SUXAMETHONIUM CHLORIDE-FRESENIUS INJECTION

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

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

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.