Anatomy and physiology
The gastrointestinal system comprises the alimentary tract, the liver, the biliary system, the pancreas and the spleen. The alimentary tract extends from the mouth to the anus and includes the oesophagus, stomach, small intestine or small bowel (comprising the duodenum, jejunum and ileum), colon (large intestine or large bowel) and rectum ( Figs 6.1 – 6.2 and Box 6.1 ).
|Liver||Upper border: fifth right intercostal space on full expiration |
Lower border: at the costal margin in the mid-clavicular line on full inspiration
|Spleen||Underlies left ribs 9–11, posterior to the mid-axillary line|
|Gallbladder||At the intersection of the right lateral vertical plane and the costal margin, i.e. tip of the ninth costal cartilage|
|Pancreas||Neck of the pancreas lies at the level of L1; head lies below and right; tail lies above and left|
|Kidneys||Upper pole lies deep to the 12th rib posteriorly, 7 cm from the midline; the right is 2–3 cm lower than the left|
The abdominal surface can be divided into nine regions by the intersection of two horizontal and two vertical planes ( Fig. 6.1C ).
Gastrointestinal symptoms are common and are often caused by functional dyspepsia and irritable bowel syndrome. Symptoms suggesting a serious alternative or coexistent diagnosis include persistent vomiting, dysphagia, gastrointestinal bleeding, weight loss, painless, watery, high-volume diarrhoea, nocturnal symptoms, fever and anaemia. The risk of serious disease increases with age. Always explore the patient’s ideas, concerns and expectations about the symptoms ( p. 5 ) to understand the clinical context.
Common presenting symptoms
Bad breath (halitosis) due to gingival, dental or pharyngeal infection and dry mouth (xerostomia) are common mouth symptoms. Rarely, patients complain of altered taste sensation (dysgeusia) or of a foul taste in the mouth (cacogeusia).
Anorexia and weight loss
Anorexia is loss of appetite and/or a lack of interest in food. In addition to enquiring about appetite, ask ‘Do you still enjoy your food?’
Weight loss, in isolation, is rarely associated with serious organic disease. Ask how much weight has been lost, over what time. Loss of < 3 kg in the previous 6 months is rarely significant. Weight loss is usually the result of reduced energy intake, not increased energy expenditure. It does not specifically indicate gastrointestinal disease, although it is common in many gastrointestinal disorders, including malignancy and liver disease. Energy requirements average 2500 kcal/day for males and 2000 kcal/day for females. Reduced energy intake arises from dieting, loss of appetite, malabsorption or malnutrition. Increased energy expenditure occurs in hyperthyroidism, fever or the adoption of a more energetic lifestyle. A net calorie deficit of 1000 kcal/day results in weight loss of approximately 1 kg/week (7000 kcal ≅ 1 kg of fat). Greater weight loss during the initial stages of energy restriction arises from salt and water loss and depletion of hepatic glycogen stores, not from fat loss. Rapid weight loss over days suggests loss of body fluid as a result of vomiting, diarrhoea or diuretics (1 L of water = 1 kg). Check current and previous weight records to confirm apparent weight loss on examination (loose-fitting clothes, for example).
Causes of sore lips, tongue or buccal mucosa include:
deficiencies, including iron, folate, vitamin B 12 or C
dermatological disorders, including lichen planus ( Fig. 6.3A )
aphthous ulcers ( Fig. 6.3B )
inflammatory bowel disease and coeliac disease, associated with mouth ulcers.
Heartburn and reflux
Heartburn is a hot, burning retrosternal discomfort.
To differentiate heartburn from cardiac chest pain, ask about associated features:
character of pain: burning
precipitating factors: lying flat or bending forward
waterbrash (sudden appearance of fluid in the mouth due to reflex salivation as a result of gastro-oesophageal reflux disease (GORD) or, rarely, peptic ulcer disease)
the taste of acid appearing in the mouth due to reflux/regurgitation.
When heartburn is the principal symptom, GORD is the most likely diagnosis.
Dyspepsia is pain or discomfort centred in the upper abdomen. In contrast, ‘indigestion’ is a term commonly used by patients for ill-defined symptoms from the upper gastrointestinal tract.
site of pain
character of pain
exacerbating and relieving factors, such as food and antacid
associated symptoms, such as nausea, belching, bloating and premature satiety.
