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Diagnosis of nonacute abdominal complaints is an important part of the general surgical clinic workload and most patients with abdominal complaints can be managed as outpatients alone. Diagnoses made in a clinic are often quite different from those in emergency surgical admissions. Nevertheless, the surgeon in the clinic must remain alert to unfamiliar presentations that more usually present acutely, for example, an appendix mass.
The principal presenting symptoms of nonacute abdominal disorders are shown in Box 18.1 . In addition, patients are often referred to a surgeon after discovery of an abdominal mass , obstructive jaundice or an iron deficiency anaemia caused by chronic blood loss. As ever, the history can provide 70% or more of the clues to the diagnosis, and so must be taken thoughtfully, accurately and with great care. As a general rule, history taking and clinical examination should be done first to reach a provisional diagnosis, and to direct any investigations.
Abdominal pain
Difficulty in swallowing (dysphagia)
Weight loss
Anorexia (loss of appetite)
Nausea or intermittent vomiting
Change in bowel habit, including rectal bleeding
Key points in taking a history of abdominal pain are summarised in Box 18.2 . Pain is highly subjective and the description will be coloured by the patient’s perception of it and its possible significance. Patients often use vague terms such as ‘indigestion’ and ‘dyspepsia’; these terms are imprecise, so what the patient actually means should be clarified by further questioning. Time-related features of the pain are often highly significant in formulating a differential diagnosis but will only be elicited by diligent enquiry. It is important to establish when a pain first began. Sometimes, asking when the patient was last completely well helps pinpoint the real onset. When presenting or writing a case history, say ‘the pain began 6 days ago’ rather than, say, ‘it began last Thursday’.
How long ago did it start (hours, days, weeks)?
Gradual or sudden onset? (sudden onset implies a mechanical cause)
Any previous similar episodes or attacks?
Does pain come in bouts recurring hourly, daily, weekly, monthly?
Predominantly daytime or night-time?
Any period free from pain?
In females, any association with menstrual cycle? Possibility of pregnancy?
Where did the pain start and where is it now, for example, central, epigastric, right or left subcostal (hypochondrial), in right or left iliac fossa, suprapubic, ‘lower abdominal’, or loin?
Is pain well or poorly localised? (i.e., well localised if parietal peritoneum involved because of its somatic innervation)
Is there any radiation of the pain? (i.e., spread to nearby areas)
Discomfort only, moderate pain or severe pain?
How much does it interfere with activities of normal living?
What descriptive words does the patient use: ‘sharp’; ‘blunt’; ‘burning’; ‘crushing’; ‘deep’; ‘gnawing’; ‘boring’; ‘bloating’; ‘knife-like’; ‘stabbing’?
Is the pain more likely to be physiological (e.g., predefaecation colic or dysmenorrhoea) or pathological?
Does the character of the pain vary during an attack, for example, constant, intermittent or episodic, ‘colicky’ (i.e., coming in severe cramp-like waves), background pain with exacerbations?
For example, improved or made worse by food, posture, exercise or drugs?
For example, vomiting, change in bowel habit, weight loss or nausea?
Patients describe pain in many different ways, and as each entity tends to have its own pattern, recognisable patterns only come to light if all aspects of the pain history are enquired into.
These, and particularly the site it first manifested, suggest likely anatomical structures involved. These are shown in Fig. 18.1 .
Gallstones and gall bladder dysfunction. Biliary colic presents with irregularly recurrent bouts of severe pain which, though described as colic, characteristically last continuously for 1 to 12 hours. Severe and prolonged episodes may bring the patient into hospital. Pain is usually located in the upper abdomen—most often on the right side—and may radiate around to the back. It is often precipitated by rich or fatty foods and may be associated with vomiting.
