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Glucose 40% w/v Intravenous Infusion BP

Active Ingredient:
dextrose monohydrate
B.Braun Medical See contact details
About Medicine
{healthcare_pro_orange} This information is for use by healthcare professionals
Last updated on emc: 28 Nov 2023
1. Name of the medicinal product

40% w/v Glucose Intravenous Infusion BP

2. Qualitative and quantitative composition

1000ml of solution contain

Dextrose monohydrate for parenteral use


(Equivalent to anhydrous dextrose


Caloric value

6700 kJ/l ≙ 1600 kcal/l

Theoretical osmolarity

2200 mOsm/l

Titration acidity (to pH 7.4)

< 1 mmol/l


3.5 - 5.5

3. Pharmaceutical form

Solution for infusion.

Clear, colourless or slightly yellowish aqueous solution

Caloric value

6700 kJ/l 1600 kcal/l

Theoretical osmolarity

2200 mOsm/l

Titration acidity (to pH 7.4)

< 1 mmol/l


3.5 - 5.5

4. Clinical particulars
4.1 Therapeutic indications

Parenteral nutrition;

High-caloric carbohydrate therapy, especially when fluid intake is restricted, as for example in renal insufficiency;


4.2 Posology and method of administration


Recommended dosage schedule

The dosage of 40 % w/v Glucose Intravenous Infusion depends on the patient's individual glucose requirements.

Fluid balance, serum glucose, and other electrolytes may need to be monitored before and during administration, especially in patients with increased non-osmotic vasopressin release (syndrome of inappropriate antidiuretic hormone secretion, SIADH) and in patients co-medicated with vasopressin agonist drugs due to the risk of hyponatraemia.

Monitoring of serum sodium is particularly important for physiologically hypotonic fluids. 40% w/v Glucose Intravenous Infusion BP may become hypotonic after administration due to glucose metabolisation in the body (see sections 4.4. 4.5 and 4.8).

Recommended dose for adults:

Up to 15 ml/kg body weight (BW)/day corresponding to 6 g of glucose/kg BW/day.

In the presence of metabolic disorders, e.g. postoperative/post-traumatic stress, hypoxia, organ insufficiencies, glucose oxidation may be impaired, which is associated with hyperglycaemia and insulin resistance and possibly with an increased mortality. In such cases, reduction of the glucose intake to 2 - 4 g of glucose/kg BW/day may be required. The blood glucose level should not exceed 110 mg/100 ml (6.1 mmol/l).

Maximum infusion and drop rate:

Up to 0.62 ml/kg BW/h, corresponding to 0.25 g of glucose/kg BW/h.

The corresponding maximum drop rate is 0.2 drops/kg BW/min.

Thus for a patient weighing 70 kg the infusion rate is 43 ml/h corresponding to 14 drops/min or 17.5 g of glucose/h.

Only in exceptional cases the total fluid intake may exceed 40 ml/kg BW/day in the setting of parenteral nutrition.

Children (from the 6th year of life onward):

Maximum daily doses of glucose:

6th – 10th year: up to 10 g of glucose/kg BW, corresponding to 25 ml/kg BW

10th – 14th year: up to 8 g of glucose/kg BW, corresponding to 20 ml/kg BW

When determining the dose, care should be taken that total parenteral fluid administration does not exceed the following values:

6th – 10th year: 60 – 80 ml per kg BW per day

11th – 14th year: 50 – 70 ml per kg BW per day.

Method of administration

Intravenous infusion via central venous catheter.

It should be noted that these solutions constitute only one component of parenteral nutrition. In total parenteral nutrition, glucose infusions should always be accompanied by infusion of sufficient quantities of amino acid solutions, lipid emulsions, electrolytes, vitamins, and trace elements.

4.3 Contraindications

– Hyperglycaemia, not responding to insulin doses of up to 6 units insulin/hour

– Decompensated diabetes mellitus, diabetic coma

– Untreated diabetes insipidus

– Acute states of shock or collapse

– Intracranial or spinal haemorrhage

– Metabolic acidosis

– Renal failure (oligo- or anuria) in absence of renal replacement therapy

– Hyperhydration

– Pulmonary oedema

– Acute cardiac failure

4.4 Special warnings and precautions for use

40% w/v Glucose Intravenous Infusion BP is a hypertonic solution. In the body, however, glucose containing fluids can become extremely physiologically hypotonic due to rapid glucose metabolization (see section 4.2).

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.


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

Administration of glucose solutions is not recommended after acute ischaemic strokes as hyperglycaemia was reported to worsen ischaemic brain damage and impair recovery.

This solution should be used with caution in patients with hypervolemia, renal insufficiency and impending or manifest cardiac decompensation.

