Module 2: Clinical Presentation of Salicylate Toxicity

2.1 Common Sources and Causes of Salicylate Poisoning

Salicylate toxicity most often occurs from accidental or intentional overdose of aspirin tablets. Other potential sources include oil of wintergreen which contains up to 98% methyl salicylate, bismuth subsalicylate tablets such as Pepto-Bismol, and topical salicylates in wart removers, acne treatments and muscle rubs.

In the pediatric population, unsupervised ingestion of salicylate-containing products is a major concern. In adolescents and adults, purposeful overdose in suicide attempts accounts for many clinically significant exposures. Prescription misuse and therapeutic errors also occur, especially in older adults with cognitive decline and multiple comorbidities.

The formulation and preparation of the salicylate product can significantly impact absorption and clinical toxicity. Enteric coated tablets that retard dissolution are associated with delayed absorption and peak concentrations occurring hours to days post-ingestion. In contrast, chewing tablets, powders and oil of wintergreen are rapidly absorbed. Large acute ingestions are more likely to result in toxicity compared to chronic repeated smaller ingestions over several days. However, chronic accumulation can also lead to adverse outcomes.

2.2 Identifying Symptoms and Signs of Acute and Chronic Salicylate Toxicity

In acute salicylate poisoning, early symptoms of nausea, vomiting, tinnitus and tachypnea manifest within 1-2 hours postingestion. As toxicity progresses over the next 6-24 hours, more severe manifestations emerge including agitation, delirium, hyperthermia, dehydration, pulmonary edema, cerebral edema, seizures, coma and cardiovascular collapse. Mortality is high once patients develop multiple organ failure.

Chronic salicylate toxicity follows a more insidious course and often goes unrecognized for days before manifesting with nonspecific constitutional symptoms. Presentations mimicking sepsis, pneumonia, delirium, and primary cardiac or neurologic disorders are common. Altered mental status, respiratory distress, vomiting, diarrhea, edema and fever are frequent signs. Patients with chronic toxicity can develop severe illness even with lower serum salicylate concentrations compared to acute ingestions.

2.3 Factors Influencing Clinical Presentation

Age significantly impacts the clinical trajectory in salicylate toxicity. Infants and young children absorb salicylates efficiently and manifest more severe toxicity from relatively small ingested doses owing to lower body mass. At the other end of the spectrum, elderly patients have reduced drug clearance as a result of declining hepatic and renal function. Their risk for adverse reactions is compounded by polypharmacy, drug interactions and chronic comorbidities that impair compensatory responses.

Pre-existing impairment of renal, hepatic, pulmonary or cardiac function predisposes patients to more severe clinical effects from salicylate poisoning by compromising elimination and physiologic compensation. Similarly, baseline cerebral edema, chronic respiratory disease or metabolic acidosis reduces reserves to tolerate further insult from toxicity. Careful monitoring and aggressive treatment is warranted in these high risk groups based on their limited capacity to tolerate exposure.