The gastrointestinal history

oesophagus, caustic damage to the oesophagus or oesophageal perforation.

If the patient complains of difficulty initiating swallowing, fluid regurgitating into the nose or choking on trying to swallow, this suggests that the cause of the dysphagia is in the pharynx (pharyngeal dysphagia). Causes of pharyngeal dysphagia can include neurological disease (e.g. motor neurone disease, resulting in bulbar or pseudobulbar palsy).

If the patient complains of food sticking in the oesophagus, it is important to consider a number of anatomical causes of oesophageal blockage.¹ Ask the patient to point to the site where the solids stick. If there is a mechanical obstruction at the lower end of the oesophagus, most often the patient will localise the dysphagia to the lower retrosternal area. However, obstruction higher in the oesophagus may be felt anywhere in the retrosternal area. If heartburn is also present, for example, this suggests that gastro-oesophageal reflux with or without stricture formation may be the cause of the dysphagia. The actual course of the dysphagia is also a very important part of the history to obtain. If the patient states that the dysphagia is intermittent or is present only with the first few swallows of food, this suggests either a lower oesophageal ring or oesophageal spasm. However, if the patient complains of progressive difficulty swallowing, this suggests a stricture, carcinoma or achalasia. If the patient states that both solids and liquids stick, then a motor disorder of the oesophagus is more likely, such as achalasia or diffuse oesophageal spasm.

Diarrhoea

The symptom diarrhoea can be defined in a number of different ways. Patients may complain of frequent stools (more than three per day being abnormal) or they may complain of a change in the consistency of the stools, which have become loose or watery. There are a large number of possible causes of diarrhoea.

Some patients pass small amounts of formed stool more than three times a day because of an increased desire to defecate. The stools are not loose and stool volume is not increased. This is not true diarrhoea. It can occur because of local rectal pathology, incomplete rectal emptying, or because of a psychological disturbance that leads

to an increased interest in defaecation.

When a history of diarrhoea is obtained, it is also important to determine if this has occurred acutely or whether it is a chronic problem. Acute diarrhoea is more likely to be infectious in nature, while chronic diarrhoea has a large number of causes.

Clinically, diarrhoea can be divided into a number of different groups based on the likely disturbance of physiology.²

Constipation

It is important to determine what patients mean if they say they are constipated.³ Constipation is a common symptom and can refer to the passage of infrequent stools (fewer than three times per week), hard stools or stools that are difficult to evacuate. This symptom may occur acutely or may be a chronic problem. In many patients, chronic constipation arises because of habitual neglect of the impulse to defecate, leading to the accumulation of large, dry faecal masses. With constant rectal distension from faeces, the patient may grow less aware of rectal fullness, leading to chronic constipation. Constipation may arise from ingestion of drugs (e.g. codeine, antidepressants and aluminium or calcium antacids), and with various metabolic or endocrine diseases (e.g. hypothyroidism, hypercalcaemia, diabetes mellitus, phaeochromocytoma, porphyria, hypokalaemia) and neurological disorders (e.g. aganglionosis, Hirschsprung’s^b disease, autonomic neuropathy, spinal cord injury, multiple sclerosis). Constipation can also arise after partial colonic obstruction from carcinoma; it is, therefore, very important to determine whether there has been a recent change in bowel habit, as this may indicate development of a malignancy. Patients with very severe constipation in the absence of structural disease may be found on a transit study to have slow colonic transit; such slow-transit constipation is most common in young women.

Constipation is common in the later stages of pregnancy.

Difficulty with evacuation of faeces may occur with disorders of the pelvic floor muscles or nerves, or anorectal disease (e.g. fissure, or stricture). Patients with this problem may complain of straining, a feeling of anal blockage or even the need to self-digitate to perform manual evacuation of faeces.

A chronic but erratic disturbance in defaecation (typically alternating constipation and diarrhoea) associated with abdominal pain, in the absence of any structural or biochemical abnormality, is very common; such patients are classified as having the irritable bowel syndrome.⁴ Patients who report abdominal pain plus two or more of the following symptoms—abdominal pain relieved by defaecation, looser or more frequent stools with the onset of abdominal pain, passage of mucus per rectum, a feeling of incomplete emptying of the rectum following defaecation and visible abdominal distension—are more likely to have the irritable bowel syndrome than organic disease.

Mucus

The passage of mucus (white slime) may occur because of a solitary rectal ulcer, fistula or villous adenoma, or in the irritable bowel syndrome.

Bleeding

Patients may present with the problem of haematemesis (vomiting blood), melaena (passage of jet-black stools) or haematochezia (passage of bright-red blood per rectum). Sometimes patients may present because routine testing for occult blood in the stools is positive (page 183). It is important to ensure that if vomiting of blood is reported, this is not the result of bleeding from a tooth socket or the nose, or coughing up of blood.

Haematemesis indicates that the site of the bleeding is proximal to or at the duodenum. Ask about symptoms of peptic ulceration; haematemesis is commonly due to bleeding chronic peptic ulceration, particularly from a duodenal ulcer. Acute peptic ulcers often bleed without abdominal pain. A Mallory-Weiss tear usually occurs with repeated vomiting; typically the patient reports first the vomiting of clear gastric contents and then the vomiting of blood. Less-common causes of upper gastrointestinal bleeding are presented in Table 6.3.

TABLE 6.3 Causes of acute gastrointestinal bleeding

CRST = calcinosis, Raynaud’s phenomenon, sclerodactyly and telangiectasia.

^* George Kenneth Mallory (b. 1900), professor of pathology, Boston, and Soma Weiss (1898–1942), professor of medicine, Boston City Hospital described this syndrome in 1929.

^† Georges Dieulafoy (1839–1911), Paris physician.

^‡ Edvard Ehlers (1863–1937), German dermatologist, described the syndrome in 1901, and Henri Alexandre Danlos (1844–1912), French dermatologist, described the syndrome in 1908.

^§ Pierre Ménétrier (1859–1935), French physician.

^# Johann Friedrich Meckel the younger (1781–1833), Professor of Surgery and Anatomy at Halle. His father and grandfather were also professors of anatomy.

Haemorrhoids and local anorectal diseases such as fissures will commonly present with passing small amounts of bright-red blood per rectum. The blood is normally not mixed in the stools but is on the toilet paper, on top of the stools or in the toilet bowl. Melaena usually results from bleeding

from the upper gastrointestinal tract, although right-sided colonic and small bowel lesions can occasionally be responsible. Massive rectal bleeding can occur from the distal colon or rectum, or from a major bleeding site higher in the gastrointestinal tract. With substantial lower gastrointestinal tract bleeding, it is important to consider the presence of angiodysplasia or diverticular disease (where bleeding more often occurs from the right rather than the left colon, even though diverticula are more common in the left colon). Less-common causes of lower gastrointestinal bleeding are presented in Table 6.3.

Spontaneous bleeding into the skin, or from the nose or mouth, can be a problem for patients with coagulopathy resulting from liver disease.

Jaundice

Usually the relatives notice a yellow discoloration of the sclerae or skin before the patient does. Jaundice is due to the presence of excess bilirubin being deposited in the sclerae and skin. The causes of jaundice are described on page 185. If there is jaundice, ask about the colour of the urine and stools; pale stools and dark urine occur with obstructive or cholestatic jaundice because urobilinogen is unable to reach the intestine. Also ask about abdominal pain; gallstones, for example, can cause biliary pain and jaundice.⁵

Pruritus

This symptom means itching of the skin, and may be either generalised or localised. Cholestatic liver disease can cause pruritus which tends to be worse over the extremities. Other causes of pruritus are discussed on page 445.

Abdominal bloating and swelling

A feeling of swelling (bloating) may be a result of excess gas or a hypersensitive intestinal tract (as occurs in the irritable bowel syndrome). Persistent swelling can be due to ascitic fluid accumulation; this is discussed on page 175. It may be associated with ankle oedema.

Lethargy

Tiredness and easy fatiguability are common symptoms for patients with acute or chronic liver disease, but the mechanism is not known. This can also occur because of anaemia due to gastrointestinal or chronic inflammatory disease. Lethargy is also very common in the general population and is not a specific symptom.

Treatment

The treatment history is very important. Traditional non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, can induce bleeding from acute or chronic damage to the gastrointestinal tract. As described above, many drugs can result in disturbed defaecation. A large number of drugs are also known to affect the liver. For example, acute hepatitis can occur with halothane, phenytoin or chlorothiazide. Cholestasis may occur from a

hypersensitivity reaction to chlorpromazine or other phenothiazines, sulfonamides, sulfonylureas, phenylbutazone, rifampicin or nitrofurantoin. Anabolic steroids and the contraceptive pill can cause dose-related cholestasis. Fatty liver can occur with alcohol use, tetracycline, valproic acid or amiodarone. Large blood-filled cavities in the liver called peliosis hepatis can occur with anabolic steroid use or the contraceptive pill. Acute liver cell necrosis can occur if an overdose of paracetamol (acetaminophen) is taken.

Past history

Surgical procedures can result in jaundice from the anaesthesia (e.g. multiple uses of halothane), hypoxaemia of liver cells (hypotension during the operative or postoperative period) or direct damage to the bile duct during abdominal surgery. A history of relapsing and remitting epigastric pain in a patient who presents with severe abdominal pain may indicate that a peptic ulcer has perforated. A past history of inflammatory bowel disease (either ulcerative colitis or Crohn’s disease) is important as these are chronic diseases that tend to flare up.

Social history

The patient’s occupation may be relevant (e.g. healthcare workers may be exposed to hepatitis). Toxin exposure can also be important in chronic liver disease (e.g. carbon tetrachloride, vinyl chloride). If a patient has symptoms suggestive of liver disease, ask about recent travel to countries where hepatitis is endemic.

The alcohol history is very important, particularly as alcoholics often deny or understate the amount they consume (see Table 1.3, page 7).⁶ Contact with anybody who has been jaundiced should always be noted. The sexual history should be obtained. A history of any injections (e.g. intravenous drugs, plasma transfusions, dental treatment or tattooing) in a patient who presents with symptoms of liver disease is important, particularly as hepatitis B or C may be transferred in this way.

Family history

A family history of colon cancer, especially of familial polyps, or inflammatory bowel disease is important. Ask about coeliac disease in the family. A positive family history of jaundice, anaemia, splenectomy or cholecystectomy may occur in patients with haemolytic anaemia (due to haemoglobin abnormalities or auto-immune disease) or congenital or familial hyperbilirubinaemia.

The gastrointestinal examination

Examination of the gastrointestinal system includes a complete examination of the abdomen. It is also important to search for the peripheral signs of gastrointestinal and liver disease. Some signs are more useful than others.⁷

Examination anatomy

An understanding of the structure and function of the gastrointestinal tract and abdominal organs is critical for the diagnosis of gastrointestinal disease (Figure 6.1). The mouth is the gateway to the gastrointestinal tract. It and the anus and rectum are readily accessible to the examiner, and both must be examined carefully in any patient with suspected abdominal disease. The position of the abdominal organs can be quite variable, but there are important surface markings which should be kept in mind during the examination.

Figure 6.1 MRI scans of the abdomen

(a) Front. (b) Back.

Courtesy M Thomson, National Capital Diagnostic Imaging, Canberra.

The liver is the largest organ in the abdomen; it comprises a large right lobe and smaller left lobe divided into eight segments, including the caudate lobe (segment I) squeezed in between. The lower border of the liver extends from the tip of the right tenth rib to just below the left nipple. Normally the liver is not palpable but it may just be possible to feel the lower edge in healthy people.

The spleen is a lymphoid organ that underlies the ninth, tenth and eleventh ribs posteriorly on the left. It is usually not palpable in health.

The kidneys lie anteriorly 4 finger-breadths from the midline and posteriorly under the twelfth rib. Normally, the right kidney extends 2.5 cm lower than the left. In thin patients, the lower pole of the right kidney may be palpable in health.

