •Diseases resulting in achlorhydria increase risk as they encourage bacterial colonisation of stomach, thus increasing conversion of nitrates to carcinogenic nitrosamines; e.g. chronic gastritis and partial gastrectomy (3)

Presentation Symptoms • Dyspepsia • Dysphagia • Vomiting • Weight loss • Anaemia • Abdominal pain

Signs • Epigastric pain • Hepatomegaly • Ascites • Troisier’s sign (Virchow’s node) • Sister Mary Joseph’s Nodule (periumbilical nodule) • Acanthosis Nigrans


Surgery • Localised disease may be treated with curative gastrectomy - Tumours in distal 2/3rds of stomach, partial gastrectomy may suffice - Proximal tumours may need total gastrectomy • A 5cm margin proximal and distal to the lesion is traditionally maintained • D2 resections (excision of tumour + perigastric and lymph nodes surrounding coeliac axis) have been found to be worse prognostically than D1 resections (excision of tumour + perigastric nodes) • Endoscopic mucosal resection (EMR) is used to treat early tumours that are confined to the mucosa, this is much less invasive Neo-adjuvant Chemotherapy • Combination chemotherapy of epirubicin, cisplatin + 5-flourouracil has improved 5-year survival rate from 23% to 36%

•Gastric neoplastic polyps •Gastric ulcers •Smoking, alcohol


Adenocarcinoma of stomach

• 95% of gastric carcinomas are adenocarcinomas. Commonly develop on background of chronic gastritis and intestinal metaplasia/dysplasia. Most cancers are ‘intestinal’, arising from intestinal metaplasia, whilst some are ‘diffuse’, arising from normal gastric mucosa (2).


• 3 morphologies (3): • Fungating tumours - polypoid, may be large, have a better prognosis • Malignant ulcers - broader than most peptic ulcers • Infiltrating carcinomas - spread beneath mucosa and invade muscular layer, may cause ‘leather bottle’ stomach with thickened and rigid wall and reduced capacity

For staging and metastatic lesions: • Endoscopic US • CT abdomen/pelvis • CXR • Staging laparoscopy

•OGD with biopsies

Billroth II gastrectomy


Total gastrectomy with Rouxen-Y reconstruction

Subtotal gastrectomy with Roux-en-Y reconstruction

• Gastric carcinoma carries a very poor prognosis • Unfortunately many tumours are metastatic or unresectable due to local extension and surgery is therefore not suitable for consideration • <10% 5 year survival overall • This is increased to nearly 20% for patients undergoing radical surgery

Gallstones Dean Chatterjee, Jennifer Rickard, Charlie Mitchell, Medical Students Epsom & St Helier University Hospitals NHS Trust

Saint’s Triad Josephine Cassell, Hemali Chauhan, Andrew Howe, Lee Hudson, 3 rd Year Medical Students (2010) Epsom & StCassell, Helier University Hospitals NHS Trust Josephine Hemali Chauhan, Andrew Howe, Lee Hudson St George’s, University of London

“The concomitant occurrence of hiatus hernia, colonic diverticula and cholelithiasis” Charles F.M. Saint

Philosophy of Saint’s Triad

• Charles F.M. Saint of Saint’s Triad (1886-1973) was born in Bedlington, England • He obtained his medical degree from the University of Durham and then served as assistant to the surgeon Rutherford Morisson (of Morisons’ pouch, incision and forceps, former assistant of Lister) • After services as a medical officer in World War 1 Saint was appointed head of surgery at the new faculty of medicine at University of the Cape, South Africa • He remained professor there for the rest of his working life, and died at the age of 86 • Interestingly Saint’s triad was never actually published by Saint. It was instead first cited by one of his students C.J.B. Miller who created the eponym based on the teaching he had received from Saint

• Saint’s Triad highlights the concurrence of hiatus hernia, gallstones, and diverticula of the colon • Here Saint is saying that these conditions can occur at the same time and this compound diagnosis can explain complex symptoms • This challenges the usual method of trying to attribute symptoms/signs to one cause (Occam’s Razor) • Saints triad is therefore an example of Hickam’s Dictum, most well phrased as: “Patients can have as many diseases as they… please“

Hiatus Hernia

Colonic Divericula


• Sliding (common): Gastric mucosa moves upwards into the thorax through an enlarged oesphageal hiatus (natural fissure) in the diaphragm (gastro-oesophageal junction above diaphragm) • Rolling (uncommon): Portion of gastric fundus enters thorax alongside oesophagus through a weakness in the diaphragm (gastrooesophageal junction below diaphragm)

• A diverticulum is an outpouching of the colon wall, most frequently in the sigmoid but can occur in the whole colon • Diverticulosis means that diverticula are present, and diverticular disease implies that they are symptomatic • Diverticulitis refers to inflammation of a diverticulum

• Can occur anywhere within the gallbladder and biliary tree • Most commonly cholesterol and pigment stones made of bilirubin and calcium • Usually asymptomatic until they reach a size where they become irritant or obstructive to surrounding structures • Obstruction can cause signs and symptoms of biliary colic which include intense sporadic right upper quadrant pain and nausea. Gallstones can also lead to pancreatitis • Raised cholesterol predisposes to cholesterol gallstones, as can obesity. Low-fibre diets are implicated in stone formation, as is low intake of certain nutrients including vit C • The 4 “F”s – Fat, Forty, Female and Fertile Pre-menopausal women or those exposed to high oestrogen levels (pregnancy/contraceptives) can form cholesterol stones due to the possibility of oestrogen raising bile cholesterol levels and reducing gallbladder motility

• Symptoms are associated with gastro-oesphageal reflux (heartburn and regurgitation) • Due to incompetence of the lower oesphageal sphincter • Dysphagia, painful swallowing and bleeding can occur • Large hiatus hernias can lead to gastric volvulus and/or intrathoracic gastric dilation

• Diverticula occur in 50% of patients over the age of 50 years • Diverticular disease is asymptomatic in 95% of cases and is usually discovered incidentally on a barium enema • Related to the low-fibre diet eaten in developed countries • Pathophysiology: Thickening of muscle layer → High intraluminal pressures → Weakened areas of muscle wall → Outpouching of mucosa through muscle wall

Surgical Jaundice Ben Blackman, 4th Year Medical Student (2012) Epsom & St Helier University Hospitals NHS Trust Definition 1 Surgical Jaundice, also known as obstructive or posthepatic jaundice, is an elevation in serum bilirubin resulting from obstruction of the biliary tract distal to the bile canaliculi.

Table: Differentiation of Common Causes of Surgical Jaundice Condition

Differential Diagnosis 1,2,3,4 Surgical Jaundice usually results from diseases of the bile duct system or of the pancreas. The most common causes are: • Choledocholithiasis (i.e. gallstones in the common bile duct) • Malignancy- either of the head of the pancreas or of the bile duct itself • Biliary strictures, secondary to the above causes, previous cholecystectomy, Primary Sclerosing Cholangitis, Primary Biliary Cirrhosis or Pancreatitis Other causes include: • Drug induced (OCP, erythromycin, anabolic steroids, chlorpromazine) • Pregnancy • Biliary parasites (such as clonorchis sinensis, common in the far East) • Congenital biliary atresia (in newborn children) • Compression of the porta hepatis or common hepatic duct by: • Gallstones (Mirizzi’s Syndrome) • Cancer (1º or metastases) in the liver • Lymphadenopathy. • Dubin-Johnson Syndrome/ Rotor Syndrome (hereditary defects in excretion of conjugated bilirubin) This page focuses on differentiating between the most common causes.



Hx Gallstone disease Increasing age Female sex Obesity Ileal disease/resection

RUQ pain, Murphy’s sign, episodic jaundice

US abdomen ERCP

Initial stenting may be appropriate if patient is severely unwell Definitive treatment is endoscopic removal of stones ± laparoscopic cholecystectomy

Ca Head of Pancreas

Increasing age Smoking

Jaundice w/o biliary colic, vague upper abdo pain radiating to back, palpable gallbladder (see Courvoisier’s Law), Cachexia, VTE, polyarthritis, skin nodules

US abdomen CT/MR abdomen ?ERCP Tumour marker: Ca19-9

Surgical resection (e.g. see Whipple’s procedure) may be used to attempt cure, but commonly resection is used palliatively to remove obstruction. However, prognosis is dire, so treatment is palliative of symptoms and pancreatic failure

Primary Sclerosing Cholangitis

Hx Inflammatory bowel disease (75%) Male sex Mean age 40

Hx of fluctuating symptoms of pruritus, jaundice and cholangitis

ERCP/MRC (beading of ducts) US liver- (no gallstones) Serum pANCA (60%) Liver Bx: biliary scarring

If predominantly extrahepatic ducts affected, dilatation/stenting may improve symptoms Otherwise, liver transplantation is only curative treatment

Primary Biliary Cirrhosis

Female sex Predominantly aged 4050 Hx autoimmune conditions

Often asymptomatic hepatomegaly with raised ALP Fatigue and pruritus may be presenting symptoms

Liver Bx: cirrhosis and lymphocytic infiltrate surrounding portal tracts Bloods: Raised serum IgM, +ve antimitochondrial antibody, raised cholesterol

Ursodeoxycholic acid improves biochemical values Malabsorption and hyperlipidaemia should be treated The only curative measure is liver transplantation

This obstruction leads to a build up of conjugated bilirubin in the bloodstream, leading to jaundice and pruritus. Water-soluble conjugated bilirubin is passed in the urine, giving a dark appearance, but reduced bile salts reach the gut, leading to pale stools. Blood tests will reveal raised serum conjugated bilirubin and markedly raised ALP, but other LFTs will be less abnormal. Urine testing will reveal bilirubin but not raised urobilinogen, as the problem is of excretion, not production.

Clinical Features


Clinical Presentation 1,2 The classic picture of obstructive jaundice is of pale stools and dark urine in addition to the typical jaundice symptoms of icteric skin and sclerae, and pruritus.

Risk factors


Basic Algorithm: Surgical Management


Courvoisier’s Law


This law, observed by Ludwig Courvoisier in 1890, states that if the gallbladder is palpable in a case of painless jaundice, the cause is unlikely to be gallstones. Courvoisier’s law holds because chronic cholelithiasis leads to sclerosis of the gallbladder and renders it indistensible. A palpable gallbladder therefore rules out a history of cholelithiasis and implies a different pathology. 50%–70% of patients with periampullary cancer or Ca head of pancreas have painless jaundice and a palpable gallbladder, but an impalpable gallbladder does not exclude non-gallstone pathology.

