"Late presenters" after paracetamol self poisoning

Abstract

The popularity of paracetamol as a drug for self poisoning has increased dramatically since the early 1980s 1 2 ; nowadays almost 50% of episodes of self poisoning presenting to hospital involve the ingestion of paracetamol or paracetamol containing drugs. [3][4][5] It is estimated that about 70 000 episodes of paracetamol self poisoning occur each year in Britain. 6 Although serious morbidity and deaths are rare, 6 7 these usually result from late presentation, which reduces the eVectiveness of available antidotes. 8 9 The epidemiology of paracetamol self poisoning has not previously been described in detail in relation to recorded delays in presentation for treatment. We studied, retrospectively, all episodes of paracetamol self poisoning occurring at either of the two acute hospital units in Nottingham during the first six months of 1996. These included patients seen only in the accident and emergency department, as well as those admitted for inpatient care. Methods and resultsIn Nottingham all patients presenting with suspected or confirmed self poisoning involving paracetamol undergo testing for plasma paracetamol concentrations. The results are routinely recorded in a computerised laboratory database from which all positive tests (>5 mg/l) were identified and subsequently confirmed by reference to the clinical records of each person. During the first six months of 1996 we noted 417 episodes involving 361 people; data on time of ingestion and presentation were available for 330 episodes (79.1%) involving 294 people (81.4%). To avoid bias caused by repeat attenders, only the first presentation by each person during the study period was used in the analysis. Persons in whom the time of ingestion was unknown were more likely to be male (51% versus 42%) but this diVerence was not significant ( 2 =1.9 with 1 df, p=0.17). Similarly, no significant diVerences were detected with respect to age group (0-24 years versus 25-44 versus >45: 2 =2.0 with 2 df, p=0.37); however, persons were more likely to be admitted to hospital when time of ingestion was unknown (67% versus 42%, 2 =14.1 with 1 df, p=0.0002). It was not possible to compare the amounts ingested by these two groups, because of the large number of cases in which both time and amount were unknown. In 132 of 361 cases (36.6%) paracetamol was ingested as a constituent of a fixed ratio combination product, in 110 cases (30.5%) together with other separate pharmaceutical products, and in 133 cases (36.8%) with alcohol. Serum paracetamol concentrations measured less than four hours after ingestion are unlikely to represent peak concentration; therefore unless the amount ingested has been very large or the time of ingestion cannot be determined, treatment is not started until the four hour concentration is known. Accordingly, we designated presentation times within four hours as "optimal", but any longer than this as potentially delaying the onset of eVective treatment. While we found that the majority of patients who had taken a paracetamol overdose (71.1%) presen...

Ease of access is a principal factor in the frequency of paracetamol overdose

“…21 It appears that men more than women place themselves at increased risk before presenting for treatment after paracetamol overdose. 22 In our study, we encountered more females following paracetamol overdose. However, males were more likely to take significantly larger amounts, delay longer before presentation and take the overdose with alcohol.…”

Paracetamol, alcohol and the liver

“…However, alcoholics may appear to be more susceptible to the hepatotoxicity of paracetamol because they often present late. Patients who present late are more severely poisoned and have a much worse prognosis than those who come to hospital early, regardless of alcohol intake [106–109]. In addition, the apparent association of severe liver damage and excessive alcohol intake largely reflects a population which is likely to take overdoses [108].…”

“…Thus alcohol inhibited the toxic metabolic activation of paracetamol by human liver microsomes [71] and it produced a major reduction in the fractional urinary excretion of the cysteine and mercapturic acid conjugates of paracetamol in healthy nonalcoholic volunteers [144–147] as well as in heavy drinkers [148]. A substantial proportion of patients who take overdoses of paracetamol have also taken alcohol at the same time [18, 107, 109, 112, 149] and this appears to protect them against liver damage [111, 150]. The protective action of alcohol taken at the time of an overdose probably adds significantly to the large individual variation in susceptibility to the toxicity of paracetamol.…”