From the Guidelines
Bicarbonate levels may remain low even after DKA improves due to the time required for the body to regenerate bicarbonate stores, renal tubular mechanisms, and potential concurrent conditions like acute kidney injury or volume depletion. The primary reason is that while ketone production has decreased and glucose levels have normalized, the body needs time to correct the severe metabolic acidosis that occurred during DKA, as bicarbonate was consumed to buffer the excess ketoacids 1. Additionally, the kidneys require 24-48 hours to fully regenerate bicarbonate through renal tubular mechanisms. Concurrent conditions like acute kidney injury, which often accompanies DKA, can delay this recovery process by impairing the kidney's ability to excrete acid and regenerate bicarbonate. Volume depletion may also persist despite initial fluid resuscitation, affecting renal perfusion and bicarbonate regeneration. In some cases, hyperchloremic metabolic acidosis develops during treatment as chloride-rich IV fluids replace bicarbonate-poor body fluids, creating a new acid-base disturbance that maintains a low bicarbonate level despite resolution of ketosis.
- Key factors to consider include:
- Time required for bicarbonate regeneration
- Renal function and potential acute kidney injury
- Volume status and potential for hyperchloremic metabolic acidosis
- Ongoing monitoring of electrolytes and acid-base status Patients should continue to receive appropriate fluid resuscitation and insulin therapy while monitoring electrolytes and acid-base status until bicarbonate levels normalize, as recommended by recent guidelines 1. It is also important to note that the use of bicarbonate in patients with DKA has been shown to make no difference in the resolution of acidosis or time to discharge, and its use is generally not recommended 1.
From the Research
Possible Reasons for Low Bicarb after DKA Improves
- The severity of metabolic acidosis on presentation can predict the severity of subsequent hypophosphataemia and potentially low bicarbonate levels 2
- Profound hypophosphataemia can be associated with serious complications, and clinicians should recognize the likelihood of this biochemical derangement in those DKA patients presenting with profound acidosis 2
- Initial hyperphosphataemia is reflective of intravascular volume depletion and pre-renal renal impairment, which may also affect bicarbonate levels 2
- DKA treatment involves fluid and electrolyte replacement, insulin, treatment of precipitating causes, and close monitoring to adjust therapy and identify complications, which may not immediately correct low bicarbonate levels 3, 4, 5
- The use of sodium-glucose cotransporter-2 inhibitors can increase the risk of DKA and euglycemic DKA, which may have different effects on bicarbonate levels 3
- Combined acid-base disturbances, such as those caused by profuse vomiting, can mask the expected acidosis and affect bicarbonate levels 6