Acta anaesth. scand. 1975, 19, 159-168

Serum Cholinesterase Activity in Burned Patients I: Biochemical Findings J. VIBY-MOGENSEN, H. K. HANEL,E. HANSEN, B. S0RENSEN and J. GRAAE Department of Anaesthesia, Rigshospitalet, Department of Clinical Chemistry, Bispebjerg Hospital, Department of Anaesthesia, Municipal Hospital, Department of Plastic Surgery and the Burns Unit, Municipal Hospital; all University Hospitals of Copenhagen University, Copenhagen, Denmark

The purpose of the study was to determine the magnitude and the aetiology of alterations in serum cholinesterase activity (pseudocholinesterase) in burned patients. Sixty burned patients with an estimated area of burn between 3 and 72% of body surface were investigated. Serum cholinesterase activity, serum albumin concentration and serum bilirubin were measured a t various time intervals. The magnitude as well as the rate of fall of serum cholinesterase activity was found to be closely correlated with the severity of burn injury. Minimum levels were often reached 5 to 6 days after the burn injury, at which time the activity might have been depressed by more than 80 per cent. In the most severely burned patients, the activity sometimes remained low for months despite wound healing. Apart from the severity of the burn injury in the individual patient, several important factors determined the level of serum cholinesterase activity at a given time. These included the presence or absence of local or systemic infections, the event of recent surgery such as slough removal or skin grafting, and blood transfusions. The decrease in serum albumin concentration following the burn injury occurred earlier than the decrease in serum cholinesterase activity. Minimum levels were often reached during the first 24 h, after which time the concentration rose to reach fairly constant but decreased levels after 4 to 5 days. Apart from this initial phase, the changes in serum albumin concentration were roughly proportional to the changes in serum cholinesterase activity. The possible reasons for these findings are discussed.

Received 10 October 1974. acceptedf o r publication 22 Junuury 1975

Hyperkalaemia associated with various cardiac arrhythmias following the administration of suxamethonium is a well known complication of anaesthesia in burned patients (TOLMIE et al. 1967, BIRCHet al. 1969). I t has been suggested that this abnormal increase in serum potassium arises from an increased sensitivity of muscle to suxamethonium, possibly caused by denervation or disuse et al. 1973, SIKERet al. atrophy (GRONERT 1969). The effect of suxamethonium, i.e., the duration of apnoea after intravenous injection, depends, however, upon the serum cholinesterase activity. Low serum cholinesterase activity in burned patients has been

reported (BUSH1964, LAING& BARTON1966, ARTURSON 1967, PRICEet al. 1970), but it is not known whether this low activity influences the changes in serum potassium after suxamethonium administration. The main purpose of our study was to determine the magnitude and the aetiology of alterations in serum cholinesterase activity in burned patients and to correlate the enzyme activity with the reaction to intravenous injection of suxamethonium during anaesthesia. The present report concerns the changes in enzyme activity. The relevance of these changes to anaesthetic management of the burned patient will be discussed in a subsequent paper.

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J, VIBY-MOGENSEN, H. K. HANEL, E. HANSEN, B. S0RENSEN AND J. GRAAE

MATERIAL AND METHODS Patients and therapy Sixty patients admitted to the Burns Unit, Municipal Hospital, Copenhagen during the period from March 1, 1972 to October 31, 1973 were studied. Of these patients, 20 were female and 40 were male with an average age of 38 years (range: 11-82). The estimated area of burn (E.A.B.) varied between 3 and 72% of the body surface area. The main principle of topical therapy was exposure of all burned areas (SBRENSEN & THOMSEN 1968). Patients who required anti-shock therapy (adults with an E.A.B. exceeding 15% and children with an E.A.B. exceeding 10%) were given Dextrana or Ringer's lactate (HALL& SBRENSEN 1973). Whole blood was given when necessary, but plasma or plasma derivatives were never used to correct hypoproteinaemia. A careful check was kept on the calorie and protein intake, and a balance sheet was kept by the Hospital Laboratory of Nutritional Physiology. The patients were divided into three groups according to their burn indexes (B.I.) estimated according to the following formula : B.I. = Per cent area full skin thickness burn+ 4x per cent area partial thickness burn. Group 1 included 31 patients whose B.I. was less than 15. Group 2 consisted of 15 patients whose B.I. ranged from 15 to 30. Group 3 included 14 patients whose B.I. was more than 30 (maximum 62). The patients were classified according to their physical activity as: a) ambulant (five patients), b) confined to bed but more or less mobile with active physiotherapy (53 patients), and c) confined to bed mostly or totally immobile without active physiotherapy (two patients).

