II. Epidemiology
- Incidence: 0.5 to 1% of Diabetic Ketoacidosis patients
III. Pathophysiology
- Osmotic Theory (historically accepted theory)
- Prolonged Hyperglycemia results in hyperosmolarity
- Rapid osmolar shift occurs with large fluid bolus
- However, fails to explain Cerebral Edema in DKA patients who did not receive IV fluids
- Vasogenic Theory (more recent theory gaining acceptance)
- Free fluid crosses the brain barrier more easily in severe acidosis and Dehydration
IV. Risk Factors
- Younger children (<5 years old, and esp. age <3 years)
- New onset of diabetes
- Longer duration of DKA symptoms
- Severe acidosis
- Rapid hydration has been postulated as cause
- Precautions regarding fluid rate and amount are standard of care in Diabetic Ketoacidosis management (see below)
- However large study did not show an association with fluid rate or amount
- Glaser (2001) N Engl J Med 344(4): 264-9 [PubMed]
- Insulin given in first hour of DKA Management
- Elevated Blood Urea Nitrogen
- Decreased pCO2
- Bicarbonate administration
- Failure of Serum Sodium to rise despite correction of Hyperglycemia
V. Symptoms: Initial Symptoms
- Headache
- Refractory Vomiting
- Hypertension
- Bradycardia
- Lethargy
VI. Precautions: Children under age 5 years old with DKA
- Avoid large fluid boluses beyond initial 10-20 cc/kg if at all possible
- Avoid dropping Serum Osmolality (calc) >3 mOsms/hour
VII. Management
- See Diabetic Ketoacidosis Management in Adults
- See Diabetic Ketoacidosis Management in Children
- Emergent management of acute cerebral edema
- Raise the head of bed
- Administer Hypertonic Saline 3% (5 ml/kg) OR Mannitol IV (0.5 to 1 mg/kg)
VIII. Prognosis
- Mortality: 21-24% (50% in some studies)
- Persistent vegatative state in up to one third of surviving children
IX. References
- Aurora and Menchine in Herbert (2014) EM:Rap 14(1): 10-11
- Fahlsing and Ponce (2024) Crit Dec Emerg Med 38(3): 18-9