Annals of Burns and Fire Disasters - vol. XII - n° 2 - June 1999

Jackson described three concentric zones of thermal injury in the burn wound, thus providing a practical basis for discussing local burn injury. The central area is termed the zone of coagulation. Extending concentrically from the central zone lies the labile area of injured cells which, under the most ideal circumstances, have the potential ability to survive. The progressive injury that results from dermal ischaernia occurs in this zone, designated by Jackson the zone of stasis. Before the mechanism of progressive dennal ischaemia was understood, cells in this zone routinely progressed to necrosis within 24-48 h post-burn. Lying further peripherally is the zone of hyperaernia, where injury is minimal. A clear relationship between the state of intravascular thrombosis and the degree of burn can be shown by means of cinephotomicrography, for the visualization and photography of the microcirculation of the burn wound. The problems of evaluating the source of coagulation defects in burn patients are numerous. The idea that the progressive changes in the burn wound might be related to inflammation led investigators to study the possible role of inflammatory mediators, especially prostaglandins. Thromboxane is a potent platelet aggregator and vasoconstrictor, which was isolated from burn blister fluid. When the thromboxane response is prevented pharmacologically, platelet adherence is reduced and vasoconstriction is prevented.
Burn patients present significant thromboeytopenia, attributed to the utilization of platelets in the burn area, and toxic depression of the blood-forming organs in response to products arising from tissue destruction and bacterial infection. Thermal injury is known to result in decreased survival and circulatory half-life of the platelets, fibrinogen, and procoagulant factors V and IX, while activated platelets can be detected in the circulation.
The level of platelets is greater in burn patients than in non-burn patients in the pre-surgical period. The increased number of platelets results from stimulation of acute phase reaction protein synthesis by the inflammatory reaction of the burn wound and the secondary messengers, such as cytokines and tymphokines, originating from the burn wound.

Aspirin is a non-steroidal anti-inflammatory salicylate. It irreversibly inhibits the enzyme cyclo-oxygenase, which in platelets is responsible for the conversion of arachidonic acid to thromboxane A2- In vascular wall cells, it is responsible for the conversion of arachidonic acid to prostaglandin 12 (PGI2). Thromboxane A2 induces platelet aggregation and vasoconstriction, while PGI2 inhibits platelet recruitment and induces vasodilatation.
Aspirin is absorbed rapidly in the stomach and upper intestine, with peak plasma levels occurring after 14 to 20 min and inhibition of platelet function within I h. Although aspirin in plasma has a half-life of 15 to 20 min the platelet inhibitory effect lasts for the platelet's life-span (9 to 10 days) because of the irreversible acetylation of platelet cyclo-oxygenase. Graham et al. postulated that since the side-effects of aspirin are dose-dependent and many of the clinical conditions in which aspirin is effective require long-term use ofthe drug, the lowest effective dose should be administered, Aspirin administered in doses of approximately 100 mg/day inhibits both platelet thromboxane A2 synthesis and vascular PGI2 synthesis. According to Herd et al. the recommended antithrombotic dose of aspirin is 150 mg per day. The possible side-effects of aspirin include benign gastric (but not duodenal) ulcer, an increase in the incidence of stomach pain, heart burn, nausea, constipation, and occult gastrointestinal blood loss.
All these conditions may occur at a dose of 900 mg per day or more.

This study was carried out at the Burn Unit of Assiut University Hospital (Egypt) in the period December 1996February 1998. The study regarded twenty patients suffering from recent burns of varying degree covering 15 to 40% TBSA (mean, 27.0 17.3%). The ages ranged from 15 to 45 yr (mean, 26.5 10.5 yr). The patients had no pre-existing medical pathology. The period of study lasted 17 days. Laboratory results were compared with those of a control group comprising 16 healthy subjects. The data were analysed by Student's t-test and the chisquare lest.
The patients were divided into two groups of ten patients each. Patients in the first group (defined as the classic group) received only classical burn management, while those in the second group (defined as the aspirin group) received aspirin in an antithrombotic dose of 150 mg per day in addition to classic burn management. Patient data are presented in Table I.

Assessment was by clinical observation and laboratory tests. The geographical distribution of the wound was observed every other day. Changes in burn depth were determined clinically under the supervision of two physicians with at least ten years experience in burn management. A drug monitoring sheet was used to study any complications related to the medication used.
With regard to laboratory studies, bedside samples of blood were taken from peripheral veins in each patient with two days' time interval between samples. The first sample was obtained within 24 h of the burn and the last on day 17 post-burn. The blood samples were used for the following investigations, which were also effected in the controls: 1. complete blood picture, including haemoglobin, haematocrit, and platelet count; 2. screening tests for coagulation, e.g. prothrombin time and activated partial thromboplastin time; 3. screening tests for fibrinolysis, e.g. fibrinogen and fibrinogen degradation products; 4. specific tests for platelets, i.e. platelet aggregation, platelet size distribution, and B-thromboglobulin.

The patients' demographic data are presented in Table I, which shows that as regards age, sex, and percentage of burn the difference between the classic and the aspirin groups was insignificant. Table II indicates that the difference between the groups as regards the percentage of different degrees of burn on admission was also insignificant.

However, the percentage of healing was significantly better in the aspirin group than in the classic group. This difference was manifest from day 13 postburn until the end of the study (Table III).

The aspirin and the classic group presented insignificant differences as regards the values of the haemoglobin level and haernatocrit.With regard to platelet count (Table IV), the classic and the aspirin group showed a significant increase in comparison with control starting from day 7 post-burn until the end of the study, while aspirin had no effect on platelet count in comparison with the classic group.