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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The postoperative courses of 26 patients admitted to an Intensive Care Unit after different types of surgery on their portal tree are studied. All were diagnosed as having portal hypertension secondary to chronic liver disease and had presented one or more episodes of bleeding. Those complications of greater risk with an important early mortality rate are: 1) recurrence of the gastrointestinal hemorrhage, independently of the type of lesion which originates it; 2) recurrence of ascites because these patients more often develop dehiscence of the abdominal wall, serious dilutional hyponatremia and severe functional renal insufficiency; 3) acute renal failure, both functional or caused by an organic tubulo-interstitial nephropathy; 4) peritonitis; 5) persistent hepatolytic episode; 6) hyperdynamic heart failure; and 7) re-operations in general, independently of the causes. The frequency of these complications and the greater or lesser seriousness of their development in the postoperative period are dependent on: 1) the age of the patient with a better prognosis for those under 50; 2) the histopathologic type of the hepatic lesion, with hepatic fibrosis having a more favourable evolution in comparison with cirrhosis; 3) the degree of decompensation of the hepatopathy immediately before the operation, evaluating signs of functional hepatic deficit, cytolysis and degree of portal hypertension. The greater the preoperative activity, the worse the postsurgical prognosis. 4) The elective or urgent character of the surgery. During the postoperative course of emergency surgery all types of complications may appear. The emergency operation which has effectively achieved the stopping of the esophageal bleeding has been the porto-azygos disconnection, which allows later a portosystemic shunt with a greater probability of success. 5) The type of anastomosis carried out. Radicular shunts were those which had a lower postoperative mortality rate and those which progressed better because of the small number of problems occurring in the early postoperative period.
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PMID:[Postoperative care in portal hypertension surgery (author's transl)]. 43 Nov 56

Through real time ultrasonography, it is possible to display the splenic vein, the superior mesenteric vein, the vena porta, and the intrahepatic portal and systemic veins. In jaundice, it is of the utmost importance to carefully identify the vena porta before making a diagnosis of common bile duct enlargement. It is also necessary, when confronted with a pattern of apparently enlarged intrahepatic ducts, to conduct a thorough study of possible confluences of the ducts with the vena porta or vena cava to be certain that the ducts are not part of the portal or systemic venous network. Without such differentiation, portal enlargement caused by portal hypertension, systemic venous enlargement caused by cardiac insufficiency, or even nonpathological wide veins may lead to an erroneous diagnosis of obstructive jaundice.
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PMID:Ultrasonic study of venous patterns in the right hypochondrium: an anatomical approach to differential diagnosis of obstructive jaundice. 80 81

Leucocidin from Pseudomonas aeruginosa causes cardiovascular failure in rats and mice. The time between i.v. injection and death depends on the dose. After injection of high doses (500 mug/kg) the arterial blood pressure decreases rapidly and cardiac irregularities and AV block occur within about 5 min. In contrast to endotoxin shock no pulmonary hypertension was observed, whereas portal hypertension was seen in our experiments. Injection of lower doses (less than 200 mug/kg) caused peripheral vascular damage with lung oedema, vascular disturbances in various tissues, exudation and bleeding. Finally cardiac insufficiency predominated. Dexamethasone delayed the symptoms but did not prevent death in either rats or mice. Heparin was ineffective in this type of shock.
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PMID:Cardiovascular reactions induced by leucocidin from Pseudomonas aeruginosa. 82 38

Two hundred twelve Italian patients with genetic hemochromatosis (181 men, mean age 50 +/- 11 yr; and 31 women, mean age 49 +/- 10 yr) were followed for a median period of 44 mo (range = 3 to 218 mo). Alcohol abuse was present in 31 subjects (15%), and chronic HBV and HCV infection were seen in 19 (9%) and 35 (24%) of 145 cases tested, respectively. Twenty-four patients (11%) had concomitant beta-thalassemia trait. Liver biopsy revealed cirrhosis in 146 and a noncirrhotic pattern in the other 66. Perls' stain was degree III in 37 patients and IV in 171 patients. One hundred eighty-five patients underwent weekly venesection, and iron depletion was achieved in 122 cases after total iron removal of 3 to 41 gm. Death occurred in 44 patients after 3 to 198 mo and was due to hepatocellular carcinoma in 20 cases, liver failure in 10, extrahepatic cancer in six, heart failure in three and hemochromatosis unrelated causes in five. Cancer has developed in seven other patients still alive (hepatocellular in five and extrahepatic in two). No deaths were observed among noncirrhotic patients; cumulative survival rates in cirrhotic patients were 85%, 75%, 60% and 47% at 3, 5, 8 and 10 yr, respectively. Univariate analysis in the 146 cirrhotic patients showed that age greater than 60 yr, alcohol abuse, cardiomyopathy, skin pigmentation, portal hypertension, hypoalbuminemia, hypergammaglobulinemia and Child class B or C had significant negative prognostic value. At multivariate analysis, only alcohol abuse, gamma-globulins greater than 2.0 gm/dl and Child class B or C maintained their negative prognostic values (p less than 0.01, hazard ratio 2.7; p less than 0.001, hazard ratio 2.8; and p less than 0.001, hazard ratio 4.3, respectively).
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PMID:Survival and prognostic factors in 212 Italian patients with genetic hemochromatosis. 131 85

