Depolarizing Neuromuscular Blockade

Depolarizing Neuromuscular Blockade


suxamethonium mimics the action of acetylcoline and produces a sustained depolarization of the postjunctional membrane. Skeletal muscle paralysis occurs because a depolarized postjunctional membrane and inactivated sodium channels cannot respond to subsequent release of ach. Muscle twitching (fasciculation) is noted when it is administered to a patient. Unlike ACh, however, these drugs are not metabolized by acetylcholinesterase, and their concentration in the synaptic cleft does not fall as rapidly, resulting in a prolonged depolarization of the muscle end-plate.

Suxamethenium is the only depolarizing NMBD used clinically. Furthermore, it is the only NMBD with both a rapid onset and ultra short duration of action. Typically, doses of 0.5 to 1.5 mg/kg intravenously are administered and produce a rapid onset of skeletal muscle paralysis (30 to 60 seconds) that lasts 5 to 10 minutes. IM dose is 2.5-4 mg/kg. These characteristics make SCh ideal for providing rapid skeletal muscle paralysis to facilitate tracheal intubation. Succinylcholine is metabolized by plasma cholinesterase after 3-5 minutes. A genetic defect (pseudocholinesterases abnormalities) will affect a small percentage of the populations' ability to metabolize succinylcholine. This will result in prolonged paralysis. The patient may require artificial ventilation by an endotracheal tube for several hours. The effect will eventually wear off. Low pseudocholinesterase levels occur in liver disease, severe anemia, malnutrition, the second half of pregnancy and after contamination with organic phosphorous insecticides

Side Effects of Suxamethonium

  • Repeated administration may result in severe bradycardia and even cardiac arrest. Atropine may help prevent this. If possible, repeated doses should be minimized or avoided. When administering succinylcholine airway equipment should always be available including a bag mask-valve device or anesthesia circuit, oral airways, oxygen, and intubating equipment. Atropine may be administered prior to succinylcholine in children up to 8 years of age. This may prevent bradycardia.
  • If there is a family history of malignant hyperthermia, succinylcholine and inhaled anesthetics should be avoided.
  • Succinylcholine will increase the patients' potassium level in the blood by 0.3-0.5 meq/L. Higher levels of potassium are released in patients with recent burn injuries and a history of neurological diseases such as multiple sclerosis, muscular dystrophy, and paralysis. It can cause a large release of potassium, resulting in cardiac arrest.
  • May result in muscle aches and pain after administration (Myalgia).
  • The routine use of succinylcholine for pediatric patients is not recommended. This is due to the rare reports of cardiac arrest secondary to high potassium levels in pediatric patients with undiagnosed muscular dystrophy. Succinylcholine should be reserved for emergency intubation, rapid sequence induction, laryngospasm, and other emergent situations.


  • Family or patient history of malignant hyperthermia.
  • Family or patient history of prolonged paralysis after the administration of succinylcholine.
  • Neurological diseases or injuries such as multiple sclerosis, muscular dystrophy, and paralysis. Open globe injuries in salvageable eyes.
  • Recent, extensive burn injuries.
  • Patients with hyperkalemia.
Last modified: Wednesday, 16 November 2016, 2:04 PM