Immediate apnea after acute head trauma is a concept that has received renewed focus lately. BIA/IBA (Brain Impact Apnea or as some call it, Impact Brain Apnea) was described in animal models as far back as 1874 by Koch and Filehne (1). A number of subsequent studies (2-5) have established a clear link between severity of impact and duration of centrally mediated apnea. In one of these studies, cranial trauma lead to a sustained cessation of spontaneous breathing, followed by a catecholamine surge (2). It is now well understood that increased pCO2 levels (secondary to apnea), together with an elevated blood pressure, both seem to contribute to cerebral oedema and increased ICP.

A growing body of anecdotal evidence, gathered especially in the prehospital field, lends support to the thesis that this penomenon may contribute significantly to morbidity and mortality in head injured patients. Case reports have been published citing full and rapid recovery from apparent lifelessness after brain impact, simply through immediate airway management and ventilation (6). Conversely, a significant number of TBI patients have been reported to have had either radiological or post-mortem evidence of anoxic brain injury, in the absence of other parenchymal brain damage to explain death or poor neurological outcomes (7,8). The hypothesis has thus been that these findings are due to anoxia secondary to sustained apnea, and not necessarily structural brain injury per se. Furthermore, as this may be an entirely reversible process if recognized and managed expeditiously, it certainly warrants our attention.

The subject has also been covered very well in the St. Emlyn´s podcast (interview with London HEMS´ Gareth Davies) and Life in The Fast Lane. An excellent overview article by Atkinson et al can be read here. Many of the references below are courtesy of that very article, published in 2000 in the Mayo Clin Proc.

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