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Acidosis, Metabolic: Treatment & Medication

Author: Margaret A Priestley, MD, Assistant Professor of Clinical Anesthesiology and Critical Care, University of Pennsylvania School of Medicine; Clinical Director, Pediatric Intensive Care Unit, The Children's Hospital of Philadelphia
Contributor Information and Disclosures

Updated: Jun 25, 2009

Treatment

Medical Care

A metabolic acidosis is a biochemical derangement resulting from one of many different disease processes; therefore, the key to successful treatment lies in appropriately managing the underlying disorder. For example, insulin administration is necessary in cases of diabetic ketoacidosis, and restoration of adequate perfusion with crystalloid administration is necessary in cases of dehydration.

  • In instances in which the serum bicarbonate level is only mildly to moderately depressed (>10-12 mEq/L), bicarbonate replacement may not be necessary. If the underlying disease is treated appropriately, the kidneys are able to replenish bicarbonate stores within 3-4 days, unless significant renal dysfunction is present.
  • In some disease states, the use of bicarbonate therapy is clearly indicated. For patients with chronic renal failure or renal tubular acidosis (RTA), bicarbonate replacement is necessary because of known ongoing bicarbonate losses. In salicylate intoxication, short-term therapy with bicarbonate to create an alkalemic environment enhances toxin elimination.
  • If serum bicarbonate levels are less than 8 mEq/L, significant myocardial and CNS dysfunction can occur and emergent treatment may be needed.
  • Calculating the amount of bicarbonate replacement necessary must take into account the effect of non-bicarbonate buffers on exogenously administered bicarbonate. Multiply the desired increase in plasma bicarbonate concentration by the apparent volume of distribution and weight. The bicarbonate deficit can be calculated as follows:
      (Desired Bicarbonate – Measured Bicarbonate) X Weight (kg) X 0.6
    The general recommendation is to replace only half of the total bicarbonate deficit during the first few hours of therapy.
    • Do not overestimate or overcorrect the bicarbonate deficit. Rapid infusion of bicarbonate and overcorrection of the metabolic acidosis can lead to complications such as tetany, seizures, and hypokalemia by worsening the preexisting hypocalcemia and hypokalemia.
    • Doses of bicarbonate exceeding 1 mEq/kg per dose may lead to an alkaline overshoot. For each 0.1 increase in pH, oxygen availability may decrease by 10% because of the shift of the oxygen-hemoglobin dissociation curve to the left.
    • Administered bicarbonate is dissociated into carbon dioxide and water.
    • Carbon dioxide diffuses through the blood-brain barrier, whereas bicarbonate does not; this may lead to a paradoxical CNS acidosis.
    • Parenteral forms of sodium bicarbonate are available as 4% (1/2 strength) or 8% solutions. The sodium load can be significant when multiple bolus doses are administered.
    • If hypernatremia is a concern, consider continuous infusion of sodium bicarbonate as part of the maintenance intravenous solution. For example, 34 mEq/L of sodium bicarbonate can be added to a 0.22% sodium chloride solution to make up a 0.45% salt solution for maintenance intravenous therapy.
  • Hemodialysis is another option for correcting a severe metabolic acidosis associated with renal failure or intoxication with methanol or ethylene glycol.
  • Thiamine deficiency is a rare disorder in developed countries; it can occur in breastfed infants of mothers who have inadequate thiamine intake or in patients with unsupplemented total parenteral nutrition.
    • Thiamine is an essential vitamin for brain development in infants. Thiamine acts as a cocarboxylase, catalyzing decarboxylation of pyruvic acid and acetyl-coenzyme A (acetyl-CoA). It also acts as a coenzyme for pyruvate dehydrogenase activity and oxidative decarboxylation of alpha-ketoglutarate to succinyl-CoA.
    • Thiamine deficiency causes excess pyruvate levels and impaired fatty acid metabolism through the Krebs cycle. Generation of nicotinamide adenine dinucleotide (NADH) in the Krebs cycle is also impaired, stimulating anaerobic glycolysis and leading to increased lactate production.
    • The clinical presentation of thiamine deficiency is characterized by a severe lactic acidosis and shock, which is often resistant to inotropic agents and volume resuscitation. It can produce a polyneuropathy, weakness, paralysis, cardiac failure, or a combination thereof. Lack of thiamine intake can lead to depleted stores within 10 days.
    • Thiamine deficiency is a likely diagnosis for a patient on total parenteral nutrition without multivitamins for 2 or more weeks, who then develops a metabolic acidosis, lactic acidosis, and shock resistance to inotropic support. Thiamine administration rapidly corrects the clinical symptomatology.
  • THAM (tromethamine; tris [hydroxymethyl]-aminomethane) is a buffer that can be used to treat acidosis when concerns exist regarding carbon dioxide accumulation from the metabolism of administered sodium bicarbonate. THAM increases serum bicarbonate predictably:
    • THAM + H2 CO3 ® THAM-H + HCO3
    • H2 CO3 ® CO2 + H2 O
    • Dose: 1 mEq/kg
  • The use of sodium bicarbonate therapy in cases of diabetic ketoacidosis and lactic acidosis is controversial. In 2001, an article published by Glaser et al reported that patients with diabetic ketoacidosis who were treated with sodium bicarbonate were at increased risk for cerebral edema.1
  • A recent study concluded that albumin was not more effective than normal saline in initial hydration of dehydrated term infants with metabolic acidosis due to acute diarrhea.2

