Metabolic acidosis medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

A pH under 7.1 is an emergency, due to the risk of cardiac arrhythmias, and may warrant treatment with intravenous bicarbonate. Bicarbonate is given at 50-100 mmol at a time under scrupulous monitoring of the arterial blood gas readings. This intervention however, is not effective in case of lactic acidosis. If the acidosis is particularly severe and/or there may be intoxication, consultation with the nephrology team is considered useful, as dialysis may clear both the intoxication and the acidosis.

General Management:

Aim is to Maintain adequate tissue oxygenation & Hemodynamic stability.

ECLS Approach to Management of Metabolic Acidosis

	ECLS Approach to Management of Metabolic Acidosis
Emergency:	intubation and ventilation for airway or ventilatory control; Cardiopulmonary resuscitation: Severe hyperkalemia
Cause:	Treat the underlying disorder as the primary therapeutic goal. Consequently, an accurate diagnosis of the cause of metabolic acidosis is very important.
Losses:	Replace losses (e.g. fluids and electrolytes) where appropriate. Other supportive care (oxygen administration) is useful. In most cases, IV sodium bicarbonate is not necessary, and may even be harmful so is not generally recommended.
Specifics:	There are often specific problems or complications associated with specific causes or specific cases that require specific management. For example, Ethanol blocking treatment with methanol ingestion; rhabdomyolysis requires management by IV fluids and uricosurics agents for preventing acute renal failure; hemodialysis can remove some nephrotoxins

Specific Treatment:

Treatment of the cause should be our primary aim. Administration of bicarbonates and dialysis is required for metabolic acidosis that is associated with Renal failure.

Restoration of adequate intravascular volume and proper peripheral perfusion is necessary for metabolic acidosis caused by lactic acidosis.

Alcohol Intoxication:

Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication.

Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications.

Base administration in the treatment of acute metabolic acidosis	Benefits	Description	side-effects
Intravenous sodium bicarbonate	Inexpensive Simple to use bicarbonate	It should be administered slowly as an isosmotic solution to avoid hyperosmolality and minimize the extent of intracellular acidosis	Might exacerbate intracellular acidosis; can provide large sodium load
Intravenous THAM	Buffers protons without generating CO2 penetrates cells to buffer pH,	Given as 0.3M solution, best to give through a central vein; serum potassium and PCO2 should be monitored carefully during therapy	hyperkalaemia, hypercapnia, liver necrosis in newborns
Intravenous carbicarbonate	It preserves cardiac contractility in animal studies, human practice not done.	Under-study	under-study
Dialysis	Can provide large quantities of the base while preventing volume overload or hyperosmolality; continuous renal replacement therapy can deliver base over 24 hour period at a low rate. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in the treatment of several of the alcohol-related intoxications	Continuous renal replacement therapy is preferred over intermittent hemodialysis	Requires use of dialysis equipment and personnel; hypotension can occur during procedure

Treatment of Diabetic-ketoacidosis

• DKA is managed in an intensive care unit during the first day is always advisable
• Fluid, Insulin and electrolyte replacement are most crucial for DKA management.
• Correction of fluid loss with intravenous fluids only , Correction of hyperglycemia with insulin, Correction of electrolyte disturbances, particularly potassium loss is < 5.5, Correction of acid-base balance by bicarbonate if <7.1, Treatment of concurrent infection by antibiotics, if present.

	MANAGEMENT OF DKA AND HHS
IV fluids	Hight flow 0.9% normal saline is recommended and should be continued until corrected sodium is <135 mg/dl. Switch to .45% normal saline when Sodium >135 mg/dl. Add dextrose into 0.45% normal saline when serum glucose <200 mg/dl and sodium <135.
Insulin	Initiate continuous IV regular insulin infusion Switch to subcutaneous basal-bolus insulin for the following : able to eat glucose <200 mg/dl anion gap <12 mEq/L serum bicarbonate > 15 mEq/L pH > 7.3 Overlap subcutaneous and IV insulin by 1-2 hours.
Potassium	Add IV potassium if serum potassium <5.2 mEq/L Hold insulin for serum potassium <3.3 mEq/L Nearly all patients are potassium depleted, even with hyperkalemia
Bicarbonates	Consider for patients with pH<6.9, Bicarbonate<5 and severe hyperkalemia. But mostly it is avoided as it is cause of cerebral edema in children.
phosphate	Consider for serum phosphate <1 mg/dl, cardiac dysfunction, or respiratory depression Monitor serum calcium frequently

Renal Tubular Acidosis

type 1 and type 2 RTA	Type 4 RTA
The treatment of type 1 and type 2 RTA is relatively simple.	Type 4 RTA may require treatment with fludrocortisone.
It requires the use of sodium bicarbonate or the slightly more palatable compound Shohl solution/Bicitra, which contains citric acid and sodium citrate as a source of alkali.	To reverse the hyperkalemia that characterizes the metabolic acidosis of type 4 RTA, dietary potassium restriction and orally administered potassium binders, Kalexate, Kionex, Lokelma, patiromer, sodium polystyrene sulfonate, sodium zirconium cyclosilicate may be needed.
Polycitra K solutions contain potassium citrate to provide equal amounts of alkali and potassium i-e 2 mEq/mL of alkali and 2 mEq/mL of potassium, to correct both the acidosis and hypokalemia	Finally, to increase renal excretion of potassium use diuretics like chlorothiazide, and furosemide may be required to correct hyperkalemia.
	To neutralize the metabolic acidosis, bicarbonate therapy can also be used

Lactic Acidosis:

• Treatment for Lactic Acidosis starts with Identification of the primary illness and correction of that disturbance.
• Restoration of tissue oxygen delivery through hemodynamic and/or respiratory support is the key therapeutic goal in type A lactic acidosis.
• The use of sodium bicarbonate in lactic acidosis is controversial, particularly in patients with circulatory and respiratory failure. Despite the controversy most physicians support administration of NaHCO3 for very severe acidemia and will give small amounts of NaHCO3 to maintain the arterial pH above 7.10.
• Administration of Bicarbonates in a pH beyond 7.1 will promote the development of arrhythmias and cardiac depression.

Experimental treatment:

Small animal studies of various models of shock and lactic acidosis demonstrated improved cardiac function, reduced mortality, and decreased generation of pro-inflammatory cytokines; human studies yet to be performed, so options include as follows:

1. Dichloroacetate
2. Administration of selective inhibitors Na+-H+ Exchanger 1 or amiloride analogues
3. Administration of inhibitors of transient receptor potential vanilloid 1
4. Administration of selective inhibitors acid sensing Ion channel la
5. Administration of inhibitors of mitogen activated protein kinase

Contraindicated medications

Metabolic acidosis is considered an absolute contraindication to the use of the following medications:

• Glyburide and Metformin
• Saxagliptin hydrochloride and Metformin hydrochloride
• Topiramate