Can Diabetic Ketoacidosis (DKA) lead to seizures?

Diabetic Ketoacidosis (DKA) and Seizures

Yes, diabetic ketoacidosis (DKA) can lead to seizures through several mechanisms, including cerebral edema, electrolyte disturbances, and severe hypocapnia. Seizures represent a serious neurological complication that can significantly increase morbidity and mortality in patients with DKA.

Mechanisms of DKA-Related Seizures

• Cerebral edema: This is a rare but potentially fatal complication of DKA, occurring in 0.7-1.0% of children with DKA. Neurological deterioration may be rapid, with seizures, incontinence, pupillary changes, bradycardia, and respiratory arrest. Once clinical symptoms beyond lethargy occur, mortality is high (70%), with only 7-14% of patients recovering without permanent morbidity 1.

• Electrolyte disturbances:

  • Severe hypophosphatemia during DKA treatment can trigger seizures and even lead to respiratory failure and cardiac dysfunction 2, 3.
  • Hypokalemia due to insulin administration and treatment of acidosis with bicarbonate can contribute to neurological complications including seizures 1.

• Hypocapnia: Sudden severe hypocapnia during DKA treatment may lower the seizure threshold and precipitate seizure activity 4.

• Hyperosmolality: Rapid changes in serum osmolality during treatment can trigger seizures. The mechanism likely involves osmotically driven movement of water into the central nervous system when plasma osmolality declines too rapidly 1.

Risk Factors for DKA-Related Seizures

• Children with newly diagnosed diabetes are at higher risk for cerebral edema and subsequent seizures 1.
• Young people in their twenties with DKA may also develop cerebral edema 1.
• Rapid correction of hyperglycemia and osmolality (>3 mOsm kg⁻¹ H₂O h⁻¹) increases risk 1.
• Patients with severe acidosis (pH <7.0) may be at higher risk for neurological complications 1.

Prevention of DKA-Related Seizures

• Gradual correction of osmolality: Limit the reduction in osmolality to no more than 3 mOsm kg⁻¹ H₂O h⁻¹ in hyperosmolar patients 1.

• Careful fluid management:

  • Add dextrose to hydrating solution once blood glucose reaches 250 mg/dL 5.
  • Maintain glucose between 150-200 mg/dL until DKA resolution 5.

• Electrolyte monitoring and replacement:

  • Monitor potassium levels closely and maintain serum K+ between 4-5 mmol/L 5.
  • Consider phosphate replacement in patients with cardiac dysfunction, anemia, respiratory depression, or serum phosphate <1.0 mg/dL 1, 2.

• Continuous monitoring: Regularly assess neurological status during DKA treatment to rapidly identify changes that might indicate iatrogenic complications 1.

Management of DKA-Related Seizures

• Immediate evaluation to determine underlying cause 4.

• If cerebral edema is suspected:

  • Reduce the rate of fluid administration 1.
  • Elevate the head of the bed 1.
  • Consider mannitol or hypertonic saline if severe 1.

• For electrolyte-related seizures:

  • Correct severe hypophosphatemia with 20-30 mEq/L potassium phosphate added to replacement fluids when indicated 1, 3.
  • Maintain potassium in the normal range 6.

Important Caveats and Pitfalls

• Do not discontinue insulin therapy prematurely: Interruption of insulin therapy before ketoacidosis resolves can lead to recurrence and worsening of DKA 5.

• Avoid overly rapid correction of hyperglycemia: This can precipitate cerebral edema and seizures 1.

• Don't overlook phosphate levels: Although routine phosphate replacement is not recommended, severe hypophosphatemia (<1.0 mg/dL) should be corrected to prevent neurological complications 1, 2.

• Consider alternative causes of seizures: In patients with DKA and seizures, also evaluate for intracerebral hemorrhage, cerebrovascular occlusive disease, and other neurological conditions 7.

DKA-related seizures represent a medical emergency with high morbidity and mortality. Early recognition of risk factors and careful management of fluid, electrolyte, and glucose levels are essential to prevent this serious complication.