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

The hepatopulmonary syndrome results from erythrocytes bypassing the lung without oxygenation. In addition to ventilation-perfusion mismatching, the hypoxemia may result from portapulmonary shunting, passage around alveoli through pleural and hilar blood vessels, and intrapulmonary vascular dilatations. Dilated vascular channels between arteries and veins on the pleural surface are seen more often than dilated intrapulmonary capillaries in chronic liver disease. These anastomoses appear grossly as vascular "spider nevi" on the pleura. Portal vein-to-pulmonary vein anastomoses could produce arterial hypoxemia because the deoxygenated portal venous blood can mix with oxygenated pulmonary venous blood. There is an association of esophageal varices with the hepatopulmonary syndrome and anastomoses between the portal veins and pulmonary veins have been found in both animals and humans. As portal pressures increase, the mediastinal veins enlarge, enhancing the chance that they may penetrate the pleura and drain into pulmonary veins. Direct splenic injections in patients, however, suggest that this shunt pathway is uncommon and small. Pulmonary artery injection studies have demonstrated dilated intrapulmonary vascular segments in humans and animals. Dilation of capillaries may allow a more rapid flow through the lung and the greater distance between the erythrocyte and alveolar wall may make it more difficult to oxygenate rapidly passing erythrocytes. Pulmonary capillary dilation can explain the abnormalities of the perfusion lung scan and contrast echocardiogram that portapulmonary shunting cannot. Pulmonary hypertension may occur in chronic liver disease even without arterial hypoxemia, but it is rare. The prevalence of hypertensive pulmonary vascular disease in patients with cirrhosis of the liver is less than 1%, although a higher percentage (2%) has been found when patients with portal hypertension were studied by cardiac catheterization. The hypertensive pulmonary vascular disease (pulmonary arteriopathy with plexiform lesions) that occurs in patients with liver disease appears identical to that encountered in patients with congenital cardiac shunts and unexplained (primary) pulmonary hypertension.
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PMID:Structural and pathologic changes in the lung vasculature in chronic liver disease. 866 83

We report three patients with cystic fibrosis and one patient with primary biliary cirrhosis and plexogenic pulmonary hypertension who have undergone heart-lung-liver transplantation as a combined procedure. Liver transplantation was necessary in the three patients with cystic fibrosis because of portal hypertension secondary to either hepatic fibrosis or established cirrhosis in addition to their advanced lung disease. Three of the four patients were alive at 20, 50, and 100 months after transplantation (one patient with cystic fibrosis died on day 16 of pneumonia) with well-preserved pulmonary function (forced expiratory volume in 1 second 110%, 49%, and 100% predicted, respectively), normal hepatic function and New York Heart Association class 1 performance status. Heart-lung and concurrent liver transplantation is a feasible and successful procedure with a satisfactory long-term outcome in selected patients with advanced pulmonary and hepatic disease.
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PMID:Heart-lung-liver transplantation. 877 10

Primary pulmonary hypertension (PPH) in patients with hepatic cirrhosis is often considered an unacceptable condition for liver transplantation because of increased morbidity and mortality during the procedure. We studied the incidence, characteristics, and final outcome of patients with PPH undergoing liver transplantation in our institution. Among the 226 patients undergoing 257 liver transplantations, eight (3.5%) fulfilled the conditions of PPH and responded to vasodilator therapy. Nitroglycerin 1.5 micrograms/kg produced a decrease in pulmonary vascular resistance index (PVRI) and mean pulmonary arterial pressure (MPAP) of 20% and 15%, respectively. Patients with PPH when compared with a matched group of patients without PPH had markedly increased hemodynamic changes in PVRI (P = 0.004) and MPAP (P = 0.0001) during and after the procedure. All patients with PPH required pulmonary vasodilator therapy after reperfusion of the new liver, while none in the group of patients without PPH required this therapy. Furthermore, after graft reperfusion, patients with PPH in which venovenous bypass was not used (n = 3), had a more compromised right ventricular function with a greater increase of central venous pressure (CVP) (90%) and MPAP (140%) when compared with patients with bypass or preservation of the recipient's vena cava (n = 5) in whom the increase of CVP and MPAP was 50% and 60%, respectively. Moderate PPH without a fixed level of pulmonary hypertension in patients undergoing liver transplantation is not related to an adverse outcome.
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PMID:Moderate primary pulmonary hypertension in patients undergoing liver transplantation. 883 2

