Overview
The Clinical Pattern
Salicylate poisoning is not simply “too much aspirin.” Salicylates stimulate the medullary respiratory center, so the patient breathes rapidly and removes excess carbon dioxide.
Salicylate poisoning is not simply “too much aspirin.” Salicylates stimulate the medullary respiratory center, so the patient breathes rapidly and removes excess carbon dioxide. This produces an early primary respiratory alkalosis. At the same time, salicylates disrupt cellular energy production and increase the generation of organic acids. The result is an anion gap metabolic acidosis. The classic laboratory picture is therefore mixed respiratory alkalosis and metabolic acidosis, not isolated respiratory alkalosis. This acid-base pattern explains a dangerous clinical shift. Tachypnea may initially help maintain the blood pH. As toxicity worsens, metabolic acid production can exceed that compensation. Falling pH increases the nonionized fraction of salicylate, allowing more drug to enter the central nervous system and intensify neurologic toxicity. A patient who becomes acidemic, confused, or less able to sustain rapid breathing can deteriorate quickly. Salicylates also impair heat production and hearing pathways. Tinnitus, nausea, vomiting, diaphoresis, fever, tachycardia, dehydration, and tachypnea are common clues. Severe poisoning may cause altered mental status, seizures, pulmonary edema, renal failure, hypotension, or circulatory collapse. Acute toxicity is expected after ingestion of more than 150...