The mechanism of action of acetylcysteine in the treatment of carbon tetrachloride poisoning is unclear, but it may serve as a free radical scavenger or may maintain intracellular glutathione stores (Chyka et al., 2000) and its early use may protect against carbon tetrachloride toxicity (Mathieson et al., 1985; ATSDR, 1992a). Acetylcysteine is relatively safe and easily available and should be considered for serious carbon tetrachloride poisoning.
In a study of 19 patients with acute carbon tetrachloride poisoning (confirmed by laboratory analysis), 13 were treated with acetylcysteine and had evidence of milder hepatic damage than the 6 patients who did not receive this treatment (Ruprah et al., 1985). In another case successfully treated with acetylcysteine, this patient's serum carbon tetrachloride concentrations remained elevated for several days post ingestion (probably due to re-entry into the circulation from adipose tissue). Consequently it is recommended that acetylcysteine is given for longer than the regimen (20 hours) used in paracetamol poisoning (Mathieson et al., 1985).
• Hyperbaric oxygen
It is thought that elevated hepatic oxygen tensions may potentially alter the metabolism of carbon tetrachloride. In theory, oxygen may inhibit the NADPH-dependent reducing enzyme system resulting in formation of less ^CCl3 free radical, by shifting the conversion of ^CCl3 towards the CCl3OO^ pathway. It is proposed that the highly reactive CCl3OO^ (compared with •CC^), may destroy the enzyme system thereby preventing production of further free radical intermediates (Kubic and Anders, 1980; Truss and Killenberg, 1982; Burkhart et al., 1991). Hyperbaric oxygen therapy has been recommended for potentially lethal doses of carbon tetrachloride (Burkhart et al., 1991). However, other authors have stated that, due to the free radical nature of the toxic intermediates in carbon tetrachloride metabolism, hyperbaric oxygen is contraindicated (ATSDR, 1992a)
• Free radical scavengers
Treatment of carbon tetrachloride poisoning with free radical scavengers such as ascorbic acid or vitamin E, has been shown to be effective only if administered before or simultaneously with exposure to carbon tetrachloride (Truss and Killenberg, 1982). Consequently, these are unlikely to be of benefit in the clinical situation.
Carbon tetrachloride liver cirrhosis results from the accumulation of bile acids that are not being detoxified in the enterohepatic circulation. In rat studies, administration of cholestyramine, which has a strong affinity for bile acids in the intestine, decreases the induction of cirrhosis (De Heer et al., 1980). This is only an experimental therapy and human case data are lacking.
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