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Chapter 57: Status Epilepticus

INTRODUCTION

  • Status epilepticus (SE) is any seizure lasting more than 30 minutes, whether or not consciousness is impaired or recurrent seizures without an intervening period of consciousness. SE is a medical emergency, and aggressive treatment of seizures that last 5 minutes or more is strongly recommended. Seizure duration of greater than 30 minutes is associated with increasing risk of long-term consequences. Table 57–1 shows the classification of SE. This chapter focuses on generalized convulsive status epilepticus (GCSE), the most common and severe form.

  • The four stages of GCSE are (1) impending, (2) established, (3) refractory, and (4) superrefractory.

TABLE 57–1abcdInternational Classification of Status Epilepticus
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TABLE 57–1 International Classification of Status Epilepticus
Convulsive Nonconvulsive
International Traditional terminology International Traditional terminology

Generalized SE

  • Tonic–Clonica,b

  • Tonicc

  • Clonicc

  • Myoclonicb

  • Erraticd

 Grand mal, epilepticus convulsivus Absencec Petit mal, spike-and-wave stupor, spike and-slow-wave or 3/s spike-and-wave, epileptic fugue, epilepsia minora continua, epileptic twilight, minor SE

Secondary generalized SEa,b

  • Tonic

  • Partial seizures with secondary generalization

Partial SEa,b

Simple partial

Somatomotor

Dysphasic

Other types

Complex partial

Focal motor, focal sensory, epilepsia partialis continua, adversive SE

Elementary

Temporal lobe, psychomotor, epileptic fugue state, prolonged epileptic stupor, prolonged epileptic confusional state, continuous epileptic twilight state

(SE, status epilepticus.)

a

Most common in older children.

b

Most common in adolescents and adults.

c

Most common in infants and young children.

d

Most common in neonates.

PATHOPHYSIOLOGY

  • Seizure initiation is likely caused by an imbalance between excitatory (eg, glutamate, calcium, sodium, substance P, and neurokinin B) and inhibitory (γ-aminobutyric acid [GABA], adenosine, potassium, neuropeptide Y, opioid peptides, and galanin) neurotransmission.

  • GCSE is largely caused by glutamate acting on postsynaptic N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate receptors. Sustained depolarization can result in neuronal death.

  • GABAA receptors may become less responsive to endogenous GABA and GABA agonists.

  • During phase I of GCSE, each seizure produces marked increases in plasma epinephrine, norepinephrine, and steroid concentrations that may cause hypertension, tachycardia, and cardiac arrhythmias. Muscle contractions and hypoxia can cause acidosis, hypotension, shock, rhabdomyolysis, and secondary hyperkalemia, and acute tubular necrosis may ensue.

  • In phase II, beginning 30 minutes into the seizure, the patient begins to decompensate and may become hypotensive with compromised cerebral blood flow. Serum glucose may be normal or decreased, and hyperthermia, respiratory deterioration, hypoxia, and ventilatory failure may develop.

  • In prolonged seizures, motor activity may cease, but electrical seizures may persist.

MORBIDITY AND MORTALITY

  • Younger children, the elderly, and those with preexisting epilepsy have a higher propensity for sequelae.

  • Recent estimates suggest a mortality rate up to 16% in children, 20% in adults, and 38% in the elderly. Neonates have a higher mortality and more neurologic sequelae.

  • Variables affecting outcome are (1) the time between onset of GCSE and the ...

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