The gallbladder is a pear-shaped organ and the fundus (top) is at the tip of the right ninth costal cartilage; it cannot be felt in health. The pancreas is situated in the retroperitoneum (behind the peritoneum), with the head tucked into the C-shaped duodenum and the tail snuggling into the spleen. A huge pancreatic mass may rarely be large enough to be palpable.

The aorta lies in the midline and terminates just to the left of the midline at the level of the iliac crest. A pulsatile mass in the middle of the abdomen is likely to be arising from the aorta and may indicate an aneurysm.

The stomach is usually J-shaped and lies in the left upper part of the abdomen over the spleen and pancreas; it connects with the duodenum. The small intestine ranges from 3 to 10 metres in length and comprises the upper half (duodenum and jejunum) and the lower half (ileum). The small intestine lies over the middle section of the abdomen but is usually impalpable.

The colon is approximately 1.5 metres in length, and from right to left consists of the caecum, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending colon, sigmoid colon, rectum and anal canal (anorectum). The appendix usually lies in the right lower abdominal area, arising posterior-medially from the caecum. The caecum and ascending colon lie on the right side of the abdomen, the transverse colon runs across the upper abdomen from right to left, and then the descending colon and sigmoid and rectum lie on the left side of the abdomen. Rarely, masses arising from the colon will be felt in the abdomen.

Other important anatomical areas include the inguinal canal and the anorectum which will be described later in this chapter in relation to examination of hernias and the rectal examination.

Positioning the patient

For the proper examination of the abdomen it is important that the patient be lying flat with the head resting on a single pillow (Figure 6.2). This relaxes the abdominal muscles and facilitates abdominal palpation. Helping the patient into this position affords the opportunity to make a general inspection.

Figure 6.2 Gastrointestinal examination: positioning the patient

General appearance

Jaundice

The yellow discoloration of the sclerae (conjunctivae) and the skin that results from hyperbilirubinaemia is best observed in natural daylight (page 185). Whatever the underlying cause, the depth of jaundice can be quite variable.

Weight and wasting

The patient’s weight must be recorded. Failure of the gastrointestinal tract to absorb food normally may lead to loss of weight and cachexia. This may also be the result of gastrointestinal malignancy or alcoholic cirrhosis. Folds of loose skin may be visible hanging from the abdomen and limbs. These suggest recent weight loss. Obesity can cause fatty infiltration of the liver (non-alcoholic steatohepatitis) and result in abnormal liver function tests. Anabolic steroid use can induce increase in muscle bulk (sometimes considered desirable) and various liver tumours, including adenomas or hepatocellular carcinomas.

Skin

The gastrointestinal tract and the skin have a common origin from the embryoblast. A number of diseases can present with both skin and gut involvement (Figures 6.3–6.8, Table 6.4).⁸

Figure 6.3 (above) Glucagonoma: migratory rash involving the groin

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

Figure 6.4 (right) Dermatitis herpetiformis

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

Figure 6.5 Peutz-Jeghers syndrome, with discrete brown-black lesions of the lips

Figure (a) from Jones DV et al, in Feldman M et al, Sleisenger & Fordtran’s gastrointestinal disease, 6th edn, Chapter 112. Philadelphia: WB Saunders, 1998, with permission. Figure (b) from McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

Figure 6.6 Acanthosis nigricans: (a) axilla; (b) chest wall

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

Figure 6.7 (right) Hereditary haemorrhagic telangiectasia involving the lips

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

Figure 6.8 Porphyria cutanea tarda—scarring from photosensitivity

TABLE 6.4 The skin and the gut

Pigmentation

Generalised skin pigmentation can result from chronic liver disease, especially in haemochromatosis (due to haemosiderin-stimulating melanocytes, to produce melanin). Malabsorption may result in Addisonian-type pigmentation (‘sunkissed’ pigmentation) of the nipples, palmar creases, pressure areas and mouth (page 311).

Peutz-Jeghers^c syndrome

Freckle-like spots (discrete, brown-black lesions) around the mouth and on the buccal mucosa (Figure 6.5) and on the fingers and toes, are associated with hamartomas of the small bowel (50%) and colon (30%), which can present with bleeding or intussusception. In this autosomal dominant condition the incidence of gastrointestinal adenocarcinoma is increased.

Acanthosis nigricans

These are brown-to-black velvety elevations of the epidermis due to confluent papillomas and are usually found in the axillae and nape of the neck (Figure 6.6). Acanthosis nigricans is associated rarely with gastrointestinal carcinoma (particularly stomach) and lymphoma, as well as with acromegaly, diabetes mellitus and other endocrinopathies.

Hereditary haemorrhagic telangiectasia (Rendu-Osler-Weber syndrome^d)

Multiple small telangiectasia occur in this disease. They are often present on the lips and tongue (Figure 6.7), but may be found anywhere on the skin. When they are present in the gastrointestinal tract they can cause chronic blood loss or even, occasionally, torrential bleeding. An associated arteriovenous malformation in the liver may be present. This is an autosomal dominant condition and is uncommon.

Porphyria cutanea tarda

Fragile vesicles appear on exposed areas of the skin and heal with scarring (Figure 6.8). The urine is dark in this chronic disorder of porphyrin metabolism associated with alcoholism, liver disease and hepatitis C.

Systemic sclerosis

Tense tethering of the skin in systemic sclerosis is often associated with gastro-oesophageal reflux and gastrointestinal motility disorders (page 285).

Mental state

Assess orientation (page 380). The syndrome of hepatic encephalopathy, due to decompensated advanced cirrhosis (chronic liver failure) or fulminant hepatitis (acute liver failure), is an organic neurological disturbance. The features depend on the aetiology and the precipitating factors (page 188). Patients eventually become stuporous and then comatose. The combination of hepatocellular damage and portosystemic shunting due to disturbed hepatic structure (both extrahepatic and intrahepatic) causes this syndrome. It is probably related to the liver’s failure to remove toxic metabolites from the portal blood. These toxic metabolites may include ammonia, mercaptans, short-chain fatty acids and amines.

The hands

Even the experienced gastroenterologist must restrain his or her excitement and begin the examination of the gastrointestinal tract with the hands. The signs that may be elicited here give a clue to the presence of chronic liver disease. Whatever its aetiology, permanent diffuse liver damage results in similar peripheral signs. However, none of these signs alone is specific for chronic liver disease.

Nails

Leuconychia

When chronic liver or other disease results in hypoalbuminaemia, the nail beds opacify (the abnormality is of the nail bed and not of the nail), often leaving only a rim of pink nail bed at the top of the nail (Terry’s nails;^eFigure 6.9). The thumb and index nails are most often involved. The exact mechanism is uncertain. It may be that the explanation is compression of capillary flow by extracellular fluid.

Figure 6.9 Leuconychia—Terry’s nails

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

Muehrcke’s lines (transverse white lines) can also occur in hypoalbuminaemic states, including cirrhosis. Blue lunulae may be seen in patients with Wilson’s disease (hepatolenticular degeneration).

Clubbing

Up to one-third of patients with cirrhosis may have finger clubbing. In at least some cases, this may be related to arteriovenous (AV) shunting in the lungs, resulting in arterial oxygen desaturation. Cyanosis may be associated with severe long-standing chronic liver disease. The cause of this pulmonary AV shunting is unknown. Conditions such as inflammatory bowel disease and coeliac disease, which cause long-standing nutritional depletion, can also cause clubbing.

The palms

Palmar erythema (‘liver palms’)

This is reddening of the palms of the hands affecting the thenar and hypothenar eminences. Often the soles of the feet are also affected. This can be a feature of chronic liver disease. While the finding has been attributed to raised oestrogen levels, it has not been shown to be related to plasma oestradiol levels, so the aetiology remains uncertain. Palmar erythema can also occur with pregnancy, thyrotoxicosis, rheumatoid arthritis, polycythaemia and rarely with chronic febrile diseases or chronic leukaemia. It may also be a normal finding, especially in women, and like spider naevi can occur in pregnancy.

Anaemia

Inspect the palmar creases for pallor suggesting anaemia, which may result from gastrointestinal blood loss, malabsorption (folate, vitamin B₁₂), haemolysis (e.g. hypersplenism) or chronic disease.

Dupuytren’s contracture^f

This is a visible and palpable thickening and contraction of the palmar fascia causing permanent flexion, most often of the ring finger. It is often bilateral and occasionally affects the feet. It is associated with alcoholism (not liver disease), but is also found in some manual workers; it may be familial. The palmar fascia of these patients contains abnormally large amounts of xanthine, and this may be related to the pathogenesis.

Hepatic flap (asterixis^g)

Before leaving the hands one should ask the patient to stretch out the arms in front, separate the fingers and extend the wrists for 15 seconds. Jerky, irregular flexion–extension movement at the wrist and metacarpophalangeal joints, often accompanied by lateral movements of the fingers, constitute the flapping of hepatic encephalopathy. It is thought to be due to interference with the inflow of joint position sense information to the reticular formation in the brainstem. This results in rhythmical lapses of postural muscle tone. Occasionally the arms, neck, tongue, jaws and eyelids can also be involved. It can be demonstrated if the patient is asked to close the eyes forcefully or to protrude the tongue. The flap is usually bilateral, tends to be absent at rest, and is brought on by sustained posture. The rhythmic movements are not synchronous on each side and the flap is absent when coma supervenes.

Although this flap is a characteristic and early sign of liver failure, it is not diagnostic: it can also occur in cardiac, respiratory and renal failure, as well as in hypoglycaemia, hypokalaemia, hypomagnesaemia or barbiturate intoxication.

An apparent tremor (really a form of choreoathetosis, page 399) may occur in Wilson’s disease. A fine resting tremor is common in alcoholism.

The arms

Inspect the upper limbs for bruising. Large bruises (ecchymoses) may be due to clotting abnormalities. Hepatocellular damage can interfere with protein synthesis and therefore the production of all the clotting factors (except factor VIII, which is made elsewhere in the reticuloendothelial system). Obstructive jaundice results in a shortage of bile acids in the intestine, and therefore may reduce absorption of vitamin K (a fat-soluble vitamin), which is essential for the production of clotting factors II (prothrombin), VII, IX and X.

Petechiae (pinhead-sized bruises) may also be present. Chronic excessive alcohol consumption can sometimes result in bone marrow depression, causing thrombocytopenia, which may be responsible for petechiae. In addition, splenomegaly secondary to portal hypertension can cause hypersplenism, with resultant excessive destruction of platelets in the spleen; in severe liver disease (especially acute hepatic necrosis), diffuse intravascular coagulation can occur.

Look for muscle wasting, which is often a late manifestation of malnutrition in alcoholic patients. Alcohol can also cause a proximal myopathy (page 391).

Scratch marks due to severe itch (pruritus) are often prominent in patients with obstructive or cholestatic jaundice. This is commonly the presenting feature of primary biliary cirrhosis^h before other signs are apparent. The mechanism of pruritus is thought to be retention of an unknown substance normally excreted in the bile, rather than bile salt deposition in the skin as was earlier thought.

Spider naeviⁱ (Figure 6.10) consist of a central arteriole from which radiate numerous small vessels which look like spiders’ legs. They range in size from just visible to half a centimetre in diameter. Their usual distribution is in the area drained by the superior vena cava, so they are found on the arms, neck and chest wall. They can occasionally bleed profusely. Pressure applied with a pointed object to the central arteriole causes blanching of the whole lesion. Rapid refilling from the centre to the legs occurs on release of the pressure.

Figure 6.10 A large crop of spider naevi

The finding of more than two or three spider naevi anywhere on the body is likely to be abnormal. Spider naevi can be caused by cirrhosis, most frequently due to alcohol. In patients with cirrhosis the number of spider naevi may increase or decrease as the patient’s condition changes, as does palmar erythema. They may occur transiently with viral hepatitis. During the second to fifth months of pregnancy, spider naevi frequently appear, only to disappear again within days of delivery. It is not known why they occur only in the upper part of the body, but it may be related to the fact that this is the part of the body where flushing usually occurs. Like palmar erythema they are traditionally attributed to oestrogen excess. Part of the normal hepatic function is the inactivation of oestrogens, which is impaired in chronic liver disease. Oestrogens are known to have a dilating effect on the spiral arterioles of the endometrium, and this has been used to explain the presence of spider naevi, but changes in plasma oestradiol levels have not been found to correlate with the appearance and disappearance of spider naevi.

