Massive posttraumatic bleeding: epidemiology, causes, clinical features, and therapeutic management

Giuseppe Lippi, Emmanuel J Favaloro, Gianfranco Cervellin

Research output: Contribution to journalReview articlepeer-review

14 Citations (Scopus)


Bleeding typically results as a consequence of derangements of primary hemostasis, secondary hemostasis, or both, and can be dramatically amplified by the presence of other predisposing conditions, especially inherited bleeding disorders. Life-threatening hemorrhages are, however, almost exclusively caused by penetrating wounds, blunt traumas of chest and abdomen, suicide attempts, amputations, bone fractures with concomitant injury to internal organs and blood vessels, and shearing forces from sudden rotation, violent flexion, extension, or deceleration injuries. The pathogenesis of posttraumatic bleeding is complex and multifaceted. The most dramatic phenomenon that always accompanies major hemorrhages is the abrupt and considerable loss of intravascular volume, that further leads to hypovolemic shock, also known as hemorrhagic shock, culminating with peripheral ischemia, especially in those tissues where oxygen delivery is more critical (i.e., central nervous system and myocardium). The mortality rate of severe posttraumatic bleeding can be as high as 50%, especially when an appropriate treatment is not established in a timely manner. The damage control sequence basically entails a four-step approach including damage control surgery, damage control resuscitation with fluid restoration, and hemocomponents administration, as well as correction of the coagulopathy with platelets, antifibrinolytic (e.g., tranexamic acid), and/or procoagulant agents such as fresh frozen plasma, prothrombin complex concentrate, or recombinant-activated Factor VII.

Original languageEnglish
Pages (from-to)83-93
Number of pages11
JournalSeminars in Thrombosis and Hemostasis
Issue number1
Publication statusPublished - Feb 2013


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