Pulmonary hypertension is now recognized to be a rare association of liver disease and portal hypertension. This report describes the slow resolution of symptomatic pulmonary hypertension in a 33-year-old woman with cirrhosis who underwent isolated liver transplantation. The patient survived the surgery and perioperative period without significant haemodynamic compromise. After liver transplantation, the patient was monitored with regular Doppler echocardiography. By 27 months the pulmonary hypertension had almost completely resolved. This observation is important, as it suggests that patients with severe pulmonary hypertension who survive the perioperative period may have an excellent outcome, although resolution may be slow.
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PMID:Case report: delayed resolution of severe pulmonary hypertension after isolated liver transplantation in a patient with cirrhosis. 887 70

The association between portal venous hypertension and pulmonary arterial hypertension has received scarce attention in the italian medical literature. Nevertheless the association is relatively frequent, it needs a multidisciplinary approach and it is a stimulus for the search of causes of so-called primary pulmonary hypertension. The purpose of the article is to review the frequency of the association, the main pathogenetic hypothesis formulated to explain the appearance of pulmonary hypertension, the clinical and the laboratory findings, the evolution of the association and to present briefly a personal series of cases. The pulmonary arterial hypertension has been found in approximately 2% of patients with portal hypertension due to either hepatic cirrhosis or extraepatic lesions. Microembolism from the portocavat system or a number of vasoactive substances which enter the pulmonary circulation without being inactivated by the liver have been held responsible for the appearance of pulmonary hypertension in predisposed patients. Clinical and laboratory findings do not differ from those a patients with primary pulmonary hypertension. Also the prognosis is similar. In conclusion on accurate examination of the pulmonary circulation by noninvasive methods, in particular by echocardiography, appears to be mandatory in patients with chronic hepatic lesions. When pulmonary arterial hypertension is detected the study of the biochemical factors which at present are known to determine pulmonary hypertension may be warranted. The study may enhance our knowledge of the pathogenesis of the so-called primary pulmonary hypertension.
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PMID:[Association of pulmonary and portal hypertension]. 896 90

We investigated the long-term efficacy and the contraindications of single-session percutaneous ethanol injection (PEI) under general anesthesia in hepatocellular carcinoma (HCC). One hundred patients were treated from October, 1991, to April, 1996: 24 patients had a single capsulated HCC, 4.5 to 10 cm phi (group A); 62 had a single infiltrating tumor or multiple lesions (3 to 6), with 10 cm maximum phi (group B); 14 patients were in an advanced stage because of Child class C or of infiltrating tumors with portal thrombosis, with 14 cm lesion maximum phi (group C). Group A patients were treated because they were not operable or refused surgery. Three to 22 injections were performed (mean: 13) depending on tumor size and ethanol spread. The maximum injected volume of ethanol was 190 ml (mean: 57 ml). The procedure took 20 to 50 minutes (mean: 30 minutes). The mean hospital stay was 3.5 days. Tumor necrosis was complete in 58% of encapsulated tumors and > 70% in infiltrating lesions. The greatest lesion with complete post-PEI necrosis was 8.2 cm phi. A transient and variable increase in transaminase, bilirubin, white cell and D-dimer levels and a decrease in red cell, platelet, hemoglobin, fibrinogen and haptoglobin levels were observed. These changes were due to hepatic cell necrosis, hemolysis and focal thrombosis. One death (bleeding esophageal varices in the Child C patient)(1%) and four major complications (one peritoneal bleeding, one liver decompensation, two chemical segmentectomies with pain)(4%) were observed. 1, 2, 3 year survival rates for groups A, B and C were: 80, 63, 63%; 70, 50, 30% and 58, 14 and 0% respectively. In our experience, PEI was an efficacious procedure. The risk conditions are: superficial lesion site with severe coagulation defects, severe portal and/or pulmonary hypertension, esophageal varices at risk of bleeding, cardiac ischemia, advanced cirrhosis.
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PMID:[Single-session alcohol administration for hepatocarcinoma]. 942 44

