Portacaval Shunt PCS

Portacaval Shunt Surgery

Fig. 4. Small-diameter portacaval shunt.

Inferior A^ vena \

cava Pancreas Duodenum

Fig. 4. Small-diameter portacaval shunt.

The overall postoperative morbidity averages about 30%. Complications include perioperative bleeding requiring multiple transfusions, postoperative ascites (including chylous ascites), pancreatitis from operative trauma to the gland, sepsis, and portal vein thrombosis. Specific complications from portasystemic shunting include postoperative hepatic encephalopathy, deterioration of liver function, and recurrent variceal hemorrhage.

Worsening of ascites following DSRS is due to the maintenance of portal hypertension, and the interruption of retroperitoneal lymphatics. Most surgeons feel that the presence of significant ascites is a contraindication for this procedure; the small-diameter MCS or PCS may be a better alternative. Medical management is successful in most cases: sodium restriction before and after surgery, using fresh frozen plasma or salt-poor albumin for maintaining plasma volume, spironolactone for diuresis, and restricting dietary fat to 30 g/d to minimize the risk of chylous ascites. Refractory cases may require paracentesis or rarely peritoneo-venous shunting.

Hepatic encephalopathy is defined as mental confusion related by the patient or family, or the detection of disorientation and asterixis by the physician. Subclinical encephalopathy, which is part of the spectrum, is characterized by elevated blood ammonia levels, electroencephalographic changes and abnormal psychometric tests. The emergence of postshunt encephalopathy occurs over time, necessitating close follow-up of patients after surgery. The incidence of this complication has been reduced with recognition of the importance of preserving hepatic portal blood flow, and avoiding shunt surgery in patients with severe liver dysfunction. Prospective, randomized studies have shown that portal blood flow preserving procedures have a reduced incidence of encephalopathy, and improved survival compared to total shunts (23,24). Treatment of hepatic encephalopathy includes control of precipitating factors (sepsis, electrolyte abnormalities, and hypovolemia), restricting protein intake to 40 g/d, use of oral neomycin and lactulose, and in refractory cases, ligation of the shunt.

Recurrent variceal bleeding after portasystemic shunt surgery occurs in less than 10% of cases, and is usually caused by shunt thrombosis. There is evidence to suggest that prosthetic grafts have a higher thrombosis rate compared to autogenous splenorenal shunts (25). Clinical manifestations of a thrombosed DSRS include left upper quadrant pain, splenomegaly, ascites, and recurrent variceal formation. When identified early (within 2 wk of occurrence), it may be salvaged by thrombolytic therapy or reoperation. Early rebleeding after DSRS may also occur despite a patent shunt, and is caused by inadequate decompression of the varices. Development of an adequate outflow (via the short gastric, splenic, left renal veins, and the inferior vena cava) for complete gastroesophageal decompression may take up to 4-6 wk in some patients. One study showed that 24% of patients had inadequate immediate decompression 1-2 wk after DSRS (26). Hence, the use of this shunt in the acute setting of active variceal hemorrhage is controversial. Management of rebleeding in such patients should be nonoperative: vasopressin, balloon tamponade, and sclerotherapy. Prosthetic shunts also have a higher likelihood of causing portal vein diameter reduction or thrombosis compared to DSRS (25).

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