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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The intra- and early postoperative courses of 142 consecutive patients who underwent liver resections using vascular occlusions to reduce bleeding were reviewed. In 127 patients, the remnant liver parenchyma was normal, and 15 patients had liver cirrhosis. Eighty-five patients underwent major liver resections: right, extended right, or left lobectomies. Portal triad clamping (PTC) was used alone in 107 cases. Complete hepatic vascular exclusion (HVE) combining PTC and occlusion of the inferior vena cava below and above the liver was used for 35 major liver resections. These 35 patients had large or posterior liver tumors, and HVE was used to reduce the risks of massive bleeding or air embolism caused by an accidental tear of the vena cava or a hepatic vein. Duration of normothermic liver ischemia was 32.3 +/- 1.2 minutes (mean +/- SEM) and ranged from 8 to 90 minutes. Amount of blood transfusion was 5.5 +/- 0.5 (mean +/- SEM) units of packed red blood cells. There were eight operative deaths (5.6%). Overall, postoperative complications occurred in 46 patients (32%). The patients who experienced complications after surgery had received more blood transfusion than those with an uneventful postoperative course (p less than 0.001). The length of postoperative hospital stay was also correlated with the amount of blood transfused during surgery (p less than 0.001). On the other hand, there was no correlation between the durations of liver ischemia of up to 90 minutes and the lengths of postoperative hospital stay. The longest periods of ischemia were not associated with increased rates of postoperative complications, liver failures, or deaths. There was no difference in mortality or morbidity after major liver resections performed with the use of HVE as compared with major liver resections carried out with PTC alone, although the lesions were larger in the former group. It is concluded that the main priority during liver resections is to reduce operative bleeding. Vascular occlusions aim at achieving this goal and can be extended safely for up to 60 minutes.
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PMID:Vascular occlusions for liver resections. Operative management and tolerance to hepatic ischemia: 142 cases. 291 65

Liver biopsy results and clinical records from 13 patients with sickle cell anemia were reviewed to assess the relative importance of local ischemia or of factors unrelated to sickling as a cause of their liver disease. Two of the biopsy specimens were normal and one showed cirrhosis. Nine patients had received multiple blood transfusions and nine had cholelithiasis, of whom two also had choledocholithiasis. Seven had both risk factors. Five had lobular cholestasis and four had acute or chronic hepatitis. One biopsy specimen showed changes of the Budd-Chiari syndrome. Another showed clear portal tract changes of large bile duct obstruction but no mechanical blockage of the biliary system; this suggests the thickened bile as postulated by Muirhead. Otherwise the changes observed were those to be expected in a heavily transfused population with a high prevalence of gallstones.
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PMID:Histopathologic features of liver biopsy specimens in sickle cell disease. 334 26

An enhanced frequency and morbidity of urinary tract infections (UTI) have been observed in association with alcoholism and liver disease. The causes of these phenomena may relate, in part, to the defects in humoral and cellular immune mechanisms that occur in alcoholism. Urinary catheterization is the most common cause of UTI in hospitalized alcoholics. The severity of the sequelae of UTI in alcoholism is demonstrated by the unusually frequent occurrence of renal papillary necrosis (RPN) in conjunction with pyelonephritis in these patients. Indeed, in over 90% of the reported cases of RPN occurring with alcoholism or liver disease, pyelonephritis has been a contributing factor. The proclivity to medullary ischemia and RPN in this patient group may be, at least in part, a result of interstitial renal edema secondary both to infection and the effect of ethanol per se and to renal arterial vasoconstriction that occurs in cirrhosis. The frequency with which death due to sepsis or renal failure occurs in association with UTI in alcoholics obliges the physician to exercise caution in the prevention and treatment of UTI in these patients.
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PMID:Urinary tract infections and renal papillary necrosis in alcoholism. 370 22

Thirty-four adult patients with portomesenteric venous occlusion (PVO) were reviewed. In 11 with hepatic cirrhosis, PVO was usually heralded by worsening ascites often with varix hemorrhage; mortality was high. Four with isolated portal block had varix hemorrhage without ascites. All of these patients survived despite recurrent hematemesis when portal decompression was not feasible in two patients. Eight others (5 agnogenic and 3 with hypercoagulability), experienced sudden abdominal pain with a clot typically propagated into mesenteric tributaries with ileojejunal infarction; survival was related to the promptness of operation and the extent of bowel ischemia. Of five patients with intraabdominal sepsis and pylephlebitis, only one survived. In the final six patients, PVO occurred with intraabdominal carcinoma. Five had progressive ascites, cachexia, and an early death. Imaging techniques included plain and contrast roentgenograms, ultrasonography, and for definitive diagnosis direct portography (operative or splenoportogram), indirect portography (splanchnic arteriovenogram), and computed tomography. Thirteen of 34 patients had ascites, and in nine of 11 patients examined, protein concentration of ascitic fluid was extremely low (less than 0.6 g/dl). Clinical presentation of PVO varies, depending on acuteness and extent of visceral venous blockade, severity of portal hypertension, auxiliary venous collateralization, and regional lymph flow. Inciting factors include endothelial damage and blood hypercoagulability from trauma, infection, stagnant circulation, blood dyscrasia, and malignancy. Improved imaging now allows early diagnosis.
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PMID:Protean manifestations of pylethrombosis. A review of thirty-four patients. 387 12

