1. AN UNUSUAL CAUSE OF DELAYED
RECOVERY FROM
NEUROMUSCULAR PARALYSIS
DURING GENERAL ANAESTHESIA
Dr. Ankit Raiyani
Medicine Dept.
LTMMC & GH

2. • 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 .

3. • Anesthesia used during the present surgery
included induction with propofol and
maintenance on O2 + N2O + sevoflurane +
atracurium.
• Neuromuscular paralysis was attained with
succinylcholine .

4. • 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 .

5. • 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.

6. • 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] .

7. • 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.

8. • A final diagnosis of pseudocholinesterase
deficiency causing delayed neuromuscular
recovery from general anesthesia was made.

9. • 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.

10. Pseudocholinesterase(Butyrylcholinesterase)
deficiency may be caused by
1. Acquired physiological condition like –Neonates,
Pregnant women, elderly individual
2. Pathological condition –chronic infection like T.B,
Extensive burn injuries, liver diseases, Malignancy,
malnutrition, Organophosphate insecticide poisoning,
uremia
3. Iatrogenic causes- Anticholinesterase inhibitor,
Bambuterol, Chlorpromazine, Oral contraceptives,
Cyclophosphamide, Ecothiopate eye drops,
Hexafluorenium, Glucocorticoids, MAO inhibitor,
metoclopromide, Pancuronium,
4. Inherited Pseudocholinesterase deficiency

11. 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 550–552
1Valle AM, Radid Z, Rana BK, et al. The cholinesterases: analysis by pharmacogenomics in man. Chem Biol
Interact 2008; 175:343–345.

12. 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 silent
butyrylcholinesterase in the Vysya community of India. Clin Chim Acta 2007; 378:128–135.

13. 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.

14. 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

15. Drugs to be avoided
• Choline esters:
Succinylcholine(SCh), Mivacurium, Procaine, c
ocaine, benzocaine
• Pilocarpine
• Galantamine, Donepezil, Huperzine A

16. Thank you!!