Clusters of symptoms are used to classify dyspepsia:
reflux-like dyspepsia (heartburn-predominant dyspepsia)
ulcer-like dyspepsia (epigastric pain relieved by food or antacids)
dysmotility-like dyspepsia (nausea, belching, bloating and premature satiety).
Often there is no structural cause and the dyspepsia is functional. There is considerable overlap, however, and it is impossible to diagnose functional dyspepsia on history alone without investigation. Dyspepsia that is worse with an empty stomach and eased by eating is typical of peptic ulceration. The patient may indicate a single localised point in the epigastrium (pointing sign), and complain of nausea and abdominal fullness that is worse after fatty or spicy meals. ‘Fat intolerance’ is common with all causes of dyspepsia, including gallbladder disease.
Odynophagia is pain on swallowing, often precipitated by drinking hot liquids. It can be present with or without dysphagia (see below) and may indicate oesophageal ulceration or oesophagitis from gastro-oesophageal reflux or oesophageal candidiasis. It implies intact mucosal sensation, making oesophageal cancer unlikely.
Characterise the pain using SOCRATES (see Box 2.2 ). Ask about the characteristics described here.
Visceral abdominal pain from distension of hollow organs, mesenteric traction or excessive smooth-muscle contraction is deep and poorly localised in the midline. The pain is conducted via sympathetic splanchnic nerves. Somatic pain from the parietal peritoneum and abdominal wall is lateralised and localised to the inflamed area. It is conducted via intercostal nerves.
Pain arising from foregut structures (stomach, pancreas, liver and biliary system) is localised above the umbilicus ( Fig. 6.4 ). Central abdominal pain arises from midgut structures, such as the small bowel and appendix. Lower abdominal pain arises from hindgut structures, such as the colon. Inflammation may cause localised pain: for example, left iliac fossa pain due to diverticular disease of the sigmoid colon.
Pain from an unpaired structure, such as the pancreas, is midline and radiates through to the back. Pain from paired structures, such as renal colic, is felt on and radiates to the affected side ( Fig. 6.5 ). Torsion of the testis may present with abdominal pain ( p. 232 ). In females, consider gynaecological causes like ruptured ovarian cyst, pelvic inflammatory disease, endometriosis or ectopic pregnancy ( p. 218 ).
Sudden onset of severe abdominal pain, rapidly progressing to become generalised and constant, suggests a hollow viscus perforation (usually due to colorectal cancer, diverticular disease or peptic ulceration), a ruptured abdominal aortic aneurysm or mesenteric infarction.
Torsion of the caecum or sigmoid colon (volvulus) presents with sudden abdominal pain associated with acute intestinal obstruction.
Colicky pain lasts for a short time (seconds or minutes), eases off and then returns. It arises from hollow structures, as in small or large bowel obstruction, or the uterus during labour.
Biliary and renal ‘colic’ are misnamed, as the pain is rarely colicky; pain rapidly increases to a peak and persists over several hours before gradually resolving. Dull, constant, vague and poorly localised pain is more typical of an inflammatory process or infection, such as salpingitis, appendicitis or diverticulitis ( Box 6.2 ).
Pain radiating from the right hypochondrium to the shoulder or interscapular region may reflect diaphragmatic irritation, as in acute cholecystitis (see Fig. 6.5 ). Pain radiating from the loin to the groin and genitalia is typical of renal colic. Central upper abdominal pain radiating through to the back, partially relieved by sitting forward, suggests pancreatitis. Central abdominal pain that later shifts into the right iliac fossa occurs in acute appendicitis. The combination of severe back and abdominal pain may indicate a ruptured or dissecting abdominal aortic aneurysm.
Anorexia, nausea and vomiting are common but non-specific symptoms. They may accompany any very severe pain but conversely may be absent, even in advanced intra-abdominal disease. Abdominal pain due to irritable bowel syndrome, diverticular disease or colorectal cancer is usually accompanied by altered bowel habit. Other features such as breathlessness or palpitation suggest non-alimentary causes ( Box 6.3 ).
|Dissecting aortic aneurysm|
|Acute vertebral collapse|
|Salpingitis or tubal pregnancy|
|Torsion of testis/ovary|
Hypotension and tachycardia following the onset of pain suggest intra-abdominal sepsis or bleeding: for example, from a peptic ulcer, a ruptured aortic aneurysm or an ectopic pregnancy.
