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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Serie: Lecture Notes
- Sprache: Englisch
Gastroenterology and Hepatology Lecture Notes is a comprehensive yet easy-to-read overview of luminal gastroenterology and hepatology. Covering the epidemiology, causes, clinical features, investigation, treatment and prognosis of all the main gut and liver conditions, it is ideal for both exam preparation and fact finding.
Key features include:
- A full range of new illustrations, including clinical photographs and scans, that clearly demonstrate signs and symptoms
- Sections on anatomy, physiology, pharmacology, and epidemiology – written to enhance understanding of clinical features
- Essential information highlighted throughout the text
- Case-based self-assessment for each chapter helps retention of knowledge and puts it in its clinical context
- A new section of "best answer" MCQs
- New chapters on inflammatory bowel disease and different diagnosis of the upper GI tract
- Includes a companion website at www.lecturenoteseries.com/gastroenterology featuring 16 in-depth case studies
Whether learning the basics of the gastrointestinal system, starting a general medical or gastroenterological placement, or looking for a quick-reference overview to revise key concepts, Gastroenterology and Hepatology Lecture Notes is an ideal resource for medical students, MRCP or FRACP candidates, and junior doctors.
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Veröffentlichungsjahr: 2016
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Table of Contents
Cover
Title Page
Preface to the second edition
Preface to the first edition
About the companion website
Part I: Clinical Basics
1 Approach to the patient with abdominal pain
Chronic abdominal pain
Acute abdominal pain
2 Approach to the patient with liver disease
Epidemiology
Clinical features
Assessment of the severity of liver disease
3 Approach to the patient with luminal disease
Dysphagia
Nausea and vomiting
Constipation
Diarrhoea
Anal incontinence
Weight loss
Iron-deficiency anaemia
4 Nutrition
Nutritional physiology
Evaluation of nutritional status
Nutritional support
Parenteral nutrition
Enteral nutrition
Physiology of starvation
The refeeding syndrome
Intestinal failure
5 Gastrointestinal infections
Oral infections
Oesophageal infections
Helicobacter pylori
infection
Acute gastroenteritis
Intestinal tuberculosis
Miscellaneous gut infections
Anal infections
Gut symptoms in HIV infection
6 Gastrointestinal investigations
Structural tests
Physiological tests
Part II: Gastrointestinal Emergencies
7 Acute gastrointestinal bleeding
Acute upper gastrointestinal bleeding
Acute lower gastrointestinal bleeding
8 Acute upper and lower gastrointestinal emergencies
Acute total dysphagia
Oesophageal rupture
Acute diarrhoea
Gut obstruction and ileus
Foreign bodies
9 Acute liver failure
Epidemiology and causes
Pathophysiology
Clinical features
Management
10 Pancreatobiliary emergencies
Acute pancreatitis
Clinical features
Acute cholangitis
Part III: Regional Gastroenterology
11 Oral cavity
Oral ulcers
Oral cancer
Oral manifestations of inflammatory bowel disease
Dental enamel erosion
Hereditary haemorrhagic telangiectasia
Gardner syndrome
Peutz–Jegher’s syndrome
12 Oesophagus
Gastro-oesophageal reflux disease (GORD)
Caustic oesophagitis
Oesophageal motility disorders
Oesophageal tumours
Oesophageal endoscopic abnormalities
13 Stomach and duodenum
Gastritis
Ménétrier’s disease
Peptic ulcer disease
Gastric and duodenal ulcer
Zollinger–Ellison syndrome
Gastroparesis
Gastric carcinoma
Gastric lymphoma
Other gastric tumours
14 Small intestine
Malabsorption
Intestinal failure
Coeliac disease
Tropical sprue
Small intestinal bacterial overgrowth
Bile acid malabsorption
Whipple’s disease
Protein-losing enteropathy
Intestinal infections
Small intestine tumours
Miscellaneous intestinal disorders
15 Small and large bowel disorders
Inflammatory bowel diseases (IBDs)
Microscopic colitis
Functional gastrointestinal disorders
Ischaemia of the gut
Radiation enterocolitis
16 Colon
Colorectal tumours
Miscellaneous colonic disorders
17 Anorectum
Haemorrhoids
Anal fissure
Anal fistula
Anal pain and itch
Anal cancers
Rectal prolapse
Solitary rectal ulcer syndrome
18 Pancreatic diseases
Pancreatic anatomy
Physiology
Chronic pancreatitis
Pancreatic tumours
19 Biliary diseases
Embryology
Biliary anatomy
Biliary physiology
Biliary microbiology
Cholelithiasis
Cholecystitis
Acalculous biliary pain
Structural bile duct abnormalities
Cholangiocarcinoma
20 Consequences of chronic liver disease
Anatomy of the liver
Physiology of the liver
Jaundice
Portal hypertension
Ascites
Spontaneous bacterial peritonitis
Oesophageal and gastric varices
Hepatic encephalopathy
Hepatorenal syndrome
Hepatopulmonary syndrome
21 Liver transplantation
Indications and contraindications
The operation
Postoperative care
Strategies to maximise donor pool
22 Alcoholic liver disease
Epidemiology and causes
Clinical features
Investigations
Management
23 Non-alcoholic fatty liver disease
Epidemiology and cause
Clinical features
Management
Prognosis and natural history
24 Viral hepatitides
Hepatitis A
Hepatitis E
Hepatitis B
Hepatitis D
Hepatitis C
Other viral hepatitides
25 Drug-induced liver injury
26 Autoimmune hepatitis
Epidemiology and cause
Clinical features
Investigations
Management
Prognosis
27 Liver tumours and lesions
Epidemiology and causes
Clinical features
Investigations
Management and prognosis
28 Vascular liver diseases
Embryology
Vascular anatomy of the liver
Budd–Chiari syndrome
Hepatic veno-occlusive disease
Congestive hepatopathy and cardiac cirrhosis
Portal vein thrombosis
29 Pregnancy-related liver disease
HELLP syndrome
Acute fatty liver of pregnancy
Obstetric cholestasis
Hyperemesis gravidarum
30 Hereditary and congenital liver diseases
Hereditary haemochromatosis
Wilson’s disease
Alpha-1-antitrypsin deficiency
Alagille’s syndrome
Hereditary hyperbilirubinaemias
Autoimmune polyglandular syndromes
The porphyrias
Glycogen storage diseases
Biliary atresia
Part IV: Study Aids and Revision
Gastrointestinal history check-list
Abdominal examination routine
Rectal examination routine
Common OSCE cases
Surgical sieve
Part V: Self-Assessment: Answers
Self-assessment: answers
Chapter 1
Chapter 2
Chapter 3
Chapter 4
Chapter 5
Chapter 6
Chapter 7
Chapter 8
Chapter 9
Chapter 10
Chapter 12
Chapter 13
Chapter 14
Chapter 15
Chapter 16
Chapter 17
Chapter 18
Chapter 19
Chapter 20
Chapter 21
Chapter 23
Chapter 24
Chapter 25
Chapter 26
Chapter 27
Chapter 28
Chapter 29
Chapter 30
Index
End User License Agreement
List of Tables
Chapter 01
Table 1.1 Extraintestinal manifestations of hepatogastrointestinal diseases.
