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Difficulty: MediumNephrology

A 52-year-old woman is evaluated on postoperative day 4 following a small bowel resection for severe intestinal strictures. Since the surgery, she has been receiving continuous low-wall suction via a nasogastric tube, which has drained 1.5 to 2 liters of bilious fluid daily. Over the last 12 hours, she has developed significant weakness, muscle cramps, and dizziness upon sitting up. Her temperature is 37.1°C (98.8°F), blood pressure is 96/60 mm Hg, heart rate is 110/min, and respiratory rate is 10/min. Physical examination reveals dry mucous membranes, flat jugular veins, and decreased skin turgor. Laboratory studies show the following:

- Serum sodium: 136 mEq/L
- Serum potassium: 2.8 mEq/L
- Serum chloride: 88 mEq/L
- Serum bicarbonate: 36 mEq/L
- Blood urea nitrogen: 42 mg/dL
- Serum creatinine: 1.6 mg/dL

Arterial blood gas (room air):
- pH: 7.52
- pCO 2_2: 49 mm Hg
- pO 2_2: 86 mm Hg

Urine chloride is 8 mEq/L. Which of the following is the most appropriate next step in management?

  1. Intravenous administration of 0.9% sodium chlorideAnswer
  2. B
    Intubation and mechanical ventilation
  3. C
    Intravenous administration of acetazolamide
  4. D
    Intravenous administration of 5% dextrose in water
  5. E
    Initiation of broad-spectrum antibiotics

Answer

The most appropriate next step is intravenous administration of 0.9% sodium chloride to correct the volume deficit and provide the necessary chloride to reverse the alkalosis.
The correct answer is intravenous administration of 0.9% sodium chloride. This patient has a severe metabolic alkalosis secondary to gastric acid (HCl) and volume loss from continuous nasogastric suctioning. The resulting volume depletion activates the renin-angiotensin-aldosterone system (RAAS), which promotes sodium reabsorption in the distal tubule at the expense of potassium and hydrogen ion excretion (perpetuating the alkalosis). Because the primary drivers are volume and chloride depletion, this is termed a 'saline-responsive' metabolic alkalosis, confirmed by a urine chloride level of < 20 mEq/L. Administering isotonic saline expands the intravascular space, deactivates RAAS, and provides the chloride necessary for the kidneys to excrete excess bicarbonate.

Step-by-Step Solution

1
Analyze the acid-base status on the arterial blood gas.
The pH is 7.52 (alkalemia). The elevated serum bicarbonate (36 mEq/L) identifies this as a primary metabolic alkalosis.
Establishing the primary acid-base disorder is required to interpret the compensatory mechanisms.
2
Calculate expected respiratory compensation for the metabolic alkalosis.
Expected pCO 2_2 = 40+0.7×(36−24)=48.440 + 0.7 \times (36 - 24) = 48.4 mm Hg. The measured pCO 2_2 of 49 mm Hg represents perfect physiological compensation.
This confirms there is no superimposed primary respiratory disorder, and the hypoventilation is appropriately compensatory.
3
Determine the etiology of the metabolic alkalosis using patient history and urine studies.
NG suction causes massive loss of H +^+ and Cl −^- (gastric acid) along with fluid. The low urine chloride (< 20 mEq/L) and elevated BUN/Cr ratio (> 20:1) confirm severe volume depletion.
Differentiating between saline-responsive (urine Cl < 20) and saline-resistant (urine Cl > 20) metabolic alkalosis dictates the treatment.
4
Select the optimal therapeutic intervention.
Volume resuscitation with 0.9% sodium chloride (normal saline).
Isotonic saline simultaneously expands the intravascular volume (turning off aldosterone) and replaces the depleted chloride, allowing the kidneys to excrete bicarbonate.

Key Concept

Patients with significant upper gastrointestinal fluid losses (via vomiting or nasogastric suction) develop a hypochloremic, hypokalemic metabolic alkalosis. Because this is a 'saline-responsive' alkalosis (urine Cl < 20 mEq/L), the definitive treatment is restoration of intravascular volume and chloride with intravenous 0.9% sodium chloride.
Estimated Time:1m 30s
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Nephrology

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