Metabolic Acidosis Medication
- Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...
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.
Acute metabolic acidosis is usually treated with alkali therapy to raise plasma pH and to maintain it at greater than 7.20.
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.
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).
Carbonic Anhydrase Inhibitors
Agents in this class may be used to induce alkaline diuresis.
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.
These agents are used for the treatment of ketoacidosis.
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.
These agents may be used in methanol or ethylene glycol poisoning.
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.
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.
Hamm LL, Nakhoul N, Hering-Smith KS. Acid-Base Homeostasis. Clin J Am Soc Nephrol. 2015 Dec 7. 10 (12):2232-42. [Medline].
Reddy P, Mooradian AD. Clinical utility of anion gap in deciphering acid-base disorders. Int J Clin Pract. 2009 Oct. 63(10):1516-25. [Medline].
Noritomi DT, Soriano FG, Kellum JA, et al. Metabolic acidosis in patients with severe sepsis and septic shock: a longitudinal quantitative study. Crit Care Med. 2009 Oct. 37(10):2733-9. [Medline].
Mehta AN, Emmett JB, Emmett M. GOLD MARK: an anion gap mnemonic for the 21st century. Lancet. 2008 Sep 13. 372(9642):892. [Medline].
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].
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].
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].
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].
Kraut JA, Madias NE. Metabolic Acidosis of CKD: An Update. Am J Kidney Dis. 2015 Oct 15. [Medline].
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].
|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.|