Pradip K Datta MBE, MS, FRCS (Ed, Eng, Irel, Glasg), Honorary Consultant Surgeon, Caithness General Hospital, Wick, Member of Council and College Tutor, Royal College of Surgeons of Edinburgh
Christopher J K Bulstrode MCh, FRCS (Orth), Professor and Honorary Consultant Trauma and Orthopaedic Surgeon, University of Oxford, Member of Council, Royal College of Surgeons of Edinburgh
B V Praveen MS, FRCS (Ed, Eng, Glasg, Irel, Gen), Consultant Surgeon and Associate Director of Medical Education, Southend University Hospital, Honorary Senior Lecturer, Queen Mary, University of London
First published in Great Britain in 2010 by Hodder Arnold, an imprint of Hodder Education, part of Hachette UK, 338 Euston Road, London NW1 3BH
All rights reserved. Apart from any use permitted under UK copyright law, this publication may only be reproduced, stored or transmitted, in any form, or by any means with prior permission in writing of the publishers or in the case of reprographic production in accordance with the terms of licences issued by the Copyright Licensing Agency. In the United Kingdom such licences are issued by the Copyright Licensing Agency: Saffron House, 6—10 Kirby Street, London EC1N 8TS.
Whilst the advice and information in this book are believed to be true and accurate at the date of going to press, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. In particular, (but without limiting the generality of the preceding disclaimer) every effort has been made to check drug dosages; however it is still possible that errors have been missed. Furthermore, dosage schedules are constantly being revised and new side-effects recognized. For these reasons the reader is strongly urged to consult the drug companies’ printed instructions before administering any of the drugs recommended in this book.
British Library Cataloguing in Publication Data
A catalogue record for this book is available from the British Library
Library of Congress Cataloging-in-Publication Data
A catalog record for this book is available from the Library of Congress
ISBN 978-0-340-98580-9
1 2 3 4 5 6 7 8 9 10
Commissioning Editor: Gavin Jamieson
Project Editor: Francesca Naish
Production Controller: Joanna Walker
Cover Design: Helen Townson
Indexer: Laurence Errington
Typeset in 9.5/11.5 Formata Light Condensed by MPS Limited, A Macmillan Company. Printed and bound in India by Replika Press
What do you think about this book? Or any other Hodder Arnold title? Please visit our website: www.hodderarnold.com
Foreword
This innovative companion volume will certainly be considered as an essential complement to Bailey & Love’s Short Practice of Surgery. The authors and contributors have recognised the fundamental changes that have occurred in surgical training and assessment where greater knowledge must be acquired in a shorter period of time, not only to ensure success in examinations but also to provide the comprehensive foundations on which to build clinical expertise. The Silver Jubilee edition of Bailey & Love in 2008 emphasised its enduring importance for generations of surgeons internationally. MCQs and EMQs in Surgery will define the indispensable elements for today’s surgical practitioners.
John D Orr, FRCS (Ed)
Contributors
Sanjay De Bakshi MS FRCS (Eng & Ed)
Consultant Surgeon, Calcutta Medical Research Institute (CMRI), Kolkata, India
Brian W Fleck FRCS (Ed), MD Consultant Ophthalmic Surgeon, Princess Alexandra Eye Pavilion and Royal Hospital for Sick Children, Edinburgh
Professor Pawanindra Lal MS DNB MNAMS FRCS (Ed & Eng)
Professor of Surgery, Maulana Azad Medical College, New Delhi, India
Professor Peter McCollum MCh, FRCS (Ed), FRCSI Professor of Vascular Surgery, Hull/York Medical School
John C McGregor BSc (Hons) MBChB (with commendation) FRCS, FRCS (Edin)
Former Consultant in Plastic, Reconstructive and Cosmetic Surgery, St John’s Hospital, West Lothian
Lynn Myles BSc (Hons), MB ChB, MD, FRCS (SN)
Consultant Neurosurgeon, Department of Clinical Neurosciences, Western General Hospital, Edinburgh
Dumbor L Ngaage MB BS FRCS (Ed), FWACS, FRCS (C-Th), FETCS (Cardiovascular), FETCS (Thoracic), MS
Specialist Registrar in Cardiothoracic Surgery, Castle Hill Hospital, Hull. Honorary Clinical Tutor, Hull York Medical School, Universities of Hull & York
Iain J. Nixon MBChB FRCS (Edin.) Specialist Registrar in Otolaryngology
Head and Neck Surgery, West of Scotland Rotation. Clinical Research Fellow, Memorial Sloan Kettering Cancer Center, New York, USA
Charles S Perkins FDSRCS, FFDRCSI, FRCS
Consultant Oral and Maxillofacial Surgeon, Gloucestershire Royal and Cheltenham General Hospitals, Gloucestershire
Nandini P Rao, MRCP, Msc
Specialist Registrar in Chemical Pathology/Metabolic Medicine, Royal Free Hospital, London
Professor N R Webster MB ChB PhD FRCA FRCP FRCS Institute of Medical Sciences, Foresterhill, Aberdeen
Preface
First published in 1932, Bailey & Love’s Short Practice of Surgery has stood the test of time. Perhaps this is an understatement, considering that all three of us have used the book as medical students! This book has been the result of good foresight on the part of Hodder Arnold to keep up with the changing trends in the pattern of surgical examinations, both at undergraduate and postgraduate levels. The publishers should be congratulated in bringing out this book – converting the original Silver Jubilee (25th) edition – all 77 chapters of it – as Multiple Choice Questions (MCQs) and Extended Matching Questions (EMQs).
The book is aptly titled as a companion to Bailey & Love. We would therefore hope that the reader, specifically preparing for a written examination, would use this book as the major reading material, referring to the original for detailed elucidation of a particular point or operative detail.
Most of the contributors are different from Bailey & Love’s Short Practice of Surgery except for chapters 5, 25 the section on orthopaedics and part of trauma. Thus while retaining the essence of the original material, this book has been seasoned by different authors, thus giving it a fresh flavour without losing any of its original ingredients. We are grateful to all the contributors for their prompt response in spite of the pressures of work in the National Health Service.
