Canadian Journal of Anesthesia, Vol 25, 231-235, Copyright © 1978 by Canadian Anesthesiologists' Society

A Propos D'Un Cas D'deme Pulmonaire D'Origine Centrale

¹ Département d'Anesthésie-Réanimation, I'Université de Montréal. Anesthésiste, Département d'Anesthésie, Hôpital Sainte-Justine, 3175, Chemin de la Côte Sainte-Catherine, Montréal, Québec, Canada H3T 1C7

A case of centrogenic pulmonary oedema is reported in a young boy without other disease. The problems that occurred in the operating room and the anaesthetic management are presented. The pathophysiology of this entity is briefly explained. Haemodynamic studies have shown that a moderate degree of intracranial hypertension leads to sympathetic stimulation where beta activity predominates, thus reducing peripheral resistance and increasing the cardiac output.^{2-4, 20, 27} The alveolo-arterial gradient is increased and the arterial PO₂ reduced, triggering the ischaemic reflex in the cerebral circulation described by Cushing⁹.

According to Sarnoff^31,32 and Ducker^8,9 more severe intracranial hypertension leads to sympathetic hyperactivity where the alpha adrenergic system predominates. This "adrenergic storm" causes generalized vasoconstriction with massive pooling of the blood in the pulmonary circulation. The combined effects of increased pre-load and after-load, leads to left heart failure and pulmonary oedema.

Alpha blocking agents were used with relative success by many authors.^{1,5,22,25,26,29} However, this management appears more efficient to prevent the "adrenergic storm" than actually to treat it. On the other hand, beta blockers and hypotensive drugs like trimetaphan or sodium nitroprusside have been recommended, but the danger of secondary hypotension in such a situation cannot be over-emphasized. Phenothiazines and butyrophenones, in our opinion, would appear to be a good choice: they possess central sympatholytic action, alpha blocking properties at the periphery and they reduce the activity of the central nervous system.

During this case an episode of ventricular fibrillation occurred which we believe is related to surgical manipulation in close proximity to vaso-motor centres.

It is interesting to underline that as early as four hours after the acute phase, the radiological evidence of pulmonary oedema was already regressing to disappear completely 18 hours following the surgical decompression.