Picture: Whipple’s Procedure 1,9 Picture showing upper gastrointestinal tract before and after proximal pancreaticoduodenectomy. 20% of malignant tumours of the pancreas are suitable for resection, but 5 year survival rates are as low as 2%.

Abbreviations: ALP: Alkaline Phosphatase, LFTs: Liver Function Tests, OCP: Oral Contraceptive Pill, Hx: History, RUQ: Right Upper Quadrant, ERCP: Endoscopic Retrograde Cholangio-Pancreatography, VTE: Venous Thromboembolism MRC: Magnetic Resonance Cholangiogram, Bx: Biopsy, pANCA: p-Anti-Neutrophil Cytoplasmic Antibody, PTC:Percutaneous Transhepatic Cholangiography

Acute Pancreatitis

Shaun Davey, Fatima Neves Ferreira, Nimalan Sanmugalingam (Final Year Medical Students, July 2007) Epsom & St Helier University Hospitals NHS Trust Investigations

Definition Acute pancreatitis is the condition in which activated pancreatic enzymes leak into the substance of the pancreas and initiate the autodigestion of the gland.

Causes • • • • • • • • •

GETSMASHED Gallstones Ethanol Trauma Steroids Mumps Autoimmune (PAN, SLE) Scorpion Venom (rare in UK) Hyperlipidaemia –

(Hyperparathyroidism, hypothermia,hereditary causes)

Serum amylase – This is the standard laboratory test carried out to confirm the diagnosis. It is measured within 24 hours of the onset of pain. If serum amylase is greater than three times the upper limit of normal, usually diagnostic of acute pancreatitis. Degree of elevation doesn’t bear any clear relationship to the severity of the pancreatitis. Amylase levels gradually fall back towards normal over the next 3-5 days.

Urinary amylase levels – maybe diagnostic as these remain over a longer period of time

Serum lipase levels – raised in acute pancreatitis and these remain elevated for a longer period of time

Other baseline investigations – Full blood count and CRP, urea and electrolytes, blood glucose, liver biochemistry, plasma calcium and arterial blood gases

Erect Chest X –ray is necessary to exclude gastroduodenal perforation which can also raise serum amylase. Abdominal film may show gallstones or pancreatic calcification.

Abdominal Ultrasound scan is used as a screening test to identify a possible biliary cause of pancreatitis. USS may demonstrate pancreatic swelling and necrosis.

Spiral CT with contrast can assess degree of pancreatic damage.

MRI can assess gallstones in common bile duct


• ERCP (also emboli) –

(endoscopic retrograde cholangiopancreatography)

Ranson’s Criteria for Acute Pancreatitis One point for each variable; a score of 3 or more points indicates severe pancreatitis • • • • • •

At admission Age greater than 55 years Blood glucose> 11 mmol/l Serum LDH> 500IU/l AST> 200IU/I White blood count> 16 X 109/l

• • • • • •

At 48 h after admission Haematocrit fall> 10% Blood urea> 16mmol/l Serum calcium < 2 mmol/l Arterial pO2 < 8kPa Base deficit < 4 mmol/l N.B. Serum amylase is not included in criteria.

• Drugs (Azathioprine, mercaptopurine)

Management of Severe Pancreatitis Initial Management • • • • • •

HDU or ITU Iv fluids, oxygen (baseline ABG needed) , analgesia Nil by mouth, NG tube only if vomiting Fluid balance chart Urinary catheter – monitor urine output hourly (Large amounts iv fluids needed + maintain urine output above 30 ml/h

Subsequent Management •


• •

• Gradual/sudden onset severe epigastric/central abdominal pain (radiating to back) • Vomiting prominent (in severe cases multi-organ failure) • Sitting forward may relieve the pain


• • • • • • • • •

Tachycardia Fever Jaundice Shock Ileus rigid abdomen +/- Epigastric tenderness and periumbilical discolouration (Cullen’s sign or at the flanks, Grey Turner’s sign)

• •

Assessment of Disease Severity •

Assessment of severity is carried out by a multifactorial scoring system such as the Ranson’s scoring system. Alternatively measurement of the C reactive protein can also provide an accurate assessment of severity.

Nasogastric suction – prevents abdo distension & vomiting (therefore preventing aspiration pneumonia) Nutrition – enteral via nasojejunal tube Analgesia – Pethidine & tramadol usually via a patient controlled system. Avoid morphine derivatives as can cause sphincter of Oddi contraction. Prophylactic Antibiotics for 7days. Commonly used Antibiotics (dependent on culture): Meropenem, Imipenen, Ciprofloxacin, Cefuroxime PPI or H2 receptor antagonist Gallstones present - Elective laparoscopic cholecystectomy – to prevent further attacks Biliary Cause of severe pancreatitis – urgent endoscopic sphincterotomy Infected pancreatic necrosis – radiological drainage. Open surgery with necrosectomy & postoperative cavity irrigation or retroperitoneal endoscopic necrosectomy or transgastric endoscopic necrosectomy (if walled-off collection behind stomach) Positive pressure ventilation & renal support if multi-organ failure develops

Laparoscopic cholecystectomy: gallbladder is dissected free and removed. Sphincterotomy in progress during ERCP.

Complications Intra-abdominal: • Pancreatic "collections": phlegmon, pseudocyst, abscess, necrosis • Intestinal: paralytic ileus; gastrointestinal haemorrhage from stress ulceration, gastric varices due to splenic vein obstruction, or rupture of pseudoaneurysm; necrotising obstruction or fistulisation of colon • Hepatic - obstructive jaundice due to oedematous narrowing of common bile duct • Spleen - rupture or haematoma, from spread of peripancreatic inflammation Systemic: • Minor pyrexia to rapidly fatal, multiple organ-system failure. • Circulatory shock - kinin activation, haemorrhage • Disseminated intravascular coagulation • Respiratory insufficiency: mild e.g. hypoxaemia, atelectasis, pleural effusion; severe e.g. adult respiratory distress syndrome • Acute renal failure • Metabolic: hypocalcaemia; hyperglycaemia / diabetes mellitus; hypertriglyceridaemia • Pancreatic encephalopathy - confusions, delusions, coma • Retinal arteriolar obstruction causing sudden blindness: Purtscher's retinopathy • Metastatic fat necrosis Prognosis • Majority with mild – moderate will fully recover with no long term sequelae • Recurrent episodes can occur (esp. if long term ductal damage) • Severe may cause exocrine (malabsorption) & endocrine (diabetes) insufficiency

Pancreatic Cancer Rabiya Aseem 4th Year Medical Student Epsom & St Helier University Hospitals NHS Trust Introduction

Clinical Presentation


Pancreatic Cancer is the 4th leading cause of cancer deaths in men and women, particularly affecting the elderly. It is notoriously problematic to diagnose early hence has a very poor prognosis. At the time of diagnosis, unfortunately 52% of patients have distant disease and 26% have regional spread. The 1-year survival rate is 24%, and the overall 5-year survival is 5% (1). Pancreatic cancer is twice as common in men and over 80% of cases occur between 60-80yrs of age. 95% of cases are exocrine tumours; 75% of tumours occur in the head of the pancreas, 20% occur in the body and 5% in the tail.

The presenting symptoms of pancreatic cancer depend on the location of the tumour within the gland, and the stage of the disease. Presenting features include:

Surgery is the preferred treatment for pancreatic cancer. However, chemotherapy and/or radiation therapy also play a vital role in patients with unresectable disease and improve overall survival.


•Significant weight loss (80%) and anorexia •Epigastric pain, radiating to the back (Absent in 40% of patients) •Obstructive jaundice (dark urine and pale stools) with pruritus (Obstruction of the biliary system-50%) •Courvoisier's law- Painless jaundice with palpable gallbladder. •Ascites •Nausea & vomiting Uncommonly steatorrhoea, thrombophlebitis migraines, GI haemorrhage caused by duodenal erosion and symptoms of hypoglycaemia.

Surgery A thorough preoperative workup is needed, after which the surgical approach for resectability of the tumour can be assessed. Factors affecting resection include tumour size (<4 cm), invasion of SMA or portal vein and the presence of ascites, nodal, peritoneal or liver metastases. Curative resection options include: 1.Pancreaticoduodenectomy (Whipple procedure)- This is the most common procedure used for removing cancer of the exocrine pancreas. The procedure has a mortality rate of 6.6%. Complications include; delayed gastric emptying, haemorrhage, abscess formation and formation of a pancreatic fistula (4).

Diagnosis and Investigations •Biochemistry; Increased serum bilirubin and ALP in obstructive jaundice. Impaired glucose tolerance or diabetes may be observed. •Tumour markers; CA19-9 (serum levels of CA19-9 used at time of diagnosis and during follow-up) and CEA (may be raised if hepatic metastases). Imaging

Fig 1. Dissection representing parts of the pancreas and surrounding structures.

The pancreas is a gland with both endocrine and exocrine functions. It is a retroperitoneal organ that lies approximately at the L2 level.

•USS (80% sensitivity) •ERCP or trans-hepatic percutaneous cholangiography •CT/MRI scan is the most reliable method of diagnosis (sensitivity >95%) and helps to recognise metastases and stage of cancer. •CT or US guided biopsy can confirm the diagnosis (2).

Aetiology 40% of cases are sporadic. Known risk factors include: •Smoking is the most common environmental risk factor. Smokers have a 2 fold greater risk than non-smokers. •Central obesity has been associated with a greater risk of developing early onset pancreatic cancer. •Chronic diabetes mellitus •Chronic Pancreatitis (<5% cases), .frequenty in alcoholics, is associated with increased risk of developing pancreatic cancer. •Genetic predisposition (5-10%) Mutations have been recognised in the KRAS2, CDKN2, p53 and Smad4 genes.

Figure 2. Whipple’s Procedure (Before and after). The head of the pancreas, part of the small intestine, and some of the nearby tissues are removed.

2.Total pancreatectomy- used in cases where the tumour involves the neck of the pancreas and has a higher mortality than Whipple procedure. These patients get insulin-dependent diabetes. 3.Distal pancreatectomy- This procedure is most commonly used for islet cell (endocrine) cancer of the pancreas. The body and tail of the pancreas are removed. Palliation

Table 1: Pancreatic Cancer staging and survival (3).

85% of patients are not suitable for curative resection. The aim of intervention is symptomatic relief e.g. Endoscopic stenting can relieve jaundice or a gastrojejunostomy can be performed to prevent duodenal obstruction. Coeliac plexus blocks can be used for pain relief. Palliative chemotherapy (e.g. gemcitabine) is useful but controversial.

