Metabolic alkalosis causes: Difference between revisions
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{{Metabolic alkalosis}} | {{Metabolic alkalosis}} | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}} {{MMT}} | ||
==Overview== | ==Overview== | ||
Causes of Metabolic Alkalosis are Vomiting, Diarrhea, Diuretics, Cystic Fibrosis, Primary Hyperaldosteronism, Secondary hyperaldosteronism, laxative use, CKD, elactrolyte and nutritional imbalances, Milk-alkali syndrome, Blood transfusion, Genetic diseases for instances Bartter, Liddle, Gitelman syndrome etc. Among them, life threatening causes are | |||
loss of gastric acid, excessive use of loop and thiazide diuretics. | |||
==Causes== | |||
There are several causes of metabolic alkalosis. | |||
Life threatening causes of severe [[Metabolic alkalosis|metabolic alkalosis (]]<nowiki/>pH 7.55 to 7.65) may result in death (45% to 80%) or permanent disability within 24 hours if left untreated.<ref name="pmid20436691">{{cite journal |vauthors=Tripathy S |title=Extreme metabolic alkalosis in intensive care |journal=Indian J Crit Care Med |volume=13 |issue=4 |pages=217–20 |date=October 2009 |pmid=20436691 |pmc=2856150 |doi=10.4103/0972-5229.60175 |url=}}</ref> | |||
*[[Gastric acidity reduced|Loss of gastric acid]] | |||
*[[Loop diuretics|Loop]] or [[thiazide diuretics]] | |||
===Common Causes=== | |||
*'''[[Chloride]] depletion''' o[[Gastrointestinal|r '''Gastrointestinal''']] '''loss of [[hydrogen]]''' | |||
**[[Gastrointestinal tract|GI]] loss: [[Vomiting]] (most commonly seen in [[pyloric stenosis]]), [[Nasogastric tube|NG suction]] , [[Zollinger-Ellison syndrome|Zollinger-ellison]] syndrome, [[Bulimia nervosa|Bulimia]].<ref name="pmid1928424">{{cite journal |vauthors=Galla JH, Gifford JD, Luke RG, Rome L |title=Adaptations to chloride-depletion alkalosis |journal=Am J Physiol |volume=261 |issue=4 Pt 2 |pages=R771–81 |date=October 1991 |pmid=1928424 |doi=10.1152/ajpregu.1991.261.4.R771 |url=}}</ref> | |||
**[[Diuretic|Diuretics]]: [[Loop diuretic|Loop]] and [[thiazide diuretics]]. | |||
**[[Diarrhea]] | |||
**[[Cystic fibrosis]].<ref name="pmid7618650">{{cite journal |vauthors=Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-Jäggi C, Bianchetti MG |title=Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis |journal=Am J Nephrol |volume=15 |issue=3 |pages=245–50 |date=1995 |pmid=7618650 |doi=10.1159/000168839 |url=}}</ref> | |||
**[[Chloride]] deficient [[Infant formula|infant formula.]] | |||
*'''[[Potassium]] depletion''' or '''[[Mineralocorticoids]] excess''' or '''[[Renal]] loss of [[hydrogen]]''' | |||
**Dietary [[potassium]] depletion.<ref name="pmid8648937">{{cite journal |vauthors=Sabatini S |title=The cellular basis of metabolic alkalosis |journal=Kidney Int |volume=49 |issue=3 |pages=906–17 |date=March 1996 |pmid=8648937 |doi=10.1038/ki.1996.125 |url=}}</ref> | |||
**[[Primary Hyperaldosteronism|Primary hyperaldosteronism]]: [[Conn syndrome]] or [[adenoma]], [[hyperplasia]], [[carcinoma]], [[renin]] or [[glucocorticoid]] responsive. | |||
**[[Secondary hyperaldosteronism]]: [[Renovascular hypertension|Reno vascular hypertension]], [[edema]] ([[cirrhosis]], [[heart failure]], [[Nephrotic syndrome|nephrotic syndrome)]], [[Juxtaglomerular apparatus|juxtaglomerular cell]]([[Renin-secreting tumors|renin producing) tumor]], [[renal cell carcinoma]], [[nephroblastoma]] | |||
**[[Mineralocorticoid]] excess due to primary decorticosterone excess ([[11β-hydroxylase deficiency|11 beta]], [[17 alpha-hydroxylase deficiency|17 alpha hydroxylase deficienc]]<nowiki/>y), [[licorice]]([[glycyrrhetinic acid]]) <ref name="pmid1731223">{{cite journal |vauthors=Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, Lalouel JM |title=A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension |journal=Nature |volume=355 |issue=6357 |pages=262–5 |date=January 1992 |pmid=1731223 |doi=10.1038/355262a0 |url=}} | |||
**[[Laxative]] | |||
*'''Reduced [[Glomerular filtration rate]]''' | |||