The differential diagnosis of spider naevi includes Campbell de Morgan^jspots, venous stars and hereditary haemorrhagic telangiectasia. Campbell de Morgan spots are flat or slightly elevated red circular lesions that occur on the abdomen or the front of the chest. They do not blanch on pressure and are very common. Venous stars are 2- to 3-cm lesions that can occur on the dorsum of the feet, legs, back and the lower chest. They are due to elevated venous pressure and are found overlying the main tributary to a large vein. They are not obliterated by pressure. The blood flow is from the periphery to the centre of the lesion, which is the opposite of the flow in the spider naevus. Lesions of hereditary haemorrhagic telangiectasia (page 228) occasionally resemble spider naevi.

Palpate the axillae for lymphadenopathy (page 229). Look in the axillae for acanthosis nigricans.

The face

Eyes

Look first at the sclerae for signs of jaundice (Figure 6.11) or anaemia. Bitot’s^k spots are yellow keratinised areas on the sclera (Figure 6.12). They are the result of severe vitamin A deficiency due to malabsorption or malnutrition. Retinal damage and blindness may occur as a later development. Kayser-Fleischer rings^l (Figure 6.13) are brownish green rings occurring at the periphery of the cornea, affecting the upper pole more than the lower. They are due to deposits of excess copper in Descemet’s membrane^m of the cornea. Slit-lamp examination is often necessary to show them. They are typically found in Wilson’s disease,ⁿ a copper storage disease that causes cirrhosis and neurological disturbances. The Kayser-Fleischer rings are usually present by the time neurological signs have appeared. Patients with other cholestatic liver diseases, however, can also have these rings. Iritis may be seen in inflammatory bowel disease (page 191).

Figure 6.11 Scleral icterus

Figure 6.12 Bitot spot: focal area of conjunctival xerosis with a foamy appearance

From Mir MA, Atlas of Clinical Diagnosis, 2nd edn. Edinburgh: Saunders, 2003, with permission.

Figure 6.13 Kayser-Fleischer rings

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

Xanthelasma are yellowish plaques in the subcutaneous tissues in the periorbital region and are due to deposits of lipids (see Figure 4.19, page 57). They may indicate protracted elevation of the serum cholesterol. In patients with cholestasis, an abnormal lipoprotein (lipoprotein X) is found in the plasma and is associated with elevation of the serum cholesterol. Xanthelasma are common in patients with primary biliary cirrhosis.

Periorbital purpura following proctosigmoidoscopy (‘black eye syndrome’) is a characteristic sign of amyloidosis (perhaps related to factor X deficiency) but is exceedingly rare (Figure 6.14).

Figure 6.14 Amyloidosis causing periorbital purpura

Note the periorbital purpura that followed a proctoscopic examination, a characteristic (albeit rare) sign.

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

Salivary glands

Next inspect and palpate the cheeks over the parotid area for parotid enlargement (Table 6.5). Ask the patient to clench the teeth so that the masseter muscle is palpable; the normal parotid gland is impalpable but the enlarged gland is best felt behind the masseter muscle and in front of the ear. Parotidomegaly that is bilateral is associated with alcoholism rather than liver disease per se. It is due to fatty infiltration, perhaps secondary to alcohol toxicity with or without malnutrition. A tender, warm, swollen parotid suggests the diagnosis of parotiditis following an acute illness or surgery. A mixed parotid tumour (a pleomorphic adenoma) is the commonest cause of a lump. Parotid carcinoma may cause a facial nerve palsy (page 343). Feel in the mouth for a parotid calculus, which may be present at the parotid duct orifice (opposite the upper second molar). Mumps also causes acute parotid enlargement which is usually bilateral.

TABLE 6.5 Causes of parotid enlargement

Bilateral 1. Mumps (can be unilateral) 2. Sarcoidosis or lymphoma, which may cause painless bilateral enlargement 3. Mikulicz* syndrome: bilateral painless enlargement of all three salivary glands. This disease is probably an early stage of Sjögren’s syndrome 5. Alcohol-associated parotitis 6. Malnutrition 7. Severe dehydration: as occurs in renal failure, terminal carcinomatosis and severe infections

Unilateral

1. Mixed parotid tumour (occasionally bilateral)

2. Tumour infiltration, which usually causes painless unilateral enlargement and may cause facial nerve palsy

3. Duct blockage, e.g. salivary calculus

^* Johann von Mikulicz-Radecki (1850–1905), professor of surgery, Breslau. He described this condition in 1892.

Submandibular gland enlargement is most often due to a calculus. This may be palpable bimanually (Figure 6.15). The examiner’s gloved index finger is placed on the floor of the mouth beside the tongue, feeling between it and fingers placed behind the body of the mandible. It may also be enlarged in chronic liver disease.

Figure 6.15 Examination of the submandibular gland

The mouth

The teeth and breath

The very beginning of the gastrointestinal tract is, like the very end of the tract, accessible to inspection without elaborate equipment.⁹ Look first briefly at the state of the teeth and note whether they are real or false. False teeth will have to be removed for a complete examination of the mouth. Note whether there is gum hypertrophy (Table 6.6) or pigmentation (Table 6.7). Loose-fitting false teeth may be responsible for ulcers and decayed teeth may be responsible for fetor (bad breath).

TABLE 6.6 Causes of gum hypertrophy

1 Phenytoin

2 Pregnancy

3 Scurvy (vitamin C deficiency: the gums become spongy, red, bleed easily and are swollen and irregular)

4 Gingivitis, e.g. from smoking, calculus, plaque, Vincent’s* angina (fusobacterial membranous tonsillitis)

5 Leukaemia (usually monocytic)

^* Jean Hyacinthe Vincent (1862–1950), professor of forensic medicine and French Army bacteriologist, described this in 1898.

TABLE 6.7 Causes of pigmented lesions in the mouth

1 Heavy metals: lead or bismuth (blue-black line on the gingival margin), iron (haemochromatosis—blue-grey pigmentation of the hard palate)

2 Drugs: antimalarials, the oral contraceptive pill (brown or black areas of pigmentation anywhere in the mouth)

3 Addison’s disease (blotches of dark brown pigment anywhere in the mouth)

4 Peutz-Jeghers syndrome (lips, buccal mucosa or palate)

5 Malignant melanoma (raised, painless black lesions anywhere in the mouth)

Other causes of fetor are listed in Table 6.8. These must be distinguished from fetor hepaticus which is a rather sweet smell of the breath. It is an indication of severe hepatocellular disease and may be due to methylmercaptans. These substances are known to be exhaled in the breath and may be derived from methionine when this amino acid is not demethylated by a diseased liver. Severe fetor hepaticus that fills the patient’s room is a bad sign and indicates a precomatose condition in many cases. The presence of fetor hepaticus in a patient with a coma of unknown cause may be a helpful clue to the diagnosis.

TABLE 6.8 Causes of fetor (bad breath)

1 Faulty oral hygiene

2 Fetor hepaticus (a sweet smell)

3 Ketosis (diabetic ketoacidosis results in excretion of ketones in exhaled air, causing a sickly sweet smell)

4 Uraemia (fish breath: an ammoniacal odour)

5 Alcohol (distinctive)

6 Paraldehyde

7 Putrid (due to anaerobic chest infections with large amounts of sputum)

8 Cigarettes

Unless the smell is obvious one should get a patient to exhale through the mouth while one sniffs a little of the exhaled air.

The tongue

Thickened epithelium with bacterial debris and food particles commonly causes a coating over the tongue, especially in smokers. It is rarely a sign of disease and is more marked on the posterior part of the tongue where there is less mobility and the papillae desquamate more slowly. It occurs frequently in respiratory tract infections, but is in no way related to constipation or any serious abdominal disorder.

Lingua nigra (black tongue) is due to elongation of papillae over the posterior part of the tongue, which appears dark brown because of the accumulation of keratin. There is no known cause and apart from its aesthetic problems it is symptomless. Bismuth compounds may also cause a black tongue.

Geographical tongue is a term used to describe slowly changing red rings and lines that occur on the surface of the tongue. It is not painful, and the condition tends to come and go. It is not usually of any significance, but can be a sign of riboflavin (vitamin B₂) deficiency.

Leucoplakia is white-coloured thickening of the mucosa of the tongue and mouth; the condition is premalignant. Most of the causes of leucoplakia begin with ‘S’: sore teeth (poor dental hygiene), smoking, spirits, sepsis or syphilis, but often no cause is apparent. Leucoplakia may also occur on the larynx, anus and vulva.

The term glossitis is generally used to describe a smooth appearance of the tongue which may also be erythematous. The appearance is due to atrophy of the papillae, and in later stages there may be shallow ulceration. These changes occur in the tongue often as a result of nutritional deficiencies to which the tongue is sensitive because of the rapid turnover of mucosal cells. Deficiencies of iron, folate and the vitamin B group, especially vitamin B₁₂, are common causes. Glossitis is common in alcoholics and can also occur in the rare carcinoid syndrome. However, many cases, especially those in elderly people, are impossible to explain.

Enlargement of the tongue (macroglossia) may occur in congenital conditions such as Down syndrome (page 314) or in endocrine disease, including acromegaly (page 307). Tumour infiltration (e.g. haemangioma or lymphangioma) or infiltration of the tongue with amyloid material in amyloidosis can also be responsible for macroglossia.

Mouth ulcers

This is an important topic because a number of systemic diseases can present with ulcers in the mouth (Table 6.9). Aphthous ulceration is the commonest type seen (Figure 6.16). This begins as a small painful vesicle on the tongue or mucosal surface of the mouth, which may break down to form a painful, shallow ulcer. These ulcers heal without scarring. The cause is completely unknown. They usually do not indicate any serious underlying systemic disease, but may occur in Crohn’s^o disease or coeliac disease. HIV infection may be associated with a number of mouth lesions (page 457). Angular stomatitis refers to cracks at the corners of the mouth; causes include deficiencies in vitamin B₆, vitamin B₁₂, folate and iron.

TABLE 6.9 Causes of mouth ulcers

Common Aphthous Drugs (e.g. gold, steroids) Trauma

Uncommon

Gastrointestinal disease: Crohn’s disease, ulcerative colitis, coeliac disease

Rheumatological disease: Behçet’s^* syndrome, Reiter’s^† syndrome

Erythema multiforme

Infection: viral—herpes zoster, herpes simplex; bacterial—syphilis (primary chancre, secondary snail track ulcers, mucous patches), tuberculosis

Self-inflicted

^* Halusi Behçet (1889–1948), Turkish dermatologist. He described the disease in 1937.

^† Hans Reiter (1881–1969), Berlin bacteriologist, described this in 1916.

Figure 6.16 Aphthous ulceration

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

The neck and chest

Palpate the cervical lymph nodes. It is particularly important to feel for the supraclavicular nodes, especially on the left side. These may be involved with advanced gastric or other gastrointestinal malignancy, or with lung cancer. The presence of a large left supraclavicular node (Virchow’s node) in combination with carcinoma of the stomach is called Troisier’s sign.^p Look for spider naevi.

In males, gynaecomastia may be a sign of chronic liver disease. Gynaecomastia may be unilateral or bilateral and the breasts may be tender (Figure 6.17). This may be a sign of cirrhosis, particularly alcoholic cirrhosis, or of chronic autoimmune hepatitis. In chronic liver disease, changes in the oestradiol-to-testosterone ratio may be responsible. In cirrhotic patients, spironolactone, used to treat ascites, is also a common cause. Gynaecomastia may also occur in alcoholics without liver disease because of damage to the Leydig cells^q of the testis from alcohol. A number of drugs may rarely cause gynaecomastia (e.g. digoxin, cimetidine).

