Suxamethonium chloride 50mg/ml injection

Indications

• Neuromuscular blockade during surgery
• Facilitation of intubation

Dosage

Children: Neonate: 2 mg/kg by intravenous injection, producing effects lasting 5–10 minutes.

Adults: 1–1.5 mg/kg by intravenous injection.

Mechanism of action

Suxamethonium chloride acts by binding to nicotinic acetylcholine receptors at the neuromuscular junction, leading to prolonged depolarization of the motor end plate. Unlike acetylcholine, which is rapidly hydrolyzed by acetylcholinesterase, suxamethonium is hydrolyzed much more slowly, resulting in sustained depolarization and subsequent neuromuscular blockade.

Pharmacodynamics

The primary pharmacodynamic effect of suxamethonium is the induction of muscle relaxation through neuromuscular blockade. This effect occurs rapidly, typically within 30 to 60 seconds of administration, and lasts for about 5 to 10 minutes. The drug is particularly useful for procedures requiring rapid onset of muscle paralysis while minimizing exposure time.

Pharmacokinetics

Suxamethonium chloride is rapidly distributed and eliminated from the bloodstream. It is metabolized by plasma cholinesterase, leading to its short duration of action. Variability in plasma cholinesterase activity, such as in patients with atypical cholinesterase or liver disease, can affect the drug's clearance and lead to prolonged neuromuscular blockade. The drug is primarily excreted in urine.

Contra-indications

• Hypersensitivity to suxamethonium chloride or any of its components
• Myasthenia gravis (may be resistant to suxamethonium chloride)
• Atypical plasma cholinesterase
• Neuromuscular disease (e.g. Duchenne muscular dystrophy)
• Severe burns (may develop resistance)
• Severe sepsis (risk of hyperkalaemia)
• Severe respiratory disease

Adverse effects

• Apnoea
• Bradycardia
• Arrhythmias
• Hyperkalemia
• Cardiac arrest
• Malignant hyperthermia
• Trismus
• Hypersensitivity reactions

Interactions

• Non-depolarising neuromuscular blocking drugs can have additive effects
• Certain antibiotics may potentiate neuromuscular blockade
• Cholinesterase inhibitors may antagonize the effects of suxamethonium
• Magnesium salts may enhance neuromuscular blockade

Precautions

• Should only be administered by, or under the direct supervision of, personnel experienced in its use
• Patients with cardiovascular disease (reduce rate of administration)
• Electrolyte disturbances (response unpredictable)
• Fluid disturbances (response unpredictable)
• Burns and major trauma (risk of resistance)
• Neurogenic disease (acute phase may be unpredictable)

Pregnancy

Suxamethonium is unlikely to cross the placenta in significant amounts, but caution is advised due to potential risks.

Breast-feeding

Non-depolarising neuromuscular blocking drugs are ionised at physiological pH and are unlikely to be present in milk in significant amounts.

Storage

Store in a cool, dry place. Protect from light. Do not freeze.

Formulations

• Suxamethonium chloride 50 mg per 1 ml solution for injection
• Suxamethonium chloride 100 mg/2 ml solution for injection

Indications

• Administration of intravenous medications
• Preparation of injectable solutions
• Adjustment of drug concentrations for pediatrics
• Facilitation of oral drug administration in patients with difficulty swallowing

Dosage

Children: Refer to specific drug guidelines for appropriate dilution protocols as dosages vary based on the drug and therapeutic context.

Adults: Refer to specific drug guidelines for appropriate dilution protocols as dosages vary based on the drug and therapeutic context.

Mechanism of action

The mechanism of action of dilute solutions typically involves the principle of concentration gradients. When a drug is diluted, it is distributed more evenly throughout the solvent, allowing for more uniform absorption and reduced toxicity. This can enhance the drug's efficacy while minimizing adverse effects associated with higher concentrations.

