Ascites Examination OSCE — Shifting Dullness, Fluid Thrill, SAAG, and Causes

Why This Station Is Tested

Ascites is a common finding in abdominal OSCE examinations, most frequently in the context of chronic liver disease, malignancy, or heart failure. Examiners test your ability to detect ascites with two clinical techniques (shifting dullness and fluid thrill), interpret findings, generate a differential, and discuss management including diagnostic paracentesis.

Before You Begin

Introduce yourself, confirm patient identity, obtain consent, and position the patient supine with one pillow. Expose the abdomen from nipples to groin. Ask about pain before touching. The examination follows the standard look-feel-move framework.

Inspection

Stand at the end of the bed and observe systematically:

• Abdominal distension: ascites typically produces a central or diffuse distension that is full in the flanks (compared to gaseous distension, which is more central/tympanitic)
• Everted umbilicus: suggests raised intra-abdominal pressure from significant ascites
• Caput medusae: dilated periumbilical veins indicating portal hypertension — blood flows away from the umbilicus
• Distended flank veins: if inferior vena cava obstruction — blood flows upward
• Jaundice, spider naevi, palmar erythema, leukonychia, clubbing, Dupuytren's contracture: stigmata of chronic liver disease
• Scratch marks: pruritus from jaundice (cholestasis)
• Gynecomastia: in liver disease (reduced oestrogen metabolism)
• Peripheral oedema: suggests hypoalbuminaemia or heart failure

Palpation

Palpate gently in all nine quadrants — feel for hepatomegaly, splenomegaly (both enlarged in portal hypertension), and any masses. In massive ascites, solid organs may be difficult to palpate (dipping technique: rapid firm pressure to displace fluid and feel the organ beneath).

Percussion — Detecting Ascites

Shifting Dullness (Routine Test for Ascites)

1. 1Percuss from the umbilicus laterally — ascitic fluid is dull in the flanks (fluid pools by gravity), tympanitic centrally (gas-filled bowel floats)
2. 2Note where dullness begins on the right side — keep your finger at this point
3. 3Ask the patient to roll towards you (left lateral decubitus) — wait 15–30 seconds for fluid to redistribute
4. 4Percuss again at the same point — if ascites is present, the dullness shifts to resonance (fluid has moved away from that point following gravity)
5. 5Repeat on the left side to confirm

Shifting dullness detects approximately 1500 mL of ascitic fluid. Sensitivity ~83%, specificity ~56%.

Fluid Thrill (Large Ascites Only)

1. 1Place the patient's own hand (or an assistant's hand) in the midline of the abdomen to dampen any transmitted vibrations through fat
2. 2Place your left hand flat on one flank
3. 3Flick or tap the opposite flank with your right hand
4. 4A positive fluid thrill = palpable impulse transmitted across the abdomen through the fluid to your receiving hand

Fluid thrill only positive with large volumes (typically >3.5 L). Sensitivity ~60%, specificity ~90%.

Causes of Ascites — Differential

SAAG — Serum Ascites Albumin Gradient

SAAG = Serum albumin − Ascitic fluid albumin

SAAG has replaced the exudate/transudate classification for ascitic fluid. Exudate vs transudate (Light's criteria) applies to pleural fluid, not ascites.

Diagnostic Paracentesis — Indications and Technique

Indications for diagnostic paracentesis: new-onset ascites (diagnosis), suspected spontaneous bacterial peritonitis (SBP — fever, abdominal pain, or deteriorating hepatic encephalopathy in a cirrhotic), clinical deterioration.

Procedure: ultrasound-guided preferred (reduces complications); site is the left iliac fossa (avoids liver, gallbladder, inferior epigastric vessels); using aseptic technique, a 22-gauge needle or paracentesis kit aspirates 10–20 mL fluid for analysis.

Ascitic fluid analysis:

• White cell count: >250 polymorphonuclear (PMN) cells/mm³ = SBP (treat immediately with cefotaxime)
• Culture and sensitivity: inoculate blood culture bottles at the bedside (increases yield)
• Albumin: for SAAG calculation
• Total protein: <25 g/L suggests cirrhotic transudate
• Cytology: to look for malignant cells
• Glucose, LDH, amylase if appropriate

Completing the Examination

Offer to: check for hepatic flap (asterixis — indicates hepatic encephalopathy), assess for pleural effusion (dullness at lung bases), check for peripheral oedema, assess JVP (raised in cardiac ascites/cardiac failure), perform PR examination if indicated. State you would organise abdominal ultrasound, liver function tests, clotting (PT/INR), albumin, and renal function.

Frequently Asked Questions

"How do I perform and interpret shifting dullness correctly in the OSCE?"

Shifting dullness is the most reliable bedside test for ascites. Begin by percussing from the umbilicus towards the right flank — in ascites, you will find a transition from tympanic (gas-filled bowel floating centrally) to dull (fluid in the flank). Mark this point with your finger. Ask the patient to roll 45° towards you and wait 30 seconds for the fluid to redistribute with gravity. Now re-percuss at the same point — if ascites is present, the area that was dull is now resonant because fluid has shifted away. Repeat on the left side. A common mistake is not waiting long enough for the fluid to redistribute, or percussing from flank to centre rather than centre to flank. Always confirm both resonance centrally and dullness in the flank first, otherwise you cannot interpret the shift. Sensitivity is approximately 83% and specificity 56% — not perfect, but the standard clinical test. In the OSCE, narrate each step and state what you are looking for.

"What is SAAG and how does it help differentiate causes of ascites?"

