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Query: UMLS:C0023890 (cirrhosis)
 42,195 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

A patient with clinical and serological manifestations of systemic lupus erythematosus (SLE) without renal or neurological manifestations was managed conservatively for 4 1/2 years. At this time she developed ascites and abnormal liver function tests, and was found to have severe chronic active hepatitis (CAH) with cirrhosis and portal hypertension. No clinical or biochemical evidence of liver disease was documented over the first 3 1/2 years of her illness, though no tests were performed in the 12 months before diagnosis. This case emphasizes the value of monitoring liver function tests over extended periods in such patients, since appropriate immunosuppressive therapy may benefit CAH, and as in this case, systemic manifestations of CAH may simulate SLE and precede clinical liver disease.
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PMID:Chronic active hepatitis in a patient presenting with clinical and serological evidence of SLE. 43 9

The course and possible risks of pregnancy in 7 women between the ages of 20 and 30 yr with chronic-persistent hepatitis (CPH) were evaluated. Ten pregnancies occurred in these women during the follow-up period which ranged from 3 to 8 yr. Four of the fetuses were aborted electively for nonmedical reasons. The other six pregnancies resulted in normal spontaneous vaginal deliveries at term. Each of the women experienced uneventful pre- and postnatal courses, and the neonates were all healthy and developmentally normal at birth. There was no biochemical or clinical evidence to suggest worsening liver disease during pregnancy. Normal menstrual patterns when not pregnant and normal biphasic basal body temperature patterns in 4 women suggested that ovulation and fertility were not impaired significantly. Pregnancy in women with CPH appears safe to both mother and fetus alike. This finding contrasts with the morbidity and mortality some authors have found to be associated with cirrhosis and with portal hypertension. We speculate that our findings may be relevant to women with other portal lesions resembling CPH such as resolving acute hepatitis and chronic active hepatitis in sustained remission.
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PMID:Chronic-persistent hepatitis and pregnancy. 45 47

Sodium and water retention is constant in decompensated cirrhosis with ascites and edema. Sodium retention is due to several factors. Renal hemodynamic disturbances appear first: decrease in glomerular filtration and renal plasmatic perfusion, redistribution of renal perfusion to the juxtamedullar area where the longer nephrons reabsorb more sodium. Metabolic disorders of estrogens, natriuretic hormonal factor, prostaglandins and the kallikrein-kinin system contribute to greater sodium retention. Water retention is secondary to greater sodium reabsorption and to hyperactivity of the antidiuretic hormone. Sodium and water retention, associated with portal hypertension, with reduced oncotic pressure and with dynamic lymphatic insufficiency, is responsible for the production of ascites. The latter results in a decrease in the effective plasmatic volume, with non-suppression of the renin-angiotensin system, increased aldosterone production and additional sodium retention.
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PMID:[The physiopathology of ascites]. 46 62

A man of 37 years of age developed portal hypertension which was observed on radiological examination as a mediastinal opacity having the appearance of a tumor. No oesophageal varices were seen on barium meal examination or by endoscopy. A smooth liver was seen during laparoscopy. Pre-operative hemodynamic studies showed that there was no sinus block. Thoracotomy revealed an aneurysm of the azygos veins. Exploratory laparotomy after coelio-mesenteric arteriography confirmed the diagnosis of diffuse nodular hyperplasia of the liver, cirrhosis, and portal hypertension. The findings in 16 cases of mediastinal opacity from portal hypertension reported in the published literature are discussed.
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PMID:[False tumor of the posterior mediastinum in a case of portal hypertension (author's transl)]. 46 46

Estimates were made of the arsenic concentration in liver specimens from nine patients having idiopathic portal hypertension (IP), and in four livers these were found to be significantly higher than those in patients with cirrhosis and in control subjects. The splenovenogram revealed extensive portosystemic collateral circulation. Corrected sinusoidal pressure and blood flow studies showed higher levels in four patients than in normal subjects. Microscopic examination of liver tissues revealed periportal fibrosis. The higher hepatic arsenic levels that were found were due to the inadvertent drinking of water contaminated with arsenic, adulterated opium, and indigenous medicines. A history of opium intake was not forthcoming but two patients had drunk water contaminated with arsenic and two others had taken bhasams (Ayurvedic medicines prepared by repeated oxidation of ores). Though the aetiology of idiopathic portal hypertension is not known, it is possible that arsenic intake may be one of the factors.
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PMID:Chronic oral arsenic intoxication as a possible aetiological factor in idiopathic portal hypertension (non-cirrhotic portal fibrosis) in India. 46 68

