Abdominal Examination Routine — Viva Defence

Viva — The Abdominal Examination Short-Case Defence

The routine (examiner: "Examine this patient's abdomen")

I would introduce myself, confirm the patient's identity, explain what I am going to do, request permission, position the patient supine with one pillow and the arms at the sides, and expose the abdomen from xiphisternum to symphysis pubis. I would ensure good lighting and a chaperone if appropriate. [1]

I perform the twelve-step head-to-toe routine: [1]

End of bed. I observe the patient's general appearance — cachectic, with obvious scleral icterus. I note the body habitus, the skin colour (jaundice), the breathing pattern, and the bedside clues. [1]

Hands. I examine for clubbing (present — primary biliary cholangitis is a GI cause of clubbing), palmar erythema (present — liver palms), Dupuytren contracture (absent), nail signs (leuconychia from hypoalbuminaemia), and a liver flap (asterixis — I ask the patient to hold their hands out with wrists dorsiflexed for 30 seconds). [1]

Arms. I look for bruising (coagulopathy), needle marks, AV fistula, excoriations (pruritus from cholestasis — a hallmark of PBC, often preceding jaundice). [1]

Face. I examine the eyes (scleral icterus present, xanthelasma present — PBC causes disordered lipid metabolism, and the patient has periorbital xanthomata), the mouth (angular cheilitis from cholestasis-related fat-soluble vitamin malabsorption), and the lips. [1]

Neck. I palpate for a Virchow node (absent — no sentinel sign of malignancy) and the cervical chain. [1]

Chest. I examine for spider naevi (more than ten, in the SVC distribution above the nipple line — I confirm by blanching with a glass slide), gynaecomastia, and loss of axillary hair. I note that spider naevi are significant when above five and in the SVC territory. [1]

Inspection. The abdomen is distended with the flanks filled and the umbilicus everted — a distribution suggesting ascites. There is no visible peristalsis. I note caput medusae (dilated periumbilical veins from portal hypertension). There is no surgical scar. [1]

Auscultation BEFORE palpation. I listen in all four quadrants for a full minute each, starting in the right iliac fossa. Bowel sounds are present and normal. There is no bruit. I listen for a succession splash (absent). [1]

Palpation. I start with light palpation away from any tender area, assessing for guarding, rigidity and tenderness. Then deep palpation. On deep palpation, the liver edge is palpable 4 cm below the costal margin in the midclavicular line, firm, with an irregular surface and a hard edge — consistent with cirrhosis. The spleen is palpable 3 cm below the left costal margin, smooth, with a notch. I confirm this is the spleen: I cannot get above it, it is dull to percussion, and it has a notch. [1]

Percussion. I measure the liver span by percussion — the upper border is at the sixth intercostal space and the lower border is 4 cm below the costal margin, giving a span of approximately 14 cm (mildly enlarged). I test for shifting dullness: the midline is tympanic and the flanks are dull, and the transition point shifts when the patient rolls onto her side — positive for ascites. I test for a fluid thrill: positive, indicating tense large-volume ascites. [1]

Additional. I would complete my examination by examining the hernial orifices, performing a digital rectal examination, and examining the external genitalia. [1]

Legs. I examine for peripheral oedema (bilateral pitting oedema to the mid-shin — from hypoalbuminaemia) and signs of DVT. [1]

The presentation (examiner: "Present your findings")

My findings are: chronic liver disease with portal hypertension. The constellation of palmar erythema, spider naevi in the SVC distribution, xanthelasma, gynaecomastia, pruritus, and jaundice is consistent with chronic cholestatic liver disease. The likely aetiology, given the xanthelasma, the pruritus, and the clubbing, is primary biliary cholangitis. The patient has cirrhosis (hard, irregular liver edge), portal hypertension (splenomegaly, caput medusae), and tense ascites (shifting dullness and fluid thrill). I would confirm the diagnosis with antimitochondrial antibodies, an IgM level, liver function tests, an abdominal ultrasound with Doppler, and a FibroScan. [1]

Probing questions

Q: What is the pathophysiology of the pruritus in this patient? [1]

The pruritus of primary biliary cholangitis is cholestatic pruritus — it is caused by the deposition of bile salts (or more precisely, pruritogens such as lysophosphatidic acid and autotaxin) in the skin. It characteristically precedes the onset of visible jaundice, sometimes by months or years. The pruritus is often worse at night, affects the limbs and back, and produces linear excoriations. It is not a histamine-mediated itch, so antihistamines are often ineffective. Treatment options include cholestyramine (bile acid sequestrant), rifampicin, naltrexone (opioid antagonist), and sertraline. In refractory cases, MARS (molecular adsorbent recirculating system) dialysis or liver transplantation may be required. [1]

Q: How do you confirm that the mass in the left upper quadrant is the spleen and not the kidney? [1]

Three features confirm splenomegaly. First, I cannot get above the mass — the spleen arises from under the costal margin and its upper border is continuous with the diaphragm. A kidney arises retroperitoneally, so I can palpate above a ballotable kidney. Second, the spleen is dull to percussion — it is a solid organ behind the gas-filled stomach. A kidney is resonant to percussion because of the overlying stomach or splenic flexure. Third, the spleen has a notch on its medial border — the splenic notch — which I may feel with careful palpation. The Grover systematic review found these manoeuvres have moderate sensitivity, and a non-palpable spleen does not exclude splenomegaly, particularly in obese patients [2].

Q: What volume of ascites is required for shifting dullness, and how does this compare with the fluid thrill? [1]

Shifting dullness requires approximately 1000 mL or more of free intraperitoneal fluid. The fluid thrill requires a larger volume — typically over 2000 mL of tense ascites. The fluid thrill is less sensitive than shifting dullness but more specific for large-volume ascites [1].

Q: What would a pulsatile liver indicate? [1]

A pulsatile liver indicates tricuspid regurgitation — the regurgitant systolic wave is transmitted through the vena cava, hepatic veins, and into the liver. If I felt a pulsatile liver, I would examine the JVP for giant v-waves and listen for the pansystolic murmur of tricuspid regurgitation. In a patient with cirrhosis, this is not the typical finding — but cirrhosis itself can cause a palpable but non-pulsatile liver. [1]

Q: Name the four gastrointestinal causes of clubbing. [1]

Inflammatory bowel disease (especially Crohn disease), cirrhosis (any cause, classically primary biliary cholangitis), coeliac disease, and malabsorption syndromes. [1]