eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic

Metabolic Acidosis: Treatment & Medication

Author: Antonia Hipp, DO, Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate Medical Center/Kings County Hospital Center; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Coauthor(s): Richard Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Contributor Information and Disclosures

Updated: Sep 11, 2008

Treatment

Emergency Department Care

The initial therapeutic goal for patients with severe acidemia is to raise the systemic pH above 7.1-7.2, a level at which dysrhythmias become less likely and cardiac contractility and responsiveness to catecholamines will be restored.

Metabolic acidosis can be reversed by treating the underlying condition or by replacing the bicarbonate. The decision to give bicarbonate should be based upon the pathophysiology of the specific acidosis, the clinical state of the patient, and the degree of acidosis.

  • Treating the underlying conditions in high AG states usually is sufficient in reversing the acidosis.
    • Treatment with bicarbonate is unnecessary, except in extreme cases of acidosis when the pH is less than 7.1-7.2.
    • For all cases of diabetic ketoacidosis, the role of bicarbonate is controversial, regardless of the pH or bicarbonate level.
    • In hyperchloremic acidosis, the central problem is with the reabsorption or regeneration of bicarbonate. In these conditions, therapy with bicarbonate makes physiologic sense and is prudent in patients with severe acidosis.
  • Caution with bicarbonate therapy is indicated because of its potential complications, including the following:
    • Volume overload
    • Hypokalemia
    • CNS acidosis
    • Hypercapnia
    • Tissue hypoxia via leftward shift of hemoglobin-oxygen dissociation curve
    • Alkali stimulation of organic acidosis (lactate)
    • Overshoot alkalosis

Consultations

Metabolic acidosis secondary to ingestions (eg, salicylate, methanol, ethylene glycol) often requires dialysis therapy, and a nephrologist should be consulted early in the case management. Toxicologic consultation should also be considered in such cases. Dialysis is the preferred treatment for patients with significant metabolic acidosis in the setting of renal failure.

Medication

Many drugs may be used in the management of a patient with metabolic acidosis. They range from antibiotics for septic shock to toxin antidotes. These agents are discussed in detail under the specific articles for the disease. Bicarbonate is an agent that is considered across the numerous differentials of metabolic acidosis. Its use generally is limited to severe cases of acidosis (pH <7.1-7.2).

Alkalinizing agent

This agent is used in the treatment of metabolic acidosis.


Sodium bicarbonate (Neut)

Bicarbonate ion is produced when it dissociates and neutralizes the hydrogen ions and raises urinary and blood pH.

Adult

Total bicarbonate deficit = Base deficit X bicarbonate (0.5-0.8) X body weight (kg)
Although this represents total bicarbonate deficit, replacement of this amount is never necessary since the unmeasured anions will be converted back to bicarbonate once the underlying condition is treated; the goal of IV bicarbonate is only to emergently raise the pH above 7.1-7.2; this generally can be accomplished by small boluses of IV bicarbonate equalling 50-100 mEq; continuous monitoring of pH and electrolytes is required to judge the adequacy of bicarbonate therapy

Pediatric

The following formula may be used to estimate dose to be administered in children: HCO3 - (mEq) = 0.5 X weight (kg) X [24 - serum HCO3 - (mEq/L)]
Formula has many limitations, but practitioner can roughly determine amount of bicarbonate required and subsequently titrate against pH and anion gap

Urinary alkalinization, induced by increased sodium bicarbonate concentrations, may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases 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

Sodium bicarbonate should only be used to treat documented metabolic acidosis and hyperkalemia-induced cardiac arrest; can cause alkalosis, decreased plasma potassium, hypocalcemia, and hypernatremia; caution in electrolyte imbalances (eg, CHF, cirrhosis, edema, corticosteroid use, renal failure); when administering, avoid extravasation because can cause tissue necrosis

More on Metabolic Acidosis

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

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Further Reading

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Keywords

metabolic acidosis, increase in total body acid, acidemia, pH <7.10, renal tubular acidosis, RTA, tachypnea, hyperpnea, Kussmaul respiration, hyperventilation, chronic metabolic acidosis, uremia, renal failure, hypoaldosteronism, lactic acidosis, ketoacidosis

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Contributor Information and Disclosures

Author

Antonia Hipp, DO, Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate Medical Center/Kings County Hospital Center; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Antonia Hipp, DO is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Richard Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Erik D Schraga, MD, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Howard A Bessen, MD, Professor of Medicine, Department of Emergency Medicine, UCLA School of Medicine; Program Director, Harbor-UCLA Medical Center
Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

 
 
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