Peptic ulcer disease. Typically, there is intermittent ‘boring’ epigastric pain which recurs several times a year and lasts for days or weeks at a time. It is not as severe as biliary colic unless there is perforation, which presents acutely. Retrosternal ‘burning’ occurs in peptic oesophagitis and tends to occur after large meals and on lying down. The relationship of pain with food varies according to the site of the ulcer disease: duodenal ulcer pain is relieved by bland food and recurs 3 to 4 hours afterwards, typically in the early morning, whereas the pain of gastric ulcer and oesophagitis tends to be aggravated by food, especially if acidic or spicy. Peptic pain is generally relieved by antacids and virtually always by H 2 -blocking drugs (e.g., ranitidine) or proton-pump inhibitors (e.g., omeprazole), this ‘trial of treatment’ providing evidence towards a diagnosis.
Chronic pancreatitis and carcinoma of pancreas. Both are typically associated with severe ‘gnawing’, persistent and poorly localised central pain which usually radiates through to the back and is often associated with anorexia and weight loss. The pain may be relieved by leaning forwards (‘the pancreatic position’). Early carcinoma of the pancreas, however, is usually painless.
Irritable bowel syndrome and constipation. These may cause a chronic symptom complex mimicking partial bowel obstruction and manifested by episodes of colicky pain. This is poorly localised, often ‘bloating’ pain, particularly postprandially (after meals). Its intensity varies and it is often associated with transient disturbances of bowel function, particularly alternating diarrhoea and constipation. Passage of flatus or stool often temporarily relieves the symptoms
Diverticular disease and Crohn disease. Partial bowel obstruction can occur with sigmoid diverticular disease or with small bowel Crohn disease. Symptoms are similar to those of complete bowel obstruction but more low key. In incomplete bowel obstruction, there is often passage of some flatus or even faeces but the patient otherwise appears obstructed.
Chronic renal outflow obstruction (hydronephrosis). Causes include stones, tumour (urothelial carcinoma), ureteric stricture, extrinsic ureteric compression (i.e., retroperitoneal fibrosis) or pelviureteric junction obstruction from an aberrant crossing vessel. Patients may report a ‘dull’, poorly defined, fairly constant loin pain, which can radiate to the groin or genitalia. Pain is often aggravated acutely by high fluid intake. Associated urinary symptoms may include haematuria or dysuria.
Gynaecological conditions. Chronic pelvic pain may be caused by pelvic inflammatory disease, endometriosis and ovarian tumours. These may reach the general surgeon because of poorly defined lower abdominal pain. A gynaecological history should be taken in female patients; pelvic examination may reveal the cause and ultrasound is usually diagnostic.
Nonsurgical (i.e., ‘medical’) disorders causing abdominal pain. These include liver congestion in heart failure (common), splenic infarcts or diabetes (both uncommon but important), acute intermittent porphyria, sickle-cell anaemia or tertiary syphilis (very rare). Patients sometimes present with abdominal pain for which no organic cause can be found despite extensive investigation. In these, irritable bowel syndrome or sensitivity to certain foods, for example, gluten or wheat protein, need to be considered. Only as a last resort should the pain be attributed to psychological disturbances.
This is common. The main organic causes are: ‘infantile colic’ (sometimes caused by cow’s milk allergy), irritable bowel syndrome in older children, chronic inflammatory bowel disease, recurrent streptococcal infections, and sometimes hydronephrosis caused by urinary tract obstruction. Childhood ‘periodic syndromes’ include recurrent episodes of poorly defined and inconsistent abdominal pain and/or recurrent vomiting, sometimes sufficiently severe for the child to require admission and intravenous fluids; these are often described as a precursor to migraine. ‘Abdominal migraine’ describes abdominal pain with or without nausea, pallor, and photophobia which lasts for up to 3 days, is most common in the years before puberty, and is not usually associated with a headache. Psychosomatic abdominal pain may be the explanation if organic causes have been excluded and thus psychological, environmental and social factors, including the possibility of child neglect and abuse, should be explored (see Chapter 51 ).
A differential diagnosis must first be made on clinical grounds ( Box 18.3 and see Fig. 18.1 ). The choice (and order) of investigations should be efficient and economical, after considering how each will support or help eliminate the most probable (and common) diagnoses and how it might influence management.
Well-looking or ill (thin, emaciated, weak)?
Alert and responding normally or obtunded and slumped in bed?
Dehydrated (poor skin tone, sunken cheeks)?
