Neurointensive Care of Traumatic Brain Injury Patients Based on Coagulation and Fibrinolytic Parameter Monitoring

Abstract

Coagulopathy, a common complication of traumatic brain injury (TBI), is characterized by a hypercoagulable state developing immediately after injury, with hyperfibrinolysis and bleeding tendency peaking 3 h after injury, followed by fibrinolysis shutdown. Reflecting this timeframe, the coagulation factor fibrinogen is first consumed and then degraded after TBI, its concentration rapidly decreasing by 3 h post-TBI. The fibrinolytic marker D-dimer reaches its maximum concentration at the same time. Hyperfibrinolysis in the acute phase of TBI is associated with poor prognosis via hematoma expansion. In the acute phase, the coagulation and fibrinolysis parameters must be monitored to determine the treatment strategy. The combination of D-dimer plasma level at admission and the level of consciousness upon arrival at the hospital can be used to predict the patients who will "talk and deteriorate." Fibrinogen and D-dimer levels should determine case selection and the amount of fresh frozen plasma required for transfusion. Surgery around 3 h after injury, when fibrinolysis and bleeding diathesis peak, should be avoided if possible. In recent years, attempts have been made to estimate the time of injury from the time course of coagulation and fibrinolysis parameter levels, which has been particularly useful in some cases of pediatric abusive head trauma patients.

A metabolomic and proteomic analysis of pathologic hypercoagulability in traumatic brain injury patients after dura violation

“…The proteomic data additionally showed key increases in antiplasmin and fibrinogen, which correlated to hypercoagulability on thrombelastography. Fibrinogen is known to increase immediately after TBI before a precipitous decline and is believed to participate in destruction of the blood-brain barrier and neuroinflammation 36 . The release of antiplasmin as a result of TBI may be a compensatory mechanism to mitigate intracerebral hemorrhage progression, as previous proteomic work has identified an inversed relationship between antiplasmin and progressive hemorrhagic injury 50 …”

“…This association between fibrinolytic shutdown and TBI may ultimately be driven by tPA resistance and elevated PAI-1 levels 35 . The process of an initial thrombin and fibrin burst following by conversion to fibrinolytic shutdown in TBI is further suggested by a gradual decrease in fibrinogen and D-dimer during the first 3 hours following brain injury, 36 a distinct process from the tissue factor-drive DIC.…”

“…Fibrinogen is known to increase immediately after TBI before a precipitous decline and is believed to participate in destruction of the blood-brain barrier and neuroinflammation. 36 The release of antiplasmin as a result of TBI may be a compensatory mechanism to mitigate intracerebral hemorrhage progression, as previous proteomic work has identified an inversed relationship between antiplasmin and progressive hemorrhagic injury. 50 Limitations to this study include a reliance on steady-state measurements for the omic observations; therefore, conclusions on aberrant metabolic fluxes through glycolysis, Krebs cycle, purine oxidation, and fatty acid/amino acid oxidation, in addition to protein cascades, will require further validation with flux analysis studies based on incubation with stable isotope-label tracers.…”

Age, admission platelet count, and mortality in severe isolated traumatic brain injury: A retrospective cohort study

“…Platelets play a role in the early restoration of the blood–brain barrier after TBI 36 . A relationship between the extent of endothelial injury and the available platelet number at the time of injury is plausible.…”

“…Platelets play a role in the early restoration of the blood-brain barrier after TBI. 36 A relationship between the extent of endothelial injury and the available platelet number at the time of injury is plausible. Since the first explorations of trauma-associated coagulopathy in the early 2000's, studies have suggested that early platelet repletion may have an independent role in survival after TBI, 37,38 though this has never been confirmed.…”