150 ML glucose 50 MG/ML Injection

INDICATIONS AND USAGE 25% Dextrose Injection is indicated in the treatment of acute symptomatic episodes of hypoglycemia in the neonate or older infant to restore depressed blood glucose levels and control symptoms. Other drugs, such as epinephrine and glucagon, should be considered in patients unresponsive or intolerant to dextrose (glucose). Oral feeding of dextrose may be necessary in infants with frequently recurring hypoglycemic episodes or to prevent recurrences due to hyperinsulinemia. 25% Dextrose Injection also provides a minimal source of carbohydrate calories.

DOSAGE AND ADMINISTRATION • Pharmacy Bulk Package. Not for direct intravenous infusion. ( 2.1 ) • For slow intravenous infusion only into a: ( 2.2 ) o Central vein, if final dextrose concentration is greater than 5% or osmolality is greater than 900 mOsm/L approximately. o Peripheral vein, if final dextrose concentration 5% or less and osmolality is less than 900 mOsm/L approximately. • Individualize dosage based on the patient’s clinical condition, body weight, nutritional/fluid requirements, as well as additional energy given orally/enterally. ( 2.3 ) • Discontinue infusion of concentrated dextrose solutions slowly. ( 2.4 ) 2.1 Preparation Instructions Prior to Administration Dextrose Injection is supplied as a pharmacy bulk package for admixing only and is not for direct intravenous infusion. Dextrose Injection is intended for use in the preparation of sterile, intravenous admixtures. Prior to administration, Dextrose Injection must be transferred to a separate PN container , diluted with other compatible intravenous fluids and used as an admixture in PN solutions. • Do not remove from overpouch until ready to use. • Tear protective overwrap at slit and remove solution container. Small amounts of moisture may be found on the solution container from water permeating from inside the container. The amount of permeated water is insufficient to affect the solution significantly. If larger amounts of water are found, the container should be checked for tears or leaks. • Inspect Dextrose Injection prior to use. Opacity of the container may be observed due to moisture absorption during the sterilization process. This is normal and does not affect the solution quality or safety. The opacity will diminish gradually. Evaluate the following: o If the outlet port protector is damaged, detached, or not present, discard container as solution path sterility may be impaired. o Check for minute leaks by squeezing the inner container firmly. If leaks are found, discard solution as sterility may be impaired. o Do not use unless solution is clear and container is intact. • Because additives may be incompatible, evaluate all additions for compatibility and stability of the resulting preparation. Consult with a pharmacist, if available. If it is deemed advisable to introduce additives, use aseptic technique and mix thoroughly. • Calcium and phosphate ratios must be considered. Excess addition of calcium and phosphate, especially in the form of mineral salts, may result in the formation of calcium phosphate precipitates [see Warnings and Precautions (5.1)] . Preparation for Admixing 1. The Pharmacy Bulk Package is to be used only in a suitable work area such as a laminar flow hood (or an equivalent clean air compounding area). 2. Suspend container from eyelet support. 3. Remove plastic protector from outlet port at bottom of container. 4. Attach solution transfer set. Refer to complete directions accompanying set. Note: The closure shall be penetrated only one time with a suitable sterile transfer device or dispensing set which allows measured dispensing of the contents. 5. The VIAFLEX plastic container should not be written on directly since ink migration has not been investigated. Affix accompanying label for date and time of entry notation. 6. Once container closure has been penetrated, withdrawal of contents should be completed without delay. After initial entry, maintain contents at room temperature (25°C/77°F) and dispense within 4 hours. 