• Accidental ingestion (Board, 1866; Storms, 1973) and inhalation (Allan et al., 1988)

• Intravenous injection (Timm and Moser, 1975; Rao et al., 1993)

• Clinical anaesthesia (Payne 1981; Thorpe and Spence, 1997)

• Criminal use, e.g., robbery, assault, homicide (McGee et al., 1987; McIntyre, 1988; Nashelsky et al., 1995; Vendura et al., 1996).

Ingestion of as little as 10 ml may cause CNS depression and death (Baselt, 2000). A 17 year old male survived ingestion of 4 ounces (114 ml) of chloroform (Schroeder, 1965), but the same quantity was fatal in a 42 year old (Board, 1866). Three ounces (84 ml) was survived by a 19 year old female (Waterston and Robinson, 1898). In a more recent case an adult survived ingestion of 230 ml of chloroform after treatment with acetylcysteine (Boyer et al., 1998). Intravenous injection of 0.5 ml of chloroform in a 21 year old man caused hepatotoxicity and lung changes, but he recovered within 3 days (Timm and Moser, 1975).

There has been concern over the risk of delayed chloroform poisoning (onset usually 2 days) after anaesthesia. This is usually attributed to liver damage and clinical effects include vomiting, jaundice, restlessness, delirium, coma and death. However, after reviewing the literature on 'delayed chloroform poisoning' from the mid-19th century onwards, Thorpe and Spence (1997) concluded that the risk was not as great as originally thought. Many reported cases did not stand up to scrutiny and the clinical features were not consistent with liver failure. Nine studies comparing the toxicity of various anaesthetics did not show a clinically significant difference in liver damage with chloroform. However, the numbers were small in most studies. Other causes of liver damage in these patients may have included hypoxia and hypercapnia. There may also have been predisposing factors such as dehydration, acidosis and alcoholism.

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