Coagulopathy post peritoneovenous shunt.

In 1942, 53% of medically treated patients with cirrhosis were dead 6 months after the onset of ascites. Only 30% survived 1 year. This dismal outlook has improved only slightly with advances in medicine. Yet, some internists reject the peritoneovenous shunt (PVS) for this fatal condition even if they are aware that a diminished blood volume causes the abnormal sodium retention responsible for ascites. Their objections are based on life-threatening complications of PVS, especially post shunt coagulopathy (PSC). Blood shed into the peritoneal cavity becomes incoagulable. Such blood is immediately coagulated by a protocoagulant (soluble collagen) and concurrently lysed by tissue plasminogen activator (TPA) secreted by the peritoneal serosa. Wide zones of lysis surround peritoneal tissue placed on fibrin plates. Large volumes of ascitic fluid infused into circulating blood simulates the fate of blood shed into the peritoneal cavity with lysis playing the major role. Addition of ascitic fluid to normal platelet-rich plasma in vitro initiates clot lysis on thromboelastogram (TEG). Epsilon-aminocaproic acid (EACA) counteracts this lysis. EACA and clotting factors normalize the TEG and arrest PSC. Disposal of ascitic fluid at surgery prevents or ameliorates PSC. Mild PSC was encountered only twice in 150+ consecutive patients (1.3%) with only one case being clinically significant (0.6%). Severe PSC occurred seven times in 98 early shunt patients whose ascitic fluid was not discarded. Severe PSC requires shunt interruption and control of bleeding with clotting factors and EACA. Peritoneal lavage with saline prevents the recurrence of PSC on reopening the shunt. In four patients, EACA and clotting factors were adequate to arrest coagulopathy. Three earlier patients died of PSC before its cause and treatment were understood. Proper management eliminates this life-threatening complication, and PSC cannot be considered a deterrent to PVS. Disseminated intravascular coagulopathy (DIC) is produced in experimental animals only by the injection of thrombin or thromboplastin. PSC is a distinct entity differing from DIC; EACA and not heparin is the antidote for PSC.

Peritoneovenous shunt occlusion. Etiology, diagnosis, therapy.

Electronic pressure testing of every LeVeen valve has practically eliminated mechanical malfunction as a cause of shunt failure. Nonetheless, failures do occur and in a series of 240 cases, early or late shunt failure occurred in 29 patients. Thirty-five additional cases of failures were either referred by other physicians over a period of 6 years or information and x-rays were accumulated by direct contact. Shunt failure becomes manifest by a sudden reaccumulation of ascites in patients with a previously functioning shunt. In immediate failure, the ascites may fail to disappear after surgery or reaccumulate if removed. Ideally, caval clotting should be first excluded by x-ray visualization of the superior vena prior to injection of the shunt with contrast agent. Shuntograms are done with fine-bore needles. The venous pressure is also measured. The entry of contrast into the vena cava without pooling indicates a patent venous limb. The contrast will empty from the venous tubing with forceful inspiration if the entire system is patent. The venous tube will not clear if the valve or peritoneal collecting tubes are blocked. Only the valve and collecting tube need then be replaced if contrast enters the cava but does not leave the venous tubing. Occluded valves must not be flushed to restore patency since inflammatory exudate and cellular debris are erroneously identified as "fibrin flecks." Histology and culture are mandatory. Immediate and early failure are often caused by malposition of the venous tubing. Malplacements can often be diagnosed simply by chest x-rays. Intraoperative injection of methylene blue into the venous tubing establishes a satisfactory washout prior to wound closure. Fresh clots in the vena cava can be dissolved by the slow injection of streptokinase into the venous tubing. Other patent veins are chosen for access. Patients having repeat surgery after clotting must be heparinized to prevent a similar recurrence. Flushing blood clots from the cava can be fatal.

Management of ascites with hydrothorax.

Hydrothorax occurs in 5.3 percent of ascitic patients. Our experience with 22 cases forms the basis of this report. Of the 22 cases, 21 were spontaneous and 1 was due to transdiaphragmatic incision. Eighteen occurred on the right side. Usually fluid enters the chest through tiny defects in the diaphragm. These defects are often covered by pleuroperitoneum, but the high abdominal pressure raises a bleb on the superior surface of the diaphragm. Rupture produces hydrothorax. The ascites is often relieved with the onset of the hydrothorax. Blockage of the thoracic duct has produced chylous ascites. The thoracoabdominal communication is immediately confirmed by a scan of the chest and abdomen after intraperitoneal injection of technetium-99 colloid. Fluid is tapped from the chest immediately before intraperitoneal injection. The rate at which the technetium-99 enters the chest is related to the size of the defect in the diaphragm. A significant transfer should occur within 12 hours. Immediate transfer occurs with large defects. The ruptured blister on the diaphragm forms a one-way valve. Intrathoracic injection does not migrate into the peritoneal cavity. The valvular characteristics of the leak force ascitic fluid into the thorax because the differential pressure between the abdominal and pleural cavities is intensified by inspiration. If tension hydrothorax has occurred, urgent thoracocentesis and paracentesis may be required. A chest tube should not be introduced. The main principle of surgery is to supply a low resistance pathway for the return of fluid to the venous system and to eliminate the diaphragmatic defect by obliteration of the pleural space. A LeVeen peritoneovenous shunt is performed after emptying the abdomen of its fluid load. After completion of the shunt operation, the chest is emptied of fluid, and a sclerosing agent (tetracycline or nitrogen mustard) is injected into the pleural cavity. Closure of the defect is verified by technetium-99 labeled scans which also confirm shunt patency. With this regime, the defect closed or was rendered insignificant in 18 of 22 patients. One patient had a post-transdiaphragmatic surgical defect which was too extensive to be closed by the aforementioned procedures. One patient remained well but did not have closure of the defect, one patient with a ruptured hiatal hernia did not have closure, and one patient who had previous placement of a chest tube could not be closed. Therefore, 18 of 22 patients were successfully treated.