Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Metabolic Alkalosis Clinical Presentation

  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Jul 21, 2016
 

History

Symptoms of metabolic alkalosis are not specific. Because hypokalemia is usually present, the patient may experience weakness, myalgia, polyuria, and cardiac arrhythmias.

Hypoventilation develops because of inhibition of the respiratory center in the medulla. Symptoms of hypocalcemia (eg, jitteriness, perioral tingling, muscle spasms) may be present.

The clinical history is helpful in establishing the etiology. Important points in the history include the following:

  • Vomiting or diarrhea - Gastrointestinal (GI) losses of hydrochloric acid (HCl)
  • Age of onset and family history of alkalosis - Familial disorders (eg, Bartter syndrome, which starts during childhood)
  • Renal failure - Alkali-loading alkalosis develops only when impairment of renal function occurs
  • Drug use (eg, loop or thiazide diuretics; licorice; tobacco chewing; carbenoxolone; fludrocortisone; glucocorticoids; antacids [eg, magnesium hydroxide]; calcium carbonate)
  • Previous GI surgery [4] (eg, ileostomy [5] )
Next

Physical Examination

The physical signs of metabolic alkalosis are not specific and depend on the severity of the alkalosis. Because metabolic alkalosis decreases ionized calcium concentration, signs of hypocalcemia (eg, tetany, Chvostek sign, Trousseau sign), change in mental status, or seizures may be present.

Physical examination is helpful to establish the cause of metabolic alkalosis. Important aspects of the physical examination include the evaluation of hypertension and of volume status.

Hypertension accompanies several causes of metabolic alkalosis (see Etiology). Volume status assessment includes evaluation of orthostatic changes in blood pressure and heart rate, mucous membranes, presence or absence of edema, skin turgor, weight change, and urine output. Volume depletion usually accompanies chloride-responsive alkalosis, while volume expansion accompanies chloride-resistant alkalosis.

Bulimia

Because patients with bulimia frequently self-induce vomiting, they may have erosions of teeth enamel and dental caries because of repeatedly exposing their teeth to gastric acid.

Cushing syndrome

Findings associated with Cushing syndrome include the following:

  • Obesity
  • Moon face
  • Buffalo hump
  • Hirsutism
  • Violaceous skin striae
  • Acne

Congenital adrenal hyperplasia

Congenital adrenal hyperplasia (CAH): Infants with CAH secondary to 11-hydroxylase deficiency have hypertension and growth retardation. Male infants have premature sexual development, while female infants develop virilization. In 17-hydroxylase deficiency, males develop sexual ambiguity, while females have sexual infantilism.

Complications

Alkalosis may lead to tetany, seizures, and decreased mental status. Metabolic alkalosis also decreases coronary blood flow and predisposes persons to refractory arrhythmias. Metabolic alkalosis causes hypoventilation, which may cause hypoxemia, especially in patients with poor respiratory reserve, and it may impair weaning from mechanical ventilation. By increasing ammonia production, it can precipitate hepatic encephalopathy in susceptible individuals.

Previous
 
 
Contributor Information and Disclosures
Author

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Departments of Pediatrics and Obstetrics and Gynecology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, Royal College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Sameer Yaseen, MD Staff Nephrologist, Department of Internal Medicine, Division of Nephrology, Mercy Hospital of Des Moines

Sameer Yaseen, MD is a member of the following medical societies: Renal Physicians Association, American Society of Nephrology

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Acknowledgements

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Mehler PS, Walsh K. Electrolyte and acid-base abnormalities associated with purging behaviors. Int J Eat Disord. 2016 Mar. 49 (3):311-8. [Medline].

  2. Medarov BI. Milk-alkali syndrome. Mayo Clin Proc. 2009 Mar. 84(3):261-7. [Medline]. [Full Text].

  3. Tentori F, Karaboyas A, Robinson BM, Morgenstern H, Zhang J, Sen A, et al. Association of dialysate bicarbonate concentration with mortality in the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis. 2013 Oct. 62(4):738-46. [Medline]. [Full Text].

  4. Gennari FJ, Weise WJ. Acid-base disturbances in gastrointestinal disease. Clin J Am Soc Nephrol. 2008 Nov. 3(6):1861-8. [Medline].

  5. Weise WJ, Serrano FA, Fought J, Gennari FJ. Acute electrolyte and acid-base disorders in patients with ileostomies: a case series. Am J Kidney Dis. 2008 Sep. 52(3):494-500. [Medline].

  6. Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol. 2007 Jan. 2(1):162-74. [Medline]. [Full Text].

  7. Stewart PA. How to understand acid-base: a quantitative acid-base primer for biology and medicine. [AcidBase.org]. Available at http://www.acidbase.org/index.php?show=sb. Accessed: Aug 10, 2009.

  8. Kaplan LJ, Cheung NH, Maerz L, et al. A physicochemical approach to acid-base balance in critically ill trauma patients minimizes errors and reduces inappropriate plasma volume expansion. J Trauma. 2009 Apr. 66(4):1045-51. [Medline].

  9. Fontana V, Santinelli S, Internullo M, Marinelli P, Sardo L, Alessandrini G, et al. Effect of acetazolamide on post-NIV metabolic alkalosis in acute exacerbated COPD patients. Eur Rev Med Pharmacol Sci. 2016. 20 (1):37-43. [Medline].

  10. Gennari FJ. Pathophysiology of metabolic alkalosis: a new classification based on the centrality of stimulated collecting duct ion transport. Am J Kidney Dis. 2011 Oct. 58(4):626-36. [Medline].

 
Previous
Next
 
Algorithm for metabolic alkalosis.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.