Structural alterations to the pulmonary circulation in fulminant hepatic failure.
Like patients with chronic liver disease, those with coma due to fulminant hepatic failure may show arterial hypoxaemia even in the absence of pulmonary complications, and in both it is attributed to increased intrapulmonary arteriovenous admixture. This study is concerned with the structural alterations in the pulmonary circulation of patients who have died from fulminant hepatic failure. Precise quantitative morphometric techniques applied to the injected and inflated lung have shown the major abnormality to be a diffuse dilatation of the pulmonary vascular bed affecting arteries and veins of all structural types. At an intra-acinar level the diameter of arteries accompanying respiratory bronchioles was 232.97 micron (+/-SD 46.35) compared with 177.76 micron (+/-SD 30.43) in controls (P less than 0.01). In two-thirds of the patients pleural spider naevi were seen and, throughout the lung, similar significant dilatation of precapillary vessels; but in only one patient were precapillary anastomoses shown. While intrapulmonary venous admixture undoubtedly contributes to hypoxia in fulminant hepatic failure, its exact relation to the structural changes is not yet determined.
D000293:Adolescent; D000328:Adult; D001158:Arteries / Q000473:pathology; D002196:Capillaries / Q000473:pathology; D004108:Dilatation, Pathologic; D005260:Female; D006501:Hepatic Encephalopathy / Q000473:pathology*; D006801:Humans; D008107:Liver Diseases / Q000473:pathology*; D008168:Lung / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011652:Pulmonary Circulation