The images and pictures are mostly different to those in the original book, giving this tome an added attraction. While the MCQs test knowledge, the EMQs with the illustrations give a good format for a self-assessment exercise. The chapters are specifically geared towards helping the reader with preparation for the written papers of the MRCS and FRCS(Gen) examinations. The undergraduate will also find this book equally stimulating for the same reasons. In surgical examinations in the English-speaking world, where essays have been replaced by shortanswer questions (short notes of yesteryear), the reader will find the EMQs ideal preparation.
Any book must be dynamic, much more so a new venture such as this. It was said in the preface of the parent book, “Whereas the past informs the present, it must never enslave the future.” As authors of this very exciting project we can stay true to the spirit of this statement only with help from you – our readers. Therefore we look forward to your suggestions and constructive criticisms for the next edition.
Pradip K Datta
Christopher J K Bulstrode
B V Praveen November 2009
Acknowledgements
An email from Gavin Jamieson to one of us (PKD) was the inspiration behind this publication, he being the catalyst who set alight our enthusiasm to write this book. Thus to him we owe a huge debt of gratitude for getting this project off the ground. Indeed it is a tribute to all concerned that this book was published in just over a year since the idea was born as his brainchild.
All the contributors have done a tremendous job not only in producing comprehensive chapters but also delivering them on time – and this, in spite of the pressures of the present-day National Health Service; to them we are grateful. Francesca Naish, as editorial manager, has kept the team on track by liaising with us all on a regular basis, thus bringing our efforts to fruition. We give our thanks to her. To Jane Utting we are grateful for her meticulous proofreading. Thanks are also due to Adam Campbell for his efficient and prompt copy-editing.
We are very grateful to Mr John D Orr, immediate Past President of the Royal College of Surgeons of Edinburgh for writing the foreword. Finally, our great appreciation goes to our families (Swati, Sandip, Victoria, Harry, John-James, Jenny, Nandini and Prakruti) for their encouragement and support. We dedicate this book to them.
PKD
CJKB
BVP
List of Abbreviations Used
5-FU 5-fluorouracil
5-HIAA 5-hydroxyindoleacetic acid
AAAs abdominal aortic aneurysms
ABCD airways, breathing, circulation and disability
ABGs arterial blood gases
ACS abdominal compartment syndrome
ACTH adrenocorticotrophic hormone
ADH antidiuretic hormone
ADP adenosine diphosphate
AF atrial fibrillation
AFP alpha-fetoprotein
AIN anal intraepithelial neoplasia
ALG antilymphocytic globulin
ALP alkaline phosphatase
ALS antilymphocytic serum
ALT alanine transaminase
ANCA antineutrophil cytoplasmic antibodies
ANDI aberrations of normal development and involution
TNM classification of malignant tumours (tumour, nodes, metastasis)
TPN total parenteral nutrition
TPO thyroid peroxidase antibodies
TRUS transrectal ultrasound-guided biopsy
TSH thyroid-stimulating hormone
TURP transurethral resection of the prostate
U&E urea and electrolytes
UC ulcerative colitis
UICC Union Internationale Contre le Cancer
US ultrasound
UTI urinary tract infection
VAC vacuum-assisted closure
VATS video-assisted thoracoscopy
VP ventriculoperitoneal
VPC vapour pulse coagulation
WCC white cell count
WHO World Health Organization
Introduction
Bailey & Love’s Short Practice of Surgery celebrated the publication of its Silver Jubilee edition in 2008. It has certainly come a long way since the first edition was published in 1932. As authors of this book (CJKB being one of the editors of Bailey & Love), dare we say that the title of the book is a misnomer. It is anything but a ‘Short Text Book’. Editions of yesteryear consisted of some 1300 pages of single column text. The current edition consists of over 1500 pages, each containing a double column.
Arguably Bailey & Love is not just a text book. Many students and teachers of surgery the world over use it as a reference book too. Today both postgraduate and undergraduate examinations lay emphasis on knowledge rather than presentation and the nuances of essay writing. Thus for many years, the candidate’s test of theory knowledge in examinations has been based on Multiple Choice Questions (MCQs) and Extended Matching Questions (EMQs), sometimes supplemented by Single Best Answers (SBAs).
Therefore for the first time in this book, all 77 chapters of Bailey & Love have been converted into MCQs and EMQs. We, as authors, along with the other contributors, have reproduced the original text in this form of MCQs and EMQs. We hope that we have accurately mirrored the subject matter. Most of the images in this book are not from Bailey & Love, but are from the personal collection of one of the authors (PKD). We hope that this book will be useful for medical students studying surgery in the English-speaking world and for those doing MRCS and FRCS (Gen) examinations in the UK. As authors of the very first such undertaking, we would welcome suggestions for future editions from our readers.
This page intentionally left blank
1 The metabolic response to injury
Multiple choice questions
➜ Homeostasis
1. Which of the following statements about homeostasis are false?
A It is defined as a stable state of the normal body.
B The central nervous system, heart, lungs, kidneys and spleen are the essential organs that maintain homeostasis at a normal level.
C Elective surgery should cause little disturbance to homeostasis.
D Emergency surgery should cause little disturbance to homeostasis.
E Return to normal homeostasis after an operation would depend upon the presence of co-morbid conditions.
➜ Stress response
2. In stress response, which of the following statements are false?
A It is graded.
B Metabolism and nitrogen excretion are related to the degree of stress.
C In such a situation there are physiological, metabolic and immunological changes.
D The changes cannot be modified.
E The mediators to the integrated response are initiated by the pituitary.
➜ Mediators
3. Which of the following statements about mediators are true?
A They are neural, endocrine and inflammatory.
B Every endocrine gland plays an equal part.
C They produce a model of several phases.
D The phases occur over several days.
E They help in the process of repair.
➜ The recovery process
4. With regard to the recovery process, identify the statements that are true.
A All tissues are catabolic, resulting in repair at an equal pace.
B Catabolism results in muscle wasting.
C There is alteration in muscle protein breakdown.
D Hyperalimentation helps in recovery.
E There is insulin resistance.
➜ Optimal perioperative care
5. Which of the following statements are true for optimal perioperative care?
A Volume loss should be promptly treated by large intravenous (IV) infusions of fluid.
B Hypothermia and pain are to be avoided.
C Starvation needs to be combated.
D Avoid immobility.
E Helpful measures can be taken.
