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Metabolic Alkalosis Treatment & Management

  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Jul 26, 2016
 

Approach Considerations

The management of metabolic alkalosis depends primarily on the underlying etiology and on the patient’s volume status. In the case of vomiting, administer antiemetics, if possible. If continuous gastric suction is necessary, gastric acid secretion can be reduced with H2-blockers or more efficiently with proton-pump inhibitors. In patients who are on thiazide or loop diuretics, the dose can be reduced or the drug can be stopped if appropriate. Alternatively, potassium-sparing diuretics or acetazolamide can be added. Acetazolamide also appears safe and effective in patients with metabolic alkalosis following treatment of respiratory acidosis from exacerbations of chronic obstructive pulmonary disease.[9]

For a discussion of metabolic alkalosis in children, see Pediatric Metabolic Alkalosis. For a general review of acid-base regulation, see Metabolic Acidosis.

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Chloride-Responsive Alkalosis

If chloride-responsive alkalosis occurs with volume depletion, treat the alkalosis with an intravenous infusion of isotonic sodium chloride solution. Because this type of alkalosis is usually associated with hypokalemia, also use potassium chloride to correct the hypokalemia.

If chloride-responsive alkalosis occurs in the setting of edematous states (eg, congestive heart failure [CHF]), use potassium chloride instead of sodium chloride to correct the alkalosis and avoid volume overload. If diuresis is needed, a carbonic anhydrase inhibitor (eg, acetazolamide) or a potassium-sparing diuretic (eg, spironolactone, amiloride, triamterene) can be used to correct the alkalosis.

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Chloride-Resistant Metabolic Alkalosis

Management of chloride-resistant metabolic alkalosis is based on the specific cause.

Primary hyperaldosteronism

Metabolic alkalosis is corrected with the aldosterone antagonist spironolactone or with other potassium-sparing diuretics (eg, amiloride, triamterene). If the cause of primary hyperaldosteronism is an adrenal adenoma or carcinoma, surgical removal of the tumor should correct the alkalosis. In glucocorticoid-remediable hyperaldosteronism, metabolic alkalosis and hypertension are responsive to dexamethasone.

Cushing syndrome

Potassium-sparing diuretics should correct the alkalosis until surgical therapy is performed. Definitive therapy includes transsphenoidal microresection of adrenocorticotropic hormone (ACTH)–producing pituitary adenomas and adrenalectomy for adrenal tumors.

Syndrome of apparent mineralocorticoid excess

Metabolic alkalosis in the syndrome of AME may be treated with potassium-sparing diuretics. On the other hand, dexamethasone may be used to suppress cortisol production by inhibiting ACTH. Unlike cortisol and some synthetic glucocorticoids, dexamethasone does not activate the mineralocorticoid receptor.

Licorice ingestion

Discontinuation of licorice ingestion corrects the alkalosis; however, because full recovery of the enzyme 11B-HSD may take as long as 2 weeks following long-term licorice use, potassium-sparing diuretics can be used during this interval.

Bartter syndrome and Gitelman syndrome

Metabolic alkalosis can be corrected partially with potassium supplementation, potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs, or ACE inhibitors.

Liddle syndrome

Metabolic alkalosis can be treated with amiloride or triamterene but not with spironolactone. Both amiloride and triamterene inhibit the apical sodium ion channel in the collecting duct. Spironolactone, which is a mineralocorticoid receptor antagonist that works upstream of the defective sodium ion channel, does not correct the alkalosis or the hypertension.

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Specialized Therapies in All Types of Metabolic Alkalosis

Hydrochloric acid

Intravenous HCl is indicated in severe metabolic alkalosis (pH >7.55) or when sodium or potassium chloride cannot be administered because of volume overload or advanced renal failure. HCl may also be indicated if rapid correction of severe metabolic alkalosis is warranted (eg, cardiac arrhythmias, hepatic encephalopathy, digoxin cardiotoxicity). Seek the advice of a nephrologist when severe alkalosis is present and HCl therapy or dialysis is contemplated.

Dialysis

Both peritoneal dialysis and hemodialysis can be used with certain modifications of the dialysate to correct metabolic alkalosis. The main indication of dialysis in metabolic alkalosis is in patients with advanced renal failure, who usually have volume overload and are resistant to acetazolamide.

With hemodialysis, metabolic alkalosis may be corrected by using a low-bicarbonate dialysate (bicarbonate can be as low as 18 mmol/L). Otherwise, acetate-free biofiltration (buffer-free dialysate), in which bicarbonate is not present in the dialysate but is infused separately as needed, may be used. In peritoneal dialysis, dialysis can be performed using isotonic sodium chloride solution as the dialysate.

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Consultations

Seek the advice of a nephrologist when severe alkalosis is present and HCl therapy or dialysis is contemplated.

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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
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  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].

 
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Algorithm for metabolic alkalosis.
 
 
 
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