Figure 6.17 Gynaecomastia with prominent breasts and unassociated with confounding obesity

From Mir MA, Atlas of Clinical Diagnosis, 2nd edn. Edinburgh: Saunders, 2003, with permission.

The abdomen

Self-restraint is no longer required and it is now time to examine the abdomen itself.

Inspection

The patient should lie flat, with one pillow under the head and the abdomen exposed from the nipples to the pubic symphysis (see Figure 6.2). It may be preferable to expose this area in stages to preserve the patient’s dignity.

Does the patient appear unwell? The patient with an acute abdomen may be lying very still and have shallow breathing (page 186).

Inspection begins with a careful look for abdominal scars, which may indicate previous surgery or trauma (Figure 6.18). Look in the area around the umbilicus for laparoscopic surgical scars. Older scars are white and recent scars are pink because the tissue remains vascular. Note the presence of stomata (end-colostomy, loop colostomy, ileostomy or ileal conduit) or fistulae. There may be visible abdominal striae following weight loss.

Figure 6.18 Abdominal scars

Note: Laparoscopic surgical scars are now common. Most of these procedures include a port about 2 cm in length, just above the umbilicus.

1. Upper midline

2. Right subcostal (Kocher’s)

3. Right paramedian

4. Lower midline

5. Nephrectomy

6. Appendicectomy (Gridiron)

7. Transplanted kidney

8. Suprapubic (Pfannensteil)

9. Left inguinal

10. Umbilical port—laparoscopic surgery

Generalised abdominal distension (Figure 6.19) may be present. All the causes of this sound as if they begin with the letter ‘F’: fat (gross obesity), fluid (ascites), fetus, flatus (gaseous distension due to bowel obstruction), faeces, ‘filthy’ big tumour (e.g. ovarian tumour or hydatid cyst) or ‘phantom’ pregnancy. Look at the shape of the umbilicus, which may give a clue to the underlying cause. An umbilicus buried in fat suggests that the patient eats too much. However, when the peritoneal cavity is filled with large volumes of fluid (ascites) from whatever cause, the abdominal flanks and wall appear tense and the umbilicus is shallow or everted and points downwards. In pregnancy the umbilicus is pushed upwards by the uterus enlarging from the pelvis. This appearance may also result from a huge ovarian cyst.

Figure 6.19 Abdomen distended with ascites: umbilicus points downwards, unlike cases of distension due to a pelvic mass

Local swellings may indicate enlargement of one of the abdominal or pelvic organs. A hernia is a protrusion of an intra-abdominal structure through an abnormal opening; this may occur because of weakening of the abdominal wall by previous surgery (incisional hernia), a congenital abdominal wall defect, or chronically increased intra-abdominal pressure.

Prominent veins may be obvious on the abdominal wall. If these are present, the direction of venous flow should be elicited at this stage. A finger is used to occlude the vein and blood is then emptied from the vein below the occluding finger with a second finger. The second finger is removed and, if the vein refills, flow is occurring towards the occluding finger (Figure 6.20). Flow should be tested separately in veins above and below the umbilicus. In patients with severe portal hypertension, portal to systemic flow occurs through the umbilical veins, which may become engorged and distended (Figure 6.21). The direction of flow then is away from the umbilicus. Because of their engorged appearance they have been likened to the mythical Medusa’s hair after Minerva had turned it into snakes; this sign is called a caput Medusae (head of Medusa) but is very rare (Figure 6.22). Usually only one or two veins (often epigastric) are visible. Engorgement can also occur because of inferior vena caval obstruction, usually due to a tumour or thrombosis but sometimes because of tense ascites. In this case the abdominal veins enlarge to provide collateral blood flow from the legs, avoiding the blocked inferior vena cava. The direction of flow is then upwards towards the heart. Therefore, to distinguish caput Medusae from inferior vena caval obstruction, determine the direction of flow below the umbilicus; it will be towards the legs in the former and towards the head in the latter. Prominent superficial veins can occasionally be congenital.

Figure 6.20 Detecting the direction of flow of a vein

(a) Place two fingers firmly on the vein. (b) The second finger is moved along the vein to empty it of blood and keep it occluded. (c) The second finger is removed but the vein does not refill. (d) At repeat testing and removing the first finger, filling occurs, indicating the direction of flow.

Adapted from Swash M, ed. Hutchison’s clinical methods, 20th edn. Philadelphia: Baillière Tindall, 1995, with permission.

Figure 6.21 Distended abdominal veins in a patient with portal hypertension

From Mir MA, Atlas of Clinical Diagnosis, 2nd edn. Edinburgh: Saunders, 2003, with permission.

Figure 6.22 Prominent veins on the abdominal wall

1 = thin veins over the costal margin—not of clinical relevance. 2 = caput Medusae. 3 = inferior vena caval obstruction.

Based on Swash M, ed. Hutchison’s clinical methods, 20th edn. Philadelphia: Baillière Tindall, 1995.

Pulsations may be visible. An expanding central pulsation in the epigastrium suggests an abdominal aortic aneurysm. However, the abdominal aorta can often be seen to pulsate in normal thin people.

Visible peristalsis may occur occasionally in very thin normal people; however, it usually suggests intestinal obstruction. Pyloric obstruction due to peptic ulceration or tumour may cause visible peristalsis, seen as a slow wave of movement passing across the upper abdomen from left to right. Obstruction of the distal small bowel can cause similar movements in a ladder pattern in the centre of the abdomen.

Skin lesions should also be noted on the abdominal wall. These include the vesicles of herpes zoster, which occur in a radicular pattern (they are localised to only one side of the abdomen in the distribution of a single nerve root). Herpes zoster may be responsible for severe abdominal pain that is of mysterious origin until the rash appears. The Sister Joseph^r nodule is a metastatic tumour deposit in the umbilicus, the anatomical region where the peritoneum is closest to the skin. Discoloration of the umbilicus where a faintly bluish hue is present is found rarely, in cases of extensive haemoperitoneum and acute pancreatitis (Cullen’s sign^s—the umbilical ‘black eye’). Skin discoloration may also rarely occur in the flanks in severe cases of acute pancreatitis (Grey-Turner’s sign^t).

Stretching of the abdominal wall severe enough to cause rupture of the elastic fibres in the skin produces pink linear marks with a wrinkled appearance, which are called striae. When these are wide and purple-coloured, Cushing’s syndrome may be the cause (page 309). Ascites, pregnancy or recent weight gain are much more common causes of striae.

Next, squat down beside the bed so that the patient’s abdomen is at eye level. Ask him or her to take slow deep breaths through the mouth and watch for evidence of asymmetrical movement, indicating the presence of a mass. In particular a large liver may be seen to move below the right costal margin or a large spleen below the left costal margin.

Palpation

This part of the examination often reveals the most information. Successful palpation requires relaxed abdominal muscles. To this end, reassure the patient that the examination will not be painful and use warm hands. Ask the patient if any particular area is tender and examine this area last. Encourage the patient to breathe gently through the mouth. If necessary, ask the patient to bend the knees to relax the abdominal wall muscles.

For descriptive purposes the abdomen has been divided into nine areas or regions (Figure 6.23). Palpation in each region is performed with the palmar surface of the fingers acting together. For the palpation of the edges of organs or masses, the lateral surface of the forefinger is the most sensitive part of the hand.

Figure 6.23 (a) Regions of the abdomen (b) Quadrants of the abdomen

Palpation should begin with light pressure in each region. All the movements of the hand should occur at the metacarpophalangeal joints and the hand should be moulded to the shape of the abdominal wall. Note the presence of any tenderness or lumps in each region. As the hand moves over each region, the mind should be considering the anatomical structures that underlie it. Deep palpation of the abdomen is performed next, though care should be taken to avoid the tender areas until the end of the examination. Deep palpation is used to detect deeper masses and to define those already discovered. Any mass must be carefully characterised and described (Table 6.10).

TABLE 6.10 Descriptive features of intra-abdominal masses

For any abdominal mass all the following should be determined:

1 Site: the region involved

2 Tenderness

3 Size (which must be measured) and shape

4 Surface, which may be regular or irregular

5 Edge, which may be regular or irregular

6 Consistency, which may be hard or soft

7 Mobility and movement with inspiration

8 Whether it is pulsatile or not

9 Whether one can get above the mass

Guarding of the abdomen (when resistance to palpation occurs due to contraction of the abdominal muscles) may result from tenderness or anxiety, and may be voluntary or involuntary. The latter suggests peritonitis. Rigidity is a constant involuntary contraction of the abdominal muscles always associated with tenderness and indicates peritoneal irritation. Rebound tenderness is said to be present when the abdominal wall, having been compressed slowly, is released rapidly and a sudden stab of pain results. This may make the patient wince, so the face should be watched while this manoeuvre is performed. It strongly suggests the presence of peritonitis and should be performed if there is doubt about the presence of localised or generalised peritonitis. The patient with a confirmed acute abdomen should not be subjected to repeated testing of rebound tenderness because of the distress this can cause. Be careful not to surprise your patient by a sudden jabbing and release movement: rebound tenderness should be elicited slowly. If you suspect the patient may be feigning a tender abdomen, test for rebound with your stethoscope after telling the patient to lie still and quiet so that you can hear.

The liver

Feel for hepatomegaly (Figure 6.24).¹⁰ With the examining hand aligned parallel to the right costal margin, and beginning in the right iliac fossa, ask the patient to breathe in and out slowly through the mouth. With each expiration the hand is advanced by 1 or 2 cm closer to the right costal margin. During inspiration the hand is kept still and the lateral margin of the forefinger waits expectantly for the liver edge to strike it.

Figure 6.24 Abdominal examination: the liver

If the liver edge has been identified, an attempt should be made to feel the surface of the liver. The edge of the liver and the surface itself may be hard or soft, tender or non-tender, regular or irregular, and pulsatile or non-pulsatile. The normal liver edge may be just palpable below the right costal margin on deep inspiration, especially in thin people. The edge is then felt to be soft and regular with a fairly sharply defined border and the surface of the liver itself is smooth. Sometimes only the left lobe of the liver may be palpable (to the left of the midline) in patients with cirrhosis.

If the liver edge is palpable the total liver span can be measured. Remember that the liver span varies with height and is greater in men than women, and that inter-observer error is quite large for this measurement. The normal upper border of the liver is level with the sixth rib in the midclavicular line. At this point the percussion note over the chest changes from resonant to dull (Figure 6.25a). To estimate the liver span (Figure 6.25b), percuss down along the right midclavicular line until the liver dullness is encountered and measure from here to the palpable liver edge. Careful assessment of the position of the midclavicular line will improve the accuracy of this measurement. The normal span is less than 13 cm. Note that the clinical estimate of the liver span usually underestimates its actual size by 2 to 5 cm.

Figure 6.25 Percussing the liver span: (a) upper border; (b) lower border

Other causes of a normal but palpable liver include ptosis due to emphysema, asthma or a subdiaphragmatic collection, or a Riedel’s lobe.^u The Riedel’s lobe is a tongue-like projection of the liver from the right lobe’s inferior surface; it can be quite large and rarely extends as far as the right iliac fossa. It can be confused with an enlarged gallbladder or right kidney.

Many diseases cause hepatic enlargement and these are listed in Table 6.11. Detecting the liver edge below the costal margin clinically is highly specific (100%) but insensitive (48%)—positive LR 2.5, negative LR 0.5.^10,11 Remember, the diseased liver is not always enlarged; a small liver is common in advanced cirrhosis, and the liver shrinks rapidly with acute hepatic necrosis (due to liver cell death and collapse of the reticulin framework).