Answers: Multiple choice questions
➜ Homeostasis
1. D
The normal physiological state of the human body is referred to as homeostasis – a normal internal environment (the milieu intérieur of Claude Bernard). All the vital organs – the brain, heart, lungs, kidneys and, to a lesser extent, the spleen – play an important role in its maintenance. These organs are interdependent and thus help to maintain a normal fluid and acid–base balance.
In the elective situation, the patient is always optimised prior to any operation, thereby minimising the homeostatic disturbance. The extent of surgery also plays a part. Disturbance in the homeostasis to some degree occurs in emergency surgery; this depends upon the extent of injury, presence of sepsis and any ongoing insults. If the patient has co-morbid conditions, postoperatively the return to normal homeostasis would take longer than in those with no co-morbidity. In such cases, care in a high-dependency or intensive care unit (ICU) is essential.
➜ Stress response
2. D
The stress response is graded according to the injury inflicted. An elective operation in a fit patient, such as a laparoscopic cholecystectomy in a 30-year-old female, will elicit a minor transient stress response from which the patient recovers quite quickly. On the other hand, a severely injured patient of 70 will elicit a major response, requiring care in the ICU (see Fig. 1.1). There is an increase in metabolism and nitrogen excretion in direct proportion to the injury. There are immunological and metabolic changes which are reflected in the physiology – pyrexia, tachycardia and tachypnoea. The body’s innate defence mechanisms can combat mild stress, and return to normal physiology occurs very soon.
Stress response depends upon
Severity of injury Type of injury
To get speedy resolution avoid (‘SO’)
Secondary insults – 3 Is: Ischaemia
Infection
Inadequate oxygenation (hypoxia)
Ongoing trauma, e.g. compartment syndrome (abdominal/limb)
Figure 1 .1 Metabolic response to severe trauma.
In severe injury, the stress response can be modified by anticipating complications and preventing them by judicious management in an ICU, i.e. attention to nutrition and anticipation and prevention of secondary insults such as ischaemia, infection, hypoxia and compartment syndrome.
The pituitary gland, rightly referred to as ‘the leader in the endocrine orchestra’ (Sir Walter Langdon-Brown, 1931), sets in motion the entire synchronous response. The body will bring into play neural, endocrine and inflammatory responses. The neural response that initiates and acts in concert with the endocrines is referred to as the neuroendocrine response to trauma.
➜ Mediators
3. A, B, E
Stress from injury travels along afferent pathways of the spinal cord to the hypothalamus which secretes the corticotrophin-releasing factor (CRF) that acts on the pituitary to secrete adrenocorticotrophic hormone (ACTH) and growth hormone (GH). This creates the ‘flight or fight’ response. The pancreas increases glucagon secretion. Other endocrines, thyroid and gonads play a minor role. This concerted neuroendocrine response results in lipolysis, hepatic gluconeogenesis, protein breakdown, pyrexia and hypermetabolism. Cytokines, interleukins (IL-1, IL-6) and tumour necrosis factor-alpha (TNF ) are simultaneously released (see Fig. 1.2).
Catecholamine-mediated ‘fight or flight’ response
Adrenal medulla
Adrenaline
Hypothalamus
Noradrenaline from peripheral nerves
Neurohormonal response
Cytokines
Inflammatory response
Cortisol-releasing hormone (CRH)
Anterior pituitary
Adrenocorticotrophic hormone
Cortisol and glucocorticoids
Stress response to injury
Figure 1.2 Neuroendocrine response to trauma.
A model of two phases, ‘ebb and flow’, is created. The term was coined by Sir David Cuthbertson in 1930. The ebb, or early, phase helps initiate a ‘holding pattern’ within the first 12 hours (clinically manifesting as shock). The flow phase lasts much longer depending upon the extent of damage. It can be divided into a catabolic phase lasting several days, followed by a recovery and repair phase lasting several weeks. The time factor depends upon the extent of initial injury and any ongoing insults. The mediators do help in the repair process by endogenous cytokine antagonists, which controls the proinflammatory response, commonly called the systemic inflammatory response syndrome (SIRS). If the response to SIRS is inadequate, multiple organ dysfunction syndrome occurs (MODS), which is just a step away from death.
The recovery process
4. B, C, E
Catabolism is an important aspect of recovery. However, the body’s stress response has a capacity to triage the catabolic effect. The catabolic effect concentrates away from the peripheries, such as muscle fat and skin, to the more important parts – the liver, the immune system and the wound. During catabolism, muscle wasting occurs from muscle protein breakdown and a decrease in muscle protein synthesis. The major site for such a change is peripheral skeletal muscle; sometimes respiratory muscles are affected, resulting in hypoventilation with resultant pulmonary problems; gut muscle may be affected to produce paralytic ileus. Therefore, clinically, patients are weak with malaise and function suboptimally with increased risk of hospital-acquired infections.
Hyperalimentation is not advisable as it enhances the metabolic stress. Nutritional support should therefore be at a modest level. Hyperglycaemia is a normal response to stress. This is due to increased glucose production and decreased uptake in peripheral tissues as a result of insulin resistance, a temporary effect of stress. The severity of the stress determines the duration of the hyperglycaemic state – stress-induced diabetes. The patient is therefore at increased risk of diabetic complications: sepsis, renal impairment and polyneuropathy. Intravenous insulin infusion in the ICU setting using a sliding scale has been shown to reduce morbidity and mortality.
➜ Optimal perioperative care
5. B, C, D, E
As a result of hypovolaemia, receptors in the carotid artery, aortic arch and left atrium act to release aldosterone and antidiuretic hormone (ADH). Aldosterone is also released by the renin–angiotensin system activated by the juxtaglomerular apparatus (see Fig. 1.3). Aldosterone and ADH help in sodium and water retention. Therefore large volumes of fluid infusion should not be used, as it will result in oedema, peripheral and visceral, the latter causing delayed gastric emptying.
Fluid and electrolyte conservation
Hypovolaemia from haemorrhage (’The three-line whip’)
CNS (hypothalamus)
Aortic and carotid body pressure receptors
Atrial stretch receptors
Posterior pituitary ADH ↑
Atrial natriuretic peptide (ANP) ↓
Renin-angiotensin system
Aldosterone ↑
Conservation of sodium and water at renal tubule
Figure 1 .3 Hypovolaemia in trauma.
