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+; hold insulin if K+ <3.3 and replete.
- Begin insulin infusion; monitor anion gap and glucose; add dextrose as glucose ~200.
- Transition to SC insulin when ketoacidosis resolves; address precipitant and education.
                                        Clinical Synopsis & Reasoning
            DKA presents with hyperglycemia, ketosis, and metabolic acidosis. Begin balanced crystalloids, correct potassium, and start insulin infusion after K+ ≥3.3 mEq/L. Add dextrose as glucose approaches 200 mg/dL and continue insulin until ketoacidosis resolves (anion gap closes). Search for 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 | 
|---|
                
                  | Serum glucose, β-hydroxybutyrate/ketones, ABG/VBG | Diagnosis | Ketoacidosis with anion gap | Severity staging | 
| Electrolytes (K+, Na+, bicarbonate), phosphate | Safety | Insulin lowers K+; risk of hypophosphatemia | Frequent labs | 
| Infection/MI workup | Precipitant | Common triggers | Treat source | 
                
              
             
                                        High-Risk & Disposition Triggers
            
              
                | Trigger | Why it matters | Action | 
|---|
                
                  | Shock, AMS, or refractory acidosis (pH <7.0) | High mortality | ICU; cautious fluids and insulin; address precipitant | 
| Serum K+ <3.3 mEq/L | Arrhythmia risk | Hold insulin; replete K+ first | 
| Cerebral edema signs (headache, bradycardia, AMS) | Catastrophic complication | Slow correction; mannitol/hypertonic; neuro consult | 
| Pregnancy or ESRD | Complex kinetics | ICU; specialist input | 
| No improvement of anion gap by 6–8 h | Treatment failure | Reassess diagnosis/dosing; evaluate infection/MI | 
                
              
             
                                        Pharmacology
            
              
                | Medication/Intervention | Mechanism | Onset | Role in Therapy | Limitations | 
|---|
                
                  | Balanced crystalloids then 0.45% NaCl as needed | Fluids | Hours | Restore volume; correct Na+ | Avoid rapid shifts | 
| Regular insulin 0.1 U/kg/h (no bolus) after K+ ≥3.3 | Insulin | Hours | Clear ketones and close gap | Add dextrose when glucose ~200 | 
| Potassium and phosphate repletion per protocols | Electrolytes | Hours | Prevent arrhythmia/weakness | Monitor Mg2+ | 
                
              
             
                                        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 DKA guidance — Link