2.2 Important Administration Instructions • Dextrose Injection is for admixing use only and is not for direct intravenous infusion . Prior to administration, Dextrose Injection must be diluted with other compatible intravenous fluids and used as an admixture in PN solutions . • To prevent air embolism, use a non-vented infusion set or close the vent on a vented set, avoid multiple connections, do not connect flexible containers in series, fully evacuate residual gas in the container prior to administration, do not pressurize the flexible container to increase flow rates, and if administration is controlled by a pumping device, turn off pump before the container runs dry. • When Dextrose Injection is admixed, the choice of a central or peripheral venous route should depend on the osmolarity of the final infusate. Solutions with an osmolarity of 900 mOsm/L or greater must be infused through a central venous catheter [see Warnings and Precautions (5.4)] . • Prior to infusion, visually inspect the PN solution to ensure precipitates have not formed during the mixing or addition of additives. Discard container if precipitates are observed. • If admixed or infused with lipid emulsion, do not use administration sets and lines that contain di-2-ethylhexyl phthalate (DEHP). Administration sets that contain polyvinyl chloride (PVC) components have DEHP as a plasticizer. 2.3 Dosing Instructions Caution: Dextrose Injection is not for direct intravenous infusion. Prior to administration, Dextrose Injection must be diluted with other compatible intravenous fluids or used as an admixture in PN solutions. Dextrose Injection is a part of the parenteral nutrition (PN) regimen which also includes amino acids, electrolytes, and possibly lipid emulsion. Protein, caloric, fluid and electrolyte requirements all need to be taken into consideration when determining individual patient dosage needs. Individualize the dosage of Dextrose Injection based on the patient’s clinical condition (ability to adequately metabolize dextrose), body weight, nutritional and fluid requirements, as well as additional energy given orally or enterally to the patient. Vitamins and trace elements and other components (including amino acids, electrolytes, and lipid emulsion) can be added to the PN solution to meet nutrient needs and prevent deficiencies and complications from developing. The administration rate should be governed, especially during the first few days of therapy, based on the patient’s tolerance to dextrose. Daily intake of amino acids and dextrose should be increased gradually to the maximum required dose as indicated by frequent determinations of blood glucose levels. In many patients, provision of adequate calories in the form of hypertonic dextrose may require the administration of exogenous insulin to prevent hyperglycemia and glycosuria. 2.4 Discontinuation of Dextrose Injection To reduce the risk of hypoglycemia, a gradual decrease in flow rate in the last hour of infusion should be considered [see Warnings and Precautions (5.2) , Use in Specific Populations (8.4)] .

WARNINGS AND PRECAUTIONS • Pulmonary Embolism due to Pulmonary Vascular Precipitates : If signs of pulmonary distress occur, stop the infusion and initiate a medical evaluation. ( 5.1 ) • Hyperglycemia or Hyperosmolar Hyperglycemic State : Monitor blood glucose and administer insulin as needed. ( 5.2 ) • Hypersensitivity Reactions : Monitor for signs and symptoms and discontinue infusion if reactions occur. ( 5.3 ) • Vein Damage and Thrombosis : Administer solutions containing more than 5% dextrose as the final concentration or solutions with an osmolarity of approximately 900 mOsm/L or greater through a central vein. ( 2.2 , 5.4 ) • Hyponatremia: Monitor serum sodium to minimize the risk of hypo- or hyperosmotic hyponatremia. ( 5.5 ) • Risk of Infection : Monitor for signs and symptoms and laboratory parameters. ( 5.6 ) • Refeeding Syndrome : Monitory laboratory parameters. ( 5.7 ) • Hepatobiliary Disorders : Monitor liver function parameters and ammonia levels. ( 5.8 ) • Aluminum Toxicity : Dextrose Injection contains aluminum that may be toxic. Adult patients with impaired renal function and preterm infants are at higher risk. Limit aluminum to less than 4 mcg/kg/day ( 5.9 , 8.4 ) • Parenteral Nutrition Associated Liver Disease : Increased risk in patients who receive parenteral nutrition for extended periods of time, especially preterm infants; monitor liver function tests, if abnormalities occur consider discontinuation or dosage reduction. ( 5.10 , 8.4 ) • Electrolyte Imbalance and Fluid Overload : Monitor daily fluid balance, blood electrolyte levels, correct