Syndrome of postoperative depression of vital functions in poor-risk patients: its treatment.
Loss of proprioception due to depressed neuromuscular transmitter following continued action of skeletomuscular relaxant drugs may not be the main cause of stupor, respiratory depression, and suppression of motor and sensory reflex activity in the immediate or delayed post-operative period in surgical patients. Those with a chronic history of suffering (termed poor-risk types because of other associated derangements in electrolytes, body water, etc.), hyper-react to surgical stress as well as postoperative pain and apprehension. This leads to the release of large quantities of stress products (noradrenaline and its cognates) into the central nervous system (CNS), thus inducing a phase of depression of the cerebral cortex and other vulnerable parts of the CNS in such a way that the stupor analgesic stage is induced in the affected persons (called the "syndrome of post-operative depression of vital functions"). Treatment of such a syndrome thus involved removal of the stress products from the CNS as well as from peripheral circulation by extraction therapy (20% mannitol administration), coupled with judicious use of atropine and neostigmine to stimulate the CNS itself, i.e., the production of acetylcholine in the mesencephalic reticulo-activating system.[1]References
- Syndrome of postoperative depression of vital functions in poor-risk patients: its treatment. Rao, L.N., Venkatakrishna-Bhatt, H. International journal of clinical pharmacology, therapy, and toxicology. (1981) [Pubmed]
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