Ver el código de «Metabolic alkalosis»

==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 [[hypovolemia|loss of volume]])

==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==
===Chloride-Responsive===
'''Urine Cl < 20 mEq/L'''
#Loss of gastric secretions;
#*[[Vomiting]]
#*NG suction
#*[[Bulimia nervosa|Bulimia]]
#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 syndrome|Refeeding alkalosis]]
*[[Massive transfusion|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 [[Hypokalemia|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
#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

==Disposition==
*Admit for:
**Severe alkalosis (pH >7.55) - risk of arrhythmias and seizures
**Symptomatic patients (confusion, tetany, arrhythmia)
**Underlying cause requiring inpatient management (GI losses, diuretic excess)
*Discharge with close follow-up for:
**Mild alkalosis (pH 7.45-7.50) with identified correctable cause
**Asymptomatic patients with stable vitals

==See Also==
*[[Acid-base disorders]]

==References==
<references/>
[[Category:FEN]]
[[Category:Toxicology]]