Ascites - Case Viva Questions & Answers

Q1. Define Ascites.

• Harrison's Principles of Internal Medicine 22E, p.2758

Q2. What are the causes of ascites? How do you classify them?

Q3. What is the pathogenesis of ascites in cirrhosis?

1. Cirrhosis → increased intrahepatic resistance → portal hypertension
2. Portal hypertension → splanchnic arterial vasodilation (mediated by nitric oxide)
3. Vasodilation → arterial underfilling (perceived hypovolemia)
4. Compensatory activation of RAAS + SNS → aldosterone excess + sympathetic activation → sodium and water retention
5. Increased portal venous inflow + increased splanchnic lymph production
6. Hypoalbuminemia → reduced plasma oncotic pressure → fluid leaks into peritoneal cavity
7. Net result: fluid accumulates in the peritoneal cavity faster than it can be reabsorbed

Q4. What are the clinical features of ascites?

• Symptoms: Increase in abdominal girth, abdominal fullness/discomfort, dyspnea (if massive), fatigue, early satiety. At least 1-2 L of fluid must accumulate before the patient notices.
• Signs on examination:
  • Abdominal distension
  • Bulging flanks
  • Shifting dullness - most sensitive bedside test (moves with position)
  • Fluid wave / fluid thrill - requires large amounts of fluid; a helper must press in the midline to block fat-wave transmission
  • Everted umbilicus (umbilical hernia in massive ascites)
  • Pedal edema

Q5. How do you diagnose ascites? What is the first investigation you would do?

• Clinical examination (shifting dullness, fluid wave)
• Ultrasound abdomen - can detect as little as 100 mL; most sensitive imaging
• Diagnostic paracentesis is mandatory when ascites is first detected - to characterize the fluid and rule out SBP

• SAAG calculation (serum albumin - ascitic albumin)
• Cell count with differential
• Total protein
• Glucose
• LDH
• Gram stain + culture (inoculate blood culture bottles at bedside)
• Cytology (if malignancy suspected - send ≥50 mL)
• Amylase (if pancreatic ascites suspected)

Q6. What is the SAAG? How is it calculated and interpreted?

• SAAG reflects the pressure in hepatic sinusoids and correlates with the hepatic venous pressure gradient (HVPG)
• SAAG does not change with diuresis (unlike older transudate/exudate classification)
• SAAG is superior to the exudate-transudate concept

Q7. What is the gross appearance of ascitic fluid and its significance?

Q8. What does the cell count of ascitic fluid tell you?

• Neutrophil (PMN) count ≥ 250 cells/mm³ → Spontaneous Bacterial Peritonitis (SBP) - treat empirically
• Lymphocytosis in ascitic fluid → Tuberculosis peritonitis or malignancy
• WBC >500, PMN >250 with multiple organisms on culture → Secondary bacterial peritonitis (perforated viscus)

Q9. How do you differentiate SBP from secondary bacterial peritonitis?

Q10. What is the management of ascites?

• Dietary sodium restriction: 2 g/day (avoid canned/processed foods)
• Diuretics:
  • Spironolactone 100 mg/day (first-line - blocks aldosterone)
  • Add Furosemide 40 mg/day (especially if peripheral edema)
  • Ratio maintained at 100:40 (spironolactone:furosemide) to maintain normokalemia
  • Max doses: Spironolactone 400 mg/day, Furosemide 160 mg/day

• Target weight loss: 0.5 kg/day (without edema); 1 kg/day (with edema)

• Large-Volume Paracentesis (LVP): For ≥5 L removal, give IV 25% albumin 6-8 g per liter removed to prevent circulatory dysfunction / post-paracentesis circulatory dysfunction (PPCD)
• TIPS (Transjugular Intrahepatic Portosystemic Shunt): Effective but does not improve survival; increases risk of hepatic encephalopathy
• Liver transplantation: Definitive treatment; should be considered since <50% of patients with cirrhotic ascites survive 2 years

Q11. What is the prognosis of cirrhotic ascites?

Q12. What drugs should be avoided in cirrhotic ascites?

• NSAIDs - cause renal vasoconstriction, precipitate AKI/hepatorenal syndrome
• Aminoglycosides - nephrotoxic
• ACE inhibitors / ARBs - use with great caution; can cause hypotension and worsen renal function
• Beta-blockers - need reassessment; in patients with SBP or refractory ascites, beta-blockers may worsen survival and circulatory dysfunction (viva hot topic!)

Q13. What is Spontaneous Bacterial Peritonitis (SBP)?

• Spontaneous infection of ascitic fluid without an identifiable intraabdominal source
• Occurs in up to 30% of hospitalized cirrhotic patients with ascites
• In-hospital mortality: ~25%
• Mechanism: bacterial translocation - gut flora traverse intestinal wall → mesenteric lymph nodes → bacteremia → seeding of ascites
• Most common organisms: E. coli, Klebsiella, Streptococcus pneumoniae (gram-negatives predominate)
• Treatment: Cefotaxime IV (3rd-generation cephalosporin); albumin infusion (1.5 g/kg at diagnosis, 1 g/kg on day 3) reduces risk of hepatorenal syndrome and mortality
• Prophylaxis: Norfloxacin or Trimethoprim-sulfamethoxazole for secondary prevention

Q14. What is hepatic hydrothorax?