The solution should also be administered with caution to patients with increased serum osmolarity.

Disorders of fluid and electrolyte balance like hypotonic dehydration or pathologically low levels of serum electrolytes, must be corrected prior to administration of Glucose 40 % w/v solution for infusion.

Special attention must be paid to hypokalaemia. Then supplementation of potassium is absolutely mandatory.

Unstable metabolism (e.g. postoperatively or after injuries, hypoxia, organ insufficiencies) impairs oxidative metabolism of glucose and may lead to metabolic acidosis.

States of hyperglycaemia should be adequetely monitored and treated with insulin. The application of insulin causes additional shifts of potassium into the cells and may therefore cause or increase hypokalaemia.

Solutions containing glucose should be used with caution in patients with manifest or known subclinical diabetes mellitus or carbohydrate intolerance for any reason.

Profound hypoglycemia may follow sudden discontinuation of high glucose infusion rates because of the accompanying high serum insulin concentrations. This applies especially to children less than 2 years of age, patients with diabetes mellitus and other disease states with impaired glucose homeostasis. In obvious cases the glucose infusion should be tapered off within the last 30 – 60 minutes of the infusion. As a precaution it is recommended that each individual patient be monitored for 30 minutes for hypoglycemia on the first day of abrupt discontinuation of parenteral nutrition.

Refeeding or repletion of malnourished or depleted patients may in particular cause hypokalaemia, hypophosphataemia and hypomagnesaemia. Adequate supplementation of electrolytes according to deviations from normal values is necessary.

Clinical monitoring should include blood glucose, serum electrolytes, fluid and acid-base balance in general. Frequency and kind of laboratory testing depend on the overall condition of the patient, the prevailing metabolic situation and the administered dose. Also monitor total volume and amount of glucose administered.

Electrolytes and vitamins should be supplied as necessary. Vitamin B, especially thiamine, is needed for glucose metabolism.

Glucose infusions should not be administered through the same infusion equipment, simultaneously with, before, or after administration of blood, because of the possibility of pseudo-agglutination.

4.5 Interaction with other medicinal products and other forms of interaction

Interactions with medicinal products with an influence on glucose metabolism should be considered.

Drugs leading to an increased vasopressin effect.

The below listed drugs increase the vasopressin effect, leading 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.: Chlorpropamide, clofibrate, carbamazepine, vincristine, selective serotonin reuptake inhibitors, 3.4-methylenedioxy-N-methamphetamine, ifosfamide, antipsychotics, narcotics

• Drugs potentiating vasopressin action, e.g.: Chlorpropamide, 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.

4.6 Fertility, pregnancy and lactation

For 40 % w/v Glucose Intravenous Infusion no controlled clinical data on exposed pregnancies are available. Animal studies with parenterally administered glucose do not indicate direct or indirect harmful effects with respect to pregnancy, embryonal/foeta1 development, parturition or postnatal development.

Yet caution should be exercised when prescribing to pregnant or nursing women and careful monitoring of blood glucose is necessary.

40% w/v Glucose Intravenous Infusion BP should be administrated 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).

4.7 Effects on ability to drive and use machines

No effects to be expected.

4.8 Undesirable effects

Provided the product is used in accordance with the directions given, undesirable effects are not to be expected.

The following side effects, which are not directly related to the product but to the conditions of administration, underlying disorders or accompanying treatment, may occur:

Metabolism and nutrition disorders

– Hypokalemia may be related to insulin therapy. In addition, hypokalaemia, hypomagnesaemia and hypophosphataemia may be caused by refeeding with glucose especially in malnourished patients.

– Abrupt discontinuation and/or insulin application may cause rebound hypoglycemia, especially in patients with glucose tolerance disorders.

Frequency not known: Hospital Acquired Hyponatraemia**

Neurological disorders:

Frequency not known: Hyponatraemic encephalopathy**

**Hospital acquired hyponatraemia may cause irreversible brain injury and death due to development of acute hyponatraemic encephalopathy (see sections 4.2 and 4.4).

Vascular disorders

Thrombophlebitis may be caused by osmolarities above 800 mmol/l. The osmolarity of the added medication should be kept in mind.

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: or search for MHRA Yellow Card in the Google Play or Apple App Store.

4.9 Overdose


Overdose may cause hyperglycaemia, glucosuria, serum hyperosmolarity, possibly leading to hyperosmotic and hyperglycaemic coma, further hyperhydration and electrolyte disorders.

Emergency treatment, antidotes

The disorders mentioned above can be corrected by reduction of the glucose intake, administration of insulin and/or appropriate supplementation of electrolytes.

