Case #11: Heart Pills
Author: Neeraj Chhabra, MD
Peer Reviewer: Navneet Cheema, MD
An 18 year old male with no known past medical history presents to the emergency department via ambulance two hours after ingesting a bunch of his father’s “heart pills”. Upon arrival, he is alert, oriented, and in mild respiratory distress. He is tachypneic but able to speak in full sentences. He had two episodes of non-bloody, non-bilious emesis in the ambulance and complains of tinnitus. His father soon arrives carrying an empty bottle of aspirin.
Vitals: Temp: 98.6, HR: 100, RR: 28, BP: 130/70, O2 sat: 100% on RA
Describe the pathophysiology of aspirin toxicity. How does it affect the acid-base status?
Aspirin causes a direct stimulatory effect on the respiratory center of the medulla oblongata resulting in a respiratory alkalosis. Aspirin also uncouples oxidative phosphorylation, interfering with aerobic metabolism and resulting in a metabolic acidosis. Thus, aspirin causes both a primary respiratory alkalosis and a primary metabolic acidosis, leading to a mixed acid-base disorder.
What method of GI decontamination would be most beneficial for this patient?
Activated charcoal (AC) is effective in decreasing the amount of aspirin that is absorbed. In order to be a candidate for AC, patients must be protecting their airway, tolerating PO, and have a preserved mental status. Repeated doses of AC are safe and result in reduced salicylate levels. Whole-bowel irrigation is not recommended secondary to lack of evidence and poor patient tolerance. Bezoars are common with enteric-coated aspirin and can result in fluctuating serum salicylate levels and prolonged GI absorption.
The patient’s initial serum salicylate level returns at 63mg/dL. All other lab assessments are normal. What treatment should be considered at this point?
Urine and serum alkalinization are important treatments for salicylate toxicity. Alkalinization reduces conversion of the acetylsalicylic acid (ASA, aspirin) from the charged (ionic) to the uncharged (nonionic) state. The uncharged ion is not able to cross the blood-brain barrier and cannot be reabsorbed from the urinary system, resulting in “ion trapping”. Alkalinization is accomplished by adding 3 ampules of NaHCO3 and 40mEq of KCl to 1 liter of D5W and titrating to a urinary pH ≥ 8.
One of your colleagues suggests using a nomogram to guide treatment. What are the pitfalls of the nomogram?
The Done nomogram was published in 1960 to aid decision-making in acute aspirin ingestion. It was developed in pediatric patients. It has been demonstrated to have very little application in aspirin-poisoned adults, chronic ingestions, and ingestions less than 6 hours old. It is almost never used clinically by medical toxicologists.
What are the risks associated with endotracheal intubation in aspirin overdose patients?
Endotracheal intubation removes the patient’s ability to hyperventilate and compensate for the metabolic demands of salicylate toxicity. It is best to maximize other therapies before progressing to intubation. If endotracheal intubation is required, remember to match the patient’s spontaneous minute ventilation with the ventilator settings, especially while the patient remains paralyzed.
What are the indications for hemodialysis in salicylate toxicity?
-Severe refractory acidosis or hypotension.
-Inability to tolerate the fluids required for alkalinization (i.e. renal failure, congestive heart failure, acute lung injury).
-Persistent CNS disturbances: altered mental status, seizures, agitation.
-High serum aspirin concentration (Acute: >100 mg/dL, Chronic: > 60 mg/dL; Note: Remember that dialysis should be considered at lower levels if the above conditions exist.)
References:
Dargan PI, Wallace CI, Jones AL. An evidence based flowchart to guide the management of acute salicylate (aspirin) overdose. Emerg Med J. 2002 May;19(3):206-9.
O’Malley GF. Emergency department management of the salicylate-poisoned patient. Emerg Med Clin North Am. 2007 May;25(2):333-46
Worthley LI. Clinical toxicology: part I. Diagnosis and management of common drug overdosage. Crit Care Resusc. 2002 Sep;4(3):192-215.
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