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Harrison’s Manual of Medicine





Cirrhotic Ascites


Accumulation of fluid within the peritoneal cavity. Small amounts may be asymptomatic; increasing amounts cause abdominal distention and discomfort, anorexia, nausea, early satiety, heartburn, flank pain, and respiratory distress.
PHYSICAL EXAMINATION   Bulging flanks, fluid wave, shifting dullness, “puddle sign” (dullness over dependent abdomen with pt on hands and knees). May be associated with penile or scrotal edema, umbilical or inguinal herniation, pleural effusion. Evaluation should include rectal and pelvic examination, assessment of liver and spleen. Palmar erythema and spider angiomata seen in cirrhosis. Periumbilical nodule (Sister Mary Joseph’s nodule) suggests metastatic disease from a pelvic or GI tumor.
ULTRASONOGRAPHY/CT   Very sensitive; able to distinguish fluid from cystic masses.
Diagnostic paracentesis (50–100 mL) essential; use 22-gauge needle in linea alba 2 cm below umbilicus or with “Z-track” insertion in LLQ or RLQ. Routine evaluation includes inspection, protein, albumin, glucose, cell count and differential, culture, cytology; in selected cases check amylase, LDH, triglycerides, culture for TB. Rarely, laparoscopy or even exploratory laparotomy may be required. Ascites due to CHF (e.g., pericardial constriction) may require evaluation by right-sided heart catheterization.
DIFFERENTIAL DIAGNOSIS   More than 90% of cases due to cirrhosis, neoplasm, CHF, tuberculosis.
1.   Diseases of peritoneum: Infections (bacterial, tuberculous, fungal, parasitic), neoplasms, connective tissue disease, miscellaneous (Whipple’s disease, familial Mediterranean fever, endometriosis, starch peritonitis, etc.).
2.   Diseases not involving peritoneum: Cirrhosis, CHF, Budd-Chiari syndrome, hepatic venocclusive disease, hypoalbuminemia (nephrotic syndrome, protein-losing enteropathy, malnutrition), miscellaneous (myxedema, ovarian diseases, pancreatic disease, chylous ascites).
PATHOPHYSIOLOGIC CLASSIFICATION USING SERUM-ASCITES ALBUMIN GRADIENT   Difference in albumin concentrations between serum and ascites as a reflection of imbalances in hydrostatic pressures: Low gradient (serum-ascites albumin gradient <1.1): 2° bacterial peritonitis, neoplasm, pancreatitis, vasculitis, nephrotic syndrome. High gradient (serum-ascites albumin gradient >1.1 suggesting increased hydrostatic pressure): cirrhosis, CHF, Budd-Chiari syndrome.

Table 24-1 Representative Fluid Characteristics

PATHOGENESIS   Contributing factors: (1) portal hypertension, (2) hypoalbuminemia, (3) increased hepatic lymph formation, (4) renal sodium retention—secondary to hyperaldosteronism, increased sympathetic nervous activity (renin-angiotensin production). Initiating event may be peripheral arterial vasodilation triggered by endotoxin and cytokines and mediated by nitric oxide; results in decreased “effective” plasma volume and activation of compensatory mechanisms to retain renal Na and preserve intravascular volume. In severe ascites, plasma atrial natriuretic factor levels are high but insufficient to cause natriuresis.

Maximum mobilization ~700 mL/d (peripheral edema may be mobilized faster).

Rigid salt restriction (400 mg Na/d).

Fluid restriction of 1–1.5 L only if hyponatremia.

Diuretics if no response after 1 week or if urine Na concentration <25 meq/L; spironolactone (mild, potassium-sparing, aldosterone-antagonist) 100 mg/d PO increased by 100 mg q4–5d to maximum of 600 mg/d; furosemide 40–80 mg/d PO or IV may be added if necessary (greater risk of hepatorenal syndrome, encephalopathy), can increase by 40 mg/ d to maximum of 240 mg/d until effect achieved or complication occurs. If still no diuresis, add hydrochlorothiazide 50–100 mg PO qd.

Monitor weight, urinary Na and K, serum electrolytes, and creatinine.

Repeated large-volume paracentesis (5 L) with IV infusions of albumin (10 g/L ascites removed) is preferable for initial management of massive ascites because of fewer side effects than diuretics.

In refractory cases, consider transjugular intrahepatic portosystemic shunt (TIPS), though 20–30% risk of encephalopathy and high rate of shunt stenosis and occlusion. Peritoneovenous (LeVeen, Denver) shunt (high complication rate—occlusion, infection, DIC) and side-to-side portacaval shunt (high mortality rate in end-stage cirrhotic pt) have fallen out of favor. Consider liver transplantation in appropriate candidates (Chap. 155).

SPONTANEOUS BACTERIAL PERITONITIS   Suspect in cirrhotic pt with ascites and fever, abdominal pain, worsening ascites, ileus, hypotension, worsening jaundice, or encephalopathy; low ascitic protein concentration (low opsonic activity) is predisposing factor. Diagnosis suggested by ascitic fluid PMN cell count >250/µL and symptoms or PMN count >500/µL; confirmed by positive culture (usually Enterobacteriaceae, group D streptococci, Streptococcus pneumoniae, S. viridans). Initial treatment: Cefotaxime 2 g IV q8h; efficacy demonstrated by marked decrease in ascitic PMN count after 48 h; treat 5–10 days or until ascitic PMN count is normal. Risk of recurrence can be reduced with norfloxacin 400 mg PO qd, trimethoprim-sulfamethoxazole 1 double-strength PO bid 5 days a week, or possibly ciprofloxacin 750 mg PO once a week. Consider prophylactic therapy (before first episode of peritonitis) in pts with cirrhotic ascites and an ascitic albumin level <10 g/L (<1 g/dl).
HEPATORENAL SYNDROME   Progressive renal failure characterized by azotemia, oliguria with urinary sodium concentration <10 mmol/L, hypotension, and lack of response to volume challenge. May be spontaneous or precipitated by bleeding, excessive diuresis, paracentesis, or drugs (aminoglycosides, NSAIDs, ACE inhibitors). Thought to result from altered renal hemodynamics, elevated serum thromboxane and endothelin levels, and decreased urinary prostaglandin levels. Prognosis poor. Treatment: Trial of plasma expansion; TIPS of doubtful benefit; liver transplantation in selected cases.

For a more detailed discussion, see Glickman RM: Abdominal Swelling and Ascites, Chap. 46, p. 260, and Podolsky DK: Cirrhosis and Its Complications, Chap. 299, p. 1754, in HPIM-15.

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