POLYTRAUMA AND MASSIVE BLEEDING – CASE REPORT

Trauma je vodeći uzrok smrti i invalidnosti u osoba ispod 45 godina života te ujedno i najčešći razlog za primjenu masivne transfuzije. U ovom radu prikazujemo bolesnika ozlijeđenog nakon naleta vlaka, u teškom hemoragičnom šoku s pratećom traumatskom ozljedom mozga kod kojeg je primijenjen koncept kontrole štete resuscitacijom. Tijekom zahvata bolesnik je primio 6500 mL kristaloidnih i 1500 mL koloidnih otopina, 22 doze KE, 17 doza svježe smrznute plazme (SSP), 20 doza trombocita (Tr) i 5 doza krioprecipitata. Ordinirana je traneksamična kiselina te rekombinantni faktor VII. Uz obilnu nadoknadu krvi i krvnih pripravaka, vazoaktivnu potporu noradrenalinom, sistolički tlak se održavao između 50 i 90 mm Hg. Kontrolni laboratorijski nalazi ukazivali su na zadovoljavajuću krvnu sliku, ali uz progresiju koagulopatije te izraženu metaboličku acidozu. Usprkos masivnoj transfuziji i intenzivnoj terapiji bolesnik je preminuo zbog sekundarnog intracerebralnog krvarenja, edema i hernijacije mozga kao posljedica izravne traume mozga, a djelomično zbog razvoja koagulopatije. Zbrinjavanje politraumatiziranih bolesnika zahtijeva multidisciplinski pristup usmjeren na brzu kontrolu krvarenja, sprječavanje razvoja koagulopatije te održavanje odgovarajuće perfuzije mozga i ostalih organa. Poseban oprez potreban je kod bolesnika s pridruženom traumatskom ozljedom mozga koja dodatno povećava učestalost koagulopatije, a time i mortaliteta, te je i dalje značajan izazov u kliničkoj praksi.Trauma is the leading cause of death in patients under 45 years of age, and also the most common reason for massive transfusion. In this paper, we report on the management of a polytraumatized patient admitted to emergency department with severe hemorrhagic shock and concomitant traumatic brain injury, in which the damage control resuscitation (DCR) approach was used to promote hemostatic resuscitation. During the procedure, the patient received 6500 mL of crystalline and 1500 mLl of colloid solutions, 22 doses of red blood cells, 17 doses of fresh frozen plasma, 20 doses of platelets and 5 doses of cryoprecipitate. Tranexamic acid and recombinant factor VII were also administered. Systolic pressure was maintained between 50 and 90 mm Hg with abundant administration of packed red blood cells, other blood components and vasoactive support of noradrenaline. Control lab test results showed satisfactory hemoglobin levels with progression of coagulopathy and pronounced metabolic acidosis. Despite massive transfusion and intensive therapy, the patient died due to secondary intracerebral hemorrhage, edema and brain herniation partly as a result of direct brain trauma and partly due to the development of coagulopathy. Treatment of polytrauma patients requires a multidisciplinary approach aimed at rapid control of bleeding, prevention of the development of coagulopathy and maintenance of appropriate perfusion of the brain and other organs. Particular care is needed in patients with associated traumatic brain injury that further increases the incidence of coagulopathy and thus mortality, and remains a major challenge in clinical practice