Pancreatic Pseudocysts Gregory Landon and Lynn Wong,4th Year Medical Students (May 2011) Epsom & St Helier University Hospitals NHS Trust Definition

Clinical Presentation

A pancreatic pseudocyst is a localised collection of pancreatic juice. It may be within, adjacent to, or remote from the pancreas. Pancreatic pseudocysts are formed by pancreatic secretions escaping from a ruptured duct. They do not have an epithelial lining, but are enclosed in a wall consisting of fibrous and granulation tissue. Occasionally they contain small amounts of necrotic debris. Persistence of the pseudocyst indicates continuing communication with the duct. [1]

Common symptoms are abdominal pain (76–94%), early satiety, nausea and vomiting (50%) and weight loss (20–51%). Physical examination may reveal upper abdominal tenderness and epigastric fullness. Large cyst can be palpated as a mass felt above the umbilicus that is fixed, tender and classically, tense, with illdefined borders. Other findings may include fever, sclera icterus and pleural effusion. [4]

Aetiology Pancreatic pseudocysts most often develop after an episode of severe, acute pancreatitis. Typically, acute pancreatitis causes pseudocyst formation in 50% of cases with first symptoms evolving four weeks after the episode [1], It may also occur after trauma to the abdomen, more often in children, and in someone with chronic pancreatitis [2]. A study [3] of 69 pseudocysts found: 78% were due to alcoholic pancreatitis 7% were related to complicated gallstone pancreatitis 6% were of unknown causation (idiopathic) 3% each were caused by trauma, hyperlipidemia or a recent surgical operation

Up to 40% of acute pseudocysts will resolve within approximately one week. Supportive treatment is all that is required in this time. [1] Intervention is indicated for symptomatic and enlarging pseudocysts greater than 6cm that persist for longer than 6 weeks This is due to the likelihood of spontaneous rupture and secondary complications such as haemorrhage and infection as time passes. [4]

Investigations CT scan is the gold standard of investigation for pancreatic pseudocysts. It has a sensitivity of 90100% and is not operator dependent. [5]


Pathophysiology The main mechanism leading to pseudocyst formation is thought to be the pancreatic duct disruption during the episode of pancreatitis. Leakage and activation of pancreatic enzymes evolve into autodigestion and necrosis of pancreatic parenchyma. This subsequently evokes an inflammatory response, causing a pseudocyst wall consisting of granulation and fibrous tissue. 40% of pancreatic pseudocysts resolve spontaneously. However, some may persist without symptoms, or progress to complications. Post-chronic pancreatitis pseudocysts are more likely to persist compared to those caused by acute pancreatitis. A pseudocyst may enlarge, causing pain with biliary or pyloric obstruction. About 10% become infected, forming an abscess. If ruptured into the peritoneum, it will lead to ascites. A pseudocyst may also erode a vessel, causing haemorrhage. [4]


Classification Acute pancreatitis Type I normal duct/no communication Type II normal duct/with communication Type III normal duct with stricture/no communication Type IV normal duct with stricture/with communication Type V normal duct/complete obstruction Chronic pancreatitis Type VI abnormal duct/no communication Type VII abnormal duct/with communication

Catheter drainage •Percutaneous aspiration is useful only to establish a diagnosis or as a temporising measure. It has a 54% failure rate and a 63% recurrence rate. This technique has a relatively high risk of infecting the pseudocyst. •Percutaneous catheter drainage is the procedure of choice for treating infected pseudocysts, allowing for rapid drainage of the cyst and identification of any microbial organism. Endoscopic drainage may be either transpapillary (via ERCP) or transmural. •Transpapillary drainage, while safer and more effective than transmural drainage, requires cyst communication with the pancreatic duct. This technique may be technically challenging because it requires wire passage and stenting through the pancreatic duct to the pseudocyst. The success rate is about 80%. The recurrence rate is 10-14%, and, in most series, the complication rate (mainly pancreatitis) is approximately 13%. •Endoscopic transmural drainage involves cutting through the gastric or duodenum wall, and a series of pigtail stents are placed through the resulting communication. The method has an 82-89% success rate in very experienced hands. The recurrent rate is 6-18%. The complication rate is 20%, with the most feared complication being bleeding. Surgical drainage is the standard against which all therapies are measured. •Internal drainage is the procedure of choice. A laparoscopic approach has been used in some cases with good results. •In most series, the mortality rate is 3%, and the complication rate is approximately 24%. •The success rate is 85-90%. •Recent work suggests that a laparoscopic approach to drainage has a high success rate and a low morbidity rate. [5]

Lower GastroIntestinal Surgery

Acute Appendicitis Pavandeep Singh Sandhu, 4th Year, Medical Student(2011) Epsom & St Helier University Hospitals NHS Trust



Acute appendicitis is the most common abdominal emergency in the UK, affecting 1/6th of the British population. It is more common in those on a Western diet.

Perforation This is more likely if a faecolith is present, and also in younger children as diagnosis can be delayed in this age group.

Pathology The lumen of the appendix becomes obstructed by, most commonly, lymphoid hyperplasia, or a faecolith. Filarial worms may also be responsible if infection is present. Bacteria, if present, then proliferate in the lumen and begin to invade the appendix wall. This leads to inflammation, pressure necrosis, and eventually perforation if an appendicectomy is not promptly performed.

Appendix Mass Here, the inflamed appendix is walled off due to adhesions with the omentum. Initial treatment is conservative, with 80% of cases resolving spontaneously. An appendicectomy is then performed after 3 months to allow the inflammation to settle. Appendix abscess This results from an unresolved appendix mass. Drainage of the abscess is required.

Patient presentation Acute appendicitis


Patients usually present with the following symptoms: •Peri-umbilical pain moving to the RIF


•Anorexia •Nausea •Fever

Localised abscess

Generalised peritonitis

An inflamed appendix might resolve on its own, but in this case, a further attack is likely. Appendicitis may also occur in a non-obstructed appendix, such as when there is direct infection of the lymphoid follicles from the appendix lumen. If bacteria are not present within the lumen, a mucocele of the appendix may result, due to continuous secretion of mucus from the goblet cells in the mucosal wall.

•Diarrhoea or constipation A retrocaecal appendix may cause flank or RUQ pain. Similarly, an appendix in the pelvic position may cause suprapubic pain with urinary frequency as the bladder is irritated. On examination, special clinical tests may be employed to help further determine the diagnosis, and also to help identify the position of the inflamed appendix: Rovsing’s Sign Pain >in RIF than in LIF when the LIF is pressed. Psoas Sign Pain on extending hip if retrocaecal appendix.

Cope Sign Pain on flexion and internal rotation of right hip if the appendix tip is close to obturator internus.

Investigations An FBC will usually show a neutrophil leucocytosis. An elevated CRP is also a common finding. A urine dipstick should be performed in all cases of acute abdominal pain. An ultrasound scan can be performed as well as a diagnostic laparoscopy if uncertainty still exists.

The Alvarado Score The Alvarado score is a scoring system used to aid in the diagnosis and management of acute appendicitis. It consists of three symptoms, three signs and two laboratory findings: Migratory RIF pain Anorexia Nausea or vomiting Tenderness in the RIF Rebound tenderness in the RIF Fever >37.3 °C Leucocytosis (>10 x 109/l) Neutrophilia (shift to the left >75%)

(2) (1) (1) (1) (1) (1) (2) (1)

Score 1-4 = Acute appendicitis very unlikely, keep under observation. Score 5-6 = May be acute appendicitis, keep for regular observation. Score 7-8 = Probable acute appendicitis, operate. Score 9-10 = Definite acute appendicitis, operate.


The treatment of acute appendicitis is a prompt appendicectomy which is nowadays performed laparoscopically.

Appropriate Colonoscopy? Laura Corbett and Ian Alberts – 4th Year Medical Students(2010) Epsom & St Helier University Hospitals NHS Trust



Colonoscopy is the endoscopic examination of the colon and the distal part of the small bowel with a CCD camera or a fibre optic camera on a flexible tube passed through the anus. It may provide a visual diagnosis (e.g. ulceration, polyps) and grants the opportunity for biopsy or removal of suspected lesions.

Recently, there have been a number of guidelines produced to indicate when colonoscopy may be appropriate published by: • National Institute of Clinical Excellence (NICE) • British Society of Gastroenterology

Indication 1: CANCER Diagnosis: Altered bowel habit to loose stool ; > 6/52 duration; ≥ 60 yrs old Rectal bleeding ; > 6/52 duration; ≥ 60 yrs old Unexplained iron deficient anaemia Rectal mass Right sided abdominal mass Surveillance After removal of adenomatous polyp: 1-2 adenomas and all <1cm  No surveillance or 5 years 3-4 adenomas or 1 >=1cm  3 year surveillance >5 small or >=3 at least 1 >= 1cm  I year surveillance Screening If family history of CRC

Summary Necessary - Iron-def anaemia Inappropriate colonoscopies -

Indication 2: IBD Screening programme for history of IBD

Abdominal pain, bloating, chronic diarrhoea, pt less than 45yrs are likely to have an unhelpful examination. BUT.........reassuring factor

Colorectal Cancer Luise Brown, Aled Daniels, Daniel Griffin and Joseph Tait, 3 rd Year Medical Students (May 2010) Epsom & St Helier University Hospitals NHS Trust Epidemiology (1,2) • • • •

Presentation (4, 5)

Left-Sided •Change in bowel habit • Weight loss • Rectal bleeding - clots • Pain • Tenesmus (annular forms)

Lifetime risk: ♂ = 1 in 16; ♀=1 in 20 More common in developed countries. UK incidence (2007): 16,851(♂); 13,876(♀) UK mortality (2008): 16,259

Rectal • Rectal bleeding – streaks • Mucus – progressive amounts • Alternating diarrhoea & constipation • Tenesmus • Weight loss

Aetiology (2) • Unknown although most colorectal carcinoma arises from pre-existing, benign adenomatous polps,(surg bk).

