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Difficulty: EasyNephrology

A 4242-year-old male is evaluated in the urgent care clinic for persistent nausea and non-bilious emesis that has occurred multiple times daily over the past four days. He reports feeling profoundly weak and dizzy when standing up. His blood pressure is 98/6098/60 mm Hg while supine and drops to 82/5082/50 mm Hg upon standing. Heart rate is 112112/min. Physical examination reveals dry oral mucosa and decreased skin turgor. Laboratory studies show:

Na+Na^+: 137137 mEq/L
K+K^+: 2.82.8 mEq/L
Cl−Cl^-: 8686 mEq/L
HCO3−HCO_3^-: 3636 mEq/L
BUNBUN: 4242 mg/dL
Creatinine: 1.31.3 mg/dL

Arterial blood gas reveals a pHpH of 7.537.53 and a pCO2pCO_2 of 4646 mm Hg.

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

  1. A
    Intravenous 5%5\% dextrose in water
  2. B
    Intravenous acetazolamide
  3. Intravenous 0.9%0.9\% sodium chlorideAnswer
  4. D
    Intravenous sodium bicarbonate
  5. E
    Oral spironolactone

Answer

Intravenous 0.9%0.9\% sodium chloride
The correct intervention is administering intravenous isotonic normal saline. This patient has a classic saline-responsive metabolic alkalosis secondary to severe and recurrent vomiting. The profound loss of gastric fluid leads to a hypochloremic, hypokalemic metabolic alkalosis complicated by severe intravascular volume depletion (evidenced by his orthostatic hypotension, tachycardia, and elevated BUN-to-creatinine ratio). The body's response to hypovolemia is to activate the renin-angiotensin-aldosterone system. Aldosterone acts on the distal nephron to aggressively reabsorb sodium to maintain blood pressure, but this occurs at the obligate expense of excreting potassium and hydrogen ions. Therefore, the kidneys cannot excrete the excess bicarbonate until the volume and chloride deficits are corrected. Intravenous 0.9%0.9\% sodium chloride restores the intravascular volume and provides the necessary chloride, which deactivates the aldosterone surge and allows the kidneys to excrete bicarbonate, naturally resolving the alkalosis.

Step-by-Step Solution

1
Assess the patient's volume status and acid-base derangement from the clinical presentation and laboratory results.
The patient has marked orthostatic hypotension and dry mucosa indicating severe volume depletion, alongside a hypokalemic, hypochloremic metabolic alkalosis.
Recurrent emesis causes significant loss of gastric fluid, which is rich in hydrochloric acid and potassium.
2
Determine the pathophysiological mechanism maintaining the alkalosis.
Volume and chloride depletion trigger the activation of the renin-angiotensin-aldosterone system.
Aldosterone promotes aggressive renal sodium reabsorption at the expense of potassium and hydrogen ion excretion, meaning the kidneys prioritize volume preservation over correcting the acid-base balance.
3
Select the appropriate therapy to break the maintenance cycle.
Administration of isotonic normal saline.
Restoring intravascular volume with a chloride-rich fluid deactivates aldosterone secretion, which allows the kidneys to safely excrete the excess bicarbonate and correct the alkalosis.

Key Concept

Saline-responsive metabolic alkalosis caused by vomiting is maintained by volume depletion and hypochloremia, and is treated initially with intravenous 0.9% sodium chloride.
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Topics

Nephrology

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