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Ascites - Practical Viva Questions & Answers
(Based on Goldman-Cecil Medicine, Harrison's Principles of Internal Medicine, Sleisenger & Fordtran's GI and Liver Disease, and Frameworks for Internal Medicine)
1. What is ascites?
Ascites is the pathological accumulation of free fluid (>25 mL) in the peritoneal cavity. It is the most common complication of cirrhosis and a marker of decompensated liver disease.
2. What are the causes of ascites?
| Category | Examples |
|---|---|
| Most common (80%) | Cirrhosis |
| Cardiac | Congestive cardiac failure, constrictive pericarditis |
| Malignant (10%) | Peritoneal carcinomatosis (colon, gastric, pancreatic, ovarian, breast) |
| Infectious | Peritoneal tuberculosis, chlamydia |
| Others | Nephrotic syndrome, pancreatitis, hypothyroidism, hypoalbuminemia, Budd-Chiari syndrome |
Cirrhosis accounts for ~84% of ascites cases; cardiac, malignant and "mixed" ascites make up most of the remaining 10-15%. - Harrison's Principles of Internal Medicine 22E
3. What is the pathophysiology of ascites in cirrhosis?
Key mechanism: Sinusoidal portal hypertension
- Portal hypertension increases hydrostatic pressure in hepatic sinusoids
- Splanchnic vasodilation (due to nitric oxide) causes effective arterial hypovolemia
- Activation of RAAS, ADH, and sympathetic nervous system leads to sodium and water retention
- Fluid leaks from the hepatic sinusoids and splanchnic capillaries into the peritoneal cavity
- Hypoalbuminemia (reduced oncotic pressure) worsens fluid accumulation
4. How do you clinically detect ascites on examination?
Inspection:
- Abdominal distension with fullness of flanks ("frog belly")
- Everted umbilicus
- Prominent dilated abdominal veins (caput medusae if portal hypertension)
- Scrotal/pedal edema
Percussion:
- Flank dullness - fluid settles in flanks due to gravity (bowel floats up, dullness is in flanks)
- Shifting dullness - most reliable clinical sign; dullness shifts to dependent side when patient is turned; confirms free fluid
- Puddle sign - for very small amounts (<120 mL), patient on hands and knees, dullness at umbilicus
Palpation:
- Fluid thrill (fluid wave) - examiner places one hand on one flank; assistant places edge of hand in midline to block fat wave; flicking the other flank transmits an impulse - detects large amounts of fluid
The most reliable clinical sign is shifting dullness on percussion. - Harrison's Principles of Internal Medicine 22E
5. What is the minimum amount of fluid needed to detect ascites clinically vs. on imaging?
| Method | Minimum detectable |
|---|---|
| Clinical examination (shifting dullness) | ~500 mL |
| Ultrasound | 100 mL |
| CT scan | ~10 mL |
6. What is diagnostic paracentesis? When should it be done?
Paracentesis is a bedside procedure where a needle or catheter is inserted transcutaneously to extract ascitic fluid. It should be performed in:
- Every patient with new-onset ascites
- Cirrhotic patients admitted to hospital (to exclude spontaneous bacterial peritonitis - SBP)
- Any patient with ascites who clinically deteriorates
Site: Left lower quadrant preferred (greater depth of ascites, thinner abdominal wall). It is safe even in patients with coagulopathy. - Goldman-Cecil Medicine
7. What tests are done on ascitic fluid?
Routine (sent in every case):
- Albumin (+ simultaneous serum albumin for SAAG)
- Total protein
- Cell count and differential (PMN count)
- Gram stain and culture (inoculate blood culture bottles at bedside)
- Cytology (if malignancy suspected)
Selective:
- Glucose and LDH (if secondary bacterial peritonitis suspected)
- AFB smear and culture (if TB peritonitis suspected)
- Amylase (if pancreatic ascites suspected)
- Triglycerides (if chylous ascites suspected)
- Bilirubin (if biliary tract perforation suspected)
8. What is SAAG? How is it calculated and interpreted?
SAAG = Serum Albumin - Ascitic Fluid Albumin (specimens on same day)
| SAAG | Interpretation | Causes |
|---|---|---|
| ≥1.1 g/dL (High) | Portal hypertension-related | Cirrhosis, cardiac failure, Budd-Chiari, portal vein thrombosis |
| <1.1 g/dL (Low) | Non-portal hypertension | Peritoneal carcinomatosis, TB peritonitis, nephrotic syndrome, pancreatitis |
SAAG is ~97% accurate in diagnosing portal hypertension.
