Evaluate preoperative patients for succinylcholine (suxamethonium) anesthetic sensitivity, genetic or secondary to insecticide exposure, in appropriate circumstances. To prevent or evaluate prolonged anesthetic effect, prolonged apnea, after surgery. Very small amounts (0.04−0.06 mg/kg) of succinylcholine are needed to obtain 90% of neuromuscular blockade in patients with low levels of plasma cholinesterase activity.
Monitor organophosphorous or carbamate insecticide poisoning, in which level is decreased; establish patient's baseline value before exposure. Indications include such pesticide exposure, especially with miosis, blurred vision, muscle weakness, twitching, and fasciculation, bradycardia, nausea, diarrhea, vomiting, salivation, sweating, pulmonary edema, arrhythmias, and convulsions. The value of assessing risk status in persons exposed to organophosphate insecticides on the basis of plasma or serum cholinesterase levels alone has been called into question. Are normal levels indicative of no exposure or of a genetic variant with or without exposure? There are interpretive problems with low or high values.
Family studies may be done when an individual with a genetically abnormal type is documented by serum pseudocholinesterase deficiency and, ideally, confirmed by phenotyping.
Ambient (preferred) - 14 days
Refrigerated - 14 days
Frozen - 14 days
Spectrophotometry (Ellman) - kinetic
1 day – 5 yrs: Not established
6 – 17 years: 1396−3282 U/L
18 – 70 years: 1801−3537 U/L
≥ 71 years: 903−2964 U/L
1 day – 1 yr: Not established
2 – 12 years: 1649−2940 U/L
13 - 50 years: 1247−2978 U/L
51 - 80 years: 1355−3299 U/L
≥ 81 years: Not established
Two types of cholinesterase are found in blood: “true” cholinesterase (acetylcholinesterase) in red cells and “pseudocholinesterase” (acylcholine acylhydrolase) in serum (plasma). Low serum cholinesterase activity may relate to exposure to insecticides or to one of a number of variant genotypes. Dibucaine and fluoride numbers are useful to phenotype such homozygous and heterozygous individuals, who are genetically sensitive to succinylcholine.
One patient in 1500 is susceptible to succinyldicholine anesthetic mishap. Evans and Wroe suggest that an enzyme level in serum below 2.5 standard deviations will pick up 90% of sensitive individuals using propionylthiocholine as substrate.4 Rather marked inhibition can be found without symptoms.
Plasmapheresis has been noted to decrease the level of plasma cholinesterase. Patients with abnormally low cholinesterase activity after transfusion of blood or plasma will experience temporary augmentation of enzyme level.5 In estimating the duration of this enhanced activity, measures of plasma cholinesterase half-life have been utilized. The true half-life value has, however, been uncertain. A half-life value determined by measuring the rate of disappearance after intravenous injection of human cholinesterase has provided an average value of 11 days.
A low level of activity of pseudocholinesterase has been demonstrated in cerebrospinal fluid, at about 1/20 to 1/100 the activity present in the corresponding plasma. With clinical conditions characterized by bleeding into the CSF, pseudocholinesterase activity increases to one-fourth to one-half that of plasma.
Patients with a variety of carcinomas have been reported to accumulate an embryonic type of cholinesterase activity in their sera. Such novel cholinesterase activity was found only in the sera of patients undergoing antitumor therapy (eg, chemotherapy or radiation therapy and/or hormone therapy).
Increase in acetylcholinesterase activity, notably, in an acetylcholinesterase:butyrylcholine esterase ratio (histochemical study, not as measured in serum) has provided discriminatory diagnostic value in some cases of Hirschsprung disease.