A 70 kg old athlete was posted for surgery, Patient was administered succinylcholine due to unavailability of vecuronium. It was administered in intermittent dosing (total 640 mg). During recovery patient was not able to respire spontaneously & move limbs. What is the explanation ?
B i.e. Phase 2 blockade produced by succinylcholine - Sch is depolarizing/ non competitiveQ M.R. with shoest duration of actionQ (3-5 min) d/t rapid hydrolysis by pseudo cholinesteraseQ. It causes dual/ biphasic blockQ. It increases K. (ie hyperkalemiaQ 1/t diastolic cardiac arrest), intraocular & intragastric pressure and temperature (l/t) malignant Hypehermia)Q - Depolarizing block (phase I & II) caused by Succinyl cholineQ is also called Dual or Biphasic Block. In contrast to phase II depolarization block & Non depolarizing block, phase I depolarization block does not exhibit fade during tetanus or train-of-four, neither does it demonstrate post tetanic potentiation. Phase I block is potentiated by isoflurane, Mg, Li & Anticholine-esterase while phase II block is potentiated by enflurane. - The onset of paralysis by succinylcholine is signaled by visible motor unit contractions called fasciculation.Q Patients who have received suxamethonium have an increased incidence of postoperative myalgiaQ. This is more common in healthy female outpatients. Pregnancy & extremes of age seem to be protective. Succinylcholine releases a metabolite succinylmonocholine, causing excitation of the cholinergic receptors in the sinoatrial node resulting in bradycardia. Q Intravenous atropine is given prophylactically (paicularly in children, who are more susceptible) in children and always before a second dose of sch. - Prolonged apnea after suxamethonium is best managed by providing mechanical ventilation, maintaining anesthesia and continuous monitoring until muscle function returns to normal.Q Transfusion of fresh frozen plasma is beneficial (as it provides pseudocholinesterase) its infectious risks outweigh its potential benefits -Morgan Administration of purified pseudocholinesterase, blood or plasma may antagonize the block. However because of the risk associated with their use, infusion of banked blood or fresh frozen plasma cannot be recommended - Churchill. - Succinylcholine & mivacurium are metabolized by pseudocholinesterase, while esmolol and remifentanyl are metabolized by RBC es terase.(2 - Pseudo cholinesterase deficiency causes prolonged residual paralysis at normal Sch dose (1-2 mg/kg)Q whereas, phase 2 non-depolarization blockade occurs after administration of higher doses >6 (7-10) mg/kgQ Despite large decrease in pseudo cholinesterase activity (level) there is only moderate increase in duration of action of Sch. In contrast to the doubling or tripling of blockade duration seen in patients with low pseudo cholinesterase enzyme levels or hetozygous atypical enzyme, patients with homozygous atypical enzyme will have a very blockade (4-8 hrs) following Sch administration.
Pseudocholinesterase deficiency increasing action of syccinylcholine
Phase 2 blockade produced by succinylcholine
Undiagnosed muscular dystrophy and muscular weakness
Muscular weakness due to fasciculation produced by succinylcholine