TABLE 6.11 Differential diagnosis in liver palpation

Hepatomegaly 1. Massive • Metastases • Alcoholic liver disease with fatty infiltration • Myeloproliferative disease • Right heart failure • Hepatocellular cancer 2. Moderate • The above causes • Haemochromatosis • Haematological disease—e.g. chronic leukaemia, lymphoma • Fatty liver—secondary to e.g. diabetes mellitus, obesity, toxins • Infiltration—e.g. amyloid 3. Mild • The above causes • Hepatitis • Biliary obstruction • Hydatid disease • Human immunodeficiency virus (HIV) infection

Firm and irregular liver

Hepatocellular carcinoma

Metastatic disease

Cirrhosis

Hydatid disease, granuloma (e.g. sarcoid), amyloid, cysts, lipoidoses

Tender liver

Hepatitis

Rapid liver enlargement—e.g. right heart failure, Budd-Chiari^* syndrome (hepatic vein thrombosis)

Hepatocellular cancer

Hepatic abscess

Biliary obstruction/cholangitis

^* George Budd (1808–1882), professor of medicine, King’s College Hospital, London, described this in 1845. Hans Chiari (1851–1916), professor of pathology, Prague, described it in 1898.

The gallbladder

The gallbladder is occasionally palpable below the right costal margin where this crosses the lateral border of the rectus muscles. If biliary obstruction or acute cholecystitis is suspected, the examining hand should be oriented perpendicular to the costal margin, feeling from medial to lateral. Unlike the liver edge, the gallbladder, if palpable, will be a bulbous, focal, rounded mass which moves downwards on inspiration. The causes of an enlarged gallbladder are listed in Table 6.12.

TABLE 6.12 Gallbladder enlargement

^* Abraham Vater (1684–1751), Wittenberg anatomist and botanist.

^† Henri Hartmann (1860–1952), professor of surgery, Paris.

Murphy’s sign^v should be sought if cholecystitis is suspected (Good signs guide 6.1). On taking a deep breath, the patient catches his or her breath when an inflamed gallbladder presses on the examiner’s hand, which is lying at the costal margin. Other signs are less helpful.

GOOD SIGNS GUIDE 6.1 Cholecystitis

NS = not significant.

From McGee S, Evidence-based physical diagnosis, 2nd edn. St Louis: Saunders, 2007.

The clinician examining for an enlarged gallbladder must always be mindful of Courvoisier’s law,^w which states that, if the gallbladder is enlarged and the patient is jaundiced, the cause is unlikely to be gallstones. Rather, carcinoma of the pancreas or lower biliary tree resulting in obstructive jaundice is likely to be present. This is because the gallbladder with stones is usually chronically fibrosed and therefore incapable of enlargement. Note that if the gallbladder is not palpable, and the patient is jaundiced, some cause other than gallstones is still possible, as at least 50% of dilated gallbladders are impalpable (Good signs guide 6.2).

GOOD SIGNS GUIDE 6.2 Gallbladder

From McGee S, Evidence-based physical diagnosis, 2nd edn. St Louis: Saunders, 2007.

The spleen

The spleen enlarges inferiorly and medially (Figure 6.26). Its edge should be sought below the umbilicus in the midline initially. A two-handed technique is recommended. The left hand is placed posterolaterally over the left lower ribs and the right hand is placed on the abdomen below the umbilicus, parallel to the left costal margin (Figure 6.27a). Don’t start palpation too near the costal margin or a large spleen will be missed. As the right hand is advanced closer to the left costal margin, the left hand compresses firmly over the rib cage so as to produce a loose fold of skin (Figure 6.27b); this removes tension from the abdominal wall and enables a slightly enlarged soft spleen to be felt as it moves down towards the right iliac fossa at the end of inspiration (Figure 6.27c).

Figure 6.26 Massive splenomegaly: note the splenic notch

Figure 6.27 Palpation of the spleen

(a) Palpation begins in the lower mid-abdomen and finishes up under the left costal margin.

(b) The examiner’s hand supports the patient’s side…

(c) …and then rests over the lower costal margin to reduce skin resistance.

(d) If the spleen is not palpable when the patient is flat, he or she should be rolled towards the examiner.

If the spleen is not palpable, the patient must be rolled onto the right side towards the examiner (the right lateral decubitus position) and palpation repeated. Here one begins close to the left costal margin (Figure 6.27d). As a general rule, splenomegaly becomes just detectable if the spleen is one-and-a-half to two times enlarged. Palpation for splenomegaly is only moderately sensitive but highly specific. The positive LR of splenomegaly when the spleen is palpable is 9.6 and the negative LR of splenomegaly if the spleen is not palpable is 0.6.¹¹ The causes of splenomegaly are listed in Table 8.8 (page 230). The causes of hepatosplenomegaly are listed in Table 6.13.

TABLE 6.13 Causes of hepatosplenomegaly

The kidneys

The first important differential diagnosis to consider, if a right or left subcostal mass is palpable, must be a kidney. An attempt to palpate the kidney should be a routine part of the examination. The bimanual method is the best. The patient lies flat on his or her back. To palpate the right kidney, the examiner’s left hand slides underneath the back to rest with the heel of the hand under the right loin. The fingers remain free to flex at the metacarpophalangeal joints in the area of the renal angle. The flexing fingers can push the contents of the abdomen anteriorly. The examiner’s right hand is placed over the right upper quadrant.

First an attempt should be made to capture the kidney between the two hands. It is more often possible to feel a kidney by bimanual palpation (this is traditionally called ballotting, although this term should probably be reserved for the palpation of an organ or mass in a fluid medium). In this case the renal angle is pressed sharply by the flexing fingers of the posterior hand. The kidney can be felt to float upwards and strike the anterior hand. The opposite hands are used to palpate the left kidney.

When palpable, the kidney feels like a swelling with a rounded lower pole and a medial dent (the hilum). However, it is unusual for a normal kidney to be felt as clearly as this. The lower pole of the right kidney may be palpable in thin, normal persons. Both kidneys move downwards with inspiration. The causes of kidney enlargement are listed in Table 7.8 (page 210).

It is particularly common to confuse a large left kidney with splenomegaly. The major distinguishing features are: (i) the spleen has no palpable upper border—the space between the spleen and the costal margin, which is present in renal enlargement, cannot be felt; (ii) the spleen, unlike the kidney, has a notch that may be palpable; (iii) the spleen moves inferomedially on inspiration while the kidney moves inferiorly; (iv) the spleen is not usually ballottable unless gross ascites is present, but the kidney is, again because of its retroperitoneal position; (v) the percussion note is dull over the spleen but is usually resonant over the kidney, as the latter lies posterior to loops of gas filled bowel; (vi) a friction rub may occasionally be heard over the spleen, but never over the kidney because it is too posterior.

Other abdominal masses

The causes of a mass in the abdomen, excluding the liver, spleen and kidneys, are summarised in Table 6.14.

TABLE 6.14 Causes of abdominal masses

Stomach and duodenum

Although many clinicians palpate the epigastrium to elicit tenderness in patients with suspected peptic ulcer, the presence or absence of tenderness is not helpful in making this diagnosis. With gastric outlet obstruction due to a peptic ulcer or gastric carcinoma (page 194), the ‘succussion splash’ (the sign of Hippocrates) may occasionally be present but unfortunately this entertaining sign is more of historical interest than practical use now. In a case of suspected gastric outlet obstruction, after warning the patient what is to come, grasp one iliac crest with each hand, place your stethoscope close to the epigastrium and shake the patient vigorously from side to side. The listening ears eagerly await a splashing noise due to excessive fluid retained in an obstructed stomach. The test is not useful if the patient has just drunk a large amount of milk or other fluid for his or her ulcer; the clinician must then return 4 hours later, having forbidden the patient to drink anything further.

Pancreas

A pancreatic pseudocyst following acute pancreatitis may, if large, be palpable as a rounded swelling above the umbilicus. It is characteristically tense, does not descend with inspiration and feels fixed. Occasionally a pancreatic carcinoma may be palpable in thin patients.

Aorta

Arterial pulsation from the abdominal aorta may be present, usually in the epigastrium, in thin normal people. The problem is to determine whether such a pulsation represents an aortic aneurysm (usually due to atherosclerosis) or not. Measure the width of the pulsation gently with two fingers by aligning these parallel to the aorta and placing them at the outermost palpable margins. With an aortic aneurysm, the pulsation is expansile (i.e. it enlarges appreciably with systole) (Figure 6.28). If an abdominal aortic aneurysm is larger than 5 cm in diameter, it usually merits surgical repair. The sensitivity of examination for finding an aneurysm of 5 cm or larger is 82%.^12,13 The sensitivity of the examination for detecting an aneurysm increases pari passu with the size of the aneurysm. The overall LR for a significant aneurysm when one is suspected on palpation is 2.7, with a negative LR of 0.43 if the examination is normal.¹¹

Figure 6.28 Detecting an expansile impulse

A = no impulse; B = transmitted pulsation from a neighbouring artery; C = expansile impulse, the sign of an aneurysm.

Adapted from Clain A, ed. Hamilton Bailey’s Physical signs in clinical surgery, 17th edn. John Wright & Sons, 1986.

Bowel

Particularly in severely constipated patients with soft abdominal walls and retained faeces, the sigmoid colon is often palpable. Unlike other masses, faeces can usually be indented by the examiner’s finger. Rarely, carcinoma of the bowel may be palpable, particularly in the caecum where masses can grow to a large size before they cause obstruction. Such a mass does not move on respiration. In the examination of children or adults with chronic constipation and a megarectum, the enlarged rectum containing impacted stool may be felt above the symphysis pubis, filling a variable part of the pelvis in the midline.

Bladder

An empty bladder is impalpable. If there is urinary retention, the full bladder may be palpable above the pubic symphysis. It forms part of the differential diagnosis of any swelling arising out of the pelvis. It is characteristically impossible to feel the bladder’s lower border. The swelling is typically regular, smooth, firm and oval-shaped. The bladder may sometimes reach as high as the umbilicus. It is unwise to make a definite diagnosis concerning a swelling coming out of the pelvis until you are sure the bladder is empty. This may require the insertion of a urinary catheter.

Inguinal lymph nodes

These are described on page 229.

Testes

Palpation of the testes should be considered if indicated during the abdominal examination (page 215). Testicular atrophy occurs in chronic liver disease (e.g. alcoholic liver disease, haemochromatosis); its mechanism is believed to be similar to that responsible for gynaecomastia.

Anterior abdominal wall

The skin and muscles of the anterior abdominal wall are prone to the same sorts of lumps that occur anywhere on the surface of the body (Table 6.15). So to avoid embarrassment it is important not to confuse these with intra-abdominal lumps. To determine whether a mass is in the abdominal wall, ask the patient to fold the arms across the upper chest and sit halfway up. An intra-abdominal mass disappears or decreases in size, but one within the layers of the abdominal wall will remain unchanged.

TABLE 6.15 Some causes of anterior abdominal wall masses

Pain can arise from the abdominal wall; this can cause confusion with intra-abdominal causes of pain. To test for abdominal wall pain, feel for an area of localised tenderness that reproduces the pain while the patient is supine. If this is found, ask the patient to fold the arms across the upper chest and sit halfway up, then palpate again (Carnett’s test: described by JB Carnett in 1926). If the tenderness disappears, this suggests that the pain is in the abdominal cavity (as tensed abdominal muscles are protecting the viscera), but if the tenderness persists or is greater, this suggests that the pain is arising from the abdominal wall (e.g. muscle strain, nerve entrapment, myositis).^14–16 However, the Carnett test may occasionally be positive when there is visceral disease with involvement of the parietal peritoneum producing inflammation of the overlying muscle (e.g. appendicitis).

Percussion

Percussion is used to define the size and nature of organs and masses, but is most useful for detecting fluid in the peritoneal cavity, and for eliciting tenderness in patients with peritonitis.

