Introduction: Peak serum levels following overdose with immediate‐release formulations of carbamazepine have been reported to occur up to 2 days postingestion. We report a case of poisoning with carbamazepine controlled‐release resulting in peak levels 96 h postingestion. Case Reports: A 31‐year‐old female presented following a suspected polypharmacy overdose. She was haemodynamically stable with a Glasgow Coma Scale score of 3 and was endotracheally intubated in the emergency department. A single‐dose of activated charcoal was administered on admission and her neurological status improved gradually. Results of qualitative urine drug screen available 24 h postadmission to the intensive care department revealed benzodiazepines and carbamazepine. The serum carbamazepine concentration at this time was 66 µmol/L (therapeutic 17–42 µmol/L). A history of therapy with controlled‐release carbamazepine was discovered. Repeat‐dose activated charcoal and whole‐bowel irrigation were commenced, but poorly tolerated. Serum carbamazepine levels continued to rise and gastrointestinal tract decontamination was ceased due to the presence of an ileus. By day 4, the serum carbamazepine concentration peaked at 196 µmol/L. This was associated with coma, generalized intermittent seizure activity and hypotension. Charcoal haemoperfusion was commenced due the presence of end‐organ toxicity and failed gastrointestinal tract decontamination. Serum carbamazepine concentrations fell from 176 to 106 µmol/L after 1 h of haemoperfusion and the patient was rousable to voice and could obey commands at this time. She confirmed ingestion of 300 Tegretol‐CR® (200 mg) on extubation and was discharged without long‐term sequelae. Conclusion: Unrecognized poisoning with controlled‐release carbamazepine has the potential to produce significant delayed carbamazepine toxicity and delayed peak serum carbamazepine concentrations. This may occur much later than previously reported with immediate‐release carbamazepine preparations.

Aim: To compare the clinical features of cyclic antidepressant and newer, non‐cyclic, serotonin‐specific antidepressant poisoning. Methods: Comparitive, descriptive study of all antidepressant overdose patients admitted to a hospital toxicology service from February 1997 to April 2001. Patient data were entered prospectively into a dedicated toxicology database for subsequent analysis. Results: There were 256 admissions for antidepressant poisoning (17.5% of all poisoning admissions). Cyclic antidepressant poisoning comprised 43% of antidepressant admissions. Statistically significant differences between the two groups included: cyclic antidepressant group had longer median length of stay (23.1 vs 15.9 h, P = 0.0008), greater need for endotracheal intubation (31%vs 4%, OR = 11.5, P < 0.0001) and higher incidence of seizures (7.2%vs 0.7%, OR = 10.4, P = 0.01), faster median pulse rate, longer QRS‐interval on admission, and longer intensive care unit stays. However, non‐cyclic, serotonin‐specific antidepressant poisonings involved larger doses of antidepressants and were more likely to ingest other medications along with these. Serotonin syndrome was only seen in non‐cyclic, serotonin‐specific poisoning (10.3%, OR = 26.6, P = 0.0002). Patients with serotonin syndrome had a longer median hospital stay (46 vs 16 h, P < 0.0002) compared to other non‐cyclic, serotonin‐specific patients. There were no deaths during the study period. Conclusions: Cyclic antidepressants still comprise a significant proportion of antidepressant poisoning and result in more significant morbidity than non‐cyclic, serotonin‐specific poisoning. Clinicians should also be aware that non‐cyclic, serotonin‐specific poisoning may result in the development of serotonin syndrome. This was the most significant toxic effect noted following non‐cyclic, serotonin‐specific poisoning in this study.

Collett's snake envenoming is characterized by early generalized systemic effects (nausea, vomiting, abdominal pain, diarrhoea and headache) and an anticoagulant coagulopathy, followed in some cases by rhabdomyolysis and acute renal failure in untreated patients within 24 h. Early initiation of fluid therapy and treatment with black snake antivenom should be undertaken in all envenomed patients.

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Pure triethylene glycol poisoning results in coma and metabolic acidemia and may be treated with alcohol dehydrogenase inhibitors such as ethanol.