++
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.
++
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) or supraclavicular node (Virchow’s node) suggests an abdominal malignancy.
++
Very sensitive; able to distinguish fluid from cystic masses.
++
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
++
Cirrhosis counts for 84% of cases of ascites. Cardiac ascites, peritoneal carcinomatosis, and “mixed” ascites resulting from cirrhosis and a second disease account for 10–15%.
++
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. 43-1).
++
++
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
Rigid salt restriction (<2 g Na/d).
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 [HRS], encephalopathy), can increase to maximum of 120–160 mg/d until effect achieved or complication occurs.
Monitor weight, urinary Na and ...