Hypothermia, due to increased production of adrenal steroids and catecholamines, causes greater risk of cardiac arrythmias. Therefore all efforts must be made to conserve heat in the stressed patient.
As a result of starvation, the body needs to produce glucose to sustain cerebral function. This is done by mobilising glycogen stores by hepatic gluconeogenesis. Fat is mobilised from adipose tissue followed by loss of lean tissue. At least 2 L of 5 per cent dextrose intravenously provides 100 g of glucose a day; this has a protein-sparing effect. Early institution of nutrition by the most appropriate route will avoid loss of body mass.
Immobility should be avoided as it induces muscle wasting. Inactivity of skeletal muscle impairs protein synthesis. Early mobilisation therefore helps in preventing muscle wasting besides minimising the dreaded complications of deep vein thrombosis and pulmonary embolism.
Perioperative care can be optimised by attention to feeding and preventing fluid overload. Epidural analgesia not only reduces stress from pain but also reduces the insulin resistance, by blocking the cortisol stress response. Beta-blockers and statins have a role in improving long-term survival after recovery from a major stress response.
2 Shock and blood transfusion
Multiple choice questions
➜ Cell metabolism
1. Which of the following statements are true?
A Cells change from aerobic to anaerobic metabolism when perfusion to tissues is reduced.
B The product of aerobic respiration is lactic acid.
C The product of anaerobic respiration is carbon dioxide.
D The accumulation of lactic acid in the blood produces systemic respiratory acidosis.
E Lack of oxygen and glucose in the cell will eventually lead to failure of sodium/ potassium pumps in the cell membrane and intracellular organelles.
➜
Hypovolaemic shock
2. Which of the following statements regarding hypovolaemic shock are true?
A It is associated with high cardiac output.
B The vascular resistance is high.
C The venous pressure is low.
D The mixed venous saturation is high.
E The base deficit is low.
➜ Ischaemia-reperfusion
syndrome
3. Which of the following statements about ischaemia-reperfusion syndrome is correct?
A This refers to the cellular injury because of the direct effects of tissue hypoxia.
B It is seen after the normal circulation is restored to the tissues following an episode of hypoperfusion.
C The increased sodium load can lead to myocardial depression.
D This is influenced by the duration and extent of tissue hypoperfusion.
E It usually does not cause death.
➜ Responses in shock
4. In which of the following cases might tachycardia accompany shock?
A Hypovolaemia due to gastrointestinal (GI) bleeds
B Patients on alpha-blockers
C Patients with implanted pacemakers
D Fit young adults with normal pulse rate of 50/min
E Cardiogenic shock.
5. Which of the following regarding blood pressure in shock are false?
A Elderly patients who are normally hypertensive may present with a ‘normal’ blood pressure.
B Children and fit young adults are able to maintain blood pressure until the final stages of shock.
C Hypotension is one of the first signs of shock.
D Beta-blockers may prevent a tachycardic response.
E Blood pressure is increased by reduction in stroke volume and peripheral vasoconstriction.
➜ Compensated shock
6. Which of the following statements about compensated shock are false?
A The preload is preserved by the cardiovascular and endocrinal compensatory responses.
B Tachycardia and cool peripheries may be the only clinical signs.
C The perfusion to the skin, muscle and GI tract is increased.
D Systemic respiratory acidosis is seen.
E Patients with occult hypoperfusion for more than 12 hours have a significantly higher mortality rate.
➜ Resuscitation in shock
7. Which of the following statements are false?
A Administration of inotropic agents to an empty heart will help to increase diastolic filling and coronary perfusion.
B In all cases, regardless of classification, hypovolaemia and preload must be addressed first.
C Long, wide-bore catheters allow rapid infusion of fluids.
D The oxygen-carrying capacity of both colloids and crystalloids is zero.
E Hypotonic solutions are poor volume expanders and should not be used in shock except in conditions of free water loss or sodium overload.
➜ Inotropic support in shock
8. Which of the following are true regarding inotropic support in shock?
A This is the first-line therapy in hypovolaemic shock.
B Phenylephrine and noradrenaline are indicated in distributive shock states.
C Dobutamine is the agent of choice in cardiogenic shock or septic shock complicated by low cardiac output.
D Vasopressin may be used when the vasodilatation is resistant to catecholamines.
E Use in the absence of adequate preload may be harmful.
➜ Mixed venous saturation
9. Which of these statements about mixed venous saturation are false?
A The percentage saturation of oxygen returning to the heart from the body is a measure of the oxygen delivery and extraction by the tissues.
B The normal mixed oxygen saturation levels are 30–40 per cent.
C Accurate measurements are via analysis of blood drawn from a line placed in the superior vena cava (SVC).
D Levels below 50 per cent indicate inadequate oxygen delivery consistent with hypovolaemic shock.
E High mixed venous saturation levels are seen in sepsis.
➜ Reactionary haemorrhage
10. Which of the following about reactionary haemorrhage are false?
A This is delayed haemorrhage occurring within 24 h after operation.
B It is usually caused by dislodgement of clot, normalisation of blood pressure or slippage of ligature.
C It is associated with infection.
D It can be significant, requiring re-exploration.
E It is usually venous.
➜ Blood transfusion
11. Which of the following about blood transfusion are false?
A A haemoglobin level of 10 g/dL or less is now considered a typical indication.
B Fresh frozen plasma (FFP) is considered as the first-line therapy in coagulopathic haemorrhage.
C Cryoprecipitate is useful in lowfibrinogen states and in factor VIII deficiency.
D Platelets have a shelf life of 3 weeks.
E Patients can pre-donate blood up to 3 weeks before surgery for autologous transfusion.
12. Which of the following is a complication of massive blood transfusions?
A Coagulopathy
B Hypercalcaemia
C Hyperkalaemia
D Hypokalaemia
E Hypothermia.
Extended matching questions
➜
1. Types of shock
A Septic shock
B Cardiogenic shock
C Hypovolaemic shock – haemorrhagic
D Neurogenic shock
E Anaphylactic shock
F Endocrinal shock
G Hypovolaemic shock – non-haemorrhagic
Choose and match the correct diagnosis with each of the scenarios given below:
1 A 7-year-old boy with nut allergy develops stridor and collapses after eating a snack. He requires airway and breathing support. His BP is 60/38 mmHg.
