Important clinical lessons about the effects and prognosis of convulsive SE have emerged from studies:
Convulsive SE can cause numerous complications.Table: Complications of SE Cardiac and autonomic changes, which can be severe, include hypertension, tachycardia, arrhythmias, diaphoresis, hyperthermia, and vomiting. Cardiac arrhythmias may be precipitated by lactic acidosis and elevated catecholamines. Hyperthermia may result from excessive convulsive muscle contractions as well as from hypothalamic effects. The electrocardiogram (ECG) may show conduction abnormalities or ischemic patterns. Autonomic dysfunction and cardiac arrhythmias may explain much of the mortality of SE and some other unexplained sudden death in epilepsy patients.
Cerebral blood flow and metabolism are elevated in early SE but decline eventually, and the excessive metabolism of discharging neurons may outstrip the oxygen and glucose supply. As seizures continue, autoregulation may break down and contribute to cerebral edema, particularly in children. Compensatory physiologic changes in early SE appear to break down after about 30 minutes, with subsequent hypotension, hypoxemia, hypoglycemia, and increasing acidosis and hyperkalemia. Hypotension and bradycardia may be worsened further by anticonvulsants and other medications. Hypotension or volume depletion may complicate medical and metabolic disorders or lead to venous stasis and even cerebral venous thrombosis.
Inhibitory GABA receptors are progressively lost, which may help to determine the critical period at which SE becomes more refractory to treatment and more dangerous physiologically.
SE prompts cortisol and prolactin release, although prolactin may become exhausted and return to normal levels in prolonged SE.
Leukocytosis and spinal fluid pleocytosis may occur, but these problems should not be attributed to the SE itself until infection or some other cause of inflammation has been excluded.
Aspiration pneumonia is common if airway protection is not assured. Respiratory failure is probably more often due to medications than to SE itself. Pulmonary edema may also occur.
Rhabdomyolysis can occur after repeated convulsive seizures. Together with hypotension, it may result in renal failure.
Patients may exhibit an orderly sequence of electroencephalogram (EEG) changes in SE:
Clinical convulsions abate as the EEG progresses through these stages. Patients in later EEG stages have seizures that are particularly refractory to the usual anticonvulsants and have a worsened prognosis.
Persistent EEG discharges generally are a sign of continuing and damaging SE, so an EEG is necessary when a patient's convulsions have ended and the patient has not awakened. The EEG can show whether comatose patients are in a postictal state or still having seizures. Even without motor phenomena, EEG evidence of SE warrants aggressive treatment.
Abundant experimental animal evidence indicates that convulsive SE (whether induced by electrical stimulation, kainic acid, or lithium and pilocarpine) leads to neuronal damage due directly to the neuronal epileptic activity. The cellular activity of SE releases excitatory amino acids, which are neurotoxic in excessive amounts. Hippocampal damage and a subsequent recurrent seizure disorder are among the consequences. Systemic factors, however, especially hypotension, respiratory failure, and hypoxia, worsen the prognosis and contribute to cerebral damage.
Repetitive electrical stimulation produces SE after 30 minutes or so-the same time at which human homeostasis appears to deteriorate during convulsive SE. Thus, both clinical and experimental data implicate 30 minutes as a critical time before which convulsive status should be interrupted if damage is to be avoided. Experimental data using electrical stimulation-induced SE also suggest that phenobarbital is far more effective than phenytoin at breaking this SE. These effects are more difficult to substantiate in humans, but pyramidal cell loss in the hippocampus has been identified after SE in humans.
It has become increasingly clear that SE in patients with prior epilepsy and SE in those with a new diagnosis are almost different conditions. Patients who have had prior epilepsy or whose SE has been precipitated by withdrawal from an anticonvulsant or another medication do far better. The reason may be earlier detection and diagnosis, partial treatment from earlier anticonvulsants, or the absence of acute severe insults that worsen the prognosis in other patients.
Children also fare far better than adults, perhaps because older patients often have underlying illnesses with a higher associated morbidity and mortality.
The underlying disease is the most important prognostic factor in generalized convulsive SE. Mortality has declined in recent decades and should be below 2% from the SE itself with reasonable treatment. Mortality due to the condition causing the convulsive SE may be substantially higher, often about 30%. Underlying conditions predicting a worse outcome include:
The presence of more than one medical complication, especially cardiac arrhythmias, hypotension, kidney or liver failure, and intracranial hypertension, also predicts a worsened outcome.
Studies have found other factors that influence outcome:
SE may cause subsequent intellectual impairment, but studies suggesting that this is the case have generally been retrospective and have usually included only subjects who have had prolonged SE, who have had prior substantial neurologic and intellectual impairment, and who were taking several anticonvulsants. SE may worsen chronic epilepsy.
Reviewed and revised January 2004 by Thaddeus Walczak, MD, MINCEP® Epilepsy Care, Minneapolis, MN
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