Surgical Care

  • Tissue ischemia or necrosis from bowel obstruction or necrotizing enterocolitis, with or without peritonitis, may lead to metabolic acidosis.
  • Especially in newborns with necrotizing enterocolitis, this may be the first laboratory abnormality associated with a surgical abdomen.

Consultations

Consultations depend on the underlying etiology of metabolic acidosis.

  • Consult with a nephrologist for children with renal failure, who may or may not require dialysis.
  • Consult with a geneticist for inborn errors of metabolism.
  • Consult with a surgeon if the underlying cause of metabolic acidosis is surgical in nature (necrotizing enterocolitis, malrotation, volvulus, ruptured appendicitis).
  • Consult with an endocrinologist for children whose metabolic acidosis is caused by diabetic ketoacidosis.

Diet

  • The underlying disease state (eg, diabetes, renal failure) may require diet modification.

Medication

Specific therapies are directed at the underlying disease process that causes metabolic acidosis.

Alkalinizing agents

Sodium bicarbonate is used as a gastric, systemic, and urinary alkalinizer and has been used in the treatment of acidosis resulting from metabolic and respiratory causes, including, diarrhea, kidney disturbances, and shock. Alternatively, THAM is a buffering agent that increases pH without increasing levels of PaCO2. It may be used to correct metabolic acidosis if sodium bicarbonate is contraindicated.


Sodium bicarbonate

Buffering agent for metabolic acidosis when significant bicarbonate losses have occurred.

Adult

1-2 mEq/kg/dose IV

Pediatric

Bicarbonate deficit = (Desired bicarbonate – measured bicarbonate) X weight (kg) X 0.6 Replace only one half of total deficit initially over several hours, then reassess
Dosage range: 0.5-1 mEq/kg/dose IV

Urinary alkalinization induced by increased sodium bicarbonate concentrations may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; may cause increased levels of amphetamines, pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine

Alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema; unknown abdominal pain

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Only used to treat documented metabolic acidosis and hyperkalemia-induced cardiac arrest; can cause alkalosis, decreased plasma potassium level, hypocalcemia, and hypernatremia; caution in electrolyte imbalances such as CHF, cirrhosis, edema, corticosteroid use, or renal failure; when administering, avoid extravasation because tissue necrosis can result


Tromethamine (THAM)

Also called tris (hydroxymethyl)-aminomethane. Combines with hydrogen ions to form bicarbonate buffer. Used to prevent and correct systemic acidosis. Available as 0.3-mol/L IV solution containing 18 g (150 mEq) per 500 mL (0.3 mEq/mL).

Adult

Not established

Pediatric

0.5-1 mEq/kg/dose IV (ie, 1.66-3.33 mL/kg/dose)
Alternatively, may calculate dose with the following formula:
mL of 0.3 mol/L tromethamine = body weight (kg) X base deficit (mEq/L) X 1.1 (factor of 1.1 accounts for about a 10% reduction in buffering capacity due to presence of sufficient acetic acid to lower pH of the 0.3-mol/L solution to approximately 8.6)
Typical initial dose: 3-16 mL/kg/h IV; titrate according to serum pH

Documented hypersensitivity; renal failure; uremia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May induce respiratory depression and hypoglycemia, which may require ventilatory assistance and administration of glucose; reduce dose in renal impairment; monitor serum and urine pH.

Vitamins

Thiamine deficiency is a rare disorder in developed countries; it can occur in breastfed infants of mothers who have inadequate thiamine intake or in patients with unsupplemented total parenteral nutrition.


