Abdominal Examination Routine — DCE Clinical Case

Clinical Case — Station 3 Abdominal Examination

Patient brief (for the candidate)

Mrs Patricia H is a 54-year-old woman. She is known to the gastroenterology service. The examiner asks you to examine her abdomen. [1]

The examination (candidate performs the twelve-step routine)

The candidate introduces themselves, positions the patient, and performs the systematic head-to-toe routine: [1]

End of bed. The patient is cachectic, with obvious yellow discolouration of the sclera. She is comfortable at rest. [1]

Hands. Finger clubbing is present (Schamroth window lost). Palmar erythema of the thenar and hypothenar eminences. Leuconychia. No Dupuytren contracture. No asterixis. [1]

Arms. Multiple linear excoriations on the extensor surfaces (pruritus). Several bruises on the forearms. No needle-track marks. [1]

Face. Scleral icterus. Periorbital xanthelasma (yellow lipid deposits on the eyelids). Oral cavity: angular cheilitis, smooth atrophic tongue (glossitis from B12 and iron deficiency). No mucosal telangiectasia. No pigmented lip macules. [1]

Neck. No Virchow node. No cervical lymphadenopathy. [1]

Chest. More than ten spider naevi in the SVC distribution (face, neck, upper chest, shoulders) — confirmed by blanching with a glass slide. Gynaecomastia. Loss of axillary hair. [1]

Inspection. The abdomen is distended with the flanks filled and an everted umbilicus. There are dilated radiating veins around the umbilicus (caput medusae). No surgical scars. No visible peristalsis. No stoma. [1]

Auscultation (before palpation). Bowel sounds present and normal in all four quadrants. No bruit. No succession splash. [1]

Palpation. Light palpation: no guarding, no rigidity, no focal tenderness. Deep palpation: the liver edge is palpable 4 cm below the right costal margin in the midclavicular line, firm, irregular, with a hard edge. The spleen is palpable 3 cm below the left costal margin, smooth, with a notch — confirmed as the spleen (cannot get above it, dull to percussion). No ballotable kidneys. No expansile pulsation in the epigastrium. [1]

Percussion. Liver span approximately 14 cm (upper border at the sixth intercostal space). Shifting dullness positive (midline tympanic, flanks dull, transition point shifts on rolling). Fluid thrill positive. [1]

Additional (offered). Hernial orifices, digital rectal examination, genitalia. [1]

Legs. Bilateral pitting oedema to the mid-shin. [1]

The presentation

"I examined Mrs Patricia's abdomen. At the end of the bed, she is cachectic with scleral icterus. In the hands, there is finger clubbing, palmar erythema, and leuconychia. There are excoriations consistent with pruritus and bruising on the forearms. On the face, there is scleral icterus, periorbital xanthelasma, angular cheilitis, and glossitis. There is no Virchow node. On the chest, there are more than ten spider naevi in the SVC distribution, gynaecomastia, and loss of axillary hair. The abdomen is distended with the flanks filled and an everted umbilicus, with caput medusae. Bowel sounds are normal. On palpation, the liver is enlarged 4 cm below the costal margin, firm and irregular. The spleen is enlarged 3 cm below the costal margin, smooth, with a notch. There is shifting dullness and a fluid thrill, confirming tense large-volume ascites. There is no expansile pulsation. There is bilateral pitting oedema to the mid-shin. My findings are of chronic liver disease with portal hypertension and cirrhosis. The likely aetiology, given the xanthelasma, the pruritus preceding the jaundice, and the clubbing, is primary biliary cholangitis. I would confirm with antimitochondrial antibodies, IgM, liver function tests, an ultrasound with Doppler, and a FibroScan." [1]

Probing questions

Q: Why primary biliary cholangitis specifically? [1]

