Role of thiopentone infusion for management of intractable status epilepicus in pediatric patients
© BioMed Central Ltd. 2004
Published: 15 March 2004
Intractable status epilepticus not responding to conventional pharmacotherapy is a medical emergency. Deeper suppression of cortical activity, documented electrocerebral silence and titrable length of time during which such electrocerebral silence can be maintained all make thiopentone the ideal drug for initial management of status epilepticus [1, 2]. A long-lasting anti-epileptic drug regimen can be established during thiopentone-induced burst suppression, which can then be tapered and discontinued with minimal chances of recurrence.
Twenty-one pediatric patients suffering from idiopathic generalized tonic clonic disorder with age of onset of 12 months–2 years were included in the study. All patients were admitted to the pediatric ICU after initial management in the emergency room. Rapid sequence intubation with cricoid pressure was done with an induction dose of 4 mg/kg thiopentone intravenously (IV) and 1.5 mg/kg succinylcholine IV. Additional boluses of 4 mg/kg thiopentone were administered at 5–30 min intervals until complete areflexia was achieved, while a continuous intravenous thiopentone infusion (0.5–4 mg/kg/hour) was maintained and titrated to obtain electroencephalogram (EEG) burst suppression. Continuous single channel processed EEGs using a cerebral function analyzing monitor and an intermittent multichannel electroencephalogram (EEG) were done. After control of clinical and electroencephalographic seizure activity, patients were started on phenytoin and phenobarbitone. Thiopentone infusion was progressively tapered over 24 hours and finally discontinued once therapeutic serum levels were achieved for these anti-epileptic medications. Statistical values were obtained from 2 × 2 tables of outcome versus EEG suppression employing Fisher's exact test with significance quantified as P < 0.05.
Out of the 21 patients, 16 showed burst suppression and five showed a 'flat' record. Two patients in the burst suppression category showed recurrence of seizure activity after being controlled initially, and none in the flat one. In these two patients, EEG seizures recurred earlier than clinical seizures, which were rapidly controlled with increasing the rate of thiopentone infusion. More sustained control of seizure activity was achieved by adding valproic acid to the anti-epileptic regimen in these two patients.
We conclude that, tightly controlled by serum levels, carefully monitored with EEG for therapeutic efficiency, initiating and tapering of thiopentone infusion in the ICU setting with mechanical ventilation and hemodynamic monitoring will allow the physician to establish therapeutic serum levels of conventional anti-epileptic agents, to reduce the relapse rate, and to avoid the mortality and long-term morbidity associated with this life-threatening medical emergency.