Hepatopulmonary syndrome: prevalence and predictive value of various cut offs for arterial oxygenation and their clinical consequences

Background: The hepatopulmonary syndrome (HPS) is defined as the triad of liver disease, arterial deoxygenation, and pulmonary vascular dilatation. The reported prevalence of HPS in cirrhotic patients varies between 4% and 19%, and various threshold values defining arterial deoxygenation have been u...

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Published in:	Gut Vol. 51; no. 6; pp. 853 - 859
Main Authors:	Schenk, P, Fuhrmann, V, Madl, C, Funk, G, Lehr, S, Kandel, O, Müller, C
Format:	Journal Article
Language:	English
Published:	London BMJ Publishing Group Ltd and British Society of Gastroenterology 01-12-2002 BMJ BMJ Publishing Group Ltd BMJ Publishing Group LTD Copyright 2002 by Gut
Subjects:	AaDO2 Age Aged Alcohol alveolar-arterial difference for the partial pressure of oxygen Arteries Biological and medical sciences Blood Gas Analysis Colleges & universities Confidence intervals contrast echocardiography Echocardiography Embolisms Female FEV1 forced expiratory volume in one second Gastroenterology. Liver. Pancreas. Abdomen Heart hepatopulmonary syndrome Hepatopulmonary Syndrome - blood Hepatopulmonary Syndrome - diagnosis HPS Humans Hypertension hypoxaemia Liver cirrhosis Liver Cirrhosis - blood Liver Disease Liver diseases Liver. Biliary tract. Portal circulation. Exocrine pancreas Lung diseases Male Medical sciences Middle Aged OLT orthotopic liver transplantation Other diseases. Semiology Oxygen - blood PaCO2 PaO2 partial pressure of arterial carbon dioxide partial pressure of arterial oxygen portal hypertension Predictive Value of Tests Prevalence pulmonary vasodilation Respiratory Function Tests TLC total lung capacity Ultrasonic imaging Human Lung disease Prevalence Respiratory disease Liver Lung Cardiovascular disease Hepatic disease Statistical study Standards Vascular disease Arterial blood Cirrhosis Dilatation Blood vessel Deoxygenation Digestive diseases Complication
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Summary:	Background: The hepatopulmonary syndrome (HPS) is defined as the triad of liver disease, arterial deoxygenation, and pulmonary vascular dilatation. The reported prevalence of HPS in cirrhotic patients varies between 4% and 19%, and various threshold values defining arterial deoxygenation have been used and recommended previously. However, it is not known how the prevalence of HPS differs using different cut off values for arterial deoxygenation. Methods: We studied 127 patients for the presence of HPS using transthoracic contrast echocardiography for detection of pulmonary vasodilation, pulmonary function tests, and blood gas analysis. Results: Ninety eight patients were included in the study, of whom 33 (34%) had a positive contrast echocardiography. Using an increased alveolar-arterial difference for the partial pressure of oxygen (AaDO2) as an indication of hypoxaemia, the prevalence of HPS was considerably higher (>15 mm Hg, 32%; >20 mm Hg, 31%; and >age related threshold, 28%) than using reduced partial pressure of arterial oxygen (PaO2) as a threshold (<80 mm Hg, 19%; <70 mm Hg, 15%; and <age related threshold, 15%). For AaDO2 as the cut off, the positive predictive value for a diagnosis of HPS was low (34%, 37%, and 53%, respectively). In contrast, PaO2 as a cut off had considerably higher positive predictive values (44%, 93%, and 94%, respectively). Introducing PaO2 <65 mm Hg as the cut off, the positive predictive value increased to 100%. Dyspnoea was more often present in patients with “clinically significant” HPS (57%) compared with “subclinical HPS” (8%), and patients without HPS (6%). The Child-Pugh score correlated significantly with the severity of HPS. Two of five liver transplanted patients with “subclinical HPS” had embolic brain infarcts, possibly induced by venous emboli passing through dilated intrapulmonary vessels. Conclusions: Defining arterial hypoxaemia in HPS by different, previously used, cut off values for arterial oxygenation leads to a wide variation in the prevalence of HPS in the same sample of cirrhotic patients.
Bibliography:	PMID:12427789 ark:/67375/NVC-XM728GDL-F local:0510853 href:gutjnl-51-853.pdf istex:A89CD71DA24073D037F9B604AE43E32111CA96A5 Correspondence to:  Dr P Schenk, Department of Internal Medicine IV, Intensive Care Unit 13 H1, University of Vienna, Allgemeines Krankenhaus, Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria;  Peter.Schenk@akh-wien.ac.at ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Correspondence to: Dr P Schenk, Department of Internal Medicine IV, Intensive Care Unit 13 H1, University of Vienna, Allgemeines Krankenhaus, Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria; Peter.Schenk@akh-wien.ac.at
ISSN:	0017-5749 1468-3288 1458-3288
DOI:	10.1136/gut.51.6.853