Why We Should Avoid Routine Bicarbonate Use in DKA?

In the management of diabetic ketoacidosis (DKA), the use of bicarbonate therapy remains a highly debated topic. Despite its theoretical benefits, it is rarely recommended in routine practice. Here’s why:

1. Potential for Intracellular Acidosis

? Bicarbonate increases CO2 production, which diffuses rapidly into cells.

? Inside cells, CO2 combines with water to form carbonic acid, lowering intracellular pH.

? Paradoxically, this can worsen intracellular acidosis despite improvements in arterial pH.

2. Impairment of Oxygen Delivery

? Rapid bicarbonate administration can induce alkalosis, leading to a leftward shift in the oxygen-hemoglobin dissociation curve.

? This reduces tissue oxygen release, impairing oxygen delivery to already stressed tissues.

? In cases of impaired CO2 elimination (e.g., lung disease), bicarbonate may lead to paradoxical respiratory acidosis, further complicating oxygen delivery.

3. No Proven Mortality Benefit

? Studies have shown no significant improvement in morbidity or mortality with bicarbonate use in DKA, even at pH <7.0.

? In one trial, bicarbonate did not accelerate pH correction or improve clinical outcomes compared to a placebo in patients with moderate acidosis (pH 6.9–7.14).

4. Slowing Ketosis Resolution

? Alkali therapy may delay the recovery of ketosis by inhibiting the acid-mediated breakdown of ketoacids.

? In some cases, bicarbonate-treated patients experienced delayed clearance of serum ketones.

5. Risk of Overcorrection

? Post-treatment metabolic alkalosis is a common complication, particularly as insulin therapy naturally generates bicarbonate.

? Insulin alone is often sufficient to correct metabolic acidosis.

6. Hyperkalemia Management Concerns

? While bicarbonate may drive potassium into cells during hyperkalemia, its effect is temporary. Addressing the underlying cause with insulin and fluid therapy is more effective and safer .

When Should Bicarbonate Be Considered?

? Severe acidosis (pH <7.0) with associated hemodynamic instability (e.g., decreased cardiac contractility, vasodilation).

? Life-threatening hyperkalemia with ECG changes.

In these scenarios, bicarbonate administration must be cautious, monitored closely, and given with potassium supplementation if serum potassium is <5.0 mEq/L.

Dose and monitoring :

For patients with a pH <7.0, 100 mmol of sodium bicarbonate is administered in 400 mL of sterile water over two hours. If the serum potassium level is <5.0 mEq/L, 20 mEq of potassium chloride (KCl) should be added to the solution. Since bicarbonate therapy can further lower serum potassium, more aggressive potassium replacement may be required if levels drop. Venous pH and bicarbonate concentrations should be monitored every two hours, and bicarbonate doses can be repeated until the pH rises above 7.0.

Key Takeaway:

Bicarbonate therapy should be reserved for specific, life-threatening situations?in DKA.?Fluid resuscitation, insulin therapy, and electrolyte correction remain the cornerstones of DKA management.