Table 1.2 Approach to differential diagnosis and directed investigation for Ms AP.
Table 1.3 Historical features in acute abdominal pain examination.
Chapter 02
Table 2.1 Glasgow Coma Scale.
Table 2.2 Stigmata of chronic liver disease (progressing through the hands, face, abdomen and legs).
Table 2.3 Differential diagnosis based on features of the liver examination.
Table 2.4 Child−Turcotte–Pugh scoring system.
Table 2.5 Prognosis related to Child−Turcotte–Pugh scoring system.
Table 2.6 Model for End-stage Liver Disease (MELD) score.
Chapter 03
Table 3.1 Historical features of help in identifying the cause of dysphagia.
Table 3.2 Causes of dysphagia, classified by frequency of occurrence.
Table 3.3 Secondary causes of constipation.
Table 3.4 Physiology of fluid fluxes in the gut.
Table 3.5 Causes of diarrhoea.
Table 3.6 Causes of weight loss.
Table 3.7 Likelihood ratio (LR) of iron-deficiency anaemia with different ferritin levels.
Chapter 04
Table 4.1 Clinical manifestations of specific deficiency states.
Table 4.2 Nutrient deficiencies in refeeding syndrome: Their consequences and management.
Chapter 05
Table 5.1 Features of oesophageal infections.
Table 5.2 Disorders associated with
Helicobacter pylori
infection.
Table 5.3 Diagnostic methods to detect
Helicobacter pylori
.
Table 5.4 Infectious causes of acute diarrhoea.
Chapter 07
Table 7.1 Rockall score – initial.
Table 7.2 Rockall score – post-endoscopy.
Chapter 08
Table 8.1 Causes of gut obstruction.
Table 8.2 Symptoms, investigation and management of gut obstruction according to site of obstruction.
Chapter 09
Table 9.1 Grading of hepatic encephalopathy.
Table 9.2 King’s College criteria of poor prognosis in acute liver failure.
Chapter 10
Table 10.1 Causes of acute pancreatitis.
Chapter 12
Table 12.1 Clinical features of gastro-oesophageal reflux.
Table 12.2 Clinical features of achalasia.
Chapter 13
Table 13.1 Features of gastritides.
Table 13.2 Features differentiating gastric and duodenal peptic ulcers.
Chapter 14
Table 14.1 Potential investigations in patients with malabsorption (malabsorption factor being assessed, if not obvious, given in parentheses).
Table 14.2 Causes of small bowel bacterial overgrowth.
Table 14.3 Conditions causing protein-losing enteropathy.
Table 14.4 Classification of chronic intestinal pseudo-obstruction. Those in bold have myopathic causation; others have neuropathic causation.
Chapter 15
Table 15.1 Extraintestinal manifestations of IBD.
Table 15.2 Truelove and Witts’ criteria for assessing acute colitis severity.
Table 15.3 Therapies used to induce remission vs maintain remission.
Table 15.4 Characteristics of 5-ASA compounds. As 5-ASA is easily absorbed from the small bowel, the molecule needs modification to be released at the site of inflammation.
Chapter 16
Table 16.1 Dukes’ staging for colorectal cancer.
Table 16.2 TNM staging for colorectal cancer.
Chapter 17
Table 17.1 Management of haemorrhoids.
Table 17.2 Management of anal fissure.
Table 17.3 Clinical features and management of conditions causing anal pain.
Chapter 19
Table 19.1 Characteristics of different gallstone types.
Chapter 20
Table 20.1 Classification of jaundice by cause, symptoms and investigation features.
Table 20.2 Grading of hepatic encephalopathy.
Table 20.3 Precipitants of encephalopathy in chronic liver disease.
Table 20.4 Classification of hepatorenal syndrome (HRS).
Chapter 21
Table 21.1 Mechanism of action and adverse effects of orthotopic liver transplantation immunosuppressive drugs.
Table 21.2 Pathogenesis and management of post–liver transplantation complications.
Table 21.3 Post–liver transplantation cancer complications.
Chapter 24
Table 24.1 Hepatitis viruses.
Table 24.2 Epidemiology and modes of transmission of hepatitis B virus infection.
Chapter 25
Table 25.1 Causes of drug-induced liver injury.
Chapter 26
Table 26.1 Drugs implicated in the aetiogenesis of autoimmune hepatitis (AIH).
Chapter 27
Table 27.1 Cardinal features of the commonest liver tumours.
Chapter 28
Table 28.1 Clinical features and classification of Budd–Chiari syndrome (BCS).
Chapter 30
Table 30.1 Genetic variants of alpha-1-antitrypsin deficiency.
Table 30.2 Clinical features of the familial hyperbilirubinaemias.
Table 30.3 Clinical features of the autoimmune polyglandular syndromes.
Table 30.4 Clinical features and investigation findings of the porphyrias.
Table 30.5 Clinical features of the glycogen storage diseases.
List of Illustrations
Chapter 01
Figure 1.1
Left
: Mechanism of referred pain.
Right
: Location of pain in relation to organic pathology.
Figure 1.2 Likely pathologies according to location of acute pain.
Chapter 03
Figure 3.1 Shape study for colonic transit. The number of shapes and where they are in the colon 4 and 7 days after ingestion are added up to give a transit time across the colon.
Figure 3.2 Pathophysiology of faecal incontinence. The most common disorders are indicated with an asterisk. IBD, inflammatory bowel disease; IBS, irritable bowel syndrome; MS, multiple sclerosis.
Figure 3.3 Wireless endoscopy capsule.
Chapter 04
Figure 4.1a Feeding: An abundance of glucose triggers insulin release and its resultant storage as glycogen in the liver and muscle. Glucose is also converted to triglycerides in adipose tissue for storage when in excess.
Figure 4.1b Fasting and starvation: When insulin levels in the portal tract fall, insulin secretion decreases and gluconeogenesis and glycogenolysis are induced. Fatty acids now become the major energy substrate for the body.
Figure 4.2 Range of options for nutritional support. ONS: oral nutritional supplementation
Chapter 06
Figure 6.1 Normal endoscopic retrograde cholangiopancreatography (the lucency at the distal end of the bile duct is an inflated balloon).
Figure 6.2 Stationary oesophageal manometry trace showing normal peristalsis in upper four graphs and relaxation of lower oesophageal sphincter in lower four graphs. Each horizontal division represents 5 s.
