Evaluation of metabolic alkalosis

Diseases

Summary

Definition

Metabolic alkalosis is indicated by an increase in plasma bicarbonate (HCO₃) level. Arterial pH >7.45 defines alkalosis.

It is the consequence of disorders that cause either a loss of hydrogen ions from the body or an increase in plasma HCO₃. The severity of alkalosis depends on the severity of the underlying disorder; it may be more severe if both metabolic and respiratory alkalosis are present.

Pathophysiology

The main mechanisms involved can be one, or a combination, of the following:

Loss of hydrogen ions from the body. Hydrogen ions can be lost from the body either through the gastrointestinal tract or through the kidneys. In the body, hydrogen ions may shift from the extracellular fluid into the cells. If the loss of hydrogen ions exceeds production by the diet and metabolism, the serum HCO₃ level increases, leading to metabolic alkalosis.[1] Loss of hydrogen ions through the stomach and kidneys is accompanied by the production of HCO₃.
Administration of HCO₃, addition of HCO₃-generating substances, or intake of HCO₃ or substances (citrate, acetate, or lactate) that increase HCO₃ production in excess of hydrogen ion production will lead to metabolic alkalosis. This is usually compensated by the kidneys with normal function by renal excretion of HCO₃.[1]
Severe circulating volume contraction. This leads to loss of extracellular fluid and relative increase in HCO₃ concentration.

Metabolic alkalosis generally requires an initiation factor that starts the process and a maintenance factor that continues the imbalance by preventing renal excretion of excess HCO₃. Sometimes, the same factor may be responsible for both initiation and maintenance.[2] [3]

Citations

Key Articles

Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000 Feb;11(2):369-75.[Abstract][Full Text]
Khanna A, Kurtzman NA. Metabolic alkalosis. J Nephrol. 2006 Mar-Apr;19(Suppl 9):S86-96.[Abstract]
Royal College of Pathologists of Australasia. Alkalosis. 2014 [internet publication].[Full Text]

Referenced Articles

1. Tinawi M. Pathophysiology, evaluation, and management of metabolic alkalosis. Cureus. 2021 Jan 21;13(1):e12841.[Abstract][Full Text]
2. Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000 Feb;11(2):369-75.[Abstract][Full Text]
3. Garella S, Chang BS, Kahn SI. Dilution acidosis and contraction alkalosis: review of concept. Kidney Int. 1975 Nov;8(5):279-85.[Abstract]
4. Online Mendelian Inheritance in Man (OMIM). Liddle syndrome. MIM#177200. March 2016 [internet publication].[Full Text]
5. Khanna A, Kurtzman NA. Metabolic alkalosis. J Nephrol. 2006 Mar-Apr;19(Suppl 9):S86-96.[Abstract]
6. Morineau G, Sulmont V, Salomon R, et al. Apparent mineralocorticoid excess: report of six new cases and extensive personal experience. J Am Soc Nephrol. 2006 Nov;17(11):3176-84.[Abstract][Full Text]
7. Fleseriu M, Auchus R, Bancos I, et al. Consensus on diagnosis and management of Cushing's disease: a guideline update. Lancet Diabetes Endocrinol. 2021 Dec;9(12):847-75.[Abstract][Full Text]
8. Online Mendelian Inheritance in Man (OMIM). Bartter syndrome, type 4A. MIM#602522. May 2016 [internet publication].[Full Text]
9. Online Mendelian Inheritance in Man (OMIM). Gitelman syndrome. #263800. November 2012 [internet publication].[Full Text]
10. Blanchard A, Bockenhauer D, Bolignano D, et al. Gitelman syndrome: consensus and guidance from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2017 Jan;91(1):24-33.[Abstract][Full Text]
11. Naesens M, Steels P, Verberckmoes R, et al. Bartter's and Gitelman's syndromes: from gene to clinic. Nephron Physiol. 2004;96(3):65-78.[Abstract]
12. Gennari FJ. Hypokalemia. N Engl J Med. 1998 Aug 13;339(7):451-8.[Abstract]
13. Hearing SD. Refeeding syndrome. BMJ. 2004 Apr 17;328(7445):908-9.[Abstract][Full Text]
14. Hihnala S, Höglund P, Lammi L, et al. Long-term clinical outcome in patients with congenital chloride diarrhea. J Pediatr Gastroenterol Nutr. 2006 Apr;42(3):369-75.[Abstract]
15. Bates CM, Baum M, Quigley R. Cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent. J Am Soc Nephrol. 1997 Feb;8(2):352-5.[Abstract]
16. Dave S, Honney S, Raymond J, et al. An unusual presentation of cystic fibrosis in an adult. Am J Kidney Dis. 2005 Mar;45(3):e41-4.[Abstract]
17. Schuman CA, Jones HW 3rd. The 'milk-alkali' syndrome: two case reports with discussion of pathogenesis. Q J Med. 1985 May;55(217):119-26.[Abstract]
18. Javaheri S, Nardell EA. Severe metabolic alkalosis: a case report. Br Med J (Clin Res Ed). 1981 Oct 17;283(6298):1016-7.[Abstract][Full Text]
19. Royal College of Pathologists of Australasia. Alkalosis. 2014 [internet publication].[Full Text]
20. Miller RB. Central nervous system manifestation of fluid and electrolyte disturbances. Surg Clin North Am. 1968 Apr;48(2):381-93.[Abstract]
21. Morrison RS. Management of emergencies: metabolic acidosis and alkalosis. N Engl J Med. 1966 May 26;274(21):1195-7.[Abstract]
22. Kassirer JP, Berkman PM, Lawrenz DR. The critical role of chloride in the correction of hypokalemic alkalosis in man. Am J Med. 1965;38:172-181.[Abstract]
23. Rountas C, Vlychou M, Vassiou K, et al. Imaging modalities for renal artery stenosis in suspected renovascular hypertension: prospective intraindividual comparison of color Doppler US, CT angiography, GD-enhanced MR angiography, and digital substraction angiography. Ren Fail. 2007;29(3):295-302.[Abstract][Full Text]
24. Palermo M, Shackleton CH, Mantero F, et al. Urinary free cortisone and the assessment of 11 beta-hydroxysteroid dehydrogenase activity in man. Clin Endocrinol (Oxf). 1996 Nov;45(5):605-11.[Abstract]