5. Pharmacological properties
5.1 Pharmacodynamic properties

Glucose is metabolised ubiquitously as the natural substrate of the cells of the body. Under physiological conditions glucose is the most important energy-supplying carbohydrate with a caloric value of approx. 17 kJ or 4 kcal/g. Neural tissue, erythrocytes and medulla of the kidneys are amongst the tissues with an obligate requirement for glucose. The concentration of glucose in the blood is 60 – 100 mg/100 ml, or 3.3 – 5.6 mmol/l (fasting).

One the one hand, glucose serves for the synthesis of glycogen as the storage form of carbohydrates and, on the other hand, it is subject to glycolysis to pyruvate and lactate for energy production in the cells. Glucose also serves to maintain the blood sugar level and for the synthesis of important body components. It is primarily insulin, glucagon, glucocorticoids and catecholamines that are involved in the regulation of the blood sugar concentration.

A normal electrolyte and acid-base status is a prerequisite for the optimal utilisation of administered glucose. So acidosis, in particular, can indicate an impairment of oxidative glucose metabolism.

There are close metabolic relationships between the electrolytes and carbohydrate metabolism. So, most importantly, the utilisation of glucose is associated with an increased demands for potassium. Without adequate potassium supply, considerable hypokalaemia may result, which can, amongst other things, lead to - sometimes severe - cardiac arrhythmia.

Glucose utilisation can be impaired e.g. in the following pathological conditions: Diabetes mellitus and states of metabolic stress (e.g. intra-, and postoperatively, severe disease, injury), or hormonally induced depression of glucose tolerance, which can lead to hyperglycaemia even without exogenous supply of the substrate. Hyperglycaemia can - depending on its degree - lead to osmotically induced renal fluid losses with consecutive hypertonic dehydration, to hyperosmotic disorders up to hyperosmotic coma.

In situations of impaired glucose utilisation, e.g. postoperatively or post-traumatically, very high glucose doses may cause marked aggravation of the existing disorder and, as a result of the limitation of oxidative glucose utilisation, to an increased conversion of glucose into lipids. This in turn can be associated, amongst other things, with an increased carbon dioxide load of the body (problems with weaning from the respirator) and increased fatty infiltration of the tissues, particularly the liver. Patients with skull and brain injury and cerebral oedema are particularly at risk from disturbances of glucose homeostasis. Here even slight increases of the blood glucose concentration and the associated increase of plasma (serum) osmolality may lead to a considerable increase in the degree of cerebral damage.

5.2 Pharmacokinetic properties

Infused glucose primarily adds to the blood glucose content and is then incorporated in the endogenous glucose pool.

In glycolysis, glucose is metabolised to pyruvate or to lactate. Lactate can be partially re-introduced into the glucose metabolism (Cori cycle). Under aerobic conditions pyruvate is completely oxidised to carbon dioxide and water. The final products of the complete oxidation of glucose are eliminated via the lungs (carbon dioxide) and the kidneys (water).

Practically no glucose is excreted renally by healthy persons. In pathological metabolic conditions (e.g. diabetes mellitus, postaggression metabolism) associated with hyperglycaemia (blood glucose concentrations of more than 120 mg/100 ml or 6.7 mmol/l), glucose is also excreted via the kidneys (glucosuria) when the maximum tubular resorption capacity (180 mg/100 ml or 10 mmol/l) is exceeded.

5.3 Preclinical safety data

There are no pre-clinical data of relevance to the prescriber which are additional to the safety instructions already stated in other sections of the SPC.

6. Pharmaceutical particulars
6.1 List of excipients

Hydrochloric acid (for pH adjustment), water for injections.

6.2 Incompatibilities

Because of its acid pH, the solution may be incompatible with other medicaments.

6.3 Shelf life

In the unopened container the product has a shelf life of 3 years

6.4 Special precautions for storage

This medicinal product does not require any special storage conditions.

6.5 Nature and contents of container

Polyethylene containers;

contents: 500 ml.

available in packs of:

10 x 500 ml

6.6 Special precautions for disposal and other handling

Single-dose container. Discard unused contents.

Only to be used if the solution is clear and the container or its closure do not show visible signs of damage.

7. Marketing authorisation holder

B. Braun Melsungen AG

Carl-Braun-Straße 1

34212 Melsungen


8. Marketing authorisation number(s)

PL 03551/0063

9. Date of first authorisation/renewal of the authorisation

1 August 2001 / 17/03/2009

10. Date of revision of the text


B.Braun Medical
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Brookdale Road, Thorncliffe Park Estate, Chapeltown, Sheffield, South Yorkshire, S35 2PW
0114 225 9000
Medical Information Direct Line
0800 298 0299
Medical Information e-mail
[email protected]
Stock Availability
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