Metabolic alkalosis: Difference between revisions

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

Weakness/Fatigue
Vomiting or diarrhea
Hypoventilation

Differential Diagnosis

Chloride-Responsive

Urine Cl < 20 mEq/L

Loss of gastric secretions;
- Vomiting
- NG suction
- 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 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
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

References

Authors:

@@ Line 1: / Line 1: @@
-==Pathophysiology==
+==Background==
-*Chloride-Responsive (volume depletion)
+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-.
-**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
-*Chloride-Resistant
-**Excess mineralocorticoid activity leads to same cascade as above
-***No hypovolemia so urine chloride is generally normal
-==DDX==
+===Main Causes===
-#Chloride-Responsive (urine Cl < 20 mEq/L)
+*Hydrogen ion loss (via [[vomiting]])
-##Loss of gastric secretions
+*Shift of hydrogen ions intracellularly (from [[hypokalemia]])
-###vomiting
+*Bicarbonate administration
-###NG suction
+*Contraction alkalosis ([[Diuretic]] administration, [[diarrhea]], or any excessive [[hypovolemia|loss of volume]])
-###bulemia
-##Loss of colonic secretions
-###congenital chloridorrhea
-###villous adenoma
-##Thiazides/loop after D/C
-##Post hypercapnia
-##Cystic fibrosis
-#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
-##Without HTN
-###Bartter syndrome^
-###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
+==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
-==Treatment==
+==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
+#*[[Normal saline]]
-###Repletion of extracellular volume decr need for Na reaborption
+#**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 -> acidosis
+#*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
-##Must give a reabsorbable anion to replace HCO3
+#*Must give a reabsorbable anion to replace HCO3
 #Correct mineralocorticoid excess
-##Aldostorone antagonists if indicated (i.e. spironolactone)
+#*Aldosterone antagonists if indicated (i.e. [[spironolactone]])
-*Note: if pt is edematous (CHF, cirrhosis), do NOT give NS
-**If pt is hypokalemic KCl will correct both hypoK AND alkalosis
+*Note: if patient is edematous (CHF, cirrhosis), do NOT give normal saline
+**If patient is hypokalemic, KCl will correct both hypoK AND alkalosis
-==Source ==
+==See Also==
-Emedicine, Tintinalli, UpToDate, Kaji 2011
+*[[Acid-base disorders]]
+==References==
+<references/>
 [[Category:FEN]]
-[[Category:Tox]]
+[[Category:Toxicology]]