During the first 1–2 hours after perforation, a ‘silent interval’ may occur when abdominal pain resolves transiently. The initial chemical peritonitis may subside before bacterial peritonitis becomes established. For example, in acute appendicitis, pain is initially periumbilical (visceral pain) and moves to the right iliac fossa (somatic pain) when localised inflammation of the parietal peritoneum becomes established. If the appendix ruptures, generalised peritonitis may develop. Occasionally, a localised appendix abscess develops, with a palpable mass and localised pain in the right iliac fossa.
Change in the pattern of symptoms suggests either that the initial diagnosis was wrong or that complications have developed. In acute small bowel obstruction, a change from typical intestinal colic to persistent pain with abdominal tenderness suggests intestinal ischaemia, as in strangulated hernia, and is an indication for urgent surgical intervention.
Abdominal pain persisting for hours or days suggests an inflammatory disorder, such as acute appendicitis, cholecystitis or diverticulitis.
Exacerbating and relieving factors
Pain exacerbated by movement or coughing suggests inflammation. Patients tend to lie still to avoid exacerbating the pain. People with colic typically move around or draw their knees up towards the chest during spasms.
Excruciating pain, poorly relieved by opioid analgesia, suggests an ischaemic vascular event, such as bowel infarction or ruptured abdominal aortic aneurysm. Severe pain rapidly eased by potent analgesia is more typical of acute pancreatitis or peritonitis secondary to a ruptured viscus.
Features of the pain can help distinguish between possible causes ( Box 6.3 ).
The acute abdomen
The majority of general surgical emergencies are patients with sudden severe abdominal pain (an ‘acute abdomen’). Patients may be so occupied by recent and severe symptoms that they forget important details of the history unless asked directly. Seek additional information from family or friends if severe pain, shock or altered consciousness makes it difficult to obtain a history from the patient. Note any relevant past history, such as acute perforation in a patient with known diverticular disease. Causes range from self-limiting to severe life-threatening diseases ( Box 6.4 ). Evaluate patients rapidly, and then resuscitate critically ill patients immediately before undertaking further assessment and surgical intervention. Parenteral opioid analgesia to alleviate severe abdominal pain will help, not hinder, clinical assessment. In patients with undiagnosed acute abdominal pain, reassess their clinical state regularly, undertake urgent investigations and consider surgical intervention before administering repeat analgesia.
|Acute appendicitis||Nausea, vomiting, central abdominal pain that later shifts to right iliac fossa||Fever, tenderness, guarding or palpable mass in right iliac fossa, pelvic peritonitis on rectal examination|
|Perforated peptic ulcer with acute peritonitis||Vomiting at onset associated with severe acute-onset abdominal pain, previous history of dyspepsia, ulcer disease, non-steroidal anti-inflammatory drugs or glucocorticoid therapy||Shallow breathing with minimal abdominal wall movement, abdominal tenderness and guarding, board-like rigidity, abdominal distension and absent bowel sounds|
|Acute pancreatitis||Anorexia, nausea, vomiting, constant severe epigastric pain, previous alcohol abuse/cholelithiasis||Fever, periumbilical or loin bruising, epigastric tenderness, variable guarding, reduced or absent bowel sounds|
|Ruptured aortic aneurysm||Sudden onset of severe, tearing back/loin/abdominal pain, hypotension and past history of vascular disease and/or high blood pressure||Shock and hypotension, pulsatile, tender, abdominal mass, asymmetrical femoral pulses|
|Acute mesenteric ischaemia||Anorexia, nausea, vomiting, bloody diarrhoea, constant abdominal pain, previous history of vascular disease and/or high blood pressure||Atrial fibrillation, heart failure, asymmetrical peripheral pulses, absent bowel sounds, variable tenderness and guarding|
|Intestinal obstruction||Colicky central abdominal pain, nausea, vomiting and constipation||Surgical scars, hernias, mass, distension, visible peristalsis, increased bowel sounds|
|Ruptured ectopic pregnancy||Premenopausal female, delayed or missed menstrual period, hypotension, unilateral iliac fossa pain, pleuritic shoulder-tip pain, ‘prune juice’-like vaginal discharge||Suprapubic tenderness, periumbilical bruising, pain and tenderness on vaginal examination (cervical excitation), swelling/fullness in fornix on vaginal examination|
|Pelvic inflammatory disease||Sexually active young female, previous history of sexually transmitted infection, recent gynaecological procedure, pregnancy or use of intrauterine contraceptive device, irregular menstruation, dyspareunia, lower or central abdominal pain, backache, pleuritic right upper quadrant pain (Fitz-Hugh–Curtis syndrome)||Fever, vaginal discharge, pelvic peritonitis causing tenderness on rectal examination, right upper quadrant tenderness (perihepatitis), pain/tenderness on vaginal examination (cervical excitation), swelling/fullness in fornix on vaginal examination|
Patients with dysphagia complain that food or drink sticks when they swallow.
