D is the correct answer. Why?

Explanation

Salicylate, in its various forms including aspirin, is found in a multitude of over-the-counter and prescription products. Toxicity may be from an acute overdose, usually intentional, or from chronic use due to its ubiquity in various medications. Aspirin, or acetylsalicylic acid, is generally hepatically metabolized to salicylate with a significant amount being protein-bound. In acute overdoses, unbound salicylate concentrations increase due to liver metabolism and protein-binding sites becoming saturated, forcing kidney clearance as the main route of elimination via zero-order kinetics. 

Salicylate stimulates the brain’s respiratory center to induce respiratory alkalosis early in toxicity. This is replaced by a wide anion gap metabolic acidosis later in the course of toxicity due to the inhibition of oxidative phosphorylation, increased fatty acid metabolism resulting in ketone bodies, and kidney retention of inorganic acids. Thus, mixed respiratory alkalosis and metabolic acidosis is classically recognized in salicylate or aspirin toxicity.

Early clinical features of an acute overdose include nausea, vomiting, tinnitus, and tachypnea. Chronic toxicity is frequently misdiagnosed and can present with a nebulous and often more severe array of symptoms and occurs generally in older patients who are on long-term medications containing salicylate. Altered mental status, seizures, pulmonary edema, hypotension, kidney injury, and hyperthermia portend a poor prognosis in salicylate toxicity. 

Evaluation of all patients with suspected salicylate poisoning should, at the minimum, include electrolyte measurements, blood gases, and trending salicylate levels. Along with resuscitation and supportive care, the treatment of salicylate toxicity is multifaceted. Activated charcoal binds salicylate and is beneficial even in late presentations. Whole bowel irrigation and multiple-dose activated charcoal can be used for sustained-release medications or massive ingestions. 

Urinary alkalinization is the mainstay of treatment for salicylate toxicity. Administration of a sodium bicarbonate drip increases salicylate excretion via “ion-trapping.” Hypokalemia must be corrected as this may interfere with effective urinary alkalinization. Hemodialysis is indicated for patients with severe toxicity, with indications including kidney injury, coma or seizure, salicylate level ≥ 100 mg/dL in acute toxicity (≥ 40 mg/dL in chronic toxicity), severe acidosis, acute lung injury, or a rising salicylate level despite urinary alkalinization. 

Intubation should be avoided in these patients until absolutely necessary due to the possible interruption of the patient’s compensatory respiratory alkalosis. If intubated, proper ventilation management is crucial with a focus on maintaining a high minute ventilation. Failing to do so can result in worsening acidosis and cardiac arrest.

Forced diuresis (A) with diuretics is ineffective and can actually cause clinical deterioration and hemodynamic instability.

Hemodialysis (B) is the first-line treatment for severe salicylate toxicity, but the patient above does not meet any criteria as his salicylate level is only 38 mg/dL, and he does not have evidence of other indications at this time. A salicylate level of 40 mg/dL is used to determine the need for dialysis in chronic toxicity as opposed to 100 mg/dL in acute toxicity.

Intubation (C) should be avoided if at all possible. It is very difficult to match the patient’s compensatory tachypnea and minute ventilation and resulting respiratory alkalosis. During intubation and mechanical ventilation, the patient can become hemodynamically unstable and arrest due to a worsening metabolic acidosis after blunting the patient’s ability to compensate effectively.