Nitrates have been used for the last 130 years to treat and control the symptoms of angina pectoris. Within the last 15 years, nitrates also have been shown to limit infarct size and to be beneficial in the treatment of patients with severe intractable heart failure, cardiogenic shock, severe mitral and aortic regurgitation, hypertensive episodes, and portal hypertension. The adequate use of nitrates to treat these disorders requires the ability to document a hemodynamic response and to closely monitor the adverse consequences of this therapy. Nitrates work by directly relaxing smooth muscle in resistance and capacitance vessels, thereby causing generalized dilation. Nitrates reduce preload and, at higher doses, reduce systemic vascular resistance and afterload. This chapter reviews the physiologic mechanisms that underlie nitrate therapy, the appropriate indications for nitrate use, the usefulness of specific agents, and their appropriate nursing implications.
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PMID:Nitrates. 157 38

Hemangioendotheliomas and arteriovenous malformations (AVMs) of the liver often cause congestive heart failure in babies, but embolization of the hepatic artery is not always effective. Six newborns and infants (four with hemangioendotheliomas and two with AVMs) underwent abdominal aortography, hepatomesenteric arteriography, and angiography of arterial and portal collateral vessels prior to embolization of the hepatic artery for heart failure (n = 5) and portal hypertension (n = 1). In addition, extrahepatic arteries were embolized in one patient and a portal vein branch in another. Extrahepatic arterial collaterals from the superior mesenteric, intercostal, phrenic, and adrenal arteries were seen in five patients; portal vein connections, in two patients. Embolization was therapeutically most effective in the baby with the least collateral supply and in the two patients in whom arterial collaterals or portal venous connections were embolized. Angiographic documentation and possibly embolization of collateral flow is required to improve treatment planning and success in these severely ill patients.
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PMID:Multiple collaterals to hepatic infantile hemangioendotheliomas and arteriovenous malformations: effect on embolization. 194 71

Measurement of fibronectin in ascites has been proposed for the differentiation of ascites either due to malignant growth in the peritoneal cavity or liver cirrhosis with portal hypertension. The high ascitic fibronectin concentration in patients with peritoneal carcinomatosis was thought to be due to the synthesis of this protein by neoplastic cells. Therefore in ascites of malignant origin cellular fibronectin should be present as it is synthesized by neoplastic cells. On the other side the transsudative ascites due to liver cirrhosis with portal hypertension should mainly contain plasma-fibronectin, which is secreted by hepatocytes into the bloodstream. With the aid of two different monoclonal antibodies and immunoblotting of partially digested or intact ascitic fibronectin, cellular fibronectin could be demonstrated in ascitic fluid of 10 patients with peritoneal carcinomatosis, 13 patients with liver cirrhosis, one patient with right-sided heart failure and one patient with Budd-Chiari-Syndrome. As determined by a specific ELISA 8 out of 10 samples of malignant ascites contained more than 30 mg/l of cellular fibronectin, whereas 10 out of 13 samples of ascites due to liver cirrhosis contained less than 10 mg/l. Whereas in ascites of malignant origin cellular fibronectin represented about 20% of total fibronectin, in portal ascites fibronectin represented sometimes more than 50% of total fibronectin. Cellular fibronectin of non-malignant origin is probably produced by mesothelial cells or peritoneal macrophages. Therefore, fibronectin accumulating in peritoneal carcinomatosis is only to some extent locally produced, but mainly caused by an unhindered exsudation of plasma-fibronectin.
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PMID:[Genesis of fibronectin in ascites--detection of cellular and plasma fibronectin in portal and malignant ascites]. 205 24

Hepatic aneurysms, pseudoaneurysms and fistulas (arterial biliary and arterial portal) causing bleeding or portal hypertension, and arteriovenous malformations causing high output cardiac failure in adults can be successfully managed by embolization techniques. Results of embolization in infantile hemangioendotheliomas are less uniform and tumors with massive arteriovenous shunting are difficult to manage. Transjugular intrahepatic portal systemic shunts using expendable stents have been successfully created in patients and have effectively controlled portal hypertension and variceal bleeding.
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PMID:Interventional treatment of hepatic arterial and venous pathology: a commentary. 212 46

Echographic examination of 3900 patients showed enlargement of the gallbladder wall in 3.5%. It was seen not only in cholecystitis but also in diffuse liver injury, portal hypertension, chronic heart failure and in other pathological conditions. Examples are given of 3 different sonographic versions of enlargement of the gallbladder wall. In some patients' groups (with diffuse liver injury, chronic heart failure, portal hypertension), a correlation was established between the thickness of the gallbladder wall and the diameter of the portal vein. It is assumed that echographic demonstration of the enlarged gallbladder wall in patients with diffuse liver injury may serve an early sign of portal hypertension.
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PMID:[Diffuse thickening of the gallbladder wall detectable during echography]. 218 98

Severe bleeding from gastric varices occurred in an 18-year-old male known, since he was three years old, to have liver cirrhosis with beginning protal hypertension. The cause of the portal hypertension was chronic cholestasis due to hypoplasia of the interlobular bile ducts. There was also peripheral pulmonary stenosis with pulmonary hypertension (106 mmHg systolic), and a posterior embryotoxon (arcus juvenilis). Skeletal anomalies, particularly of the vertebrae, and a striking facial dysmorphism provided the features of arteriohepatic dysplasia, Alagille's syndrome, an autosomal dominant disease generally becoming manifest during childhood. As the patient's liver functions were only slightly abnormal, liver transplantation was not indicated and a shunt operation performed. A septicaemia developed on the third postoperative day after an at first complication free course, and he died from right-heart failure.
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PMID:[The Alagille syndrome in an adult]. 239 Sep 42


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