Pharmacodynamics

Pharmacodynamics of diluted drugs often reflect the relationship between the drug concentration and its therapeutic effect. Diluted drugs may exhibit altered pharmacological activity due to changes in receptor binding, absorption rates, and bioavailability. Lower concentrations can result in reduced receptor activation, which may be beneficial in minimizing side effects or achieving a more controlled therapeutic effect.

Pharmacokinetics

The pharmacokinetics of diluted drugs can vary based on the solubility and stability of the drug in the chosen solvent. Factors such as absorption rate, distribution volume, metabolism, and excretion can be influenced by dilution. For instance, a diluted drug may have a faster absorption rate due to lower viscosity, but its overall bioavailability may be affected depending on the concentration of the active ingredients and the solvent used.

Pregnancy

Consult healthcare provider before use. Safety in pregnancy has not been established.

Breast-feeding

Consult healthcare provider before use. Safety during lactation has not been established.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Adjustment of pH in pharmaceutical formulations
• Facilitation of drug absorption
• Used in sterile preparations

Dosage

Children: Refer to specific product guidelines for dosing information, as hydrochloric acid is typically used in a controlled setting based on formulation requirements.

Adults: Refer to specific product guidelines for dosing information, as hydrochloric acid is typically used in a controlled setting based on formulation requirements.

Mechanism of action

Hydrochloric acid dissociates in aqueous solution to release hydrogen ions (H+), leading to a decrease in pH. This acidic environment promotes the activation of pepsinogen to pepsin, an enzyme essential for protein digestion. Additionally, the acidity aids in the absorption of certain minerals and drugs that require an acidic environment for optimal bioavailability.

Pharmacodynamics

The primary pharmacodynamic action of hydrochloric acid is the maintenance of gastric acidity, which is essential for normal digestive processes. The acidic environment helps in denaturing proteins, activating digestive enzymes, and providing a barrier against pathogenic microorganisms. Its effects can influence the absorption and efficacy of various medications, particularly those that are pH-dependent.

Pharmacokinetics

Hydrochloric acid does not undergo significant systemic absorption when used in its normal contexts, as it acts locally within the gastrointestinal tract. The amount of hydrochloric acid produced by the stomach varies with food intake and physiological needs. It is secreted by parietal cells in the gastric mucosa, and its secretion is regulated by neural, hormonal, and local factors. The half-life of hydrochloric acid is not applicable as it is continuously produced and neutralized within the gastrointestinal tract.

Contra-indications

• Hypersensitivity to hydrochloric acid or any of its components
• Severe renal impairment
• Active gastrointestinal bleeding

Adverse effects

• Abdominal pain
• Diarrhea
• Nausea
• Vomiting
• Esophageal irritation
• Gastric mucosal irritation
• Electrolyte imbalances

Interactions

• May interact with alkaline substances, potentially neutralizing hydrochloric acid
• Caution with antacids as they may affect the efficacy of hydrochloric acid

Precautions

• Use with caution in patients with a history of gastritis or gastric ulcers
• Monitor electrolytes in prolonged use
• Use cautiously in patients with respiratory conditions due to potential aspiration risks

Pregnancy

Hydrochloric acid is classified as a category C drug. Use during pregnancy only if clearly needed and the potential benefits justify the risks to the fetus.

Breast-feeding

There is limited data on the excretion of hydrochloric acid in human milk. Use with caution during breastfeeding.

Storage

Store in a cool, dry place away from direct sunlight and heat. Ensure the container is tightly closed.

Formulations

• Oral solutions
• Injectable forms
• Tablets

Indications

• Pain management
• Vaccination
• Antibiotic therapy
• Hormonal therapies
• Anesthesia
• Nutritional support
• Chemotherapy

Dosage

Children: Refer to specific drug guidelines for paediatric dosing, as it requires careful consideration of weight and age.

Adults: Refer to specific drug guidelines for adult dosing, as it varies widely depending on the medication and clinical condition.

