Key Points
- Use the highest‑yield diagnostic test early; do not let testing delay time‑critical therapy.
- Set objective targets and reassess frequently.
- Plan definitive source control or disease‑specific therapy when indicated; document follow‑up and patient education.
Algorithm
- Start fluids; check K+. If K+ <3.3 → replete before insulin.
- Begin insulin infusion; add dextrose when glucose ~200 mg/dL to continue ketone clearance.
- Replace K+/Mg2+/phosphate as needed; monitor glucose/electrolytes closely.
- Identify and treat precipitant (infection, insulin omission, MI); transition to SC insulin when AG closed and patient eating.
Clinical Synopsis & Reasoning
DKA presents with hyperglycemia, anion gap metabolic acidosis, and ketonemia/ketonuria. Begin isotonic fluids, correct potassium before insulin if K+ <3.3, start insulin infusion when safe, and transition to subcutaneous insulin once gap closes. Identify and treat precipitants.
Treatment Strategy & Disposition
Stabilize ABCs. Initiate guideline‑concordant first‑line therapy with precise dosing and continuous monitoring. Escalate to advanced/procedural interventions based on explicit failure criteria. Define ICU, step‑down, and ward disposition triggers; involve specialty teams early.
Epidemiology / Risk Factors
- Risk varies by comorbidity and precipitants; see citations for condition‑specific data.
Investigations
| Test | Role / Rationale | Typical Findings | Notes |
|---|
| BMP, anion gap, β-hydroxybutyrate/ketones | Diagnosis/severity | High anion gap, ketonemia | Trend closure |
| VBG/ABG and calculated serum osmolality | Acid-base | Acidemia; HHS overlap | Guide therapy |
| Electrolytes (K+, Mg2+, phosphate) and glucose hourly | Safety | Hypokalemia risk during therapy | Replete proactively |
High-Risk & Disposition Triggers
| Trigger | Why it matters | Action |
|---|
| K+ <3.3 mEq/L or severe acidosis (pH <7.0) | Arrhythmia/respiratory failure risk | Hold insulin; replete K+ aggressively; ICU |
| Cerebral edema signs (headache, AMS, bradycardia) | Life-threatening complication | Hypertonic saline/mannitol; neuro consult; imaging |
| Refractory hypotension or hypoxemia | Shock/ARDS risk | ICU; vasopressors; ventilatory support |
| Pregnancy or severe comorbidity | Fetal/maternal risk | Multidisciplinary care; fetal monitoring |
| Failure of anion gap to close or rising β‑hydroxybutyrate | Treatment failure | Reassess insulin/fluids; search precipitant |
Pharmacology
| Medication/Intervention | Mechanism | Onset | Role in Therapy | Limitations |
|---|
| Normal saline or balanced crystalloids (1–1.5 L in first hour) | Resuscitation | Immediate | Restore volume | Switch based on Na+/osmolality |
| Regular insulin: 0.1 U/kg IV bolus then 0.1 U/kg/h infusion (or no bolus with 0.14 U/kg/h) | Insulin | Minutes | Stop ketogenesis | Add dextrose when glucose ~200 mg/dL |
| Potassium chloride per protocol (10–20 mEq/h) | Electrolyte | Hours | Keep K+ 4.0–5.0 | Hold insulin if K+ <3.3 |
| Phosphate repletion (selected) | Electrolyte | Hours | If severe hypophosphatemia or respiratory/cardiac dysfunction | — |
| Bicarbonate (rare; pH <6.9) | Buffer | Immediate | Severe acidosis only | Controversial |
Prognosis / Complications
- Outcome depends on timeliness of diagnosis and definitive therapy; monitor for complications.
Patient Education / Counseling
- Provide red‑flag education, adherence guidance, and explicit return precautions; arrange timely specialty follow‑up.
References
- ADA/Endocrine Society consensus on DKA/HHS management — Link