Insulin + Dextrose for Hyperkalemia

Clinical guide, protocols, and safety pearls to rapidly shift K+ intracellularly while minimizing hypoglycemia.

Onset ≈ 15 min · Peak 30–60 min · Duration 4–6 h Typical ΔK+: 0.6–1.2 mEq/L (10U) Highest risk: CKD/ESRD, low BMI, elderly

When to Treat

Serum K+ ≥ 6.0 mEq/L (regardless of ECG)
K+ 5.5–6.0 mEq/L with ECG changes (peaked T, PR↑, QRS↑, loss of P, sine wave)
Hemodynamic instability/arrhythmia/cardiac arrest → treat immediately
Sequence matters: 1) IV Calcium (membrane stabilization), then 2) Insulin + Dextrose (redistribution), plus adjuncts and definitive K+ removal as indicated.

Mechanism & Time Course

Na⁺/K⁺-ATPase activation via insulin signaling (APK pathway); K+ shifts into cells independent of glucose transport.
Onset ~15 min · Peak 30–60 min · Duration ~4–6 h. Renal dysfunction prolongs action → ↑ hypoglycemia risk.
Dose–response: 10U regular insulin typically lowers K+ by ~0.6–1.2 mEq/L in 15–20 min.
FYI Maximal K-shift needs far higher insulin levels than glycemic control → prolonged hypoglycemia possible.

Evidence‑Based Insulin Dosing

Standard (many settings)

  • Regular insulin 10U IV + dextrose (see right).
  • Effective for K+ lowering, but higher hypoglycemia rates.

High‑Risk (CKD/ESRD, low BMI, elderly)

  • 5U IV often adequate; ~50% ↓ hypoglycemia vs 10U with similar ΔK+ (slightly less).
  • Consider 0.1 U/kg in underweight or frail patients.

Formulation

  • Regular insulin most used.
  • Rapid‑acting analogs (aspart/lispro) may shorten tail; limited data.

Administration

  • IV bolus standard in ED/ICU.
  • Continuous infusion reserved for extreme, refractory cases with expert monitoring.

Dextrose Strategies

Goal
Prevent hypoglycemia while insulin drives K+ shift (effect outlasts a single bolus).

Common Options

  • D50W 25–50 g IV bolus. Many centers give 50 g up‑front.
  • D10W infusion (e.g., 500 mL over 4 h) → matches insulin duration; gentler osmolality.
  • Sequential dosing: 25 g now + 25 g at 1 h to blunt delayed dips.
  • If baseline glucose >250–300 mg/dL, initial dextrose may be deferred with close monitoring.

Hypoglycemia Prevention

Risk factors: CKD/ESRD (↓ clearance), low BMI, advanced age, low baseline glucose, non‑diabetic status.

Mitigation

  • Use 5U (or weight‑based) in high‑risk patients.
  • Prefer 50 g D50W or D10W infusion / scheduled second bolus at 1 h.
  • Give dextrose immediately before insulin if feasible.
  • Have rescue D50W at bedside; treat glucose <70 mg/dL (urgent if <50).

Monitoring Protocol

Glucose

  • POC checks q15–30 min × 2 h, then q1h × 4–6 h.
  • Delayed events up to 6–8 h, esp. renal dysfunction.

Potassium

  • Re‑check at ~1 h to gauge response.
  • Repeat at 2–4 h if severe or ongoing therapies.
Document values, timing, symptoms, and treatments in EHR; enable alerts/order sets when available.

At‑a‑Glance Algorithm

1) Stabilize
  • IV Calcium (chloride/gluconate) for ECG changes/instability.
  • Continuous cardiac monitoring.
2) Shift K+
  • Insulin IV (10U standard; 5U or 0.1 U/kg if high risk) + dextrose strategy.
  • Consider inhaled β‑agonist; bicarbonate if severe acidosis.
3) Remove K+
  • Loop diuretics, cation exchangers (patiromer/SZC), dialysis when indicated.

Special Populations

  • Diabetes: Often lower hypoglycemia risk overall but beware unawareness; tailor dextrose to baseline glucose.
  • CKD/ESRD: Prefer dose‑reduced insulin; action prolonged; close monitoring.
  • ICU/CRRT: Coordinate with nephrology; dialysate glucose may modify needs.
  • Pediatrics: Use ~0.1 U/kg regular insulin with proportionate dextrose; monitor closely.
  • Pregnancy: Standard therapy acceptable; consider increased insulin resistance; obstetric input as needed.

Quality Improvement Wins

  • Standardized order sets with 5U for CKD/ESRD.
  • Built‑in glucose monitoring schedule & alerts.
  • Education + pharmacist review → ~50–60% ↓ hypoglycemia in reports.

Future Directions

  • Ultra‑low insulin doses (2–3U) in select high‑risk patients.
  • More data on rapid/ultra‑rapid analogs.
  • Integration of novel binders (patiromer, SZC) for sustained control.
  • Decision support & potential use of CGM in high‑risk monitoring.

Safety Pearls

Match the tail
Insulin outlasts a D50W bolus. Add a second bolus at 1 h or run D10W for 4–6 h in high‑risk patients.
Risk‑stratify the dose
CKD/ESRD, elderly, or low BMI → choose 5U (or 0.1 U/kg). Keep rescue glucose at bedside.
Don’t skip monitoring
POC glucose q15–30 min × 2 h, then q1h × 4–6 h. Check K+ at ~1 h, then as needed.

Pathophysiology Snapshot

  • Insulin triggers APK pathway → ↑ Na⁺/H⁺ exchange → ↑ intracellular Na⁺ → stimulates Na⁺/K⁺‑ATPase → K+ moves into cells.
  • Effect independent of glucose transport; preserved in insulin resistance/diabetes.
  • Renal dysfunction: ↓ insulin clearance + ↓ gluconeogenesis → prolonged hypoglycemia risk.
Clinical impact: Expect meaningful K+ drop within 30–60 min; maintain vigilance for 6–8 h for delayed hypoglycemia, especially if GFR ↓.