Massive Posttraumatic Bleeding: Epidemiology, Causes, Clinical Features, and Therapeutic Management

Abstract

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.

Role of Monocyte-to-lymphocyte Ratio, Mean Platelet Volume-to-Platelet Count Ratio, C-Reactive Protein and Erythrocyte Sedimentation Rate as Predictor of Severity in Secondary Traumatic Brain Injury: A Literature Review

“…This leads to platelets being nonresponsive to AA stimulation. Overactivation of coagulation leads to consumptive coagulopathy and decreased of hyperactive platelet [73], [74]. In the other hand, to maintain the hemostasis balance, plasmin is activated and causing fibrinolysis and clot lysis [60].…”

Main Complications of AECHB and Severe Hepatitis B (Liver Failure)

“…D-dimer will have an apparent increase with the occurrence of secondary fibrinolysis, but D-dimer test shows negative when primary hyperfibrinolysis occurs. Monitoring the above molecular markers dynamically is helpful to estimate therapeutic efficacy and guide treatment [ 154 ].…”

Diagnosis and Management of Ischemic Heart Disease

“…The abrupt onset of irreversible ischemic injury is most frequently associated with erosion, fissuration, or rupture of a coronary plaque, which is followed by intracoronary thrombosis (i.e., AMI type 1, "spontaneous"). 2 Nonvascular conditions that can contribute to ischemia include a negative imbalance between blood demand and supply (AMI type 2) 2 or coronary artery spasm (i.e., variant angina), 3 infections, 4 massive bleeding, 5 social drugs such as marijuana and cocaine, 4,6 complications of revascularization procedures (AMI types 4 and 5), or other severe illness. Finally, AMI type 3 is defined as cardiac death due to myocardial infarction.…”