SENSOCAIN SPINAL 0.5%

Indications

• Infiltration anaesthesia in dentistry
• Nerve blocks for surgery
• Epidural anaesthesia
• Post-operative pain management

Dosage

Adults: Bolus doses of 1.5 mL/kg over 1 minute, with intervals of 5 minutes, and maximum cumulative doses should not exceed 12 mL/kg. For continuous infusion, the rate may

Mechanism of action

Bupivacaine hydrochloride acts by blocking voltage-gated sodium channels on the neuronal cell membrane, which inhibits the influx of sodium ions, leading to a decrease in depolarization and action potential generation. This mechanism results in reversible loss of sensation in the targeted area. The effect is dose-dependent and varies based on the route of administration.

Pharmacodynamics

Bupivacaine exhibits a high lipid solubility, which facilitates its action at the nerve membrane. The onset of action is typically within 10 to 20 minutes, with a duration of effect that can last from 2 to 8 hours, depending on the dosage and the method of administration. The drug provides effective analgesia, making it a preferred choice for procedures requiring prolonged pain relief. However, caution is advised as high concentrations can lead to systemic toxicity, primarily affecting the central nervous and cardiovascular systems.

Pharmacokinetics

Bupivacaine is rapidly absorbed following parenteral administration, with peak plasma concentrations occurring within 30 minutes to 2 hours. The drug is extensively metabolized in the liver by cytochrome P450 enzymes and excreted in the urine as metabolites. Its half-life ranges from 2.5 to 6 hours in healthy individuals, but it can be prolonged in patients with hepatic impairment. Due to its extensive protein binding (approximately 95%), the free fraction available for action is reduced in conditions affecting protein levels.

Contra-indications

• Hypersensitivity to bupivacaine or any of its components
• Application to damaged skin
• Severe hypertension
• Unstable cardiac rhythm

Adverse effects

• Face oedema
• Gingivitis
• Headache
• Nausea
• Abnormal sensation

Interactions

• Concurrent use of sympathomimetics may increase cardiovascular effects
• Adrenaline should be used with caution; total dose should not exceed 5 micrograms/kg
• Avoid using propofol as an alternative to lipid emulsion treatment

Precautions

• Use with caution in patients with hepatic impairment due to increased risk of toxicity
• Use with caution in patients with renal impairment
• Requires monitoring of blood pressure and ECG during administration
• Should only be administered by trained personnel experienced in its use

Pregnancy

Use only if potential benefit outweighs risk; no information available.

Breast-feeding

Avoid breastfeeding for 48 hours after administration.

Storage

Store at room temperature, away from light. Do not freeze.

Formulations

• Solution for injection cartridges
• Injectable preparation

Indications

• Regional anesthesia for surgical procedures
• Pain management in obstetric settings (e.g., epidural analgesia during labor)
• Postoperative analgesia
• Nerve blocks for pain control

Dosage

Children: Refer to the BNF for Children for specific dosing information in paediatric patients.

Adults: For infiltration anesthesia, the typical dose is 5 to 10 mL of a 0.25% to 0.5% solution. For epidural anesthesia, a dose of 10 to 20 mL of a 0.25% to 0.5% solution may be used, depending on the procedure.

Mechanism of action

Bupivacaine acts by inhibiting voltage-gated sodium channels in the neuronal cell membrane. This inhibition prevents the initiation and propagation of action potentials, leading to a reversible loss of sensation in the area supplied by the affected nerves. It predominantly affects small unmyelinated fibers, which are responsible for pain and temperature sensation.

Pharmacodynamics

The onset of action for bupivacaine is dose-dependent, with effects typically observed within 10 to 30 minutes after administration, depending on the route of administration. The duration of action can last from 2 to 8 hours, with longer durations noted for higher doses or when used in conjunction with vasoconstrictors. Bupivacaine is more potent than lidocaine and provides a longer duration of anesthesia.

Pharmacokinetics

Bupivacaine is well-absorbed after injection, with peak plasma concentrations occurring within 30 minutes. It is metabolized primarily in the liver by cytochrome P450 enzymes, and its metabolites are excreted in the urine. The elimination half-life ranges from 2.5 to 6 hours, depending on the route of administration and patient-specific factors.

Contra-indications

• Hypersensitivity to bupivacaine or any component of the formulation
• Severe heart block
• Severe hepatic impairment
• Uncontrolled hypotension

Adverse effects

• Cardiovascular collapse
• Hypotension
• Bradycardia
• Nausea
• Vomiting
• Dizziness
• Headache
• Numbness
• Paresthesia
• Tremors

Interactions

• Concurrent use with other local anesthetics may increase the risk of toxicity
• Caution advised when used with agents that can affect the cardiovascular system

Precautions

• Use with caution in patients with cardiovascular disease
• Monitor for signs of systemic toxicity, particularly in high doses or accidental intravascular injection
• Ensure resuscitation equipment and trained personnel are available during administration

Pregnancy

Bupivacaine can be used during pregnancy when the potential benefits justify the risks. Consult relevant clinical guidelines.

Breast-feeding

Bupivacaine is excreted in breast milk. Caution is advised when administering to nursing mothers.

Storage

Store at room temperature, away from light and moisture. Do not freeze.