2 A 78-year-old man with known ischaemic heart disease (IHD) complains of chest pain and collapses. His pulse is irregular and BP is 74/48 mmHg. ECG shows features of an anterolateral myocardial infarction (MI).
3 A 76-year-old male is brought to the hospital with persistent diarrhoea and vomiting for the past 4 days. He has been unable to keep his food down and feels very tired. On examination he is very dehydrated. His pulse is 128/min and his BP is 88/52 mmHg.
4 A 55-year-old woman with poorly controlled hypothyroidism is found comatose. She is hypothermic. Her pulse is irregular and her BP is 96/70 mmHg.
5 An 86-year-old male has been complaining of increasing lower abdominal pain for the past week. On examination he looks very unwell with warm peripheries. He has signs of generalised peritonitis. His pulse is 130/min and his BP 84/50 mmHg.
6 A 28-year-old motorist is brought to the A&E after a road traffic accident (RTA). He has sustained an isolated injury to his back and has motor and sensory deficits in both lower limbs. His pulse is 122/min and his BP 100/62 mmHg.
7 A 19-year-old male is brought to the hospital after sustaining an abdominal injury while playing rugby. He is complaining of left upper abdominal pain and has some bruising over the same area. His pulse is 140/min and his BP is 100/82 mmHg.
➜ 2. Vasopressor and inotropic support in shock
A Noradrenaline
B No role for vasopressor or inotropic agent
C Phenylephrine
D Dobutamine
E Vasopressin
Choose and match the correct intervention with each of the scenarios given below:
1 Cardiogenic shock when myocardial depression complicates shock state.
2 Distributive shock due to sepsis.
3 Vasodilatation resistant to catecholamines due to relative or absolute steroid deficiency.
4 Hypovolaemic shock due to splenic injury.
5 Distributive shock due to spinal cord injury.
3. Complications of blood transfusion
A Haemolytic transfusion reaction due to incompatibility
B Fluid overload
C Disseminated intravascular coagulation (DIC)
D Hypocalcaemia
E Infection
Choose and match the correct diagnosis with each of the scenarios given below:
1 A 86-year-old woman is admitted with a haemoglobin (Hb) of 5.6 g/dL. The HO prescribes 4 units of blood. These 4 units are transfused over a period of 6 h. Four hours later the patient is found to be having difficulty in breathing. Chest examination reveals fine creps bilaterally. Chest X-ray confirms pulmonary oedema.
2 A 28-year-old male is taken to a nearby hospital after sustaining injuries while on a safari in Africa. He has lost a lot of blood and is hence given 2 units of blood transfusion. He develops fever and chills with rigors the next day. Peripheral blood smear demonstrates malarial parasite.
3 A 38-year-old man requires several units of blood transfusion due to multiple injuries sustained as a result of a fall. He develops tetany and complains of cicumoral tingling.
4 A 34-year-old motorcyclist sustains multiple injuries after an RTA. He is brought to the hospital in severe shock and requires multiple blood transfusions. It is observed that the bleeding is still uncontrolled and the blood fails to clot.
5 The ward is very busy and quite a few staff have phoned in sick. There are two patients (with the same surnames) needing blood transfusions. The staff nurse points to the blood units on the table and asks the HCA to start them as she is just going off for her break. The blood transfusion is started. Within a few minutes the patient is unwell and his urine is haemorrhagic. He collapses and becomes anuric. He is also found to be jaundiced.
Answers: Multiple choice questions
➜ Cell metabolism
1. A, E
Cells switch from aerobic to anaerobic metabolism when deprived of oxygen. The product of aerobic respiration is carbon dioxide. This is eliminated efficiently through the lungs. The product of anaerobic respiration is lactic acid. When enough tissue is underperfused, the accumulation of lactic acid in the blood produces systemic metabolic acidosis. As tissue ischaemia progresses, the immune and complement systems are activated. This also results in the complement and neutrophil priming with the generation of oxygen-free radicals and cytokines. This leads to injury of the epithelial and endothelial cells, which leads to loss of integrity and ‘leaky’ walls. The resultant oedema further increases tissue hypoxia. As glucose within the cells is exhausted, anaerobic respiration ceases and there is a failure of the sodium/potassium pump. Intracellular lysosomes release autodigestive enzymes and cell lysis ensues. Intracellular contents, including the potassium, are released into the bloodstream.
During the period of reperfusion, cellular and organ damage progresses as a result of direct effects of tissue hypoxia and local activation of inflammation. Further injury occurs once the normal circulation is restored. This is termed ischaemia-reperfusion syndrome. The acid and potassium load that has built up can lead to direct myocardial depression, vascular dilatation and further hypotension. The cellular and humoral components flushed back into circulation cause further endothelial injury and organ damage. This can lead to multiple organ failure (MOF) and death. Ischaemia-reperfusion injury can be reduced by limiting the extent and duration of tissue hypoperfusion.
➜ Responses in shock
4. A, B
Tachycardia is an early warning sign in hypovolaemic shock. The tachycardic response is not seen in patients on beta-blockers.
5. C, E
Hypotension may not be seen until the shock is well established. The heart compensates initially to maintain cardiac output by increasing both the rate and the stroke volume.
➜ Compensated shock
6. C, D
Systemic metabolic acidosis is seen in shock (also see Table 2.2)
Resuscitation should not be delayed in order to definitively diagnose the cause of the shocked state. The first-line therapy is intravenous (IV) access administration of IV fluids using short, wide-bore catheters that allow rapid infusion of fluids. Hypotonic fluids are poor volume
expanders and should not be used in the treatment of shock (an exception is free water loss, as in diabetes insipidus and sodium overload, e.g. cirrhosis). If there is an initial doubt about the cause of shock, it is safer to assume that it is hypovolaemia and begin with fluid resuscitation, followed by an assessment of the response. In patients who are actively bleeding (major trauma, ruptured abdominal aortic aneurysm, GI bleed), it is counterproductive to institute high-volume fluid therapy without controlling the site of bleeding. Resuscitation should proceed in parallel with surgery. Conversely, a patient with bowel obstruction and hypovolaemic shock should be adequately resuscitated before undergoing surgery. Administration of inotropic agents to an empty heart will rapidly and permanently deplete the myocardium of oxygen stores and dramatically reduce diastolic filling and therefore coronary perfusion.