**[[Chronic kidney disease]] | |||
*'''[[Extracellular fluid|ECF volume]] depletion/ [[Volume depletion|Volume contraction]]''' | |||
**[[Hypovolemia]] or [[Diuresis|massive diuresis]] with [[loop diuretics]]. | |||
*'''Miscellanous''' | |||
**[[Hypercalcemia]] due to [[Milk-alkali syndrome]] or [[bone metastasis]]. | |||
**Massive [[blood transfusion]]. | |||
**[[Acetate]] containing [[Colloid|colloid sollution]]. | |||
**[[Exogenous]] [[alkali]] admintration. | |||
**Combined [[antacid]] and cation exchange resin administration. | |||
**Sodium [[Penicillin|penicillins]]. | |||
===Less common causes=== | |||
== | |||
=== | **[[Villous adenoma]]<ref name="pmid5927076">{{cite journal |vauthors=Babior BM |title=Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances |journal=Am J Med |volume=41 |issue=4 |pages=615–21 |date=October 1966 |pmid=5927076 |doi=10.1016/0002-9343(66)90223-3 |url=}}</ref> | ||
**[[congenital chloride diarrhea]]<ref name="pmid8896562">{{cite journal |vauthors=Höglund P, Haila S, Socha J, Tomaszewski L, Saarialho-Kere U, Karjalainen-Lindsberg ML, Airola K, Holmberg C, de la Chapelle A, Kere J |title=Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea |journal=Nat Genet |volume=14 |issue=3 |pages=316–9 |date=November 1996 |pmid=8896562 |doi=10.1038/ng1196-316 |url=}}</ref> | |||
** [[ | **[[Bartter syndrome|Bartter]] and [[Gitelman syndrome]]. <ref name="pmid9767561">{{cite journal |vauthors=Kurtz I |title=Molecular pathogenesis of Bartter's and Gitelman's syndromes |journal=Kidney Int |volume=54 |issue=4 |pages=1396–410 |date=October 1998 |pmid=9767561 |doi=10.1046/j.1523-1755.1998.00124.x |url=}}</ref> | ||
** | **[[Liddle's syndrome|liddle syndrome]]</ref> <ref name="pmid9452995">{{cite journal |vauthors=Warnock DG |title=Liddle syndrome: an autosomal dominant form of human hypertension |journal=Kidney Int |volume=53 |issue=1 |pages=18–24 |date=January 1998 |pmid=9452995 |doi=10.1046/j.1523-1755.1998.00728.x |url=}}</ref> | ||
**[[hemangiopericytoma]] | |||
** [[ | **Gastrocystoplasty <ref name="pmid7609133">{{cite journal |vauthors=Plawker MW, Rabinowitz SS, Etwaru DJ, Glassberg KI |title=Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty |journal=J Urol |volume=154 |issue=2 Pt 1 |pages=546–9 |date=August 1995 |pmid=7609133 |doi=10.1097/00005392-199508000-00066 |url=}}</ref> | ||
**Post hypercapneic [[metabolic alkalosis]]. | |||
** [[ | |||
** | |||
** [[ | |||
===Causes by Organ System=== | ===Causes by Organ System=== | ||
Latest revision as of 04:02, 1 February 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Marufa Marium, M.B.B.S[2]
Overview
Causes of Metabolic Alkalosis are Vomiting, Diarrhea, Diuretics, Cystic Fibrosis, Primary Hyperaldosteronism, Secondary hyperaldosteronism, laxative use, CKD, elactrolyte and nutritional imbalances, Milk-alkali syndrome, Blood transfusion, Genetic diseases for instances Bartter, Liddle, Gitelman syndrome etc. Among them, life threatening causes are loss of gastric acid, excessive use of loop and thiazide diuretics.