onset: recent or longstanding
nature: intermittent or progressive
difficulty swallowing solids, liquids or both
the level the patient feels food sticks at
any regurgitation or reflux of food or fluid
any associated pain (odynophagia), heartburn or weight loss.
Do not confuse dysphagia with early satiety, the inability to complete a full meal because of premature fullness, or with globus, which is a feeling of a lump in the throat. Globus does not interfere with swallowing and is not related to eating.
Neurological dysphagia resulting from bulbar or pseudobulbar palsy ( p. 129 ) is worse for liquids than solids, and may be accompanied by choking, spluttering and fluid regurgitating from the nose.
Neuromuscular dysphagia, or oesophageal dysmotility, presents in middle age, is worse for solids and may be helped by liquids and sitting upright. Achalasia, when the lower oesophageal sphincter fails to relax normally, leads to progressive oesophageal dilatation above the sphincter. Overflow of secretions and food into the respiratory tract may then occur, especially at night when the patient lies down, causing aspiration pneumonia. Oesophageal dysmotility can cause oesophageal spasm and central chest pain, which may be confused with cardiac pain.
A pharyngeal pouch may cause food to stick or be regurgitated, and may lead to recurrent chest infections due to chronic silent aspiration.
‘Mechanical’ dysphagia is often due to oesophageal stricture but can be caused by external compression. With weight loss, a short history and no reflux symptoms, suspect oesophageal cancer. Longstanding dysphagia without weight loss but accompanied by heartburn is more likely to be due to benign peptic stricture. Record the site at which the patient feels the food sticking; this is not a reliable guide to the site of oesophageal obstruction, however.
Nausea and vomiting
Nausea is the sensation of feeling sick. Vomiting is the expulsion of gastric contents via the mouth. Both are associated with pallor, sweating and hyperventilation.
relation to meals and timing, such as early morning or late evening
associated symptoms, such as dyspepsia and abdominal pain, and whether they are relieved by vomiting
whether the vomit is bile-stained (green), blood-stained or faeculent
associated weight loss
the patient’s medications.
Nausea and vomiting, particularly with abdominal pain or discomfort, suggest upper gastrointestinal disorders. Dyspepsia causes nausea without vomiting. Peptic ulcers seldom cause painless vomiting unless they are complicated by pyloric stenosis, which causes projectile vomiting of large volumes of gastric content that is not bile-stained. Obstruction distal to the pylorus produces bile-stained vomit. Severe vomiting without significant pain suggests gastric outlet or proximal small bowel obstruction. Faeculent vomiting of small bowel contents (not faeces) is a late feature of distal small bowel or colonic obstruction. In peritonitis, the vomitus is usually small in volume but persistent. The more distal the level of intestinal obstruction, the more marked the accompanying abdominal distension and colic.
Vomiting is common in gastroenteritis, cholecystitis, pancreatitis and hepatitis. It is typically preceded by nausea but in raised intracranial pressure may occur without warning. Severe pain may precipitate vomiting, as in renal or biliary colic or myocardial infarction.
Anorexia nervosa and bulimia are eating disorders characterised by undisclosed, self-induced vomiting. In bulimia, weight is maintained or increased, unlike in anorexia nervosa, where profound weight loss is common.
