Clinicopathological observations on metastasis in man studied in patients treated with peritoneovenous shunts.
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Fourteen patients with inoperable cancer treated with peritoneovenous shunts for malignant ascites were studied post mortem. Clinical observations and findings at necropsy indicated that peritoneovenous shunting does not result in the establishment of clinically important haematogenous metastases and that metastases do not necessarily develop even when large numbers of viable tumour cells regularly enter the blood. Peritoneovenous shunting provides a unique opportunity for collecting data on the spread of tumours in man. (+info)
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. (+info)
Peritoneovenous shunt therapy for leaking ascites in the cirrhotic patient.
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Review of clinical and operative records of 86 patients at the Minneapolis VA Medical Center and Mount Sinai Hospital undergoing peritoneovenous (PV) shunt for intractable ascites revealed a subgroup of patients (n = 9) who developed leaking ascites prior to shunting. The etiology of leaking ascites was as follows: 1) ruptured umbilical hernia ( UH ) (four patients), 2) repeated paracentesis (three patients), and 3) postoperative incisional ascitic fluid leak (two patients). Initial therapy included local sterile compression dressing, intravenous antibiotics, and management of fluid and electrolytes. All nine patients underwent subsequent closure of the fascial defect and PV shunt to prevent reaccumulation of ascites (simultaneous procedures were performed in five patients). No patient developed postoperative septic complications, organ failure, gastrointestinal bleeding, or encephalopathy. There were no early deaths; however, three late deaths (18 months, 2, and 4 years) were due to variceal bleeding and/or liver failure. Ascites was well controlled in seven patients with PV shunt alone, the other two ultimately responding to medical therapy. We conclude that peritoneal fluid leaks can be treated successfully by repairing the fascial defect and placing a PV shunt. In the absence of infected ascites and clinical peritonitis, PV shunt may be performed simultaneously with closure of UH , thus preventing the reaccumulation of ascites during the immediate postoperative period. (+info)
Mechanisms of human tumor metastasis studied in patients with peritoneovenous shunts.
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The technique of peritoneovenous shunting for the alleviation of abdominal pain and distension in malignant ascites due to inoperable cancer, returns the fluid to the circulation via a one-way, valved, anastomosis between the peritoneum and the jugular vein. Surprisingly, although the patients treated with this technique receive direct infusions of malignant tumor cells into the blood, this study of 29 patients, 15 of whom came to autopsy, shows that they did not all develop metastases, some being completely free of such lesions despite long survival. Even when metastases do form, they are small and clinically asymptomatic, and the technique is therefore not hazardous. In some patients, inert tumor cells identifiable by natural markers were recognized in the tissues, but no growing metastases were observed. In others, the distribution of secondary deposits was unexpected in that metastases did not form in the organ containing the first capillary bed encountered, although hematogenous metastases had formed in other organs. Despite the fact that various factors such as (a) the small numbers of patients treated with the technique; (b) the sensitive nature of studies on terminally ill patients; and (c) the absence of consistency in the sample population with regard to factors such as length of survival and site of neoplasm, combine to reduce the number of suitable cases for study, the approach has unrivaled power and interest for those seeking to understand mechanisms underlying tumor metastasis in humans. (+info)
Coagulopathy of peritoneovenous shunts: studies on the pathogenic role of ascitic fluid collagen and value of antiplatelet therapy.
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The role of ascitic fluid collagen in the pathogenesis of the coagulopathy that follows peritoneovenous shunting was examined. Collagen was partially purified from ascitic fluid and infused into rabbits. All animals developed changes in their haemostatic profile consistent with intravascular coagulation. Aspirin therapy, for five days before the collagen infusion, prevented these changes. Seven patients undergoing a total of eight peritoneovenous shunts for intractable ascites received antiplatelet therapy (aspirin and dipyridamole) in the immediate pre- and postoperative period. After six shunts no thrombocytopenia or prolongation of clotting times developed to suggest decompensated consumptive coagulopathy. Complicating factors may have contributed to the deterioration in haemostasis in the other two patients. There was no early shunt occlusion. The results support the hypothesis that ascitic fluid collagen is important in the pathogenesis of intravascular coagulation postascitic fluid infusion and indicate that antiplatelet drugs may be of value in preventing this complication. (+info)
Management of spontaneous umbilical hernia disruption in the cirrhotic patient.