Measurements Blood samples for measuring serum cholinesterase activity, serum albumin concentration and serum bilirubin were drawn immediately upon admission and twice weekly thereafter. I n 28 patients, serum glutamic oxalacetic transaminase (S-GOT), serum glutamic pyruvic transaminase (S-GPT) and serum lactic dehydrogenase (S-LDH) were measured on the second day post-burn and if abnormal monitored twice weekly until normal. The alterations in serum albumin and serum cholinesterase represented changes from the patients normal values expressed in per cent. Normal values were determined in 50 patients from steady values obtained 3 to 9 months after recovery. Therefore, these 50 patients acted as their own controls. I n ten patients, follow-up was impossible. I n these cases, changes were calculated on the basis of means taken from a normal population.

Drugs, which were potential cholinesterase inhibitors, and blood transfusions were recorded and correlated with the cholinesterase activity.

AnalysiJ Serum cholinesterase (acylcholine acyl hydrolasc) was measured according to the procedure described by KALOW & GENEST (1957). I n a recording spectrophotometer with a thermostat setting of 25"C, the changes in light absorbance at 240 nm were plotted against reaction time. Enzymatic activity was then calculated from the slope of the straight line representing micromoles split benzoylcholine versus reaction time in minutes. The activity was calculated per litre of serum (Ujl). Serum albumin was measured according to the method described by DOUMAS (1972). Serum bilirubin was measured using the method OfJENDRASSIK & GROF (1938) modified as described by NOSSLIN(1960) and MICHAELSON (1961). Glutamic oxalacetic transaminase (GOT, Daspartat: 2-oxyglutarate aminotransferase) and glutamic pyruvic transaminase (GPT, L-alanine : 2-oxyglutarate aminotransferase) were assayed by the method of KARMENet al. (1955) and serum lactate dehydrogenase (LDH, L-lactate: NAD-oxyreductase) according to WROBLEWSKI & LADUE(1955).

RESULTS

Serum albumin Fig. 1 shows the levels of serum albumin in all three groups in relation to time after injury. The serum albumin concentration fell immediately following the injury. This initial fall in all three groups as well as the difference between the groups was statistically significant (P

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Fig. 1. Variation in serum albumin expressed as per cent of the patients' normal values in relation to time after injury. Mean values+ s.d. and ranges are shown. Numbers represent the number of observations.

162

J. VIBY-MOGENSEN, H. K. HANEL, E. HANSEN, B. SORENSEN AND J. GRAAE

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163

SERUM CHOLINESTERASE AND BURNS

Serum cholinesterase Inhibitor studies with dibucaine showed all patients to have the normal serum cholinesterase enzyme. Fig. 2 shows the serum cholinesterase activity which decreased in all three groups. This decrease as well as the difference between the groups was statistically significant (P 15), the average activity after 6 days was 32% of normal (range: 15 to 56%). Several patients in all three groups received blood transfusions in connection with surgical procedures at about the 10th to 16th day. I n these patients,

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SERUM CHOLINESTERASE AND BURNS

transfusions. Infections, whether local or systemic, always tended to depress enzyme activity. Slough removal was normally followed by a transient decrease in activity, whereas successful grafting resulted in increasing activity. A transient increase was often seen after blood transfusions. Fig. 4 illustrates the importance of these factors, showing the alterations in serum cholinesterase activity in a patient with B.I. of 28. Neither sex nor age influenced the changes occurring in serum cholinesterase activity. Our study did not provide the basis for any conclusion concerning the possible connection between physical activity and serum cholinesterase depression. However, in five ambulatory patients we found the same percentage of decrease in activity as in other nonambulatory patients with the same degree of burn injury.

Liver function Four of the 60 patients (6.6%) showed a transient increase in serum bilirubin (maximum: 3.2 mg/l00 ml; normal: 0.4-1.0 mg/ 100 ml). This increase was found on the 2nd

day post-burn in two patients (Table 3) and on the 5th and 14th day, respectively, for the other two patients. I n all four patients, a normal serum bilirubin was regained within 10 days. Tables 2 and 3 show the values for S-GOT, S-GPT, S-LDH and serum bilirubin found on the second day post-burn in ten of the 28 patients investigated. I n the remaining

Table 2 Connection between burn index and the finding of abnormal values on the second post-burn day for one or more of the following parameters: serum glutamic oxalacetic transaminase (S-GOT), serum glutamic pyruvic transaminase (S-GPT), serum lactic dehydrogenase (S-LDH) and serum bilirubin. Burn index (B.I.)