Summary Table - Ascitic Fluid Interpretation

EXPANDED: Inspection and Palpation in Ascites

INSPECTION

1. General Look (from foot of bed)

• Increased abdominal girth - the most obvious finding
• Protuberant / distended abdomen - look from the side; ascites produces a "full, rounded" contour
• Flanks: Look for bulging flanks - fluid settles by gravity into the flanks when supine; this gives the abdomen a "frog-belly" appearance
• Peripheral edema - pitting edema of ankles and legs is commonly associated

2. Umbilicus

• Everted (protruding) umbilicus - hallmark of significant ascites; umbilical hernia can develop from raised intraabdominal pressure
• Compare with a gaseous distension where the umbilicus remains central but does NOT evert

3. Abdominal Wall Veins

• Caput medusae - dilated, tortuous periumbilical veins radiating from the umbilicus outward like spokes; pathognomonic of portal hypertension
• Caput medusae vs. IVC obstruction: In portal hypertension, blood flows away from umbilicus in all directions. In IVC obstruction, veins on the lower abdomen carry blood upward (cephalad flow below umbilicus)
• Also look for distended veins on the flanks

4. Skin Signs of Chronic Liver Disease (look for the underlying cause)

• Jaundice - best seen in sclerae (scleral icterus), sublingual mucosa, hard palate; detectable when bilirubin >2.5-3.0 mg/dL
• Spider telangiectasias - above the nipple line; >5 is significant in liver disease
• Palmar erythema
• Leukonychia (white nails), Terry's nails
• Excoriations from pruritus
• Gynecomastia, testicular atrophy (in men; due to hyperestrogenism)

5. Respiratory Effect

• In massive ascites, the diaphragm is pushed up, causing visible increased respiratory rate, reduced chest expansion, or paradoxical breathing

6. Grading of ascites (clinically)

PALPATION

1. General Tenderness

• Uncomplicated cirrhotic ascites - abdomen is non-tender
• Tenderness on palpation - raises concern for SBP, secondary peritonitis, or another acute process
• Guarding / rigidity - suggests peritonitis (more likely secondary than SBP)

2. Fluid Wave (Fluid Thrill)

• Patient lies supine
• An assistant (or the patient) places the ulnar border of one hand firmly in the midline of the abdomen (to dampen a fat-transmitted wave)
• The examiner places one hand flat on one flank
• The other hand gives a sharp tap / flick on the opposite flank
• Positive test: A transmitted impulse (thrill/wave) is felt on the receiving hand

• Indicates large volume ascites (usually >2-3 L)
• Likelihood ratio LR+ = 5.3 - the best single sign for ascites
• LR- = 0.57 - a negative fluid wave does NOT reliably rule out ascites
• The midline hand is essential - without it, a wave in a fat abdomen is indistinguishable from ascites

3. Shifting Dullness

• LR+ = 2.1, LR- = 0.4
• Technique: Percuss from umbilicus toward flanks; mark the dullness-to-resonance border. Turn the patient 45° to the side - wait 30-60 seconds for fluid to shift. Re-percuss - if the dull area moves toward the dependent flank (i.e., dullness shifts), the test is positive
• Detects fluid as small as 1.5 L
• More sensitive than fluid wave but less specific

4. Puddle Sign (for minimal ascites)

• Patient lies prone for 5 minutes, then rises to elbows and knees
• Fluid pools in the most dependent region (umbilicus)
• Percuss from flanks toward umbilicus - a dull area appears centrally
• Can detect as little as 120 mL of fluid
• Rarely used clinically; mainly of academic/exam importance

5. Liver Palpation

• In early cirrhosis: liver may be enlarged and firm
• In advanced cirrhosis: liver may be small and shrunken (not palpable)
• Tender, enlarged liver → hepatic congestion (cardiac failure), hepatitis, biliary obstruction
• Non-tender, enlarged liver → malignant infiltration

6. Spleen Palpation

• Splenomegaly in the presence of ascites strongly suggests portal hypertension
• Always palpate from the right iliac fossa moving toward the left hypochondrium
• Percussion (Traube's space dullness) - dullness in the left 9th-11th intercostal space suggests splenomegaly

7. Dipping (Ballottement) in Ascites

• When massive ascites is present, organs like the liver, spleen, or a tumor may not be palpable normally
• Ballottement technique: Apply a quick dipping pressure with the fingertips - the organ sinks through fluid then bounces back ("dipping sign")
• Useful to feel a mass or organ in a tense, fluid-filled abdomen

8. Hernias

• Check for umbilical hernia (very common with tense ascites)
• Check for inguinal hernia and other hernias - all worsen with raised intraabdominal pressure

Key Viva Point: Inspection vs. Palpation Signs Summary

Q. What is the minimum fluid to detect ascites by each method?