Six hundred sixty-two consecutive patients with acetaminophen overdoses were evaluated. Those at risk on the basis of their acetaminophen blood levels, as plotted on the study nomogram, were treated with oral acetylcysteine. Statistically significant differences in severity of hepatic toxicity were observed between patients treated within 16 hours after ingestion and those treated between 16 and 24 hours after ingestion. No deaths occurred among patients treated within 24 hours of ingestion, except for one patient who was an alleged gunshot homicide. Seven percent of patients with plasma acetaminophen levels in the potentially toxic range and treated with acetylcysteine within ten hours of ingestion showed transient SGOT level elevations, whereas 29% of those treated between ten and 16 hours after ingestion and 62% of those treated between 16 and 24 hours after ingestion showed such transient toxicity. No consistent difference in hepatotoxicity could be demonstrated between those patients with a history of chronic alcohol use and those patients with no history of chronic alcohol use. Acute alcohol use resulted in less severe toxic reactions than in those patients without acute alcohol use.

Acetaminophen (paracetamol in British literature) is a metabolite of phenacetin which has become increasingly popular as a substitute for salicylates.1 The popularity of acetaminophen has been encouraged by the medical profession because it is allegedly safer than aspirin.2 However, experience in Britain indicates that acute acetaminophen overdosage is both common and significantly more toxic than of salicylates.3-7 Although it is widely used in the United States, only one report describing a single American patient has appeared in the literature.8 This is a puzzling situation. It is axiomatic that if you do not look for something you will not diagnose it. This may provide the answer as there is apparently a general lack of knowledge in the United States concerning the toxicity of acetaminophen. Indeed, one of us (B.H.R.) contacted nine American University poison services in the spring of 1973 and discovered that none had clinical experience or analytical methods in operation. During the past year, however, with a high index of suspicion in Denver, 156 ingestions with four fatalities have been recorded. Because of the nonspecific initial features of acute overdosage, the lack of coma, the delay in onset of jaundice and the rapid fall in detectable plasma levels of acetaminophen, the cause-and-effect relationship may be missed in even a floridly ill or dying patient. Hepatoxicity is the most remarkable feature and the question must be raised as to how many cases of "jaundice of unknown etiology" are actually due to this drug. This review is intended to provide an understanding of the current knowledge of this drug. It should be noted that although toxicity and fatalities have occurred in the adolescent age group, only one death in younger children has been recorded.

No abstract

Acetaminophen overdose was studied in 416 patients as part of a nationwide multiclinic open study. Twenty-seven percent of the patients were toxic by plasma acetaminophen level. The 12- to 21-year-old age group had the highest incidence of toxic blood levels (47%). Children under age 5 had the mildest toxicity of any age group; only two of 16 patients had toxic blood levels. No relationship to subsequent Reye's syndrome could be demonstrated. Acetylcysteine is a safe, effective treatment if administered within the first ten hours; it has some efficacy with no toxicity if used after ten hours. Acetylcysteine has advantages over both cysteamine and methionine. All patients in this study recovered with no sequelae.