DKA
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Diabetic Ketoacidosis (DKA)
Definition
DKA is defined by a triad of three fundamental biochemical abnormalities:
- Hyperglycemia (glucose typically >250 mg/dL, though can be variable)
- Ketonemia/ketonuria (urine ketones 2+ or more, or serum ketones ≥3.0 mmol/L)
- Metabolic acidosis (arterial or venous pH <7.3, serum HCO₃ <18 mmol/L)
- Goldman-Cecil Medicine, p. 2483
Pathophysiology
The core problem is insulin deficiency + counter-regulatory hormone excess (glucagon, cortisol, catecholamines, growth hormone):
| Axis | Mechanism | Consequence |
|---|---|---|
| Carbohydrate | Decreased glucose uptake, increased gluconeogenesis | Hyperglycemia |
| Fat | Hormone-sensitive lipase activated → ↑ free fatty acids → hepatic ketogenesis (β-hydroxybutyrate, acetoacetate, acetone) | Ketoacidosis |
| Protein | Accelerated proteolysis, ↑ amino acids to liver | Further gluconeogenesis |
| Renal | Osmotic diuresis from glycosuria | Dehydration, electrolyte loss |
| Respiratory | Kussmaul breathing to compensate acidosis | Lowers pCO₂, consumes bicarbonate |
Glucose and ketones are released into the circulation faster than they are utilized. The resulting osmotic diuresis causes profound dehydration (typically 3-5 L fluid deficit in adults, sometimes up to 10 L in severe cases), with losses of sodium (5-10 mmol/kg), potassium (5-7 mmol/kg), phosphorus, and magnesium.
- Rosen's Emergency Medicine, p. 2542-2543
- Goldman-Cecil Medicine, p. 2483-2484
Precipitants
Most common:
- Infections (especially pneumonia, UTI)
- Inadequate insulin / non-adherence
- New-onset type 1 diabetes (~25% of DKA episodes)
- Acute coronary syndrome
Other precipitants:
- Cerebrovascular accident, pulmonary embolism, pancreatitis
- Drugs: corticosteroids, SGLT-2 inhibitors, clozapine, olanzapine, cocaine, sympathomimetics, thiazides
- Endocrinopathies: Cushing syndrome, thyrotoxicosis, acromegaly
- Burns, hyperthermia/hypothermia
Clinical Features
Symptoms (typically evolve over hours to days):
- Polyuria, polydipsia, polyphagia
- Weakness, lethargy, weight loss
- Nausea, vomiting, anorexia
- Abdominal pain (~50% of patients, especially children - usually resolves with treatment; in adults, more likely to represent a true abdominal precipitant)
Signs:
- Kussmaul breathing - deep, rapid respirations to compensate acidosis
- Fruity/acetone breath
- Tachycardia, orthostatic hypotension or frank hypotension
- Dry skin and mucous membranes (dehydration)
- Depressed sensorium - degree correlates with osmolality
- Elevated temperature usually signals infection (DKA itself rarely causes fever)
Diagnosis & Lab Findings
| Parameter | Typical Finding |
|---|---|
| Glucose | >350 mg/dL (DKA); can be normal in euglycemic DKA (e.g., SGLT-2i) |
| pH | <7.3 (mild: 7.20-7.30; severe: <7.00) |
| HCO₃ | <18 mmol/L |
| Anion gap | Elevated (proportional to HCO₃ drop) |
| Ketones | ↑↑ (β-hydroxybutyrate preferred) |
| Sodium | Often low (dilutional + osmotic shift); correct for glucose: add 1.6 mEq/L per 100 mg/dL glucose above normal |
| Potassium | Normal or HIGH initially (acidosis shifts K⁺ extracellularly), but total body K⁺ is depleted - correct: subtract 0.6 mEq/L per 0.1 pH decrease |
| WBC | Elevated (reflects ketosis severity, not necessarily infection; only band neutrophilia indicates infection) |
| Creatinine | May be falsely elevated on autoanalyzer |
| Lipase | Preferred over amylase if pancreatitis suspected (must be >3x ULN for diagnosis) |
| Hematocrit | Elevated (hemoconcentration) |
Key pitfall: The serum K⁺ may appear normal or high at presentation but will drop sharply once insulin is started. Never begin insulin if K⁺ <3.3 mEq/L - replace first.