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S-LDH

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% of the patient’s U/l

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normal value

S-GPT = serum glutamic pyruvic

166

J. VIBY-MOGENSEN, H. K . HANEL, E. HANSEN, B. S0RENSEN AND J. GRAAE

18 patients, all values measured were normal. S-LDH always returned to normal within 6 to 7 days, whereas raised values for S-GOT and S-GPT were found more than 30 days post-burn.

S-GOT and S-GPT, probably because of a release of these enzymes from burned tissue cells. Abnormal values for S-GOT, S-GPT, S-LDH and serum bilirubin were found in the present study on the second day post-burn (Tables 2 and 3 ) . T o what extent these abnormal values were due to liver cell DISCUSSION damage or to damage of other tissue cells is difficult to determine. Serum albumin concentration However, the serum cholinesterase activity The fall in serum albumin concentration was decreased on the second day post-burn during the first 24 hours may be due to an irrespective of the values for S-GOT, initial extravascular distribution of albumin, S-GPT, S-LDH and serum bilirubin. I n 11 wound losses and a dilution effect due to patients with B.I. below 15 and with otherfluid therapy (ARTURSON 1961, BIRKEet al. wise normal enzymes, the mean serum 1957, 1968) The increase in concentration cholinesterase activity on the second postafter this time is probably attributable to re- burn day was 85% (range: 50 to 100%). absorption of albumin from the interstitial Four out of eight patients with B.I. between space (BIRKEet al. 1968). The most likely 15 and 30 showed abnormal values for explanations for the persistent low albumin S-GOT, S-GPT, S-LDH and serum biliconcentration after the initial phase seem rubin (Table 3). The mean serum cholinto be defective synthesis, increased destruc- esterase activity on the same day in these tion and, in spite of meticulous monitoring of patients was 69% (range: 51 to 88%). the calorie and protein intake, insufficient The corresponding value for the remaining exogenous supply (BIRKEet al. 1968, DAVIES four patients with otherwise normal serum et al. 1962). enzymes was 58% (range: 23 to 85%). As the normal turnover of serum cholinSerum cholinesterase activity esterase is 10 to 14 days (COHEN& WARThe most likely causes of the decrease in RINGA 1957, JENKINS et al. 1967), even a serum cholinesterase activity are : 1) decreased total cessation of enzyme production or enzyme synthesis in or release from the liver release could not in two days cause a fall in due to hepatocellular damage, 2) an initial serum cholinesterase activity to the abovedilution effect due to fluid therapy, 3) mentioned values. Therefore, it seems unincreased catabolism, and 4) increased likely that the rapid initial fall in serum transcapillary losses. choIinesterase activity is due to liver cell damage. Hepatocellular damage. Serum cholinesterase is synthesised in the liver, and hepatocellular Dilution efect and catabolism increase. A more damage therefore influences the serum likely explanation is that this initial fall is & WAL- due at least partly to a dilution effect. cholinesterase activity. ARTURSON LENIUS (1963) have shown that severe burns I n some patients with large fluid infusions, in rats and dogs are followed by liver cell we did in fact find the lowest serum cholindamage. This finding was based on morpho- esterase activity within the first 24 hours. logical and biochemical changes in the liver Cholinesterase metabolism in burned as well as on changes in the activity of orni- patients has to our knowledge not yet been thine carbomyl transferase, GOT, G P T and investigated, but an increased catabolism as alkaline phosphatase in serum, bile and has beenshown to occurwith albumin (DAVIES lymph. Following minor burns, Arturson and et al. 1962, BIRKE et al. 1960) cannot be Wallenius found only a moderate increase in ruled out.

