Harrisons Manual of Medicine, 18th Ed.

CHAPTER 49. Ascites

DEFINITION

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.

DETECTION

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.

EVALUATION

Diagnostic paracentesis (50–100 mL) essential. Routine evaluation includes gross inspection, protein, albumin, glucose, cell count and differential, Gram’s and acid-fast stains, culture, cytology; in selected cases check amylase, LDH, triglycerides, culture for tuberculosis (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, TB.

Diseases of peritoneum: Infections (bacterial, tuberculous, fungal, parasitic), neoplasms, connective tissue disease, miscellaneous (Whipple’s disease, familial Mediterranean fever, endometriosis, starch peritonitis, etc.).

Diseases not involving peritoneum: Cirrhosis, CHF, Budd-Chiari syndrome, hepatic venoocclusive disease, hypoalbuminemia (nephrotic syndrome, protein-losing enteropathy, malnutrition), miscellaneous (myxedema, ovarian diseases, pancreatic disease, chylous ascites).

Pathophysiologic Classification Using Serum-Ascites Albumin Gradient (SAAG)

Difference in albumin concentrations between serum and ascites as a reflection of imbalances in hydrostatic pressures and can be used to differentiate between potential causes of ascites (Fig. 49-1).

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FIGURE 49-1 Algorithm for the diagnosis of ascites according to the serum-ascites albumin gradient (SAAG). IVC, inferior vena cava.

CIRRHOTIC ASCITES

Pathogenesis

Contributing factors: (1) portal hypertension, (2) hypoalbuminemia, (3) hepatic lymph, (4) renal sodium retention–secondary to hyperaldosteronism, increased sympathetic nervous system activity (renin-angiotensin production). Initiating event may be peripheral arterial vasodilation triggered by endotoxin and cytokines and mediated by nitric oxide.

TREATMENT Cirrhotic Ascites

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

1. Rigid salt restriction (<2 g Na/d).

2. For moderate ascites, diuretics usually necessary; spironolactone 100–200 mg/d PO (can be increased to 400 mg/d if low-sodium diet is confirmed and fluid not mobilized); furosemide 40–80 mg/d PO or IV may be added if necessary (greater risk of hepatorenal syndrome, encephalopathy), can increase to maximum of 120–160 mg/d until effect achieved or complication occurs.

3. Monitor weight, urinary Na and K, serum electrolytes, and creatinine. If ascites is still present with the above measures this is defined as refractory ascites. Treatment modalities include:

a. Repeated large-volume paracentesis (5 L) with IV infusions of albumin (10 g/L ascites removed).

b. Consider transjugular intrahepatic portosystemic shunt (TIPS). While TIPS manages the ascites, it has not been found to improve survival and is often associated with encephalopathy.

Prognosis for pts with cirrhotic ascites is poor with <50% survival 2 years after onset of ascites. Consider liver transplantation in appropriate candidates with the onset of ascites (Chap. 165).

COMPLICATIONS

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; confirmed by positive culture (usually Escherichia coli and other gut bacteria; however, gram-positive bacteria including Streptococcus viridans, Staphylococcus aureus, and Enterococcus spp. also can be found). Initial treatment: Cefotaxime 2 g IV q8h. Risk is increased in pts with variceal bleeding and prophylaxis against spontaneous bacterial peritonitis is recommended when a pt presents with upper GI bleeding.

Hepatorenal Syndrome (HRS)

Functional renal failure without renal pathology; occurs in 10% of pts with advanced cirrhosis or acute liver failure. Thought to result from altered renal hemodynamics. Two types: type 1 HRS–decrease in renal function within 1–2 weeks of presentation; type 2 HRS–associated with a rise in serum creatinine but is associated with a better outcome. Often seen in pts with refractory ascites. Treatment: midodrine along with octreotide and IV albumin. For either type 1 or 2 HRS, prognosis is poor in the absence of liver transplantation.

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For a more detailed discussion, see Corey KE, Friedman LS: Abdominal Swelling and Ascites, Chap. 43, p. 330; and Bacon BR: Cirrhosis and Its Complications, Chap. 308, p. 2592, in HPIM-18.