What is the management approach for a 4-month pregnant patient with diabetic ketoacidosis (DKA), convulsions, and a normal magnetic resonance imaging (MRI) scan?

Management of DKA with Convulsions in 4-Month Pregnancy with Normal MRI

Immediately initiate continuous intravenous insulin infusion alongside 10% dextrose, even with normal or mildly elevated glucose, while aggressively managing convulsions and correcting electrolyte abnormalities—this dual approach is critical because pregnancy creates a ketogenic state where DKA occurs at lower glucose levels and the fetus requires continuous glucose supply. 1

Immediate Priorities for Convulsion Management

• Secure the airway and administer benzodiazepines (lorazepam 4mg IV or diazepam 10mg IV) as first-line treatment for active seizures, while simultaneously assessing for underlying metabolic causes 1, 2
• Check serum glucose, electrolytes (particularly sodium, potassium, calcium, magnesium), arterial blood gases, and β-hydroxybutyrate levels immediately—convulsions in DKA may result from severe metabolic derangements including hyponatremia, hypocalcemia, or cerebral edema 1, 3
• Obtain continuous fetal monitoring given the high risk of fetal distress and mortality (up to 35% historically) associated with maternal DKA 2, 3, 4
• The normal MRI helps exclude structural causes but does not rule out metabolic encephalopathy from DKA itself 5

Aggressive Fluid Resuscitation Protocol

• Begin with 1-2 liters of 0.9% normal saline over the first 1-2 hours to restore intravascular volume and tissue perfusion 1, 6, 4
• After initial resuscitation, switch to dextrose-containing fluids (10% dextrose) to meet the higher carbohydrate demands of the placenta and fetus in the third trimester, even while continuing insulin therapy 1, 7
• Aim for gradual reduction in osmolality (maximum 3 mOsm/kg H2O/hour) to prevent cerebral edema, which may have contributed to the convulsions 1
• Monitor urine output closely, targeting ≥0.5 mL/kg/hour to confirm adequate renal perfusion before aggressive potassium replacement 8, 3

Insulin and Dextrose Co-Administration

• Start continuous IV insulin infusion at 0.1 units/kg/hour (typically 5-10 units/hour) immediately, regardless of glucose level—do not wait for hyperglycemia confirmation 1, 7, 2
• Simultaneously administer 10% dextrose IV to prevent hypoglycemia and meet fetal metabolic needs while insulin resolves ketosis 1, 7
• This dual approach is non-negotiable in pregnancy: insulin stops ketogenesis while dextrose prevents maternal hypoglycemia and maintains fetal glucose supply 1, 5
• Adjust insulin rate based on ketone clearance (β-hydroxybutyrate reduction), not just glucose levels 1, 5

Critical Electrolyte Management

• Potassium replacement is paramount: Check serum potassium before starting insulin if possible, as insulin drives potassium intracellularly and can precipitate life-threatening hypokalemia, respiratory paralysis, and ventricular arrhythmias 8, 1, 7
• Add 20-40 mEq/L potassium (2/3 KCl and 1/3 KPO4) to IV fluids once serum potassium falls below 5.5 mEq/L and adequate urine output is established 1, 8
• Monitor serum potassium every 2-4 hours during acute management—hypokalemia occurs in approximately 50% of DKA cases and severe hypokalemia (<2.5 mEq/L) is associated with increased mortality 7, 1
• Check and correct magnesium levels (target >0.6 mmol/L), as hypomagnesemia makes hypokalemia resistant to correction 1, 9
• Monitor calcium levels, as hypocalcemia can lower seizure threshold and contribute to convulsions 1

Monitoring Requirements

• Measure β-hydroxybutyrate levels (preferred over urine ketones) every 2-4 hours to monitor treatment response—resolution of acidosis or reduction in blood β-hydroxybutyrate marks successful treatment 1, 5
• Check arterial blood gases, serum glucose hourly, and electrolytes every 2-4 hours during acute management 1, 3
• Continuous cardiac monitoring is essential given the risk of arrhythmias from electrolyte shifts 1, 8
• Continuous fetal heart rate monitoring throughout acute management, as fetal distress may occur even with improving maternal status 3, 4

Pregnancy-Specific Pathophysiology Considerations

• Euglycemic DKA is common in pregnancy (up to 35% of cases)—do not rely solely on glucose levels for diagnosis, as DKA can occur with glucose <200 mg/dL or even normal levels 1, 2, 5
• Pregnancy creates accelerated starvation, insulin resistance, and respiratory alkalosis that promote ketosis at lower glucose thresholds 1, 2, 4
• Look for classic symptoms: nausea, vomiting, abdominal pain, Kussmaul respirations, altered mental status, and dehydration—though presentation may be atypical 1, 3
• The placenta and fetus have continuous high carbohydrate demands that persist even during maternal ketoacidosis, necessitating dextrose administration alongside insulin 1, 7

Post-Delivery Considerations

• Anticipate dramatic improvement in insulin sensitivity and rapid resolution of ketoacidosis after delivery of the fetus and placenta 1, 7
• Insulin requirements drop precipitously postpartum—reduce insulin infusion rate by 50-75% immediately after delivery to prevent hypoglycemia 7

Prevention of Recurrence

• Prescribe ketone test strips and provide clear instructions to check ketones regularly, especially during illness, poor oral intake, or hyperemesis 1, 7
• Educate the patient that even with normal glucose levels, ketones can indicate impending DKA in pregnancy 1, 5
• Instruct to seek emergency care immediately if ketones are moderate to large, even with normal glucose 1, 5

Common Pitfalls to Avoid

• Do not wait for hyperglycemia to diagnose DKA in pregnancy—euglycemic DKA is common and can be missed if relying solely on glucose levels 1, 2, 5
• Never give insulin without dextrose in pregnant women with DKA—this fails to meet fetal metabolic needs and can perpetuate ketosis 1, 7
• Do not assume convulsions are solely from DKA—aggressively treat seizures while correcting metabolic abnormalities 2, 3
• Avoid over-aggressive glucose lowering—the goal is ketone clearance, not rapid glucose normalization 1, 5
• Do not neglect potassium monitoring and replacement—hypokalemia is the most common cause of mortality during DKA treatment 7, 1, 8