Endocrinology
Diabetic Ketoacidosis
당뇨성케톤산증
Insulin deficiency + counter-regulatory hormones cause ketoacidosis and hyperglycemia
- How common
- Common T1DM complication
- Typical age
- Mostly T1DM patients
What is it?
Insulin deficiency + counter-regulatory hormones cause lipolysis → ketones → acidosis.
Commonly affected: Systemic (metabolism, CV, brain)
How it develops
- Insulin deficiency + stressInfection, insulin omission, new T1DM
- Counter-reg hormone surgeGlucagon, cortisol, epinephrine rise
- Lipolysis → ketogenesisFFA → β-hydroxybutyrate + acetoacetate
- AG acidosis + dehydrationpH <7.3, HCO3 <15, osmotic diuresis
Symptoms
- Kussmaul respirationDeep rapid breathing (compensatory)
- Severe dehydrationDry mucosa, tachycardia
- Abdominal pain/vomitingCommon in children; mimics acute abdomen
- Altered mental statusMild → coma
- Fruity breathAcetone breath odor
How it is examined
- ABG + electrolytespH <7.3, HCO3 <15, AG >12
- Serum/urine ketonesβ-hydroxybutyrate ≥3 mmol/L
- Workup for triggerInfection, MI workup (CBC, CXR, ECG, cultures)
Imaging
CXR to evaluate precipitants like pneumonia.
- Pneumonia
- Congestion
Brain CT/MRI if cerebral edema suspected (esp. children).
- Cerebral edema
Non-surgical care
- IV fluids (NS 1 L/hr)Aggressive first 1–2h, then 0.45% NS
- IV regular insulin 0.1 U/kg/hrAdd D5W when glucose reaches 250
- Potassium replacementStart when K <5.2 (insulin shifts K intracellularly)
- Treat precipitantAntibiotics for infection, ACS care if MI
- Monitor anion gapContinue IV insulin until AG normalizes
Conservative options are generally tried first. Medications listed here can have side effects — discuss them with your prescriber.
When surgery is considered
None
Outlook
Mortality <5% with treatment; pediatric cerebral edema 20–50%.