Abdominal Swelling and Ascites¶
Chapter 53 | Part 2: Cardinal Manifestations and Presentation of Diseases
KEY CLINICAL POINTS¶
- Abdominal swelling can result from increased intestinal gas (flatus), fat accumulation, fluid (ascites), pregnancy (fetus), fecal retention, or abdominal masses (fatal growth).
- Ascites is classified by serum-ascites albumin gradient (SAAG) ≥ 1.1 g/dL (portal hypertension) vs. <1.1 g/dL (nonportal causes).
- Diagnosis of ascites requires paracentesis with SAAG calculation, ascitic fluid analysis, and differential for spontaneous bacterial peritonitis (SBP).
- Management of cirrhotic ascites includes sodium restriction, spironolactone/furosemide diuretics, and TIPS for refractory cases.
- SBP is a life-threatening complication of cirrhotic ascites, treated with third-generation cephalosporins.
1. DEFINITION & OVERVIEW¶
Abdominal swelling encompasses distension from gas, fluid (ascites), or solid masses. Ascites is fluid accumulation in the peritoneal cavity. Causes include the six Fs: flatus, fat, fluid, fetus, feces, and fatal growth (masses).
Table 52-3: Causes of Extrahepatic Cholestasis¶
| Malignant Causes | Benign Causes |
|---|---|
| Pancreatic cancer | Choledocholithiasis |
| Gallbladder cancer | IgG4-associated cholangitis |
| Ampullary carcinoma | Primary biliary cirrhosis |
| Cholangiocarcinoma | Biliary atresia |
1.1 Subtopic¶
Abdominal swelling may be due to increased intestinal gas (flatus), fat accumulation, ascites, pregnancy, fecal retention, or abdominal masses. Ascites is fluid accumulation in the peritoneal cavity, often associated with portal hypertension or other systemic conditions.
2. EPIDEMIOLOGY¶
Infections are leading causes of jaundice in developing countries, while extrahepatic biliary obstruction and drugs are common in developed countries. Cirrhosis accounts for 84% of ascites cases. Ascites prevalence increases with age and in patients with chronic liver disease.
2.1 Risk Factors¶
Excessive alcohol use, viral hepatitis, malnutrition, nephrotic syndrome, and chronic infections (e.g., tuberculosis) increase risk. Obesity and metabolic syndrome contribute to abdominal fat accumulation.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Ascites in cirrhosis results from portal hypertension and renal sodium retention. Non-cirrhotic ascites may arise from peritoneal carcinomatosis, infections, or hypoalbuminemia. Pathogenesis involves increased hepatic resistance, splanchnic vasodilation, and impaired oncotic pressure.
SAAG Classification of Ascites¶
| SAAG ‡1.1 g/dL | SAAG <1.1 g/dL |
|---|---|
| Portal hypertension (cirrhosis, Budd-Chiari syndrome) | Nonportal causes (hepatitis, nephrotic syndrome, TB) |
| Ascitic protein ‡2.5 g/dL | Ascitic protein <2.5 g/dL |
3.1 Portal Hypertension Mechanisms¶
Hepatic fibrosis disrupts sinusoidal flow, while hepatic stellate cell activation and reduced eNOS production cause vasoconstriction. Splanchnic vasodilation leads to effective hypovolemia, triggering antidiuretic hormone release and sodium retention.
4. CLINICAL FEATURES¶
Symptoms include bloating, abdominal fullness, and discomfort. Signs of ascites include distension, umbilical hernia, and dull percussion. Complications include spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, and renal dysfunction.
4.1 Ascites Presentation¶
Marked abdominal distension, shifting dullness, and fluid wave. In severe cases, respiratory compromise from diaphragmatic pressure. Ascitic fluid may be turbid (infection), milky (chylous), or dark (biliary leak).
5. DIFFERENTIAL DIAGNOSIS¶
Differential includes intestinal obstruction, bowel tumors, ovarian masses, and peritoneal infections. Consider TB, carcinomatosis, and pancreatic ascites. Ascitic fluid analysis helps distinguish causes.
5.1 Key Differentiators¶
SBP (PMN ≥ 250/ µ L), chylous ascites (triglycerides >200 mg/dL), and tuberculous peritonitis (lymphocytic ascites).
6. INVESTIGATIONS & DIAGNOSIS¶
Paracentesis with SAAG calculation, ascitic fluid analysis, and imaging (CT/MRI). Laboratory tests include serum albumin, BUN/creatinine, and amylase. Ultrasound detects ascites ≥ 100 mL.
Ascitic Fluid Analysis¶
| Parameter | Normal Findings | Abnormal Findings |
|---|---|---|
| Albumin | ‡25 g/L | Low in nonportal ascites |
| Parameter | Normal Findings | Abnormal Findings |
|---|---|---|
| PMN | £250/mL | ‡250/mL (SBP) |
| Amylase | £1000 U/L | >1000 U/L (pancreatic ascites) |
| Lactate | Normal | Elevated in secondary peritonitis |
6.1 Diagnostic Algorithm¶
- Confirm ascites via ultrasound. 2. Perform paracentesis for fluid analysis. 3. Calculate SAAG and ascitic protein. 4. Test for infection (Gram stain, culture), TB (AFB smear/culture), and malignancy (cytology).
7. MANAGEMENT & TREATMENT¶
Cirrhotic ascites: sodium restriction (2 g/d), spironolactone/furosemide diuretics. Refractory cases require TIPS or albumin infusions. SBP treated with cefotaxime. Malignant ascites managed with paracentesis, chemotherapy, or shunts.
7.1 Diuretic Therapy¶
Spironolactone (100 mg) + furosemide (40 mg) in 40:100 ratio. Monitor for hypokalemia and hypernatremia. Albumin infusions (6–8 g/L) reduce post-paracentesis circulatory dysfunction.
8. PROGNOSIS & COMPLICATIONS¶
SBP mortality is 20–40% without treatment. Complications include hepatic encephalopathy, spontaneous bacterial peritonitis, and renal failure. Ascites recurrence is common in cirrhosis.
8.1 SBP Management¶
Early paracentesis (within 12 hours) reduces mortality. Antibiotics (cefotaxime 2 g q12h) for 5 days. Repeat paracentesis to confirm PMN reduction ≥ 25%.
9. SPECIAL CONSIDERATIONS¶
Pregnancy: abdominal distension from uterine growth. Elderly: increased risk of SBP and renal dysfunction. Celiac disease: bloating from malabsorption. Tuberculosis: lymphocytic ascites with TB history.
9.1 Pediatric Considerations¶
Ascites in children may result from nephrotic syndrome, congenital infections, or tumors. Monitor for growth failure and malnutrition.
10. KEY POINTS & CLINICAL PEARLS¶
- Use SAAG to differentiate portal vs. nonportal ascites.
- Paracentesis is essential for diagnosis and management.
- SBP is a medical emergency requiring prompt antibiotics.
- Diuretics must be used cautiously in cirrhosis to avoid renal failure.