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Umbilical hernia is a common finding in cirrhotic patients with ascites. Spontaneous disruption of the hernia and attendant discharge of ascitic fluid is an unusual and rarely reported complication in these patients and is associated with an overall mortality rate of nearly 30%. During the 5-year period 1977-1982, nine patients with hepatic cirrhosis and ascites were treated for spontaneous rupture of an umbilical hernia. Ascites was attributed to alcoholic cirrhosis in all cases and was present for an average of 21 months prior to rupture. In two cases, failed peritoneovenous shunts resulted in reaccumulation of massive ascites. Initial management included sterile occlusive dressings, fluid repletion, and intravenous antibiotic administration. Hernia repair was performed an average of 4.2 days after rupture. General anesthesia was used in eight cases and local anesthesia in one case. In one instance, the hernia became incarcerated and required urgent repair. Postoperative complications, including wound infection and colonic dilatation, occurred separately in two patients (22%). One patient died of hepatic failure 28 days after operation, for an overall mortality rate of 11%. Surviving patients have been followed for an average of 8 months, and most have done well. Spontaneous rupture of umbilical hernia in patients with ascites occurs uncommonly. Operative management is indicated uniformly and can be conducted safely when the patient's condition has stabilized. The prognosis is favorable for patients with good hepatic reserve. (+info)
Ten of 11 patients undergoing peritoneovenous (LeVeen) shunt placement for intractable ascites had disseminated intravascular coagulation (DIC) following the shunt procedure. Intraoperative ascitic fluid specimens revealed fibrin split products (FSP) in high titer (1:100-1:1600) in all patients. Endotoxin was found in 6 of 11 ascitic fluid samples but in no plasma samples. Activated clotting factors, clot inhibitors, excess protein, and fibrinolytic activity were not found in ascitic fluid. Clotting factor levels were much lower than in plasma. Bleeding occurred after operation in two patients; this appeared to be related to the severity of liver dysfunction as demonstrated by elevations of bilirubin, serum glutamic oxalocetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), and preoperative DIC. It is concluded that the LeVeen shunt coagulopathy is DIC, and may be related to exposure of the systemic circulation to FSP-rich ascitic fluid that may activate the coagulation mechanism. Bleeding complications do not appear to be related to the severity of the post shunt coagulopathy, but rather to the severity of liver dysfunction and presence of preoperative DIC (probably caused by the liver disease). (+info)
Hemodynamics of LeVeen shunt pulmonary edema.
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In order to characterize the circulatory changes which may lead to pulmonary edema following the surgical placement of a LeVeen peritoneovenous shunt, intraoperative hemodynamic studies were performed on five consecutive patients without clinical evidence of cardiac disease undergoing shunt insertion. Within 30 minutes after opening the peritoneovenous shunt, there was a marked increase in pulmonary capillary wedge pressure, cardiac output, and stroke work index, and a sharp decline in both pulmonary and systemic vascular resistances. In three patients, pulmonary edema did not occur; in one patient, pulmonary edema occurred transiently but responded to furosemide administration. In these four patients, systemic vascular resistance continued to drop over the ensuing hours and the elevated pulmonary capillary wedge pressure also decreased appropriately with furosemide. The fifth patient developed persistent pulmonary edema. In this subject, systemic vascular resistance continued to rise and the elevated pulmonary capillary wedge pressure did not respond to intravenous furosemide. This study suggests that uncomplicated LeVeen peritoneovenous shunt insertion may result in a drop in systemic vascular resistance which lowers left ventricular afterload, and, thus, may protect most patients from pulmonary edema. In contrast, a continued rise in systemic vascular resistance and afterload may contribute to pulmonary edema refractory to diuretic therapy and should probably be treated with a parenteral afterload-reducing agent. (+info)