Figure 6.3 High-resolution oesophageal manometry: normal water swallow. The two bands of high pressure correspond to the UOS and LOS. The UOS relaxes at the start of the swallow, and the LOS relaxes as the contraction front traverses the oesophageal body (x-axis: distance from LOS to UES, y-axis: time, the intraoesophageal pressure is represented by colours [red: higher, green: lower, blue: background pressure]).
Chapter 08
Figure 8.1 Imaging in diagnosis of acute GI obstruction in a patient with small bowel obstruction. (a) Plain abdominal radiograph. (b) Computer tomography.
Chapter 10
Figure 10.1 Development and normal anatomy of the pancreas.
Chapter 12
Figure 12.1 (a) Normal distal oesophagus and proximal stomach; (b) Distal oesophagus and proximal stomach with hiatus hernia (LOS, lower oesophageal sphincter).
Figure 12.2 Stationary oesophageal manometry study showing simultaneous contractions in upper four traces and non-relaxing high-pressure
lower oesophageal sphincter
(LOS) in lower four traces.
Chapter 14
Figure 14.1 Endoscopic (a) and histopathologic view (b) of coeliac disease.
Chapter 15
Figure 15.1 Algorithm for the treatment of microscopic colitis proposed by the European Microscopic Colitis Group.
Chapter 16
Figure 16.1 Adenoma−carcinoma sequence
APC
, adenomatous polyposis coli;
DCC
, deleted in colon cancer (this
DCC
gene has the least strong evidence of involvement in this sequence).
Figure 16.2 Possible presentations with colonic diverticula. IBS, irritable bowel syndrome.
Chapter 17
Figure 17.1 (a) A superficial fistula, the commonest type, tracks below both the internal anal sphincter and external anal sphincter complexes and presents as perianal abscess. Classification of anal fistula. (b) Type 1. An intersphincteric fistula tracks between the internal anal sphincter and the external anal sphincter in the intersphincteric space. Type 2. A transsphincteric fistula tracks from the intersphincteric space through the external anal sphincter. Type 3. A suprasphincteric fistula leaves the intersphincteric space over the top of the puborectalis and penetrates the levator muscle before tracking down to the skin. Type 4. An extrasphincteric fistula tracks outside of the external anal sphincter and penetrates the levator muscle into the rectum.
Chapter 18
Figure 18.1 Pancreatic acinar structure.
Figure 18.2 Pancreatoduodenal anatomy showing the developing ductal systems.
Figure 18.3 CT of chronic pancreatitis. CT showing pancreatic calculi in an atrophic pancreas (long arrow) and a pseudocyst at the tail of the pancreas (short arrow).
Figure 18.4 CT showing large pancreatic pseudocyst and endoscopic procedure to drain it. This large pancreatic pseudocyst developed after an episode of severe gallstone pancreatitis. The pseudocyst was putting pressure on the stomach and causing early satiety and pain. It was drained by endoscopically puncturing the pseudocyst, using contrast to outline the cyst as in the X-ray shown here, and placing multiple plastic stents through the wall of the stomach and into the cyst. The cyst decompressed very quickly and on repeat CT 3 months later, the stents had fallen out and the pseudocyst resolved.
Chapter 19
Figure 19.1 Human embryo at 3 mm length stage, showing developmental structures of the biliary tree.
Figure 19.2 Anatomy of biliary system with detail of liver lobule.
Figure 19.3 Plain abdominal X-ray showing porcelain gallbladder.
Figure 19.4 ERCP picture showing primary sclerosing cholangitis.
Figure 19.5 ERCP picture showing Klatskin cholangiocarcinoma causing biliary stricturing at the level of the porta-hepatis and following insertion of an expanding metal stent for palliation.
Chapter 20
Figure 20.1 Functional anatomy of the liver.
Figure 20.2 Schematic drawing of the major veins that may form portal systemic collateral routes.
Figure 20.3 Portal hypertensive gastropathy.
Figure 20.4 (a) Oesophageal varices. (b) Gastric varices at endoscopy.
Figure 20.5 Primary management of oesophageal varices.
Figure 20.6 Sengstaken tube for tamponade of bleeding varices.
Figure 20.7 Secondary management of oesophageal varices. FU: follow-up.
Figure 20.8 Diagnosis of hepatopulmonary syndrome (HPS). ABG, arterial blood gas; CT, computer tomography; CXR, chest X-ray; MAA, macroaggregated albumin scan; PFT, pulmonary function test.
Chapter 22
Figure 22.1 Pathophysiological consequences of alcohol on the liver.
Chapter 23
Figure 23.1 NASH, non-alcoholic steatohepatitis.Spectrum of non-alcoholic fatty liver disease (NAFLD).
Figure 23.2 Acanthosis nigricans.
Chapter 24
Figure 24.1 Natural history of hepatitis A. ALT, alanine aminotransferase; HAV, hepatitis A virus.
Figure 24.2 Serological and clinical course of hepatitis E virus infection.
Figure 24.3 Serological and clinical course of hepatitis D co-infection (upper panel) and superinfection (lower panel).
Figure 24.4 HCV genome and targets for drug discovery. The HCV RNA genome serves as a template for viral replication and as a viral messenger RNA for viral production. It is translated into a polyprotein that is cleaved by proteases. All the HCV enzymes – NS2-3 and NS3-4A proteases, NS3 helicase and NS5B RdRp – are essential for HCV replication and are therefore potential drug discovery targets.
Chapter 26
Figure 26.1 Interface hepatitis. Mononuclear inflammatory infiltrate disrupts the limiting plate of the portal tract and extends into parenchymal tissue (haematoxylin and eosin stain, original magnification × 100).
Chapter 27
Figure 27.1 ERCP picture showing Caroli’s disease.
Figure 27.2 MRI of HCC before (a) and after (b) treatment with radiofrequency ablation. The contrast-enhancing lesion seen in the dome of the liver in image A was treated with radiofrequency ablation. At a 3-month follow-up scan the lesion had lost its contrast enhancement. The enhancement and size of the lesion had not changed at MRI 2 years after original therapy.
Chapter 28
Figure 28.1 Normal arterial (a) and venous (b) anatomy of the liver.
Figure 28.2 Cross-section of a portal canal.
Figure 28.3 Nutmeg liver.
Figure 28.4 Degree of hepatic enzyme elevation over time after hypotensive injury.
Chapter 30
Figure 30.1 Causes of neonatal jaundice.