Risk Factors (2) • • • • • •

Age > 60 Family history IBD (duration dependent) Dietary (↑ animal fat, ↓ fibre and folate) Obesity (33% increased risk) Pre-existing adenomatous polyps

Caecal and Right-Sided Presentation is often late with: • Pain – obstruction • Faecal occult blood • Iron deficiency anaemia (indicates colonoscopy) • Weight loss

Surgical Treatment (3,7): Investigation (3) • Mandatory digital rectal examination • Sigmoidoscopy with biopsy of any abnormal mucosa • Colonoscopy • CT Colography • Barium enema (rarely)

Screening • In the UK a Faecal Occult Blood (FOB) test is sent to all those aged between 60 -75 years every two years. • People with a positive FOB test are then referred for colonoscopy A normal test does not rule out cancer.

Non-surgical Non-surgicalTreatment Treatment(3,6): (3,6): Adjuvant Adjuvanttherapy: therapy: →Role →Roleof ofthis thisin incolorectal colorectalcancer cancerisisstill stillunclear. unclear. →At →Atpresent presentitit appears appears that thatsystemic systemicchemo chemowith with55fluorouracil fluorouraciland andlevamisole levamisoleleads leads to toincreased increasedsurvival survivaland and decreased decreasedrecurrence recurrencein inpatients patientswith withDukes Dukes CCCancers. Cancers. →The →Therole roleof of chemotherapy chemotherapyin inDukes DukesBBCancers Cancers isisless lessclear clear

Pathogenesis (8) • Colorectal cancer originates from epithelial cells lining the GI tract, as a result of inherited or acquired genetic mutations. • The most common causative mutation is within the APC gene. • This gene encodes a protein without which there is DNA overactivation by Beta-catinin • Mutations can also occur in several onco-genes and genes responsible for apoptosis.

Spread Metastases of colon cancer are normally found within the liver, as this is the normal route of blood drainage, but they can also be found in the lung, brain and bones.

Staging (8) • TMN staging (replacing the conventional Dukes classification).

Radiotherapy: Radiotherapy: →Generally →Generallyof oflittle littlevalue valuein incolon coloncancer cancer(the (thetumour tumournot not particularly particularlyradiosensitive) radiosensitive)but buthas has been beenshown shownto toimprove improve outcome outcomefor forsome somepatients. patients.

Right hemicolectomy: tumours of the right colon and caecum

Hartmann’s (I) & Anterior resection(II): tumours of the sigmoid colon and mid and upper rectum

Transverse colectomy: tumours of the transverse colon (extended right hemicolectomy also an option)

Left hemicolectom y: tumours of the descending colon

Abdominoperi neal resection (AP resection): tumours of the lower rectum

Prognosis (8) 5 yr survival using Dukes classification: A: 93%, B: 77%, C: 48%, D:7%

Non-Malignant Causes of Large Bowel Obstruction Anna Clark & Eleanor Dodson, 4th Year Medical Students (2011) Epsom & St Helier University Hospitals NHS Trust DEFINITION 1


Significant impairment or complete obstruction of the passage of intestinal contents.

AETIOLOGY 2-6 •90% are due to underlying malignancy •Non-malignant causes of bowel obstruction include: • 5% Volvulus • 3% Benign strictures due to inflammatory or ischemic disease • 2% due to other causes including pseudo obstruction and faecal impaction Volvulus: Loop of bowel becomes twisted around its mesenteric axis, forming a closed loop obstruction. Common sites include caecum and sigmoid. •Risk factors: chronic constipation, laxative abuse, extremes of age, embryological anomalies resulting in hypermobile segments of bowel Pseudo Obstruction: impaired motility of the large bowel, leading to a functional obstruction. •Common causes: Metabolic disorders (DKA/Na+), anticholinergic drugs, pelvis trauma, neurological disease

The section of bowel beyond obstruction collapses The section of bowel above obstruction, or within closed loop, dilates (due to accumulation of gastric secretions and air) and becomes hyperactive (causing colicky pain) Fluid and electrolytes shift into bowel wall causing dehydration (3rd space loss) and electrolyte imbalance The bowel wall stretches which results in compromised blood supply leading to ischemia and necrosis


Colicky abdominal pain

Usually not tender, rebound tenderness = ?peritonitis

Bloated abdomen

Abdominal distension

Absolute constipation (no faeces or flatus)

Increased bowel sounds (tinkling) in volvulus. Absent in pseudo-obstruction

Vomiting (later sign)

Signs of dehydration Tachycardia and hypotension



WCC? Anaemia?


Electrolyte imbalances, Assess renal function, dehydration?




 INR can occur in sepsis

Group & Save

Prep for surgery

Erect CXR

Air under the diaphragm?


Dilated loops of bowel?

Bacteria proliferate in the obstructed bowel -ABG ?lactate -Laparoscopy -Biopsy

Perforation can occur, resulting in faecal contamination of peritoneal cavity, sepsis and possible death



MANAGEMENT 2,4,5,10, GENERAL MEASURES: • Assess the patient fully and identify the cause • “DRIP & SUCK” = Insert NG tube – make the patient NBM and start IV fluids •Decompression with colonoscopy successful in 7090% of volvulus & pseudo-obstruction •Surgical intervention is indicated if:  Failed decompression  Signs of ischemia/perforation



‘Coffee bean sign’ = dilation of closed loop obstruction

Dilated (>6cm) large bowel (haustra visible)

CONSTIPATION as cause: •Ensure there is no other underlying cause •Laxative options include: • Stool softeners: Arachis oil enema • Osmotic: Macrogols (movicol/laxido) 6 sachets/1L H2O/6hrs • Stimulants: Glycerin suppositories, Senna, Sodium picosulphate (dulcolax oral/suppositories) •Disimpaction under sedation

Small Bowel Obstruction Hannah Newham, Medical Student (2008) Epsom & St Helier University Hospitals NHS Trust Classification of SBO: • Mechanical / functional • Partial / complete • Simple / strangulated Mechanical obstruction = physical blockage of passage of bowel contents, caused by: • External compression of the bowel (extrinsic). • Lesions arising in the wall of the bowel (intrinsic). • Lesions arising within the lumen (luminal).

Functional obstruction = atony / loss of normal peristalsis, in the absence of a mechanical cause. In the small intestine = paralytic ileus In the large intestine = pseudo-obstruction

Symptoms: • Colicky abdominal pain • Nausea • Vomiting (associated with more proximal obstructions) • Early diarrhoea & flatus • Late constipation & absence of flatus Signs: • Fever & tachycardia (occur late and with strangulation) • Scars from previous abdominal surgery (→adhesions) • Distension (associated with more distal obstructions) • Hyperactive bowel sounds early, then hypoactive bowel sounds. • Exclude hernias. • Rectal examination: blood (suggests strangulation or malignancy), masses.

Atony can be generalised or localised.

Most common causes of SBO: • Post-op adhesions (60%) • Malignant tumour (20%) • Other hernias (10%) • Inflammatory bowel disease (5%) • Volvulus (3%) • Miscellaneous causes (2%)

Investigations Bloods:

Management Conservative

•FBC: ↑ WCC may indicate strangulation ↑ haematocrit (volume depletion

If strangulation is not suspected, a period of non-operative treatment is commenced:

•U&Es: ↑ creatinine (vol. depletion ↑ electrolytes (vol. depletion)

• Nil by mouth

• Group & save (patient may require emergency surgery)


• Urinalysis (to exclude UTI) • LFTs (to exclude biliary & hepatic disease) Imaging • Abdominal X-ray (supine & upright): - Central gas shadows - Small bowel dilatation (>2.5cm in diameter) - Air-fluid levels - No gas in the colon • CT: - Transition point of bowel dilatation to collapse may be visible - Gastrografin follow-through

(nb. Small bowel has valvulae conniventes which completely cross the lumen whereas the haustra in the large bowel do not)

•NG tube: “drip and suck” • IV fluids •Monitor U&Es and correct electrolyte imbalances. If SBO does not resolve after 2-3 days, or if strangulation is suspected, surgery is required. Surgical procedure depends on cause of obstruction: • Adhesiolysis • Tumour resection • Hernia repair • Resection of non-viable bowel

Pathophysiology: • Impaired gut absorption → net loss of water & electrolytes → dehydration & hypovolaemia → decreased skin turgor, hypotension & tachycardia. • Proximal bowel dilates due to accumulation of secretions → stimulates cell secretory activity → more fluid accumulation → bowel wall lymphoedema • Bowel dilatation causes reflex contraction → 1. colicky abdominal pain & distension 2. frequent loose stools and flatus early on. • Distal bowel collapses & peristalsis ceases. • Eventually, reflex bowel contraction ceases → atony

Strangulation = impairment of the blood supply to or from the bowel wall which leads to bowel ischaemia and necrosis. If not diagnosed and properly treated, this will lead to perforation, peritonitis and death. It is therefore a surgical emergency. As many as 40% of patients have strangulated obstructions. The following features may indicate strangulation: • Guarding • Rebound tenderness • Tachcardia despite Rx of hypovolaemia • Pyrexia • Elevated white cell count • Colicky pain replaced by a continuous dull ache If surgery is performed within 36 hours, mortality = 8%. This increases to 25% if surgery is delayed beyond 36 hours.

Diverticular Disease Lucy Ashken, Alice Brooks, Hannah Harris – MBBS year 4 Epsom & St Helier University Hospitals NHS Trust Aetiology The exact aetiology of diverticular disease is unknown; however, there are several risk factors which are thought to lead to the presence of diverticula: • A low fibre diet increases intraluminal pressure which leads to the herniation of mucosa through muscle layers of the bowel wall. • Constipation results in an increase in intraluminal pressure. • Increasing age is accompanied by a fall in tensile strength of collagen fibres in the colon submucosa. • Connective tissue disorders result in weaknesses in the colon wall.

Acute diverticulitis is managed conservatively via fluids and antibiotics (a combination chosen from metronidazole, penicillin, gentamicin, and ciprofloxacin).

Clinical Presentation Diverticular Disease



• Change in bowel habits • Bloating, nausea, flatulence • LLQ pain (relieved by defecation)

An outpouching of the gut wall at a site of potential weakness that corresponds to the supplying vessels to the colon.


• Perforation o Peritonitis o Ileus o Shock • Haemorrhage o Large o Painless rectal bleeding • Fistulae o UTI o Vaginal infection o Pneumaturia


Diverticulosis Presence of diverticula in the colon, most commonly the sigmoid, but may extend into the rest of the left side and the transverse colon. Occasionally they are found in the right colon. The rectum is never involved.

• Above + fever • LLQ tenderness • Localized/generalized peritonism

Diverticular Disease


This implies symptomatic diverticulosis. Diverticula are thought to be present in 30% of Westerners over 60, but the majority will remain asymptomatic.

• Abdominal examination and PR.

