Generic Name

Dextrose

Mechanism

Dextrose (glucose‑6‑phosphate) is the primary energy substrate for all mammalian cells.
• Rapid uptake by GLUT‑4 transporters on muscle and adipose cells and by GLUT‑1 on the blood‑brain barrier.
• Metabolism to ATP via glycolysis → Krebs cycle → oxidative phosphorylation.
• In the bloodstream, it clocks glucose sensors (glucose‑dependent insulinotropic peptide, glucagon, insulin) to maintain normoglycemia.
• In critical‑care settings, high‑concentration dextrose prevents ketosis and catabolism by satisfying metabolic demands.

Pharmacokinetics

• Absorption: IV; 100 % bioavailability.
• Distribution: Rapid placental and cerebrospinal fluid penetration; equilibrium ≈ 10 min.
• Metabolism: Oxidative phosphorylation and glycogen synthesis; hepatic gluconeogenesis is suppressed indirectly by insulin release.
• Elimination: Metabolites excreted renally; clearence roughly proportional to renal perfusion.
• Half‑life: ~ 30–60 min for 5 % solutions; longer with higher concentrations due to slower tissue extraction.

Indications

• Treating hypoglycemia (rapid rise of plasma glucose).
• Energy maintenance for patients on total parenteral nutrition (TPN).
• Preventing catabolism in critically ill or postoperative patients.
• Adjunct in vasoactive drug solutions (e.g., epinephrine, norepinephrine).
• Diagnostic glucose‑tolerance studies (IV glucose challenge).

Contraindications

• Hyperglycemia or uncontrolled diabetes—avoid 5 %+ solutions unless blood glucose can be monitored.
• Renal or hepatic impairment—monitor for azotemia and fluid overload.
• Severe metabolic acidosis—high‑osmolar dextrose may worsen acidosis.
• Intrathecal/epidural use is contraindicated—risk of neurotoxicity.
• Pregnancy: Generally safe; monitor fetal blood glucose if maternal hypoglycemia is treated.

Dosing

• Check glucose 5 min after IV push; titrate based on labs.
• For continuous infusions, monitor glucose hourly.

Adverse Effects

• Common: Hyperglycemia, hypocalcemia (calcium precipitation with high‑osmolar solutions), fluid overload.
• Serious:
• Thromboembolic events (if large volumes used).
• Ketoacidosis exacerbation if dextrose is given rapidly.
• Infection at IV sites—sterile technique essential.
• Hypocalcemia due to calcium phosphate precipitation with high‑osmolar solutions.

Monitoring

• Blood glucose: baseline and every 15–30 min for first 2 h, then hourly.
• Serum electrolytes: Na⁺, K⁺, Ca²⁺, Mg²⁺ (especially with continuous infusions).
• Fluid balance: hourly input/output; adjust as needed.
• Labored vasopressor infusion: monitor hemoglobin and hematocrit to rule out hemolysis.
• Kidney function: BUN/creatinine twice daily with large volumes or renal impairment.

Clinical Pearls

• “Push‑and‑watch” rule: For emergency hypoglycemia, administer 10 % dextrose IV push (100 mg) and re‑check BG after 5 min—avoid over‑correction.
• Odorless, clear, 5–10 % solutions are preferred in ICU; concentrations > 20 % increase viscosity and osmolarity, raising the risk of central line thrombosis.
• Use a dedicated line for dextrose when mixing vasopressors to avoid accidental dilution and osmolarity shifts.
• In diabetics: Switch to 5 % dextrose infusion when on insulin pumps—prevent low‑grade hyperglycemia and catheter occlusion.
• Ethanol‑mediated hypoglycemia (e.g., alcohol use disorder) is effectively countered with 5–10 % dextrose; monitor for delayed hypoglycemia once ethanol is metabolized.

*For deeper pharmacodynamic nuances or registry data, refer to recent critical‑care guidelines (e.g., Surviving Sepsis Campaign).*

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