Guide
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This new edition is also available as an e-book. For more details, please see www.wiley.com/buy/9781118728123 or scan this QR code:
Gastroenterology and Hepatology
Lecture Notes
Stephen Inns
MBChB FRACPSenior LecturerClinical Lecturer in GastroenterologyOtago School of Medicine, WellingtonConsultant GastroenterologistHutt Valley Hospital, WellingtonNew Zealand
Anton Emmanuel
BSc MD FRCPSenior Lecturer in Neurogastroenterologyand Consultant GastroenterologistUniversity College HospitalLondon, UK
Second Edition
This edition first published 2017 © 2011, 2017 by John Wiley & Sons, LtdFirst edition published 2011 by Blackwell Publishing, Ltd
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Preface to the second edition
He who studies medicine without books sails an uncharted sea, but he who studies medicine without patients does not go to sea at all.
William Osler 1849–1919
Let the young know they will never find a more interesting, more instructive book than the patient himself.
Giorgio Baglivi 1668–1707
With the first edition of Lecture notes in Gastroenterology and Hepatology we strove to create a book that read just as we teach, incorporating the important and pertinent parts of anatomy, physiology and pathology into the structure of the lesson. In this way the building blocks of clinical understanding can illuminate rather than distract, or worse yet bore, the student or aspiring gastroenterologist. With this edition we have attempted to augment and clarify this concept by using a very uniform structure. Each section, where it is at all appropriate, is divided into subsections on the epidemiology, causes, clinical features, investigation, treatment and prognosis of the condition being considered. We hope this will help with understanding the material and integrating it into practice, as well as improve the textbook as a reference source or revision aid. Icons that alert the reader to those aspects of a disease that we believe are especially important, whether it be from a basic science, clinical or emerging topic perspective, have been added to focus the reader further.
This textbook is intended as a source of information and advice for all who are starting out in the important work of assisting people with disturbances of gastroenterological and hepatological function, from the most junior of medical students to those preparing for specialist exams. To this end we have added ‘key point’ summaries to each chapter, as an aid to revision and understanding. We have also added an extensive ‘best answer’ multi-choice question section, in the style of the MRCP and FRACP examinations. These questions remain very clinically focused and draw heavily on our own clinical experiences. We believe that those early in their training will find them just as illuminating as those further along will find them challenging. Additionally, we have added further line diagrams and clinical images, with the aim of illustrating the important concepts without cluttering the book.
We firmly believe that our patients are the people who teach us the most. However, guidance from our colleagues and sources such as this book help light the path that each of us must walk to become the best clinician we can. We hope this book guides you in the same way that writing it has us.
Stephen Inns and Anton Emmanuel
Preface to the first edition
Science is the father of knowledge, but opinion breeds ignorance.
Hippocrates 460–357 BCE
Specialised knowledge will do a man no harm if he also has common sense; but if he lacks this he can only be more dangerous to his patients.
Oliver Wendell Holmes 1809–94
The content of any textbook has, by definition, got to be factual. There are two potential consequences of this. The first, and most important, is that medical fact is based on science, and we have based this book on the anatomical, physiological and pathological basis of gastrointestinal practice. The second potential consequence of a factual focus is that the text can become rather dry and list like. To limit this we have tried to present the information from a clinical perspective – as the patients present in outpatients or casualty.
Gastroenterology is well suited to such an approach. It is a fundamentally practical speciality, with a strong emphasis on history, examination and endoscopy. The importance of integrating clinical assessment with investigation – both anatomical and physiological – is emphasised by the curiously limited range of symptoms despite the complexity of the gastrointestinal tract. The gut contains about three-quarters of the body’s immune cells; it produces a wider range of hormones than any single endocrine organ; it has almost as many nerves as the spinal cord; it regulates the daily absorption of microgram quantities of vitamins simultaneously with macronutrients in 100 million times that amount.
We have tried to combine a didactic approach to facts alongside recurrently occurring themes to aid memory. For example, we have referred to the principles of embryology of the gut to give a common-sense reminder of how abdominal pain is referred and how the blood supply can be understood; approached lists of investigations by breaking them down to tests which establish the condition, the cause or the complications; approached aetiological lists by breaking down into predisposing, precipitating and perpetuating ones. We have eschewed ‘introductory chapters’ on anatomy, physiology and biochemistry as these are frequently skipped by readers who are often studying gastroenterology alongside some other subject. Rather, we have included preclinical material in the practical context of relevant disease areas (fluid absorption physiology in the section on diarrhoea, haemoglobin biochemistry in that on jaundice, etc.). Ultimately, we hope the reader uses this book as a source of material to help understand a fascinating speciality, pass exams in it, but above all be able to get as much as possible out of each patient seen with a gastrointestinal complaint.
Anton Emmanuel and Stephen Inns
About the companion website
Gastroenterology and Hepatology Lecture Notes is accompanied by a companion website, featuring 16 in-depth case studies:
www.lecturenoteseries.com/gastroenterology
Part IClinical Basics
1Approach to the patient with abdominal pain
In gastroenterological practice, patients commonly present complaining of abdominal pain. The clinician’s role is to undertake a full history and examination, in order to discern the most likely diagnosis and to plan safe and cost-effective investigation. This chapter describes an approach to this process. The underlying diagnoses and pathological mechanisms encountered in chronic pain are often quite different from those seen in acute pain, and for this reason each is considered in turn here.
Chronic abdominal pain
Anatomy and physiology of abdominal pain
Pain within the abdomen can be produced in two main ways: irritation of the parietal peritoneum or disturbance of the function and/or structure of the viscera (Box 1.1). The latter is mediated by autonomic innervation to the organs, which respond primarily to distension and muscular contraction. The resulting pain is dull and vague. In contrast, chemical, infectious or other irritation of the parietal peritoneum results in a more localised, usually sharp or burning pain. The location of the pain correlates more closely with the location of the pathology and may give important clues as to the diagnosis. However, once peritonitis develops, the pain becomes generalised and the abdomen typically becomes rigid (guarding).
Referred pain occurs due to the convergence of visceral afferent and somatic afferent neurons in the spinal cord. Examples include right scapula pain related to gallbladder pain and left shoulder region pain from a ruptured spleen or pancreatitis.
Box 1.1 Character of visceral versus somatic pain
Visceral
Originates from internal organs and visceral peritoneum
Results from stretching, inflammation or ischaemia
Described as dull, crampy, burning or gnawing
Poorly localised
Somatic
Originates from the abdominal wall or parietal peritoneum
Sharper and more localised
Clinical features
History taking
Initially the approach to the patient should use open-ended questions aimed at eliciting a full description of the pain and its associated features. Useful questions or enquiries include:
‘Can you describe your pain for me in more detail?’
‘Please tell me everything you can about the pain you have and anything you think might be associated with it.’
‘Please tell me more about the pain you experience and how it affects you.’
Only following a full description of the pain by the patient should the history taker ask closed questions designed to complete the picture.
In taking the history it is essential to elucidate the presence of warning or ‘alarm’ features (Box 1.2). These are indicators that increase the likelihood that an organic condition underlies the pain. The alarm features guide further investigation.
