Salicylate poisoning is a toxic condition resulting from an overdose or excessive accumulation of salicylate compounds in the body. The most common source is aspirin, also known as acetylsalicylic acid. Other sources include oil of wintergreen, bismuth subsalicylate found in medications like Pepto-Bismol, and various topical analgesics and liniments. Poisoning can occur from acute overdose or chronic overuse of these medications.
Salicylate poisoning presents with a range of clinical manifestations. Early symptoms include tinnitus, which is ringing in the ears, along with nausea and vomiting. As poisoning progresses, patients develop hyperpnea, characterized by deep and rapid breathing due to respiratory stimulation. Fever and sweating are common due to the effect on temperature regulation. Neurological symptoms include confusion and agitation, which can progress to seizures and coma in severe cases. These symptoms result from salicylate's effects on multiple body systems, including the central nervous system, respiratory system, and metabolic processes.
The pathophysiology of salicylate poisoning involves several key mechanisms. Salicylates uncouple oxidative phosphorylation in mitochondria, leading to increased metabolic rate and heat production. This explains the fever seen in patients. Early in poisoning, direct stimulation of the respiratory center causes hyperventilation, leading to respiratory alkalosis with an elevated blood pH. As poisoning progresses, the uncoupling of oxidative phosphorylation leads to accumulation of organic acids and metabolic acidosis, causing the pH to drop. Other effects include altered glucose metabolism, electrolyte imbalances particularly involving potassium, and dehydration from increased insensible losses and vomiting.
Diagnosing salicylate poisoning relies on clinical history, serum salicylate levels, arterial blood gas analysis, and electrolyte panels. The Done nomogram helps assess severity based on serum salicylate levels and time since ingestion, categorizing cases as mild, moderate, or severe. Management begins with supportive care to maintain vital functions. For recent ingestions, activated charcoal can reduce absorption. Urine alkalinization with sodium bicarbonate enhances salicylate excretion by trapping ionized salicylate in the urine. Fluid and electrolyte replacement addresses dehydration and imbalances. In severe cases, especially with renal failure, altered mental status, or very high salicylate levels, hemodialysis is the most effective method for rapidly removing salicylates from the bloodstream.
To summarize what we've learned about salicylate poisoning: It results from overdose or excessive accumulation of salicylate compounds, most commonly aspirin. The classic symptoms include tinnitus, hyperventilation, fever, and altered mental status, which can progress to seizures and coma in severe cases. The underlying pathophysiology involves uncoupling of oxidative phosphorylation, leading to respiratory alkalosis in early stages followed by metabolic acidosis as poisoning progresses. Diagnosis relies on clinical history, serum salicylate levels, and assessment of acid-base status. Treatment approaches include supportive care, activated charcoal for recent ingestions, urine alkalinization to enhance excretion, and hemodialysis for severe cases. Early recognition and appropriate management are essential to prevent serious complications and improve outcomes.