A 28-year-old woman ingested 20 g of hydroxychloroquine sulphate for suicidal attempt. She developed hypotension, cardiac conduction disturbance, hypokalemia and hypoglycemia. Despite treatment with mechanical ventilation, epinephrine, sodium bicarbonate, diazepam and potassium replacement, she succumbed 10 hours post-overdose. Previous case reports of hydroxychloroquine overdose are summarised and the therapeutic choices are discussed. (Hong Kong j.emerg.med. 2007;14:53-57) (Figure 1). Twenty grams of dextrose given intravenously brought her GCS to 15/15 and blood glucose to 13.4 mmol/L. The BP was improved to 80/50 mmHg after infusion of 1 L of normal saline. Gastrointestinal decontamination was performed with 50 g of oral activated charcoal but gastric lavage was not done.She was later transferred to the Intensive Care Unit. She remained conscious but the BP and central venous pressure were 57/35 mmHg and 26 cmH 2 O respectively. She was intubated and put on synchronised intermittent mandatory ventilation mode of mechanical ventilation. The medications given included intravenous diazepam 60 mg followed by infusion of 2 mg/h, epinephrine 20 µg/min and sodium bicarbonate 100 mmol. The serum potassium three hours after the overdose was 1.5 mmol/L. Potassium chloride of 20 mmol was given over one hour followed by a maintenance infusion of 1.6 mmol/h.Her BP was sustained well above systolic 100 and diastolic 60 mmHg one hour after starting the epinephrine drip. At six hours post-overdose, the QRS

To identify and analyse the characteristics of carbon monoxide (CO) poisoning due to burning charcoal in our locality. Methods: This was a 3-year retrospective study. All patients presenting with CO poisoning by burning charcoal from August 1999 to December 2002 were recruited. The demographic data, initial vital signs, blood results, treatment regimens and outcomes were collected. Association between clinical outcomes and parameters were calculated. Results: The study identified 148 patients (mean age 34.7 years) suffering from CO poisoning by burning charcoal. One hundred and forty-six cases (98.6%) were suicidal. Twenty-five patients (16.9%) were unconscious (GCS ≤ 8) on arrival. The mean initial carboxyhaemoglobin (COHb) level was 21.0%. The mortality rate was 5.4%. Fifteen cases (10.1%) required intensive care. Twelve cases (8.1%) had neurological complications and five (3.4%) suffered from delayed neurological sequelae. Initial blood results showing hyperkalemia and acidosis were associated with likelihood of unconsciousness on arrival (p = 0.007, p = 0.019 respectively). Hyperkalemia and unconsciousness on arrival were associated with longer hospital stay (p < 0.001, p < 0.001 respectively) as well as likelihood of systemic complication (p < 0.001, p < 0.001 respectively). There was no relationship between co-ingestion, age, initial COHb level, initial systolic and diastolic blood pressure with consciousness level on arrival (p = 0.188, p = 0.846, p = 0.264, p = 0.224, p = 0.755 respectively). Age, initial COHb level, acidosis, initial systolic and diastolic blood pressure did not correlate with the duration of hospital stay (p = 0.679, p = 0.176, p = 0.501, p = 0.313, p = 0.868 respectively). Conclusion: Suicide almost accounted for all the CO poisonings by burning charcoal in our study group. It caused significant mortality and morbidity. Hyperkalemia, unconscious state and acidosis had prognostic values.

Butoxyethanol intoxication has seldom been reported. We describe a case of ingestion of butoxyethanolcontaining cleaner resulting in high anion gap metabolic acidosis, which resolved after treatment with ethanol and haemodialysis. The presentations and treatments of previous cases are highlighted. Discussion is centred on the toxicological pathway of butoxyethanol and the role of alcohol dehydrogenase inhibitor. (Hong Kong