Box 1.2 Alarm features precluding a diagnosis of irritable bowel syndrome (IBS)
History
Weight loss
Older age
Nocturnal wakening
Family history of cancer or IBD
Examination
Abnormal examination
Fever
Investigations
Positive faecal occult blood
Anaemia
Leucocytosis
Elevated ESR or CRP
Abnormal biochemistry
Historical features that it is important to elicit include those in the following sections.
Onset
Gradual or sudden?
Pain of acute onset may result from an acute vascular event, obstruction of a viscus or infection. Pain resulting from chronic inflammatory processes and functional causes is more likely to be gradual in onset.
Frequency and duration
Colicky pain (which progresses and remits in a crescendo–decrescendo pattern)?
Usually related to a viscus (e.g. intestinal, renal and biliary colic), whereas constant intermittent pain may relate to solid organs (
Box 1.3
).
How long has the pain been a problem?
Pain that has been present for weeks is unlikely to have an acutely threatening illness underlying it and very longstanding pain is unlikely to be related to malignant pathology.
Box 1.3 Characteristic causes of different patterns of abdominal pain
Chronic intermittent pain
Mechanical:
Intermittent intestinal obstruction (hernia, intussusception, adhesions, volvulus)
Gallstones
Ampullary stenosis
Inflammatory:
Inflammatory bowel disease
Endometriosis/endometritis
Acute relapsing pancreatitis
Familial Mediterranean fever
Neurological and metabolic:
Porphyria
Abdominal epilepsy
Diabetic radiculopathy
Nerve root compression or entrapment
Uraemia
Miscellaneous:
Irritable bowel syndrome
Non-ulcer dyspepsia
Chronic mesenteric ischaemia
Chronic constant pain
Malignancy (primary or metastatic)
Abscess
Chronic pancreatitis
Psychiatric (depression, somatoform disorder)
Functional abdominal pain
Location: Radiation or referral (Figure 1.1 right)
Figure 1.1Left: Mechanism of referred pain. Right: Location of pain in relation to organic pathology.
Source: Frederick H. Millham, in Feldman M, Friedman L, Brandt L (eds) (2010) Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 9th edn, Philadelphia, PA: Saunders, Figure 10.1. Reproduced with permission of Elsevier.
Poorly localised?
Usually related to a viscus (e.g. intestinal, renal and biliary colic).
Located to epigastrium?
Disorders related to the liver, pancreas, stomach and proximal small bowel (from the embryological foregut).
Located centrally?
Disorders related to the small intestine and proximal colon (from the embryological midgut).
Located to suprapubic area?
Disorders related to the colon, renal tract and female reproductive organs (from the embryological hindgut).
Radiation of pain may be useful in localising the origin of the pain. For example, renal colic commonly radiates from the flank to the groin and pancreatic pain through to the back.
Referred pain (Figure 1.1 left) occurs as a result of visceral afferent neurons converging with somatic afferent neurons in the spinal cord and sharing second-order neurons. The brain then interprets the transmitted pain signal to be somatic in nature and localises it to the origin of the somatic afferent, distant from the visceral source.
Character and nature
Dull, crampy, burning or gnawing?
Visceral pain: related to internal organs and the visceral peritoneum.
Sharp, pricking?
Somatic pain: originates from the abdominal wall or parietal peritoneum (
Box 1.1
).
One process can cause both features, the classic example being appendicitis, which starts with a poorly localised central abdominal aching visceral pain; as the appendix becomes more inflamed and irritates the parietal peritoneum, it progresses to sharp somatic-type pain localised to the right lower quadrant.
Exacerbating and relieving features
Patients should be asked if there are any factors that ‘bring the pain on or make it worse’ and conversely ‘make the pain better’. Specifically:
Any dietary features, including particular foods or the timing of meals?
Patients with chronic abdominal pain frequently attempt dietary manipulation to treat the pain. Pain consistently developing soon after a meal, particularly when associated with upper abdominal bloating and nausea or vomiting, may indicate gastric or small intestinal pathology or sensitivity.
Relief of low abdominal pain by the passage of flatus or stool?
This indicates rectal pathology or increased rectal sensitivity.
The effect of different forms of analgesia or antispasmodic when used may give clues as to the aetiology of the pain.
Simple analgesics such as paracetamol may be more effective in treating musculoskeletal or solid organ pain, whereas antispasmodics such as hyoscine butylbromide (Buscopan) or mebeverine may be more beneficial in treating pain related to hollow organs.
Pain associated with twisting or bending?
More likely related to the abdominal wall than intra-abdominal structures.
Pain severity
may be affected by stress in functional disorders, but increasing evidence shows that psychological stress also plays a role in the mediation of organic disease, such as inflammatory bowel disease (IBD).
Any associated symptoms?
The presence of associated symptoms may be instrumental in localising the origin of the pain.
Relationship to bowel habit: frequency, consistency, urgency, blood, mucus and any association of changes in the bowel habit with the pain are important.
Fluctuation in the pain associated with changes in bowel habit is indicative of a colonic process and is typical of irritable bowel syndrome (IBS).
Vomiting or upper abdominal distension?
Suggestive of small bowel obstruction or ileus.
Haematuria?
Indicates renal colic.
Palpable lump in the area of tenderness?
Suggests an inflammatory mass related to transmural inflammation of a viscus, but may simply be related to colonic loading of faeces.
Examination technique
The physical examination begins with a careful general inspection.
Does the patient look unwell?
Obvious weight loss or cachexia is an indicator of malabsorption or undernourishment.
Is the patient comfortable? If in acute pain, are they adopting a position to ease the pain?
The patient lying stock still in bed with obvious severe pain may well have peritonitis, whereas a patient moving about the bed, unable to get comfortable, is more likely to have visceral pain such as obstruction of a viscus.
Observation of the skin
may demonstrate jaundice, pallor associated with anaemia, erythema ab igne (reticular erythematous hyperpigmentation caused by repeated skin exposure to moderate heat used to relieve pain) or specific extraintestinal manifestations of disease (
Table 1.1
). Leg swelling may be an indicator of decreased blood albumin related to liver disease or malnutrition.
Observe the abdomen
for visible abdominal distension (caused by either ascites or distension of viscus by gas or fluid).
Vital signs, including the temperature
, should be noted.
Examination of the hands
may reveal clues to intra-abdominal disease. Clubbing may be related to chronic liver disease, IBD or other extra-abdominal disease with intra-abdominal consequences. Pale palmar creases may be associated with anaemia. Palmar erythema, asterixis, Dupytren’s contractures and spider naevi on the arms may be seen in chronic liver disease.
Inspection of the face
may reveal conjunctival pallor in anaemia, scleral yellowing in jaundice, or periorbital corneal arcus indicating hypercholesterolaemia and an increased risk of vascular disease or pancreatitis.
