Metabolic alkalosis: Difference between revisions

Line 11: Line 11:


==Differential Diagnosis==
==Differential Diagnosis==
*Chloride-Responsive (urine Cl < 20 mEq/L)
===Chloride-Responsive===
**Loss of gastric secretions
'''Urine Cl < 20 mEq/L'''
***[[vomiting]]
#Loss of gastric secretions;
***NG suction
#*[[Vomiting]]
***bulemia
#*NG suction
**Loss of colonic secretions
#*[[Bulemia]]
***congenital chloridorrhea
#Loss of colonic secretions
***villous adenoma
#*Diarrhea
**Thiazides/loop after D/C
#*Congenital chloridorrhea
**Post hypercapnia
#*Villous adenoma
**Cystic fibrosis
#Thiazides/loop diuretics
*Chloride-resistant (urine Cl > 20 mEq/L)
#Cystic fibrosis
**With HTN
===Chloride-resistant===
***Primary hyperaldo
'''Urine Cl > 20 mEq/L'''
****adrenal adenoma
*Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
****bilateral adrenal
*[[Milk alkali syndrome]]
****hyperplasia
*[[Hypercalcemia]] (inability to concentrate urine leads to hypovolemia)
****adrenal carcinoma
*Intravenous [[penicillin]]
***11B-HSD2
*Refeeding alkalosis
****genetic, licorice
*[[Massive blood transfusion]]
****chewing tobacco
*Primary hyperaldosteronism
****carbenoxolone
*CAH (11-Hydroxylase or 17-hydroxylase deficiency)
***CAH (11-Hydroxylase or 17-hydroxylase deficiency)
*[[Cushing syndrome]]
***Current diuretics + HTN
*Exogenous steroids
***[[Cushing syndrome]]
*Liddle syndrome
***Exogenous steroids
*Renovascular HTN
***Liddle syndrome
*Bartter syndrome (pediatrics)
***Renovascular HTN
*Gitelman syndrome (pediatrics)
**Without HTN
*Severe K+ depletion
***Bartter syndrome^
*[[Hypomagnesemia]]
***Gitelman syndrome^
***Severe K+ depletion
***Current thiazides/loop
***[[Hypomagnesemia]]
*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==
==Diagnosis==

Revision as of 02:32, 5 April 2016

Background

Metabolic alkalosis generally occurs as a primary increase in serum bicarbonate (HCO3-) concentration, which can occur due to loss of H+ from the body or a gain in HCO3-.

Main Causes

  • Hydrogen ion loss (via vomiting)
  • Shift of hydrogen ions intracellularly (from hypokalemia)
  • Bicarbonate administration
  • Contraction alkalosis (Diuretic administration, diarrhea, or any excessive loss of volume)

Clinical Features

Differential Diagnosis

Chloride-Responsive

Urine Cl < 20 mEq/L

  1. Loss of gastric secretions;
  2. Loss of colonic secretions
    • Diarrhea
    • Congenital chloridorrhea
    • Villous adenoma
  3. Thiazides/loop diuretics
  4. Cystic fibrosis

Chloride-resistant

Urine Cl > 20 mEq/L

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

  1. Correct volume depletion
    • Normal Saline
      • Repletion of extracellular volume decr need for Na reaborption
      • Delivery of Cl to distal tubule increases Cl/bicarb exchange
  2. Correct potassium depletion
    • Giving K+ leads to movement of H+ out of cells -> acidosis
    • Giving K+ stops hypokalemia-induced distal H+/K+ pump
  3. Correct chloride depletion
    • Must give a reabsorbable anion to replace HCO3
  4. 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

References