Spleen

Percussion over the left costal margin may be more sensitive than palpation for detection of enlargement of the spleen. Percuss over the lowest intercostal space in the left anterior axillary line in both inspiration and expiration with the patient supine (Figure 6.29). Splenomegaly should be suspected if the percussion note is dull or becomes dull on complete inspiration. Percussion appears to be more sensitive than palpation for the detection of splenomegaly. If the percussion note is dull, palpation should be repeated.

Figure 6.29 Percussion of the spleen

Ascites

The percussion note over most of the abdomen is resonant, due to air in the intestines.¹⁷ The resonance is detectable out to the flanks. When peritoneal fluid (ascites) collects, the influence of gravity causes this to accumulate first in the flanks in a supine patient. Thus, a relatively early sign of ascites (when at least 2 litres of fluid have accumulated) is a dull percussion note in the flanks (Good signs guide 6.3). With gross ascites, the abdomen distends, the flanks bulge, umbilical eversion occurs (see Figure 6.19) and dullness is detectable closer to the midline. However, an area of central resonance will always persist. Routine abdominal examination should include percussion starting in the midline with the finger pointing towards the feet; the percussion note is tested out towards the flanks on each side.

GOOD SIGNS GUIDE 6.3 Ascites

Sign	Positive LR	Negative LR
Inspection
Bulging flanks	1.9	0.4
Oedema	3.8	0.2
Palpation and percussion
Flank dullness	NS	0.3
Shifting dullness	2.3	0.4
Fluid wave	5.0	0.5

NS = not significant.

From McGee S, Evidence-based physical diagnosis, 2nd edn. St Louis: Saunders, 2007.

If (and only if) dullness is detected in the flanks, the sign of shifting dullness should be sought.¹⁷ To detect this sign, while standing on the right side of the bed percuss out to the left flank until dullness is reached (Figure 6.30a). This point should be marked and the patient rolled towards the examiner. Ideally 30 seconds to 1 minute should then pass so that fluid can move inside the abdominal cavity and then percussion is repeated over the marked point (Figure 6.30b).

Figure 6.30 Shifting dullness

(a) Percuss out to the left flank until the percussion note becomes dull. Mark this spot with your finger.

(b) Roll the patient towards you, wait 30 seconds. Shifting dullness is present if the left lateral dull area is now resonant.

Shifting dullness is present if the area of dullness has changed to become resonant. This is because peritoneal fluid moves under the influence of gravity to the right side of the abdomen when this is the lowermost point. Very occasionally, fluid and air in dilated small bowel in small intestinal obstruction, or a massive ovarian cyst filling the whole abdomen, can cause confusion.

To detect a fluid thrill (or wave) the clinician asks an assistant (or the patient) to place the medial edges of both palms firmly on the centre of the abdomen with the fingers pointing towards each other. The examiner flicks the side of the abdominal wall, and a pulsation (thrill) is felt by the hand placed on the other abdominal wall. A fluid thrill is of more value when there is massive ascites. Interestingly, it may also occur when there is a massive ovarian cyst or a pregnancy with hydramnios.

The presence of bulging in the flanks has good sensitivity and specificity for the detection of ascites. Shifting dullness has both good sensitivity and specificity. The presence of ankle oedema increases the likelihood of ascites. (See Good signs guide 6.3.)

The causes of ascites are listed in Table 6.16.

TABLE 6.16 Classification of ascites by the serum ascites to albumin concentration gradient

High gradient (>11g/L) 1. Cirrhosis* 2. Alcoholic hepatitis 3. Budd-Chiari syndrome (hepatic vein thrombosis) or veno-occlusive disease 4. Fulminant hepatic failure 5. Congestive heart failure, constrictive pericarditis (cardiac ascites) 6. Myxoedema (rare)

Low gradient (<11g/L)

1. Peritoneal carcinomatosis

2. Tuberculosis

3. Pancreatic ascites

4. Nephrotic syndrome

^* Patients with a high serum-to-ascites albumin gradient most often have portal hypertension (97% accuracy).

When significant ascites is present, abdominal masses may be difficult to feel by direct palpation. Here is the opportunity to practise dipping. Using the hand placed flat on the abdomen, the fingers are flexed at the metacarpophalangeal joints rapidly so as to displace the underlying fluid. This enables the fingers to reach a mass covered in ascitic fluid. In particular, this should be attempted to palpate an enlarged liver or spleen. The liver and spleen may become ballottable when gross ascites is present.

Auscultation

While some cardiologists believe that the sounds produced in the abdominal cavity are not as varied or as interesting as those one hears in the chest, they have some value.

Hernias

Hernias are of surgical importance and should not be missed during an abdominal examination. They are very frequently the focus of student assessment examinations. This section will be restricted to examination of groin hernias, which comprise inguinal and femoral hernias.

The principal sign of a hernia is that of a lump in the groin region. Naturally, not all lumps in the region are hernias (Table 6.17). A lump that is present on standing or during manoeuvres that raise intra-abdominal pressure (such as coughing or straining), and that disappears on recumbency, is easily identified as a hernia. Some hernias, however, are irreducible. Another term used for irreducible is incarcerated, but this term is probably best avoided. Some irreducible hernias contain bowel, which may become obstructed, giving rise to symptoms of small bowel obstruction in addition to the irreducible lump. Sometimes the bowel contents’ blood supply becomes jeopardised, and these are known as strangulated hernias; they are usually painful, red, tense and tender.

TABLE 6.17 Differential diagnosis of a solitary groin lump

Inguinal hernias

Inguinal hernias typically bulge above the crease of the groin. They arise from a deficiency above the inguinal ligament and this is where they are usually felt (Figure 6.31). The inguinal ligament lies between the anterior superior iliac spine and the pubic tubercle. The pubic tubercle is just above the attachment of the adductor longus tendon to the pubic bone (feel the upper medial aspect of the thigh to palpate the tendon). The internal inguinal ring lies 2 cm above the midpoint of the inguinal ligament.

Figure 6.31 Note the elliptical swelling of an indirect inguinal hernia descending into the scrotum on the right side. Also note the globular swelling of a direct inguinal hernia on the left side

An indirect inguinal hernia protrudes through the deep inguinal ring. The best surface marking for this point is just above the midpoint of the inguinal ligament, which is halfway between the pubic tubercle and the anterior superior iliac spine (it is the position where the spermatic cord structures enter the inguinal canal). This is lateral to the inferior epigastric vessels. A direct hernia, on the other hand, pushes into the inguinal canal posteriorly through a region of weakness known as Hesselbach’s triangle.^z This triangle is bounded inferiorly by the inguinal ligament, laterally by the inferior epigastric vessels and medially by the lateral border of the rectus sheath.

The student may be asked to differentiate between direct and indirect inguinal hernias. However, clinically this is difficult and the true nature of an inguinal hernia can often be determined only at the time of operation. The muscular defect in a direct hernia is usually larger than that of an indirect hernia, and as such direct hernias are typically easier to demonstrate and usually reduce immediately and spontaneously. An indirect hernia may often be felt on palpation to slide along the direction of the inguinal canal under the examining fingers.

A large inguinal hernia may descend through the external ring immediately above the pubic tubercle into the scrotum. Gentle invagination of the scrotum with the tip of the gloved little finger in the external ring may be performed to confirm an indirect hernia in men but this can be difficult to interpret without substantial experience (Figure 6.32). A maldescended testis can be confused with an inguinal hernia; always confirm that there is a testis in each scrotum. A large inguinal hernia may present as a lump in the scrotum. It is important initially in this situation to ascertain whether one can get above the lump. If so, the lump is of primary intrascrotal pathology and is not a hernia.

Figure 6.32 To examine the inguinal canal in a male, the scrotum can be invaginated as shown (always wear gloves)

Rectal examination (Figure 6.33)

Figure 6.33 The rectal examination: regional anatomy

From Talley NJ, American Journal of Gastroenterology. 2008; 108: 802–803, with permission.

The abdominal examination is not complete without the performance of a rectal examination.^18,19 It should be considered in all patients admitted to hospital who are over the age of 40, unless the examiner has no fingers, the patient no anus, or acute illness such as myocardial infarction presents a temporary contraindication.

The patient’s permission must be obtained and if indicated a chaperone introduced to the patient. Privacy must be ensured for the patient throughout the examination. Following an explanation as to what is to happen and why, the patient lies on his or her left side with the knees drawn up and back to the examiner. This is called the left lateral position. The examination can be performed with the patient standing and in the bent-over position. This may help provide good information about the prostate, but makes assessment of rectal function more difficult.

The examiner dons a pair of gloves and begins the inspection of the anus and perianal area by separating the buttocks. The following must be looked for:

Next ask the patient to strain and watch the perineum: look for incontinence and leakage of faeces or mucus, abnormal descent of the perineum or the presence of a patulous anus. The presence of a gaping anus often correlates with lower resting pressures on anorectal manometry. Internal haemorrhoids can prolapse in the right anterior, right posterior and left lateral positions.

If there is rectal prolapse, straining may cause a dark red mass to appear at the anal verge; mucosal prolapse causes the appearance of radial folds and concentric folds are a sign of complete prolapse. This mass is continuous with the perianal skin and is usually painless. In cases of mucosal rectal prolapse, the prolapsed mucosa can be felt between the examiner’s thumb and forefinger.

Now test the anal wink. Stroke a cotton pad in all four quadrants around the anus. Usually you will see a brisk anal contraction which indicates the sacral nerve pathways are intact. Sometimes the response is weak in healthy people. However, the complete absence of an anal wink, particularly in the setting of faecal incontinence, suggests that there is a spinal cord problem and indicates the need to perform a more detailed neurological examination and consider further investigations accordingly.

Now the time for action has come. The tip of the gloved right index finger is lubricated and placed over the anus. Ask the patient to breathe in and out quietly through the mouth, as a distraction and to aid relaxation. If there is excruciating pain at the start of the examination, this strongly suggests that there is an anal fissure and the remainder of the rectal examination should be abandoned. Often the fissure can be seen on inspection. An anal fissure can precipitate constipation but may be secondary to constipation itself. By liberally lubricating the rectum with lignocaine jelly, it may still be possible to complete the rest of the examination, but usually it is better to perform anoscopy under appropriate sedation for these patients. Other causes of significant anal pain during palpation include recently thrombosed external haemorrhoids, an ischiorectal abscess, active proctitis, or anal ulceration from another cause.

Slowly increasing pressure is applied with the pulp of the finger until the sphincter is felt to relax slightly. At this stage the finger is advanced into the rectum slowly. During entry, sphincter tone should be assessed as normal or reduced. The accuracy of this assessment has been questioned in the past, but more recently has been shown to correlate well with anorectal manometry measurements.²⁰ This resting tone is predominantly (70%–80%) attributable to the internal anal sphincter muscle. Reduced sphincter tone may indicate a sphincter tear. A high anal resting tone may contribute to difficulties with evacuation.

Palpation of the anterior wall of the rectum for the prostate gland in the male and for the cervix in the female is performed first. The normal prostate is a firm, rubbery bilobed mass with a central furrow. It becomes firmer with age. With prostatic enlargement, the sulcus becomes obliterated and the gland is often asymmetrical. A very hard nodule is apparent when a carcinoma of the prostate is present. The prostate is boggy and tender in prostatitis. A mass above the prostate or cervix may indicate a metastatic deposit on Blumer’s shelf.^aa

The finger is then rotated clockwise so that the left lateral wall, posterior wall and right lateral wall of the rectum can be palpated in turn. Then the finger is advanced as high as possible into the rectum and slowly withdrawn along the rectal wall. A soft lesion, such as a small rectal carcinoma or polyp, is more likely to be felt this way^bb (Table 6.18). Ask the patient to squeeze your finger with the anal muscles as a further test of anal tone.

TABLE 6.18 Causes of a palpable mass in the rectum

Note: Faeces, while palpable, also indent.

^* James Douglas (1675–1742), Scottish anatomist and male midwife, physician to Queen Caroline (wife of George II) in London.

Ask the patient to strain again when the examiner’s finger is rotated anteriorly. In this position a rectocele (a defect in the anterior wall of the rectum) may be palpable.