Diverticulitis Inflammation of a diverticulum which presents with features of infection such as pyrexia, raised white cell count and CRP/ESR in conjunction with a tender colon. This can lead to complications such as perforation, haemorrhage, fistulae, abscesses and strictures.

• FBC (anaemia, infection), U&E, CRP, ESR. • Barium enema (reveals diverticula, strictures and fistulae – typical ‘sawtooth’ appearance). • Sigmoidoscopy, colonoscopy (visualize diverticula and exclude differentials). • CT (assess complications).


Diverticulitis complicated by formation of an abscess requires percutaneous drainage; a perforated abscess needs laparoscopic lavage and drainage. The affected section of bowel may then be resected. Perforation of diverticulum can lead to generalised peritonitis and requires urgent surgical intervention. Laparotomy is performed and the colon resected with the formation of an end colostomy and intraperitoneal rectal stump, usually via the Hartmann’s procedure. Chronic diverticular disease may be managed conservatively where symptoms are mild and carcinoma has been excluded. In this case, the bowels are regulated with lubricant laxatives (e.g. Milpar) and a high-fibre diet. If disease is severely symptomatic, laparotomy and resection of the affected colon is performed.

Fistula in Ano Oliver Bendall & Sindy Lee – 4th Year Medical Students Epsom & St Helier University Hospitals NHS Trust

Definition A fistula is “an abnormal connection between two epithelial surfaces”. An anal fistula has a primary internal opening to the anal canal and a secondary external opening onto the skin. There may be multiple external openings originating from one opening in the anal canal.


Goodsall’s Rule

1. High and Low fistulae

Fistulas anterior to the anus open to the anus in straight line

‘High’: crosses the sphincters above the dentate line ‘Low’: does not cross the sphincters above dentate line

Fistulas posterior to anus have curving track and open in midline posteriorly

Aetiology Unlike other benign anorectal diseases such as anal abscesses and haemorrhoids, anal fistulas are relatively rare. One study from Finland estimated the incidence to be 9 / 100,000 (1). Most anal fistulae develop from perianal abscess. These abscesses originate from the anal glands. If the outlet of these glands becomes blocked, an abscess can form which can eventually point to the skin surface. The tract formed by this process is the fistula. Other causes of anal fistulae include Crohn’s disease, carcinoma, radiotherapy and TB

Management ‘Low’ fistula - Lay open: insert metal probe and incise tissue down to probe.

2. Parks Classification Clinical Presentation Pain, peri-anal discharge (a small discharging sinus may be noted by the patient), itching, swelling and the noticing of an external opening are reported symptoms. History of causal conditions (see above) should be noted.

An alternative, more anatomically precise classification method which has 4 categories (2): intersphincteric 75% transphincteric 20% suprasphincteric 4% extrasphincteric 1%

High’ fistula – Seton: Cannot lay open high fistulae as would lead to sphincter damage so use seton method (see right). A thread is passed through fistula track and tied outside. Tightened gradually and cuts through to the surface, allowing time for healing so that is sphincter integrity is maintained.

Breast & Endocrine Surgery

Benign Breast Lumps Nida Pasha, 4th Year Medical Student (2012) Epsom & St Helier University Hospitals NHS Trust Introduction

Clinical Presentation


Breasts are made up of fat, connective tissue, glandular tissue and ducts (Figure 1). The majority of women who present with a lump have a benign disease. Common presenting complaints include: lump, breast enlargement, discharge or pain. All lumps should be investigated thoroughly to exclude malignancy. Common causes benign single lumps: Fibroadenoma, Cyst Common causes benign Multiple lumps: Fibroadenoma, Fibrocystic changes, Cysts.

The most common site for all benign breast lumps is in the upper outer quadrant.

All breast lumps should be investigated using the triple assessment:

Aetiology Fibroadenomas: The exact cause remains unknown. They appear to be influenced by oestrogen as they are most prevalent in premenopausal, pregnant women, or in postmenopausal women who are taking HRT. Fibrocystic: The exact causes are not fully understood, however it is known to be related to the levels of oestrogen, progesterone, prolactin. As the condition is known to regress with menopause and the symptoms are strongly related to the menstrual cycle. Many other hormones such as TSH, Insulin, Growth factors and GH are thought to exert direct and indirect effects amplifying or regulating cell growth1.

Fibroadenomas: Most common type of benign breast lumps found in women under 30 years. It is hard, smooth with well defined edges, painless. These lumps are highly mobile and are therefore often described as breast mice. Fibrocystic: symptoms commonly change with menstrual cycle. Commonly found in women between 25-45. present with: cyclical breast pain, multiple or single lumps often described as a lumpy cobblestone texture. Lumps are smooth with defined edges, mobile, may produce a green/ yellow/ brown discharge. Breast Cysts: commonly seen in women aged 40-60 years. They are fluctuant, soft, painful. The cysts may become larger and tender during menstruation.

3.Biopsy: Fine needle aspiration will help distinguish benign from malignant cells.

Management Conservative management •Lifestyle changes: Supportive brassière can help reduce discomfort. Other changes include a diet low in saturated fats or sodium, reduced caffeine intake, weight reduction if obese, and decreasing levels of stress. •Evening primrose oil: First line treatment for mild mastalgia. The active component of evening primrose oil is gammalinolenic acid, a fatty acid that is thought to modulate hormone-receptor interaction in breast tissue. •Hormonal treatments: Can be used for pain which does not respond to conservative therapy. Danazol and bromocriptine are the only licensed medications for use in severe mastalgia.

Fibrocystic: When confirmed by ultrasound patients with diffuse, bilateral nodularity are reassured of their benign disease course and are managed symptomatically.


Breast cysts: This is caused by an overgrowth of glands and connective tissue of the breast which eventually block the milk ducts causing them to dilate and fill.

2.Imaging: mammography (women >35 years) or, ultrasound scan (women <35 years)

Surgical management Fibroadenomas: (Figure 3) Malignant potential is very low therefore excision is not routinely preformed unless it is more than 4cm in diameter, diagnosed in over 40s or is enlarging. In which case excision is usually recommended to exclude malignancy. Open excision is the preferred option for large size fibroadenomas. Several multi-institutional trials have demonstrated cryoablation to be a successful option for the resolution of fibroadenomas without surgical excision. The Results of cryoablation have been followed out to 4 years and demonstrate the procedure to be safe and durable2.

Breast Cysts: The exact cause of breast cysts remains unknown. Evidence suggests that excess oestrogen plays an important role.

Fibroadenomas: These consist of epithelium and stroma. The epithelial proliferation appears in a single terminal ductal unit which becomes encased in a fibroblastic stroma. Fibrocystic: This is caused cyst formation due to an overgrowth of glands and connective tissue of the breast which eventually block the milk ducts causing them to dilate and fill. This is followed by the formation of scar-like fibrous tissue. There is also considerable hyperplasia of the lining of the milk ducts, eventually leading to the enlargement of breast lobules (Figure 2).

1.Clinical examination

Figure 1: Structure of breast tissue

Figure 2: Diagram of Fibrocystic breast

Breast Cysts: When confirmed by ultrasound scan (Figure 4) the aspiration of these cysts can be attempted, using a small green needle and syringe. The aspirate of the cyst can be discarded unless the cyst fluid is bloody in which case it is sent to cytology

Figure 3 Ultrasound scan demonstrating a 4cm fibroadenoma

Figure 4 Ultrasound scan demonstrating two simple breast cysts

Breast Cancer (Triple Assessment) Rajiv Atchuthanaikabahu, 4th Year Medical Student (2011) Epsom & St Helier University Hospitals NHS Trust This is termed ‘ductal carcinoma in situ’ (DCIS). It may present as a lump in a manner similar to invasive cancer, or with nipple discharge or be picked up on screening as it is often associated with microcalcification (unifocal or widespread) on mammography (3). When carcinoma cells migrate along the ducts to the nipple they produce skin changes known as Pagets disease (3). Non-invasive lobular CIS is rarer and tends to be multifocal. Invasive ductal carcinoma is most common (70%), whereas invasive lobular carcinoma accounts for 10-15% of breast cancer (2). Medullary cancers (5%) tend to affect younger patients while colloid/mucoid (2%) tend to affect the elderly. Other cancers of the breast include papillary, tubular and adenoid-cystic (2).

Concluding examination: Further examination should be suggested if evidence of metastases by palpating liver for hepatomegaly, vertebrae for pain and auscutating the lungs (5).


Clinical features: History and Examination


The exact cause of breast cancer is not well understood. However, in addition to the risk factors outlined below, two genes have been identified: BRCA 1 and BRCA 2. 2% of women with breast cancer have the BRCA gene (3). A strong familial history along with germline mutation of these genes accounts for most cases of familial breast cancer and over half of ovarian cancers (4). BRCA genes are crucial for DNA repair. BRCA 1 and 2 proteins bind to the DNA repair enzyme Rad51 to make it functional in repairing DNA breaks. Mutations in the BRCA genes will lead to accumulation of unrepaired mutations in tumour suppressor genes and crucial oncogenes (4).

Classically on presentation the patient notices a painless lump. The size of the lump when first noticed does not give an accurate indication of how long it has been present. A lump may be found in the axilla if there are lymph gland metastases (3). The patient may notice a skin dimple (peau d’orange) caused by tethering. The nipple may become inverted, secrete discharge or even be destroyed. The breast may be noticed to be harder or have changed shape. Swelling of the arm caused by lymphatic or venous obstruction in the axilla is an uncommon but significant presentation (3). Backache, caused by secondary infiltration and collapse of lumbar vertebrae, with nerve root pains radiating down the back of the legs is a common symptom of advanced disseminated disease, but an uncommon mode of presentation as are respiratory symptoms from pleural effusions or malignant infiltration (3). A cerebral metastasis may cause a fit and a pathological fracture may be the first indication of the presence of disease. Interestingly the general symptoms commonly associated with cancer such as malaise, weight loss and cachexia are rare in patients with breast cancer (3).

Depends on the stage of the cancer. Stage 1: confined to the breast, mobile. Stage 2: growth confined to the breast, mobile, LNs in ipsilateral axilla. Stage 3: Tumour fixed to muscle (but not chest wall), ipsilateral LNs matted and may be fixed, skin involvement larger than tumour. Stage 4: complete fixation of tumour to chest wall, distant metastases (2).

Definition Breast cancer consists of cancer that forms in tissues of the breast, usually the ducts (tubes that carry milk to the nipple) and lobules (glands that make milk). It occurs in both men and women, although male breast cancer is rare(1).

