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Metabolic Acidosis Medication

  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Dec 18, 2015
 

Medication Summary

As previously stated, sodium bicarbonate (NaHCO3) is the agent most commonly used to correct metabolic acidosis. Also as previously mentioned, the role of alkali therapy is controversial in the treatment of lactic acidosis, with some evidence suggesting that HCO3- therapy produces only a transient increase in the serum HCO3- level and that this can lead to intracellular acidosis and worsening of lactic acidosis.

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Alkalinizing Agents

Class Summary

Acute metabolic acidosis is usually treated with alkali therapy to raise plasma pH and to maintain it at greater than 7.20.

Sodium bicarbonate

 

Sodium bicarbonate is a systemic and urinary alkalinizer used to increase serum or urinary HCO3- concentration and raise pH. Dosing is based on the clinical setting, blood pH, serum HCO3- level, and PaCO2.

Tromethamine (THAM)

 

THAM combines with hydrogen ions to form a bicarbonate buffer. It is used to prevent and correct systemic acidosis. It is available as 0.3-mol/L IV solution containing 18 g (150 mEq) per 500 mL (0.3 mEq/mL).

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Carbonic Anhydrase Inhibitors

Class Summary

Agents in this class may be used to induce alkaline diuresis.

Acetazolamide (Diamox)

 

This agent is used in the treatment of salicylate poisoning. It reduces the reduction of hydrogen ion secretion at the renal tubule and increases excretion of sodium, potassium, bicarbonate, and water. The goal is to maintain the urine pH at greater than 7.5 until the salicylate level falls below 30-50 mg/dL.

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Antidiabetic Agents

Class Summary

These agents are used for the treatment of ketoacidosis.

Insulin

 

Insulin is administered, to facilitate cellular uptake of glucose, reduce gluconeogenesis, and halt lipolysis and production of ketone bodies. In addition, normal saline is administered to restore extracellular volume; potassium and phosphate replacement also may be necessary.

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Detoxification Agents

Class Summary

These agents may be used in methanol or ethylene glycol poisoning.

Fomepizole (Antizol)

 

Begin fomepizole treatment immediately upon suspicion of ethylene glycol ingestion based on patient history or anion gap metabolic acidosis, increased osmolar gap, oxalate crystals in urine, or documented serum methanol level.

Activated charcoal (Actidose-Aqua, Requa Activated Charcoal)

 

This agent can be used to increase the excretion of salicylate. It is used in the emergency treatment of poisoning caused by drugs and chemicals. The network of pores present in activated charcoal absorbs 100-1000 mg of drug per gram of charcoal. It prevents absorption by adsorbing the drug in the intestine. Multidose charcoal may interrupt enterohepatic recirculation and enhance elimination by enterocapillary exsorption. Theoretically, by constantly bathing the GI tract with charcoal, the intestinal lumen serves as a dialysis membrane for reverse absorption of the drug from intestinal villous capillary blood into the intestine. It does not dissolve in water.

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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)

Khaled Hamawi, MD, MHA Director, Multi Organ Transplant Center, King Fahad Specialist Hospital, Dammam

Khaled Hamawi, MD, MHA is a member of the following medical societies: American Society of Transplantation, American Society of Nephrology

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

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.

Additional Contributors

James W Lohr, MD Professor, Department of Internal Medicine, Division of Nephrology, Fellowship Program Director, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, Central Society for Clinical and Translational Research

Disclosure: Partner received salary from Alexion for employment.

References
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  4. Mehta AN, Emmett JB, Emmett M. GOLD MARK: an anion gap mnemonic for the 21st century. Lancet. 2008 Sep 13. 372(9642):892. [Medline].

  5. Maciel AT, Park M. Differences in acid-base behavior between intensive care unit survivors and nonsurvivors using both a physicochemical and a standard base excess approach: a prospective, observational study. J Crit Care. 2009 Dec. 24(4):477-83. [Medline].

  6. Morimatsu H, Toda Y, Egi M, et al. Acid-base variables in patients with acute kidney injury requiring peritoneal dialysis in the pediatric cardiac care unit. J Anesth. 2009. 23(3):334-40. [Medline].

  7. Walsh SB, Shirley DG, Wrong OM, Unwin RJ. Urinary acidification assessed by simultaneous furosemide and fludrocortisone treatment: an alternative to ammonium chloride. Kidney Int. 2007 Jun. 71(12):1310-6. [Medline].

  8. Pereira PC, Miranda DM, Oliveira EA, Silva AC. Molecular pathophysiology of renal tubular acidosis. Curr Genomics. 2009 Mar. 10(1):51-9. [Medline]. [Full Text].

  9. Starke A, Corsenca A, Kohler T, Knubben J, Kraenzlin M, Uebelhart D, et al. Correction of metabolic acidosis with potassium citrate in renal transplant patients and its effect on bone quality. Clin J Am Soc Nephrol. 2012 Sep. 7(9):1461-72. [Medline]. [Full Text].

  10. Kraut JA, Madias NE. Metabolic Acidosis of CKD: An Update. Am J Kidney Dis. 2015 Oct 15. [Medline].

  11. Abramowitz MK, Melamed ML, Bauer C, Raff AC, Hostetter TH. Effects of oral sodium bicarbonate in patients with CKD. Clin J Am Soc Nephrol. 2013 May. 8(5):714-20. [Medline]. [Full Text].

  12. Goraya N, Simoni J, Jo CH, Wesson DE. A comparison of treating metabolic acidosis in CKD stage 4 hypertensive kidney disease with fruits and vegetables or sodium bicarbonate. Clin J Am Soc Nephrol. 2013 Mar. 8(3):371-81. [Medline]. [Full Text].

 
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Table. Comparison of Types 1, 2, and 4 RTA
Characteristics Proximal (Type 2) Distal (Type 1) Type 4
Primary defect Proximal HCO3 - reabsorption Diminished distal H+ secretion Diminished ammoniagenesis
Urine pH < 5.5 when serum HCO3 - is low >5.5 < 5.5
Serum HCO3 - >15 mEq/L Can be < 10 mEq/L >15 mEq/L
Fractional excretion of HCO3 - (FEHCO3) >15-20% during HCO3 - load < 5% (can be as high as 10% in children) < 5%
Serum K+ Normal or mild decrease Mild-to-severe decrease* High
Associated features Fanconi syndrome ... Diabetes mellitus, renal insufficiency
Alkali therapy High doses Low doses Low doses
Complications Osteomalacia or rickets Nephrocalcinosis, nephrolithiasis ...
*K+ may be high if RTA is due to volume depletion.
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