Dynamics of Ultrasound and Histological Changes in Determining the Rate of Spleen Damage injured in the Absence of Alcohol Intoxication

The article presents data from literary sources and the statistical analysis on the nature, mechanisms and prescription of spleen injury in case of mechanical trauma and the absence of alcohol intoxication in order to improve the diagnosis, treatment and prevention of spleen injuries. According to the literature the frequency of spleen injuries ranges from 15 to 33%. Ultrasound and histological methods are usually used in the long-term follow-up of spleen injuries. The purpose of the work was to study the dynamic changes of ultrasound indexes and histological parameters of injured spleen tissues in various types of mechanical injury, depending on the period of injury. Material and methods. We studied the spleen tissues of 56 people aged from 20 to 60, with known and unknown time of injury, and death occurrence both with and without alcohol intoxication. These people underwent an autopsy in the anatomical department of the Forensic Medical Examination Bureau. In the conducted research we used histological and histochemical techniques to detect dynamic processes of regeneration, and histological parameters of the injured spleen tissues. We also performed statistical analysis of the results. To detect pathological changes in organs and tissues we used ultrasound with frequency from 0.5 to 1.5 million vehicles fluctuations on Sonoace 8000 (South Korea), Sonosite Titan (USA). The abdomen and retroperitoneal area examination was conducted while registering 51 injured people to hospitals, as well as in the dynamics of 1, 2, 3 and 5 days after injury. Results and discussion. The obtained results showed that the mechanical injury of spleen ruptures often developed capsule and parenchyma with a hemorrhage in the area of injury. During the first 6 hours after injury histological examination of the spleen showed orange hematoma in a cluster of erythrocytes with clear contours, central pieces of hematoma had hemolysis of erythrocytes. Closer to the edges of hematoma we observed single leukocytes, and fibrin strands. We also noted that perifocal edema increased by the contours of hematoma. Lekocytic stasis and perifocal accumulation of leukocytes were observed in vessels. Nearby vessels, sinuses, sometimes in the damaged areas showed small clusters of leukocytes not associated with blood vessels. 6-12 hours after injury most red blood cells in the center of injury had vague outlines, some intact erythrocytes were just on the edges of hematoma, the number of granulocytes in hematoma increased and began their destruction. The periphery of hematoma continued accumulation of decaying granulocytes, there appeared strands of fibrin to form clusters for the torus demarcationis which clearly marked areas of damaged parenchyma intact. The sinuses perifocal zone showed focal accumulation of granulocytes. We observed hemolyzed erythrocytes and completely destroyed granulocytes 12-24 hours after the injury. The torus demarcationis was represented with destroyed granulocytes, macrophages with hemosiderin intracellular grains, fibrin strands on the edge of the hematoma intact tissues. Blood clots were detected in the blood vessels. Further, after 2-3 days, there began resorption of erythrocyte destruction products and formation of siderophages. The proliferation of histio-fibroblastic cells and platelets organization in the vessels (the appearance of fibroblasts and blood clots in the blood vessels) started on the border of hematoma with intact tissue. The formation of torus demarcationis continued in the form of fuzzy mass of fibrin strands which form delicate collagen fibers including many hemosiderophages.