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

  1. Insulin deficiency + stressInfection, insulin omission, new T1DM
  2. Counter-reg hormone surgeGlucagon, cortisol, epinephrine rise
  3. Lipolysis → ketogenesisFFA → β-hydroxybutyrate + acetoacetate
  4. 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%.

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