Etiologies-of-Metabolic-Alkalosis

Saline responsive

UCl <25

• GI loss of H+:
  • emesis, NGT suction, villous adenoma, chloridorrhea
• Renal loss:
  • loop/thiazide, ↓ Cl intake, milk-alkali, Pendred syndrome
• Posthypercapnia(bilevel positive airway pressure for chronic obstructive pulmonary disease AE),
  • sweat losses in cystic fibrosis

Saline resistant

UCl >40

Hypertensive (mineralocorticoid excess)

• Primary Hyperaldosteronism

• Secondary Hyperaldosteronism

• Non-aldo (Cushing syndrome, Liddle syndrome, exogenous mineralocorticoids, licorice)

• Normotensive

• Severe hypokalemia (K<2); exogenous alkali load (w/ AKI or ↓ vol)

• Bartter’s syndrome (loop-like); Gitelman’s syndrome (thiazide-like)

summary of metabolic alkalosis