Acute metabolic emergency of insulin deficiency producing hyperglycemia, ketonemia, and anion-gap acidosis.
Also known as: DKA, diabetic ketoacidosis, ketoacidosis, euglycemic DKA
Overview
Life-threatening complication of insulin deficiency defined by the triad of hyperglycemia (>250 mg/dL, or near-normal in euglycemic DKA), ketonemia/ketonuria, and high anion-gap metabolic acidosis (pH <7.30, bicarbonate <18 mEq/L).
Epidemiology
Annual incidence ~8 per 1,000 patients with diabetes. Most common in T1DM but increasingly seen in T2DM (~10-30% of DKA admissions), particularly with SGLT2 inhibitors. In-hospital mortality <1% with modern care; higher in elderly and those with comorbid sepsis.
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Uremic acidosis — Advanced CKD with elevated BUN/creatinine; non-ketotic anion gap acidosis
Diagnostic workup
Diagnostic criteria
ADA criteria: glucose >250 mg/dL (or <250 in euglycemic DKA), arterial pH <7.30, bicarbonate <18, anion gap >12, positive serum/urine ketones. Severity: mild (pH 7.25-7.30), moderate (7.00-7.24), severe (<7.00).
Labs
POC glucose, then serum glucose (>250 mg/dL; may be normal in euglycemic DKA)
VBG or ABG: pH <7.30, HCO3 <18 mEq/L
Anion gap >12 (calculate: Na − [Cl + HCO3])
Serum or urine ketones; β-hydroxybutyrate is the preferred quantitative marker
BMP: serum K may be normal or elevated initially despite total-body depletion; phosphate, magnesium often low
CBC (leukocytosis common even without infection), lipase, urinalysis, blood/urine cultures if infection suspected
ECG to assess for hyperkalemia and ischemic precipitants
Pregnancy test in women of reproductive age
Imaging
CXR if infection suspected
CT head only if focal deficits or persistent altered mentation despite metabolic correction (cerebral edema risk in pediatrics)
Diagnostic algorithm
Parameter
DKA
HHS
Typical population
T1DM (any age)
Elderly T2DM
Glucose
>250 mg/dL (may be normal in euglycemic DKA)
>600 mg/dL
pH
<7.30
>7.30
Bicarbonate
<18 mEq/L
>18 mEq/L
Anion gap
>12 (high)
Variable, usually normal
Ketones (serum/urine)
Strongly positive
Mild or absent
Effective osmolarity
Variable
>320 mOsm/kg
Mental status
Alert → drowsy → coma
Often profoundly altered
Onset
Hours to 1-2 days
Days to weeks
Mortality
<1%
5-20%
Comparison of DKA vs HHS — overlap exists; mixed presentations occur.
Treatment
First-line
IV fluids — 0.9% NaCl 15-20 mL/kg in the first hour, then transition to 0.45% NaCl if corrected serum Na normal/elevated; switch to D5-0.45% NaCl when glucose <200-250 to allow continued insulin infusion
Insulin — IV regular insulin 0.1 unit/kg bolus then 0.1 unit/kg/hr infusion (omit bolus in pediatrics); titrate to lower glucose 50-75 mg/dL/hr
Potassium — check before insulin: if K <3.3, HOLD insulin and replace K (10-40 mEq/hr) first; if 3.3-5.2, add 20-30 mEq KCl per liter of fluid; if >5.2, no K replacement initially but recheck q2h
Bicarbonate — only if pH <6.9 (controversial; consider 100 mEq in 400 mL water over 2 h)
Identify and treat precipitating cause (infection, MI, missed insulin)
Complications
Cerebral edema — feared complication in pediatric DKA (mortality up to 25%); presents 4-12 h into treatment with headache, bradycardia, altered mental status; treat with mannitol or hypertonic saline; avoid overly rapid fluid resuscitation
Hypokalemia, hypophosphatemia, hypomagnesemia during insulin therapy
Hypoglycemia from prolonged insulin infusion without dextrose
Mucormycosis (rhinocerebral) — rare but devastating; consider in immunocompromised DKA patient with facial pain or black eschar
PANCE pearls
Euglycemic DKA (glucose <250) — increasingly common with SGLT2 inhibitors; hold SGLT2i during illness and 3-4 days before surgery.
Pseudohyponatremia: each 100 mg/dL of glucose above normal lowers measured Na by ~1.6 mEq/L; corrected Na guides fluid choice.
Total-body potassium is depleted even when serum K is normal/high — insulin will rapidly drive K intracellularly causing dangerous hypokalemia.
Anion gap closure (not bicarbonate normalization) is the marker of resolution; bicarbonate may lag due to hyperchloremic acidosis from saline.
Always overlap subcutaneous insulin BEFORE stopping the infusion — failing to overlap is the most common cause of rebound DKA.
References
ADA 2025 — American Diabetes Association Standards of Care in Diabetes—2025: Diabetes Technology and Hyperglycemic Crises (Diabetes Care 2025; 48 Suppl 1)
ADA Consensus 2024 — Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (Umpierrez et al., Diabetes Care 2024)
ISPAD 2022 — ISPAD Clinical Practice Consensus Guidelines 2022: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State
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