Key Points
- Stabilize ABCs; begin targeted evaluation without delaying life-saving therapy.
- Use system-specific risk tools to guide testing and disposition.
- Order high-yield tests first; escalate imaging when indicated.
- Start evidence-based initial therapy and reassess frequently.
Algorithm
- Primary survey and vitals; IV access and monitors.
- Focused history/physical; identify red flags and likely etiologies.
- Order system-appropriate labs and imaging (see Investigations).
- Initiate guideline-based empiric therapy (see Pharmacology).
- Reassess response; arrange consultation and definitive management.
Clinical Synopsis & Reasoning
DKA is precipitated by insulin deficiency and counter‑regulatory surge, producing hyperglycemia, ketonemia, and anion‑gap acidosis. Confirm diagnosis with glucose, β‑hydroxybutyrate/ketones, pH, and bicarbonate; assess volume depletion and precipitating factors (infection, insulin omission, MI, stroke). Expect total body potassium deficit despite initial normal/elevated K⁺. Frequent bedside reassessment and point‑of‑care tests are critical to guide safe correction and detect cerebral edema risk.
Treatment Strategy & Disposition
Resuscitate with balanced crystalloids, begin insulin infusion after verifying K⁺ ≥3.3 mEq/L, and replace electrolytes proactively, especially potassium and phosphate as indicated. Once glucose reaches ~200–250 mg/dL with persistent ketosis, add dextrose to avoid hypoglycemia while clearing ketones; transition to basal‑bolus when anion gap closes and patient can eat. Treat precipitants (e.g., antibiotics for infection) and provide sick‑day education. ICU admission for severe acidosis, altered mental status, or need for continuous insulin/electrolyte titration; otherwise step‑down with protocolized monitoring.
Epidemiology / Risk Factors
- Diabetes and endocrine disorders depending on topic
Investigations
| Test | Role / Rationale | Typical Findings | Notes |
|---|---|---|---|
| BMP | Electrolytes/anion gap | Derangements | |
| Ketones (if DKA) | Ketoacidosis | Positive | |
| ABG/VBG | Acid–base status | Acidosis/alkalosis |
DKA Severity (Adult)
| Severity | pH | HCO3 (mEq/L) | Anion Gap | Mental Status |
|---|---|---|---|---|
| Mild | 7.25–7.30 | 15–18 | Elevated | Alert |
| Moderate | 7.00–7.24 | 10–15 | Elevated | Drowsy |
| Severe | <7.00 | <10 | Elevated | Stupor or coma |
Pharmacology
| Medication | Mechanism | Onset | Role in Therapy | Limitations |
|---|---|---|---|---|
| Regular insulin (IV) | Anabolic/anti-ketotic | Minutes | Correct hyperglycemia/ketosis | Hypoglycemia, hypokalemia |
| Potassium chloride | Electrolyte repletion | Hours | Prevent hypokalemia | Overcorrection arrhythmia |
| Isotonic fluids | Volume expansion | Immediate | Restore perfusion and osmolar balance | Fluid overload in CHF/CKD |
| Sodium bicarbonate | Buffer | Hours | Severe acidemia (pH ≤6.9) | Alkalemia, hypokalemia |
| Phosphate (select cases) | Electrolyte repletion | Hours | Severe depletion | Hypocalcemia |
Prognosis / Complications
- Improves with derangement correction; recurrence if triggers persist
Patient Education / Counseling
- Explain red flags and when to seek emergent care.
- Reinforce medication adherence and follow-up plan.
Electrolyte Notes
Replace potassium aggressively; monitor every 2–4 hours. Bicarbonate is rarely indicated and reserved for profound acidosis with hemodynamic compromise.