Metabolic alkalosis: Difference between revisions
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==Differential Diagnosis== | ==Differential Diagnosis== | ||
===Chloride-Responsive=== | |||
'''Urine Cl < 20 mEq/L''' | |||
#Loss of gastric secretions; | |||
#*[[Vomiting]] | |||
* | #*NG suction | ||
#*[[Bulemia]] | |||
** | #Loss of colonic secretions | ||
* | #*Diarrhea | ||
#*Congenital chloridorrhea | |||
#*Villous adenoma | |||
#Thiazides/loop diuretics | |||
#Cystic fibrosis | |||
* | ===Chloride-resistant=== | ||
* | '''Urine Cl > 20 mEq/L''' | ||
* | *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]] | |||
*Primary hyperaldosteronism | |||
*CAH (11-Hydroxylase or 17-hydroxylase deficiency) | |||
*[[Cushing syndrome]] | |||
*Exogenous steroids | |||
*Liddle syndrome | |||
*Renovascular HTN | |||
*Bartter syndrome (pediatrics) | |||
*Gitelman syndrome (pediatrics) | |||
*Severe K+ depletion | |||
*[[Hypomagnesemia]] | |||
==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
- Loss of gastric secretions;
- Loss of colonic secretions
- Diarrhea
- Congenital chloridorrhea
- Villous adenoma
- Thiazides/loop diuretics
- Cystic fibrosis
Chloride-resistant
Urine Cl > 20 mEq/L
- 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
- Primary hyperaldosteronism
- CAH (11-Hydroxylase or 17-hydroxylase deficiency)
- Cushing syndrome
- Exogenous steroids
- Liddle syndrome
- Renovascular HTN
- Bartter syndrome (pediatrics)
- Gitelman syndrome (pediatrics)
- Severe K+ depletion
- Hypomagnesemia
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
