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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.1
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.2 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.2
Family studies may be done when an individual with a genetically abnormal type is documented by serum pseudocholinesterase deficiency and, ideally, confirmed by phenotyping.
Serum cholinesterase may be decreased in patients on estrogens and oral contraceptives.3 Fluoride interferes.
Pseudocholinesterase is low also in some instances of liver disease, including decompensated cirrhosis, hepatitis, metastatic carcinoma, CHF, and in malnutrition, but not sufficiently consistently enough to be a useful clinical test for such disorders.
Genetic atypical enzyme does not explain every instance of prolonged postsurgical apnea. Red cell cholinesterase is more useful for chronic insecticide exposure. Carbamate-poisoned persons can appear to have near normal or normal levels of pseudocholinesterase.
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.6
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.7
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).8
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.9
1. Hickey DR, O'Connor JP, Donati F. Comparison of atracurium and succinylcholine for electroconvulsive therapy in a patient with atypical plasma cholinesterase. Can J Anaesth. 1987 May; 34(3 Pt 1):280-283. PubMed 3581397 2. Alexiou NG, Williams JF, Yeung HW, Husting EL. Paradoxical elevation of plasma cholinesterase. Am J Prev Med. 1986 Jul-Aug; 2(4):235-238. PubMed 3502583
3. Ladenson JH. Nonanalytical sources of variation in clinical chemistry results. In: Sonnenwirth AC, Jarett L, eds. Gradwohl's Clinical Laboratory Methods and Diagnosis. 8th ed. St Louis, Mo: Mosby-Year Book Inc;1980:160.
4. Evans RT, Wroe J. Is serum cholinesterase activity a predictor of succinyl choline sensitivity? An assessment of four methods. Clin Chem. 1978 Oct; 24(10):1762-1766. PubMed 699286
5. Evans RT, MacDonald R, Robinson A. Suxamethonium apnoea associated with plasmapheresis. Anaesthesia. 1980 Feb; 35(2):198-201. PubMed 7386837
6. Ostergaard D, Viby-Mogensen J, Hanel HK, Skovgaard LT. Half-life of plasma cholinesterase. Acta Anaesthesiol Scand. 1988 Apr; 32(3):266-269. PubMed 3364151
7. Kambam JR, Horton B, Parris WC, Hyman SA, Berman ML, Sastry BV. Pseudocholinesterase activity in human cerebrospinal fluid. Anesth Analg. 1989 Apr; 68(4):486-488. PubMed 2929981
8. Zakut H, Even L, Birkenfeld S, Malinger G, Zizling R, Soreq H. Modified properties of serum cholinesterases in primary carcinomas. Cancer. 1988 Feb 15; 61(4):727-737. PubMed 3338035
9. Causse E, Vaysse P, Fabre J, Valdiguie P, Thouvenot JP. The diagnostic value of acetylcholinesterase/butyrylcholinesterase ratio in Hirschsprung's disease. Am J Clin Pathol. 1987 Oct; 88(4):477-480. PubMed 3661499