Epidemiology - Breast cancer affects 1 in 11 women. - Incidence: 20,000 new cases/yr in the UK and increasing. - Rare in men (1%) of all breast cancers (2).

Risk Factors The primary risk factors for breast cancer are: female sex, age, family history, and uninterrupted oestrogen exposure, hence: nulliparity, first pregnancy > 30 yrs old, early menarche, late menopause, HRT, obesity, BRCA genes, not breast feeding, the pill and past breast cancer (metachronous rate = 2%, synchronous rate = 1%) (2).

Pathophysiology Cancer of the breast is adenocarcinoma and the commonest cancer in women. There are many microscopic varieties and histological types (3). A particular feature is the variable quantity of fibrous tissue that surrounds the cancer cells. Sometimes 90% of the mass is fibrous tissue, with just a few cancer cells scattered throughout it, while at the other end of the spectrum is the cancer with no fibrous reaction (3). This variety may be so cellular, vascular and fast growing that it is clinically indistinguishable from acute inflammation. In a proportion of cases the malignant cells remain inside the ducts and there is no invasive element (3). .

Examination: Introduction: Patient should be initially sitting at 45o and exposed from the waist up and be asked if they require a chaperone. Inspection: Any asymmetry, nipple changes (retraction, discharge), skin dimpling, local depression and oedema. Then inspect::with her arms resting down by her sides, above her head and then with her arms pressing into her hips (tensing the pectoral muscles)(5). Palpation: Ask if breasts are painful and if patient has noticed a lump. Both breasts are palpated, starting with the normal breast and using the flat of the fingers (5). Assessing for breast lumps: palpate the breast using the standard ‘zig zag’ technique across each quadrant and the nipple. Assessing axillary lymph nodes (LNs): axilla palpated fully for any LNs. Repeated on both sides. Also cervical, supra and infraclavicular LNs are also examined (5).

Investigations All lumps should undergo triple assessment: 1. History and clinical examination. 2. Radiology: ultrasound (US) < 35 yrs; mammograph and US for > 35 3. Histology/cytology (FNA or core biopsy, US-guided core biopsy is best for new lumps) (2).

For stage 1 and 2 cancers: Surgery: wide local excision (WLE) or mastectomy ± breast reconstruction and axillary node sampling or surgical clearance. Radiotherapy: if at high risk of local recurrence, post op radiotherapy reduces local recurrence and may increase overall survival. Chemotherapy: improves survival especially if younger and node +ve, in recurrent disease or a neoadjuvant if large tumour e.g.. epirubicin+ 5FU+cyclophosphamide+docetaxel are used. Endocrine agents: aim to decrease oestrogen activity and is used in oestrogen receptor (ER) or progesterone receptor (PR) +ve disease. The ER blocker tamoxifen is widely used. Aromatase inhibitors targeting oestrogen synthesis are also used (2). For stage 3-4 (distant disease): Assess LFT, Ca2+, CXR, skeletal survey, bone scan, CT/MRI or PET-CT, liver US, DXT to painful bony lesions, bisphosphonates may reduce pain and fracture risk. Tamoxifen is often used in ER+ve, if relapse consider chemotherapy. Tumours positive for HER-2 protein metastasising to brain may respond to monclonal antibody Trastuzumab (Herceptin) (2).

Prognosis Depends on the tumour size, grade, LN status, ER/PR status and vascular invasion (2). Deaths from breast cancer are now at their lowest ever in 40 yrs. Prognosis is best for those with cancers that are small and have not spread. More cancers are being diagnosed and treated early due to screening with women in the UK aged between 50-70 yrs having mammography every 3 yrs (6).

Vascular Surgery

Acute Ischaemia of the Lower Limbs Vanessa Jonga, 4th Year Medical Student (2011) Epsom & St Helier University Hospitals NHS Trust


Venous Disorders of the Lower Limb Sophia Broderick, 4th Year Medical Student (2012) Epsom & St Helier University Hospitals NHS Trust Varicose VaricoseVeins Veinsare areabnormally abnormallydilated dilatedand andlengthened lengthenedveins. veins. ItItisisvery verycommon commonand andprevalence prevalenceincreases increaseswith withage. age. Aetiology Aetiology Structural Structuraldefects defects such suchas asincompetent incompetentvalves, valves,on onthe thevein vein wall, wall,causes causes dilatation dilatationininresponse responsetotoincreased increasedvenous venous pressure pressurebecause becauseofofbipedal bipedalpostures posturesand andother otherfactors. factors. Clinical Clinicalfeatures features •Majority are •Majority areAsymptomatic Asymptomatic •Discolouration •Discolourationand andcosmetic cosmeticchanges changesnear nearthe theaffected affectedveins veins •Aching and heavy legs •Aching and heavy legs •May •Maydevelop developthe thecomplications complications ofofChronic Chronicvenous venous insufficiency insufficiencysuch suchas asulcers, ulcers,haemorrhage haemorrhageand and thrombophlebitis thrombophlebitis •Percussion •Percussionover overaavarix varixwhilst whilstpalpating palpating atataalower level to trace the lower level to trace thepattern pattern •The •TheTrendelenberg Trendelenbergtest test Investigations Investigations •Hand •Handheld helddopler doplerprobe probe •Duplex •Duplexultrasound ultrasound •Contrast •Contrastvenography venography

Chronic Chronicvenous venousinsufficiency insufficiency(CVI) (CVI)isisthe thefunctional functional changes changesthat thatoccur occurininthe thelower lowerextremity extremitybecause becauseofof venous venoushypertension. hypertension. Aetiology Aetiology Chronic Chronicvalvular valvularreflux refluxdue duetotovalvular valvularincompetence incompetenceoror venous obstruction or a combination of venous obstruction or a combination ofboth bothleads leadstotoaa chronic increase in venous pressure. Congenital chronic increase in venous pressure. Congenitalabsence absence ofofvenous venousvalves valvesisisaaless lesscommon commoncause. cause.Previous Previoushistory history ofofulceration, ulceration,varicose varicoseveins, veins,surgery surgerytotothe thelegs, legs,abdomen abdomen and andpelvis pelvisand andrecurrent recurrentDVT DVTare areimportant importantrisk riskfactors factors. . Clinical Clinicalfeatures features •Malleolar •Malleolarflare flareofofankle ankle •Hyperpigmentation •Hyperpigmentation •Lipodermatosclerosis •Lipodermatosclerosis(severe) (severe) •Atrophie (severe) •Atrophieblanche blanche (severe) •Venous •Venousulcers ulcers •Dry •Dryscaly scalyeczematous eczematousskin skin Investigations Investigations •Duplex •Duplexultra ultrasound soundimaging imagingtotodefine definethe thenature natureand and distribution distributionofofvenous venousdisease disease •Ascending •Ascendingphlebography phlebography •Computed •Computedtomography tomographyand andmagnetic magneticresonance resonance venography venography

Management Management Conservative Conservativetreatment treatment such suchas aselastic elasticsupport supporthose, hose,weight weightreduction reductionand andavoidance avoidanceofofconstricting constrictinggarments garmentsand andprolonged prolonged standing . Compression therapy with graded compression stockings is the mainstay of conservative treatment. Importantly, standing . Compression therapy with graded compression stockings is the mainstay of conservative treatment. Importantly, arterial arterialdisease diseaseshould shouldbe beexcluded excludedbefore beforecompression compressiontherapy. therapy. Sclerotherapy Sclerotherapywhere whereaaliquid liquidsclerosant sclerosantisisinjected injectedinto intothe theaffected affectedvein veincausing causingaainflammatory inflammatoryreaction reactionwhich whicheventually eventuallyleads leads totoscarring scarringand andobliteration obliterationofofthe thevaricosity. varicosity.This Thisisismostly mostlyused usedfor forsuperfitial superfitialvaricosities varicositiesbelow belowthe theknee knee Surgical Surgicaltreatment treatmentwhere where the theterminal terminalbranches branchesofofthe thegreat greatsaphenous saphenousvein veinare areindividually individuallyligated ligatedand anddivided. divided.Ultrasound Ultrasound guided guidedfoam foamsclerotherapy sclerotherapyisisan analternative alternativetotosurgery surgery Other Other treatments treatmentsinclude include Radio Radiofrequency frequencyobliteration obliterationofofthe theLong Longsaphenous saphenousvein veinororShort Shortsaphenous saphenousvein vein and and Endovenous Endovenous laser treatment where an ultrasound guided laser fibre optic is used to heat the vein which obliterates the endothelium laser treatment where an ultrasound guided laser fibre optic is used to heat the vein which obliterates the endotheliumleading leadingtoto the vein to thrombose. the vein to thrombose.

Venous Venousthromboembolism thromboembolism/Deep /Deepvein veinthrombosis thrombosis Deep Deepvein veinthrombosis thrombosisdevelops developswhen whenaathrombus thrombuseither either arises arisesspontaneously spontaneouslyororisiscaused causedby byclinical clinicalconditions conditions including includingsurgery, surgery,trauma, trauma,ororprolonged prolongedbed bedrest. rest. Risk Riskfactors factors •Pregnancy •Pregnancy •Age •Age>>60 60years years •Previous •PreviousDVT DVT •Immobility •Immobility- -Surgery/Trauma Surgery/Trauma/Obesity /Obesity(BMI (BMI>>30) 30) •Varicose •Varicoseveins veins •Thrombophaelia •Thrombophaelia •OCP, •OCP,HRT HRT •Malignancy •Malignancy •One •Oneorormore moresignificant significantmedical medicalco comorbidities morbidities Clinical Clinicalfeatures features •Painful •Painfulswollen swollenleg leg •Calf •Calfwarmth, warmth,tenderness tendernessand anderythema erythema •Pitting •Pittingoedema oedema •Tenderness •Tendernessalong alongthe thedistribution distributionofofthe thedeep deepvein veinsystem system Investigations Investigations Pre Pretest testclinical clinicalprobability probabilityscore score&&D-dimer D-dimerlevels levels. .D-dimer D-dimer by itself is not accurate enough however in conjunction by itself is not accurate enough however in conjunctionwith withaa risk riskassessment assessmentisiseffective. effective. Imagine Imaginetechniques techniques Compression CompressionUltrasonography Ultrasonography Contrast ContrastVenography Venography(gold (goldstandard) standard) Management Management Stockings Stockings LMWH/Warfarin LMWH/Warfarin Thrombolysis Thrombolysis Thrombectomy Thrombectomy Vena Venacava cavafilter filter Primary Primaryprevention prevention •Low-molecular-weight •Low-molecular-weightheparin heparinfollowed followedby byvitamin vitaminKK antagonists antagonistsprior priortotosurgery, surgery, •Indefinite •Indefiniteanticoagulation anticoagulationfor forthose thosewith withrecurrent recurrentDVTs DVTsoror long term risk of DVT. long term risk of DVT.


