Trauma-Induced Coagulopathy: Overview of an Emerging Medical Problem from Pathophysiology to Outcomes

Abstract

Coagulopathy induced by major trauma is common, affecting approximately one-third of patients after trauma. It develops independently of iatrogenic, hypothermic, and dilutive causes (such as iatrogenic cause in case of fluid administration), which instead have a pejorative aspect on coagulopathy. Notwithstanding the continuous research conducted over the past decade on Trauma-Induced Coagulopathy (TIC), it remains a life-threatening condition with a significant impact on trauma mortality. We reviewed the current evidence regarding TIC diagnosis and pathophysiological mechanisms and summarized the different iterations of optimal TIC management strategies among which product resuscitation, potential drug administrations, and hemostatis-focused approaches. We have identified areas of ongoing investigation and controversy in TIC management.

Association of Platelets and White Blood Cells Subtypes with Trauma Patients’ Mortality Outcome in the Intensive Care Unit

“…The elderly and those with the comorbidities of HTN (44.5% vs. 34.6%, p < 0.001), CAD (13.3% vs. 6.6%, p < 0.001), and ESRD (9.7% vs. 2.2%, p < 0.001) had a higher risk of mortality outcome. A significantly lower GCS score (median (IQR): 5 [3][4][5][6][7][8][9][10][11][12] vs. 15 [11][12][13][14][15], p < 0.001) and higher ISS (median (IQR): 25 [25][26][27][28][29] vs. 17 [16][17][18][19][20][21][22][23][24], p < 0.001) were observed in the death group than in the survivors group. Under stratification by ISS, significantly fewer dead patients had an ISS of 1-15 and 16-24, and more dead patients had an ISS ≥ 25 than the survivors.…”

“…The immune-inflammatory response has contributed to outcome determination in critically ill patients [12,13]. Coagulopathy induced by major trauma may affect around one-third of trauma patients [14]. Of trauma patients with critical injury, 45.5% of patients had below-normal platelet response to at least one agonist ("platelet hypofunction") at admission, and 91.1% had platelet hypofunction during their stay in the intensive care unit (ICU) [15].…”

“…Of trauma patients with critical injury, 45.5% of patients had below-normal platelet response to at least one agonist ("platelet hypofunction") at admission, and 91.1% had platelet hypofunction during their stay in the intensive care unit (ICU) [15]. The development of trauma-induced coagulopathy would lead to secondary bleeding from a widespread microvascular hemorrhage that was not localized to the site of injury [14]. Many studies have demonstrated that severe trauma may also result in remarkable blood loss and lead to platelet consumption [16][17][18].…”

Mild Head Trauma (MHT) and Antiplatelet Therapy. Reply to Lorenzati et al. Comment on “Savioli et al. Mild Head Trauma: Is Antiplatelet Therapy a Risk Factor for Hemorrhagic Complications? Medicina 2021, 57, 357”

“…A recent study shows, using mouse models, BDMV's rapid release into the circulation associated with a state of systemic hypercoagulability, which rapidly evolved into consumption coagulopathy [42]. It may seem that the strong procoagulant effect may be due to an expression of the large tissue factor and phosphatidylserine, and the infusion of these substances leads to a hypercoagulable state in no-trauma mice [42]. Some reports detected fibrinogen degradation product even before the alteration of prothrombin time (PT) and partial thromboplastin time (PTT).…”

“…It can be understood as a release of substances triggered by brain damage through the affected blood–brain barrier (BBB). Through ischemic and inflammatory lesions, the trauma can increase the permeability of the BBB, the process carried out by the endothelial cell junction proteins, such as claudins [ 40 ] and junctional adhesion molecules [ 10 , 42 ]. This increase in permeability causes fluid leakage and consequent cerebral edema.…”