Other non-gastrointestinal causes of nausea and vomiting include:
drugs, such as alcohol, opioids, theophyllines, digoxin, cytotoxic agents or antidepressants
renal or liver failure
raised intracranial pressure (meningitis, brain tumour)
vestibular disorders (labyrinthitis and Ménière’s disease).
Wind and flatulence
Belching, excessive or offensive flatus, abdominal distension and borborygmi (audible bowel sounds) are often called ‘wind’ or flatulence. Clarify exactly what the patient means. Belching is due to air swallowing (aerophagy) and has no medical significance. It may indicate anxiety but sometimes occurs in an attempt to relieve abdominal pain or discomfort, and accompanies GORD.
Normally, 200–2000 mL of flatus is passed each day. Flatus is a mixture of gases derived from swallowed air and from colonic bacterial fermentation of poorly absorbed carbohydrates. Excessive flatus occurs particularly in lactase deficiency and intestinal malabsorption.
Borborygmi result from movement of fluid and gas along the bowel. Loud borborygmi, particularly if associated with colicky discomfort, suggest small bowel obstruction or dysmotility.
Abdominal girth slowly increasing over months or years is usually due to obesity but in a patient with weight loss it suggests intra-abdominal disease. The most common causes of abdominal distension are:
f at in obesity
f latus in pseudo-obstruction or bowel obstruction
f aeces in subacute obstruction or constipation
f luid in ascites (accumulation of fluid in the peritoneal cavity; Fig. 6.6 ), tumours (especially ovarian) or distended bladder
f unctional bloating (fluctuating abdominal distension that develops during the day and resolves overnight, usually occurring in irritable bowel syndrome).
Altered bowel habit
Clarify what patients mean by diarrhoea. They may complain of frequent stools or of a change in consistency of the stools. Normal frequency ranges from three bowel movements daily to once every 3 days. Diarrhoea is the frequent passage of loose stools. Steatorrhoea is diarrhoea associated with fat malabsorption. The stools are greasy, pale and bulky, and they float, making them difficult to flush away.
onset of diarrhoea: acute, chronic or intermittent
consistency: watery, unformed or semisolid
contents: red blood, mucus or pus
associated features: urgency, faecal incontinence or tenesmus (the sensation of needing to defecate, although the rectum is empty), abdominal pain, vomiting, sleep disturbance
recent travel and where to
recent medication, in particular any antibiotics.
High-volume diarrhoea (> 1 L per day) occurs when stool water content is increased (the principal site of physiological water absorption being the colon) and may be:
secretory, due to intestinal inflammation, as in infection or inflammatory bowel disease
osmotic, due to malabsorption, drugs (as in laxative abuse) or motility disorders (autonomic neuropathy, particularly in diabetes).
If the patient fasts, osmotic diarrhoea stops but secretory diarrhoea persists. The most common cause of acute diarrhoea is infective gastroenteritis due to norovirus, Salmonella species or Clostridium difficile . Infective diarrhoea can become chronic (> 4 weeks) in cases of parasitic infestations (such as giardiasis ( Giardia lamblia ), amoebiasis or cryptosporidiosis). Steatorrhoea is common in coeliac disease, chronic pancreatitis and pancreatic insufficiency due to cystic fibrosis. Bloody diarrhoea may be caused by inflammatory bowel disease, colonic ischaemia or infective gastroenteritis. Change in the bowel habit towards diarrhoea can be a manifestation of colon cancer, in particular cancer of the right side of the colon and in patients over 50 years. Thyrotoxicosis is often accompanied by secretory diarrhoea or steatorrhoea and weight loss.
Low-volume diarrhoea is associated with irritable bowel syndrome. Abdominal pain, bloating, dyspepsia and non-alimentary symptoms commonly accompany irritable bowel symptoms. Criteria have been developed to define irritable bowel syndrome more precisely, taking account of the duration of symptoms, the presence of abdominal pain and its relationship to defecation, and the frequency and consistency of stools (see Rome IV criteria for irritable bowel syndrome).
