Generic Name

Glucose

Mechanism

Glucose serves as the primary cellular substrate for energy production, feeding the tricarboxylic acid (TCA) cycle in mitochondria.
• Binding to glucose transporters (GLUTs) on cell membranes facilitates rapid cellular uptake, especially in the brain, heart, and skeletal muscle.
• Phosphorylation by hexokinase/glucokinase traps glucose inside the cell, committing it to glycolysis or glycogenesis.
• In hypoglycemia, exogenous glucose bypasses endogenous counter‑regulatory failures, rapidly restoring cytosolic ATP and correcting neuronal dysfunction.

Pharmacokinetics

• Absorption: In IV preparations, absorption is instantaneous; enteral glucose is absorbed via SGLT1 in the proximal jejunum.
• Distribution: 90 % plasma volume; small distribution into interstitial fluid; negligible CNS penetration unless blood‑brain barrier compromised.
• Metabolism: Glycolysis → pyruvate → lactate (anaerobic) or acetyl‑CoA (aerobic). Glycogen synthesis in liver and muscle follows hepatic glucokinase activity.
• Elimination: Renally excreted in urine if plasma levels exceed 10 mmol/L; renal clearance not affected by mild renal impairment (GFR > 30 mL/min).

Indications

• Acute hypoglycemia (e.g., type 1 diabetes, insulin overdose).
• Reversal of low‑glucose states in non‑diabetic patients (e.g., critical illness, accidental intrathecal insulin).
• Caloric supplementation during total parenteral nutrition (TPN).
• Maintenance of normoglycemia in high‑risk surgical or critical‑care patients receiving insulin therapy.

Contraindications

• Absolute contraindications:
• Known hypersensitivity to glucose solutions.
• Relative warnings:
• Hyperglycemia >200 mg/dL.
• Severe renal or hepatic dysfunction (risk of osmotic load).
• Shock states where fluid overload is a concern.
• Caution: In patients with diabetic ketoacidosis (DKA), high‑concentration dextrose must be paired with insulin to avoid worsening hyperglycemia.

Dosing

• Use sterile, isotonic dextrose solutions (D5W, D10W, D20W, D50W).
• Avoid rapid infusion of >50 % dextrose in patients with compromised cardiovascular stability.
• Monitor serum electrolytes when infusing concentrated dextrose to anticipate shifts.

Adverse Effects

Monitoring

• Blood glucose every 15–30 min during acute resuscitation; hourly after stabilization.
• Serum electrolytes (Na⁺, K⁺, Cl⁻, Ca²⁺, Mg²⁺) ± 4‑6 h post‑bolus in high‑dose or renal‑impaired patients.
• Urine output and renal function (Cr, BUN) when dosing >50 g.
• Fluid balance and vitals to detect edema or circulatory overload.

Clinical Pearls

• “100‑2‑2” rule: In DKA, give a 5–10 % dextrose infusion when glucose reaches 100 mg/dL to prevent rebound hypoglycemia while continuing insulin.
• Use a D10W bolus in infants (≥10 kg) for hypoglycemia; 1 mL/kg contains ~25 g glucose.
• Avoid >50 % dextrose solutions in patients with heart failure or pulmonary hypertension; opt for lower concentrations or continuous infusion.
• Pre‑mix insulin with dextrose in protocols designed to prevent severe hypoglycemia during infusion (e.g., insulin therapy × dextrose 5 %).
• Monitor electrolytes after high‑concentration dextrose because hyperglycemia can mask actual hypocalcemia or hypomagnesemia; correct with calcium gluconate or magnesium sulfate as needed.

--
• References

1. American Diabetes Association Standards of Medical Care in Diabetes, 2024.

2. Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 13th ed.

3. Bickell, R.P. *Intravenous Dextrose Therapy*, J Crit Care 2019.