Thiamine hydrochloride (Thiamilate)

Essential coenzyme that combines with ATP to form thiamine pyrophosphate. Dosage forms include a parenteral injection (l00 mg/mL) and tabs.

Adult

5-30 mg IV/IM tid for 2 wk, followed by 5-30 mg/d PO qd or divided tid for 1 mo
Wernicke syndrome: 100 mg IV for 1 dose, then 50-100 mg/d IV/IM until patient resumes normal diet

Pediatric

10-25 mg/dose IV/IM qd (if critically ill) or 10-50 mg PO qd for 2 wk, then 5-10 mg/dose PO qd for 1 mo

Neuromuscular agents may enhance effects of thiamine; high-carbohydrate diets or IV dextrose solutions may increase thiamine requirements; large doses may interfere with serum theophylline assay.

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Pregnancy category A if <1.4 mg/d (RDA), pregnancy category C if >1.4 mg/d; avoid PO dosing in patients with GI disorders that prevent absorption; administer before beginning a glucose infusion; sensitivity reactions can occur (intradermal test-dose recommended in suspected sensitivity); deaths have resulted from IV use; rash, angioedema, warmth, and tingling may occur

More on Acidosis, Metabolic

Overview: Acidosis, Metabolic
Differential Diagnoses & Workup: Acidosis, Metabolic
Treatment & Medication: Acidosis, Metabolic
Follow-up: Acidosis, Metabolic
Multimedia: Acidosis, Metabolic
References
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References

  1. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. Jan 25 2001;344(4):264-9. [Medline].

  2. Han JJ, Yim HE, Lee JH, et al. Albumin versus normal saline for dehydrated term infants with metabolic acidosis due to acute diarrhea. J Perinatol. Jun 2009;29(6):444-7. [Medline].

  3. [Guideline] Hodson E. Metabolic acidosis and growth in children. Nephrology. Dec 2005;10(S5):S221-2. [Full Text].

  4. Casaletto JJ. Differential diagnosis of metabolic acidosis. Emerg Med Clin North Am. Aug 2005;23(3):771-87, ix. [Medline].

  5. Fall PJ. A stepwise approach to acid-base disorders. Practical patient evaluation for metabolic acidosis and other conditions. Postgrad Med. Mar 2000;107(3):249-50, 253-4, 257-8 passim. [Medline].

  6. Fattal-Valevski A, Kesler A, Sela BA, et al. Outbreak of life-threatening thiamine deficiency in infants in Israel caused by a defective soy-based formula. Pediatrics. Feb 2005;115(2):e233-8. [Medline].

  7. Levraut J, Grimaud D. Treatment of metabolic acidosis. Curr Opin Crit Care. Aug 2003;9(4):260-5. [Medline].

  8. Naka T, Bellomo R. Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit--the role of renal replacement therapy. Crit Care. Apr 2004;8(2):108-14. [Medline].

  9. Szaflarski N, Hanson CW 3rd. Metabolic acidosis. AACN Clin Issues. Aug 1997;8(3):481-96. [Medline].

  10. Thauvin-Robinet C, Faivre L, Barbier ML, Chevret L, Bourgeois J, Netter JC. Severe lactic acidosis and acute thiamin deficiency: a report of 11 neonates with unsupplemented total parenteral nutrition. J Inherit Metab Dis. 2004;27(5):700-4. [Medline].

  11. Uchida H, Yamamoto H, Kisaki Y, Fujino J, Ishimaru Y, Ikeda H. D-lactic acidosis in short-bowel syndrome managed with antibiotics and probiotics. J Pediatr Surg. Apr 2004;39(4):634-6. [Medline].

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Further Reading

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Keywords

metabolic acidosis, bicarbonate, anions, cations, hydrogen, anion gap, anion gap acidosis, normal anion gap metabolic acidosis, renal tubular acidosis, RTA, acid-base disorder, plasma bicarbonate, plasma bicarbonate level, acidemia, respiratory acidosis, respiratory failure, myocardial depression, diarrhea, inborn error of metabolism, neonatal sepsis, hypoplastic left heart syndrome, renal insufficiency, renal tubular acidosis, RTA, failure to thrive, hypoglycemia, hyperammonemia, treatment, diagnosis

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Contributor Information and Disclosures

Author

Margaret A Priestley, MD, Assistant Professor of Clinical Anesthesiology and Critical Care, University of Pennsylvania School of Medicine; Clinical Director, Pediatric Intensive Care Unit, The Children's Hospital of Philadelphia
Margaret A Priestley, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Barry J Evans, MD, Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center
Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

 
 
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