Mechanism of action

The mechanism of action of injected drugs varies widely based on the specific medication being administered. Generally, injected drugs enter the bloodstream directly, allowing them to circulate rapidly throughout the body. For instance, antibiotics may work by inhibiting bacterial cell wall synthesis, while analgesics may modulate pain pathways in the central nervous system. Each drug has unique pathways through which it achieves its therapeutic effects.

Pharmacodynamics

Pharmacodynamics refers to the effects of drugs on the body and their mechanisms of action. For injectable medications, effects can be immediate or delayed, depending on the drug's formulation and route of administration. Factors influencing pharmacodynamics include receptor affinity, drug concentration, and the presence of other substances that may enhance or inhibit the drug's effects. For example, some injectable drugs may require specific receptors to exert their effects, while others may have a broader range of action.

Pharmacokinetics

Pharmacokinetics involves the absorption, distribution, metabolism, and excretion (ADME) of injected drugs. After administration, drugs are rapidly absorbed into the bloodstream, leading to quick therapeutic effects. The distribution depends on factors such as blood flow, tissue permeability, and protein binding. Drugs are metabolized primarily in the liver and excreted through the kidneys or bile. The pharmacokinetic profile can vary widely based on the drug's chemical nature, dosage, and individual patient factors.

Pregnancy

Safety during pregnancy depends on the specific injection and its active ingredients. It is essential to consult a healthcare professional for guidance.

Breast-feeding

The safety of injections during breastfeeding varies by the specific medication. It is recommended to seek advice from a healthcare provider.

Storage

Store injections as per manufacturer's guidelines, usually in a cool, dry place away from direct sunlight. Some may require refrigeration.

Indications

• Cryotherapy for the destruction of abnormal tissue
• Treatment of warts, moles, and other skin lesions
• Nitrogen narcosis in diving

Dosage

Children: Refer to the BNF for Children for appropriate dosing recommendations in paediatric patients.

Adults: For cryotherapy, the dosage and duration depend on the specific condition being treated and should be determined by the healthcare provider. Refer to specific guidelines for each condition.

Mechanism of action

In cryotherapy, the mechanism of action involves three stages: heat transfer, cell injury, and inflammation. The boiling point of liquid nitrogen is -196°C, which initiates heat transfer, leading to cell injury during the thawing process. The inflammation stage follows, characterized by edema and erythema, resulting from cellular death and contributing to local cell destruction. Additionally, nitrogen can cause direct toxic effects on brain functions, leading to nitrogen narcosis, which impairs cognitive abilities and motor functions due to its impact on nerve conduction.

Pharmacodynamics

Nitrogen's pharmacodynamics relate to its behavior in cryotherapy and asphyxiation. In cryotherapy, it induces tissue destruction through rapid cooling, leading to apoptosis of abnormal cells. In high-pressure environments, nitrogen narcosis affects the central nervous system, producing symptoms similar to alcohol intoxication, ultimately decreasing reasoning, decision-making abilities, and manual dexterity.

Pharmacokinetics

Nitrogen does not undergo metabolism in the traditional sense, as it is an inert gas at physiological conditions. Its pharmacokinetics involve physical principles of gas exchange and partial pressures. In the case of nitrogen narcosis, the effects are influenced by the partial pressure of nitrogen in the bloodstream, which increases with depth during diving. Nitrogen is primarily eliminated from the body through respiration.

Adverse effects

• Narcotic effect at high pressures
• Stupor or euphoria
• Decreased motor function and manual dexterity
• Asphyxiation due to oxygen displacement

Precautions

• Careful monitoring in environments with high nitrogen pressures
• Avoidance of rapid ascents in diving to prevent nitrogen narcosis
• Use in controlled settings to prevent asphyxiation risks

Pregnancy

Nitrogen is generally considered safe in terms of direct effects during pregnancy; however, the safety of exposure in high-pressure environments should be assessed.

Breast-feeding

Nitrogen is not known to affect breastfeeding; however, caution is recommended in environments where nitrogen levels may displace oxygen.

