A 42-year-old woman with recurrent vomiting due to gastric outlet obstruction presents with pH 7.52, PaCO₂ 48 mmHg, HCO₃⁻ 38 mEq/L, and K⁺ 2.8 mEq/L. To confirm the mechanism of metabolic alkalosis and determine the type of alkalosis (saline-responsive vs. saline-resistant), which investigation is most appropriate?

## Classification of Metabolic Alkalosis by Urine Chloride **Key Point:** Urine chloride concentration is the **gold standard** investigation to classify metabolic alkalosis into saline-responsive (Cl⁻-responsive) and saline-resistant (Cl⁻-resistant) types. This classification directly guides treatment. ## Urine Chloride-Based Classification | Type | Urine Cl⁻ | Mechanism | Examples | Treatment | |------|-----------|-----------|----------|----------| | **Saline-responsive** | < 10 mEq/L | Volume depletion + Cl⁻ loss | Vomiting, diuretics, nasogastric suction | Normal saline (0.9% NaCl) | | **Saline-resistant** | > 20 mEq/L | Ongoing Cl⁻ wasting or mineralocorticoid excess | Primary hyperaldosteronism, Cushing's, loop diuretics | Treat underlying cause; K⁺-sparing diuretics | **High-Yield:** In this patient with vomiting: - Expected urine Cl⁻ = **< 10 mEq/L** (saline-responsive) - Low K⁺ (2.8) indicates total body K⁺ depletion - Alkalosis perpetuated by volume depletion → increased proximal HCO₃⁻ reabsorption ## Pathophysiology in Vomiting-Induced Alkalosis 1. **Acute phase:** Loss of HCl → ↑ HCO₃⁻, ↑ pH 2. **Maintenance phase:** Volume depletion → ↑ aldosterone → ↑ K⁺ and H⁺ excretion → perpetuates alkalosis 3. **Urine Cl⁻ becomes low** because filtered Cl⁻ is reabsorbed in proximal tubule (volume-avid state) **Clinical Pearl:** Hypokalemia in metabolic alkalosis is a **red flag** — it indicates saline-responsive alkalosis and must be corrected with KCl supplementation alongside normal saline. **Mnemonic:** **"Low Cl⁻ in urine = Saline-Responsive"** — When urine chloride is low (< 10), the kidney is trying to conserve chloride due to volume depletion; give saline to fix it.