Two patients with liver cirrhosis and clinical and autopsy features of pulmonary hypertension are presented. Others than liver's pathology secondary causes of hypertension in pulmonary circulation were not found. In both patients pulmonary hypertension had an influence on clinical course of basic disease. Taking this complication into consideration in the explanation of pathomechanisms of symptoms allowed us better to understand the clinical manifestation of liver disease in observed in our clinic cirrhotic patients.
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PMID:[Pulmonary hypertension during the course of liver cirrhosis--presentation of two cases]. 944 Dec 91

A patient with end-stage liver disease as a result of alpha1-antitripsin deficiency presented for orthotopic liver transplantation. The liver cirrhosis was complicated by portal hypertension and hepatopulmonary syndrome resulting in varicosities and severe hypoxia (room air oxygen saturation 69%). After transplantation, the hepatopulmonary syndrome improved but, over the next 14 months, the patient developed severe pulmonary hypertension. Six years posttransplantation, his room air oxygen saturation was 95% with pulmonary artery pressures of 109 mm Hg systolic and 26 mm Hg diastolic (mean 55 mm Hg) and a pulmonary vascular resistance 688 dynes x sec x cm.
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PMID:Severe pulmonary hypertension and amelioration of hepatopulmonary syndrome after liver transplantation. 951 72

Pulmonary hypertension (PH) is a classic complication associated with intravenous drug addiction. Various pathogenic mechanisms may be involved but HIV infection now appears to be the main etiologic factor. We report herein 10 case of PH occurred in HIV+ intravenous drug abusers. Each patient had several pathogenic factors: HIV infection, pills crushed and intravenously injected (6 cases), heavy and repeated consumption of amphetamines and cocaine (6 cases), cirrhosis with portal hypertension (2 cases), anticardiolipid antibodies (2 cases). The clinical findings were similar to those reported for PH in HIV seronegative patients; however, in 5 cases, opiates could have alleviated dyspnea, which became perceptible only at the time of drug withdrawal. Because drug addicts usually exhibit a weak support for medical prescriptions, long term therapy needing regular follow-up such as anticoagulation appears to be hazardous and even dangerous. The prognosis remains poor, since the progression of PH led to the death of one third patients within the year following the diagnosis.
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PMID:[Pulmonary artery hypertension in HIV seropositive drug addicts. Apropos of 10 cases]. 955 21

Cirrhosis and portal hypertension may be associated with pulmonary hypertension and pulmonary dysfunction. However, morphological pulmonary vascular lesions in patients with cirrhosis have not been well characterized morphometrically. We morphometrically evaluated pulmonary vessels in liver transplant recipients with pretransplantation cirrhosis and correlated our findings with pretransplantation cardiopulmonary function, postoperative course, and postmortem cardiopulmonary findings. Autopsy lung slides from 23 transplant recipients with pretransplantation cirrhosis were examined. External vessel diameter, intimal thickness, and arterial medial thickness were measured with a micrometer after pentachrome staining. The percent of total diameter comprised by intima or media was calculated for each vessel. Medical records were reviewed for smoking history, pretransplantation cardiopulmonary function testing, and postoperative course. Autopsy cases without liver or significant cardiopulmonary diseases, matched for age, sex, and smoking history, served as controls. Transplant recipients had significantly more pulmonary venous intimal thickening than matched controls (P <.0001). Sixty-five percent (15 of 23) of these patients had some degree of pretransplantation pulmonary dysfunction, defined by abnormalities in pulmonary function tests, oxygen saturation, and/or increased pulmonary artery pressures. However, the severity of venous intimal thickening did not correlate with the severity of pretransplantation pulmonary dysfunction. Arterial intimal and medial thickness were not statistically significantly different from controls. Pulmonary venous intimal thickening and resultant luminal impingement are morphological findings not previously described in this population. The arterial lesion, when present, is similar to that seen in pulmonary hypertension from other causes. These pulmonary vascular lesions may be implicated in pulmonary dysfunction in patients with cirrhosis and may be associated with increased posttransplantation cardiopulmonary morbidity and mortality.
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PMID:Pulmonary vascular morphological changes in cirrhotic patients undergoing liver transplantation. 987 94


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