How do you manage a patient with metabolic alkalosis?

Management of Metabolic Alkalosis

The cornerstone of metabolic alkalosis management is identifying and treating the underlying cause while correcting volume depletion with isotonic saline and administering potassium chloride (not other potassium salts) to restore chloride and potassium deficits. 1, 2

Initial Assessment and Classification

• Obtain arterial blood gas, serum electrolytes (particularly potassium and chloride), blood urea nitrogen, creatinine, and urine chloride to classify the alkalosis 1, 3
• Measure urine chloride to distinguish chloride-responsive (<20 mEq/L) from chloride-resistant (>20 mEq/L) metabolic alkalosis, as this dictates initial treatment strategy 4, 3
• Monitor arterial pH, serum bicarbonate, and electrolytes every 2-4 hours during active treatment 1
• Assess for common precipitating factors: vomiting, nasogastric suctioning, diuretic therapy, mineralocorticoid excess, or severe hypokalemia 5, 3

Treatment Algorithm

Chloride-Responsive Metabolic Alkalosis (Most Common)

Step 1: Volume Resuscitation

• Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour during the first hour to restore effective arterial blood volume and renal perfusion 6, 3
• Volume depletion is the most common perpetuating factor—correcting this allows the kidneys to excrete excess bicarbonate 5, 7
• Continue aggressive fluid replacement until volume status is restored, as volume contraction prevents renal correction of alkalosis 3, 7

Step 2: Potassium and Chloride Repletion

• Administer potassium chloride specifically—not potassium citrate, acetate, or gluconate, as these worsen alkalosis 1, 2
• Add 20-40 mEq/L potassium chloride to IV fluids once renal function is confirmed and serum potassium is known 8, 3
• Hypokalemia both causes and perpetuates metabolic alkalosis by increasing renal bicarbonate reabsorption and generation 3, 7
• Target serum potassium of 4-5 mEq/L, as adequate potassium repletion is essential for alkalosis resolution 6, 3
• Monitor potassium closely if patient is on ACE inhibitors, ARBs, or NSAIDs, as these medications can cause potassium retention 2

Step 3: Remove Precipitating Cause

• Discontinue or reduce diuretic therapy when possible, as this is a major precipitating event 5, 3
• Stop nasogastric suctioning if feasible 5
• Treat underlying vomiting with antiemetics 3, 7

Chloride-Resistant Metabolic Alkalosis

• Evaluate for mineralocorticoid excess, severe hypokalemia, or Bartter's/Gitelman's syndromes 3, 7
• Address the specific endocrine or renal disorder driving the alkalosis 3
• Volume expansion alone will not correct these cases 7

Severe or Refractory Cases

When conventional therapy fails or cannot be tolerated:

• Acetazolamide (carbonic anhydrase inhibitor) can be used to promote renal bicarbonate excretion in patients who can tolerate diuresis 9, 3, 7
• Hemodialysis with high-chloride, low-bicarbonate dialysate is the treatment of choice for severe cases unresponsive to medical therapy, particularly in patients with renal dysfunction 9, 5
• Dilute hydrochloric acid (0.1-0.2 N) via central venous catheter may be considered in life-threatening cases (pH >7.55-7.60) when rapid correction is needed, though this carries significant risks 9, 5
• Ammonium chloride is contraindicated in hepatic or severe renal dysfunction 9

Critical Pitfalls to Avoid

• Never use potassium citrate, acetate, or gluconate—these are alkalinizing salts that worsen metabolic alkalosis 2
• Do not use alkalinizing potassium salts even in the presence of metabolic acidosis; in that setting, use potassium bicarbonate or citrate instead 2
• Avoid aggressive diuresis without adequate chloride and potassium repletion, as this perpetuates the alkalosis 3, 7
• Do not overlook volume depletion as the primary perpetuating mechanism—most cases resolve with saline and potassium chloride alone 5, 7
• Monitor for complications of severe alkalosis including cardiac arrhythmias, decreased myocardial contractility, altered mental status, and neuromuscular irritability 3, 7

Monitoring During Treatment

• Check electrolytes, particularly potassium and chloride, every 2-4 hours during active treatment 1
• Follow arterial pH and bicarbonate levels to assess response 1, 3
• Monitor urine output to ensure adequate renal function for bicarbonate excretion 3
• Assess for resolution: pH normalizing, bicarbonate declining, and clinical improvement 3, 7