Coagulopathy After Traumatic Brain Injury

Department of Neurological Surgery, University of California, San Francisco, California 94110, USA.
Neurosurgery (Impact Factor: 3.62). 02/2012; 70(6):1334-45. DOI: 10.1227/NEU.0b013e31824d179b
Source: PubMed


Traumatic brain injury has long been associated with abnormal coagulation parameters, but the exact mechanisms underlying this phenomenon are poorly understood. Coagulopathy after traumatic brain injury includes hypercoagulable and hypocoagulable states that can lead to secondary injury by either the induction of microthrombosis or the progression of hemorrhagic brain lesions. Multiple hypotheses have been proposed to explain this phenomenon, including the release of tissue factor, disseminated intravascular coagulation, hyperfibrinolysis, hypoperfusion with protein C activation, and platelet dysfunction. The diagnosis and management of these complex patients are difficult given the lack of understanding of the underlying mechanisms. The goal of this review is to summarize the current knowledge regarding the mechanisms of coagulopathy after blunt traumatic brain injury. The current and emerging diagnostic tools, radiological findings, treatment options, and prognosis are discussed.

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    • "An inhibition of coagulation and activation of fibrinolysis through activation of protein C triggered by hypotension has also been reported [11]. However , evidence for coagulopathy and abnormal fibrinolysis after severe TBI has also been documented, despite isolated head injury cases generally being accompanied by a lack of massive hemorrhage or infusion [2] [3]. The mechanism of coagulopathy and abnormal fibrinolysis after severe TBI has not been elucidated, but several hypotheses have been suggested [12]. "
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    ABSTRACT: Careful course observation is necessary for cases of mild to moderate traumatic brain injury even when disturbed consciousness is mild on admission. This is because delayed enlargement of hematoma and progression of cerebral swelling may occur and result in an emergency craniotomy. Here, we investigated coagulopathy and abnormal fibrinolysis as a predictive factor of “deterioration requiring surgery” in mild to moderate traumatic brain injury.Patients and methodsSixty-one patients with mild to moderate (Glasgow Coma Scale (GCS) score 9–15) traumatic brain injury were admitted between June 2009 and October 2010. There were 54 subjects in the study, excluding those treated with oral antiplatelet agents and anticoagulants. Patients were classified into those with deterioration requiring surgery [op(+)] or those without deterioration requiring surgery [op(−)]. This was based on whether surgical treatment was performed for hematoma expansion, and exacerbated consciousness level within 3 days after admission. Age, GCS score on admission and blood test findings (platelet count, PT-INR, APTT, fibrinogen, FDP, and d-dimer) on admission were compared.ResultsThe op(+) and op(−) groups comprised 7 (13.0%) and 47 patients (87.0%), respectively. Platelet counts (24.8 vs 18.5 × 104/μl) were decreased, and PT-INR (1.0 vs 1.2) was higher in the op(+) group. Specially, APTT (28.6 vs 39.1 s), FDP (28.9 vs 112.9 μg/ml), and d-dimer (17.3 vs 69.6 μg/ml) values were significantly higher in the op(+) group.Conclusions Coagulopathy and abnormal fibrinolysis, which are measurable in routine medical practice, is associated with deterioration requiring surgery in mild to moderate traumatic brain injury, indicating that careful course observation is necessary.
    Clinical Neurology and Neurosurgery 10/2014; 127. DOI:10.1016/j.clineuro.2014.10.007 · 1.13 Impact Factor
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    • "There has been described that coagulopathy after TBI is frequent and represents a powerful predictor related to prognosis [37]–[39]. This coagulopathy could present as hypo- and hypercoagulable state, and result in a variable degree of secondary injury via subsequent ischemic and hemorrhagic lesioning. "
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    ABSTRACT: Matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) play a role in neuroinflammation after brain trauma injury (TBI). Previous studies with small sample size have reported higher circulating MMP-2 and MMP-9 levels in patients with TBI, but no association between those levels and mortality. Thus, the aim of this study was to determine whether serum TIMP-1 and MMP-9 levels are associated with mortality in patients with severe TBI. This was a multicenter, observational and prospective study carried out in six Spanish Intensive Care Units. Patients with severe TBI defined as Glasgow Coma Scale (GCS) lower than 9 were included, while those with Injury Severity Score (ISS) in non-cranial aspects higher than 9 were excluded. Serum levels of TIMP-1, MMP-9 and tumor necrosis factor (TNF)-alpha, and plasma levels of tissue factor (TF) and plasminogen activator inhibitor (PAI)-1 plasma were measured in 100 patients with severe TBI at admission. Endpoint was 30-day mortality. Non-surviving TBI patients (n = 27) showed higher serum TIMP-1 levels than survivor ones (n = 73). We did not find differences in MMP-9 serum levels. Logistic regression analysis showed that serum TIMP-1 levels were associated 30-day mortality (OR = 1.01; 95% CI = 1.001-1.013; P = 0.03). Survival analysis showed that patients with serum TIMP-1 higher than 220 ng/mL presented increased 30-day mortality than patients with lower levels (Chi-square = 5.50; P = 0.02). The area under the curve (AUC) for TIMP-1 as predictor of 30-day mortality was 0.73 (95% CI = 0.624-0.844; P<0.001). An association between TIMP-1 levels and APACHE-II score, TNF- alpha and TF was found. The most relevant and new findings of our study, the largest series reporting data on TIMP-1 and MMP-9 levels in patients with severe TBI, were that serum TIMP-1 levels were associated with TBI mortality and could be used as a prognostic biomarker of mortality in TBI patients.
    PLoS ONE 04/2014; 9(4):e94370. DOI:10.1371/journal.pone.0094370 · 3.23 Impact Factor
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    • "We excluded patients with traumatic brain injury, ventriculitis, and meningitis from the analysis, because these inflammatory conditions of the brain are often complicated by coagulopathy and can offer significant challenges to the surgeon during the surgical procedure. A recent study reported that traumatic brain injury is related with coagulopathy in 34% of patients with severe traumatic brain injury.11,12 The relevance of the interaction between coagulation and inflammation can easily be detected as disseminated intravascular coagulation and multiple organ failure in response to severe infection, in its most extreme form. "
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    ABSTRACT: This article aimed to investigate the incidence rate and possible risk factors for catheter-induced hemorrhage (CIH) after brain parenchymal catheterization. Between January 2011 and March 2013, 381 patients (572 punctures) who underwent brain parenchymal catheterization were retrospectively evaluated. All patients were checked by computerized tomography scan for the detection of hemorrhage within 48 hours after catheter insertion. CIH was defined as any evidence of new hemorrhage on the post-procedural computerized tomography scan. The incidence rate and the possible risk factors were analyzed by surgeon (4 different surgeons performed the procedures), characteristics of the catheter device, and patient background. Of 381 patients, 572 punctures were performed and CIH developed in 122 puncture cases (122/572, 21.3%). The risk factors related to CIH were Glasgow Coma Scale (GCS) score ≤8 (p<0.01) and prothrombin time international normalized ratio (PT INR) ≥1.3 (p=0.038). The amount of hemorrhage was minimal without additional operations. A low GCS score and high PT INR are implicated as potential risk factors for CIH after brain parenchymal catheterization. Careful and delicate operative technique can help to reduce postoperative complications in these patients.
    12/2013; 49(3):113-7. DOI:10.4068/cmj.2013.49.3.113
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