Abstract
To the Editor: The suggestion that endogenous opiates might play a major role in the pathogenesis of non-cardiac pulmonary edema occurring as a result of obstructive sleep apnea is an intriguing one. If severe hypoxemia is associated with the release of endogenous opiates, as suggested by Chernick et al,1Chernick V Madansky DL Lawson EE Naloxone decreases the duration of primary apnea with neonatal asphyxia.Pediatr Res. 1980; 14: 357-359Crossref PubMed Scopus (54) Google Scholar Dr. Smitz's hypothesis is certainly quite reasonable. It is well known that overdoses of exogenous opiates may result in noncardiac pulmonary edema in some patients. Noncardiac pulmonary edema appears to be quite uncommon in patients with sleep apnea, and if the mechanism by which exogenous and endogenous opiates produce pulmonary edema is similar, one would almost have to postulate endogenous opiate “poisoning” in those patients who develop it. Since alternative mechanisms for the development of pulmonary edema in such patients seem quite plausible, it may be that multiple factors are involved. We agree with Dr. Smitz, however, that the role of endogenous opiates in the development of pulmonary edema in the patient we described2Chaudhary BA Ferguson DS Speir WA Pulmonary edema as a presenting feature of sleep apnea syndrome.Chest. 1982; 82: 122-124Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar and, indeed, in the pathogenesis of sleep apnea syndromes, deserves careful investigation.
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