Abnormal skin colour (pale, jaundiced, grey)
Signs of surgical wounds or dressings
End-of-bed charts—fever, tachycardia, fluid balance, trauma chart, pain chart, drug chart (e.g., strength and frequency of analgesia), modified early warning scores (MEWS)
‘Medical accessories’—IV infusion, urinary catheter, parenteral nutrition, monitoring equipment, oxygen mask
Fingernails for koilonychia (spoon-shaped nails in iron deficiency) and leuconychia (whiteness and opacity of nails, sometimes caused by hypoalbuminaemia)
Hands for palmar erythema and Dupuytren contracture (association with liver disease)
Eyes—yellow sclerae in jaundice, pale conjunctivae in anaemia
Mouth and tongue—for ulceration suggestive of Crohn, angular stomatitis in anaemia, dehydration, telangiectasia in hereditary haemorrhagic telangiectasia
Supraclavicular fossa palpation for enlarged lymph nodes, particularly medial left-sided Virchow node indicating upper GI malignancy (Troisier sign)
Inspect abdominal skin for jaundice and scratch marks resulting from pruritus (itching), spider naevi (indicate likely liver disease)
Chest in males for gynaecomastia in liver disease
Position the patient correctly (comfortable, near-flat, arms by sides) and expose the whole abdominal field (‘nipples to knees’, but not all at once)
Distended or scaphoid (sunken) abdominal shape?
Skin—wounds and scars, redness, purulent discharge or other signs of infection, erythema ab igne (see Fig. 18.2 in Case History)
Bruising—umbilical or flank in acute pancreatitis; cloth printing (trauma cases)
Herniation (including usual primary sites and incisional hernias)
Caput medusae—enlarged veins radiating from umbilicus indicating portal venous obstruction
Visible peristalsis—usually indicating long-standing small bowel obstruction
Gentle overall palpation for obvious abnormalities
Overall firmer palpation at a deeper level provides detailed examination of abnormal masses—relationship to abdominal wall, size, shape, position, mobility, texture, hardness, fixation posteriorly or anteriorly, tenderness. Likely site or organ of origin?
Specific organ palpation—press in first, then ask the patient to breathe in deeply; gradually relax your pressure and seek the descending lower edge of the organ; repeat at 3 cm intervals moving upwards:
Liver: start as low as it might have reached, for example, right iliac fossa, and work upwards as earlier. Map out palpable lower liver edge. If large, palpate surface for irregularities, for example, metastases. The enlarging liver usually remains in contact with the anterior abdominal wall and is dull to percussion. Percuss also for upper border to gauge liver size; auscultate a large liver for vascular bruits
Spleen: tilt patient slightly towards right side, place left hand behind lower left ribs and gently lift. Start as low as enlargement might have reached, for example, right iliac fossa, and palpate as for liver. Seek notch in lower edge. To be palpable, spleen needs to be enlarged two to three times normal. Percuss for overlying resonance caused by gas in bowel superficial to it
Kidneys: as with the liver, a renal mass usually descends with inspiration since the kidneys lie just beneath the diaphragm. Bimanual palpation enables the posteriorly placed kidney to be felt by displacing it anteriorly (see Fig. 18.3 ). Place left hand in loin and attempt to push enlarged organ forwards on to examining hand
Examination for ascites (see Fig. 18.4 )
Hernial orifices—inguinal and femoral for cough impulse; reducibility (see Ch. 32 )
Rectal and/or vaginal examination if appropriate (see Table 18.1 )
Percussion and auscultation if appropriate
Dysphagia is the term for difficulty in swallowing. The most common complaint is inability to swallow solids, which the patient describes as ‘becoming stuck’ or ‘held up’ before it passes into the stomach or is regurgitated. Fibrous foods, such as chunks of meat, usually cause the most trouble. The patient can usually indicate a precise level for the perceived obstruction. The true level of obstruction is usually some distance below that point.