SERUM CHOLINESTERASE AND BURNS

167

Transcapillary losses. Large amounts of albu- include : 1) increased cholinesterase catabolmin are lost from burns as a result of the ism, 2 ) hepatic depression of synthesis and/or increased capillary permeability that occurs release of the enzyme, 3) the presence of (NYL~N & WALLENIUS 1961, DAVIESet al. inhibiting substances in plasma, or a combina1962, BIRKE et al. 1968). Although the tion of all three factors. An increased cholinesterase catabolism at molecular weight of cholinesterase is four to five times that of serum albumin (SVENS- a time when the patient has been back at work for some time is unlikely. Therefore, MARK 1963), this capillary leak may also contribute to the decrease in serum cholin- the prolonged depression of serum cholinesterase activity. The findings of a transient esterase activity seen after wound healing in decrease in serum activity in relation to burned patients appears to be due to either slough removal, together with the increase in 2) a hepatic depression of synthesis or of activity after successful grafting, together with release of the enzyme, or 3) to the presence the highly significant inverse correlation of inhibiting substances in plasma, released between serum cholinesterase activity and for instance from burned tissue. Studies the B.I. (Fig. 3) are all consistent with this concerning the possible presence of such hypothesis. Pilot studies of cholinesterase inhibiting substances in plasma are in progress. activity and albumin content in blister fluid have also suggested that it is reasonable ACKNOWLEDGEMENTS to suppose a considerable loss of cholinThe authors wish to acknowledge the help from the esterase as well as albumin through burned Burn Unit staff physicians and the Anaesthetic areas (MOGENSEN et al., unpublished data). Department staff physicians and from the laboratory Further studies concerning this point are in technicians: Miss A. MORTENSEN, Mrs. F,. CHRISTOFFERSEN, Mrs. G. N 0 R d R D and Mrs. K. VON HAVEN. preparation. This study was supported by a grant from the Danish The increased capillary permeability is, MedicaI Research Council. however, not restricted to the burn area in moderate and severe burns (BIRKE et al. 1960, ARTURSON1961). The interstitial ZUSAMMENFASSUNG fluid volume is markedly increased, and this is Zweck dieser Untersuchung war die Erforschung des responsible for the trapping of at least a part Ausmanes und der Atiologie von Veranderungen der of the albumin lost from the vascular com- Serum-Cholinesterase-Aktivitat (Pseudocholinesterase) bei Patienten mit Verbrennungen. Es wurden 60 partment. This may also be valid for serum Verbrennungspatienten mit einem geschatzten AusmaB cholines terase. der Verbrennung zwischen 3 und 72% der KorperoberProlonged decrease. The prolonged decreased serum cholinesterase activity after the initial phase (Fig. 2) cannot, however, be explained solely as a consequence of losses through the wounds. If this were the case, the serum cholinesterase activity would be expected to be normal within at least 20 to 30 days after wound healing (cf. a turnover time of 10 to 14 days). This return to normal only applied to patients with very small burns. I n severely burned patients, the enzyme activity was often depressed for u p to 3 to 4 months after wound healing. Probable mechanisms for this prolonged depression of serum cholinesterase activity

flache untersucht. Serum-Cholinesterase-Aktivitat, Serum-Albuminkonzentration und Serum-Bilirubin wurden in verschiedenen Zeitabstanden bestimmt. Das AusmaR sowie die Geschwindigkeit des Abfallens der Serum-Cholinesterase-Aktivitat waren in enger Korrelation mit dem Schweregrad der Verbrennung. Die niedrigsten Spiegel wurden oft am 5. bis 6. T a g nach der Brandverletzung erreicht, zu welchem Zeitpunkt die Aktivitat um mehr als 80% reduziert ist. I n den allerschwersten Fallen blieb die Aktivitat manchmal trotz Wundheilung fur Monate erniedrigt. Abgesehen von der Schwere der Verbrennungsverletzung bestimmten beim individuellen Patienten einige wichtige Faktoreu die Hohe der SerumCholinesterase-Aktivitat zu bestimmter Zeit. Diese Faktoren waren das Vorliegen oder Fehlen lokaler oder allgemeiner Infektionen, kurz vorher durchgefuhrte Operationen wie Nekrosenabtragungen odcr Hauttransplantationen, sowie Bluttransfusionm.

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J. VIBY-MOGENSEN, H . K . HANEL, E. HANSEN, B. S0RENSEN AND J. GRAAE