Careful cardiac and respiratory examinations
may reveal abnormalities associated with intra-abdominal disease. For example, peripheral vascular disease may indicate that a patient is at risk for intestinal ischaemia; congestive heart failure is associated with congestion of the liver, the production of ascites and gut oedema; and pain from cardiac ischaemia or pleuritis in lower-lobe pneumonia may refer to the abdomen.
Examination of the gastrointestinal (GI) system per se begins with careful inspection of the mouth with the aid of a torch and tongue depressor
. The presence of numerous or large mouth ulcers or marked swelling of the lips may be associated with IBD. Angular stomatitis occurs in iron deficiency. Glossitis may develop in association with vitamin B
12
deficiency caused by malabsorption.
Examination of the thyroid is followed by examination of the neck and axilla
for lymphadenopathy.
Careful inspection of the abdomen is repeated and the abdominal examination is completed as described in Part IV, taking great care to avoid causing undue additional discomfort
. The examiner must be careful to ask first whether there are any tender spots in the abdomen before laying on a hand. Special care should be taken, starting with very light palpation, asking the patient to advise the examiner of any discomfort felt and by watching the patient’s expression at all times. Only if light palpation is tolerated in an area of the abdomen should deep palpation be undertaken in that area. A useful additional sign to elicit when areas of localised tenderness are found is Carnett’s sign. While the examiner palpates over the area of tenderness, the patient is asked to raise their head from the bed against the resistance provided by the examiner’s free hand on their forehead. If the palpation tenderness continues or intensifies during this manoeuvre, it is likely to be related to the abdominal wall rather than to intra-abdominal structures.
Table 1.1 Extraintestinal manifestations of hepatogastrointestinal diseases.
Disease
Dermatological
Musculoskeletal
Inflammatory bowel disease:
Crohn’s disease
Erythema nodosum, pyoderma gangrenosum
Axial arthritis more common
Ulcerative colitis
Erythema nodosum, pyoderma gangrenosum
Axial and peripheral arthritis similar in frequency
Enteric infections (Shigella, Salmonella, Yersinia, Campylobacter)
Keratoderma blennorrhagica
Reactive arthritis
Malabsorption syndromes:
Coeliac sprue
Dermatitis herpetiformis
Polyarthralgia
Viral hepatitis:
Hepatitis B
Jaundice (hepatitis), livedo reticularis, skin ulcers (vasculitis)
Prodrome that includes arthralgias; mononeuritis multiplex
Hepatitis C
Jaundice (hepatitis), palpable purpura
Can develop positive rheumatoid factor
Henoch−Schönlein purpura
Palpable purpura over buttocks and lower extremities
Arthralgias
Approach to differential diagnosis of pain and directed investigation
Following a careful history and examination, the clinician should be able to develop an idea of which organ(s) is/are likely to be involved and what the likely pathogenesis might be considering the demographics of the patient and the nature of the pain. It is important to list the most likely diagnoses based on these factors first. The differential can then be expanded by the application of a surgical sieve (as described in Part IV) to add the less likely possibilities.
Most patients should have a minimal blood panel to rule out warning features and to make any obvious diagnoses. These would include full blood count (FBC); urea, creatinine and electrolytes; liver function tests (LFTs); and coeliac antibodies, especially if there is any alteration of bowel habit. Further testing should be directed at each of the most likely diagnoses in the list of differential diagnoses. The clinician should attempt to choose the range of investigations that will most cost-effectively examine for the greatest number of likely diagnoses with the greatest sensitivity and specificity (see Clinical example 1.1).
CLINICAL EXAMPLE 1.1
HISTORY Ms AP is a 37-year-old woman who describes 1 year of intermittent right lower quadrant abdominal pain. She is Caucasian, her body mass index is 19 kg/m2 and she smokes 20 cigarettes/day. The pain first came on following an illness associated with vomiting and diarrhoea. She saw her GP and was given antibiotics, but stool culture revealed no pathogens. The diarrhoea settled spontaneously and she currently opens her bowels three times a day to soft-to-loose stool with no blood or mucus. The pain is aching and intermittent, but seems to be worse during periods of life stress. It often occurs about half an hour after meals and is associated with abdominal bloating and on occasion nausea, but no vomiting. It lasts 30 minutes to some hours at a time. There is no position in which she can get comfortable and she describes herself as ‘writhing around’ with the pain. She has reduced the size of her meals and avoids excess fibre, which seems to help. No specific foods contribute to the symptoms. Opening her bowels does not relieve the pain. She has trialled no medications. She has lost 5 kg in weight in the last year. The pain does not wake her at night and there is no nocturnal diarrhoea. There has been no change in the menstrual cycle and no association of the pain with menses. There has been no haematuria and she has never passed stones with the urine. She is on no regular medication. There is no significant family history.
EXAMINATION Observation reveals a thin woman with no hand or face signs of gastrointestinal disease; in particular, no pallor, skin lesions, angular stomatitis, mouth ulceration or tongue swelling. The abdomen is not distended. There is localised tenderness in the right lower quadrant. No mass is palpable. Carnett’s sign is negative (the tenderness disappears when the patient lifts her head from the bed). There is no organomegaly. Bowel sounds are normal.
SYNTHESIS (SEE TABLE 1.2) In considering the differential diagnosis and investigation plan, one must first consider which organ(s) might be involved, then what the possible pathologies in those organs might be, before considering the investigations that are useful for each possible pathology in each organ system. This will allow a tailored approach to directed investigation that is cost-effective and limits the potential harm to the patient.
Likely organ involved In considering the differential diagnosis, one must first consider which organ(s) might be involved. The central and aching nature of the pain, as well as the fact that it causes the patient to writhe around, suggest that it is originating in a hollow organ, perhaps the small bowel or proximal colon. The localised tenderness further localises the pain to the distal small bowel or proximal colon. The onset was associated with a probable gastroenteritis and the bowel habit is mildly disturbed, also suggesting an intestinal cause. The lack of association with menses and the absence of other urinary symptoms make conditions of the reproductive system and renal tract less likely.
Likely pathology The most likely diagnoses in this setting are inflammatory bowel disease and functional GI disease (IBS). Most patients with gastrointestinal symptoms require serological testing for coeliac disease, as it is very common and its symptoms commonly mimic other diseases. Use of a surgical sieve applied to the distal small bowel and proximal colon expands the list to include infection, neoplasia (including benign neoplasia resulting in intermittent intussusceptions) and, although unlikely in a young woman, intestinal ischaemia. Less likely causes in other organ systems include biliary colic, ovarian pain and renal colic.
