THE MANAGEMENT OF STATUS EPILEPTICUS

Status epilepticus confined to early childhood [black right triangle] Neonatal status epilepticus [black right triangle] Status epilepticus in specific neonatal epilepsy syndromes [black right triangle] Infantile spasms Status epilepticus confined to later childhood [black right triangle] Febrile status epilepticus [black right triangle] Status in childhood partial epilepsy syndromes [black right triangle] Status epilepticus in myoclonic-astatic epilepsy [black right triangle] Electrical status epilepticus during slow wave sleep [black right triangle] Landau-Kleffner syndrome Status epilepticus occurring in childhood and adult life [black right triangle] Tonic-clonic status epilepticus [black right triangle] Absence status epilepticus [black right triangle] Epilepsia partialis continua [black right triangle] Status epilepticus in coma [black right triangle] Specific forms of status epilepticus in mental retardation [black right triangle] Syndromes of myoclonic status epilepticus [black right triangle] Simple partial status epilepticus [black right triangle] Complex partial status epilepticus Status epilepticus confined to adult life [black right triangle] De novo absence status and late onset TONIC-CLONIC STATUS EPILEPTICUS The annual incidence of tonic-clonic status is estimated to be 18-28 cases per 100000 persons. The major physiological changes are related to the greatly increased cerebral blood flow and metabolism, massive autonomic activity, and cardiovascular changes Cerebral changes Systemic and metabolic changes Autonomic and cardiovascular changes Increased blood flow Hyperglycaemia Hypertension (initial) Increased metabolism Lactic acidosis Increased cardiac output Energy requirements matched by supply of oxygen and glucose (increased glucose and oxygen utilisation) Increased central venous pressure Massive catecholamine release Tachycardia Increased lactate concentration Cardiac dysrhythmia Increased glucose concentration Salivation Hyperpyrexia Vomiting Incontinence Phase 2: decompensation During this phase, the greatly increased cerebral metabolic demands cannot be fully met, resulting in hypoxia and altered cerebral and systemic metabolic patterns.