As the risk of respiratory depression is greater with more than two doses of benzodiazepines, clinicians should not disregard prehospital treatment of SE. As pre-PIC treatment of SE is inadequate in many cases, appropriate audit and modifications of standard guidelines are required.

Aims: To document the patterns of presentation and outcome of severe anticholinesterase insecticide poisoning in children requiring intensive care. Methods: Retrospective case note review of all 5541 children admitted to the paediatric intensive care unit (PICU) of a university hospital during the 10 years from January 1990 to May 2000. Fifty four children (1%) with anticholinesterase insecticide poisoning were identified. Presenting features, route of exposure, treatment, complications, and mortality were recorded. Data were analysed by the Fisher's exact and Mann-Whitney tests. Results: More children than expected were from a rural area (46% versus 25%). Decontamination occurred in 50% of children prior to PICU admission. Enteral exposure was most common (n = 27; 50%). Median pseudocholinesterase level was 185 IU/l (range 75-7404). Median total dose of atropine required to maintain mydriasis was 0.3 mg/kg (range 0.03-16.7) over a median of 10 hours (range 1-160). Complications included coma (31%), seizures (30%), shock (9%), arrhythmias (9%), and respiratory failure requiring ventilation (35%). No significant differences were detected in incidence of seizures, cardiac arrhythmias, respiratory failure, mortality, duration of ventilation, or PICU stay, according to route of exposure, or state of decontamination. Four children died (7%). Mortality was associated with the presence of a cardiac arrhythmia (likelihood ratio 8.3) and respiratory failure (likelihood ratio 3.3). Conclusion:The mortality and morbidity of severe anticholinesterase insecticide poisoning in childhood is not related to route of exposure, or to delay in decontamination. However, the presence of either a cardiac arrhythmia or respiratory failure is associated with a poor prognosis.A ccidental poisoning by acetylcholinesterase inhibitor (anticholinesterase) insecticides such as the organophosphates and carbamates remains an important public health problem in regions where these agents are in common usage.1 Effective treatment may be delayed as the constellation of nicotinic and muscarinic signs and symptoms is often incomplete, and may mimic a variety of other conditions in childhood.2 It has been suggested that the clinical manifestations of childhood anticholinesterase insecticide poisoning differ from those in adults, with a predominance of central nervous system effects.3 4 Mortality is also reported to be lower in childhood.2-4 However, contrary to previous reports, it has been our impression that children with severe anticholinesterase exposure follow a similar course to that reported in adults. 3 4 We speculated that both morbidity and mortality in this condition are more closely related to the degree of toxin exposure than to patient age. The route of contamination (enteral or transcutaneous), or delay in decontamination, might thus influence outcome by affecting the degree of toxin exposure.We present a retrospective observational study of severe anticholinesterase insecticide poisoning, with particular reference to mode of present...

Neonates with CHD may present as severe "PPHN" via the ECMO service. Poor outcome in these patients relates to the high incidence of cardiovascular collapse and end-organ dysfunction. Early echocardiography is recommended for neonates with presumed PPHN. Neonatal ECMO support should be based in centres with cardiac surgical services.

P14 Facial continuous positive airway pressure therapy for cardiogenic pulmonary oedema: a study of its efficacy in an emergency department setting within the UK

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