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The levels of marker enzymes for liver function, namely transaminases (SGPT, SGOT), creatine phosphokinase (CPK), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were estimated in the sera of burn patients by administering trypsin: chymotrypsin preparation and comparing with an untreated group. Neutrophil proteolytic activity was also measured by assaying the lysosomal enzymes, namely neutrophil elastase and cathepsin D. Our earlier studies have already proved the efficacy of the above enzyme preparation to burn patients on the enhancement of vascular responses during the acute phase of the burn injury. These beneficial responses were brought about by the modulation of acute phase proteins expressed in the liver. Hence, it is of interest to study the changes in the above mentioned liver enzymes and certain lysosomal enzymes in the serum during the first 10 days of burn injury. The levels of liver and lysosomal enzymes markedly decreased in the treated group when compared with the untreated group. The enzyme studies clearly indicated that the initial rise in the liver enzymes was minimized in the treated group when compared with the untreated group and this helped in reducing the stress to the liver in the treated cases. The increase in the activity of alpha 1-antitrypsin and alpha 2-macroglobulin and decreased levels of C-reactive protein are attributed to the reduction of proteolytic enzyme levels in the treated group and minimizing the degradative changes during wound repair.

We immunoenzymometrically measured creatine kinase (CK) isoenzyme MB in extracts of myocardium and in homogenates of five different skeletal muscles. CK-MB concentrations in the former averaged 80.9 micrograms/g wet tissue; in the skeletal muscles it varied widely, being (e.g.) 25-fold greater in diaphragm than in psoas. CK-MB in skeletal muscles ranged from 0.9 to 44 ng/U of total CK; the mean for myocardium was 202 ng/U. In sera from 10 trauma and 36 burn patients without myocardial involvement, maximum ratios for CK-MB mass/total CK activity averaged 7 (SEM 1) ng/U and 18 (SEM 6) ng/U, respectively. Except for an infant (220 ng/U), the highest ratio we found for serum after muscular damage was 38 ng/U. In contrast, the mean maximum ratio determined in 23 cases of acute myocardial infarction exceeded 200 ng/U. Among seven determinations performed 8 to 32 h after onset of symptoms, each infarct patient demonstrated at least one ratio greater than or equal to 110 ng/U. Ratios observed after infarct were unrelated to treatment received during the acute phase. We propose a CK-MB/total CK ratio of 80 ng/U as the cutoff value for differentiating myocardial necrosis from muscular injury.

In the course of a systematic study of serum enzymes activities from muscular tissues, applied to fifty six burnt patients taken at random, the authors have observed a significant and isolated raised of serum CPK in six burnt people when they were admitted to hospital. There were no known causes of raised CPK essentially due to muscular isozyme. The only common point between those six persons is that they all attempted to commit suicide by burning.

Myoglobin is released into the blood after burn injury. We measured it and other analytes in blood collected from 22 burn patients two to seven times during their recovery. There was a significant correlation between myoglobinemia and creatine kinase (CK) activity in serum (r = 0.764; p less than 0.001). In a group of 14 thermal-burn subjects a correlation was found between burn depth (clinically expressed as Unit Burn Surface) and both myoglobinemia (r = 0.825; p less than 0.01) and CK activity (r = 0.686; p less than 0.01). In eight thermal-burn patients who were recovering satisfactorily, myoglobin and CK activity measured on days 2, 4, 7, 10, and 13 after injury were significantly increased (p less than 0.05) on days 2, 4, and 7. Evidently myoglobinemia and CK activity are good biological markers of burn depth, and reflect muscle damage equally well.

Twenty-six patients were evaluated with regard to CPK values in week 1 post-burn. Patients were allocated into two groups based on the severity of burn injury. Group 1 included patients with minor electrical or thermal injury, and Group 2 those patients with deep thermal injury and objective evidence of muscle necrosis. With the exception of day 5 post-burn, Group 2 had significantly increased CPK levels as compared to Group 1. This indicates that CPK levels, especially with electrical and deep thermal burns, are sensitive tests in evaluating the depth of burn injury such that an appropriate pre-operative strategy for debriding and grafting is possible.

Medical records of 53 burn and trauma patients were reviewed to assess the possibility of myocardial damage. Except for electrophoretically detectable creatine kinase MB isoenzyme, none showed evidence of myocardial injury. Lactate dehydrogenase isoenzyme tests, electrocardiograms, myocardial pyrophosphate scans, clinical course, and results of (two) autopsies were all negative for myocardial necrosis or ischemia. Types of patient, number, mean peak value (U/L) for serum creatine kinase, and ranges of percentage MB isoenzyme were as follows. Burns from direct electrical contact: 28, 16 600, 0-29; electrical flash or other thermal burns: 10, 4340, 0-22; blunt trauma (mostly from automobile accidents): 15, 3430, 0-18; myocardial infarction: 57, 1520, 4-46. Evidently creatine kinase MB isoenzyme is nonspecific in burn and trauma patients and should not be the only test result used to assess myocardial involvement.