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  1. Discovered by Bovet.
  2. It is the dicholine ester of succinic acid.
  3. Onset of action - 20-30 sec
  4. Duration of action - 3-5 min.
  5. Dose - 1-2 mg / kg (i / v to be given very fast).
  6. Metabolism : Metabolized by plasma - pseudocholinesterase which is synthesized by liver and present in plasma.
  7. Sch. ------------------------------ succinylmonocholine ------------------------------  succinic acid + choline.
  8. Pseudo - cholinesterase levels are reduced in (so prolonging the apnea caused by sch.)
    1. Liver diseases
    2. Pregnancy
    3. Cytotoxic drugs
    4. Organophosphates
    5. Cancer
    6. Neostigmine & Pyridostigmine
    7. Pancuronium
    8. Alkylating agents
    9. Metoclopramide
    10. Uremia, hypoproteinemia, new born, alcoholics, nephrosis
Pseudocholinesterase deficiency is a clinically silent condition in individuals who are not exposed to exogenous sources of choline esters.
Patients with prolonged paralysis following administration of succinylcholine can be treated in the following ways:
  • Mechanical ventilatory support is the mainstay of treatment until respiratory muscle paralysis spontaneously resolves. Recovery eventually occurs as a result of passive diffusion of succinylcholine away from the neuromuscular junction.
  • Prophylactic transfusion of fresh frozen plasma can augment the patient's endogenous plasma pseudocholinesterase activity.
  • Administration of cholinesterase inhibitors, such as neostigmine, is controversial for reversing succinylcholine-related apnea in patients who are pseudocholinesterase deficient. The effects may be transient, possibly followed by intensified neuromuscular blockade.

Dibucaine number

  1. Dibucaine (A local anaesthetics drug) inhibits 80% of normal pseudocholinesterase only, and not the 20% abnormal pseudocholinesterase enzyme;
  2. So Dibucaine no. in normal individual is DN = 80 (which means 80% normal pseudocholinesterase are blocked by the drug).
  3. In Heterozygous patient the normal pseudocholinesterase enzyme is typically 60-70% while in homozygous the normal pseudocholinesterase enzyme is 40-60%, expecting markedly prolonged apnea up to 2 hrs.
  4. Na fluoride can be used in place of Dibucaine (fluoride number)
  5. Normal serum cholinesterase level - 80 units /ml

Mech. of action of Depolarizing agents

Drug acts like Ach; Sch attaching to Ach receptors causing depolarization & action potential --> muscle fasciculations. The time dependent sodium channels in Peri junctional zone becomes refractory & Ach. can’t overcome the inactivated sodium channels in prejunctional zone causing neuromuscular blockade
Side effects.
  1. CVS: Bradycardia (Because of cardiac muscarinic effect stimulation, so atropine should be given prior to its use. Increased chances of ventricular arrhythmia (because of hyperkalemia)
  3. Due to excessive muscular fasciculations
  4. Increases intraocular pressure (due to tonic contractions of eye muscles)
  5. Increases Intragastric pressure (due to abdominal muscle fasciculations)
  6. Increases I.C.T
  7. Muscle pains in post op period. Incidence may vary from 1% to 90% (Av. 40%) These are because of unsynchronized muscle contraction, can be  by
    1. Pre curarization with non - depolarizing agents
    2. Self taming: small amount of suxamethonium is given prior to full dose of scoline
  8. Masseter spasm - seen in children
  9. Anaphylaxis
  10. Malignant hyperpyrexia - Most commonly implicated drug
  1. Contraindication
    1. Hyperkalemia
    2. New borns (Avoid in children)
    3. Head injury
    4. Glaucoma, Penetrating eye injuries (can be used with precurarzation)
      1. Upto 3 months after trauma
      2. Upto 6 months after hemiplegia / paraplegia
      3. Upto 1 year after burns ­ chances of hyperkalemia
    5. Prolong intra - abdominal infection
    6. Renal failure (if Hyperkalemia is existing)
    7. Diagnosed case of low pseudocholinesterase level
    8. Atypical pseudocholinesterase (incidence 1:3000)
    9. If Sch is given to a patient with pseudocholinesterase
    10. Duchenne muscle dystrophy
    11. Dystrophia myotonica
  2. Phase II block: This is a prolonged block seen after sch. It is a dangerous condition seen in.
    1. Overdosage of sch. (>5 mg / kg)
    2. Atypical or low cholinesterase
    3. Anticholinesterase
    4. Features similar to nondepolarizing blockers
Reasons may be
  1. Desensitization of receptor
  2. Channel blockade
  3. Ca2+ mediated injury to end plate

Extra Junctional Receptor

seen in neonates, infants, denervated or injured muscle. These are very sensitive to depolarizing agents (but resistant to NDMR)
  1. NOTE: Acetyl cholinesterase is found at all cholinergic sites, RBCs and grey matter in brain. In contrast, pseudocholinesterase is found in plasma, liver, intestine and white. matter in brain. (MCQ) 
  2. NOTE: SCh is rapidly hydrolysed by plasma pseudocholinesterase to succinyl mono choline and then succinic acid + choline (action lasts 3-5 mm.).
  3. NOTE: In presence of genetically determined abnormality (low affinity for SCh) or deficiency of pseudocholinesterase, SCh causes dominant phase n blockade. (MCQ) 
  4. Note: Abnormal pseudocholinesterase can be detected by determining the ‘Dibucaine number’ in the serum of the individual.

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