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Pseudocholinesterase deficiency (Genetically abnormal pseudocholinesterase…
Pseudocholinesterase deficiency
Causes - reduced levels
Levels<75% needed for prolongation of Sux effect
Physiological
Pregnancy
Due to increased oestrogen
However, the duration of paralysis unchanged (increased VoD)
Neonates
Duration paralysis unchanged
Elderly
Pathological
Liver disease: must be severe before prolonged NMB occurs
Malnutrition
Pharmacological
Chemotherapeutic agents e.g. cyclophosphamide
Anticholinesterases: neostigmine, organophosphates
Metoclopramide, MAOIs
Pancuronium
OCP
Genetically abnormal pseudocholinesterase
Homozygous (Eu Eu)
Freq 96%
Dibucaine number 80
Duration 3-5mins
Heterozygous (Eu Ea)
Freq 1/480
Dibucaine number 40-60
Duration 30mins
Homozygous (Ea Ea)
Freq 1/3200
Dibucaine number 20
Duration > 3 hours
Etiology
A single cholinesterase gene is present: single amino acid subst are responsible for variants in the enzyme
Four main variants: usual, atypical (dibucaine resistant), silent (absent) and fluoride resistant
The dibucaine number reflects the genetic make up for an individual but makes no assessment of the quantity of pseudocholinesterase
In normal patients, dibucaine will inhibit 80% of enzyme activity which corresponds to dibucaine number of 80.
Consequences
Maintenance of anaesthesia and ventilation in a suitable environment
Monitoring of NM function
Possible treatments - recovery may be speeded by administering FFP (source of plasma cholinesterase)
Investigation of patient and family
Implications for future anaesthesia - including potential problems with mivacurium and ester LAs