What is the treatment for metabolic acidosis?

From the Guidelines

The treatment of metabolic acidosis should focus on addressing the underlying cause, and sodium bicarbonate therapy is generally not recommended, as shown in recent studies 1. For mild to moderate metabolic acidosis (pH > 7.2), treating the primary condition is often sufficient.

• The primary goal is to restore circulatory volume and tissue perfusion,
• resolve hyperglycemia,
• correct electrolyte imbalance, and
• address any underlying cause of the acidosis, such as sepsis or diabetic ketoacidosis.

In cases of diabetic ketoacidosis, insulin therapy is the standard of care, typically administered intravenously at 0.1 units/kg/hour, along with fluid resuscitation 1.

• The use of bicarbonate in patients with diabetic ketoacidosis has been shown to make no difference in the resolution of acidosis or time to discharge 1.
• For severe cases of metabolic acidosis, particularly with renal failure or certain toxin ingestions, hemodialysis may be necessary.
• Potassium levels should be monitored closely during treatment, as correction of acidosis can lower serum potassium.

The therapeutic approach aims to normalize the body's pH by addressing the excess acid production or inadequate acid excretion, restoring the bicarbonate buffer system, and improving cellular function that becomes compromised in acidotic states.

• Recent studies have emphasized the importance of individualizing treatment based on careful clinical and laboratory assessment 1.
• The use of subcutaneous rapid-acting insulin analogs, when combined with aggressive fluid management, has been shown to be effective in treating mild or moderate diabetic ketoacidosis 1.

From the FDA Drug Label

In cardiac arrest, a rapid intravenous dose of one to two 50 mL vials (44.6 to 100 mEq) may be given initially and continued at a rate of 50 mL (44. 6 to 50 mEq) every 5 to 10 minutes if necessary (as indicated by arterial pH and blood gas monitoring) to reverse the acidosis. In less urgent forms of metabolic acidosis, Sodium Bicarbonate Injection, USP may be added to other intravenous fluids The amount of bicarbonate to be given to older children and adults over a four-to-eight-hour period is approximately 2 to 5 mEq/kg of body weight - depending upon the severity of the acidosis as judged by the lowering of total CO2 content, blood pH and clinical condition of the patient Treatment of metabolic acidosis should, if possible, be superimposed on measures designed to control the basic cause of the acidosis - e.g., insulin in uncomplicated diabetes, blood volume restoration in shock.

The treatment for metabolic acidosis is sodium bicarbonate (IV), with the dose and administration rate depending on the severity of the acidosis and the patient's clinical condition. The initial dose in cardiac arrest is 44.6 to 100 mEq, and in less urgent cases, the dose is 2 to 5 mEq/kg of body weight over 4 to 8 hours. Treatment should be planned in a stepwise fashion, with monitoring of blood gases, plasma osmolarity, and clinical response. The goal is to improve the acid-base status of the blood without causing undue side effects, such as alkalosis 2, 2.

• Key considerations:
  • Monitor blood gases and clinical response
  • Adjust dose and administration rate as needed
  • Control the basic cause of the acidosis, if possible
  • Avoid overcorrection, which can lead to alkalosis.

From the Research

Treatment of Metabolic Acidosis

• The treatment of metabolic acidosis is aimed at diagnosis and correction of the underlying disease process 3
• Specific treatment may be required when changes in pH are severe (pH less than 7.2 or pH greater than 7.6) 3
• Treatment of severe metabolic acidosis requires the use of sodium bicarbonate, but blood pH and gases should be monitored closely to avoid an "overshoot" alkalosis 3
• The appropriate treatment of acute metabolic acidosis, in particular organic form of acidosis such as lactic acidosis, has been very controversial 4
• The only effective treatment for organic acidosis is cessation of acid production via improvement of tissue oxygenation 4
• Treatment of acute organic acidosis with sodium bicarbonate failed to reduce the morbidity and mortality despite improvement in acid-base parameters 4

Types of Metabolic Acidosis and Treatment

• Two types of nontoxic metabolic acidosis must be differentiated: the mineral metabolic acidosis and the organic metabolic acidosis 5
• Mineral acidosis is not caused by a failure in the energy metabolic pathways, and its treatment is mainly symptomatic by correcting the blood pH (alkali therapy) or accelerating the elimination of excessive mineral anions (renal replacement therapy) 5
• Organic acidosis gives evidence that a severe underlying metabolic distress is in process, and no reliable argument exists to prove that this acidosis is harmful under these conditions in humans 5
• The management of an acute organic metabolic acidosis is therefore primarily based on the cause of the acidosis, and no scientific argument exists to justify the correction of the acid-base imbalance in this context 5

Diagnostic and Therapeutic Guidance

• The correct identification of the cause, and ideally the individual acid, responsible for metabolic acidosis in the critically ill ensures rational management 6
• Diagnostic and therapeutic guidance is provided when faced with a high anion gap acidosis, for example pyroglutamate, in the common clinical scenario 'I can't identify the acid--but I know it's there' 6
• The evidence that metabolic acidosis affects outcomes and thus warrants correction is considered and management guidance including extracorporeal removal and fomepizole therapy is provided 6

Pathophysiologic Approach to Treatment

• Acute metabolic acidosis is associated with increased morbidity and mortality because of its depressive effects on cardiovascular function, facilitation of cardiac arrhythmias, stimulation of inflammation, suppression of the immune response, and other adverse effects 7
• Appropriate evaluation of acute metabolic acidosis includes assessment of acid-base parameters, including pH, partial pressure of CO(2) and HCO(3)(-) concentration in arterial blood in stable patients, and also in central venous blood in patients with impaired tissue perfusion 7
• Treatment should be directed at improving both extracellular and intracellular pH, and administration of tris(hydroxymethyl)aminomethane (THAM) improves acidosis without producing intracellular acidosis 7
• Selective sodium-hydrogen exchanger 1 (NHE1) inhibitors have been shown to improve haemodynamics and reduce mortality in animal studies of acute lactic acidosis and should also be examined further 7