Although decreases in hepatic adenosine triphosphate (ATP) levels during ischemia are thought to reflect loss of hepatic energy reserves and decreased viability, such changes have not been correlated with a clinically relevant index of hepatic function or viability. Ability to clear amino acids from plasma has been shown to correlate with function of the allograft in hepatic transplantation and survival after portal decompression in patients with hepatic cirrhosis. The effects of 60 minutes of warm ischemia in two groups of mongrel dogs were studied to assess the relationship between loss of ATP and amino acid clearance. One group (shunted) had portal decompression during the ischemic period and the other (portal stasis) did not. There was a significant correlation between loss of ATP and amino acid clearance after ischemia. Although the effects of ischemia on the liver were similar in both groups, the portal stasis group demonstrated significantly elevated SGOT levels during reperfusion that were related to impaired net adenine monophosphate synthesis and suggestive of ongoing injury. These data support the contention that loss of ATP during ischemia is associated with reduced functional capacity. In addition, they suggest that portal stasis produces toxic products that can impede hepatic recovery from ischemia.
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PMID:Alterations in amino acid clearance during ischemia predict hepatocellular ATP changes. 403 62

Portal hypertension is defined as an increase of the portal venous pressure over 20 cm H2O or 7 mm Hg, respectively. It may be induced by different types of portal venous stenosis or obstruction, primarily by cirrhosis and fibrosis of the liver and, less frequent by posthepatic disorders such as the Budd-Chiari-syndrome or congestive heart failure. Portal hypertension is followed by ectasia and phlebosclerosis of the portal vein, by splenomegaly, ascites and by various types of collateral circulation. Among these, oesophageal varices, are most important since they often lead to acute upper gastrointestinal haemorrhage, the major complication of portal hypertension. Bleeding from oesophaeal varices is essentially based on atrophy of the squamous epithelium, caused by ischemia from local hypoxia and venous stasis. Portal hypertension and the frequently compromised blood clotting mechanism due to reduced synthesis of clotting factors in the liver aggravate the bleeding. Atrophy of the esophageal mucosa presents an area of decreased resistance likely to ulcerate with easy erosion of the varices--usually lying very superficially--; with mechanical irritation by food or peptic erosion from gastroesophageal reflux being frequent inducers of hemorrhage.
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PMID:[Pathologic-anatomic reflections on portal hypertension (author's transl)]. 624 21

Evidence is presented that supports a role of oxygen free radicals in the pathogenesis of various disorders of the digestive system. In the intestine, there is evidence that oxygen radicals play an important role in the endothelial and epithelial damage associated with certain models of ischemia. The mechanism for superoxide production in this condition differs from that described for other pathologic states (i.e., oxygen toxicity and neutrophil-mediated inflammation). This mechanism involves the reaction of xanthine oxidase, hypoxanthine, and molecular oxygen to produce a burst of oxygen radicals with reperfusion of the ischemic bowel. Evidence implicating oxygen radicals in inflammatory disorders of the digestive tract (i.e., pancreatitis), radiation injury, and hepatic cirrhosis is also presented. The available data suggest that oxygen radicals appear to be a fundamental mechanism of tissue injury in the pathogenesis of various disorders of the digestive system.
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PMID:Role of oxygen-derived free radicals in digestive tract diseases. 635 11

In a randomized controlled trial, the effect of continuous intravenous administration of vasopressin was compared with Sengstaken-Blakemore balloon tamponade in 37 episodes of bleeding esophageal varices in patients with cirrhosis. The majority were Group A and B of Child's classification. Bleeding was controlled in 11 of 17 (65%) patients on vasopressin and in 14 of 20 (70%) patients on tamponade. The patients who failed to respond initially (6 episodes on vasopressin and 5 on tamponade) were treated successfully with the alternative method. Overall mortality was similar in both groups: 3 patients in the vasopressin group and 4 in the tamponade group died. Only one patient died of uncontrolled bleeding; 4 patients probably died of complications of treatment, 2 of cardiac ischemia after vasopressin and 2 of pulmonary infection after tamponade. The vasopressin group required significantly fewer blood transfusions than did the tamponade group.
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PMID:Controlled trial of vasopressin and balloon tamponade in bleeding esophageal varices. 638 98

Temporary occlusion of hepatic inflow, namely, the Pringle maneuver, was adopted for 15 patients with liver cirrhosis who underwent partial hepatectomy. The warm ischemia time ranged from 2 to 32 minutes with an average of 19 minutes. The procedure did not cause any harmful effects on systemic hemodynamic and postoperative liver function. The results in our patients were compared with those of 15 comparable control patients who had been operated on over the same period of time without inflow obstruction. The Pringle maneuver significantly diminished the estimated blood loss during surgery, intraoperative and postoperative complications, and suppressed the operative mortality rate from 20 percent to 0.
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PMID:Tolerance of the cirrhotic liver to normothermic ischemia. A clinical study of 15 patients. 673 91

Total hepatic inflow occlusion is well tolerated in pigs with normothermia for as long as two hours, provided that splanchnic venous pooling is avoided by active pumping through a splenojugular bypass. Hepatic dysfunction after 60, 90 and, even, 120 minutes of hepatic ischemia is mild and transient. Complete return to normal liver function tests is rapid. Early microscopic alterations of the liver are moderate, and no late abnormalities, such as cirrhosis or vascular changes, were observed one to three months later. Conversely, interruption of hepatic blood flow for three hours is not compatible with life. In this study, a previously unsuspected resistance of the pig liver to warm ischemia is demonstrated. These findings corroborate and extend those of recent clinical studies in which a similar tolerance of the human liver to prolonged normotherthermic ischemia is reported, thus questioning the necessity for deliberate hypothermia in operations involving the liver.
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PMID:An experimental study of survival after two hours of normothermic hepatic ischemia. 737 48


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