Acute Pulmonary Oedema, Endogenous and Exogenous Causes, with Therapy

Abstract

This paper is concerned with acute pulmonary oedema of the massive type. We define pulmonary oedema due to transudation of proteinized fluid caused by mechanical or neurogenic factors as endogenous, and that due to exudate of inflammatory fluid due to infection or irritation as exogenous. Regarding treatment, we must consider all theories of etiology. First, to reduce pulmonary stasis and blood volume we should apply serially extremity tourniquets and possibly venesection as approved by the proponents of the “mechanical” theory. Second, we should consider application of certain narcotic and sedative drugs like morphine and papaverin as well as chloretone and phenobarbital as suggested by the “neurogenic” theory. Third, we should use oxygen under positive pressure to buttress leaking pulmonary capillaries according to the exponents of the “anoxia” theory. This last and newest form of therapy is the contribution from experienced physiologists and specialists trained to meet inhalational emergencies in industry and war, those due to carbon monoxide, cadmium fume, oxides of nitrogen, or phosgene intoxication. With our need for preparedness against great fires in war targetareas involving heavy chemical industries, every physician must be familiar with oxygen equipment for positive-pressure inhalation. He must be alert for the unpredictable pulmonary oedema coming on after a latent period of several hours, following the inhalation of smoke and fumes. While many cases of acute pulmonary oedema are those seen in terminal states of hypertensive heart disease, an instance of endogenous oedema, it is our responsibility to get an accurate history of occupational exposure at once because we may be dealing with an instance of exogenous pulmonary oedema due to inhalation of a pulmonary irritant which, if recognized early, may well respond to oxygen treatment under pressure.