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.     

Dapsone poisoning

Two cases of suicidal dapsone ingestion are reported. These patients presented with marked cyanosis and had significant methaemoglobinaemia on admission. One patient also had acute psychosis and haemolytic anaemia. Both patients responded to intravenous methylene blue therapy and nasal oxygen inhalation and recovered without any sequelae.     

Chronic carbon monoxide poisoning: from smoking to accidental poisoning

The authors describe a case of furosemide possibly inhibiting the hypoprothrombinemic effect of warfarin. The initiation of furosemide dosing in a patient receiving a stable dose of warfarin was associated with an 28% decrease in the international normalized ration (INR). Using normal volunteers, two previous controlled studies of an interaction between warfarin and chlorthalidone, and between warfarin and spironolactone, assert that volume depletion produced by forced diuresis results in the inhibition of warfarin's hypoprothrombinemia. Consistent with this hypothesis, the authors found that their patient's hematocrit (believed to reflect hydration status) correlated with the INR: r2 = 0.78, p < 0.05. This case provides further evidence suggesting that acute diuresis can decrease the hypoprothrombinemic effect of warfarin.     

Thorn apple poisoning

A 20-year-old man presented with signs of thornapple intoxication: restlessness, disorientation, hallucinations, euphoria, and furthermore dry and red skin and symmetrical dilation of the pupils. Thornapple intoxication mimics atropine intoxication. Thorn apples (Datura stramonium) are seemingly becoming popular as a hallucinogenic drug. When the symptoms are mild gastric lavage leaving active charcoal in the stomach afterwards will suffice. In case of severe symptoms treatment with physostigmine is indicated.     

Melaleuca oil poisoning

A 23-month-old boy became confused and was unable to walk thirty minutes after ingesting less than 10 mL of T36-C7, a commercial product containing 100% melaleuca oil. The child was referred to a nearby hospital. His condition improved and he was asymptomatic within 5 hours of ingestion. He was discharged to home the following day. Melaleuca oil, extracted from the Melaleuca alternifolia, contains 50-60% terpenes and related alcohols. Clinical experience with products containing melaleuca oil is limited. This case report suggests that ingestion of a modest amount of a concentrated form of this oil may produce signs of toxicity.     

Acute chloroquine poisoning

HISTORY: After a quarrel with her husband a 50-year-old woman swallowed, together with some alcohol, 15 tablets of a chloroquine preparation (3.75 g chloroquine phosphate) with suicidal intent. She had no known psychiatric history. CLINICAL FINDINGS: An emergency physician called by the husband two hours after the tablet ingestion found her to be deeply comatose. After preventive nasotracheal intubation she had a grand mal seizure. On advice from a Poison Emergency Centre which was contacted while in the patient's apartment diazepam, 60 mg as a bolus, was injected intravenously, and controlled respiration was started. COURSE: After admission in hospital, gastrolavage was performed and diazepam therapy was continued with 40 mg per hour, gradually reduced until discontinued after 45 hours. The patient was transferred to an ordinary ward from the intensive care unit on the fifth day, without cardiac or neurological sequelae. CONCLUSION: The most important measures after a diagnosis of chloroquine poisoning are immediate intubation so that diazepam (1 mg/kg) can be administered intravenously as specific antidote without danger of severe respiratory failure.