➜ Inotropic support in shock
8. B, C, D, E
The first-line therapy in hypovolaemic shock is IV access and administration of fluids. Phenylephrine and noradrenaline are helpful in distributive shock states, such as those due to sepsis and neurogenic causes. These states are characterised by peripheral vasodilatation, a low systemic vascular resistance and a high cardiac output. If the vasodilatation is resistant to these agents (e.g. absolute or relative steroid deficiency), vasopressin may be used.
➜ Mixed venous saturation
9. B, C
The percentage saturation of oxygen returning to the heart from the body is a measure of the oxygen delivery and extraction by the tissues. Accurate measurement is by a long line placed in the right atrium. Samples from the SVC give slightly higher values. Normal mixed venous oxygen saturation levels are 50–70 per cent. Levels below 50 per cent indicate inadequate oxygen delivery and increased oxygen extraction by the cells. This is consistent with hypovolaemic or cardiogenic shock. High mixed venous saturation levels (>70 per cent) are seen in sepsis and some forms of distributive shock.
➜ Reactionary haemorrhage
10. C, E
The bleeding is usually arterial. It is not associated with infection, unlike secondary haemorrhage.
➜ Blood transfusion
11. A, D
The transfusion trigger was historically 10 g /dL. It is now believed, however, that a level of 6 g /dL is acceptable in patients who are not bleeding, not symptomatic and not about to undergo major surgery. Levels between 6 and 8 g /dL are selectively transfused. Also see Table 2.3.
12. A, C, D, E
Hypocalcaemia is another complication of massive transfusion. People who receive repeated transfusions over long periods of time develop iron overload.
Complications from a single transfusion include incompatibility haemolytic transfusion reaction, febrile transfusion reaction, allergic reaction, infection, air embolism, thrombophlebitis and transfusion-related acute lung injury (usually from FFP).
Another random document with no related content on Scribd:
were bringing Stanislas, and addressed one who rode in the midst, in a Frankish dress and indifferently mounted. He asked him in German where the King of Poland was. It proved to be Stanislas, whom he had not recognized in that disguise. “What,” said the King, “have you forgotten me?” Fabricius then told him of the King of Sweden’s sad condition, and of his unshaken but unsuccessful resolution.
When Stanislas came to Bender, the Pasha, who was returning from accompanying Charles, sent the King an Arabian horse with elegant trappings. He was received in Bender with a volley of artillery, and, except that he was a prisoner, had no cause to complain of his treatment there. Charles was on the way to Adrianople and the town was full of gossip about his battle. The Turks both admired him and thought him blame-worthy; but the Divan was so exasperated that they threatened to confine him in one of the islands of the Archipelago.
Stanislas, who did me the honour of informing me on most of these details, assured me also that it was proposed in the Divan that he too should be kept prisoner in one of the Greek islands, but some months later the Sultan softened and let him go.
M. Desaleurs, who could have championed him and prevented this affront to all Christian kings, was at Constantinople, as well as Poniatowski, whose resourcefulness was always feared. Most of the Swedes were at Adrianople in prison, and the Sultan’s throne seemed inaccessible to any complaints from the King of Sweden.
The Marquis of Fierville, a private envoy to Charles at Bender, from France, was then at Adrianople, and undertook a service to the Prince at a time when he was either deserted or ill-used by all. He was luckily helped in this design by a French noble of good family, a certain Villelongue, a man of great courage and small fortune, who, fascinated by reports of the King of Sweden, had come on purpose to join his service.
With the help of this youth M. de Fierville wrote a memorial from the King of Sweden, demanding justice of the Sultan for the wrong offered in his person to all crowned heads, and against the treachery of the Kan and the Pasha of Bender.
It accused the Vizir and other ministers of having been corrupted by the Russians, of having deceived the Sultan, intercepted letters, and of having employed trickery to get from the Sultan an order contrary to the hospitality of the Mussulmans, in violation of the laws of nations, and this in a manner so unworthy of a great Emperor, that a king who had none but his retinue to defend him, and who had trusted the sacred word of the Sultan, was attacked by 20,000 men.
When this memorial had been drawn up it had to be translated into Turkish, and written upon the special paper used for the Sultan’s petitions.
They tried to get it done by several interpreters, but the King’s affairs were at such a pass, and the Vizir so openly his enemy, that none of them at all would undertake it. At last they found a stranger whose hand was not known, so for a considerable fee, and a promise of profound secrecy, he translated the memorial and copied it on to the right sort of paper. Baron Ardidson counterfeited the King’s hand and Fierville sealed it with the arms of Sweden. Villelongue undertook to deliver it to the Sultan as he went to the mosque. This had been done before by people with grievances against the ministers, but that made it now the more dangerous and difficult.
The Vizir was certain that the Swedes would seek justice from his master, and knew from the fate of his predecessors what the probable sequel was. So he forbade any one to approach the Sultan, and ordered that any one seen in the neighbourhood of the Mosque with petitions should be seized.
Villelongue knew the order, and that he was risking his life; but he dressed as a Greek, and, hiding the letter in his breast, went
early to the place. He feigned madness, and danced into the midst of the two lines of janissaries, where the Sultan was to pass, and now and then dropped some money to amuse the guards.
When the Sultan was coming they wanted to push Villelongue aside; he fell on his knees and struggled with the soldiers. At last his cap blew off, and showed that he was a Frank, from his long hair: he received several blows and was ill-used.
The Sultan heard the scuffle, and asked what was the matter; Villelongue cried with all his might, “Amman, Amman” (mercy), and pulled out the letter. The Sultan commanded that he should be brought before him. Villelongue hastened forward, and embracing his stirrup gave him the paper, saying, “Sued call dan” (the King of Sweden gives it to thee). The Sultan put the letter in his breast, went on to the mosque, and Villelongue was secured in one of the out-houses of the seraglio.
