NITROUS OXIDE and oxvgen has been successfully used for general aniesthesia for many years. The pleasant induction, rapid loss of consciousness, flexibility of control, freedom from vomiting and salivation, speedy recovery, and lack of complications have given it great popularity for all types of superficial and minor operations and for many major procedures as well. Lately, however, particularly in America, nitrous oxide has been vigorously attacked on the grounds that its administration is accompanied by so much anoxia that its use should be abandoned. A formidable mass-.of evidence has been accumulated. Lowenberg (1936) and his associates at the University of Michigan, Schreiber (1939) at Detroit, Courville (1936) at Los Angeles, and workers at Johns Hopkins Hospital (Ford et al., 1937), Henry Ford Hospital (McClure et al., 1939) and others (O'Brien and Steegman, 1938; Brown et al., 1938; Stewart, 1938) have all published papers presenting similar aspects. Series of deaths under or following nitrous oxide anaesthesia have been presented. The pathologic pictures have been similar, and have been characterized by extensive capillary haemorrhage in many organs but especially of the cerebral vessels, and by cedema of the brain. Cases which have survived the aniesthesia but failed to regain consciousness have exhibited all the symptoms of decerebration with its accompanying spasm and rigidity; convulsions were common, and death occurred in a few days from pulmonary congestion and vasomotor failure. There were similar pathologic findings of diffuse cerebral capillary haemorrhage in these later cases, but in addition, there were now areas of degeneration in the cellular layers of the cerebral hemispheres and lenticulate nucleus. Less severelv damaged patients who survived had. various degrees of mental impairment, ranging from complete idiocy to transient confusion and loss of memory. Lowenberg has advanced the theory that there is something specific in the manner in which nitrous oxide attacks the cerebral cortex and claims that the lesions produced cannot be duplicated by other means. Other workers do not support this hypothesis and, pointing out the great similarity between this pathologic picture and that produced by various forms of asphyxia, including carbon monoxide poisoning, have felt that anoxia was the cause. Even Lowenberg cannot distinguish anoxia from nitrous oxide poisoning when he has no history of the case. Similar lesions can be produced in animals by anoxia; therefore, it seems to be proved that while nitrous oxide has no directly toxic effect it may sometimes produce a severe or even fatal cerebral necrosis by an accompanying anoxia. Is it possible that this danger might be present in every administration of nitrous oxide? Is anoxia necessary for nitrous oxide to produce its anaesthetic effect? Nitrous oxide is by far the mildest and least toxic of the common general anaesthetics (fig. 1). This is one of its advantages, for practically no disturbance of bodily function is produced, but it carries with it the serious disadvantage that when enough nitrous oxide is introduced into the patient to produce the required depth of anaesthesia, there may not be enough room for sufficient oxygen to maintain bodily function. Many years ago Paul Bert (1878, 1883) carried out his classic experiments to prove that nitrous oxide was actually ananaesthetic drug and that its effects were not solely caused by asphyxia. By increasing the pressures under which the gases were inhaled, he showed that it was possible to have complete anaesthesia without oxygen shortage. By thus increasing the

The Relationship of Nitrous Oxide Anaesthesia and Anoxia: (Section of Anaesthetics).

Cerebral complications following nitrous oxide anesthesia

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Cerebral complications following nitrous oxide anesthesia