Metabolic alkalosis
Background
Pathophysiology
- Chloride-Responsive (volume depletion)
- Condition that produces chloride loss also tends to reduce extracellular volume
- Reduction in extracellular volume increases mineralocorticoid activity
- Enhances Na reabsorption and K+/H+ secretion in renal tubule
- K/H+ secretion -> HCO3 generation
- Resulting urine is alkaline with little chloride (<10)
- K/H+ secretion -> HCO3 generation
- Enhances Na reabsorption and K+/H+ secretion in renal tubule
- Reduction in extracellular volume increases mineralocorticoid activity
- Condition that produces chloride loss also tends to reduce extracellular volume
- Chloride-Resistant
- Excess mineralocorticoid activity leads to same cascade as above
- No hypovolemia so urine chloride is generally normal (>10)
- Excess mineralocorticoid activity leads to same cascade as above
Clinical Features
Differential Diagnosis
- Chloride-Responsive (urine Cl < 20 mEq/L)
- Loss of gastric secretions
- vomiting
- NG suction
- bulemia
- Loss of colonic secretions
- congenital chloridorrhea
- villous adenoma
- Thiazides/loop after D/C
- Post hypercapnia
- Cystic fibrosis
- Loss of gastric secretions
- Chloride-resistant (urine Cl > 20 mEq/L)
- With HTN
- Primary hyperaldo
- adrenal adenoma
- bilateral adrenal
- hyperplasia
- adrenal carcinoma
- 11B-HSD2
- genetic, licorice
- chewing tobacco
- carbenoxolone
- CAH (11-Hydroxylase or 17-hydroxylase deficiency)
- Current diuretics + HTN
- Cushing syndrome
- Exogenous steroids
- Liddle syndrome
- Renovascular HTN
- Primary hyperaldo
- Without HTN
- Bartter syndrome^
- Gitelman syndrome^
- Severe K+ depletion
- Current thiazides/loop
- Hypomagnesemia
- With HTN
- Other causes
- Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
- Milk alkali syndrome
- Hypercalcemia (inability to concentrate urine leads to hypovolemia)
- Intravenous penicillin
- Refeeding alkalosis
- Massive blood transfusion
^in children
Diagnosis
- pH > 7.42 = alkalemia
- HCO3 > 28 = metabolic alkalosis
- Always determine if there is also a concurrent primary respiratory process
- expected pCO2 = 40 + 0.6(measured HCO3 - 24)
- if pCO2>pCO2 expected, then there is also a primary respiratory acidosis
- if pCO2<pCO2 expected, then there is also primary respiratory alkalosis
- Always calculate AG to determine if concurrent primary metabolic acidosis
Treatment
- Correct volume depletion
- Normal Saline
- Repletion of extracellular volume decr need for Na reaborption
- Delivery of Cl to distal tubule increases Cl/bicarb exchange
- Normal Saline
- Correct potassium depletion
- Giving K+ leads to movement of H+ out of cells -> acidosis
- Giving K+ stops hypokalemia-induced distal H+/K+ pump
- Correct chloride depletion
- Must give a reabsorbable anion to replace HCO3
- Correct mineralocorticoid excess
- Aldostorone antagonists if indicated (i.e. spironolactone)
- Note: if pt is edematous (CHF, cirrhosis), do NOT give normal saline
- If pt is hypokalemic KCl will correct both hypoK AND alkalosis
See Also
Source
Emedicine, Tintinalli, UpToDate, Kaji 2011