The Sultan read the letter on his return from the mosque, and resolved to examine the prisoner himself. He changed the Imperial coat and turban, and, as he often does, took the disguise of an officer of janissaries, and took an old Maltese with him as interpreter. Thanks to his disguise Villelongue had a private talk of a quarter of an hour with the Turkish Emperor, an honour that was never done to any other Christian ambassador. He did not fail to detail all the King of Sweden’s hardships, accusing the minister and demanding vengeance with the greater freedom, because he was throughout the conversation talking to the Sultan as to an equal. He had recognized the Sultan, although the prison was very dark, and this made him the bolder in his discourse. The seeming officer of the janissaries said to him, “Christian, be assured that the Sultan my master has the soul of an Emperor, and that if the King of Sweden is in the right he will do him justice.” Villelongue was soon released, and some weeks after there was a sudden change in the seraglio, which the Swedes attribute to this conference. The mufti were deprived, the Kan of Tartary banished to the Rhodes, and the serasquier Pasha of Bender to an island in the Archipelago.
The Ottoman Porte is so subject to such storms that it is hard to say whether this was an attempt to appease the King of Sweden or not; his subsequent treatment by the Porte showed little anxiety to please him.
Ali-Coumourgi, the favourite, was suspected of having made all these changes for some private ends of his own; the pretext for the banishment of the Kan and the serasquier of Bender was that they had given the King 1,200 purses against the express orders of the Sultan. He put on the Tartar throne the son of the deposed Kan of Tartary, a young man who cared little for his father and on whom Ali counted for military help. Some weeks after this the Grand Vizir Joseph was deposed, and the Pasha Soliman was declared Prime Vizir.
I must say that M. de Villelongue, and many Swedes, have assured me that the letter he gave was the cause of these changes, but M. de Fierville denies this, and I have in other cases met with contradictory accounts. Now, an historian’s duty is to tell plain matter of fact, without entering into motives, and he must relate just what he knows, without guessing at what he does not know.
In the meantime, Charles was taken to a little castle called Demirtash, near Adrianople. Crowds of Turks had collected there to see him alight. He was carried on a sofa from his chariot to the castle; but to avoid being seen by this mob he covered his face with a cushion.
It was several days before the Porte would consent to his residence at Demotica, a little town six leagues from Adrianople, near the river Hebrus, now called Marizza. Coumourgi said to the Grand Vizir, “Go and tell the King of Sweden he can stay at Demotica all his life. I warrant he will ask to move of his own accord before the year is over, and be sure you do not let him have a penny of money.”
So the King was moved to the little town of Demotica, where the Porte allowed him sufficient supplies for himself and his retinue.
They allowed him twenty-five crowns a day to buy pork and wine, a sort of provisions that the Turks do not supply, but as to the allowance of five hundred crowns a day, which he had had at Bender, it was quite withdrawn. Scarcely had he arrived at Demotica with his small court than the Grand Vizir Soliman was deposed; his place was given to Ibrahim Molla, a haughty, bold and rough man.
He had been a common sailor till the accession of Achmet III. This Emperor often disguised himself as a private citizen, a priest, or a dervish; he would then slip in the evening into the cafés and other public places of Constantinople to listen to what was said of him, and to hear the people’s opinions with his own ears. One day he heard this Molla finding fault with the Turkish ships because they never brought home any prizes, and swore that were he a captain he would never return home without some infidel ship. The next morning the Sultan gave him a ship and sent him out on a cruise. A few days later the Captain brought back a Maltese boat and a Genoese galley, and in another two years he was Admiral, and then Grand Vizir. He was no sooner appointed than he began to think that he could dispense with the favourite, and to make himself indispensable he planned to make war on the Russians; in order to do so he set up a tent near the castle where the King of Sweden was living.
He invited the King to meet him there with the new Kan of Tartary and the French ambassador. The King’s misfortunes made him feel the indignity of being sent for by a subject the more; he ordered the Chancellor Mollern to go in his place, and because he feared that the Turks might be disrespectful, and force him to compromise his dignity, he resolved to stay in bed during his stay at Demotica. This he did for ten months, just as if he had been ill. The Chancellor, Grothusen, and Colonel Dubens were his only tablecompanions. They had none of the conveniences of the Franks, all had been carried off at Bender, so that their meals lacked pomp and elegance. They waited on themselves, and Chancellor Mullern did all the cooking during that time.
While Charles was thus staying in bed, he heard news of the wreck of all his foreign dominions.
General Steinbock, famous for having driven the Danes out of Scandinavia, and for having defeated their picked troops with a band of peasants, was still maintaining the credit of the Swedish arms. He defended Pomerania, Bremen, and the King’s possessions in Germany as long as he could, but could not prevent the Saxons and Danes united from passing the Elbe and besieging Stade, a strong town near that river, and in the Duchy of Bremen. It was bombarded and burnt to ashes, and the garrison was obliged to surrender at discretion, before Steinbock could come to their assistance.
He had about 10,000 men, and half of them were cavalry, with which he pursued the enemy, though they were twice his number, and forced them to recross the Elbe. He caught them at a place called Gadebesck, on a small river of the same name, on the 20th December, 1712. The Saxons and Danes were posted with a marsh in front and a wood in the rear; they had all the advantage both in number and position, for there was no getting at them but across the marsh, through the fire of their artillery.
Steinbock led on his men, and, advancing in battle order, began one of the most bloody engagements that had ever taken place between those rival nations. After a sharp fight of three hours’ duration, the Danes and the Saxons were forced back and had to leave the field.
After this victory Steinbock could not but remember how the Danes had reduced Stade to ashes, and resolved to avenge himself on Altena, a town belonging to the King of Denmark. Altena is above Hamburg, on the river Elbe, which brings up large vessels thither. The King of Denmark had granted it great privileges, in the hope of making it a place of considerable trade. Hamburg therefore got jealous, and wished nothing but their destruction. When Steinbock came within sight of the place, he sent a herald to bid them begone at once with their possessions, for he intended to destroy their town immediately.
The magistrates came and threw themselves at his feet and offered him a ransom of 100,000 crowns. Steinbock said he must have 200,000. They begged for time to send to their correspondent at Hamburg, and promised that he should have it by the next day. The General told them that if they did not pay at once he would burn their town about their ears.
His soldiers were in the suburbs ready with their torches in their hands. The town had no defence but a poor wooden gate and a dry ditch; so that the poor wretches were forced to flee at midnight. It was on the 9th of January, 1713; the weather was severely cold, and a great north wind helped to spread the flames, and to increase the sufferings of the people exposed in the open fields.
