Biomedical subjects

B B Lystbaek

Publications and source records attributed to B B Lystbaek.

3 recordsLinked to original sources

PubMed1995

[Paracetamol poisoning].

Administration of paracetamol (acetaminophen) has analgetic and antipyretic effect. After trauma paracetamol has an anti-inflammatory activity. It was presumed that paracetamol in therapeutic doses had fewer and more acceptable side-effects than other analgetic drugs such as acetylsalicylic acid and NSAID-drugs. However, in toxic concentrations, paracetamol is more life-threatening. The toxic effects of paracetamol most often occur in the liver and kidneys. Phosphate and lactate turn-over can also be impaired. Paracetamol poisoning can induce temporary liver dysfunction or even irreversible liver failure with liver transplantation as the only therapeutic possibility. Chronic alcoholics are especially at risk, as liver damage may occur following paracetamol even in recommended doses. When intoxication with paracetamol is presumed, administration of N-acetylcysteine is vital. N-acetylcysteine therapy should be initiated not later than 15 hours after paracetamol intake. Moreover, the antitoxic effect has been observed even when N-acetylcysteine therapy is initiated 24-36 hours after presumed paracetamol intake. Measures of preventing further absorbtion of paracetamol from the gastrointestinal tract should be taken. Activated charcoal should be given if less than two hours have passed since paracetamol intake. Between two and four hours following paracetamol intake gastric lavage should be performed. During the last 10 years the incidence of paracetamol self-poisoning has increased, but death following paracetamol poisoning is relatively constant at around nine per year in Denmark. It is suggested that the incidence of serious cases of paracetamol poisoning could be reduced by simple measures. Special attention should be paid to the risk-group of chronic alcoholics.

Acetaminophen↗

PubMed1995

[A case of paracetamol retard poisoning with fatal outcome].

A case of fatal paracetamol (acetaminophen) poisoning in a 26-year-old woman who developed liver necrosis is described. The patient reported having ingested 11 g of a slow-release paracetamol preparation and a certain amount of alcohol and benzodiazepine. An unknown dose of phenobarbital (phenemal) had been ingested 24 hours previously, leading to a serum phenobarbital concentration of 0.195 mmol/l at the time of admission. The patient was initially treated with N-acetylcysteine intravenously. This treatment was discontinued after five hours due to a serum paracetamol concentration of 0.49 mmol/l, well below the "treatment line" paracetamol concentration of 0.8 mmol/l six hours after ingestion. Possible aggravating factors are discussed, including sustained high serum concentration of paracetamol due to the slow-release preparation and enzyme induction caused from concomitant phenobarbital and alcohol intake, as well as benzodiazepines displacing paracetamol from liver enzymes. These factors make serum paracetamol concentrations undependable; the importance of continuing N-acetylcysteine treatment in spite of "safe" serum concentrations in the above cases is stressed.

Acetaminophen↗

PubMed1995

[Paracetamol poisoning].

Administration of paracetamol (acetaminophen) has analgetic and antipyretic effect. After trauma paracetamol has an anti-inflammatory activity. It was presumed that paracetamol in therapeutic doses had fewer and more acceptable side-effects than other analgetic drugs such as acetylsalicylic acid and NSAID-drugs. However, in toxic concentrations, paracetamol is more life-threatening. The toxic effects of paracetamol most often occur in the liver and kidneys. Phosphate and lactate turn-over can also be impaired. Paracetamol poisoning can induce temporary liver disfunction or even irreversible liver failure with liver transplantation as the only therapeutic possibility. Chronic alcoholics are especially at risk, as liver damage may occur following paracetamol even in recommended doses. When intoxication with paracetamol is presumed, administration of N-acetylcysteine is vital. N-acetylcysteine therapy should be initiated not later than 15 hours after paracetamol intake. Moreover, the antitoxic effect has been observed even when N-acetylcysteine therapy is initiated 24-36 hours after presumed paracetamol intake. Measures of preventing further absorption of paracetamol from the gastrointestinal tract should be taken. Activated charcoal should be given if less than two hours have passed since paracetamol intake. Between two and four hours following paracetamol intake gastric lavage should be performed. During the last 10 years the incidence of paracetamol self-poisoning has increased, but death following paracetamol poisoning is relatively constant at around nine per year in Denmark. It is suggested that the incidence of serious cases of paracetamol poisoning could be reduced by simple measures. Special attention should be paid to the risk-group of chronic alcoholics.

Acetaminophen↗