Acute Cystitis & Acute Pyelonephritis Staci Boston, 4th Year Medical Student (2012) & St Helier University Hospitals NHS Trust Epsom

Acute Pyelonephritis:

Acute Cystitis Acute Cystitis:

•Infection of the urinary bladder. •Most common urinary tract infection (UTI) •Accounts for 3% of general practice consultations

Acute Pyelonephritis:

Management of suspected UTI:


Dipstick urine: +ve leucocytes and +ve nitrates are indicative of an UTI

Risk factors:

Urine culture and Microscopy (MC&S): >10 bacterial/mL + >100 WCC/µL = active bacterial infection ↓ Treat with empirical antibiotics: (Trimethoprim 200mg/12hrs PO or nitrofurantroin) for 3- 6 days and increase fluid intake whilst awaiting results of MC&S ↓ Modify antibiotics based on sensitivities 5

•Increasing age •Female sex (5:1) – shorter urethra in females •Sexually active •↓ host defence (immunocompromised, DM) •Pregnancy •Menopause •Urinary tract: Obstruction, retention, stones, catheter, malformation


Simple bacterial UTI is usually the result of bacteria ascending through the urethra from the perineum. Most common infecting organisms include: •E.Coli (80%) •Staphylococcus saprophyticus •Proteus mirabilis Rarer causes include: •Enterococcus faecalis •Klebsiella; •Enterobacter and Acinetobacter species • Pseudomonas aeruginosa •Candida albicans •Staph. Aureus

Initial investigations:

Fig 1

If recurrent/relapsing infection in women or men further investigation is needed: •Investigate renal function: Creatinine •Look for urinary tract abnormalities: Renal tract ultrasound, IVU, Cystoscopy. •Diabetes: glucose

Fig 2

Acute uncomplicated pyelonephritis most often develops as a result of: •An ascending UTI: Pathogens (most commonly E.Coli) first colonise the distal urethra and then ascend via the bladder and ureters to the kidney; thus, symptoms of cystitis often precede acute pyelonephritis. Obstruction: as a result of any cause (e.g., calculi, tumour, foreign body, BPH, or neurogenic bladder) may cause pyelonephritis • Prostatitis and BPH: These conditions may cause a urethral obstruction leading to bacteriuria and consequently pyelonephritis •Bacteraemia: Which may cause haematogenous seeding of the kidneys. Complications from pyelonephritis include renal abscess development.

Clinical features:

•High fever •Rigors •Vomiting •Loin pain and tenderness •Oligouria (if acute renal failure) •Features of cystitis, prostatis or BPH


•Urinalysis: WBCs ≥10/HPF; RBCs ≥5/HPF) •MSU: (pyuria - ≥10,000 CFU/mL, bacteruria ,micro/macroscopic haematuria) •Blood cultures: Bacteraemia is abnormal. •Renal Ultrasound : gross structural abnormalities; hydronephrosis; stones; perirenal fluid collections. •Gross abdominal film: An abdominal KUB may identify radio opaque calculi. •Contrast helical CT scan: The test of choice in adults and children when disease complications are suspected e.g. altered renal parenchymal perfusion, perinephric fluid.

Clinical features: •Dysuria •Frequency •Urgency •Suprapubic pain •Haematuria •Fever •Rigors •Foul smelling urine

A severe infectious inflammatory disease of the renal parenchyma, calices, and pelvis.


•Intravenous fluids •Antibiotics •Percutaneous or surgical drainage for renal abscess. Image 1: Contrast enhanced axial CT scan of the kidneys showing an enlargement of the right kidney and inflammatory stranding surrounding the kidney. Image 2: This Abdominal X-ray (KUB) demonstrates pyelonephritis of the right kidney.

Benign Prostatic Hyperplasia Vanessa Jonga, 4th Year Medical Student Epsom & St Helier University Hospitals NHS Trust


Outflow problems (BOO) (bladder normal)

Obstructive Sx - hesitancy - intermittency - straining - poor weak stream - terminal dribbling - incomplete bladder emptying - acute urinary retention 2. Detrusor instability / irritability problems (bladder - hypertophied, trabeculated, thickened) Irritative Sx - urgency (&urge incontinence) - frequency - nocturia - dysuria 3. Bladder failure problems (bladder - atonic, weak, insensitive, dilated) Stasis (chronic retention) Sx - overflow incontinence (leakage) - cystitis and ureteritis - renal complications - hydronephrosis - uraemia neurogenic bladder - stones UTI & prostatitis - pyelonephritis

ca prostate occ urs in str om al cell s

by 5-Îą-reductase

stromal cell

nodules formed

Differentials of obstructive urinary symptoms

ca bladder

bladder calculi


Urethral stricture/ atresia

Bladder neck contracture


Renal & Ureteric Tract Calculi Myriam Guessom, Grethe Goss Nielsen and Davina Cavallaro 4 th Year Medical Students (2010/11) Epsom & St Helier University Hospitals NHS Trust Aetiology & Pathophysiology Calcium (80%) • Precipitated with oxalate, phosphate or mixed • Tend to occur in hypercalciuric patients such as hyperparathyroidism, however the occurrence of calcium stones seems to be more related to ingestion of oxalate which plays a bigger role in the precipitation of solutes • Oxalates are found in high concentrations in strawberries, rhubarb and spinach Struvite (10-15%) • NH4MgPO4·6H2O, most often in the presence of infection by ureasplitting bacteria, which increase the pH: Proteus, Pseudomonas, Klebsiella • These stones are commonly observed in people who have factors which predispose them to UTIs owing to urinary stasis 1. spinal cord injury and other neurogenic bladder 2. ileal conduit urinary diversion 3. vesicoureteral reflux 4. obstructive uropathies • Such stones can grow rapidly, forming calyceal staghorn calculi (see picture) Uric Acid (5-10%) • Breakdown product of Purine • Low urine pH is the major determination of uric acid stone formation Cystine (rare) • Usually reabsorbed in the kidney • AR disorder reduces reabsorption promoting stone formation

Epidemiology • Renal stones are common, being present at some time in 1 in 10 of the population • The annual incidence is about 1-2 cases per 1,000 • Men are more commonly affected at of 3:1 • The peak age for developing stones is between 30 and 50, and recurrence is common

Definition Crystallisation occurring in the renal tract owing to a supersaturation of solute in the urine

Management • • •

Pain management + observation → IM diclofenac or pethidine Antibiotics and antiemetics if needed Spontaneous passage of stone depends on size of stone. < 0.5 cm → pass down ureter

Treatment is necessary if: - Stone becomes fixed → hydroureter and hydronephrosis - Infection in urine - Increasing pain and fever

Staghorn calculus

Presentation Principal symptoms – pain and haematuria The pain depends on the site of the stone: • Renal stone → dull ache in the loin • Stone in ureter → ureteric colic, moving down along the line of the ureter as the stone makes it way to the bladder • No position relieves the pain • Haematuria, usually microscopic but can be macroscopic • Nausea and vomiting

Surgical management: • Extracorporeal shock wave lithotripsy (ESWL) - shock waves are directed over the stone to break it apart. The stone particles will then pass spontaneously • Percutaneous nephrolithotomy – needle guided through back directly into the kidney → nephroscope using ultrasonic or laser probe to break up the stones → stones are suctioned out with the scope. Used for large stones (>2 cm), staghorn calculi and also cystine stones. • Ureteroscopy – scope passed through ureter. Laser are used to break up larger stones • Open surgery - rarely necessary and usually reserved for complicated cases e.g. multiple stones. < than 10% of total renal function

Investigations and diagnosis • • • • • • • • • •

Plain X-ray, IVU Urine – MC&S- red blood cells, bacteria, leukocytes, urinary casts and crystals Routine bloods - renal function Recurrent calculi – screen for: Hyperparathyroidism →↑ calcium Idiopathic hypercalciuria - ↑ gut Ca2+ absorption + ↓ renal Ca2+ reabsorption + loss of Ca2+ from bones Cystinuria – excessive excretion of the amino acid cystine Serum calcium, phosphate, oxalate and uric acid 24 hour urine collection to measure total daily urinary volume, magnesium, sodium, uric acid, calcium, citrate, oxalate and phosphate Analysis of passed or removed stones

Prevention • • • •

Increase fluid intake to 2-3 litres per day. Reduce salt intake. Reduce the amount of meat and animal protein eaten. Reduce oxalate intake (foods rich in oxalate include chocolate, rhubarb, nuts) and urate-rich foods (e.g. offal and certain fish). • Drink regular cranberry juice: increases citrate excretion and reduces oxalate and phosphate excretion.

Common Conditions of the Scrotum and Testes Rhiannon Chapman and Kate Kendrick, 3rd Year Medical Students Epsom & St Helier University Hospitals NHS Trust

Undescended testes


Testes that have stopped short of the scrotum during descent (anywhere between the abdominal cavity and top of the scrotum.) Occurs in 2% of males, and is more commonly unilateral. Treatment is with surgical correction at 2 years to allow normal spermatogenesis.

Excessive collection of serous fluid in the processus vaginalis. Primarytransluminable & difficult to feel. Secondary- smaller and due to exudate following cancer or inflammation. Do not treat in infants, but remove if they persist beyond 1 year. For adults. rule out cancer and aspirate. Surgery can be performed if recurrence occurs.

Epididymal cyst


Degeneration of the epididymal or para-epididymal structure. Typically multiple, bilateral, fluctuant and translucent swellings of the scrotum. Palpable and separate from the testes. Treatment is to remove surgically if symptomatic.

Tumour Two types- seminomatous (semniferous tubules) and non-seminomatous (usually teratoma from totipotent germ cells.) May spread to lymph nodes and then systemically to liver and lungs. Presents as a painless lump in the testes, or as metastases. Measurement of tumour markers α fetoprotein and βHCG are useful. Ultrasound, CT and CXR can be used to confirm metastases. Treat with surgical excision and radio or chemotherapy. Prognosis is good, 5 year survival rate- 98%.