Causes
There are several causes of metabolic alkalosis. Life threatening causes of severe metabolic alkalosis (pH 7.55 to 7.65) may result in death (45% to 80%) or permanent disability within 24 hours if left untreated.[1]
Common Causes
- Chloride depletion or Gastrointestinal loss of hydrogen
- GI loss: Vomiting (most commonly seen in pyloric stenosis), NG suction , Zollinger-ellison syndrome, Bulimia.[2]
- Diuretics: Loop and thiazide diuretics.
- Diarrhea
- Cystic fibrosis.[3]
- Chloride deficient infant formula.
- Potassium depletion or Mineralocorticoids excess or Renal loss of hydrogen
- Dietary potassium depletion.[4]
- Primary hyperaldosteronism: Conn syndrome or adenoma, hyperplasia, carcinoma, renin or glucocorticoid responsive.
- Secondary hyperaldosteronism: Reno vascular hypertension, edema (cirrhosis, heart failure, nephrotic syndrome), juxtaglomerular cell(renin producing) tumor, renal cell carcinoma, nephroblastoma
- Mineralocorticoid excess due to primary decorticosterone excess (11 beta, 17 alpha hydroxylase deficiency), licorice(glycyrrhetinic acid) Closing
</ref>missing for<ref>tag - congenital chloride diarrhea[5]
- Bartter and Gitelman syndrome. [6]
- liddle syndrome</ref> [7]
- hemangiopericytoma
- Gastrocystoplasty [8]
- Post hypercapneic metabolic alkalosis.
Causes by Organ System
Causes in Alphabetical Order
- ↑ Tripathy S (October 2009). "Extreme metabolic alkalosis in intensive care". Indian J Crit Care Med. 13 (4): 217–20. doi:10.4103/0972-5229.60175. PMC 2856150. PMID 20436691.
- ↑ Galla JH, Gifford JD, Luke RG, Rome L (October 1991). "Adaptations to chloride-depletion alkalosis". Am J Physiol. 261 (4 Pt 2): R771–81. doi:10.1152/ajpregu.1991.261.4.R771. PMID 1928424.
- ↑ Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-Jäggi C, Bianchetti MG (1995). "Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis". Am J Nephrol. 15 (3): 245–50. doi:10.1159/000168839. PMID 7618650.
- ↑ Sabatini S (March 1996). "The cellular basis of metabolic alkalosis". Kidney Int. 49 (3): 906–17. doi:10.1038/ki.1996.125. PMID 8648937.
- ↑ Höglund P, Haila S, Socha J, Tomaszewski L, Saarialho-Kere U, Karjalainen-Lindsberg ML, Airola K, Holmberg C, de la Chapelle A, Kere J (November 1996). "Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea". Nat Genet. 14 (3): 316–9. doi:10.1038/ng1196-316. PMID 8896562.
- ↑ Kurtz I (October 1998). "Molecular pathogenesis of Bartter's and Gitelman's syndromes". Kidney Int. 54 (4): 1396–410. doi:10.1046/j.1523-1755.1998.00124.x. PMID 9767561.
- ↑ Warnock DG (January 1998). "Liddle syndrome: an autosomal dominant form of human hypertension". Kidney Int. 53 (1): 18–24. doi:10.1046/j.1523-1755.1998.00728.x. PMID 9452995.
- ↑ Plawker MW, Rabinowitz SS, Etwaru DJ, Glassberg KI (August 1995). "Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty". J Urol. 154 (2 Pt 1): 546–9. doi:10.1097/00005392-199508000-00066. PMID 7609133.