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[Nonhemodynamic pulmonary edema due to toxins].

Authors: J P, Frejaville; Y, Tourtier; J, Susini; A, De Courcy;

pmid: 9874

[Nonhemodynamic pulmonary edema due to toxins].

Abstract

Lesional pulmonary edema caused by substances which are directly caustic for the gastrointestinal pathways (strong acids and bases, inhaled vomit) are opposed by their immediate and long-term gravity with those due to cardiotropic medicamentatous toxins or volemic overloading which lead to curable pulmonary edema. Material and human factors, in favour of accidental intoxication are compensated for by the fact that many toxins produce vapours which are strongly irritant for the upper respiratory pathways: this prevents prolonged exposure and therefore wards off edema. Drug intoxication by ingestion can lead to pulmonary edema by relative or absolute volemic overload, by allergic accidents or by immaturity of the enzyme degradation systems. It seems to us that the notions of "neurological" and "metabolic" toxic edema should be abandoned. In lesional edema the treatment is that of the acute respiratory failure. The combination of pethidine, promethazine, and chlorpromazine gives good immediate results. Owing to careful follow-up, hemodynamic pulmonary edema should most frequently be avoided.

Keywords

Male, Heart Diseases, Poisoning, Humans, Pulmonary Edema, Acute Kidney Injury, Middle Aged, Lung

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citations
The total number of citations received by all articles of the researcher of interest.
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
0
Average
Average
Average
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