A wide spectrum of clinical and morphologic changes in 32 autopsy cases of noncirrhotic portal fibrosis have been described. The disease frequently occurs in younger patients with a long history of splenomegaly, usually with a history of hematemesis. Females are affected almost equally as often as males in contrast to cirrhosis. The patients tolerate the bleeding episodes well. Death is usually due to massive hemorrhage. The diagnosis is achieved through a process of exclusion. A critical analysis of hemodynamic data, a splenoportogram, liver function tests (particularly Bromsulphalein retention) and angiographic data is mandatory. Needle biopsy of the liver appears to have limited value in making the diagnosis. The gross anatomic findings vary from a nearly normal liver to gross nodularity, seen particularly on the posteroinferior surface. In some cases these nodules are seen to physically impede the portal blood flow and contribute to portal hypertension. Phlebosclerosis of the smaller radicles of the portal vein and irregular scarring are the outstanding morphologic features of the disease. These changes are usually associated with irregular dilatation of some of the larger intrahepatic branches of the portal vein as well as fibroelastosis with or without occluding or organizing thrombi in both intra- and extrahepatic branches of the portal vein. The changes in hepatic venous radicles are characterized by irregular sclerosis, which seems to contribute significantly toward postsinusoidal block in advanced cases. The probable mode of evolution is discussed.
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PMID:The pathology of noncirrhotic portal fibrosis: a review of 32 autopsy cases. 46 24

In 19 patients with cirrhosis of the liver and portal hypertension, a catheter was inserted into the portal vein using a percutaneous transhepatic technique. The portal pressure was measured during general anaesthesia with and without halothane, and in the awake state. Addition of halothane to the N2O:O2 anaesthesia did not change portal venous pressure, in spite of a significant fall in arterial blood pressure. Portal venous pressure under general anaesthesia with complete muscle relaxation did not differ from the pressure in the resting, awake patient.
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PMID:Influence of general anaesthesia on portal pressure in liver cirrhosis and portal hypertension. 48 82

Ten male patients with cirrhosis of the liver (three with portacaval anastomosis [PCA]) and eight sex- and age-matched controls underwent an arginine infusion test followed by an intravenous glucose tolerance test. Plasma glucose and growth hormone (GH) levels were measured during a period of three hours. In the normal subjects, the peak GH response to arginine occurred 60 minutes after the start of the infusion and was followed by a progressive decline in GH concentration; dextrose injection resulted in a further rapid fall in GH concentration. In cirrhotic patients, both fasting and postarginine GH concentrations were significantly higher than in controls; in addition, the dextrose injection, after causing a transitory drop in plasma GH levels, resulted in a marked increase in plasma GH concentration. In the patients with PCA, the plasma GH increase after arginine and after dextrous was more marked. In these cirrhotic patients, the plasma GH levels correlated directly with the magnitude of the portal hypertension and inversely with the serum albumin concentration, suggesting that the abnormality of GH secretion was a reflection of the derangement in liver function.
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PMID:Altered control of growth hormone secretion in patients with cirrhosis of the liver. 48 48

In eight patients with cirrhosis of the liver and portal hypertension an intravenous infusion of lysine vasopressin induced a rapid increase in the plasma level of the fibrinolytic proenzyme plasminogen activator. In contrast, triglycyl lysine vasopressin (glypressin; GVP), in a dose known to lower portal venous pressure, produced no fibrinolytic response. This lack of fibrinolytic response represents an advantage of GVP over lysine vasopressin in addition to its longer in vivo half-life and lower cardiotoxicity. Clinical trials of GVP in the treatment of bleeding oesophageal varices are needed.
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PMID:Effects of lysine vasopressin and glypressin on the fibrinolytic system in cirrhosis. 48 51


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