Pulmonary dysfunction and hepatopulmonary syndrome in cirrhosis and portal hypertension
Article first published online: 2 SEP 2009
© 2009 John Wiley & Sons A/S
Volume 29, Issue 10, pages 1528–1537, November 2009
How to Cite
Møller, S., Krag, A., Madsen, J. L., Henriksen, J. H. and Bendtsen, F. (2009), Pulmonary dysfunction and hepatopulmonary syndrome in cirrhosis and portal hypertension. Liver International, 29: 1528–1537. doi: 10.1111/j.1478-3231.2009.02103.x
- Issue published online: 1 OCT 2009
- Article first published online: 2 SEP 2009
- Received 5 May 2009Accepted 12 July 2009
- cardiovascular dysfunction;
- central circulation time;
- diffusion abnormalities;
- hepatopulmonary syndrome;
- hyperdynamic circulation;
- oxygen inhalation
Background: Pulmonary dysfunction including the hepatopulmonary syndrome (HPS) is an important complication to cirrhosis and portal hypertension. However, the precise relation to liver dysfunction and the prevalence of HPS are unclear.
Aims: We therefore aimed to assess (i) the prevalence of HPS in consecutive alcoholic cirrhotic patients, (ii) the degree of pulmonary dysfunction in relation to liver function and (iii) the response of a 100% oxygen test on cardiopulmonary and peripheral oxygenation.
Methods: Fifty patients with cirrhosis and 12 matched healthy controls were entered in this study. All underwent haemodynamic and pulmonary investigations [lung diffusing capacity for carbon monoxide (DLCO), contrast-enhanced echocardiography and detection of extrapulmonary shunt fraction]. A 100% oxygen test was performed with the assessment of arterial oxygen tension (PaO2), the alveolar-arterial oxygen gradient (AaPO2) and peripheral transcutaneous oxygen tension (tcPO2).
Results: The prevalence of HPS was 10%. PaO2 and DLCO were reduced in 32 and 72% and AaPO2, was increased in 60% of the patients respectively. DLCO correlated with indicators of liver dysfunction (galactose elimination capacity, P<0.01, indocyanine green clearance, P<0.001), portal hypertension (post-sinusoidal resistance, P<0.01) and central hypovolaemia (central and arterial blood volume, P<0.01). After 100% oxygen inhalation, the changes in PaO2, AaPO2, tcPO2 and heart rate were abnormal in the patients compared with controls (P<0.02).
Conclusions: Pulmonary dysfunction in alcoholic cirrhosis is common and relates to different aspects of liver dysfunction, whereas the prevalence of HPS is low. The haemodynamic response to oxygen inhalation is clearly impaired and HPS and pulmonary dysfunction seem to be caused by different pathophysiological mechanisms.