Metabolic Acidosis Medication

  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Aug 30, 2011
 

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, 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 Federation for Medical Research, American Heart Association, American Society of Nephrology, American Society of Transplantation, American Thoracic Society, International Society of Nephrology, and Royal College of Physicians

Disclosure: Genzyme Grant/research funds Other

Coauthor(s)

Khaled Hamawi, MD  Medical Director, Department of Pancreatic Transplantation, Mayo clinic

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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, and Central Society for Clinical Research

Disclosure: Genzyme Honoraria Speaking and teaching

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

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

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, 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, and International Society of Nephrology

Disclosure: Nothing to disclose.

References
  1. Noritomi DT, Soriano FG, Kellum JA, Cappi SB, Biselli PJ, Libório AB, et al. Metabolic acidosis in patients with severe sepsis and septic shock: a longitudinal quantitative study. Crit Care Med. Oct 2009;37(10):2733-9. [Medline].

  2. Reddy P, Mooradian AD. Clinical utility of anion gap in deciphering acid-base disorders. Int J Clin Pract. Oct 2009;63(10):1516-25. [Medline].

  3. 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. Dec 2009;24(4):477-83. [Medline].

  4. Morimatsu H, Toda Y, Egi M, Shimizu K, Matsusaki T, Suzuki S, 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].

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

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

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Table. Comparison of Types 1, 2, and 4 RTA
CharacteristicsProximal (Type 2)Distal (Type 1)Type 4
Primary defectProximal HCO3 - reabsorptionDiminished distal H+ secretionDiminished ammoniagenesis
Urine pH< 5.5 when serum HCO3 - is low>5.5< 5.5
Serum HCO3 ->15 mEq/LCan 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 decreaseMild-to-severe decrease*High
Associated featuresFanconi syndrome...Diabetes mellitus, renal insufficiency
Alkali therapyHigh dosesLow dosesLow doses
ComplicationsOsteomalacia or ricketsNephrocalcinosis, nephrolithiasis...
*K+ may be high if RTA is due to volume depletion.
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