Dysphagia is almost always caused by disease in or near the oesophagus but occasionally the lesion is in the pharynx or stomach. Oesophageal narrowing usually causes symptoms only when the lumen is unable to expand beyond about 10 mm—the narrower the lumen, the more severe the symptoms. In many pathological conditions causing dysphagia, the lumen becomes progressively constricted and indistensible. Initially only fibrous solids cause difficulty but later this extends to all solids and eventually, even to fluids. Because narrowing is a gradual and insidious process, patients often compensate to a surprising degree (e.g., by liquidising all food) and may only present when they have difficulty swallowing fluids or even their own saliva. By this time, there is usually marked weight loss.
The common causes of dysphagia are outlined in Box 18.4 . Pain on swallowing or odynophagia (usually provoked by both food and drink, particularly if hot) is a distinctive symptom highly suspicious of carcinoma.
Peptic oesophagitis (often associated with hiatus hernia)—sometimes causes fibrous stricture
Carcinoma of oesophagus or cardia (uppermost part) of the stomach
Candida oesophagitis, particularly after major surgery
Pharyngeal pouch
Oesophageal web (Plummer–Vinson/Paterson–Kelly syndrome)
‘Oesophageal apoplexy’ caused by haematoma in the wall
Leiomyoma of the oesophageal muscle
Achalasia—uncommon
Bulbar or pseudobulbar palsy—rare
Myasthenia gravis—rare
Subcarinal lymph node secondaries from carcinoma of the bronchus—fairly common
Left atrial dilatation in mitral stenosis—rare
Dysphagia lusoria (compression from abnormally placed great arteries)—very rare
Achalasia is an exception to the usual pattern of dysphagia, in that swallowing fluids causes more difficulty than solids. In achalasia, there is idiopathic destruction of inhibitory ganglia in Auerbach (myenteric) plexus of the entire oesophagus, which results in functional narrowing of the lower oesophagus and peristaltic failure throughout its length. Thus the oesophagus becomes markedly distended and dilated, with solids settling towards the lower end and fluids spilling over into the airways causing spluttering dysphagia , particularly when the patient is lying flat. Achalasia commonly presents with chronic chest infection rather than dysphagia and the diagnosis is often reached late. Similar overspill symptoms can be caused by bulbar palsy, most commonly after a stroke.
Bolus obstruction is an acute form of dysphagia, where a lump of food sticks at a narrowed part, completely obstructing the oesophagus.
Dysphagia, particularly of recent onset, must be regarded seriously and fully investigated. A plain chest x-ray should be taken to exclude bronchial carcinoma; occasionally an oesophageal fluid level behind the heart is seen, resulting from an oesophageal stricture, hiatus hernia or achalasia. In high dysphagia, flexible pharyngoscopy followed by a barium swallow and meal is the usual sequence of investigation. In lower dysphagia, flexible endoscopy (oesophago-gastro-duodenoscopy, OGD) is usually performed, as this allows direct inspection and biopsy; however, contrast radiography can be helpful. In disorders of function, swallowing barium-soaked bread or a video record of a barium swallow may be diagnostic. Oesophageal physiology measurements using manometry and pH monitoring are helpful in reaching a diagnosis of achalasia, especially in its early stages.
Marked weight loss ( cachexia ) and loss of appetite ( anorexia ) are frequently manifestations of serious, insidious, often malignant abdominal disorders. There may be other symptoms, such as malaise, bloating, nausea, sporadic vomiting and regurgitation. These symptoms may have been unnoticed or dismissed as trivial by the patient and are only elicited by direct questioning.
The diseases which cause these symptoms may be grouped into four broad categories:
Intraabdominal malignancies , for example, carcinoma of stomach or pancreas, metastatic disease in the liver or widespread across the peritoneal cavity (arising particularly from stomach, large bowel, ovary, breast or bronchus), bowel lymphomas.
‘Medical’ conditions , for example, alcoholism and cirrhosis, viral diseases (e.g., hepatitis or infectious mononucleosis), uncontrolled diabetes or thyrotoxicosis, malabsorption, renal failure, cardiac cachexia.
Psychological disorders , for example, anxiety, depression, anorexia nervosa, bulimia.
Chronic visceral ischaemia , a very uncommon condition resulting from atherosclerotic narrowing of at least two of the three main visceral arteries—the coeliac axis and the superior mesenteric and the inferior mesenteric arteries—resulting in ‘fear of food’ and massive weight loss.
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