Severity Classification
| Mild | Moderate | Severe | |
|---|---|---|---|
| Glucose (mg/dL) | >250 | >250 | >250 |
| pH | 7.25-7.30 | 7.00-7.24 | <7.00 |
| HCO₃ (mEq/L) | 15-18 | 10-14 | <10 |
| Anion gap | >10 | >12 | >12 |
| Mental status | Alert | Alert/drowsy | Stupor/coma |
Treatment
1. Fluids (Priority #1)
- Adult: 1-2 L of 0.9% NS IV over 1-3 hours initially; then 250-500 mL/hr depending on fluid deficit. Total replacement typically 2-4 L in first 2-4 hours.
- Children: 20 mL/kg NS over the first hour.
- Switch to 0.45% NS once glucose falls to ~250-300 mg/dL; add dextrose (D5W + 0.45% NS) to prevent hypoglycemia while insulin continues.
- Avoid large amounts of normal saline (hyperchloremic acidosis risk).
2. Potassium
- If K⁺ <3.3 mEq/L: Hold insulin, replace K⁺ aggressively (IV, 20-40 mEq/hr) until ≥3.3 mEq/L
- If K⁺ 3.3-5.5 mEq/L: Add 20-40 mEq KCl per liter of fluid
- If K⁺ >5.5 mEq/L: Hold K⁺ supplementation, recheck every 2 hours
3. Insulin
- Do NOT start insulin until K⁺ ≥3.3 mEq/L
- Continuous IV regular insulin at 0.1 units/kg/hour
- When glucose drops to 250-300 mg/dL AND ketones <1.0 mmol/L: reduce to 0.05 units/kg/hour to prevent hypoglycemia
- In HHS: start IV fluid first; only add insulin when glucose stops falling on fluids alone
4. Other Electrolytes
- Phosphorus: Routine replacement generally not necessary
- Magnesium: Correct with 1-2 g MgSO₄ if low (serum levels may underestimate deficit)
5. Bicarbonate
- Routine bicarbonate use is NOT recommended
- May consider if pH <6.9 with severe hemodynamic compromise
- Correct the underlying cause (fluids + insulin) - bicarbonate corrects as ketones clear
6. Identify and Treat Precipitant
- Blood cultures, urine culture, CXR if infection suspected
- ECG (acute MI as precipitant)
- Look for occult sepsis, PE, pancreatitis
7. Monitoring
Meticulous flow sheets tracking:
- Vital signs, fluid I&O (hourly urine output)
- Serum glucose (hourly initially)
- Electrolytes, BUN/Cr, pH, HCO₃ every 2-4 hours
- Ketones (β-hydroxybutyrate or urine ketones)
8. Transition to Subcutaneous Insulin
- DKA is resolved when: glucose <200 mg/dL, pH >7.3, HCO₃ >18 mEq/L, anion gap normalized
- Overlap IV insulin with first SC dose by 1-2 hours before discontinuing IV to prevent rebound
Special Considerations
Euglycemic DKA: Can occur with SGLT-2 inhibitors (glucose may be <200 mg/dL). Clinical suspicion is key.
Intubation in DKA: Avoid if at all possible - patients have enormous respiratory drive. If intubated (e.g., comatose + vomiting), maintain hyperventilation or acidosis will worsen precipitously.
Cerebral edema: Major complication, mainly in children. Risk increased with rapid osmotic shifts. Symptoms: headache, deteriorating mental status after initial improvement.
Pregnancy: DKA can occur at lower glucose levels and is associated with high fetal mortality. Aggressive management required.
Prognosis
Mortality for DKA remains approximately 4% despite treatment - higher at extremes of age and with severe precipitating illness. HHS mortality is substantially higher (~20%).
- Goldman-Cecil Medicine, p. 2484
- Rosen's Emergency Medicine, p. 2542-2544
Recent Evidence (2024-2026)
Two recent meta-analyses are relevant to management:
- Subcutaneous vs IV insulin in DKA (PMID 39090718) - systematic review/meta-analysis suggesting subcutaneous insulin protocols may be comparable to continuous IV infusion in selected adult patients
- Early subcutaneous basal insulin with IV infusion (PMID 41208563) - 2026 meta-analysis of RCTs found early overlap with basal SC insulin during IV infusion reduces DKA recurrence and shortens transition time
These suggest evolving practice toward subcutaneous insulin protocols, though IV infusion remains standard in moderate-severe DKA.
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