From the Guidelines
Metabolic alkalosis with vomiting is best managed by addressing the underlying cause, correcting fluid and electrolyte imbalances, and providing intravenous fluid replacement with normal saline (0.9% NaCl) to restore volume status and correct chloride deficiency, as recommended by recent studies 1. The goal of treatment is to restore circulatory volume, tissue perfusion, and electrolyte balance.
- Stop any ongoing factors contributing to alkalosis, such as nasogastric suction.
- Provide intravenous fluid replacement with normal saline (0.9% NaCl) to restore volume status and correct chloride deficiency, typically at rates of 100-125 mL/hour based on clinical assessment, as suggested by studies on fluid management 1.
- Potassium chloride supplementation (typically 20-40 mEq/L in IV fluids) is essential as hypokalemia often accompanies this condition and its correction helps resolve the alkalosis.
- For severe cases (pH > 7.60 or bicarbonate > 40 mEq/L) with symptoms, acetazolamide 250-500 mg orally or IV every 6 hours may be used to increase bicarbonate excretion.
- Antiemetics such as ondansetron 4-8 mg IV/PO every 8 hours or promethazine 12.5-25 mg IV/PO every 6 hours should be given to control vomiting, as recommended by guidelines on antiemesis 1.
- In cases of persistent vomiting from gastric outlet obstruction or other mechanical issues, surgical intervention may be necessary.
- Monitoring of electrolytes, especially potassium, chloride, and bicarbonate levels, is crucial during treatment, as emphasized by recent studies on diabetes care in the hospital 1. The therapeutic approach works because chloride repletion allows the kidneys to excrete excess bicarbonate, while volume expansion reduces aldosterone secretion that contributes to maintaining the alkalosis.
From the Research
Metabolic Alkalosis with Vomiting
- Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid 2.
- Vomiting is a common cause of metabolic alkalosis, leading to the loss of acid and resulting in an increase in plasma HCO3- level and blood arterial pH 3.
- The pathogenesis of metabolic alkalosis requires both the generation of alkalosis and its maintenance, with generation due to excessive hydrogen ion loss by the gastrointestinal tract (e.g., vomiting) or by the kidney (e.g., use of loop diuretics) 3.
Management of Metabolic Alkalosis with Vomiting
- The cornerstone of treatment is the correction of existing depletions and the prevention of further losses 3.
- In vomiting-induced chloride depletion alkalosis, infusion of potassium chloride restores the excretion of bicarbonate by the kidney 3.
- High cation-gap amino acid (HCG-AA) may be more beneficial than normal saline for treating hyponatremic or hypervolemic metabolic alkalosis, as it predominantly comprises chloride and less sodium 4.
- Severe cases of metabolic alkalosis can be life-threatening, mandating both a systematic investigative approach and an early aggressive management strategy 5.
Key Factors in Management
- Evaluation of volemic status and measurement of urinary Cl- and plasma levels of renin and aldosterone are crucial to identify the cause(s) of metabolic alkalosis 3.
- Correction of hypokalemia, hypochloremia, and hypovolemia is essential in the management of metabolic alkalosis 6, 2.
- Administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis may be necessary in severe cases of metabolic alkalosis 6, 2.