Abstract
BackgroundHepatopulmonary syndrome (HPS) is defined by liver dysfunction, intrapulmonary vascular dilatations, and impaired oxygenation. The gold standard for detection of intrapulmonary vascular dilatations in HPS is contrast echocardiography. However, two small studies have suggested that patients with HPS have larger segmental pulmonary arterial diameters than both normal subjects and normoxemic subjects with cirrhosis, when measured by CT. We sought to compare CT imaging-based pulmonary vasodilatation in patients with HPS, patients with liver dysfunction without HPS, and matching controls on CT imaging.MethodsWe performed a retrospective cohort study at two quaternary care Canadian HPS centers. We analyzed CT thorax scans in 23 patients with HPS, 29 patients with liver dysfunction without HPS, and 52 gender- and age-matched controls. We measured the artery-bronchus ratios (ABRs) in upper and lower lung zones, calculated the “delta ABR” by subtracting the upper from the lower ABR, compared these measurements between groups, and correlated them with clinically relevant parameters (partial pressure of arterial oxygen, alveolar-arterial oxygen gradient, macroaggregated albumin shunt fraction, and diffusion capacity). We repeated measurements in patients with post-transplant CTs.ResultsPatients had significantly larger lower zone ABRs and delta ABRs than controls (1.20 +/- 0.19 versus 0.98 +/- 0.10, p<0.01; and 0.12 +/- 0.17 versus -0.06 +/- 0.10, p<0.01, respectively). However, there were no significant differences between liver disease patients with and without HPS, nor any significant correlations between CT measurements and clinically relevant parameters. There were no significant changes in ABRs after liver transplantation (14 patients).ConclusionsBasilar segmental artery-bronchus ratios are larger in patients with liver disease than in normal controls, but this vasodilatation is no more severe in patients with HPS. CT does not distinguish patients with HPS from those with uncomplicated liver disease.
Highlights
Hepatopulmonary syndrome (HPS) is a rare pulmonary vascular complication of liver disease, defined by hepatic dysfunction, intrapulmonary vascular dilatations (IPVDs), and impaired oxygenation
There were no significant differences between liver disease patients with and without HPS, nor any significant correlations between CT measurements and clinically relevant parameters
Basilar segmental artery-bronchus ratios are larger in patients with liver disease than in normal controls, but this vasodilatation is no more severe in patients with HPS
Summary
Hepatopulmonary syndrome (HPS) is a rare pulmonary vascular complication of liver disease, defined by hepatic dysfunction, intrapulmonary vascular dilatations (IPVDs), and impaired oxygenation. IPVDs are thought to be caused by nitric oxide-mediated vasodilatation of muscularized arterioles immediately proximal to the pulmonary capillaries, resulting in flow-mediated dilatation of alveolar septal capillaries[3] In severe cases, this leads to impairment of oxygenation, resulting in HPS. Two prior studies have suggested that patients with HPS have larger segmental pulmonary arterial diameters than both normal subjects and normoxemic subjects with cirrhosis, when measured by high resolution CT[5,6]. Both were small studies subject to methodological limitations. We sought to compare CT imaging-based pulmonary vasodilatation in patients with HPS, patients with liver dysfunction without HPS, and matching controls on CT imaging
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