Metabolic alkalosis: Difference between revisions
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===Main Causes=== | ===Main Causes=== | ||
*Hydrogen ion loss (via vomiting) | *Hydrogen ion loss (via [[vomiting]]) | ||
*Shift of hydrogen ions intracellularly (from hypokalemia) | *Shift of hydrogen ions intracellularly (from [[hypokalemia]]) | ||
*Bicarbonate administration | *Bicarbonate administration | ||
*Contraction alkalosis (Diuretic administration, diarrhea, or any excessive loss of volume) | *Contraction alkalosis ([[Diuretic]] administration, [[diarrhea]], or any excessive [[hypovolemia|loss of volume]]) | ||
==Clinical Features== | ==Clinical Features== | ||
Symptoms are nonspecific and usually result from the concomitant [[hypokalemia]] or [[hypocalcemia]]. Common signs and symptoms include | |||
*[[Weakness]]/Fatigue | |||
*[[Vomiting]] or [[diarrhea]] | |||
*Hypoventilation | |||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
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#*[[Vomiting]] | #*[[Vomiting]] | ||
#*NG suction | #*NG suction | ||
#*[[ | #*[[Bulimia nervosa|Bulimia]] | ||
#Loss of colonic secretions | #Loss of colonic secretions | ||
#*Diarrhea | #*[[Diarrhea]] | ||
#*Congenital chloridorrhea | #*Congenital chloridorrhea | ||
#*Villous adenoma | #*Villous adenoma | ||
#Thiazides/loop diuretics | #Thiazides/loop [[diuretics]] | ||
#Cystic fibrosis | #[[Cystic fibrosis]] | ||
===Chloride-resistant=== | ===Chloride-resistant=== | ||
'''Urine Cl > 20 mEq/L''' | '''Urine Cl > 20 mEq/L''' | ||
*Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids) | *Exogenous alkali (Nabicarb + [[renal failure]], metabolism of lactic acid, or ketoacids) | ||
**Potassium acetate | |||
*[[Milk alkali syndrome]] | *[[Milk alkali syndrome]] | ||
*[[Hypercalcemia]] (inability to concentrate urine leads to hypovolemia) | *[[Hypercalcemia]] (inability to concentrate urine leads to hypovolemia) | ||
*Intravenous [[penicillin]] | *Intravenous [[penicillin]] | ||
*Refeeding alkalosis | *[[Refeeding syndrome|Refeeding alkalosis]] | ||
*[[Massive blood transfusion]] | *[[Massive transfusion|Massive blood transfusion]] | ||
*Primary hyperaldosteronism | *Primary hyperaldosteronism | ||
*CAH (11-Hydroxylase or 17-hydroxylase deficiency) | *[[CAH]] (11-Hydroxylase or 17-hydroxylase deficiency) | ||
*[[Cushing syndrome]] | *[[Cushing syndrome]] | ||
*Exogenous steroids | *Exogenous [[steroids]] | ||
*Liddle syndrome | *Liddle syndrome | ||
*Renovascular | *Renovascular hypertension | ||
*Bartter syndrome (pediatrics) | *Bartter syndrome (pediatrics) | ||
*Gitelman syndrome (pediatrics) | *Gitelman syndrome (pediatrics) | ||
*Severe K+ depletion | *Severe [[Hypokalemia|K+ depletion]] | ||
*[[Hypomagnesemia]] | *[[Hypomagnesemia]] | ||
== | ==Evaluation== | ||
*pH > 7.42 = alkalemia | *pH > 7.42 = alkalemia | ||
*HCO3 > 28 = metabolic alkalosis | *HCO3 > 28 = metabolic alkalosis | ||
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*Always calculate AG to determine if concurrent primary metabolic acidosis | *Always calculate AG to determine if concurrent primary metabolic acidosis | ||
== | ==Management== | ||
#Correct volume depletion | #Correct volume depletion | ||
#*Normal | #*[[Normal saline]] | ||
#**Repletion of extracellular volume | #**Repletion of extracellular volume decreased need for Na reaborption | ||
#**Delivery of Cl to distal tubule increases Cl/bicarb exchange | #**Delivery of Cl to distal tubule increases Cl/bicarb exchange | ||
#Correct potassium depletion | #Correct [[potassium]] depletion | ||
#*Giving K+ leads to movement of H+ out of cells | #*Giving K+ leads to movement of H+ out of cells → acidosis | ||
#*Giving K+ stops hypokalemia-induced distal H+/K+ pump | #*Giving K+ stops hypokalemia-induced distal H+/K+ pump | ||
#Correct chloride depletion | #Correct chloride depletion | ||
#*Must give a reabsorbable anion to replace HCO3 | #*Must give a reabsorbable anion to replace HCO3 | ||
#Correct mineralocorticoid excess | #Correct mineralocorticoid excess | ||
#* | #*Aldosterone antagonists if indicated (i.e. [[spironolactone]]) | ||
*Note: if | *Note: if patient is edematous (CHF, cirrhosis), do NOT give normal saline | ||
**If | **If patient is hypokalemic, KCl will correct both hypoK AND alkalosis | ||
==See Also== | ==See Also== | ||
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==References== | ==References== | ||
<references/> | |||
[[Category:FEN]] | [[Category:FEN]] | ||
[[Category:Toxicology]] | [[Category:Toxicology]] | ||
Latest revision as of 18:05, 22 September 2019
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
Symptoms are nonspecific and usually result from the concomitant hypokalemia or hypocalcemia. Common signs and symptoms include
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)
- Potassium acetate
- 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 hypertension
- Bartter syndrome (pediatrics)
- Gitelman syndrome (pediatrics)
- Severe K+ depletion
- Hypomagnesemia
Evaluation
- 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
Management
- Correct volume depletion
- Normal saline
- Repletion of extracellular volume decreased 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
- Aldosterone antagonists if indicated (i.e. spironolactone)
- Note: if patient is edematous (CHF, cirrhosis), do NOT give normal saline
- If patient is hypokalemic, KCl will correct both hypoK AND alkalosis