Examination of the gastrointestinal contents

Urinalysis

Note that testing of the urine can be very helpful in diagnosing liver disease.

Strip colour tests can detect the presence of bilirubin and urobilinogen in the urine. False-positive or false-negative results can occur with vitamin C or even exposure to sunlight.

An understanding of the reasons for the presence of bilirubin or urobilinogen in the urine necessitates an explanation of the metabolism of these substances (Figure 6.34).

Figure 6.34 Schematic representation of the bilirubin pathway

Increased haemolysis (1) overwhelms the hepatocytes’ ability to conjugate bilirubin and excrete the conjugated form, leading to increased serum levels of unconjugated bilirubin. Low levels of glucuronyl transferase (2) (e.g. Gilbert’s disease) cause decreased conjugation. Hepatocellular dysfunction (3) causes decreased uptake, conjugation and excretion with increases of unconjugated bilirubin and conjugated bilirubin. Posthepatic obstruction (4) from stones or tumour prevents passage of bilirubin through the bile ducts into the bowel, leading to increased serum levels of conjugated bilirubin.

Red blood cells are broken down by the reticuloendothelial system, causing the release of haem, which is converted to biliverdin and then unconjugated bilirubin, a water-insoluble compound. For this reason, unconjugated bilirubin released with haemolytic anaemia will not appear in the urine (termed acholuric jaundice).

Unconjugated bilirubin is transported in the blood bound largely to albumin but also to other plasma proteins. Unconjugated bilirubin is then taken up by the liver cells and transported to the endoplasmic reticulum, where glucuronyl transferases conjugate bilirubin with glucuronide. This results in the formation of conjugated bilirubin, which is water-soluble. Conjugated bilirubin is then concentrated and excreted by the liver cell into the canaliculus.

Conjugated bilirubin is virtually all excreted into the small bowel; it is converted in the terminal ileum and colon to urobilinogen, and then to stercobilin. Stercobilin is responsible for the normal colour of the stools with other non-bilirubinoid dietary pigments. Up to 20% of urobilinogen is reabsorbed by the bowel, and small amounts are excreted in the urine as urinary urobilinogen. This can often be normally detected by reagent strips.

Total biliary obstruction, from whatever cause, results in absence of urinary urobilinogen, as no conjugated bilirubin reaches the bowel, resulting in pale stools (absence of stercobilin). The conjugated bilirubin, unable to be excreted (the rate-limiting step), leaks from the hepatocytes into the blood and from there is excreted into the urine (normally there is no bilirubin detected in urine). This results in dark urine (excess conjugated bilirubin). Acute liver damage, as in viral hepatitis, may sometimes initially result in excessive urinary urobilinogen, because the liver is unable to re-excrete the urobilinogen reabsorbed from the bowel. These changes are summarised in Table 6.19.

Examination of the acute abdomen

It is very important to try to determine whether a patient who presents with acute abdominal pain requires an urgent operation or whether careful observation with reassessment is the best course of action.^22,23 First, take note of the general appearance of the patient. The patient who is obviously distressed with pain or who looks unwell often is, and conversely some reassurance can be gained if a patient does not look sick and appears comfortable.

Assess the patient’s vital signs immediately and recheck these at frequent intervals. Signs of reduced circulating blood volume and dehydration, including tachycardia, postural hypotension, tachypnoea, vasoconstriction and sweating, are of great concern. These signs associated with abdominal pain are usually an indication of substantial intra-abdominal blood loss (such as a ruptured aortic aneurysm), or of substantial fluid losses (e.g. due to acute pancreatitis), or of septic shock (as with a perforated viscus or abscess). Take the patient’s temperature.

Inspect the abdomen. Look particularly for lack of movement with respiration, with splinting of the abdominal wall muscles. Note any abdominal distension, visible peristalsis or other lumps and masses, without forgetting the groin region and hernias. Note also any abdominal scars and inquire as to their nature and age.

Palpate very gently. The presence or absence of peritonism is first assessed. Peritonism is an inflammation that causes pain when peritoneal surfaces are moved relative to each other (Table 6.20; see also Good signs guide 6.4). Traditionally, rebound tenderness is used to assess whether peritonism is present or not. However, if peritonism is present, this test is far more uncomfortable (and cruel) than eliciting tenderness to light percussion. If the patient is extremely apprehensive, ask him or her first to cough; the reaction will be a guide to the degree of peritonism and also its location. Palpation is then continued slowly, but more deeply if possible and if masses are sought. Do not forget to palpate for the pulsatile mass of a ruptured aneurysm. This may be quite indistinct.

TABLE 6.20 Differential diagnosis of the acute abdomen

GOOD SIGNS GUIDE 6.4 Peritonitis

NS = not significant.

From McGee S, Evidence-based physical diagnosis, 2nd edn. St Louis: Saunders, 2007.

Then perform light percussion over areas of tenderness. If generalised peritonitis is present, this almost invariably necessitates a surgical approach, with the notable exception of acute pancreatitis.

Examine for hernias. The presence of a hernia does not necessarily mean that this is the cause of pathology, as they are quite common. However, a tender or irreducible hernia is more likely to be of significance, particularly if this has only very recently been noticed by the patient or has recently become tender.

Auscultation is now performed. In the presence of a bowel obstruction (Good signs guide 6.5), bowel sounds will be louder, more frequent and high-pitched. In an ileus from any cause, bowel sounds are usually reduced or absent.

GOOD SIGNS GUIDE 6.5 Acute bowel obstruction

NS = not significant.

From McGee S, Evidence-based physical diagnosis, 2nd edn. St Louis: Saunders, 2007.

Rectal and vaginal examinations may be very important but the findings are not helpful for the diagnosis of appendicitis or obstruction; note any tenderness (and its location), masses or blood loss. Per rectal blood should make the examiner think of acute colitis (e.g. Crohn’s disease, ulcerative colitis, ischaemic colitis or infectious colitis), or of mesenteric ischaemia. A purulent vaginal discharge suggests salpingitis.

Urinalysis may show glycosuria and ketonuria in diabetic ketoacidosis (which can cause acute abdominal pain), haematuria in renal colic, bilirubinuria in cholangitis or proteinuria in pyelonephritis (page 200).

Examine the respiratory system for signs of consolidation, a pleural rub or pleural effusion, and examine the cardiovascular system for atrial fibrillation (a major cause of embolism to a mesenteric artery) or for signs of a myocardial infarction. Examine the back for evidence of spinal disease that may radiate to the abdomen. Remember that herpes zoster may cause abdominal pain before the typical vesicles erupt.

Consider the symptoms and signs of appendicitis.²² Malaise and fever is usually associated with abdominal pain, which is at first worst in the hypogastrium and then moves to the right iliac fossa. The examination will often reveal tenderness and guarding in the right iliac fossa. The pain and tenderness are usually maximum over McBurney’s point.^dd He described this point as to 2 in (3.8 to 5.0 cm) along a line from the anterior superior iliac spine to the umbilicus. Rovsing’s sign^ee is another way of testing rebound tenderness. Press over the patient’s left lower quadrant, then release quickly; this causes pain in the right iliac fossa. The psoas sign is positive when the patient lies on the left side and the clinician attempts to extend the right hip. If this is painful and resisted, the sign is positive. When the appendix causes pelvic inflammation, rectal examination evokes tenderness on the right side. These signs are of variable usefulness (Good signs guide 6.6).

GOOD SIGNS GUIDE 6.6 Appendicitis

NS = not significant.

From McGee S, Evidence-based physical diagnosis, 2nd edn. St Louis: Saunders, 2007.

Remember that in elderly patients these signs may be reduced or absent.²³

Correlation of physical signs and gastrointestinal disease

Assessment of gastrointestinal bleeding

Haematemesis, melaena or massive rectal bleeding are dramatic signs of gastrointestinal haemorrhage. It is important in such a case to assess the amount of blood loss and attempt to determine the likely site of bleeding. Haematemesis indicates bleeding from a site proximal to, or in, the duodenum.

Assessing degree of blood loss

First take the pulse rate and the blood pressure lying and sitting. As a general rule, loss of 1.5 litres or more of blood volume over a few hours results in a fall in cardiac output, causing hypotension and tachycardia. A pulse rate of more than 100 a minute or a systolic blood pressure of less than 100 mmHg, or a 15 mmHg postural fall in systolic blood pressure, suggests significant recent blood loss. These are indications for blood transfusion. The signs depend to some extent on the state of the patient’s cardiovascular system. Those who have pre-existing cardiovascular disease will become shocked much earlier than young fit patients with a normal cardiovascular system.

Once signs of shock are present, massive blood loss has occurred. These signs include peripheral cyanosis with cold extremities, clammy skin, dyspnoea and air hunger; the patients are anxious. The blood pressure is low, with a compensating tachycardia, and the urine output is reduced or absent. These are ominous signs in patients with gastrointestinal haemorrhage. Urgent resuscitative measures must be instituted.

Determining the possible bleeding site

The causes of acute gastrointestinal haemorrhage are listed in Table 6.3, page 151.

Examine the patient with acute upper gastrointestinal bleeding for signs of chronic liver disease and portal hypertension. Part of the assessment should include inspection of the vomitus and stools (pages 183–184) and a rectal examination. Remember that, of patients with chronic liver disease and upper gastrointestinal bleeding, only about half are bleeding from varices. The others are usually bleeding from peptic ulceration (either acute or chronic). Look for evidence of a bleeding diathesis.

Finally, examine the patient for any evidence of skin lesions that can be associated with vascular anomalies in the gastrointestinal tract, although these are rare (Tables 6.3, 6.4). For example, pseudoxanthoma elasticum is an autosomal recessive disorder of elastic fibres that results in xanthoma-like yellowish nodules, particularly in the axillae or neck. These patients may also have angioid streaks of the optic fundus and angiomatous malformations of blood vessels that can bleed into the gastrointestinal tract. Ehlers-Danlos syndrome is a group of connective tissue disorders resulting in fragile and hyperextensible skin (Figure 6.35). In a number of types, blood vessels are involved. Type IV is characterised by gastrointestinal tract bleeding, spontaneous bowel perforation, minimal skin hyperelasticity and minimal joint hyperextension.

Figure 6.35 Ehlers-Danlos syndrome: (a) arms; (b) hands

Abnormal elasticity of the skin is typical of the Ehlers-Danlos syndrome. The skin may be greatly stretched and takes much longer than normal to return to its normal position. It is also more fragile than normal. Joint hypermobility occurs in type III Ehlers-Danlos syndrome.

Examine the patient with acute lower gastrointestinal bleeding as described above, paying close attention to the abdominal examination and the rectal examination. Inspect the stools and test them for blood. Colonoscopy is a key test for all these patients.

Inflammatory bowel disease

Inflammatory bowel disease refers to two chronic idiopathic diseases of the gastrointestinal tract: ulcerative colitis and Crohn’s disease.

Ulcerative colitis

In the gastrointestinal tract only the large bowel is affected. Occasionally the terminal ileum can be secondarily involved (backwash ileitis). The disease almost always involves the rectum and may extend, without skip areas, to involve a variable part of the colon.

• Abdominal signs: if there is proctitis only, there are usually no abnormal external findings (except at sigmoidoscopy and biopsy); occasionally, anal fissures are present; with colitis, in the uncomplicated case the abdominal examination may be normal or there may be tenderness and guarding over the affected colon.

• Signs of complications: local signs include the following: (i) toxic dilatation (megacolon)—one of the most feared complications in which there are signs of distension, generalised guarding and rigidity (peritonism), pyrexia and tachycardia; (ii) massive bleeding or perforation; (iii) carcinoma—there is an increased incidence of colonic cancer in extensive, long-standing ulcerative colitis.

