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Zorluk: ZorGeneral Internal Medicine

Paramedics bring an 81-year-old female to the acute care unit from her assisted living facility. Staff members called for help after noticing she was acting confused and breathing rapidly since she woke up. Her medical history is notable for severe osteoarthritis, hypertension, and diet-controlled type 2 diabetes mellitus. According to the facility's notes, she had been complaining of a constant "ringing" sound in her ears for the past 48 hours and self-administering extra over-the-counter analgesics for knee pain.

On arrival, her temperature is 37.1°C (98.8°F), blood pressure is 135/85 mm Hg, pulse is 112/min, and respirations are 28/min. Oxygen saturation is 96% on ambient air.

The patient appears mildly lethargic and is oriented only to person. Her mucous membranes are notably dry. Auscultation of the chest reveals a rapid, regular heart rate with no murmurs, and breath sounds are clear in all lung fields. The abdomen is non-tender. Trace pitting edema is noted at the ankles.

Laboratory evaluation demonstrates:
Sodium: 142 mEq/L
Potassium: 3.9 mEq/L
Chloride: 102 mEq/L
Bicarbonate: 14 mEq/L
Blood urea nitrogen: 24 mg/dL
Creatinine: 1.2 mg/dL
Glucose: 105 mg/dL

Arterial blood gas analysis on ambient air reveals:
pH: 7.42
pCO2: 20 mm Hg
pO2: 92 mm Hg

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

  1. A
    Intravenous furosemide
  2. B
    Nebulized albuterol and ipratropium
  3. C
    Intravenous piperacillin-tazobactam
  4. Intravenous sodium bicarbonateCevap
  5. E
    Intravenous 0.9% sodium chloride and supportive observation

Cevap

Intravenous sodium bicarbonate
This patient's clinical presentation (tinnitus, confusion, tachypnea) and laboratory findings (mixed high anion gap metabolic acidosis and primary respiratory alkalosis) are highly characteristic of salicylate toxicity. Salicylates directly stimulate the medullary respiratory center, causing early primary respiratory alkalosis. As toxicity progresses, the uncoupling of oxidative phosphorylation leads to the accumulation of organic acids, resulting in a concomitant high anion gap metabolic acidosis. This mixed disorder often keeps the pH near normal (e.g., 7.42). The next best step in management is to administer intravenous sodium bicarbonate. This alkalinizes the urine (target pH ≥7.5\ge 7.5), which converts lipophilic salicylic acid into its ionized, lipophobic form (salicylate). This 'ion trapping' prevents renal tubular reabsorption and significantly enhances the excretion of the toxin.

Adım Adım Çözüm

1
Calculate the anion gap.
Na+−(Cl−+HCO3−)=142−(102+14)=26 mEq/L\text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 142 - (102 + 14) = 26 \text{ mEq/L}.
To identify the presence of a primary high anion gap metabolic acidosis.
2
Apply Winter's formula to determine the expected pCO2.
Expected pCO2=(1.5×14)+8=29±2 mm Hg\text{pCO}_2 = (1.5 \times 14) + 8 = 29 \pm 2 \text{ mm Hg}. The measured pCO2\text{pCO}_2 is 20 mm Hg20 \text{ mm Hg}.
To assess whether respiratory compensation is appropriate or if a secondary acid-base disorder is present.
3
Synthesize the clinical and laboratory data.
The patient has a mixed high anion gap metabolic acidosis and primary respiratory alkalosis, accompanied by tinnitus and confusion in the setting of excessive analgesic use.
This triad of findings is pathognomonic for salicylate (aspirin) toxicity.
4
Determine the appropriate management.
Administer intravenous sodium bicarbonate.
To alkalinize the urine, which traps salicylate in its ionized form and enhances renal excretion.

Anahtar Kavram

Adults with salicylate toxicity classically present with a mixed high anion gap metabolic acidosis and primary respiratory alkalosis; the next best step in management is urine alkalinization with intravenous sodium bicarbonate.
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General Internal Medicine

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