as needed. ( 5.11 , 8.4 ) 5.1 Pulmonary Embolism due to Pulmonary Vascular Precipitates Pulmonary vascular precipitates causing pulmonary vascular emboli and pulmonary distress have been reported in patients receiving parenteral nutrition. In some cases, fatal outcomes due to pulmonary embolism have occurred. Patients, especially those with hypophosphatemia, may require the addition of phosphate. To prevent hypocalcemia, calcium supplementation should always accompany phosphate administration. Excessive addition of calcium and phosphate increases the risk of the formation of calcium phosphate precipitates. Precipitates have been reported even in the absence of phosphate salt in the solution. Precipitation following passage through an in-line filter and suspected in vivo precipitate formation has also been reported. If signs of pulmonary distress occur, stop the infusion and initiate a medical evaluation. In addition to inspection of the solution [see Dosage and Administration (2.1 , 2.2 )] , the infusion set and catheter should also periodically be checked for precipitates. 5.2 Hyperglycemia and Hyperosmolar Hyperglycemic State The use of dextrose infusions in patients with impaired glucose tolerance may worsen hyperglycemia. Administration of dextrose at a rate exceeding the patient’s utilization rate may lead to hyperglycemia, coma, and death. Hyperglycemia is associated with an increase in serum osmolality, resulting in osmotic diuresis, dehydration and electrolyte losses [see Warnings and Precautions (5.11) ] . Patients with underlying CNS disease and renal impairment who receive dextrose infusions, may be at greater risk of developing hyperosmolar hyperglycemic state. Monitor blood glucose levels and treat hyperglycemia to maintain levels within normal limits while administering Dextrose Injection. Insulin may be administered or adjusted to maintain optimal blood glucose levels during Dextrose Injection administration. 5.3 Hypersensitivity Reactions Hypersensitivity and infusion reactions including anaphylaxis have been reported with dextrose injection [see Adverse Reactions (6) ] . Stop infusion immediately and treat patient accordingly if signs or symptoms of a hypersensitivity reaction develop. Signs or symptoms may include: pruritis, bronchospasm, cyanosis, angioedema, hypotension, pyrexia, chills, and rash. 5.4 Vein Damage and Thrombosis Dextrose Injection is for admixture with amino acids or dilution with other compatible intravenous fluids. It is not for direct intravenous infusion. Administer solutions with an osmolarity of ≥ 900 mOsm/L through a central vein [see Dosage and Administration (2.2) ] . The infusion of hypertonic solutions into a peripheral vein may result in vein irritation, vein damage, and/or thrombosis. The primary complication of peripheral access is venous thrombophlebitis, which manifests as pain, erythema, tenderness or a palpable cord. Remove the catheter as soon as possible, if thrombophlebitis develops. 5.5 Hyponatremia Dextrose Injection is a hypertonic solution [see Description, Table 1 (11) ] . In the body, however, glucose containing fluids can become extremely physiologically hypotonic due to rapid glucose metabolization. Monitoring of serum sodium is particularly important for hypotonic fluids. 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 hyponatremia. The risk for hyponatremia is increased, in pediatric patients, elderly patients, postoperative patients, those with psychogenic polydipsia and in patients treated with medications that increase the risk of hyponatremia (such as certain diuretic, antiepileptic and psychotropic medications). Close clinical monitoring may be warranted. Acute hyponatremia can lead to acute hyponatremic encephalopathy characterized by headache, nausea, seizures, lethargy and vomiting. Patients with brain edema are at particular risk of severe, irreversible and life-threatening brain injury. Patients at increased risk for developing complications of hyponatremia, such as hyponatremic encephalopathy include pediatric patients; women, in particular, premenopausal women; patients with hypoxemia; and in patients with underlying central nervous system disease [see Use in Specific Populations (8.4) ] . Rapid correction of hyponatremia is potentially dangerous with risk of serious neurologic complications such as osmotic demyelination syndrome with risk of seizures and cerebral edema. To avoid complications, monitor serum sodium and chloride concentrations, fluid status, acid-base balance, and signs of neurologic complications. High volume infusion must be used with close monitoring in patients with cardiac or pulmonary failure, and in patients with non-osmotic vasopressin release (including SIADH), due to the risk of hospital-acquired hyponatremia. 