Status Epilepticus: Clinical Analysis of a Treatment Protocol Based on Midazolam and Phenytoin

Judith C.D. Brevoord MD; Koen F.M. Joosten MD, PhD; Willem F.M. Arts MD, PhD; Roos W. van Rooij MD; Matthijs de Hoog MD, PhD


J Child Neurol. 2005;20(6):476-481. 

In This Article


A total of 205 patients were admitted for generalized convulsive status epilepticus, of whom 122 patients received medication according to our treatment protocol. Eighty-three patients were excluded because of pretreatment with another antiepileptic medication (37), treatment with midazolam bolus directly followed by continuous midazolam (without prior phenytoin load) (25), receiving rectal diazepam only (13), the lack of information about which medication achieved cessation (4), or receiving other antiepileptic medication owing to previously proven effectiveness in individual cases (4). Thirty-seven of these 83 patients were transferred from other hospitals.

The results of 122 patients (71 males) were analyzed. The median age was 24.4 (0.5-197.4) months. Seventy-six percent were under the age of 5 years. The etiology of generalized convulsive status epilepticus in this study group is shown in Table 2 The predominant causes were idiopathic and febrile convulsions.

The mean Pediatric Index of Mortality score was 0.034 (range 0.01-0.19), which means a predicted probability of death of 3.4%. There was no difference in mean Pediatric Index of Mortality scores for patients needing different levels of antiepileptic therapy, indicating that the severity of the generalized convulsive status epilepticus causing illness was not a major factor in explaining differences in the need for antiepileptic therapy.

Table 3 shows the level of antiepileptic therapy needed for cessation of epileptic activity subdivided for initial rectal diazepam. Eighty-two of 122 patients (68%) received initial rectal diazepam. Cessation of epileptic activity was achieved with midazolam only (level 1) in 58 patients (48%); with midazolam and phenytoin (level 2) in 19 patients (15%); with midazolam, phenytoin, and continuous midazolam (level 3) in 32 patients (26%); and with additional barbiturates (level 4) in 13 patients (11%). There was no significant relationship between the initial treatment with diazepam and the overall level of antiepileptic therapy (χ2 P = .71) or the need for a barbiturate coma (level 4, χ2 P = .277).

The mean infusion rate in the 32 patients treated with midazolam continuously was 0.24 mg/kg/hour (range 0.05- 0.8 mg/kg/hour). In 13 patients needing a barbiturate, the mean midazolam dosage was 0.63 mg/kg/hour (range 0.1-1.0 mg/kg/hour). Table 4 shows the relationship between the etiology of generalized convulsive status epilepticus and the level of antiepileptic therapy needed. Seven of the 13 patients needing barbiturates had acute symptomatic convulsion (five had an encephalitis, one had a subdural empyema, and one had severe dehydration), and three had idiopathic, one had progressive neurologic, and two had febrile seizures. The relationship between the etiology and the level of antiepileptic therapy was not significant (χ2 P = .16). In the subgroup of patients needing barbiturates, there were significantly more patients with acute symptomatic convulsion (χ2 P = .001).

Fifty-two patients (43%) needed artificial ventilation. In 39 patients, respiratory insufficiency developed during initial therapy with midazolam (level 1). In 11 patients, a possible relationship was suggested. Three patients had an apnea, and eight patients were intubated after a bolus of midazolam. Twenty-eight patients were artificially ventilated to protect the airway; there were no signs of apnea related to administration of midazolam. In 13 patients, respiratory insufficiency was not related to initial therapy with midazolam. Endotrachael intubation and ventilatory support were indicated based on the convulsion itself in nine cases, elective before transportation to our hospital in three cases and one because of herniation of the brain stem. Hemodynamic instability, defined as fluid bolus or inotropic support, attributable to midazolam therapy was not encountered. Seven patients died (5.7%). No deaths were directly attributable to generalized convulsive status epilepticus itself ( Table 5 ). In these seven patients, epileptic activity ceased with midazolam in four patients, continuous midazolam in one patient, and pentobarbital in two patients.


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