Investigation plan Initial investigation reveals a microcytic anaemia but no abnormality of the renal and liver tests and negative coeliac antibodies. Stool culture and examination for ova, cysts and parasites are negative. Urine dipstick shows no blood. Warning features in the form of weight loss and anaemia prompt further investigation. The investigation of choice to rule out inflammatory disease in the terminal ileum and colon is ileocolonoscopy and biopsy. The standard investigation for the remaining small bowel is computed tomography (CT) or magnetic resonance imaging (MRI) enterography. This will also effectively investigate for biliary disease, ovarian disease and renal disease. More expensive and invasive investigations designed to examine for the less likely diagnoses are not utilised in the first instance (see Chapter 6).
At colonoscopy the caecum and terminal ileum are seen to be inflamed and ulcerated. Biopsies show chronic inflammation, ulceration and granuloma formation, suggestive of Crohn’s disease. CT shows no disease of the ovaries, kidneys or biliary tree, but does suggest thickening and inflammation of the terminal ileum and caecum. There is no significant lymphadenopathy. A diagnosis of probable Crohn’s disease is made and the patient treated accordingly.
Table 1.2 Approach to differential diagnosis and directed investigation for Ms AP.
Likely organ involved
Likely pathology
Investigation choices
Investigation plan
Small bowel and colon
Inflammatory bowel disease
Ileocolonoscopy CT/MRI enterography US small bowel Capsule endoscopy
Stool test Ileocolonoscopy CT (or MRI) enterography
Irritable bowel syndrome
Suggestive symptom complex in the absence of other diagnoses
Infection
Stool culture and examination for
C. difficile
, ova, cysts and parasites Specific parasitic serology if peripheral eosinophilia
Neoplasia
Ileocolonoscopy and enterography (CT/MRI) or capsule endoscopy
Ischaemia
Angiography
Biliary system
Biliary stones, neoplasia
Ultrasound abdomen MRCP Endoscopic ultrasound ERCP
Ovary
Ovarian cyst, torted ovary
Ultrasound pelvis CT pelvis
Renal
Renal stones
Ultrasound abdomen CT urogram
US, ultrasound; MRI, magnetic resonance imaging; MRCP, magnetic resonance cholangiopancreatography; ERCP, endoscopic retrograde cholangiopancreatography; CT, computed tomography scan.
Acute abdominal pain
The patient presenting with acute abdominal pain is a particular challenge to the clinician. Pain production within the abdomen is such that a wide range of diagnoses can present in an identical manner. However, a thorough history and examination still constitute the cornerstone of assessment. It is essential to have an understanding of the mechanisms of pain generation. Equally, it is important to recognise the alarm symptoms and initial investigative findings that help to determine which patients may have a serious underlying disease process, who therefore warrant more expeditious evaluation and treatment.
Clinical features
History taking
The assessment of the patient with abdominal pain proceeds in the same way whatever the severity of the pain; however, in the acute setting, assessment and management may need to proceed simultaneously and almost invariably involve consultation with a surgeon. Much debate has centred on the pros and cons of opiate analgesia in patients with severe abdominal pain, as this may affect assessment. The current consensus is that while judicious use of opiate analgesia may affect the examination findings, it does not adversely affect the outcome for the patient and is preferable to leaving a patient in severe pain.
The history (Table 1.3) gives vital clues as to the diagnosis and should include questions regarding the location (Figure 1.2), character, onset and severity of the pain, any radiation or referral, any past history of similar pain, and any associated symptoms.
Table 1.3 Historical features in acute abdominal pain examination.
Where is the pain?
See
Figure 1.2
Character of the pain?
Acute waves of sharp constricting pain that ‘take the breath away’ (renal or biliary colic) Waves of dull pain with vomiting (intestinal obstruction) Colicky pain that becomes steady (appendicitis, strangulating intestinal obstruction, mesenteric ischaemia) Sharp, constant pain, worsened by movement (peritonitis) Tearing pain (dissecting aneurysm) Dull ache (appendicitis, diverticulitis, pyelonephritis)
Past similar pain?
‘Yes’ suggests recurrent problems such as ulcer disease, gallstone colic, diverticulitis or mittelschmerz
Onset?
Sudden: ‘like a thunderclap’ (perforated ulcer, renal stone, ruptured ectopic pregnancy, torsion of ovary or testis, some ruptured aneurysms) Less sudden: most other causes
Severity of the pain?
Severe pain (perforated viscus, kidney stone, peritonitis, pancreatitis) Pain out of proportion to physical findings (mesenteric ischaemia)
Radiation/referral?
Right scapula (gallbladder pain) Left shoulder region (ruptured spleen, pancreatitis) Pubis or vagina (renal pain) Back (ruptured aortic aneurysm)
Relieving factors?
Antacids (peptic ulcer disease) Lying as quietly as possible (peritonitis)
Associated symptoms?
Vomiting precedes pain and is followed by diarrhoea (gastroenteritis) Delayed vomiting, absent bowel movement and flatus (acute intestinal obstruction; the delay increases with a lower site of obstruction) Severe vomiting precedes intense epigastric, left chest or shoulder pain (emetic perforation of the intra-abdominal oesophagus)
Figure 1.2 Likely pathologies according to location of acute pain.
Source: Frederick H. Millham, in Feldman M, Friedman L, Brandt L (eds) (2010) Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 9th edn, Philadelphia, PA: Saunders, Figure 10.3. Reproduced with permission of Elsevier.
Careful exclusion of past or chronic health problems that may have progressed to, or be associated with, the current condition is important. A patient with chronic dyspepsia may now be presenting with perforation of a duodenal ulcer. The patient with severe peripheral vascular disease, or who has had recent vascular intervention, might have acute mesenteric ischaemia. A binge drinker with past episodes of alcohol-related pain is at risk for acute pancreatitis, as is the patient with known cholelithiasis. Patients with past multiple abdominal surgeries are at risk for intestinal obstruction.
Questioning regarding current and past prescribed, illicit and complementary medicine use is necessary. The patient using non-steroidal anti-inflammatory drugs (NSAIDs) is at risk of peptic ulceration; use of anticoagulants increases the risk of haemorrhagic conditions; prednisone or immunosuppressants may blunt the inflammatory response to perforation or peritonitis, resulting in less pain than expected.
Examination
Initial assessment is aimed at determining the seriousness of the illness. A happy, comfortable-appearing patient rarely has a serious problem, unlike one who is anxious, pale, sweaty or in obvious pain. Vital signs, state of consciousness and other indications of peripheral perfusion must be evaluated.
Examination of the non-abdominal organ systems
is aimed at determining any evidence for an extra-abdominal cause for the pain:
Abdominal wall tenderness and swelling with rectus muscle haematoma. Extremely tender, sometimes red and swollen scrotum with testicular torsion.
Resolving (sometimes completely resolved) rash in post-herpetic pain.
Ketones on the breath in diabetic ketoacidosis.