• Systemic signs include: (i) chronic liver disease—primary sclerosing cholangitis or cirrhosis; (ii) anaemia—due to chronic disease per se, or blood loss, or autoimmune haemolysis; (iii) arthritis—there may be a peripheral non-deforming arthropathy affecting particularly the knees, ankles and wrists (10%), and there may be signs of ankylosing spondylitis in 3%; (iv) skin manifestations: erythema nodosum (2%) consists of tender red nodules usually on the shins (Figure 6.36); pyoderma gangrenosum (rare) starts as a tender, red raised area which becomes bullous and ulcerates (Figure 6.37)—it may occur anywhere but is often on the anterior aspects of the legs; mouth ulcers are common and are due to aphthous ulceration (5%); finger clubbing may be present; (v) ocular changes include conjunctivitis, iritis and episcleritis, which are strongly associated with arthritis and skin rash. (Conjunctivitis is an inflammation of the conjunctiva which then appears red and swollen: the eye itself is not tender. Iritis is an inflammation of the iris with central scleral injection, which radiates out from the pupil: the eye is tender. Episcleritis is a nodule of inflammation on the scleral surface.)

Figure 6.36 Erythema nodosum.

From McDonald FS, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

Figure 6.37 Pyoderma gangrenosum

From Misiewicz JJ, Bantrum CI, Cotton PB et al, Slide atlas of gastroenterology. London: Gower Medical Publishing, 1985, with permission.

Crohn’s disease

The whole of the gastrointestinal tract may be affected from the mouth to the anus. However, most commonly the terminal ileum, with or without the colon, is involved.

• Abdominal signs: if the condition affects only the terminal ileum there are often no abnormal findings, although tenderness, fullness or a mass (either soft or firm) in the right iliac fossa may be present. Occasionally there may be signs of an abdominal abscess: these patients may have a high swinging fever, localised tenderness, a palpable mass and evidence of bowel obstruction (pain, vomiting and constipation with dehydration, abdominal distension and tenderness, and an empty rectum). Anal disease is common, including skin tags, fissures, fistulae and abscesses. Colonic involvement produces the same signs as ulcerative colitis.

• Signs of complications: these are similar to those of ulcerative colitis with the following exceptions: (i) liver disease—primary sclerosing cholangitis is less common; (ii) osteomalacia and osteoporosis, which may occur in patients with extensive terminal ileal involvement, results in bone tenderness and fracture; (iii) signs of malabsorption; (iv) finger clubbing is more common; (v) signs of gastrointestinal malignancy (small bowel or colonic carcinoma) are uncommon but the incidence is increased; (vi) the incidence of gallstones and renal stones is increased; (vii) renal disease due to pyelonephritis, hydronephrosis or very rarely secondary amyloidosis may occur.

Radiography

As with the chest X-ray, the name and date should be checked. The left and right sides should be easily distinguished by the stomach gas on the left and the triangular bulky soft tissue of the liver seen in the right hypochondrium.

Review of an abdominal X-ray

• Boundaries: diaphragm, psoas muscles, the extraperitoneal fat (‘flank lines’).

• Bones: lower ribs and costal cartilages, lumbar spine, pelvis.

• Hollow viscera gas: check gas outlining the stomach, small bowel and large bowel.

• Solid organs: size of liver, spleen and kidneys.

• Pelvic organs: bladder size.

• Vascular: aortic calcification.

• Abnormalities: renal or biliary calculi, dilated bowel, free peritoneal gas (Figure 6.38).

Figure 6.38 Free peritoneal gas

The erect chest X-ray is superior to an erect abdominal film for the demonstration of free gas. On the erect chest X-ray, free peritoneal gas is seen below the hemidiaphragm (black arrows). The free gas on the left must be distinguished from gas in the gastric fundus (open arrow). This free gas (black arrow) on the left is crescentic in shape because it outlines the spleen and lies at the apex of the hemidiaphragm. It indicates a perforation of a hollow abdominal viscus unless there has been recent surgery or penetrating trauma.

Bowel dilatation

When an ileus (Figure 6.39) or obstruction (Figures 6.40 and 6.41) is present, it is possible to distinguish small- from large-bowel dilatation. The large-bowel loops are peripheral, few in number, have diameters greater than 5 cm, contain faeces, and have haustral margins that do not extend across the bowel lumen. In contrast, the small-bowel loops are central, multiple, between 3 and 5 cm in diameter, and do not contain faeces. Valvulae conniventes which extend completely across the bowel lumen are seen in the jejunal loops.

Figure 6.39 Generalised ileus.

The large bowel is filled with gas and is dilated, except in the descending colon. Dilated small bowel is also seen in the right hypochondrium (arrow). As gas is seen around to the rectum (arrow), mechanical obstruction is excluded.

Figure 6.40 Small bowel obstruction

There is gross dilatation of the small bowel. It is recognised as small bowel from its central position and its transverse mucosal bands—the valvulae conniventes (black arrow). Air–fluid levels are seen on the erect view (a). The supine view (b) gives a better view of the distribution of the dilated loops. From the number and position of the displayed dilated loops, the obstruction would be at the level of the mid-small bowel. The round radio-opaque shadow in the left hypochondrium is a tablet (open arrow).

Figure 6.41 Large bowel obstruction

The large bowel is markedly distended around to the sigmoid colon, where it abruptly stops (arrow). The common causes of obstruction are carcinoma or diverticular stricture. The increased peristalsis occurring at the onset of obstruction can remove the gas and faeces distal to the obstruction. Therefore no gas is seen in this patient.

With gastric dilatation, the stomach may be massively enlarged and distended with air (Figure 6.42).

Figure 6.42 Gastric dilatation

The stomach is massively enlarged and distended with air. When this occurs acutely, prompt nasogastric aspiration is necessary. Mechanical obstruction due to a pyloric ulcer or carcinoma needs exclusion. Atonic dilatation is usually a postoperative complication, but may occur with diabetic coma, trauma, pancreatitis or hypokalaemia.

Calcification

Calcification shows up well against the grey, soft-tissue densities.

About 90% of renal stones are calcified (Figure 7.4, page 203), whereas only 10% of gallstones are calcified. To identify radiolucent gallstones, an ultrasound examination is the test of choice.

Calcification may be seen in the pancreas in chronic pancreatitis (Figure 6.43).

Figure 6.43 Pancreatic calcification

Stippled calcification is seen in the region of the pancreas (arrow), indicating chronic calcific pancreatitis. The most likely cause is alcohol excess.

Costal cartilage calcification is commonly seen in elderly patients, projected over the hypochondrial regions.

Calcification in the walls of an abdominal aortic aneurysm may be seen on a lateral abdominal film. Splenic and renal artery aneurysms are also often calcified.

Vascular calcification is often seen in the elderly.

Summary

The gastrointestinal examination: a suggested method (Figure 6.44)

As with the other systems this examination will usually be targeted. However it cannot be performed properly, even in a busy clinic, unless the patient lies down and removes sufficient clothing—if necessary in stages and with a chaperone.

Figure 6.44 Gastrointestinal system

Lying flat (1 pillow)

1. General inspection

Jaundice (liver disease)

Pigmentation (haemochromatosis, Whipple’s disease)

Xanthomata (chronic cholestasis)

Mental state (encephalopathy)

2. Hands

3. Nails

• Clubbing

• Leuconychia

Palmar erythema

Dupuytren’s contractures (alcohol)

Arthropathy

Hepatic flap

4. Arms

Spider naevi

Bruising

Wasting

Scratch marks (chronic cholestasis)

5. Face

Eyes

• Sclerae: jaundice, anaemia, iritis

• Cornea: Kayser-Fleischer rings (Wilson’s disease)

Parotids (alcohol)

Mouth

• Breath: fetor hepaticus

• Lips: stomatitis, leucoplakia, ulceration, localised pigmentation (Peutz-Jeghers syndrome), telangiectasia (hereditary haemorrhagic telangiectasia)

• Gums: gingivitis, bleeding, hypertrophy, pigmentation, Monilia

• Tongue: atrophic glossitis, leucoplakia, ulceration

6. Cervical/axillary lymph nodes

7. Chest

Gynaecomastia

Spider naevi

Body hair

8. Abdomen

Inspect

• Scars

• Distension

• Prominent veins—determine direction of flow (caput Medusae; inferior vena cava obstruction)

• Striae

• Bruising

• Pigmentation

• Localised masses

• Visible peristalsis

Palpate

• Superficial palpation—tenderness, rigidity, outline of any mass

• Deep palpation—organomegaly (liver, spleen, kidney), abnormal masses

Roll onto right side (spleen)

Percuss

• Liver, spleen

• Ascites—shifting dullness

Auscultate

• Bowel sounds

• Bruits, hums, rubs

9. Groin

Testes

Lymph nodes

Hernial orifices (standing up)

10. Legs

Bruising

Oedema

Neurological signs (alcohol)

11. Other

Rectal examination—inspect (fistulae, tags, blood, mucus), palpate (masses)

Urine analysis (bile)

Cardiovascular system (cardiomyopathy, cardiac failure, constrictive pericarditis)

Temperature chart (infection)

Position the patient correctly with one pillow for the head and complete exposure of the abdomen. Look briefly at the general appearance and inspect particularly for signs of chronic liver disease.

Examine the hands. Ask the patient to extend his or her arms and hands and look for the hepatic flap. Look also at the nails for clubbing and for white nails, and note any palmar erythema or Dupuytren’s contractures. The arthropathy of haemochromatosis may also be present. Look now at the arms for bruising, scratch marks and spider naevi.

Then go to the face. Note any scleral abnormality (jaundice, anaemia or iritis). Look at the corneas for Kayser-Fleischer rings. Feel for parotid enlargement; then inspect the mouth with a torch and spatula for angular stomatitis, ulceration, telangiectasiae and atrophic glossitis. Smell the breath for fetor hepaticus. Now look at the chest for spider naevi and in men for gynaecomastia and loss of body hair.

Inspect the abdomen from the side, squatting to the patient’s level. Large masses may be visible. Ask the patient to take slow deep breaths and look especially for the hepatic, splenic and gallbladder outlines. Now stand up and look for scars, distension, prominent veins, striae, hernia, bruising and pigmentation.

Palpate lightly in each region for masses, having asked first if any area is particularly tender. This will avoid causing the patient pain and may also provide a clue to a site of possible pathology. Next palpate each region more deeply; then feel specifically for hepatomegaly and splenomegaly. If there is hepatomegaly, confirm this with percussion and estimate the span. If no spleen is felt, percuss over the left costal margin in the left anterior axillary line during complete expiration (dullness suggests splenomegaly). Always roll the patient onto the right side and palpate again if the spleen is not felt initially. Attempt now to feel the kidneys bimanually. Remember the important distinguishing features of a spleen as opposed to a kidney.

Percuss routinely for ascites. If the abdomen is resonant right out to the flanks, do not roll the patient over. Otherwise test for shifting dullness. This is performed by percussing away from your side of the bed until you reach a dull note. Then roll the patient towards you and, after waiting a minute or so, begin percussing again for resonance.

By auscultation note the presence of bowel sounds. Next auscultate briefly over the liver, spleen and renal areas, listening for bruits, hums and rubs.

Examine the groin next. Palpate for inguinal lymphadenopathy. Examine for hernias by asking the patient to stand and then cough. The testes must always be palpated. Now look at the legs for oedema and bruising. Neurological examination of the legs may be indicated if there are signs of chronic liver disease.

If the liver is enlarged or cirrhosis is suspected ask the patient to sit up to 45 degrees and estimate the jugular venous pressure. This will avoid missing constrictive pericarditis or chronic cardiac failure as a cause of liver disease, or haemochromatosis, which can cause a dilated cardiomyopathy. While the patient is sitting up, palpate in the supraclavicular fossae for lymph nodes and feel at the back for sacral oedema. If ascites is present, it is necessary to examine the chest for a pleural effusion. If malignant disease is suspected, examine all lymph node groups, the breasts and the lungs.

A rectal examination should always be considered and specimens of the patient’s vomitus or faeces should be inspected, if available. Perform a urinalysis (for bilirubin and urobilinogen, and glucose) and check the temperature.