A prospective evaluation of emergency protacaval shunt has been conducted in 180 unselected, consecutive patients with cirrhosis and bleeding varices who were operated on between 1963 and 1978. An extensive diagnostic work-up was completed within three to seven hours of admission to the emergency department, and the shunt operation was undertaken within a mean of 7.81 hours. A program of lifelong follow-up was conducted such that the current status of 97% of the patients is known. On each patient, 220 categories of data were collected and entered into a computer program for analysis. On admission, 49% of the patients had jaundice, 53% had ascites, 19% had encephalopathy, 30% had severe muscle wasting and 100% had abnormal BSP retention. Administration of a bolus dose of vasopressin by the systemic intravenous route temporarily controlled the varix hemorrhage in 95% of patients, and emergency shunt permanently controlled the bleeding in 98%. Maximum perfusion pressure in the portal vein prior to shunt did not correlate with survival rate or incidence of encephalopathy after shunt. The operative survival rate was 58%, the five-year actuarial survival rate is 38% and the 12-year actuarial survival rate is 30%. Encephalopathy was observed in 31.5% of the patients, but was severe enough to require chronic dietary protein restriction in only 7%. The portacaval shunt remained patent in 99% of patients. Of the survivors, 48% abstained from alcohol, 60% resumed gainful employment or housekeeping, and two-thirds were judged to be in excellent or good condition after one and five years. Preoperative factors that adversely influenced survival rate were ascites, SGOT >/= 100 units, BSP retention >50%, hypokalemic alkalosis, blood transfusion requirement >/= 5 L, and consumption of alcohol within seven day[unk] of admission. In comparison with our previous prospective studies, emergency portacaval shunt produced a significantly greater long-term survival rate than either emergency medical therapy or emergency varix ligation, followed by elective shunt. During the past four years, 80% of 49 unselected patients have survived emergency shunt, and the four year actuarial survival rate is 69%.
The existence of a stimulatory intestinal phase of gastric acid secretion has been suspected, but largely ignored, for many years. Recently, however, it has become clear that the intestinal phase plays an important role in acid production during digestion. The intestinal phase is of additional interest in relation to the profound gastric acid hypersecretion associated with portacaval shunt (PCS). Substantial evidence indicates that PCS-related gastric hypersecretion is due to unmasking of the intestinal phase by hepatic bypass of a humoral stimulant in portal blood that is normally degraded to a considerable extent by the liver. Studies in our laboratory during the past 12 years have provided strong physiologic evidence for humoral mediation of both the intestinal phase of gastric secretion and of PCS-related hypersecretion by a hormone that arises in the small intestine, particularly in the jejunum. Furthermore, our studies have demonstrated that this intestinal phase hormone (IPH) exists in humans as well as in dogs, rats, and pigs. Additionally, recent work by a number of investigators, as well as by our group, has provided convincing evidence that IPH is different from any of the known gastric stimulatory hormones. With these physiologic observations as a background, we have used a classical method for extracting acidic peptides to prepare a hog intestinal mucosa extract (HIME) that has all of the known physiologic properties of an IPH. Specifically, HIME contains a potent stimulant of gastric acid secretion that acts according to a linear dose-response relationship; that is not gastrin in any of its immunoassayable forms; that significantly augments the maximal acid secretory responses to pentagastrin, gastrin, CCK, and histamine; and that is substantially degraded by the liver, in contrast to gastrin and CCK. Efforts at isolating the gastric stimulatory substance in HIME suggest that it is a peptide of low molecular weight. Work directed at isolating IPH in pure form and identifying it is in progress.
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