Storage

Store in a cool, dry place away from heat sources; liquid nitrogen should be handled with care due to extreme cold.

Formulations

• Liquid nitrogen
• Nitrogen gas (compressed)

Indications

• Rapid sequence intubation
• Muscle relaxation during anesthesia
• Facilitation of mechanical ventilation

Dosage

Children: For children, refer to the BNF for Children for specific dosing information.

Adults: Typically, a dose of 1 to 1.5 mg/kg is administered intravenously for intubation purposes.

Mechanism of action

Suxamethonium binds to post-synaptic cholinergic receptors at the neuromuscular junction, causing initial depolarization that leads to transient muscle fasciculations followed by flaccid paralysis. Its resistance to acetylcholinesterase leads to a prolonged neuromuscular blockade, distinguishing it from competitive neuromuscular blockers.

Pharmacodynamics

The neuromuscular blockade induced by suxamethonium occurs within 60 seconds of intravenous administration, lasting approximately 4 to 6 minutes. It selectively affects skeletal muscles without impacting smooth or cardiac muscles. The paralysis progresses from facial muscles to respiratory muscles, necessitating concurrent anesthetic use as it does not alter consciousness or pain perception.

Pharmacokinetics

Suxamethonium is rapidly metabolized by plasma pseudocholinesterase, resulting in a quick onset and short duration of action. Its effects can be influenced by variations in enzyme activity among individuals. The drug is not stored in the body and is eliminated through enzymatic hydrolysis, which accounts for its brief therapeutic window.

Contra-indications

• Personal or family history of malignant hyperthermia
• Known hypersensitivity to succinylcholine or any of its components
• Severe burns or trauma
• Neuromuscular diseases such as myasthenia gravis
• Hyperkalemia

Adverse effects

• Prolonged neuromuscular blockade
• Cardiovascular adverse effects
• Transient muscle fasciculations
• Acute rhabdomyolysis
• Hyperkalemia
• Ventilation dysrhythmias
• Cardiac arrest

Interactions

• cyclophosphamide: increases risk of prolonged neuromuscular blockade
• lidocaine: increases effects
• carbamazepine: increases risk of prolonged neuromuscular blockade
• clindamycin: increases effects
• corticosteroids: decreases effects
• digoxin: increases risk of cardiovascular adverse effects
• irinotecan: increases risk of prolonged neuromuscular blockade
• intravenous magnesium: increases effects
• metoclopramide: increases effects
• piperacillin: increases effects

Precautions

• Monitor for signs of prolonged neuromuscular blockade
• Use with caution in patients with a history of cardiovascular disease
• Ensure adequate anesthesia due to lack of analgesic properties
• Assess for potential undiagnosed neuromuscular disorders

Pregnancy

Use only if clearly needed, as succinylcholine may cause fetal effects.

Breast-feeding

Not known whether succinylcholine is excreted in human milk; caution is advised.

Storage

Store below 25°C, protect from light. Do not freeze.