Pulmonary findings in pneumonia and pleuritis.
Examination of the abdomen
focuses on the detection of peritonitis, any intra-abdominal masses or organomegaly, and localisation of the underlying pathology:
Distension of the abdomen may be associated with intestinal obstruction.
Bruising at the flanks (Grey Turner’s sign) and periumbilically (Cullen’s sign) is occasionally seen in acute haemorrhagic pancreatitis.
Absent bowel sounds is indicative of ileus and in the presence of severe pain suggests peritonitis.
High-pitched or overactive bowel sounds might indicate intestinal obstruction.
Palpation
should start with very light examination well away from the area of greatest pain. Guarding, rigidity and rebound indicate peritoneal irritation. Guarding is a slow and sustained involuntary contraction of the abdominal muscles, rather than the flinching that is observed with sensitive or anxious patients. Careful exclusion of hernias at the inguinal canals and over surgical scars, as well as pelvic and rectal examination, is essential.
Investigation
Most patients will have an FBC, urea, creatinine and electrolytes, and dipstick urinalysis performed, although the results from these tests are neither sensitive nor specific. Serum lipase, however, is useful in detecting acute pancreatitis. It is essential that erect chest and abdomen and supine abdominal X-rays are performed when there is the possibility of intestinal perforation or obstruction. If the patient cannot sit up, the left lateral position may be used.
Modern imaging can detect the underlying pathology in acute abdominal pain with high sensitivity and specificity. While ultrasound examination has the benefits of portability and avoidance of radiation exposure, it is most useful in detecting disease of the gallbladder, and gynaecological and obstetric conditions. CT has emerged as the dominant imaging tool for evaluation of the patient with severe acute abdominal pain. This has come about with the frequent advent of easy access to helical CT within or adjacent to the emergency department. The proper execution and interpretation of CT in this setting have been shown to reduce the need for exploratory laparotomy and hence morbidity, mortality and medical expense.
Management and prognosis
The management and prognosis of both acute and chronic abdominal pain very much depend on the underlying cause. The management and prognosis of the individual diseases that cause abdominal pain (see Box 1.3 and Figure 1.2) are dealt with in each of the individual disease chapters of this book (Chapters 7 to 30).
KEY POINTS
Peritoneal pain localizes to the area affected, whereas visceral pain tends to be felt in the upper abdomen – foregut; central abdomen – midgut; or lower abdomen – hindgut.
Mode of onset, time course, location and radiation, character and exacerbants/relievers are essential to determining the cause of abdominal pain.
Symptoms associated with the pain are invaluable in further localising the disease process.
Develop a wide-ranging list of differential diagnoses first, then tailor the investigative strategy to that list and other factors that affect the individual patient.
SELF-ASSESSMENT QUESTION
(The answer to this question is given on p. 265)
A 45-year-old woman presents acutely with vague, cramping, right upper quadrant, epigastric and right shoulder blade pain. She has experienced similar pain on a few previous occasions over the last year, but never this severe. In the past the pain has been exacerbated by fatty meals, as on this occasion. She cannot get comfortable with the pain; it tends to come in waves but never completely abates. When it is present she finds breathing more difficult. She has taken paracetamol with minimal relief.
With regard to your initial approach to this patient, which of the following is most true?
The localisation of her pain to one area indicates that there is irritation of the parietal peritoneum.
Her scapular pain indicates that there is retroperitoneal involvement.
Her description of the pain makes a hollow organ the likely source.
The epigastric and right upper quadrant location of her pain indicate that it is likely to be coming from the midgut.
She is describing radiation of the pain to the back, which makes a pancreatic cause more likely.
2Approach to the patient with liver disease
Patients with liver disease can present with a wide range of complaints, and the clinician must remain alert at all times to the possibility of hepatic involvement in disease. Increasingly commonly, asymptomatic patients will present because of liver test abnormalities discovered incidentally. Once the presence of hepatic dysfunction has been established, the not always straightforward task of defining the underlying pathology is critical to planning appropriate management.
Epidemiology
The exact epidemiology of hepatic disease in the world is largely unknown. However, most estimates show that it is increasing out of proportion to many other chronic diseases. This is largely driven by increasing rates of obesity and non-alcoholic fatty liver disease, as well as of alcohol consumption and hepatitis B and C. Some sense of the burden of disease is given by the rates of cirrhosis and liver cancer, as they represent the end stage of liver pathology. Even across Europe the incidence of cirrhosis varies widely, with 1 in 1000 Hungarian males dying of cirrhosis each year compared with 1 in 100,000 Greek females. The World Health Organization (WHO) estimates that liver cancer is responsible for around 47,000 deaths per year in the European Union (EU).
Clinical features
History taking
Liver disease can present in a variety of ways:
Non-specific symptoms
include fatigue, anorexia, nausea and, occasionally, vomiting.
Loose, fatty stools (steatorrhoea)
can occur if cholestasis interrupts bile flow to the small intestine.
Fever (due to liver pyrogens)
may be the first feature in viral or alcoholic hepatitis.
Jaundice
becomes visible when the serum bilirubin reaches 34–43 µmol/l (2–2.5 mg/dl). While jaundice may be related to hepatic dysfunction, equally it can be a result of bilirubin overproduction. Mild jaundice without dark urine suggests unconjugated hyperbilirubinaemia (most often caused by haemolysis or Gilbert’s syndrome).
The historical features that it is important to elicit include those in the following sections.
Onset and duration
Did the symptoms come on gradually or suddenly? How long have the symptoms been a problem?
Symptoms of acute onset may result from an acute vascular event, toxic cause, obstruction of the biliary system or acute infection. Symptoms resulting from chronic inflammatory processes are more likely to be of gradual onset. The development of dark urine (bilirubinuria) due to increased serum bilirubin, from hepatocellular or cholestatic causes, often precedes the onset of visible jaundice.
Identify precipitating events
related to the onset of the symptoms. Direct questions often need to be asked regarding exposure to common causes (
BOX 2.1
), in particular:
Any association with pain that might relate to biliary obstruction?
Any use of medicines – prescribed, complementary or illicit? (NB: Antibiotic-related disease may take up to two weeks to present)
Any trauma or major stress, including surgery?
Any association with starvation (important in Gilbert’s syndrome; see
Chapter 20
)?
Any history of marked weight loss or gain?
Any association with vascular events or hypotension?
Any possible infectious contact or exposure?
Box 2.1 Common causes of liver disease
Infectious liver disease
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Epstein–Barr virus
Drug-induced hepatitis or cholestasis
Vascular disease
Ischaemic hepatitis
Portal vein thrombosis
Budd–Chiari syndrome
Nodular regenerative hyperplasia
Veno-occlusive disease of the liver
Immune hepatitis
Autoimmune hepatitis
Granulomatous hepatitis
Deposition diseases
