A 21-year-old woman is brought to the emergency department by her college roommate due to … — USMLE Step 2 CK

A $21$ -year-old woman is brought to the emergency department by her college roommate due to sudden-onset confusion, agitation, and rapid breathing. The roommate reports that the patient has been highly stressed studying for final examinations and recently complained of a continuous ringing sensation in her ears. The patient has no known past medical history and takes no medications. Her temperature is $37.9^\circ\text{C}$ ( $100.2^\circ\text{F}$ ), blood pressure is $112/70 \text{ mm Hg}$ , pulse is $118/\text{min}$ , and respirations are $32/\text{min}$ . Physical examination reveals a diaphoretic, anxious woman with deep, rapid breaths. There are no focal neurologic deficits.

Laboratory studies show the following:

Test	Result
Serum sodium	$140 \text{ mEq/L}$
Serum potassium	$3.6 \text{ mEq/L}$
Serum chloride	$104 \text{ mEq/L}$
Serum bicarbonate	$12 \text{ mEq/L}$
Blood urea nitrogen	$16 \text{ mg/dL}$
Serum creatinine	$1.0 \text{ mg/dL}$
Blood glucose	$95 \text{ mg/dL}$

Arterial blood gas on room air:

Test	Result
pH	$7.44$
$\text{PaCO}_2$	$18 \text{ mm Hg}$
$\text{PaO}_2$	$98 \text{ mm Hg}$

Which of the following is the most appropriate next step in management?

Intravenous sodium bicarbonateAnswer
B
Endotracheal intubation
C
Intravenous regular insulin and normal saline
D
Intravenous ceftriaxone and vancomycin
E
Intravenous furosemide and noninvasive positive pressure ventilation

Answer

Intravenous sodium bicarbonate is the correct management.

The patient's presentation of tinnitus, tachypnea, fever, and confusion, combined with a mixed high anion gap metabolic acidosis and primary respiratory alkalosis, is classic for acute salicylate toxicity. Salicylates directly stimulate the medullary respiratory center (causing a primary respiratory alkalosis) and uncouple oxidative phosphorylation (causing an accumulation of organic acids and a primary high anion gap metabolic acidosis). The most appropriate next step in management is the administration of intravenous sodium bicarbonate. This alkalinizes both the serum and the urine. Serum alkalinization keeps salicylates in their deprotonated (ionized) form, preventing them from crossing the blood-brain barrier and worsening central nervous system toxicity. Urine alkalinization traps the ionized salicylates in the renal tubules, significantly enhancing their renal excretion.

Step-by-Step Solution

Calculate the anion gap to identify the primary metabolic disturbance.

\text{AG} = 140 - (104 + 12) = 24 \text{ mEq/L}

, indicating a high anion gap metabolic acidosis.

An elevated anion gap is the first step in diagnosing the etiology of a metabolic acidosis.

Apply Winter's formula to determine the expected respiratory compensation.

\text{Expected PaCO}_2 = 1.5 \times 12 + 8 = 26 \pm 2 \text{ mm Hg}

This determines if the respiratory response is purely compensatory or if a secondary acid-base disorder is present.

Compare the actual

\text{PaCO}_2

to the expected

\text{PaCO}_2

The actual

\text{PaCO}_2

(

18 \text{ mm Hg}

) is significantly lower than the expected range (

24-28 \text{ mm Hg}

A lower than expected

\text{PaCO}_2

confirms the presence of a concomitant primary respiratory alkalosis.

Synthesize the mixed acid-base disorder with the clinical presentation.

The combination of tinnitus, fever, tachypnea, agitation, and a mixed high anion gap metabolic acidosis with primary respiratory alkalosis strongly indicates salicylate toxicity.

Recognizing this toxidrome is essential to avoid potentially fatal mismanagement.

Select the appropriate targeted therapy for salicylate toxicity.

Intravenous sodium bicarbonate is selected to alkalinize the blood and urine.

Alkalinization traps the salicylate ion in the renal tubules, enhancing excretion and reducing central nervous system toxicity.

Key Concept

Patients with acute salicylate toxicity present with a classic mixed acid-base disorder: a primary respiratory alkalosis (due to direct medullary stimulation) and a high anion gap metabolic acidosis (due to uncoupling of oxidative phosphorylation). Management centers on urine alkalinization with intravenous sodium bicarbonate.

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