exclusively electrolyte infusion (Ringer lactate). Scand. 3.plast. recnnstr. Surg. 7, 67. JENDRASSIK, L. & GROF,P. (1938) Verinfachte photometrische Methoden zur Bestimmung des Blutbili297, 81. rubins. Biochem. JENKINS, T., BALINSKY, D. & PATIENT,D. W. (1967) Cholinesterase in plasma: First reported absence in the bantu; half-life determination. Science 156, 1748. KALOW,W. & GENEST,K. (1957) A method for the detection of atypical forms of human serum cholinesterase. Determination of dibucaine numbers. Canad. 3. Biochem. 35, 339. KARMEN, A., WROBLEWSKI, F. & LADUE,J. S. (1955) Transaminase activity in human blood. J . din. REFERENCES Invest. 34, 126. ARIURSON, G. (1961) Pathophysiological aspects of the LAING, J. E. & BARTON, G.M. G. (1966) Serum enzyme burn syndrome with special reference to liver injury levels in burned patients. Transactions of the Second and alterations of capillary permeability. Acta chir. International Congress on Research in Burns, Edinburgh scand., Suppl. 274. 1965 ed. A. B. WALLACE & A. W. WILKINSON, ARTURSON, G. (1967) The zymogram in clinical burns. p. 98. Livingstone Ltd., Edinburgh and London. Transactions of the Fourth International Congress MICHAELSSON, M. (1961) Bilirubin determination in on Plastic and Reconstructive Surgery, Rome 1967. serum and urine. Studies on diazo methods and a Excerpta med. (Amst.) Sect, 111, 218. new copperazo pigment method. Scand. J . elin. Lab. ARTURSON, G. & WALLENIUS, G. (1963) The hepatoInvest., Suppl. 56. cellular origin of circulating enzymes in experimental NOSSLIN, B. (1960) The direct diazo reaction of bile burns. Acta chir. scand. 126, 34. pigments in serum. Experimental and clinical BIRCH,A. A., MITCHELL, G. D., PLAYFORD, G. A. & studies. Scand. 3. din. Lab. Invest., Suppl. 49. LANG, C. A. (1969) Changes in serum potassium NYLCN,B. & WALLENIUS, G. (1961) The protein loss response to succinylcholine following trauma. via exudation from burns and granulating wound J . Amer. nied. Ass. 210, 490. surfaces. Acta chir. scand. 97, 122. BIRKE,G., LILJEDAHL, S.-O., PLATIN,L.-0. & REIZEN- PRICE,W. R., WOOD,Mc. D., COOK,F. & GARODISTEIN, P. (1968) Studies on burns IX. The distribuMORE, B. (1970) Enzyme depletion in major thermal tion and losses through the wound of 13'J-albumin burns. Amer. 3. Surg., 120, 671. measured by whole-body counting. Acta chir. scand. SIKER,E. S., WOLFSON, B. & SCHANNER, P. .J. (1969) 134, 27. Muscle relaxants: advances in the last decade. Clin. BIRKE, G., LILJEDAHL,S.-O., PLATIN, L.-0. & Anaesth. 3, 415. WETTERFORS, J. (1960) Albumin catabolism in burns S0RENSEN, B. & THOMSEN, M. (1968) The burns unit and following surgical procedures. Acta chir. scand. in Copenhagen I. Principles of treatment. Scand. 3. 118, 353. plast. reconstr. Surg. 2,3. BIRKE,G., LILJEDAHL, S.-0. & TROELL, L., (1957) SVENSMARK, 0. (1963) Enzymatic and molecular Studies on burns 111. The serum protein pattern and properties of cholinesterases in human liver. Acta nitrogen metabolism. Acta chir. scand., Suppl. 228, 39. physiol. scand. 59, 378. BUSH,G. H. (1964) The use of muscle relaxants in TOLMIE, J. D., JOYCE, T . H . & MITCHELL, G. D. (1967) burnt children. Anaesthesia 19, 231. Succinylcholine danger in the burned patient. COHEN,J. A. & WARRINGA, M. G. P. J. (1957) The Anesthesiology 28, 467. labelling of human serum by 32P-diisopropyl- WROBLEWSKI, F. & LADUE,J. S. (1955) Lactic dephosphorofluoridate (DF32P). Biochimi. biophys. hydrogenase activity in blood. Proc. Soc. ex). Biol. Acta (Amst.) 25, 600. (N.T.) 90,210. DAVIES, J. W. L., RICKETTS, C. R. & BULL,J. P. (1962) Studies of plasma protein metabolism. Clin. Sci. 23, 411. Address : DOUMAS, B. T. (1972) Determination ofserum albumin. Stand. Meth. elin. Chem. 7, 175. J ~ r g e n Viby-Mogensen, M.D. GRONERT, G. A., LAMBERT, E. H. & THEYE, R. A. (1973) The response of denervated skeletal muscle to Department of Anaesthesia Rigshospitalet succinylcholine. Anesthesiology 39, 13. HALL,K. v. & SBRENSEN, B. (1973) The treatment Of Blegdamsvej 9 2 100 Copenhagcn 0 burn shock. A comparative controlled trial of treatDenmark ment by colloid infusion (Dextran-saline), and by Die Serum-Albuminkonzentration nahm nach Brandverletzungen fruher a b als die Serum-Cholinesterase-Aktivitat. Die niedrigsten Spiegel wurden oft schon wahrend der ersten 24 Stunden erreicht, dann stiegen die Werte wieder an, um nach 4-5 Tagen einen zwar erniedrigten, aber ziemlich konstanten Spiegel zu halten. Abgesehen von dieser Fruhphase verliefen die Serum-Albuminkonzentrationen ziemlich gleichlaufend mit den Veranderungen der SerumCholinesterase-Aktivitat. Die moglichen Ursachen dieser Befunde werden diskutiert.