The differential diagnosis at this point might include the following:
acute hepatitis (viral or alcohol-, chemical-, or drug-induced)
chronic active hepatitis (viral types B, C, D)
granulomatous or neoplastic infiltration
Among causes of acute hepatitis, alcohol is less likely because the SGPT level is greater than the SGOT level. With normal alkaline phosphatase, primary biliary cirrhosis or bile duct obstruction are also not probable.
Viral hepatitis should be ruled out by serologic testing. Imaging studies such as CAT, MRI, or liver-spleen scan would be appropriate. An angiogram would be helpful if angiosarcoma is suspected. Direct indicators, such as urinary thiodiglycolic acid or vinyl chloride levels, would be helpful only if exposure to vinyl chloride were recent. Negative results in tests measuring these direct indicators, however, would not rule out drinking water contamination, for example.
The differential diagnosis now most likely includes cirrhosis and malignancy. Hepatic angiosarcoma is not normally prominent in the differential diagnosis of liver function abnormalities. However, the test results thus far and the fact that this is a nonoccupational exposure to vinyl chloride (nonmalignant liver injury has not been reported in environmental exposures) make angiosarcoma of the liver a possibility. In the case of angiosarcoma of the liver, hepatic arteriography would reveal a characteristic appearance, with displacement of hepatic arteries, and a blush and “puddling” during the middle of the arterial phase. Percutaneous liver biopsy is contraindicated in cases of angiosarcoma because of the vascular nature of the tumor and the possibility of complicating thrombocytopenia or significant bleeding; laparoscopic biopsy would be more appropriate.
Hepatic angiosarcoma grows rapidly and carries a poor prognosis. If untreated, most patients die within 6 to 12 months after diagnosis. The only long-term survivors have had the tumor successfully resected. As a precaution you might suggest that the patient ventilate new cars before entering them for prolonged periods and drive with the window open to maintain ventilation. Until the drinking water at his home is tested, the family should use bottled water to avoid any possible exposure there.
Since the rest of the family and the nearby community may have had similar exposure to vinyl chloride, all should undergo periodic testing of transaminases, alkaline phosphatase, and serum bile acids to detect latent chemical injury. If these tests or an ICG clearance rate are positive for hepatic injury, biopsy may also be helpful. If the drinking water is not contaminated and there is no vinyl chloride waste disposal source to contaminate the water in the future, the exposure to the family and community has likely terminated.
Your local, county, or state health department should be contacted and notified of the possible case. Because hepatic angiosarcoma is an extremely rare disease, even one case would alert public health authorities to a potential risk to the community around this plant. Your report should initiate case-finding investigations among the former workers at the plant as well as in the community. Public health authorities may also want to evaluate the potential for groundwater contamination around the plant.
More information on the adverse effects of vinyl chloride and the treatment and management of vinyl chloride-exposed persons can be obtained from ATSDR, your state and local health departments, and university medical centers. Case Studies in Environmental Medicine: Vinyl Chloride Toxicity is one of a series. For other publications in this series, please use the order form on the back cover. For clinical inquiries, contact ATSDR, Division of Health Education, Office of Director, at (404) 639–0730.