Traumatic Coagulopathy in Dogs

Traumatska koagulopatija u pasa kao izrazito endogeno stanje razvija se rano u posttraumatskom razdoblju (≤ 1 sat). Neposredna i rana smrtnost uzrokovane traumom posljedica su primarno ozljeda mozga ili značajnog gubitka krvi (hemoragičnog šoka), dok su uzroci kasnijoj smrtnosti posljedica sekundarnih ozljeda mozga te neuspjeli imunološki odgovor organizma pacijenta. Prve nokse (hipoksija, hipotenzija, ozljede organa i mekih tkiva, frakture) a kasnije i sekundarne posljedice (ishemija, reperfuzijske ozljede, operativni zahvati, infekcije) potiču obrambeni odgovor organizma na doživljenu traumu. Obrambeni odgovor sastoji se od lokalnog i sustavnog oslobađanja proupalnih citokina, metabolita arahidonske kiseline, proteina koagulacijskog sustava, komplementa i proteina akutne faze a također i hormonalnih medijatora. Prema kliničkim parametrima, takav imunološki odgovor definira se kao sistemni upalni odgovor (SIRS). Paralelno sa proupalnim medijatorima oslobađaju se i protuupalni medijatori čineći takav odgovor kompenzatorno protuupalnim sindromom (CARS). Neravnoteža između dva navedena odgovora imunološkog sustava, smatra se uzrokom posljedične disfunkcije organa odnosno organizma kao i povećanu prijemljivost infekcijama. Akutna traumatska koagulopatija je dinamičan proces multifaktorijalne prirode. Čini se kako su opsežne ozljede tkiva u kombinaciji sa sistemnom hipoperfuzijom dva glavna pokretača ATC. Međutim aktivacija neurohormonalnog odgovora, sustavne upale i diseminiranih endotelnih oštećenja također mogu imati bitnu ulogu kao čimbenici razvoja. Hemodilucija, metabolička acidoza i hipotermija dodatno sprječavaju reanimativne napore, ali se ne smatraju pokretačima akutne traumatske koagulopatije. Oštećenje stanica endotela, nakupljanje leukocita, diseminirana intravaskularna koagulopatija (DIC) sa smetnjama u mikrocirkulaciji vode do apoptoze i nekroze stanica parenhimskih organa sa razvojem sindrome multiple organske disfunkcije (MODS) odnosno do zatajenja više organa (MOF).Traumatic coagulopathy in dogs as a highly endogenous condition develops early in the post- traumatic period (≤ 1 hour). Immediate and early trauma mortality is primarily due to brain injury or significant blood loss (hemorrhagic shock), while late mortality is caused by secondary brain injury and failure of the patients immune response. First hits (hypoxia, hypotension, organ and soft tissue injuries as well as fractures) and later, secondary hits (ischemia, reperfusion injuries, surgery interventions, infections) stimulate patients defence response to experienced trauma. The defence response consists of the local and systemic release of pro-inflammatory cytokines, arachidonic acid metabolites, proteins of the contact phase and coagulation cascade, complement and acute- phase proteins and also hormonal mediators. According to clinical parameters such an immune response is defined as a systemic inflammatory response syndrome (SIRS). In parallel with the pro-inflammatory mediators, anti- inflammatory mediators are released making such a response the compensatory anti- inflammatory syndrome (CARS). An imbalance between the two responses of the immune system is considered to be the cause of the consequent organ disfunction as well as the increased susceptibility to infections. Acute traumatic coagulopathy is a dynamic process of a multifactorial nature. Combination of the extensive tissues injuries as well as systemic hypoperfusion appear to be two major drivers of ATC. However activation of the neurohormonal response, systemic inflammation and disseminated endothelial damage may also play an essential role as development factors. Hemodilution, metabolic acidosis and hypothermia inhibit resuscitation efforts but are not considered to be the drivers od ATC. Endothelial cell damage, accumulation of leukocytes, disseminated intravascular coagulopathy with disorders of microcirculation leads to apoptosis and necrosis of parenchymal organ cells with development of multiple organ dysfunction syndrome (MODS), or multiple organ failure (MOF)