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Zorluk: KolayNephrology

A 42-year-old male patient is admitted to the intensive care unit for the management of severe acute pancreatitis. On presentation, he was tachycardic and hypotensive. Over the initial 24 hours of admission, he received 7 liters of 0.9% sodium chloride intravenously for aggressive fluid resuscitation. His vital signs are now stable. Laboratory studies obtained on hospital day 2 reveal the following:

Serum sodium: 142 mEq/L142 \text{ mEq/L}
Serum potassium: 4.2 mEq/L4.2 \text{ mEq/L}
Serum chloride: 115 mEq/L115 \text{ mEq/L}
Serum bicarbonate: 15 mEq/L15 \text{ mEq/L}
Blood urea nitrogen: 18 mg/dL18 \text{ mg/dL}
Serum creatinine: 0.9 mg/dL0.9 \text{ mg/dL}

Arterial blood gas on room air shows:
pH: 7.287.28
PaCO2PaCO_2: 30 mmHg30 \text{ mmHg}
PaO2PaO_2: 92 mmHg92 \text{ mmHg}

Which of the following is the most likely mechanism underlying this patient's current acid-base abnormality?

  1. Intravenous administration of a fluid with a supraphysiologic chloride concentrationCevap
  2. B
    Hypoperfusion-induced shift to anaerobic metabolism and lactate production
  3. C
    Inadequate ventilatory response to a primary metabolic acid-base derangement
  4. D
    Failure of the renal tubules to reabsorb filtered bicarbonate
  5. E
    Retention of unmeasured uremic anions due to acute kidney injury

Cevap

Intravenous administration of a fluid with a supraphysiologic chloride concentration
This patient has a normal anion gap metabolic acidosis. The anion gap is calculated as Na+−(Cl−+HCO3−)Na^+ - (Cl^- + HCO_3^-), which in this case is 142−(115+15)=12 mEq/L142 - (115 + 15) = 12 \text{ mEq/L} (normal is typically 8-12 mEq/L). The compensatory respiratory response is appropriate, as confirmed by Winter's formula: expected PaCO2=(1.5×15)+8=30.5±2 mmHgPaCO_2 = (1.5 \times 15) + 8 = 30.5 \pm 2 \text{ mmHg}, matching the measured value of 30 mmHg. The cause of this isolated, normal anion gap metabolic acidosis is the aggressive fluid resuscitation with 0.9% normal saline. Normal saline is actually supraphysiologic in its chloride content (154 mEq/L compared to a normal serum chloride of ~100 mEq/L). Massive infusion expands the extracellular volume and drives up serum chloride, which causes a relative decrease in serum bicarbonate to maintain electrical neutrality, resulting in hyperchloremic metabolic acidosis.

Adım Adım Çözüm

1
Identify the primary acid-base disorder.
The pH is acidemic (7.28) and the serum bicarbonate is low (15 mEq/L), indicating a primary metabolic acidosis.
Establishing the primary disorder dictates which compensatory formulas and diagnostic algorithms to use.
2
Calculate the serum anion gap.
Anion Gap = Na+−(Cl−+HCO3−)Na^+ - (Cl^- + HCO_3^-) = 142−(115+15)142 - (115 + 15) = 12 mEq/L12 \text{ mEq/L}.
Metabolic acidosis must be classified into high anion gap or normal anion gap (hyperchloremic) to narrow the differential diagnosis.
3
Calculate the expected respiratory compensation.
Using Winter's formula: Expected PaCO2=(1.5×15)+8=30.5±2PaCO_2 = (1.5 \times 15) + 8 = 30.5 \pm 2. The actual PaCO2PaCO_2 is 30 mmHg, which is perfectly compensated.
Checking compensation ensures there is no superimposed primary respiratory acid-base disorder.
4
Determine the cause of the normal anion gap metabolic acidosis.
The patient received 7 liters of 0.9% sodium chloride, which contains 154 mEq/L of chloride (supraphysiologic compared to the normal serum level of ~100 mEq/L), leading to hyperchloremic acidosis.
Correlating the calculated laboratory derangement with the clinical history provides the final diagnosis.

Anahtar Kavram

Normal saline (0.9% NaCl) contains 154 mEq/L of chloride. Large volume resuscitation with this fluid causes a hyperchloremic, normal anion gap metabolic acidosis.
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Nephrology

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