GLUCOSE 20% Solution for infusion Ref.[9426] Active ingredients: Glucose

Rapid administration of hypertonic glucose solutions may produce substantial hyperglycaemia and hyperosmolar syndrome; patients should be observed for signs of mental confusion and loss of consciousness, especially those patients with chronic uraemia or carbohydrate intolerance.

Prolonged use in parenteral nutrition may affect insulin production; blood and urine glucose should be monitored.

Glucose 20% intravenous infusion is a hypertonic solution (in vitro, in a container). In the body, however, glucose containing fluids can become extremely physiologically hypotonic due to rapid glucose metabolism (see section 4.2 and 5.2).

Depending on the tonicity of the solution, the volume and rate of infusion and depending on a patient’s underlying clinical condition and capability to metabolize glucose, intravenous administration of glucose can cause electrolyte disturbances most importantly hypo- or hyperosmotic hyponatraemia.

Hyponatraemia:

Patients with non-osmotic vasopressin release (e.g. in acute illness, pain, post-operative stress, infections, burns, and CNS disease), patients with heart, liver and kidney diseases and patients exposed to vasopressin agonists (see section 4.5) are at risk of acute hyponatraemia upon infusion of hypotonic fluids.

Acute hyponatraemia can lead to acute hyponatraemic encephalopathy (brain oedema) characterized by headache, nausea, seizures, lethargy and vomiting. Patients with brain oedema are at particular risk of severe, irreversible and life-threatening brain injury.

Children, women in the fertile age and patients with reduced cerebral compliance (e.g. meningitis, intracranial bleeding, and cerebral contusion) are at particular risk of the severe and life-threatening brain swelling caused by acute hyponatraemia.

Intravenous administration of Glucose 20% may result in other electrolyte disturbances such as: hypokalaemia, hypophosphataemia and hypomagnesaemia (see sections 4.2 and 4.8).

Special care should be taken during injection to avoid leakage into the surrounding tissue.

The effects of insulin are reversed by glucose.

Drugs increasing vasopressin effect, listed below, lead to reduced renal electrolyte free water excretion and increase the risk of hospital acquired hyponatraemia following inappropriately balanced treatment with i.v. fluids (see sections 4.2, 4.4 and 4.8):

• Drugs stimulating vasopressin release, e.g.: carbamazepine, vincristine, selective serotonin reuptake inhibitors, 3.4-methylenedioxy-N-methamphetamine, ifosfamide, antipsychotics, narcotics
• Drugs potentiating vasopressin action, e.g.: NSAIDs , cyclophosphamide
• Vasopressin analogues, e.g.: desmopressin, oxytocin, vasopressin, terlipressin

Other medicinal products increasing the risk of hyponatraemia also include diuretics in general and antiepileptics such as oxcarbazepine.

There is no, or inadequate evidence of safety of the drug in human pregnancy, but it has been in wide use for many years without apparent harmful consequence. Intravenous glucose may result in fetal insulin production, with an associated risk of rebound hypoglycaemia in the neonate. Infusions of glucose administered during Caesarean section and labour should be used with caution, and should not exceed 5-10g glucose/hour.

Glucose 20% should be administered with special caution for pregnant women during labour particularly if administered in combination with oxytocin due to the risk of hyponatraemia (see section 4.4, 4.5 and 4.8).

None known.

Very common (≥1/10); Common (≥1/100 to <1/10); Uncommon (≥1/1,000 to <1/100); Rare (≥1/10,000 to <1/1,000); Very rare (<1/10,000), Not known (cannot be estimated from the available data)

Metabolism and nutrition disorders

Not known: Hospital acquired hyponatraemia*, Hyperglycaemia**, Hypokalaemia, Hypophosphataemia, Hypomagnesaemia, Fluid and electrolyte imbalance.

Nervous system disorders

Not known: Hyponatraemic encephalopathy*

General disorders and administration site conditions

Not known: Pain at the injection site, Vein irritation, Venous thrombosis, Phlebitis

* Hospital acquired hyponatraemia may cause irreversible brain injury and death due to development of acute hyponatraemic encephalopathy (see sections 4.2 and 4.4).
** Hyperglycaemia (possibly indicated by mental confusion or loss of consciousness) and glycosuria may occur as a result of the rate of administration or metabolic insufficiency. If undetected and untreated hyperglycaemia can lead to dehydration, hyperosmolar coma and death.

The administration of glucose without adequate levels of thiamine may precipitate overt deficiency states e.g. Wernicke’s encephalopathy. Sodium retention, oedema, pulmonary oedema and congestive heart failure may be induced in patients with severe under-nutrition.

Reporting of suspected adverse reactions

Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.

Glucose solutions which do not contain electrolytes, should not be administered concomitantly with blood through the same infusion set, because of the possibilities of agglomeration.