Metabolic alkalosis causes
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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)
- 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.