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Pathophysiology
Clinical meaning
Diabetic ketoacidosis (DKA) results from absolute or relative insulin deficiency combined with counter-regulatory hormone excess (glucagon, cortisol, catecholamines, GH). Without insulin, glucose cannot enter cells, triggering hepatic gluconeogenesis and glycogenolysis (causing severe hyperglycemia) and unregulated lipolysis (releasing free fatty acids from adipose tissue). In the liver, fatty acids undergo beta-oxidation to acetyl-CoA, which is converted to ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) by ketogenesis — a process driven by glucagon excess and insulin deficiency. Ketone bodies are strong organic acids that consume bicarbonate buffers, causing high anion gap metabolic acidosis (AG = Na - Cl - HCO3; normal 8-12; DKA typically > 20). Hyperglycemia causes osmotic diuresis (glycosuria pulls water and electrolytes), leading to profound dehydration (average 5-9 L deficit), total body potassium depletion (despite possible initial hyperkalemia from transcellular shift due to acidosis and insulin deficiency), and electrolyte derangement. Cerebral edema is the most feared complication in children, occurring in 0.5-1% of pediatric DKA cases.
Diagnostics & workup:
- DKA diagnostic criteria: blood glucose > 250 mg/dL (unless euglycemic DKA), pH < 7.30, bicarbonate < 18 mEq/L, anion gap > 12, positive serum/urine ketones
- Classification: mild (pH 7.25-7.30, HCO3 15-18), moderate (pH 7.0-7.24, HCO3 10-14), severe (pH < 7.0, HCO3 < 10)
- BMP: hyperglycemia, hyponatremia (dilutional + osmotic shift — correct sodium: add 1.6 mEq/L for each 100 mg/dL glucose > 100), potassium (may be high/normal/low despite total body depletion), elevated BUN/creatinine (prerenal), low bicarbonate, elevated anion gap
- Beta-hydroxybutyrate (serum): preferred over urine ketones (more sensitive, not affected by dehydration); > 3.0 mmol/L in DKA
- ABG/VBG: metabolic acidosis with respiratory compensation (Kussmaul breathing — deep, rapid respirations to blow off CO2)
- CBC: leukocytosis (stress response — does not necessarily indicate infection; bands > 10% more suggestive of infection)
- Serum osmolality: usually 300-320 mOsm/kg (> 320 suggests concurrent HHS)
- ECG: assess for hyper/hypokalemia changes; continuous telemetry during potassium replacement
Risk factors:
- Type 1 diabetes (most common; DKA may be the initial presentation in 20-30%)
- Type 2 diabetes (increasingly recognized; DKA can occur, especially in African American and Hispanic patients with 'ketosis-prone' Type 2 DM)
- Insulin omission or pump failure (most common precipitant in known diabetics)
- Infection (second most common precipitant — UTI, pneumonia, sepsis; activates counter-regulatory hormones)
- New-onset Type 1 diabetes (no endogenous insulin production)
- SGLT2 inhibitor use (euglycemic DKA — glucose may be < 250 mg/dL but ketoacidosis is present)
- Substance use: cocaine, alcohol
- Medications: corticosteroids, atypical antipsychotics (olanzapine, clozapine)
Management
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Prescribing & monitoring
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Takeaways
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