Hepatopulmonary syndrome: A prospective study of relationships between severity of liver disease, PaO₂ response to 100% oxygen, and brain uptake after ^99mTc MAA lung scanning

Background: Because of the spectrum of intrapulmonary vascular dilation that characterizes hepatopulmonary syndrome (HPS), PaO₂ while breathing 100% oxygen varies. Abnormal extrapulmonary uptake of ^99mTc macroaggregated albumin (MAA) after lung perfusion is common. Goal: To describe relationships between (1) severity of liver disease measured by the Child-Pugh (CP) classification; (2) PaO₂ while breathing room air (RA) and 100% oxygen on 100% oxygen; and (3) extrapulmonary (brain) uptake of ^99mTc MAA after lung scanning. Methods and patients: We prospectively measured PaO₂ on RA, PaO₂ on 100% oxygen, and brain uptake after lung perfusion of ^99mTc MAA in 25 consecutive HPS patients. Results: Mean PaO₂ on RA, PaO₂ on 100% oxygen, PaCO₂ on RA, and ^99mTc MAA brain uptake were similar when categorized by CP classification. Brain uptake was abnormal (≥ 6%) in 24 patients (96%). Brain uptake was 29 ± 20% (mean ± SD) and correlated inversely with PaO₂ on RA (r = -0.57; p < 0.05) and PaO₂ on 100% oxygen (r = -0.41; p < 0.05). Seven patients (28%) had additional nonvascular pulmonary abnormalities and lower PaO₂ on 100% oxygen (215 ± 133 mm Hg vs 391 ± 137 mm Hg; p < 0.007). Eight patients (32%) died. Mortality in patients without coexistent pulmonary abnormalities was associated with greater brain uptake of ^99mTc MAA (48 ± 18% vs 25 ± 20%; p < 0.04) and lower PaO₂ on RA (40 ± 7 mm Hg vs 57 ± 11 mm Hg; p < 0.001). Conclusion: The degree of hypoxemia associated with HPS was not related to the CP severity of liver disease. HPS patients with additional nonvascular pulmonary abnormalities exhibited lower PaO₂ on 100% oxygen. Mortality was associated with lower PaO₂ on RA, and with greater brain uptake of ^99mTc MAA.