Abstract
Each fracture of long or pelvic bones as well as large contusions of subcutaneous fat tissue cause releasing of fat globules that rapidly penetrate into circulation through the ruptured veins of the injured tissue, and reach the lung circulation [1,2]. During the first phase, fat emboli block the functional lung circulation by their mechanical effect in capillaries producing so called isolated post-traumatic lung fat embolism [3]. The surface layer of a fat embolus, which is practically in liquid state, behaves as a membrane of very high density, i.e., as it is under high pressure which obstruct the blood stream [4] that is finally stopped at the level of lung blood vessels with diameter of approximately 20 mu [5]. This pathophysiological mechanism produces cor pulmonale acutum, with poor pathological findings [8]. Nowadays, the post-mortem diagnosis of lung fat embolism is based on microscopical examination of tissue specimens, usually prepared with special histological staining (Sudan III) [9]. The grading of fat embolism according to Sevitt's criteria is generally accepted [10]. Taking of slices from apicoventral areas of the lungs has been recommended [11]. With longer outliving period, the total number of fat emboli in the lung circulation gradually decreases, due to their disintegration and resorption. It has been stated that fat globules completely disappear about 4-6 weeks after injury, and that they should not be searched for microscopically in this post-traumatic phase [11]. The aim of our work was to determine whether the age of injured, their gender, total severity of trauma, outliving period, and hypovolemic shock that develops after injuring, may induce development of more severe forms of post-traumatic lung fat embolism. A prospective histological study was performed on the autopsy material of the Institute of Forensic Medicine in Belgrade. The analyzed sample consisted of individuals with injuries that might be a source of fat emboli (fractures of long bones, large contusions of subcutaneous fat tissue). The lung slices were systematically taken and stained with special fat staining (Sudan III). In each particular case, the grade of lung fat embolism was counted on the basis of microscopical appearance, according to Sevitt's criteria. The total severity of trauma was estimated by calculation of the Injury Severity Score (ISS) [13, 14]. In no cases from the analyzed sample, the fat embolism was mentioned as either singular or plural cause of death. The obtained results were analyzed by means of appropriates statistical methods (ANOVA, LSD-test, chi 2 test. Man-Whitney test, Fischer's test of correct probability). The analyzed sample included 58 fatally injured individuals, 39 males and 19 females. The average age was 54.10 years (SD = 16.56), the average value of ISS was 34.69 (SD = 5.88), and the average outliving period was 3.74 days (SD = 5.88). However, all these data look differently when the analyzed sample has been stratified and analyzed according to the estimated grade of lung fat embolism. It was not showed that severity of lung fat embolism depends on sex of the injured (chi 2 = 0.842; p > 0.05). The groups with the slightest and the most severe grade of lung fat embolism are statistically significantly different in relation to age of individuals (ANOVA, p = 0.017). By means of LSD test, it has been showed that the group with the most severe grade of lung fat embolism (grade III) is statistically significantly different comparing to other two groups (with grade I and II) in relation to the age of injured (the values are p = 0.16 and p = 0.19 respectively, and the both groups are less than p = 0.05). In the group with the most severe grade of lung fat embolism, the older individuals are statistically significantly represented comparing to other two groups. The analysis of our sample showed that the most severe grade of post-traumatic lung fat embolism (microscopical grade III according to Sevitt's criteria) was determined in older individuals, more severely injured, and with shorter outliving period. The severity of fat embolism depends neither on sex of the injured, nor on development of post-traumatic hypovolemic shock. The obtained results related to the influence of hypovolemic shock on severity of fat embolism should be accepted with a caution. Namely, sometimes there is an intention to simplify a procedure of creating of autopsy conclusion about the cause of death, so that loss of blood is not mentioned at all, in spite of fact that it could have been a concurrent cause of death, while in other cases exsanguination is designated as a sole cause of death, forgetting the possibility that fat embolism could have really been the immediate cause of death.
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