increased formation of hepatic lymph (from sinusoidal hypertension),
increased formation of splanchnic lymph,
salt and water retention by the kidneys.
Before therapy is started, paracentesis should be performed and the following examinations made on a sample of ascitic fluid:
Culture and leukocyte count: Spontaneous bacterial peritonitis is common and may be clinically silent. A white count above 250/L is highly suggestive of infection.
LDH levels: A ratio of LDH in ascites to serum that exceeds 0.6 suggests the presence of cancer or infection.
Serum amylase: A high level suggests pancreatic disease.
Albumin: The ratio of serum to ascites albumin concentrations is above 1.1 in liver disease and below 1.1 in malignant ascites.
Cytology: This is pertinent only in patients with a cancer diagnosis or a suspicion of cancer.
Medical Treatment of Ascites
In general, the intensity of medical therapy required to control ascites can be predicted from the pretreatment 24-hour urine Na+ output as follows: A Na+ output below 5 meq/24 h will require strong diuretics; 5–25 meq/24 h, mild diuretics; and above 25 meq/24 h, no diuretics. Initial treatment is usually with spironolactone, 200 mg/d. The objective is to stimulate a weight loss of 0.5–0.75 kg/d, except in patients with peripheral edema who can mobilize fluid faster. If spironolactone alone is insufficient, another drug such as furosemide should be added. A loop diuretic (eg, furosemide, ethacrynic acid) should be given only in combination with a distally acting diuretic (eg, spironolactone, triamterene). Alternatively, massive ascites may be treated by one or more large volume (eg, 5-L) paracenteses; this is often accompanied by an intravenous infusion of albumin, although the benefits of albumin are unclear. Close monitoring of serum electrolytes should be done. Salt or water restriction is recommended in refractory cases. Caution is required in patients with evidence of renal dysfunction, since aggressive fluid removal can result in renal failure.
Surgical Treatment of Ascites
A history of ascites that has been easy to control need not influence the choice of shunt operation intended to treat variceal bleeding. When ascites has been severe, however, a side-to-side shunt (eg, side-to-side portacaval, H-mesocaval, central splenorenal) may be considered, because it reduces sinusoidal as well as splanchnic venous pressure. A side-to-side portacaval shunt is rarely indicated just to treat ascites — eg, in patient in whom several LeVeen shunts have thrombosed—although the incidence of severe postoperative encephalopathy is high under these circumstances.
Refractory ascites can be treated with a LeVeen shunt. A modification called the Denver shunt contains a small chamber that can be used as a pump to clear the line by external pressure. In practice, Denver shunts become blocked more often than LeVeen shunts.
In patients with ascites due to cirrhosis, use of a LeVeen shunt should be confined to those who fail to respond to high doses of diuretics (eg, 400 mg of furosemide daily) or who repeatedly develop encephalopathy or azotemia during diuretic therapy.
Peritoneovenous shunts may also be used for ascites associated with cancer. The best results occur in patients whose ascitic fluid contains no malignant cells. A LeVeen shunt is of benefit in Budd-Chiari syndrome but is ineffective for chylous ascites. Because the incidence of complications and early shunt thrombosis is high, a LeVeen shunt is relatively contraindicated if the ascitic fluid is grossly bloody, contains many malignant cells, or has a high protein concentration (> 4.5 g/dL). The incidence of tumor embolization is low (5%).
The ascitic fluid should be cultured a few days before the shunt is inserted. Antibiotics are given pre- and postoperatively. The operation can be done with local anesthesia.
Postoperatively, the patient is outfitted with an abdominal binder, instructed to perform respiratory exercises against mild pressure to increase abdominal pressure and flow through the shunt. Dietary salt should not be restricted. A functioning LeVeen shunt alone is unable to fully eliminate the ascites, but it improves symptoms related to distention and renders the patient much more responsive to diuretics. Therefore, furosemide should be administered postoperatively.
An average of 10 kg of weight is lost during the first 10 days after the operation, and eventually the abdomen assumes a normal configuration. Nutrition, serum albumin levels often improve postoperatively. Urinary sodium excretion increases promptly, and renal function may improve in patients with the hepatorenal syndrome. Serious complications and deaths are most common in patients with hepatorenal syndrome or a serum bilirubin level greater than 4 mg/dL. Although some patients eventually bleed from varices following insertion of a LeVeen shunt, the shunt itself does not increase the risk of bleeding and actually decreases portal pressure. Thus, a previous episode of variceal bleeding is not a contraindication for this procedure. Disseminated intravascular coagulation (DIC), manifested by increased fibrin split products, decreased platelet count, etc, occurs in more than half of cases but is clinically relevant in only a few. The frequency of DIC may be minimized by emptying most of the ascitic fluid during operation and partially replacing it with Ringer’s lactate solution. Lethal septicemia may occur if the ascitic fluid is infected.
In about 10% of cases, the valve becomes thrombosed and must be replaced.
Hydrothorax may develop in patients with ascites. The fluid reaches the chest through a pinhole opening in the membranous portion of the diaphragm, a pathway that can be demonstrated by aspirating the thoracic fluid, injecting technetium Tc 99m colloid into the ascites fluid, and observing rapid accumulation of the label in the chest. If a leak persists, it may be closed surgically by thoracotomy.