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The authors note that electrocerebral inactivity (a so-called "flat EEG," one of the signs of "brain death" and thus of death itself) has been shown in drug overdoses, hypothermia (low temperature), cardiovascular shock, and metabolic abnormalities, but not yet with obstructive sleep apnea (OSA). They report such an occurrence during polysomnography in a pediatric patient with severe sleep apnea.
The patient was a 2-year-old African-American boy with Prader-Willi Syndrome, a congenital disorder characterized by short height, mental retardation, excessive eating and obesity, and sexual immaturity.
For the year previous he had been snoring with prolonged apneas, developing at the same time as excessive weight gain. An adenoidectomy yielded no improvement.His facial structure was peculiar. Neck exam showed an enlarged tongue with a lot of excess tissue of the palate and enlarged tonsils that met at the midline.
His sleep polysomnogram showed only stage 1 sleep, of 397 minutes duration, during which 207 respiratory events occured, for a Respiratory Distress Index (RDI) of 31, ordinarily indicating a moderate degree of sleep apnea, but in this case oxygen desaturations fell to remarkably low levels (5-15%), indicating a very severe disease. Apneas lasted as long as 30 seconds.
Surgery including a uvulopalatopharyngoplasty (UPPP) plus reduction of the tongue size, removal of both tonsils, trimming of the palate, and removal of the middle third of the mid- to posterior tongue and tongue base--quite an extensive procedure which on retesting with polysomnography 1 week later yielded no improvement.
At this retesting he was seen to have two apneas associated with marked reduction of cortical electrical activity, each lasting about 9 seconds and following a 30-second obstructive event with oxygen desaturation of 13-50%. Tracheostomy was recommended by the parents refused. Therefore he was fitted for continuous positive airway pressure (CPAP) at 3.5 cm H2O, the highest pressure he could tolerate, with 2 L of oxyen. Nine days later he had persistent sleep apnea during REM sleep with desaturation only into the mid-80%. However, when his pharyngeal swelling (from the surgery) cleared up several weeks later, he had marked clinical improvement.
The authors regretted that, not expecting to see electrocerebral inactivity, they had used standard EEG sensitivity on the polysomnogram and that was not sensitive enough to meet the strict definition of electrocortical silence.
However, they believed electrocortical silence may have occurred, and suggested that it was related to cerebral hypoxia (lack of oxygen to the brain). They made reference to the still uncertain cause of increased death rates among people with OSA. In children, it has been found that sudden infant death syndrome (SIDS) victims had more frequent and prolonged obstructive sleep apneas, and came from families with OSA> One 4-month-old girl died a day after she was found to have severe apneas.
Although the presence of Prader-Willi syndrome may make this case seem obscure to many of us, OSA is actually infrequent in this condition, though excessive daytime sleepiness is not. Polysomnograms of these patients generally show shortened REM latency, such as one might see in narcolepsy, and decreased breathing during REM. However, the enlarged tonsils and adenoids certain suggest the likelihood of obstructive sleep apnea.
Although this child did not die but apparently recovered from his OSA with CPAP, a flat EEG comes pretty close to death, and a blood oxygen saturation as low as 5% sounds adequate to account for that on the basis of oxygen deprivation of the brain. Probably the immediate resort to extensive surgery, and the proposal of tracheostomy, both stemmed from the critical nature of the case. However, it was interesting that CPAP did quite well--once the obstructive swelling from all the surgery subsided!
There has been a general assumption that unexplained death in OSA patients resulted from cardiac arrhythmias, perhaps triggered by low blood oxygen, but this case suggests that oxygen may at times fall low enough to result in brain death even without cardiac arrhythmias. This phenomenon has not, to my knowledge, been observed in adult OSA patients undergoing polysomnography. Life-threatening arrhythmias in the lab are also very rare. However, the lab situation represents one or two nights a year out of 356, during which no one knows what happens. A single instance of blood oxygen low enough to result in the kind of phenomenon described here could help explain the memory and attentional deficits--and anatomical brain damage--observed in some OSA patients.
What would it take to cause such a drastic fall in blood oxygen saturation in an adult with OSA who had no such phenomenon observed in the sleep laboratory? How about a severe case of infectious pharyngitis? How about heavy drinking before going to bed. How about use of too many sleeping pills? How about failure to use CPAP that night? How about a degree of unconsciousness resulting from alcohol and/or drugs that left the person unknowingly sleeping on his back? How about a combination of all of the above?
There has been some controversy lately over SIDS, with a prominent investigator retracting some of his statements as a result of coming to believed that many cases of alleged SIDS really represented a cover-up of death from child abuse. No doubt this is the case, but no doubt there are also cases of children dying from OSA, perhaps a much smaller group.
One of the most remarkable videos I have ever seen was shown to my group during a one-week course on sleep medicine at Stanford. A young girl whose parents claimed she had repeated choking episodes at night was being studied in the laboratory. Unbeknownst to the father, the study included low-light video recording. This enabled the technician--and us--to watch as the father entered the child's hospital room and proceeded to smother her with a pillow, interrupting this just short of killing her, then running out to tell the technician that the girl just had another "attack." It is unfortunate indeed if abusive parents are making use of a real disorder is children--OSA--to cover up their own abusive or even murderous actions under the label of "SIDS."
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