The combination of a cholestatic pattern (pruritus preceding jaundice, which is characteristic of bile salt deposition in the skin), xanthelasma (from disordered lipid metabolism in chronic cholestasis), clubbing (PBC is a recognised GI cause of clubbing), and a female patient in the sixth decade (PBC has a 9:1 female-to-male ratio, peak incidence 40 to 60 years) makes primary biliary cholangitis the most likely diagnosis. I would confirm with antimitochondrial antibodies (positive in 95 per cent of PBC patients), an elevated IgM, and the cholestatic liver function test pattern (raised ALP and GGT out of proportion to the transaminases). [1]

Q: What is the evidence base for the physical signs of cirrhosis you have found? [1]

The Udell systematic review in JAMA 2012 (the Rational Clinical Examination series) evaluated the diagnostic accuracy of physical examination for cirrhosis. Spider naevi and palmar erythema each had a specificity of approximately 95 per cent for cirrhosis when found in the appropriate clinical context [5]. The combination of multiple physical signs (spider naevi, palmar erythema, ascites, hepatomegaly, splenomegaly, caput medusae) increases the post-test probability of cirrhosis substantially, whereas the absence of these signs reduces the probability. The evidence for the accuracy of liver palpation specifically is summarised in the Naylor systematic review, which found significant interobserver variability and that the percussion span is the more reliable bedside measure than palpable centimetres alone [3].

Q: How would you investigate the ascites? [1]

I would perform a diagnostic ascitic tap (paracentesis) and send the fluid for: cell count and differential (a neutrophil count of 250 cells per cubic millimetre or above indicates spontaneous bacterial peritonitis), albumin (to calculate the serum-ascites albumin gradient — a gradient over 11 g/L indicates portal hypertension and is consistent with her cirrhosis), culture (in blood culture bottles), protein, and cytology (if malignancy is suspected). I would also check the patient's renal function, electrolytes, and coagulation before the tap. The management of her ascites would include sodium restriction, diuretics (spironolactone with or without furosemide at a ratio of 100:40), and if the ascites is refractory, large-volume paracentesis with albumin replacement, TIPSS, or liver transplantation assessment. [1]

Second short-case scenario — massive splenomegaly

Examiner: "Please examine this patient's abdomen. He is 48." [1]

End of bed. The patient appears well, not cachectic or icteric. No obvious end-of-bed signs. [1]

Hands and face. Unremarkable. No clubbing, no palmar erythema, no stigmata of chronic liver disease. [1]

Neck. No Virchow node. [1]

Inspection. The abdomen is not distended but there is a visible fullness in the left upper quadrant. [1]

Auscultation. Bowel sounds normal. [1]

Palpation. A large mass in the left upper quadrant, extending from the left costal margin to the level of the umbilicus and crossing the midline toward the right iliac fossa. It has a smooth surface, a firm consistency, and a palpable notch on the medial border. You cannot get above it. It is dull to percussion. This is massive splenomegaly. [1]

Presentation and discussion: [1]

"My findings are of massive splenomegaly — the spleen is palpable to the umbilicus and crosses the midline, with a smooth surface and a notch. I cannot get above it, confirming it is the spleen. The most likely cause of splenomegaly of this magnitude is a myeloproliferative neoplasm — chronic myeloid leukaemia or myelofibrosis. I would also consider chronic malaria, visceral leishmaniasis (kala-azar), lymphoma, and a storage disorder such as Gaucher disease. I would investigate with a full blood count and peripheral blood film, a bone marrow biopsy with cytogenetics (looking for the BCR-ABL translocation of CML or the JAK2 mutation of myelofibrosis), and an abdominal CT." [1]

The Grover systematic review found that the clinical assessment of splenomegaly has imperfect sensitivity — a non-palpable spleen does not exclude enlargement — but that when the spleen is massively enlarged and palpable with a notch, the clinical diagnosis is reliable [2]. The key is to demonstrate that you can differentiate the spleen from the kidney and from an enlarged liver, and to generate the correct differential for the degree of splenomegaly.