Bad blood: A coagulopathy associated with trauma and massive transfusion review

Abstract

Coagulopathy in trauma patients is a known contributor to death due to hemorrhage. In fact, it seen as frequently as 35% of the time. The complexity of the coagulopathy pathway requires a deliberate and planned approach. The methods used to assess and detect if a patient is coagulopathic remain challenging, but tools have been developed to assist the practitioner to effectively manage and even quickly reverse the coagulopathy. The purpose of this review is to educate trauma and emergency medicine staff on the currently available diagnostic tools to assess coagulopathy, to provide an overview of the coagulopathy pathway, as well as provide examples of how to intervene and treat coagulopathy, including the use of crew resource management during mass transfusion protocol activations.

Systematic Preventable Trauma Death Rate Survey to Establish the Region-based Inclusive Trauma System in a Representative Province of Korea

“…In addition, this type of problem solving may need to include a more detailed massive transfusion protocol. 23 24 …”

Factors associated with the progression of traumatic intracranial hematoma during interventional radiology to establish hemostasis of extracranial hemorrhagic injury in severe multiple trauma patients

“…[13][14][15][16][17] In isolated traumatic brain injuries, the hyperfibrinolytic state evoked by a brain injury was related to tissue factors released into the blood, microvessel failure, disruption of the blood-brain barrier, platelet-endothelial interaction, and platelet dysfunction. [18][19][20] These conditions activated the blood coagulation system and increased the consumption of blood coagulation factors. Additionally, the release of endogenous plasminogen activator was evoked and hyperfibrinolysis occurred.…”

“…Additionally, the release of endogenous plasminogen activator was evoked and hyperfibrinolysis occurred. [18][19][20] Biomarkers to predict progressive hemorrhagic brain injury in isolated traumatic brain injury have been reported reflecting these responses. 8,21 Nakae et al reported that D-dimer was an important biomarker to predict progressive hemorrhagic brain injury in isolated traumatic brain injury, reaching a peak at 3 h after injury before returning to baseline.…”

“…Previous reports have proposed mechanisms of traumatic intracranial hematoma/hemorrhagic brain contusion progression in patients with head trauma alone 13–17 . In isolated traumatic brain injuries, the hyperfibrinolytic state evoked by a brain injury was related to tissue factors released into the blood, microvessel failure, disruption of the blood–brain barrier, platelet–endothelial interaction, and platelet dysfunction 18–20 . These conditions activated the blood coagulation system and increased the consumption of blood coagulation factors.…”

“…These conditions activated the blood coagulation system and increased the consumption of blood coagulation factors. Additionally, the release of endogenous plasminogen activator was evoked and hyperfibrinolysis occurred 18–20 . Biomarkers to predict progressive hemorrhagic brain injury in isolated traumatic brain injury have been reported reflecting these responses 8,21 .…”