Formulations

• Injection: 200 mg/10 mL ampoule

Mechanism of action

In cryotherapy, mechanism of action could be classified into three stages: 1. heat transfer, 2. cell injury and 3. inflammation. Boiling point of liquid nitrogen is -196°C, which is the responsible for creating the initial stage which is heat transfer. The second stage is cell injury which is induced during thawing conditions of the cells. The last step in the cryotherapy is the inflammation stage which is characterized by edema and erythema. Inflammation occurs as a result of cellular death and it helps in local cell destruction. ... Nitrogen also has a direct toxic action of its own, affecting brain functions and inducing a stupor or euphoria. Nitrogen narcosis ("rapture of the deep" or "the martini effect") results from a direct toxic effect of high nitrogen pressure on nerve conduction and produces effects similar to alcohol intoxication. Complex reasoning, decision-making ability, motor function, and manual dexerity decrease. Individuals vary in this response widely, but it typically can be noticed among divers at depths exceeding 100 ft (30 m). For example, certain individuals experience no effect at depths of < or = 130 ft, whereas others feel some effect at around 80 ft. Nonetheless, the narcotic effect increases with increasing depth so that each additional 50 ft incrementally produces the effect of "another martini". A simple asphyxiant, nitrogen's main toxicty arises from its ability to displace O2 and generate an atmosphere that does not support the chemical reactions needed for maintenance of life. The displacement of O2 can be complete or incomplete, leading to varying degrees of hypoxia. Nitrogen is an inert substance and does not exert a direct toxicological effect. Nitrogen acts by the physiological effect of simple asphyxia on the target species within a Controlled Atmosphere Treatment (CAT) bubble. The biocide action of nitrogen is due to its displacement of oxygen from an atmospheric oxygen level of 20.8% to levels < 0.2% v/v in the CAT bubble. The level of oxygen is the critical factor. Victims exposed to atmospheres deficient in oxygen, i.e. < 19%, will begin to display signs and symptoms of oxygen-deficient exposure of air due to an increase in nitrogen.

Mechanism of action

Succinylcholine is a depolarizing neuromuscular blocker, meaning it causes a prolonged period of membrane depolarization in order to exert its therapeutic effects. It binds to the post-synaptic cholinergic receptors found on motor endplates, thereby inducing first transient fasciculations followed by skeletal muscle paralysis. ... SUCCINYLCHOLINE PRODUCES A BLOCKADE THAT COMBINES CERTAIN FEATURES OF ... THE DEPOLARIZING & THE COMPETITIVE AGENTS ... & THAT HAS SOME CHARACTERISTICS NOT ASSOC WITH EITHER; ... THIS TYPE OF ACTION /HAS BEEN TERMED/ A "DUAL" MECHANISM. ... /ITS/ INITIAL ACTION IS TO DEPOLARIZE THE MEMBRANE BY OPENING CHANNELS IN THE SAME MANNER AS ACETYL CHOLINE. HOWEVER, SINCE /IT/ PERSISTS FOR LONGER DURATIONS AT THE NEUROMUSCULAR JUNCTION, PRIMARILY BECAUSE OF THEIR RESISTANCE TO ACETYLCHOLINESTERASE, THE DEPOLARIZATION IS LONGER LASTING, RESULTING IN A BRIEF PERIOD OF REPETITIVE EXCITATION THAT MAY ELICIT TRANSIENT MUSCULAR FASCICULATIONS. THE INITIAL PHASE IS FOLLOWED BY BLOCK OF NEUROMUSCULAR TRANSMISSION AND FLACCID PARALYSIS.

Pharmacodynamics

Succinylcholine's neuromuscular blockade takes effect within 60 seconds of intravenous administration and lasts between four to six minutes. Similar to acetylcholine, it binds to cholinergic receptors of the motor endplate to induce membrane depolarization and, eventually, muscle paralysis, which may be maintained for as long as an adequate concentration of succinylcholine remains at the receptor site. Succinylcholine has no direct action on smooth or cardiac muscle, nor does it appear to act on pre-synaptic or ganglionic acetylcholine receptors. The paralysis induced by succinylcholine has been described as "progressive", first involving the muscles of the face and glottis, then the intercostals and diaphragm, then followed by other skeletal muscles. Succinylcholine has no effect on consciousness or pain threshold, and must therefore be used in conjunction with adequate anesthesia. There have been rare reports of the development of acute rhabdomyolysis with hyperkalemia - resulting in ventricular dysrhythmias, cardiac arrest, and death - after the intravenous administration of succinylcholine to apparently healthy pediatric patients who were subsequently found to have undiagnosed skeletal myopathy (most frequently Duchenne's muscular dystrophy). Infants or children experiencing seemingly idiopathic cardiac arrest soon after the administration of succinylcholine should therefore be treated immediately for hyperkalemia. Given that patients may not present with any apparent risk factors, the use of succinylcholine in pediatric patients should be restricted to emergency intubation or other situations in which a suitable alternative is unavailable.