The mortality of SE is higher in SSA than in the resource-rich countries. This may be caused by the delay in presenting to hospital, poor management of SE in hospital, and underlying etiology (Wilmshurst et al., 2011). Patients who have SE may be taken to traditional healers first (Kariuki SM, unpublished data), and/or their presentation to hospitals may be delayed even further by lack of infrastructure or transport. Many hospitals in SSA lack facilities such as infusion pumps, ventilators, and staff to manage SE appropriately (Wilmshurst et al., 2011).
In a randomized controlled trial in Malawian children, intranasal lorazepam (100 μg/kg) failed to stop acute seizures in 25%, compared to intramuscular paraldehyde (0.2 ml/kg), which failed to stop 39% (Ahmad et al., 2006). This difference may be attributed to the relatively low dose of paraldehyde used. In a randomized controlled trial in Ugandan children admitted with acute seizures to an urban hospital, rectal diazepam (0.5 mg/kg) failed to stop seizures in 43% within 10 min compared with 30% who received buccal midazolam (0.5 mg/kg) (Mpimbaza et al., 2009). Focal seizures, cerebral malaria, and blood glucose ≥11 mmol/l at presentation were independent predictors of treatment failure defined as seizures lasting >10 min or recurrence within 1 h of treatment (Mpimbaza et al., 2009). However, in an audit of the treatment of seizures in Kenyan children, 64% seizures were not terminated with intravenous diazepam (0.3 mg/kg) compared to 58% with intramuscular paraldehyde (0.4 ml/kg) (Ikumi ML, Muchohi SN, Ohuma EO, Ogutu BR, Kokwaro GO, Newton CR, unpublished data). The later study reported the findings from a District General Hospital in rural Kenya, and the lack of response could be the result of the prolonged duration of seizures before treatment is started, or the cause of the seizures, for example, malaria (Ikumi ML, Muchohi SN, Ohuma EO, Ogutu BR, Kokwaro GO, Newton CR, unpublished data). Seizures caused by falciparum malaria appear to be resistant to diazepam, possible because of decrease in the binding capacity of GABAA receptors in malaria (Ikumi et al., 2008).