Current Management of Salicylate-induced Pulmonary Edema

James K. Glisson, MD, PharmD; Telciane S. Vesa, MD; Mark R. Bowling, MD, FACP


South Med J. 2011;104(3):225-232. 

In This Article


A total of 39 publications were included in this review describing patients age 19 or older.[1–39] A total of 139 cases of possible SIPE in adults have been documented. Many of the cases published are from 1950 to the 1980's, and the amount of clinical information included often made interpretation of data difficult. The majority of excluded publications involved pediatric cases or review articles. The Table lists publications included in this review, plus a brief description.[1–39] Many pediatric cases result from accidental overdose and potentially would not have the confounder of "acute or chronic" or simply "chronic" use; therefore, pediatric cases were excluded.

Some information on SIPE was derived from retrospective chart reviews and included post-mortem data. It has been suggested that cigarette smoking, chronic salicylate ingestion, metabolic acidosis, and neurological symptoms on admission are strong risk factors for the development of SIPE in adults over 30 years of age.[18,20] However, the data is not conclusive regarding the risk of SIPE in patients who smoke. Also, Anderson et al[10] does not clearly comment on multi-drug ingestions, a possible contributor to the development of pulmonary edema. This information is especially important in cases of co-ingestion of salicylates with central nervous system (CNS) depressants. Finally, both Anderson et al[10] and Heffner and Sahn[16] briefly discuss treatment regimens of the patients included, but fail to report the use of CNS depressants or ventilator settings. Walters et al[19] makes little mention of treatment regimen, but does note the co-ingestion of acetaminophen in one patient with SIPE. Although these investigations were published about 30 years ago and are incomplete, they do provide a foundation for the medical community to build upon. Many of the publications have confounding factors and often do not include clear information on ingestion type (n = 15) or smoking history (n = 28), despite both being suggested risk factors.[1–13,15–18,22–29,32–35,39] Additional research on SIPE is needed to clearly define patients who may be at greatest risk of developing this condition.

Contributing to the perplexity of SIPE, the terminology in the literature is inconsistent with the use of terms such as "chronic," "acute," and "acute on chronic," when referring to salicylate intoxication and use. For example, a retrospective review defined acute as a single ingestion, while chronic was repetitive administration for a minimum of twelve hours.[40] A recent guideline by the American Association of Poison Control Centers suggests a standardization of these terms.[41] Acute is defined as exposure of less than eight hours, whereas chronic is defined as exposure longer than this duration. Some publications refer to "acute" toxicity when it actually occurred over several days. In this review and in the Table, these standardized definitions are utilized.[41]

Finally, the biochemical cause of pulmonary edema may be related to an increase in permeability within the capillaries of the lung leading to "protein leakage" and transudation of fluid in both renal and pulmonary tissues. The alteration in renal tubule permeability may lead to a change in colloid osmotic pressure and thus facilitate pulmonary edema. Also, an alteration of prostacyclin production, which influences capillary permeability, may play a role.[10,14,42] An investigation by Bowers et al[43] in sheep demonstrated intravenous administration of aspirin-caused noncardiogenic pulmonary edema without altering pulmonary vascular pressures. However, the exact mechanism of SIPE is yet to be completely elucidated.


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