Men and women, loaded with their property, went weeping and lamenting towards the neighbouring ice-clad hills. Paralytic old folk were carried by the young on their shoulders, women just delivered were carrying their children, and died of cold on the hillside, in sight of their burning homes. The people had not all left the town when the Swedes fired it. It burned from midnight to about ten the next morning; the houses, being mostly of wood, were easily burnt, so that by morning there was scarcely any trace of a town left. The aged, the sick, and the women of delicate health, who had refuged on the frozen ground while their houses were burning, dragged themselves to the gates of Hamburg, and begged that they would let them in and save their lives, but they were refused on the ground that there had been infectious disease among them. So that most of these poor wretches died under the walls, calling Heaven to witness the cruelty of the Swedes, and of the still more inhuman Hamburgers.
All Germany was scandalized by this violence. The ministers and generals of Poland and Denmark wrote to Steinbock, complaining of his cruelty, which was inexcusable because it was uncalled for, and must set God and man against him.
He replied that he never would have gone to these extremities were it not to show his master’s enemies how war ought to be made
—not like barbarians, but in consideration of the laws of nations; that they had committed atrocities in Pomerania to ruin that beautiful country, and sell 100,000 people to the Turks; that his torches at Altena were only a fitting return for the red-hot bullets they had used at Stade; that it was with such violence that the Swedes and their enemies made war on each other. If Charles could have appeared then in Poland, he might possibly have retrieved his former fortune. His armies, though they needed his presence among them, were yet actuated by his spirit; but when the master is away success is seldom turned to good account. Steinbock gradually lost all that he had gained in those great actions, which might have been decisive at a more fortunate time.
With all his success it was not in his power to prevent the Russians, the Saxons, and the Danes from uniting. They seized his quarters, and he lost several of his men in little skirmishes; 2,000 of them were drowned in the Oder as they were going to their winter quarters in Holstein; these were losses which could not be repaired in a country where the enemy was strong in all directions. He intended to defend the country of Holstein against Denmark, but in spite of his ruses and efforts the country was lost, the whole army destroyed, and Steinbock taken prisoner. To complete the misfortunes of the Swedes, the King persisted in his resolve of staying at Demotica, and fed his mind with vain expectations of help from Turkey.
The Vizir, Ibrahim Molla, who had been so bent on war with the Russians in opposition to the favourite, was pressed to death between two doors. The post of Vizir was now so dangerous that none dare take the office; but after it had been vacant for about six months, the favourite Ali-Coumourgi took it. Then the King of Sweden abandoned all hope. He really knew Coumourgi, because he had been of service to him when the favourite’s interest had corresponded with his own.
He had spent eleven months buried in idleness and oblivion at Demotica; this extreme idleness, following the most violent exercise,
made the illness which he had before assumed a fact. All Europe believed he was dead, and the Regency which he had settled when he left Stockholm, getting no word from him, the Senate went to the Princess Ulrica Eleanora to ask her to take the Regency during the absence of her brother. She accepted it; but when she found that the Senate were trying to force her to peace with the King of Denmark, who was attacking Sweden from all sides, and with the Czar, she resigned the Regency in the certainty that her brother would never ratify the peace, and sent a long account of the affair to him in Turkey.
The King received the dispatches at Demotica, and the despotic theories which he had inherited made him forget that Sweden had once been free, and that the Senate had formerly governed the kingdom together with the Kings. He looked on them as servants, who were usurping the government in the absence of their master; he wrote to them that if they wanted to govern he would send them one of his boots, to whom they might apply for orders. Then, to prevent any attempt to overthrow his authority in Sweden, and to defend his country, hoping for nothing further from the Ottomans, he depended on himself, and told the Grand Vizir that he would go through Germany.
Desaleurs, the French ambassador who transacted all the affairs of Sweden, made the proposal to the Vizir. “Well,” said the Vizir, “didn’t I say that the year would not pass without the King’s asking to go? Tell him that he is free to go or stay, but that he must fix his day, that we may not have a repetition of the trouble we had with him at Bender.”
Count Desaleurs softened the form of this message to the King. The day was fixed, but Charles wished, in spite of his wretched position, to show the pomp of a grand king before leaving. He made Grothusen his ambassador extraordinary, and sent him to make a formal leave at Constantinople, with a suite of fourscore persons in rich attire. But the splendour of the Embassy was not so great as the mean shifts to which he descended to provide it were disgraceful. M.
Desaleurs lent the King 40,000 crowns, Grothusen borrowed, through his agents at Constantinople, 1,000 from a Jew, at the rate of fifty per cent., besides 200 pistoles of an English merchant, and 1,000 of a Turk.
They amassed this money solely to act before the Divan the comedy of a Swedish embassy. At the Porte, Grothusen received all the honour paid to ambassadors extraordinary on their day of audience. The object of the whole thing was to get money from the Vizir, but the scheme failed. Grothusen proposed that the Porte should lend him a million. But the Vizir answered that his master could be generous when he wished, but that lending was beneath his dignity; that the King should have all necessary for his journey, and in a degree becoming to the giver; and that possibly the Porte might send him a present of uncoined gold, but that he was not to count on that.
The King began his journey on the 1st of October, 1714. A capigipasha, with six chiaoux, went to accompany him from Demirtash, whither he had removed a few days before. The presents they brought him from the Sultan were a large scarlet tent embroidered with gold, a sabre set with jewels, eight beautiful Arab horses, with fine saddles and stirrups set with massive silver. It is not beneath the dignity of history to tell that the Arabian groom, who had charge of the horses, gave the King an account of their genealogy; it is the custom there to think more of the family of a horse than of a man; which is not unreasonable, for if we are careful of the breed these animals never degenerate.
The convoy consisted of sixty chariots, laden with all sorts of provisions, and three hundred horses. The Pasha, knowing that many Turks had advanced money to the King’s suite at high rate of interest, told him that, as usury was forbidden by the law of Mahomet, he desired his Majesty to settle the debts, so that his resident at Constantinople should only pay the principal. “No,” said the King, “if my servants have given bills for a hundred crowns it shall be paid, even if they have only received ten for it.” He proposed