The SAAG correlates with sinusoidal pressure. Cirrhosis: high SAAG + low protein. Cardiac ascites: high SAAG + high protein. Malignant: low SAAG + high protein. - Goldman-Cecil Medicine
Combined SAAG + Ascitic Protein Table:
| Condition | SAAG | Ascitic Protein |
|---|---|---|
| Cirrhosis | >1.1 g/dL | <2.5 g/dL |
| Cardiac ascites | >1.1 g/dL | >2.5 g/dL |
| Malignant ascites | <1.1 g/dL | >2.5 g/dL |
| TB peritonitis | <1.1 g/dL | >2.5 g/dL |
| Nephrotic syndrome | <1.1 g/dL | <2.5 g/dL |
9. What is the gross appearance of ascitic fluid and its significance?
| Appearance | Significance |
|---|---|
| Clear, pale straw-yellow | Uncomplicated (normal) |
| Turbid / cloudy | Infection (SBP), tumor cells |
| Frankly bloody (hemorrhagic) | Trauma, hepatocellular carcinoma, coagulopathy |
| Milky white | Chylous ascites (triglycerides >200 mg/dL, often >1000); lymphatic obstruction |
| Dark brown | High bilirubin; biliary tract perforation |
| Black | Pancreatic necrosis, metastatic melanoma |
10. What is Spontaneous Bacterial Peritonitis (SBP)?
SBP is infection of ascitic fluid without an identifiable surgical source. It is defined by:
- Ascitic fluid PMN count ≥250 cells/µL (with or without positive culture)
- Most common organisms: E. coli, Klebsiella, Streptococcus pneumoniae
- Symptoms: fever, abdominal pain, altered mental status, or may be asymptomatic
- Treatment: Third-generation cephalosporins (e.g., cefotaxime); albumin infusion (1.5 g/kg on day 1, 1 g/kg on day 3) to prevent hepatorenal syndrome
SBP vs Secondary Bacterial Peritonitis:
- Secondary peritonitis (bowel perforation): ascitic glucose <50 mg/dL, LDH > serum LDH, protein >1 g/dL, polymicrobial culture
11. What are the grades of ascites?
| Grade | Description |
|---|---|
| Grade 1 | Mild, detectable only on ultrasound |
| Grade 2 | Moderate, visible distension with flank dullness |
| Grade 3 | Tense/large, marked distension with fluid thrill |
12. What is the treatment of ascites?
Step 1: Salt restriction
- Sodium intake restricted to 2 g/day (88 mEq/day). More restrictive diet is not recommended as it may compromise nutritional status.
Step 2: Diuretics
- Spironolactone (first-line): start 100 mg/day, titrate every 3-4 days to max 400 mg/day
- Furosemide: start 40 mg/day, titrate to max 160 mg/day
- Typical ratio used together: 100:40 (spironolactone:furosemide)
- Goal: Weight loss of 1 kg in first week, then 2 kg/week; no more than 0.5 kg/day (without edema) or 1 kg/day (with edema)
Step 3: Large-volume paracentesis (LVP)
- For tense/refractory ascites (10-20% of patients)
- Remove all fluid at once; give albumin 6-8 g IV per liter removed (especially when >5L drained) to prevent post-paracentesis circulatory dysfunction
Step 4: TIPS (Transjugular Intrahepatic Portosystemic Shunt)
- For refractory ascites requiring >2 LVPs/month
- More effective than LVP but higher risk of hepatic encephalopathy
Step 5: Liver transplantation - definitive therapy
Long-term albumin (40 g twice weekly for 2 weeks, then 40 g weekly) added to diuretics can reduce recurrent ascites and improve 18-month survival. - Goldman-Cecil Medicine
13. What is refractory ascites?
Ascites that fails to respond to maximum diuretic doses (spironolactone 400 mg + furosemide 160 mg/day) or that recurs rapidly after LVP. Seen in 10-20% of patients. Has poor prognosis.
14. What are the complications of ascites?
- SBP (spontaneous bacterial peritonitis)
- Hepatorenal syndrome (functional renal failure)
- Hepatic hydrothorax (ascitic fluid traverses diaphragm to pleural cavity, usually right-sided)
- Umbilical hernia with risk of rupture
- Hyponatremia (dilutional)
- Abdominal compartment syndrome (tense ascites)
- Malnutrition (early satiety, impaired oral intake)
15. What signs of chronic liver disease do you look for when examining a patient with ascites?
- Spider naevi (>5 is significant)
- Palmar erythema
- Jaundice
- Caput medusae (dilated periumbilical veins)
- Gynecomastia
- Leukonychia (white nails)
- Asterixis (liver flap - hepatic encephalopathy)
- Parotid enlargement (alcohol)
- Dupuytren's contracture (alcohol)
- Testicular atrophy
16. How do you differentiate ascites from other causes of abdominal distension?
"5 F's" of abdominal distension: Fat, Fluid, Flatus, Feces, Fetus
Ascites specifically: flanks dull on percussion + shifting dullness + fluid thrill (large ascites) + everted umbilicus. Distended abdomen from fat/gas/feces - percussion is tympanic throughout.
Summary Quick Reference Card
| Topic | Key Fact |
|---|---|
| Most common cause | Cirrhosis (84%) |
| Best bedside sign | Shifting dullness |
| Best initial investigation | Abdominal ultrasound |
| SAAG formula | Serum albumin - Ascitic albumin |
| SAAG ≥1.1 = | Portal hypertension |
| SAAG <1.1 = | Non-portal hypertension |
| SBP diagnosis | Ascitic PMN ≥250/µL |
| First-line diuretic | Spironolactone 100 mg/day |
| Albumin with LVP | 6-8 g/L of fluid removed |
| Refractory ascites next step | TIPS or liver transplant |
Sources: Goldman-Cecil Medicine (p.1619-1621), Harrison's Principles of Internal Medicine 22E (Ch. 53), Sleisenger & Fordtran's GI and Liver Disease, Frameworks for Internal Medicine (p.165)
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