Varicosities in the veins draining the testes. Can be secondary to other pathology. Produces dragging sensation in the scrotum and subfertility due to decreased spermatogenesis. On standing position, feels like a ‘bag of worms.’ Treatment is to reassure, but radiological embolisation of the testicular vein can be performed.

Torsion Torsion of the spermatic cord due to a congenital abnormality. Irreversible infarction occurs in hours unless treated. Causes pain in groin and lower abdomen, with vomiting. Examination reveals a swollen, high lying painful testis. Repair surgically, fixing the healthy testis too as a similar congenital abnormality may lead to further torsion.

Renal Cell Carcinoma Timothy Cooper Epsom & St Helier University Hospitals NHS Trust Clinical Presentation5


Staging – TNM9,10

Renal cell carcinoma (RCC) arises from the renal parenchyma or cortex. It accounts for 85% of all renal cancers

Risk Factors2

Investigations and likely results7

T1: tumour <7 cm in greatest dimension, limited to the kidney. T2: tumour >7 cm in greatest dimension, limited to the kidney. T3: tumour extends into major veins or perinephric tissues, but not into the ipsilateral adrenal gland and not beyond Gerota's fascia T4: tumour invades beyond Gerota's fascia (including contiguous extension into the ipsilateral adrenal gland). N0 – no regional lymph nodes N1 – Single lymph node metastasis N2 – > 1 regional lymph node

Epidemiology3 Most common renal tumour in adults Average age of presentation is 55yrs ♂:♀ = 2:1 15% of haemodialysis patients develop RCC

M0 – no distant metastasis M1 – distant metastasis


Radiology – Papillary RCC seen on CT8

Smoking is the most well established risk factor for RCC No clear evidence to suggest any other known aetiological agents There is a clear genetic predisposition to RCC, demonstrated by the strong association with VHL and increase in risk with a positive family history (4)

Management 11


RCC Stage 3 •Surgical candidate – Surgery •Non-surgical candidate – Palliative radiotherapy

Clear cell RCC is the most common histological type. Mutation of the tumour suppressor gene on chromosome 3p is likely responsible. Very vascular and microscopically composed of large cells containing clear cytoplasm

RCC Stage 1 or 2 •Surgical candidate – Surgery / local ablation therapy •Non-surgical candidate; <3cm and slow-growing – surveillance •Non-surgical candidate; ≥3cm and fast-growing - surveillance + palliative radiotherapy

RCC Stage 4 (metastatic disease) •Targeted molecular therapy e.g tyrosine kinase inhibitors (sunitinib) or mTOR inhibitors (Temsirolimus) •Surgery •Bisphosphonate therapy for bone metastases

Prognosis12 5 year survival > 68% (stage dependant) 5 year survival for metastatic disease <10% Symptomatic presentations have a poorer prognosis

Transitional Cell Carcinomas Neelam Parmar and Jibran S Qureshi Epsom & St Helier University Hospitals NHS Trust Epidemiology •Most common urological malignancy •90% cases are transitional cell carcinoma •Incidence: 1 in 5000 •Peak age 50-70 years •M>F •Increased in Middle East and Industrialised areas Remaining 10% are SCC, adenocarcinoma or mixed/undifferentiated

Aetiology Environmental: •Exposure to carcinogens, especially in industrial work such as rubber, printing and petrochemicals. • Smokers 2-3x more likely to develop it • For squamous cell carcinomas – chronic cystitis, bladder stones, schistosomiasis due to prolonged inflammation. • Radiotherapy for pelvic tumours • Cyclophosphamide Genetic: • Polymorphisms of various cytochrome P450 –those that oxidise arylamines more rapidly are more prone to malignancy as this is first step of activation of carcinogens • Acetylator status – slower status gives an increased risk

Clinical Presentation (1) •Painless haematuria – painless haematuria in any persons >40 yrs is bladder cancer until proven otherwise •Recurrent UTI’s •Voiding irritability •Pelvic pain •Bone pain •Weight loss

IVU imaging (4)

Diagnosis (2) •Urine - Microscopy (cancer may cause sterile pyuria) - Cytology •Cystoscopy – biopsy is diagnostic •Intavenous Urogram – filling defect in the tract •CT/MRI – staging •Bimanual examination under anaesthetic – staging

Grade Histology is important for prognosis: •1 – differentiated (better prognosis) •2 – intermediate •3 – poorly differentiated (worse prognosis)

Staging – TNM


Tis - Transitional cell carcinoma in situ


Ta - non-invasive papillary carcinoma

Filling defect within the bladder (2,5)

Tis/Ta/T1 (superficial bladder cancers) •Diathermy via transurethral cystoscopy (Transurethral resection of bladder tumour) •Intravesical chemotherapy (mitomycin C) for multiple small or ↑ grade tumours and to ↓ recurrence •Intravesical BCG – stimulates a non specific immune response used for ↑ grade tumours and Tis used to ↓ recurrence -Complications of dissemniated BCG infection therefore TB treatment may be required •Intravesical glycine – not toxic

T2/T3 (invasive bladder cancers) •Radical cystectomy ‘gold standard’ with formation of ileal conduit (stoma) -procedure whereby all of the bladder is removed as well as near-by lymph nodes, part of the urethra, the prostate (in men), and the cervix and womb (in women) •Radiotherapy (worse 5yr survival than with radical cystectomy surgery alone) •Salvage cystectomy (if radiotherapy fails) •Post-op chemo is toxic but effective (methotrexate, Vinblastine, Adriamycin and cisplatin)

• Lack of Glutathione S transferase M1 (GSTM1) allele – twice the risk of bladder cancer than those with one or both alleles.

Pathophysiology In most cases: •Carcinogens excreted in high concentration in urine.

T4 (invasion into nearby structures)

• Bladder and ureter epithelium become exposed. • “Field changes” to whole of urothelium from renal pelvis to urethra • Leads to multiple and recurrent tumours. Adenocarcinoma arises from urachal remnants in the dome of bladder

Cystoscopy imaging (4)

How bladder cancer spreads

•Usually palliative •chemotherapy and radiotherapy •Treat symptoms (this may include a cystectomy) •Long term catheter •Urinary diversions to relieve pain

Bladder  pelvic structures and lymphatic  iliac and para –aortic lymph nodes blood stream liver and lungs

Prostate Cancer Hannah Bowles, 4th Year Medical Student (2012) Epsom & St Helier University Hospitals NHS Trust NICE recommends using three classification systems (9):

Introduction Prostate cancer is a malignant tumour of glandular origin, situated in the prostate gland (1). 7% of all male cancers are prostate cancer (2) and it is the second most common cause of cancer related death in men in the UK (3). It is uncommon below the age of 50 years but after that the numbers of cases increase greatly with age (4) and therefore the desire to detect and treat prostate cancer early is increasing with an ever ageing population and the resulting increase in risk of this cancer.

1)TNM Classification • T=Tumour. T1 – Clinically unapparent, not detected by PR or imaging. T2 – Confined within prostate. T3 – Extends through prostatic capsule. T4 – Invasive tumour. (See Figure 2)

The zonal development of the cancer also influences where it may spread. Cancer in the transitional zone may spread to the bladder neck, and in the peripheral zone to the ejaculatory ducts and seminal vesicles (5).

•N=Node. N0 – No regional lymph node involvement regional lymph node metastasis. Figure 1: Zones of the prostate (1)


Clinical Presentation • Nocturia (1)

. N1 – Regional lymph N1 Figure 2: T1, T2, T3 (10)

•M=Metastasis. M0 – No metastasis. M1a – non regional lymph nodes, b – bone, c – other sites. 2) Gleason Score

• Increasing age

• Dysuria (1)

Used to classify the pattern of tumour growths found in prostate biopsies where 10-12 cores are taken from different parts of the gland. They are then graded from 3 (least aggressive) to 5 (most aggressive) and the Gleason score is the sum of the two most common patterns of growth so it can range from 6-10 (9).

• Family History, also likely to present earlier e.g. BRCA-2 mutations (5)

• Abnormal PR examination

3) Prognostic Risk Grouping

• Haematuria (1)

Using PSA level, Gleason score and clinical stage men are grouped into a category of low, intermediate or high risk (8), see Table 1.

Greatly unknown, but some risk factors have been identified:

• Obesity (6) • High animal fat diet (6) • Hormones may play a role (5) •Those of sub saharan African ancestry have greater risk whilst those of Asian ancestry have a lower risk (7) • Decreased exposure to sunlight and Vitamin D (7)


• Urinary frequency and hesitancy (1)

• Bone pain from metastases • Systemic symptoms e.g. weight loss, anorexia, lethargy (1)

There is no UK screening programme for prostate cancer however there is currently a risk management programme allowing men who wish to be screened to do so using the PSA test (3).

Like other cancers it forms when mutations occur in genes which control cell growth leading to increased cell proliferation and decreased cell death. Such genes involved are p53 and retinoblastoma gene (5).

The PSA test is the best method currently available for identifying localised prostate cancer (3) and is a simple blood test (Normal range 0-4 ng/ml). However 25% of men with prostate cancer will have normal PSA levels so a rectal examination should always be performed as well (1).

95% are adenocarcinomas, 4% have transitional cell morphology (may arise from the urothelial lining of the prostatic urethra), less than 1% are squamous cell carcinomas (5).

PSA testing can be used after cancer treatment to monitor possible recurrence.

The prostate is divided into three different zones (see Figure 1) and cancer development varies between them: • Peripheral zone – 70% cancers (5) • Central zone – 15-20% cancers (5) • Transitional zone – 10-15% cancers (5).

Table 1: Prognostic Risk Groups (8)

Prostate Specific Antigen (PSA)

Staging – TNM Depending on the clinical findings and the results of tests carried out it may be decided that a biopsy is necessary. NICE do not recommend that every suspected cancer is biopsied as men with clinically insignificant cancer are unlikely to benefit from this (8).

Management All patients should be assigned a risk category by a urological MDT (8). Active surveillance can be considered for men in both low and intermediate risk groups whereby they are continuously monitored so only those needing radical treatment go on to receive it. In localised disease radical treatment involves radical prostatectomy or radiotherapy (8) and is offered to those in the intermediate and high risk groups if it is thought this treatment would be beneficial. Brachytherapy is also an option in the low and intermediate risk groups where radioactive sources are implanted transperineally into the prostate gland (1). In locally advanced disease there are two options: radical radiotherapy with (neo)adjuvant hormone therapy or hormone therapy alone (8). Overall prognosis is good for lower risk cancers, hence why it is important to identify cases early so management can be initiated.



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Nutrition 1. 2. 3.

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