Skip to content

Diabetic Ketoacidosis (DKA)

Basics

  • Life-threatening emergency typically in type 1 diabetes.
  • Biochemical triad: hyperglycemia, ketosis, high anion gap metabolic acidosis.
  • Euglycemic DKA can occur in pregnancy or with SGLT2 inhibitors.
  • Systems affected: endocrine/metabolic, neurologic.

Epidemiology

  • Incidence by age:
  • 1-17 years: 10.1%
  • 18-44 years: 53.3%
  • 45-64 years: 27.1%
  • 65-84 years: 8.7%
  • β‰₯85 years: 0.8%

Etiology and Pathophysiology

  • Insulin deficiency impairs glucose utilization β†’ activates gluconeogenesis, glycogenolysis, proteolysis β†’ hyperglycemia.
  • Ketone production leads to ketonemia, osmotic diuresis, dehydration, electrolyte imbalance, acidosis.
  • Common precipitants:
  • Medication noncompliance
  • Infection
  • New-onset diabetes
  • MI, stroke
  • Drugs: corticosteroids, sympathomimetics, atypical antipsychotics, SGLT2 inhibitors
  • Trauma, surgery, stress, psychiatric illness
  • Alcohol, illicit drugs (cocaine)
  • Pregnancy
  • Risk factors include type 1 DM, ketosis-prone type 2 DM, COVID-19 infection.

Prevention

  • Sick day management, glucose monitoring during stress or illness.
  • Patient education on symptom recognition and insulin adherence.

Common Associated Conditions

  • 30% have features of both DKA and hyperosmolar hyperglycemic syndrome (HHS).

Diagnosis

Criteria

  • Hyperglycemia: glucose usually 250–800 mg/dL.
  • Bicarbonate ≀18 mEq/L.
  • Acidosis: pH <7.3.
  • Anion gap >10 mmol.
  • Positive serum Ξ²-hydroxybutyrate (>3 mg/dL abnormal).
  • Severity:
  • Mild: pH 7.25–7.30; HCO3 10–18; alert.
  • Moderate: pH 7.10–7.24; HCO3 5–9; alert/drowsy.
  • Severe: pH <7.1; HCO3 <5; stupor.

History

  • Recent illness, surgery, missed insulin, pump failure.
  • Polyuria, polydipsia, weight loss, weakness, nausea, vomiting, abdominal pain.

Physical Exam

  • Hypotension, tachycardia, fever or hypothermia.
  • Tachypnea, Kussmaul breathing.
  • Fruity (acetone) breath.
  • Dehydration signs: dry mucosa, poor skin turgor.
  • Altered mental status to coma.

Differential Diagnosis

  • Hyperosmolar hyperglycemic state (HHS).
  • Alcoholic ketoacidosis, starvation ketosis.
  • Lactic acidosis.
  • Toxic ingestions (salicylates, methanol).
  • Uremia, sepsis, pancreatitis.

Diagnostic Tests

  • Ξ²-hydroxybutyrate (serum preferred over urine ketones).
  • ABG or venous blood gas for pH.
  • Urinalysis: ketonuria, glycosuria.
  • Electrolytes: hypomagnesemia, hypophosphatemia, potassium abnormalities.
  • Correct sodium for hyperglycemia.
  • Serum osmolality.
  • CBC, blood/urine cultures, chest X-ray, ECG, troponin if indicated.
  • CT brain if cerebral edema or stroke suspected.

Treatment

Goals

  • Restore perfusion.
  • Normalize glucose gradually.
  • Correct acidosis and electrolyte disturbances.
  • Identify and treat precipitating cause.

General Measures

  • ICU admission for severe DKA.
  • Fluid resuscitation:
  • Initial: 0.9% saline 15–20 mL/kg or 1–1.5 L first hour.
  • Then 250–500 mL/hr adjusted by clinical status.
  • Consider 0.45% saline after initial resuscitation if hypernatremic.
  • Add dextrose when glucose <200 mg/dL to prevent hypoglycemia.

Medication

  • Insulin IV infusion after fluid resuscitation and K+ correction (>3.3 mEq/L).
  • Dose: 0.1 U/kg/hr continuous infusion; optional 0.1 U/kg bolus (not in children).
  • Aim glucose fall 50–75 mg/dL/hr.
  • Titrate insulin infusion to maintain glucose 150–200 mg/dL until ketoacidosis resolves.
  • Subcutaneous basal insulin overlap may shorten hospital stay.
  • Potassium replacement 20–30 mEq/L in IV fluids if K+ ≀5.2 mEq/L and urine output adequate.
  • Hold insulin if K+ ≀3.3 mEq/L until corrected.
  • Phosphorus replacement if <1.0 mg/dL.
  • Sodium bicarbonate reserved for pH <6.9 or severe hyperkalemia.
  • Magnesium replacement if symptomatic hypomagnesemia.

Second Line

  • SC rapid-acting insulin for mild-moderate DKA in alert patients.

Pediatric Considerations

  • Lower initial insulin infusion rate (0.05–0.1 U/kg/hr).
  • Monitor for cerebral edema (most common cause of death).

Pregnancy Considerations

  • Stabilize mother before delivery.
  • Euglycemic DKA is more common.

Admission and Discharge Criteria

  • Admit if glucose >250 mg/dL, pH <7.3, HCO3 ≀15 mEq/L, ketones present.
  • Discharge when anion gap <12, glucose <200 mg/dL, pH >7.3, bicarbonate >18, tolerating oral intake.

Ongoing Care

  • Follow-up in 1–2 weeks post-discharge.
  • Diet: initially NPO, advance as tolerated.
  • Avoid high glycemic index foods.

Patient Education

  • Glucose monitoring and goal awareness.
  • Hypoglycemia recognition and prevention.
  • Sick day management.
  • Insulin administration technique.

Prognosis

  • Worse in extremes of age, coma, hypotension.
  • Overall mortality 0.5–2%.

Complications

  • Cerebral edema (children).
  • Pulmonary edema, respiratory distress, MI.
  • Electrolyte disturbances causing arrhythmias.
  • Acute renal failure.
  • Infection.
  • Late hypoglycemia.

ICD10 Codes:
- E10.11 Type 1 diabetes mellitus with ketoacidosis with coma
- E10.10 Type 1 diabetes mellitus with ketoacidosis without coma
- E13.11 Other specified diabetes mellitus with ketoacidosis with coma

Clinical Pearls:
- Classic triad: hyperglycemia, ketosis, high anion gap acidosis.
- Potassium appears elevated due to acidosis but total body potassium is depleted; start replacement when K+ ≀5.2 and urine output adequate.
- Use insulin infusion only after correcting hypokalemia.