SAAG (Serum Ascites Albumin Gradient) is calculated by subtracting the ascitic fluid albumin from the serum albumin, both measured at the same time: SAAG = serum albumin − ascitic fluid albumin. A SAAG ≥1.1 g/dL indicates that portal hypertension is the cause of ascites — the oncotic pressure differential between serum and ascitic fluid is high, meaning the ascites formed by a hydrostatic mechanism (elevated portal pressure driving fluid into the peritoneum). Causes include cirrhosis, alcoholic hepatitis, cardiac ascites, Budd-Chiari syndrome, and portal vein thrombosis. A SAAG <1.1 g/dL indicates that portal hypertension is NOT the cause — the most common causes are peritoneal malignancy, TB peritonitis, pancreatitis, and nephrotic syndrome. SAAG has replaced the exudate/transudate classification (Light's criteria) for ascitic fluid because it is more accurate. In the OSCE, mentioning that you would calculate the SAAG using paired serum and ascitic albumin measurements demonstrates higher-level clinical knowledge.

"What are the clinical signs of portal hypertension on inspection and how do they arise?"

Portal hypertension occurs when portal venous pressure exceeds 12 mmHg, typically from cirrhosis causing intrahepatic resistance, and causes several visible signs. Caput medusae — dilated tortuous veins radiating from the umbilicus across the abdominal wall — arise because porto-systemic collateral vessels (particularly the paraumbilical veins connecting the portal system to the systemic anterior abdominal wall veins) dilate to decompress the portal system. Blood flow in caput medusae is away from the umbilicus (unlike inferior vena caval obstruction where flow is from groin to axilla). Splenomegaly occurs as the spleen enlarges due to venous congestion. Ascites develops through a combination of portal hypertension (increased hydrostatic pressure), hypoalbuminaemia (decreased oncotic pressure), and activation of the renin-angiotensin-aldosterone system causing renal sodium retention. Oesophageal varices (not visible externally but important) develop as upper porto-systemic collaterals. Rectal varices may cause lower GI bleeding.

"What is spontaneous bacterial peritonitis and how is it diagnosed and treated?"

Spontaneous bacterial peritonitis (SBP) is an infection of ascitic fluid in the absence of a clear surgically treatable source of infection. It occurs almost exclusively in patients with cirrhotic ascites and carries a 20–40% in-hospital mortality. The mechanism involves bacterial translocation from the gut lumen across the intestinal wall into the ascitic fluid, facilitated by impaired immune function in cirrhosis. Clinical presentation: fever, abdominal pain or tenderness, deteriorating hepatic encephalopathy, or acute kidney injury — but up to 30% are asymptomatic, which is why diagnostic paracentesis is indicated in any hospitalised cirrhotic with ascites. Diagnosis: PMN count >250 cells/mm³ in ascitic fluid. Cultures are positive in only 40–50% of cases. Treatment: IV cefotaxime 2g every 8 hours for 5 days (ciprofloxacin orally if mild and tolerating oral), plus IV albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 — albumin reduces the risk of hepatorenal syndrome and improves survival. Secondary prophylaxis with norfloxacin or co-trimoxazole after the first SBP episode reduces recurrence.

"What are the indications and contraindications for therapeutic paracentesis in ascites?"

Therapeutic large-volume paracentesis (LVP) is indicated for tense or refractory ascites causing respiratory compromise, discomfort, or early satiety when diuretics alone are insufficient. The standard technique removes up to the total volume of ascites in a single session (typically 5–10 litres) under ultrasound guidance. Critically, albumin infusion must be co-administered: 8 g of human albumin solution (HAS) per litre of ascites removed beyond 5 litres — this prevents post-paracentesis circulatory dysfunction (PPCD), a state of circulatory failure and renal impairment caused by rapid intravascular volume depletion. Contraindications include: coagulopathy (INR >2.5 — relative; use fresh frozen plasma or vitamin K if needed urgently), platelet count <50 × 10⁹/L (relative), active infection at the planned puncture site, pregnancy, bowel obstruction with distended bowel (increased perforation risk), and patient refusal. The preferred site is the left iliac fossa lateral to the rectus abdominis muscle, avoiding the inferior epigastric vessels, liver, spleen, and the right iliac fossa (risk of hitting the caecum or appendix).

"How does hepatic encephalopathy present and how would you assess it at the bedside?"

Hepatic encephalopathy (HE) is a spectrum of neuropsychiatric dysfunction caused by accumulation of toxins (particularly ammonia) in the systemic circulation due to portosystemic shunting and hepatocellular failure. It is graded using the West Haven criteria: Grade I — subtle personality changes, mild confusion, sleep disturbance; Grade II — lethargy, disorientation, asterixis (hepatic flap); Grade III — gross disorientation, stupor, responds to stimulation; Grade IV — coma, no response to painful stimuli. Asterixis is the key bedside sign — ask the patient to extend their wrists with arms outstretched and fingers spread ("stop traffic") for 15 seconds; a positive flap is a coarse, arrhythmic tremor caused by sudden brief lapses in postural tone. Bedside cognitive assessment: orientation to time, place, person; number connection test; handwriting analysis (ask to sign their name — deteriorating handwriting is a sensitive early sign). Precipitants include: constipation, GI bleeding, infection, electrolyte disturbance (hyponatraemia, hypokalaemia from diuretics), dehydration, excessive dietary protein, renal failure, and benzodiazepines.

Related guides: Abdominal Examination OSCE · Chronic Liver Disease History OSCE · Jaundice History OSCE · Fluid Balance OSCE · Upper GI Bleeding OSCE