Abstract
Hypoxic brain damage may occur in any situation where there is an inadequate supply of oxygen to nerve cells It is therefore a potential hazard to any patient subjected to general anaesthesia, a severe episode of hypotension, cardiac arrest, status epilepticus and carbon monoxide intoxication. The eventual degree of clinical recovery will be determined by whether or not satisfactory resuscitation can be achieved before permanent brain damage ensues. Crises of this kind are not uncommon in clinical practice but the central question as to what duration of hypoxia defines the watershed between recovery of the tissues and extensive permanent injury has not been critically defined in man (Plum, 1973). The reasons for this include the lack of precise physiological data about the patients’ cardiovascular and respiratory status at the time of crisis since the immediate priority is resuscitation, and therefore such basic information as the precise duration of the cardiac arrest or blood pressure and heart rate during severe hypotension is very rarely available. In such cases the neuropathological descriptions, however exhaustive, may well explain the final neuropsychiatric status of the patient but can at best indicate only tentatively the nature of the episode itself.
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© 1985 Plenum Press, New York
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Graham, D.I. (1985). The Neuropathology of Stagnant Hypoxia. In: Heuser, D., McDowall, D.G., Hempel, V. (eds) Controlled Hypotension in Neuroanaesthesia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2499-7_17
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DOI: https://doi.org/10.1007/978-1-4613-2499-7_17
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