Gastroenterology

Gastroenterology

Volume 131, Issue 1, July 2006, Pages 69-75
Gastroenterology

Clinical–liver, pancreas, and biliary tract
Hepatopulmonary Syndrome in Patients With Hypoxic Hepatitis

https://doi.org/10.1053/j.gastro.2006.04.014Get rights and content

Background & Aims: The hepatopulmonary syndrome (HPS) is defined as the triad of liver disease, arterial deoxygenation, and widespread pulmonary vasodilatation. Hypoxic hepatitis, also known as ischemic hepatitis, is the leading cause of acute liver impairment in hospitals. It is unknown whether HPS occurs in hypoxic hepatitis. We assessed the prevalence and clinical consequences of HPS in patients with hypoxic hepatitis. Methods: Forty-four patients with hypoxic hepatitis were screened prospectively for HPS using established criteria: (1) presence of hepatic disease, (2) increased alveolar-arterial difference for the partial pressure of oxygen greater than the age-related threshold, and (3) intrapulmonary vasodilatation detected via contrast-enhanced echocardiography. Sixty-two critically ill patients with different cardiopulmonary diseases but without hepatic disease were screened for prevalence of intrapulmonary vasodilatation as a control group. Results: Criteria of HPS were fulfilled in 18 patients with hypoxic hepatitis. HPS-positive patients had a significantly decreased partial pressure of arterial oxygen (P = .001) and partial pressure of arterial oxygen/fraction of inspired oxygen ratio (P = .034) at the time of diagnosis of HPS, a significant decreased area under the curve of the partial pressure of arterial oxygen/fraction of inspired oxygen ratio during the first 48 hours after diagnosis of hypoxic hepatitis (P = .009), and a significantly increased peak serum aspartate transaminase level (P = .028), compared with patients without HPS. Complete resolution of intrapulmonary vasodilatation was observed during follow-up evaluation. Contrast-enhanced echocardiography was negative for intrapulmonary vasodilatation in all 62 control patients. Conclusions: Intrapulmonary vasodilatation indicating HPS frequently occurs in patients with hypoxic hepatitis. It is reversible after normalization of the hepatic dysfunction. Clinicians should consider intrapulmonary vasodilatation and HPS in patients with hypoxic hepatitis.

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Patients

A total of 646 patients were admitted to our intensive care unit (ICU) between October 2003 and May 2005. Forty-four patients fulfilled the criteria of HH and were screened for the presence of HPS.

The control group consisted of all the remaining 602 patients, who fulfilled the following criteria: (1) presence of cardiogenic pulmonary edema, pneumonia, acute respiratory distress syndrome, chronic obstructive pulmonary disease, pleural effusion, atelectasis, or pulmonary embolism; (2) no sign of

Study Population

Data were collected and analyzed in a total of 44 critically ill patients with HH. Figure 1 shows the recruitment algorithm of the study patients.

The median age of the study patients was 62 years (range, 22–83 years); 29 (66%) were men and 15 (34%) were women. The mean acute physiologic and chronic health evaluation III score was 82 ± 31. Demographic data and patients’ characteristics are summarized in Table 1.

Control Population

The control group consisted of 62 critically ill patients without HH but several

Discussion

HPS is a known complication of chronic liver disease associated with increased morbidity and mortality.1, 2, 25 Most of the clinical studies focused on patients with cirrhosis. There are only a few cases reporting the occurrence of HPS in patients without cirrhosis.3, 4, 5, 6, 7, 8, 9 A histopathologic study of the lungs in patients who died of fulminant hepatic failure revealed pleural spider nevi, diffuse dilatation of the pulmonary vascular bed affecting arteries, precapillary vessels, and

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