Procoagulant activity in patients with isolated severe head trauma

Abstract

Within 6 hrs after severe isolated head trauma, systemic procoagulant overflow from the traumatized cerebral microvasculature proceeds to the thrombin level and is then inhibited by antithrombin III. Regional and systemic hypercoagulability and increased D-dimer concentrations appear to be common among head trauma patients. Increased procoagulant and consecutive fibrinolytic turnover may, therefore, spark disseminated intravascular coagulation in this patient group.

Acute Coagulopathy in Isolated Blunt Traumatic Brain Injury

“…These results correspond to prior investigations demonstrating that the magnitude of brain trauma plays an important role for the development of coagulation disorders after TBI [5,8,13,32,34]. GCS has been applied previously by several investigators to define the severity of TBI [3,8,9,32].…”

Systemic Platelet Dysfunction Is the Result of Local Dysregulated Coagulation and Platelet Activation in the Brain in a Rat Model of Isolated Traumatic Brain Injury

“…In addition, increases in thrombin-antithrombin complex have been identified in cerebrovenous blood in patients with isolated severe head injury. 4 Therefore, local activation of blood coagulation in the brain can have profound systemic effects on platelet function, and its sustained activation can lead to poor clinical outcomes.…”

“…1 This is especially the case when it occurs in the acute phase of TBI (within 12 h after injury). 2 The underlying mechanisms for the TBI-induced coagulopathy are not completely understood but may involve release of tissue factor (TF) from the brain, a rich source of this protein, 3 or even from damaged vasculature, 4 dysregulated fibrinolysis, shock, or hypoperfusion 5 with downstream effects on platelet function. Acute coagulopathy is prevalent in cases of severe TBI ( > 60%), but uncommon in mild head injury ( < 1%).…”

Coagulopathy as a parameter to predict the outcome in head injury patients – analysis of 61 cases

“…22 The accelerated PTT may be caused by the presence of tissue thromboplastin, activated coagulation factors and diminished levels of coagulation inhibitors in the plasma as a result of head injury which activate the coagulation mechanism. 23 Combined accelerated PTT and elevated D-dimer can be considered as hypercoagulation state in the early stage of coagulopathy after head injury. Fibrinogen quantification provides information about the integrity of the final common pathway to hemostasis.…”