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AN UNUSUAL CAUSE OF DELAYED RECOVERY FROM NEUROMUSCULAR PARALYSIS DURING GENERAL ANAESTHESIA
 

AN UNUSUAL CAUSE OF DELAYED RECOVERY FROM NEUROMUSCULAR PARALYSIS DURING GENERAL ANAESTHESIA

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    AN UNUSUAL CAUSE OF DELAYED RECOVERY FROM NEUROMUSCULAR PARALYSIS DURING GENERAL ANAESTHESIA AN UNUSUAL CAUSE OF DELAYED RECOVERY FROM NEUROMUSCULAR PARALYSIS DURING GENERAL ANAESTHESIA Presentation Transcript

    • AN UNUSUAL CAUSE OF DELAYED RECOVERY FROM NEUROMUSCULAR PARALYSISDURING GENERAL ANAESTHESIA Dr. Ankit Raiyani Medicine Dept. LTMMC & GH
    • • A 38 yr old woman was operated upon in march 2010 under general anesthesia for excision of tubercular sinus in right hypochondriac area .• She had completed 6 month course of first- line anti-tuberculous treatment 4 months previously, but subsequently suffered from persistent sinus tract formation in the same area .• She had had a laparoscopic cholecystectomy done under spinal anesthesia 4 years previously with an uneventful recovery .
    • • Anesthesia used during the present surgery included induction with propofol and maintenance on O2 + N2O + sevoflurane + atracurium.• Neuromuscular paralysis was attained with succinylcholine .
    • • Pre & intra operative course was uneventful. However, 3 hours post- op, she could not be extubated as voluntary respiratory activity was insufficient despite patient recovering adequately from sedation.• Patient’s vital parameters were well-maintained throughout procedure.• Patient was reversed but not extubated in view of poor tone , poor reflexes and poor power approx. grade 3 (weakness of limbs could not be precisely quantified due to the partial sedation).• She was conscious, with eye opening to command. There was no evidence of autonomic dysfunction. Secretions were not increased and no fasciculations were noted .
    • • Patient was shifted to surgical recovery room & put on volume SIMV mode 12/450/0.6/10/5• Voluntary respiratory activity was regained over a period of 8 hours post-op, and she was successfully extubated 8 hours post -op.
    • • During this period , all metabolic workup was normal- – Na 138, K 3.6, CL-100, – T3-115ng/dL ,T4-10.2ug/dl, TSH-4.53Uiu/ml.• ABG :-PH 7.303,PCO2 52.7, PO2 186, HCO3- 25.3, SPO2 97.6.• Pseudocholinesterase level done 4 hour post op was 357.30 U/L .[reference range 7000- 19000 U/L] .
    • • She was seen in neurology OPD 1 week later , at which time there were no fasciculations , motor power and reflexes were normal , and there was no clinical evidence of fatigability.• Pseudocholinesterase level repeated 6 weeks later continued to be low - 495.6 U/L. Patient was found to be asymptomatic on follow-up.
    • • A final diagnosis of pseudocholinesterase deficiency causing delayed neuromuscular recovery from general anesthesia was made.
    • • This patient represents an unusual cause of delayed recovery from anesthesia.• The usual causes of delayed recovery from anesthesia include overdose of I.V and volatile anesthetics, NM blocking drugs, opioids; hypoxia, hypothermia, electrolyte and endocrinal derangements, hyperglycemia, hypoglycemia, renal and hepatic failure.
    • Pseudocholinesterase(Butyrylcholinesterase) deficiency may be caused by1. Acquired physiological condition like –Neonates, Pregnant women, elderly individual2. Pathological condition –chronic infection like T.B, Extensive burn injuries, liver diseases, Malignancy, malnutrition, Organophosphate insecticide poisoning, uremia3. Iatrogenic causes- Anticholinesterase inhibitor, Bambuterol, Chlorpromazine, Oral contraceptives, Cyclophosphamide, Ecothiopate eye drops, Hexafluorenium, Glucocorticoids, MAO inhibitor, metoclopromide, Pancuronium,4. Inherited Pseudocholinesterase deficiency
    • Pattern of inherited pseudocholinesterase deficiency1 • Inheritance of the disorder has been localised to the butyrylcholinesterase gene on the long arm of chromosome 3, at 3q26.1–26.2.2 • Although often regarded as an autosomal recessive trait, there are more than 60 polymorphisms that broadly yield three categories of abnormal function (usual, atypical and ‘in-between’), that is both alleles are expressed, and this leads to the clinical and biochemical differences between wild-type homozygotes, heterozygotes and homozygous variants.1Pandit, Jaideep J.; Gopa, Satish; Arora, Jason, A hypothesis to explain the high prevalence of pseudo-cholinesterase deficiency in specific population groups. European Journal of Anaesthesiology: August 2011- Volume 28 - Issue 8 - p 550–5521Valle AM, Radid Z, Rana BK, et al. The cholinesterases: analysis by pharmacogenomics in man. Chem BiolInteract 2008; 175:343–345.
    • 1. Atypical/dibucaine-resistant homozygous individuals represent approximately 0.01% of the population; enzyme activity is reduced by 70% and paralysis after administration of succinylcholine lasts for approximately 2 h.2. Fluoride-resistant homozygotes are very rare (<0.001%) and have a 60% reduction in enzyme activity.3. The Kalow variant is the most common (1.5% frequency of homozygotes), but with the least significant clinical implications (only a 30% reduction in enzyme activity).4. Silent-type homozygotes occur with a frequency of 0.008% (i.e. an allele prevalence of ∼0.9% by the Hardy–Weinberg law)4 and completely lack active enzyme. In these patients, induced paralysis can last for up to 8 h.• It has been documented that the geographical prevalence of this last, silent- type, varies significantly, with rare homozygote frequencies of around 1 : 100 000 in people of European descent, but up to 1 : 25 in the Inuits (Eskimo) and Vysyas (of southern India)1 (i.e. an allele frequency of ∼20%).• The specific mutation Leu307Pro of the homozygous silent butyrylcholinesterase gene is approximately 4000-fold higher in the Vysya community than in other populations.1Manoharan I, Boopathy R, Darvesh S, et al. A medical health report on individuals with silentbutyrylcholinesterase in the Vysya community of India. Clin Chim Acta 2007; 378:128–135.
    • Pathophysiology• Pseudocholinesterase is a glycoprotein enzyme, produced by the liver, circulating in the plasma. It specifically hydrolyzes exogenous choline esters• In individuals with normal plasma levels of normally functioning pseudocholinesterase enzyme, hydrolysis and inactivation of approximately 90-95% of an intravenous dose of succinylcholine occurs before it reaches the neuromuscular junction.• In pseudo-cholinesterase-deficient individuals, therefore, significantly higher proportions of succinylcholine molecules reach the neuromuscular junction, and paralysis can last for several hours, requiring prolonged artificial ventilation of the lungs and often admission to the ICU.• There appear to be no other adverse consequences for health in the absence of choline ester drug exposure.
    • Management• This enzyme abnormality is a benign condition unless a person with pseudocholinesterase deficiency is exposed to the offending pharmacological agents.• Administration of choline esters(Succinylcholine, mivacurium) in a Pseudocholinesterase deficient patient: – Patient may require more time to come out of NM blockade and has to be ventilated for prolonged time post-operatively
    • Drugs to be avoided• Choline esters: Succinylcholine(SCh), Mivacurium, Procaine, c ocaine, benzocaine• Pilocarpine• Galantamine, Donepezil, Huperzine A
    • Thank you!!