At the onset of generalized seizure activity, sympathetic activity is suddenly and significantly increased, manifested by increased systemic and pulmonary vascular pressure.120,121 Bayne and colleagues suggested that transient pulmonary vascular hypertension, leading to transcapillary fluid flux, may explain the pulmonary edema after seizures.122,123
Neurogenic pulmonary edema has also been associated with sudden unexpected death in epileptic patients (SUDEP).124 Walczak and colleagues125 note the presence of pulmonary edema in SUDEP and suggest that neurogenic pulmonary edema may be responsible for SUDEP. The mechanism is thought to be due to increased preload and pulmonary capillary permeability. This permeability may be due to hydrostatic mechanisms or directly to an abnormal cortical discharge. This hypothesis is consistent with autopsy findings and reports that death may occur an hour or more after the witnessed seizure. A sheep model of death after bicuculline-induced status epilepticus126 found that pulmonary edema was in fact more extensive in animals that died than in animals that survived. The pulmonary edema was associated with increased left atrial and pulmonary artery pressures.
The degree of pulmonary edema was not sufficient to explain the degree of ventilatory failure observed in the animal model of SUDEP, however.126 Further studies of eight animals127 found that central apnea was at least partially responsible for two deaths, whereas cardiac failure related to massive subendocardial necrosis was responsible for the third death. These findings, together with the time course of the ventilatory failure, led to the conclusion that profound central apnea related to the seizure was more often responsible for death than pulmonary edema, at least in this model.127 A skeptic would point out that this is a model of status epilepticus. There is no evidence that seizures responsible for SUDEP are more severe than the patientís characteristic seizures.
Some degree of apnea is quite common during and after epileptic seizures in humans.128,129 Apnea appears to be central in type, but duration is not particularly long, nor is the degree of oxygen desaturation profound. Two case reports of video-EEG monitoring during SUDEP130,131 have demonstrated continuing regular heart rhythms for more than 1 minute after the termination of the seizure. An apparent respiratory arrest in one case130 responded to brief cardiopulmonary resuscitation. In both cases, intense postictal EEG suppression was noted, more profound than had been seen in other seizures with the same patient.
A SUDEP case series suggested that SUDEP was far more common in an outpatient setting than in a group home setting where staff had received vigorous training in first aid treatment of tonic-clonic seizures.132 This group has suggested that certain steps may help prevent SUDEP:
Treatment should take into consideration the risk of suppressing the respiratory drive, as with benzodiazepines and barbiturates (see Respiratory effects of antiepileptic drugs).
Reviewed and revised April 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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