5.6 Risk of Infections Patients who require parenteral nutrition are at high risk of infections because the nutritional components of these solutions can support microbial growth. Infection and sepsis may also occur as a result of the use of intravenous catheters to administer parenteral nutrition. The risk of infection is increased in patients with malnutrition-associated immunosuppression, hyperglycemia exacerbated by dextrose infusion, long-term use and poor maintenance of intravenous catheters, or immunosuppressive effects of other concomitant conditions, drugs, or other components of the parenteral formulation (e.g., lipid emulsion). To decrease the risk of infectious complications, ensure aseptic technique in catheter placement and maintenance, as well as aseptic technique in the preparation and administration of the nutritional formula. Monitor for signs and symptoms (including fever and chills) of early infections, including laboratory test results (including leukocytosis and hyperglycemia) and frequent checks of the parenteral access device and insertion site for edema, redness and discharge. 5.7 Refeeding Syndrome Refeeding severely undernourished patients may result in refeeding syndrome, characterized by the intracellular shift of potassium, phosphorus, and magnesium as the patient becomes anabolic. Thiamine deficiency and fluid ret

CONTRAINDICATIONS Dextrose Injection (50%) is contraindicated in patients with: • Intracranial or intraspinal hemorrhage because Dextrose Injection (50%) can worsen cerebral edema by causing a fluid shift across the blood-brain barrier. • Severe dehydration because of the potential to worsen the patient’s hyperosmolar state. • Alcohol withdrawal because of the potential to precipitate Wernicke encephalopathy (WE) or cardiomyopathy in thiamine-deficient patients. • Known hypersensitivity to dextrose [see Warnings and Precautions (5.2) ] . • Intracranial or intraspinal hemorrhage. ( 4 ) • Severe dehydration. ( 4 ) • Alcohol withdrawal. ( 4 ) • Known hypersensitivity to dextrose. ( 4 )

CLINICAL PHARMACOLOGY When administered intravenously, this solution restores blood glucose levels in hypoglycemia and provides a source of carbohydrate calories. Carbohydrate in the form of dextrose may aid in minimizing liver glycogen depletion and exerts a protein-sparing action. Dextrose injection undergoes oxidation to carbon dioxide and water. 25% Dextrose Injection, USP provides a concentrated solution sufficiently nonirritating for slow intravenous injection to infants for terminating acute symptomatic episodes of hypoglycemia in the neonate and in older infants (fasting blood glucose below 40 mg/100 mL). Values as low as 20 mg/100 mL are not uncommon in normal asymptomatic infants the first few days of life (longer in premature infants). Symptoms of hypoglycemia in the newborn and small infants may be difficult to evaluate and convulsions often are the first or only recognized manifestation of depressed blood glucose levels. Because of widely varied etiology, the precise cause may be difficult to establish. Hypoglycemia (deficient blood glucose) due to organic or functional hyperinsulinism, may be only temporarily abated by administration of dextrose (glucose) and may rebound to hypoglycemia levels as release of additional insulin is evoked. In addition to various other causes, an idiopathic form of hypoglycemia in infancy has been described, as well as occasional transitory hypoglycemia in the neonatal period which disappears in later infancy. Fetal hyperinsulinism in response to maternal hyperglycemia of diabetic mothers has been observed. Occasionally convulsions associated with severe hypoglycemia are observed in infants of diabetic mothers. Since glucose is the only sugar utilized for metabolic requirements of human neural tissue, it is essential to restore deficient blood glucose levels from any cause in order to prevent or correct central nervous system dysfunction.