Coagulopathy in Isolated Traumatic Brain Injury: Myth or Reality

Mathur, Rohan; Suárez, José I.

doi:10.1007/s12028-022-01647-4

Cited by 5 publications

(10 citation statements)

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“…56 57 However, some of these patients develop DIC with a fibrinolytic phenotype at an early stage of trauma, showing high t-PA levels associated with elevated FDP, D-dimer, and FDP/D-dimer ratios and low α2-antiplasmin levels. 54 58 59 Systemic pathologic hyperfibrin(ogen)olysis progresses to fibrinolysis inhibition by increased PAI-1 shortly after injury, which is consistent with DIC with a thrombotic phenotype. 54 58 Development of systemic pathologic hyperfibrin(ogen)olysis may depend on the severity of brain injuries, types of injury (with and without BBB disruption), and areas of injured brain abound with t-PA. 36 53 58…”

Section: Fibrinolytic Phenotypementioning

confidence: 96%

Phenotypes of Disseminated Intravascular Coagulation

Wada,

Gando

2023

Thromb Haemost

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Two phenotypes of disseminated intravascular coagulation (DIC) are systematically reviewed. DIC is classified into thrombotic and fibrinolytic phenotypes characterized by thrombosis and hemorrhage, respectively. Major pathology of DIC with thrombotic phenotype is the activation of coagulation, insufficient anticoagulation with endothelial injury, and plasminogen activator inhibitor-1 (PAI-1)-mediated inhibition of fibrinolysis, leading to microvascular fibrin thrombosis and organ dysfunction. DIC with fibrinolytic phenotype is defined as massive thrombin generation commonly observed in any type of DIC, combined with systemic pathologic hyperfibrinogenolysis caused by underlying disorder that results in severe bleeding due to excessive plasmin formation. Three major pathomechanisms of systemic hyperfibrinogenolysis have been considered: i) acceleration of tissue-type plasminogen activator (t-PA) release from hypoxic endothelial cells and t-PA rich storage pools, ii) enhancement of the conversion of plasminogen to plasmin due to specific proteins and receptors that are expressed on cancer cells and endothelial cells, and iii) alternative pathways of fibrinolysis. DIC with fibrinolytic phenotype can be diagnosed by DIC diagnosis followed by the recognition of systemic pathologic hyperfibrin(ogen)olysis. Low fibrinogen levels, high fibrinogen and fibrin degradation products (FDP) and the FDP/D-dimer ratio are important for the diagnosis of systemic pathologic hyperfibrin(ogen)olysis. Currently, evidence-based treatment strategies for DIC with fibrinolytic phenotypes are lacking. Tranexamic acid appears to be one of the few methods to be effective in the treatment of systemic pathologic hyperfibrin(ogen)olysis. International cooperation for the elucidation of pathomechanisms, establishment of diagnostic criteria, and treatment strategies for DIC with fibrinolytic phenotype are urgent issues in the field of thrombosis and hemostasis.

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Section: Fibrinolytic Phenotypementioning

confidence: 96%

Phenotypes of Disseminated Intravascular Coagulation

Wada,

Gando

2023

Thromb Haemost

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“…The coagulation system is finely tuned process, continuously balancing the mechanisms that promote and prevent clot formation. C-iTBI, a multifactorial entity different from coagulopathy secondary to multisystem trauma without TBI, occurs when these mechanisms are disrupted (6)(7)(8)(9)(10)39). While its pathophysiology has yet to be accurately defined, C-iTBI generally begins within 24 h of admission; the more severe the TBI, the earlier it manifests (40).…”

Section: Cpp Map Icp = −mentioning

confidence: 99%

“…Normal haemostasis involves a delicate balance between mechanisms that promote bleeding and those that try to prevent it, a balance that can be disrupted following TBI. Coagulation disorders in severe isolated TBI (C-iTBI) are common and contribute to secondary damage, mainly due to their role in facilitating the development or progression of both ischemic and haemorrhagic lesions (5)(6)(7)(8)(9)(10). TBI has increasingly come to affect older patients who often present with polypharmacy including antithrombotics and anticoagulants due to multiple comorbidities (11).…”

mentioning

confidence: 99%

“…The incidence of C-iTBI as reported in the literature averages 33%, with figures ranging from 7 to 90%. The disparities in results may be due to differences in study design, lack of uniform definition, varied cohorts, points of the parameters used to define it, concomitant presence of polytrauma, or the time it was analysed (5)(6)(7)(8)(9)(10)12). Nonetheless, based on these figures, we can posit that approximately one of three patients will develop C-iTBI, strongly suggesting its origin in the brain itself (7)(8)(9)(10)12).…”

mentioning

confidence: 99%

“…The presence of C-iTBI adds predictive power to validated prognostic scales (14,15). C-iTBI is associated with poor outcomes in terms of functionality and mortality, which explains why this factor is a key therapeutic target to consider (7)(8)(9)(10)(12)(13)(14)(15)(16). The real implications that early detection and correction of coagulation disorders have in the context of severe TBI remain unknown, however, they open up a wide range of future research possibilities.…”

mentioning

confidence: 99%

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“COAGULATION”: a mnemonic device for treating coagulation disorders following traumatic brain injury—a narrative-based method in the intensive care unit

Quintana-Diaz,

Anania,

Juárez-Vela

et al. 2023

Front. Public Health

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IntroductionCoagulopathy associated with isolated traumatic brain injury (C-iTBI) is a frequent complication associated with poor outcomes, primarily due to its role in the development or progression of haemorrhagic brain lesions. The independent risk factors for its onset are age, severity of traumatic brain injury (TBI), volume of fluids administered during resuscitation, and pre-injury use of antithrombotic drugs. Although the pathophysiology of C-iTBI has not been fully elucidated, two distinct stages have been identified: an initial hypocoagulable phase that begins within the first 24 h, dominated by platelet dysfunction and hyperfibrinolysis, followed by a hypercoagulable state that generally starts 72 h after the trauma. The aim of this study was to design an acronym as a mnemonic device to provide clinicians with an auxiliary tool in the treatment of this complication.MethodsA narrative analysis was performed in which intensive care physicians were asked to list the key factors related to C-iTBI. The initial sample was comprised of 33 respondents. Respondents who were not physicians, not currently working in or with experience in coagulopathy were excluded. Interviews were conducted for a month until the sample was saturated. Each participant was asked a single question: Can you identify a factor associated with coagulopathy in patients with TBI? Factors identified by respondents were then submitted to a quality check based on published studies and proven evidence. Because all the factors identified had strong support in the literature, none was eliminated. An acronym was then developed to create the mnemonic device.Results and conclusionEleven factors were identified: cerebral computed tomography, oral anticoagulant & antiplatelet use, arterial blood pressure (Hypotension), goal-directed haemostatic therapy, use fluids cautiously, low calcium levels, anaemia-transfusion, temperature, international normalised ratio (INR), oral antithrombotic reversal, normal acid–base status, forming the acronym “Coagulation.” This acronym is a simple mnemonic device, easy to apply for anyone facing the challenge of treating patients of moderate or severe TBI on a daily basis.

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