A 64-year-old woman is brought to the emergency department by her son due to worsening con… — USMLE Step 2 CK

A 64-year-old woman is brought to the emergency department by her son due to worsening confusion, nausea, and ringing in her ears for the past 24 hours. She has a history of chronic obstructive pulmonary disease (COPD), hypertension, and osteoarthritis, for which she frequently takes over-the-counter analgesics. She also underwent transsphenoidal resection of a pituitary macroadenoma 5 years ago.

Vital signs: Temperature 37.1°C (98.8°F), blood pressure 110/70 mmHg, heart rate 112/min, respiratory rate 28/min.

Physical examination reveals dry mucous membranes and lethargy. Lung auscultation reveals clear breath sounds bilaterally. There is no jugular venous distention.

Laboratory results:
Sodium: 141 mEq/L
Potassium: 3.9 mEq/L
Chloride: 105 mEq/L
Bicarbonate: 14 mEq/L
Blood urea nitrogen: 38 mg/dL
Creatinine: 1.8 mg/dL
Thyroid-stimulating hormone (TSH): 1.1 µU/mL (normal: 0.4–4.0 µU/mL)
Free T4: 0.5 ng/dL (normal: 0.9–1.7 ng/dL)

Arterial blood gas on room air:
pH: 7.42
$PaCO_2$ : 22 mmHg
$PaO_2$ : 96 mmHg

A urine culture sent 3 days ago from an outpatient clinic visit for mild dysuria has returned positive for $>100,000$ CFU/mL of *Escherichia coli*, which is susceptible to cephalexin and nitrofurantoin, but resistant to fluoroquinolones.

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

Intravenous sodium bicarbonateCevap
B
Intravenous 0.9% normal saline and observation
C
Intravenous furosemide
D
Intravenous piperacillin-tazobactam
E
Initiation of levothyroxine

Cevap

Intravenous sodium bicarbonate

The correct intervention is intravenous sodium bicarbonate. This patient presents with characteristic features of salicylate (aspirin) toxicity, specifically tinnitus, nausea, tachypnea, and altered mental status. Salicylates cause a classic mixed acid-base disorder. They directly stimulate the medullary respiratory center, causing hyperventilation and a primary respiratory alkalosis. Simultaneously, they uncouple oxidative phosphorylation, leading to the accumulation of unmeasured organic acids and a primary high anion gap metabolic acidosis (AG =

141 - (105 + 14) = 22

). Winter's formula shows an expected

PaCO_2

29 \pm 2

mmHg; the measured

PaCO_2

of 22 mmHg confirms a concomitant primary respiratory alkalosis. The near-normal pH of 7.42 is a typical feature of this mixed disorder. Treatment focuses on stabilizing the patient and alkalinizing the urine with continuous intravenous sodium bicarbonate. Alkalinization converts salicylic acid into its ionized, lipophobic form in the renal tubules, trapping it in the urine and significantly enhancing its excretion.

Adım Adım Çözüm

Analyze the acid-base status using the provided arterial blood gas and basic metabolic panel.

The anion gap is calculated as

141 - (105 + 14) = 22

mEq/L, indicating a primary high anion gap metabolic acidosis. The pH is unexpectedly normal (7.42).

Determining the primary disorder and calculating the anion gap are the first steps in evaluating any acid-base derangement.

Calculate expected respiratory compensation using Winter's formula.

Expected

PaCO_2 = 1.5 \times 14 + 8 \pm 2 = 29 \pm 2

mmHg. The actual

PaCO_2

is 22 mmHg, which is significantly lower than expected.

If the measured

PaCO_2

falls outside the expected range, a secondary primary acid-base disorder is present. In this case, there is a concurrent primary respiratory alkalosis.

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

A mixed high anion gap metabolic acidosis and primary respiratory alkalosis in a patient with tinnitus (ringing in ears) points to salicylate (aspirin) toxicity.

Salicylates directly stimulate the medullary respiratory center (respiratory alkalosis) and uncouple oxidative phosphorylation, leading to the accumulation of organic acids (metabolic acidosis).

Determine the definitive treatment for the identified toxicity.

Administration of intravenous sodium bicarbonate is required.

Sodium bicarbonate alkalinizes the blood and urine. Alkalemia promotes the movement of salicylates out of the central nervous system, while alkalinized urine traps the ionized form of salicylate, accelerating its excretion.

Anahtar Kavram

Patients with severe salicylate toxicity classically present with a mixed primary respiratory alkalosis and primary high anion gap metabolic acidosis. Treatment includes intravenous sodium bicarbonate to alkalinize the urine and enhance salicylate excretion.

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