Formulations

• Injection solution
• Epidural solution
• Nerve block solution

Indications

• Hypoglycemia
• Caloric supplementation in patients unable to eat
• Fluid replacement therapy
• Parenteral nutrition

Dosage

Children: Paediatric doses must be determined based on clinical condition and specific needs. Refer to the BNF for Children for appropriate dosing information.

Adults: The dosage of dextrose in adults varies based on clinical condition and route of administration. For hypoglycemia, intravenous dextrose 50% (D50W) is commonly administered. Refer to the BNF for specific dosing guidelines.

Mechanism of action

Dextrose supplies energy to tissues by generating ATP and NADH through glycolysis, where glucose is phosphorylated by hexokinase to form glucose 6-phosphate. This activates glucose for breakdown, ultimately converting glucose into energy molecules. Dextrose also plays a role in gene transcription, enzyme activity, and hormone secretion, regulating glucose homeostasis and cellular metabolic integrity.

Pharmacodynamics

Blood glucose acts as a crucial energy source for cellular activities and functions as a signaling molecule. It is oxidized into carbon dioxide and water, producing energy through glycolysis, the citric cycle, and oxidative phosphorylation. Dextrose can be converted into fat for energy storage and is stored as glycogen in the liver and muscles. Its administration, particularly orally, enhances insulin secretion due to stimulation of incretin hormones.

Pharmacokinetics

Dextrose is rapidly absorbed in the gastrointestinal tract, leading to a quick elevation of blood glucose levels. It is distributed throughout the body and can be utilized by various tissues for energy. The metabolism of dextrose primarily occurs in the liver, where it can be stored as glycogen or converted into fat. Renal excretion may occur when blood glucose levels are excessively high.

Adverse effects

• Hyperglycemia
• Fluid overload
• Hypokalemia
• Thrombophlebitis at injection site

Interactions

• Corticosteroids may increase blood glucose levels
• Beta-blockers may mask symptoms of hypoglycemia
• Diuretics may cause electrolyte imbalances

Precautions

• Use with caution in patients with diabetes mellitus
• Monitor blood glucose levels regularly
• Use cautiously in patients with renal impairment or heart failure

Pregnancy

Dextrose is generally considered safe for use during pregnancy when clinically indicated, but should be used with caution.

Breast-feeding

Dextrose can be used during breastfeeding as it is a natural sugar found in breast milk.

Storage

Store at room temperature, away from direct sunlight, and protect from freezing.

Formulations

• Dextrose 5% solution for infusion
• Dextrose 10% solution for infusion
• Dextrose 50% solution for injection
• Oral dextrose tablets

Mechanism of action

Glucose supplies most of the energy to all tissues by generating energy molecules ATP and NADH during a series of metabolism reactions called glycolysis. Glycolysis can be divided into two main phases where the preparatory phase is initiated by the phosphorylation of glucose by hexokinase to form glucose 6-phosphate. The addition of the high-energy phosphate group activates glucose for the subsequent breakdown in later steps of glycolysis and is the rate-limiting step. Products end up as substrates for following reactions, to ultimately convert C6 glucose molecule into two C3 sugar molecules. These products enter the energy-releasing phase where the total of 4ATP and 2NADH molecules are generated per one glucose molecule. The total aerobic metabolism of glucose can produce up to 36 ATP molecules. These energy-producing reactions of glucose are limited to D-glucose as L-glucose cannot be phosphorylated by hexokinase. Glucose can act as precursors to generate other biomolecules such as vitamin C. It plays a role as a signaling molecule to control glucose and energy homeostasis. Glucose can regulate gene transcription, enzyme activity, hormone secretion, and the activity of glucoregulatory neurons. The types, number, and kinetics of glucose transporters expressed depends on the tissues and fine-tunes glucose uptake, metabolism, and signal generation to preserve cellular and whole body metabolic integrity. Vascular calcification is a hallmark of type 2 diabetes. Glucose stimulates calcification in culture of vascular smooth muscle cells (VSMCs) but the underlying mechanisms remain obscure. We observed that high glucose levels stimulated mouse and human VSMC trans-differentiation into chondrocytes, with increased levels of Sox9, type II collagen, glycosaminoglycan and Runx2 expression, and increased alkaline phosphatase activity and mineralization. These effects were associated with increased expression of IL-1beta, which stimulated alkaline phosphatase and calcification, suggesting that glucose induces chondrocyte differentiation of VSMCs, possibly through IL-1beta activation.

Pharmacodynamics

Blood glucose is an obligatory energy source for humans involved in various cellular activities, and it also acts as a signaling molecule for diverse glucose-sensing molecules and proteins. Glucose undergoes oxidation into carbon dioxide, water, and yields energy molecules in the process of glycolysis and subsequent citric cycle and oxidative phosphorylation. Glucose is readily converted into fat in the body which can be used as a source of energy as required. Under a similar conversion into storage of energy, glucose is stored in the liver and muscles as glycogen. Glucose stores are mobilized in a regulated manner, depending on the tissues' metabolic demands. Oral glucose tablets or injections serve to increase the supply of glucose and oral glucose administration is more effective in stimulating insulin secretion because it stimulates the incretin hormones from the gut, which promotes insulin secretion.