Clarify what the patient means by constipation. Use the Bristol stool form scale ( Fig. 6.7 ) to describe the stools. Constipation is the infrequent passage of hard stools.
onset: lifelong or of recent onset
stool frequency: how often the patient moves their bowels each week and how much time is spent straining at stool
shape of the stool: for example, pellet-like
associated symptoms, such as abdominal pain, anal pain on defecation or rectal bleeding
drugs that may cause constipation.
Constipation may be due to lack of dietary fibre, impaired colonic motility, mechanical intestinal obstruction, impaired rectal sensation or anorectal dysfunction impairing the process of defecation. Constipation is common in irritable bowel syndrome. Other important causes include colorectal cancer, hypothyroidism, hypercalcaemia, drugs (opiates, iron) and immobility (Parkinson’s disease, stroke). Absolute constipation (no flatus or bowel movements) suggests intestinal obstruction and is usually associated with pain, vomiting and distension. Tenesmus suggests rectal inflammation or tumour. Faecal impaction can occasionally present as overflow diarrhoea.
Haematemesis is the vomiting of blood.
Colour: is the vomitus fresh red blood or dark brown, resembling coffee grounds?
Onset: was haematemesis preceded by intense retching or was blood staining apparent in the first vomit?
History of dyspepsia, peptic ulceration, gastrointestinal bleeding or liver disease.
Alcohol, non-steroidal anti-inflammatory drugs (NSAIDs) and glucocorticoid ingestion.
If the source of bleeding is above the gastro-oesophageal sphincter, as with oesophageal varices, fresh blood may well up in the mouth, as well as being actively vomited. With a lower oesophageal mucosal tear due to the trauma of forceful retching (Mallory–Weiss syndrome), fresh blood appears only after the patient has vomited forcefully several times.
Melaena is the passage of tarry, shiny black stools with a characteristic odour and results from upper gastrointestinal bleeding. Distinguish this from the matt black stools associated with oral iron or bismuth therapy.
Peptic ulceration (gastric or duodenal) is the most common cause of upper gastrointestinal bleeding and can manifest with melaena, haematemesis or both. Excessive alcohol ingestion may cause haematemesis from erosive gastritis, Mallory–Weiss tear or bleeding oesophagogastric varices in cirrhotic patients. Oesophageal or gastric cancer and gastric angioectasias (Dieulafoy lesion) are rare causes of upper gastrointestinal bleeding.
The Rockall and Blatchford scores are used to assess the risk in gastrointestinal bleeding ( Box 6.5 ). A profound upper gastrointestinal bleed may lead to the passage of purple stool or, rarely, fresh blood.
|< 60 years||0|
|> 80 years||2|
|Pulse > 100 beats per minute and systolic blood pressure > 100 mmHg||1|
|Systolic blood pressure < 100 mmHg||2|
|Heart failure, ischaemic heart disease or other major illness||2|
|Renal failure or disseminated malignancy||3|
|Mallory–Weiss tear and no visible bleeding||0|
|All other diagnoses||1|
|Upper gastrointestinal malignancy||2|
|Major stigmata of recent haemorrhage|
|Visible bleeding vessel/adherent clot||2|
|Pre-endoscopy (maximum score = 7)||Score 4 = 14% mortality pre-endoscopy|
|Post-endoscopy (maximum score = 11)||Score 8+ = 25% mortality post-endoscopy|
Establish whether the blood is mixed with stool, coats the surface of otherwise normal stool or is seen on the toilet paper or in the pan. Fresh rectal bleeding (haematochezia) usually indicates a disorder in the anal canal, rectum or colon. During severe upper gastrointestinal bleeding, however, blood may pass through the intestine unaltered, causing fresh rectal bleeding. Common causes of rectal bleeding include haemorrhoids, anal fissures (blood on the toilet paper or in the pan), complicated diverticular disease, colorectal cancer or colonic polyps, inflammatory bowel disease, ischaemic colitis and colonic angioectasias.
Jaundice is a yellowish discoloration of the skin, sclerae ( Fig. 6.8 ) and mucous membranes caused by hyperbilirubinaemia ( Box 6.6 ). There is no absolute level at which jaundice is clinically detected but, in good light, most clinicians will recognise jaundice when bilirubin levels exceed 50 µmol/L (2.92 mg/dL).
|Increased bilirubin production|
|Impaired bilirubin excretion|