SUCCINYLCHOLINE
The use of succinylcholine is not contraindicated in:
| A | Tetanus | |
| B | Closed head injury | |
| C | Cerebral stroke | |
| D | Hepatic failure |
The use of succinylcholine is not contraindicated in:
| A | Tetanus | |
| B | Closed head injury | |
| C | Cerebral stroke | |
| D | Hepatic failure |
Cerebral stroke
A 70 kg, 34-yr old athlete is undergoing emergency laparotomy. Due to non-availability of vecuronium bromide, the surgery was conducted under intermittent doses of succinylcholine (total dose: 640 mg) After surgery, there were no respiratory movements and the patient was unable to move his limbs. What was the cause?
| A |
Pseudocholinesterase deficiency causing prolonged action of succinylcholine |
|
| B |
Type II depolarizing block caused by succinylcholine |
|
| C |
Undiagnosed muscle dystrophy complicated by succinylcholine |
|
| D |
Fasciculations produced by succinylcholine |
The only depolarizing type of neuromuscular blocker in clinical use is succinylcholine (SCh).
| A |
Hypokalemia |
|
| B |
Hyperkalemia |
|
| C |
Both of the above |
|
| D |
None of the above |
Administration of succinylcholine to an otherwise well individual for an elective surgical procedure increases plasma potassium levels by approximately 0.5 mEq/dL.
This increase in potassium is due to the depolarizing action of the relaxant.
With activation of the acetylcholine channels, movement of sodium into the cells is accompanied by movement of potassium out of the cells.
| A |
Muscular Dystrophy |
|
| B |
Aortic aneurysm |
|
| C |
Abdominal Sepsis |
|
| D |
Burns |
- Burn injury
- Massive trauma
- Severe intra abdominal infection
- Spinal cord injury
- Encephalitis
- Stroke
- Guillain-Barré syndrome
- Severe Parkinson’s disease
- Tetanus
- Prolonged total body immobilization
- Ruptured cerebral aneurysm
- Polyneuropathy
- Closed head injury
- Hemorrhagic shock with metabolic acidosis
- Myopathies (eg, Duchenne’s dystrophy)
All of the following statements about neuromuscular blockage produced by succinylcholine are true, Except
| A |
No fade on Train of four stimulation |
|
| B |
Fade on titanic stimulation |
|
| C |
No post titanic facilitation |
|
| D |
Train of four ratio >0.4 |
B i.e. Fade on titanic stimulation
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 ‑
| A |
Pseudocholinesterase deficiency increasing action of syccinylcholine |
|
| B |
Phase 2 blockade produced by succinylcholine |
|
| C |
Undiagnosed muscular dystrophy and muscular weakness |
|
| D |
Muscular weakness due to fasciculation produced by succinylcholine |
B i.e. Phase 2 blockade produced by succinylcholine
– Sch is depolarizing/ non competitiveQ M.R. with shortest 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 Hyperthermia)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 (particularly 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.
| A | Succinylcholine & Halothane predisposes | |
| B |
Dantrolene usefull in all cases |
|
| C |
Ketanserine can be used as an alternative to Dantrolene |
|
| D |
a and b |
A i.e. Succinyl choline & halothane predispose B. i.e. Dantrolene useful in all cases
The use of succinylcholine is not contraindicated in:
| A |
Tetanus |
|
| B |
Closed head injury |
|
| C |
Cerebral stroke |
|
| D |
Hepatic failure |
D i.e. Hepatic failure
An eye surgery was performed using propofol as the intravenous anesthetic agent and succinylcholine as the muscle relaxant. Recovery from anesthesia was uneventful. However, after 8 hours of surgery, patient complained of pain in legs on walking. Which of the following is the most likely reason for this?
| A |
Propofol |
|
| B |
Succinylcholine |
|
| C |
Due to surgery |
|
| D |
Early mobilization |
Ans. b. Succinylcholine
Succinylcholine is a short acting depolarizing muscle relaxant, which causes initial fasciculations during induction. It can
cause muscle soreness and postoperative muscle pain.
Succinylcholine (Scoline, Suxamethonium or Diacetylcholine)
Suxamethonium chloride, a dicholine ester of acetyl choline
A clear, colorless aqueous solution of pH 3.0-5.0 with a shelf life of 2 years
Stored at 4C
spontaneous hydrolysis occurs in alkaline or warm conditions
Alternative to succinylcholine which muscle relaxant can be used while endotracheal intubation
| A |
Atracurium |
|
| B |
Pancuronium |
|
| C |
Mivacurium |
|
| D |
Vecuronium |
Ans. is ‘c’ i.e., Mivacurium
Succinylcholine causes hyperkalemia in patients with ‑
| A |
Burn |
|
| B |
Severe infection |
|
| C |
High velocity trauma |
|
| D |
All of the above |
Ans. is’d’ i.e., All of the above
Phase II block is seen with –
| A |
SCh infusion |
|
| B |
Single dose SCh |
|
| C |
Mivacurium |
|
| D |
None of the above |
Ans. is ‘a’ i.e., SCh infusion
- Under certain conditions depolarizing agents produce dual mechanism of neuromuscular blockade which can be divided into two phases :
a. Phase I block
- Rapid in onset
- Result from persistant depolarization of muscle end plate.
- Has classical features of depolarization block.
- Block is not antogonized by anticholinesterases (neostigmine).
b. Phase II block
- Slow in onset
- Results from desensitization of receptor to ACh.
- Resembles block produced by competitive blockers.
- Block is partially reversed by anticholinesterases (Neostigmine).
- In man normally only phase I block is seen -4 typical depolarizing block.
- Phase II block is seen when fluorinated anaesthetics have been given or when SCh is injected in high dose or infused continuously.
- SCh also produces phase II block in patients with atypical or deficient pseudocholinesterase.
