Salicylate overdose has made several exam appearances:
Many of these SAQs enter into protracted discussions of salicylate toxicity. The tendency of salicylates to produce a high anion gap metabolic acidosis is discussed briefly elsewhere. Additionally, the mechanisms of salicylate-induced acid base disturbance are dissected in great detail in another chapter. Here, a broad general overview is offered. The ideal online reference for this topic is the LITFL page on salicylate poisoning. Among published resources, one could do no better than Pearlman and Gambhir's article from 2009. Unless otherwise indicated, the information in this chapter is derived from this article.
Serum level 30-50mg/dL: | Serum level 50-75mg/dL: | Serum level >75mg/dL: |
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The classical trend is for these people to present with tinnitus, fever and respiratory alkalosis. One does not need to have tinnitus or hearing loss in order to be suffering from severe toxicity; conversely it can be seen even in therapeutic doses. They progress to hosing you with vomit, because of direct irritation of the gastric mucosa as well as irritation of the medullary chemoreceptor regions. The ensuing volume depletion may give rise to hypotension.
They then go on to become delirious. The mechanism for this is a combination of direct neurotoxicity, neuroglycopenia and cereberal oedema. The patient ultimately develops severe metabolic acidosis with multi organ system failure. The metabolic acidosis is a high anion gap variety, with lactate and ketones being the extra anions. The salicylic acid itself contributes very little to the anion gap, even in high doses. The acidaemia then promotes the entry of salicylate into the CNS, and the level of consciousness degenerates into profound coma with seizures.
Question 8 from the second paper of 2016 asks more generally about "haematologic abnormalities" whcih can be expected from a salicylate overdose. These were reviewed in an ancient article by Rothschild (1979)
Serial salicylate level measurement is meaningless, because:
Salicylate level may be declining because
O'Malley, Gerald F. "Emergency department management of the salicylate-poisoned patient." Emergency medicine clinics of North America 25.2 (2007): 333-346.
Pinedo, H. M., L. B. van de Putte, and E. A. Loeliger. "Salicylate-induced consumption coagulopathy." Annals of the rheumatic diseases 32.1 (1973): 66.
Shapiro, Shepard, Milton H. Redish, and Harold A. Campbell. "Studies on Prothrombin: IV. The Prothrombinopenic Effect of Salicylate in Man."Experimental Biology and Medicine 53.2 (1943): 251-254.
Pearlman, Brian L., and Rashi Gambhir. "Salicylate Intoxication." Postgraduate medicine 121.4 (2009).
Rothschild, Bruce M. "Hematologic perturbations associated with salicylate." Clinical Pharmacology & Therapeutics 26.2 (1979): 145-152.
Sanford-Driscoll, Marcia, and Leroy C. Knodel. "Induction of hemolytic anemia by nonsteroidal antiinflammatory drugs." Annals of Pharmacotherapy 20.12 (1986): 925-934.
Mandelli, M., and G. Tognoni. "Monitoring plasma concentrations of salicylate." Clinical pharmacokinetics 5.5 (1980): 424-440.
Done, Alan K. "SALICYLATE INTOXICATION Significance of Measurements of Salicylate in Blood in Cases of Acute Ingestion." Pediatrics 26.5 (1960): 800-807.
Kashani, John, and Richard D. Shih. "Salicylate Overdose." Encyclopedia of Intensive Care Medicine (2012): 2011-2014.