***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Traumatic brain injury ( TBI ) is commonly accompanied by intracranial bleeding which can worsen after hospital admission . Tranexamic acid ( TXA ) has been shown to reduce bleeding in elective surgery and there is evidence that short courses of TXA can reduce rebleeding in spontaneous intracranial haemorrhage . We aim ed to determine the effectiveness and safety of TXA in preventing progressive intracranial haemorrhage in TBI . Methods This is a double blinded , placebo controlled r and omized trial . We enrolled 238 patients older than 16 years with moderate to severe TBI ( post-resuscitation Glasgow Coma Scale ( GCS ) 4 to 12 ) who had a computerized tomography ( CT ) brain scan within eight hours of injury and in whom there was no immediate indication for surgery . We excluded patients if they had a coagulopathy or a serum creatinine over than 2.0 milligrams% . The treatment was a single dose of 2 grams of TXA in addition to other st and ard treatments . The primary outcome was progressive intracranial haemorrhage ( PIH ) which was defined as an intracranial haemorrhage seen on the second CT scan that was not seen on the first CT scan , or an intracranial haemorrhage seen on the first scan that had exp and ed by 25 % or more on any dimension ( height , length , or width ) on the second scan . Results Progressive intracranial haemorrhage was present in 21 ( 18 % ) of 120 patients allocated to TXA and in 32 ( 27 % ) of 118 patients allocated to placebo . The difference was not statistically significant [ RR = 0.65 ( 95 % CI 0.40 to 1.05 ) ] . There were no significant difference in the risk of death from all causes in patients allocated to TXA compared with placebo [ RR = 0.69 ( 95 % CI 0.35 to 1.39 ) ] and the risk of unfavourable outcome on the Glasgow Outcome Scale [ RR = 0.76 ( 95 % CI 0.46 to 1.27 ) ] . There was no evidence of increased risk of thromboembolic events in those patients allocated to TXA . Conclusions TXA may reduce PIH in patients with TBI ; however , the difference was not statistically significant in this trial . Large clinical trials are needed to confirm and to assess the effect of TXA on death or disability after TBI BACKGROUND Intracranial hemorrhage is a common complication of traumatic brain injury ( TBI ) . The purpose of this study is evaluation of the effect of tranexamic acid ( TXA ) on hemorrhagic mass growth in TBI patients . PATIENTS AND METHODS In this r and omized , double-blind clinical trial , 149 patients with TBI and any kind of blood on their computed tomography scan enrolled in the study and were r and omly allocated to receive TXA or placebo . After 24 hours , computed tomography scan was repeated for assessing the changes in hemorrhage , new bleeding , and mass effects of blood on brain tissue . The primary outcome was growth of the hemorrhagic lesion . Data were analyzed by SPSS software using Fisher exact , chi-square , and Mann-Whitney U tests , as well as linear and logistic regression models . FINDINGS The incidence of hemorrhagic lesion growth was 20.5 % in the TXA group and 22.7 % in the placebo group . The difference was not significant ( P = 0.87 , RR = 0.89 ) . The mean ( st and ard deviation ) of hemorrhagic lesion growth was 9.4 ( 15.3 ) in the TXA group and 10.2 ( 10.1 ) in the placebo group without significant difference ( P = 0.27 ) . The frequency of deaths ( 2.7 % vs. 4 % ) , adverse outcome at discharge ( 10.8 % vs. 17.3 % ) , and 3 months later ( 6.8 % vs. 14.7 % ) in the TXA group were lower than the placebo , but the difference was not statistically significant . No side effect was observed with the administration of TXA . CONCLUSION Administration of a short dose of TXA does not lead to significant prevention of growth of posttraumatic hemorrhagic lesion or improvement of clinical outcomes Purpose Traumatic brain injury ( TBI ) is a leading cause of death and disability . Intracranial hemorrhage ( ICH ) secondary to TBI is associated with a high risk of coagulopathy which leads to increasing risk of hemorrhage growth and higher mortality rate . Therefore , antifibrinolytic agents such as tranexamic acid ( TA ) might reduce traumatic ICH . The aim of the present study was to investigate the extent of ICH growth after TA administration in TBI patients . Methods This single-blind r and omized controlled trial was conducted on patients with traumatic ICH ( with less than 30 ml ) referring to the emergency department of Vali-Asr Hospital , Arak , Iran in 2014 . Patients , based on the inclusion and exclusion criteria , were divided into intervention and control groups ( 40 patients each ) . All patients received a conservative treatment for ICH , as well as either intravenous TA or placebo . The extent of ICH growth as the primary outcome was measured by brain CT scan after 48 h. Results Although brain CT scan showed a significant increase in hemorrhage volume in both groups after 48 h , it was significantly less in the TA group than in the control group ( p = 0.04 ) . The mean total hemorrhage expansion was ( 1.7 ± 9.7 ) ml and ( 4.3 ± 12.9 ) ml in TA and placebo groups , respectively ( p < 0.001 ) . Conclusion It has been established that TA , as an effective hospital-based treatment for acute TBI , could reduce ICH growth . Larger studies are needed to compare the effectiveness of different doses BACKGROUND  Intracranial hemorrhage ( ICH ) is common in traumatic brain injury ( TBI ) and a major determinant of death and disability . ICH commonly increases in size and coagulopathy has been implicated in such progression . We investigated the association between coagulopathy diagnosed by routine laboratory tests and ICH progression . METHODS Subgroup post hoc analysis from a r and omized controlled trial including adult patients with blunt severe TBI ( Glasgow Coma Scale score < or=8 ) and repeat computerized tomography scans in 48 hours . Coagulopathy was defined as international normalized ratio > or=1.3 , activated partial thromboplastin time > or=35 , or platelet count ( PLT ) < or=100 x 10/L any time in the first 24 hours . Progression was any size increase or new ICH . TBI-associated coagulopathy was investigated measuring soluble tissue factor ( TF ) and d-dimer . RESULTS The ICH progressed in 37 of 72 patients ( 51 % ) , in 80 % if any abnormal laboratory test ( coagulopathic patients ) versus 36 % in noncoagulopathic ( p = 0.0004 ) . Abnormal international normalized ratio ( odds ratio [ OR ] = 4.09 ; 95 % confidence interval [ CI ] = 1.29 - 12.95 ; p = 0.017 ) , PLT ( OR = 12.59 ; 95 % CI = 1.52 - 108.57 ; p = 0.019 ) , head Abbreviated Injury Scale ( AIS ) ( OR = 1.82 ; 95 % CI = 1.15 - 2.88 ; p = 0.011 ) were significantly associated with progression ( univariate analysis ) . In a multiple logistic regression , only head AIS ( OR = 1.81 ; 95 % CI 1.10 - 2.98 ; p = 0.0198 ) and PLT ( OR = 11.8 ; 95 % CI = 1.38 - 101.23 ; p = 0.024 ) correlated with progression . All patients with abnormal partial thromboplastin time experienced progression . ICH progression carried a 5-fold higher odds of death ; 32 % with progression died versus 8.6 % without . Age , head AIS , Injury Severity Score , and d-dimer were also associated with mortality . Tissue factor was not associated with progression or mortality . CONCLUSION This study demonstrates an association between coagulopathy , diagnosed by routine laboratorial tests in the first 24 hours , with ICH progression ; and ICH progression with mortality in patients with severe TBI . The causal relationship between coagulopathy and ICH progression will require further studies UNLABELLED The emergence of prothrombotic agents ( e.g. activated factor VII ) to treat traumatic brain injury ( TBI ) requires a better underst and ing of the association of coagulopathy with isolated head injury ( IHI ) . OBJECTIVE To investigate the association of IHI and coagulopathy . METHODS Prospect i ve , observational study in an urban level I trauma center . INCLUSION CRITERIA Adult ( > or = 13 years of age ) patients with IHI . EXCLUSION CRITERIA patients with known coagulopathies or on anticoagulant therapy . PREDICTOR VARIABLES TBI ( head abbreviated injury severity score > 2 , or brain hematoma on CT scan ) , age , gender , mechanism of injury , Glasgow Coma Score ( GCS ) , and loss of consciousness ( LOC ) . OUTCOME VARIABLES coagulopathy defined as elevated International Normalized Ratio ( INR > 1.3 ) or activated partial thromboplastin time ( PTT ) greater than 34 s. We divided IHI subjects into two groups of patients with and without TBI . STATISTICAL ANALYSIS Fisher 's exact test and Mann-Whitney U were used to compare data where appropriate ( alpha : 0.05 , two-tailed ) . RESULTS From July 2005 to December 2006 , 276 patients with IHI were studied . The median age was 35 years ( interquartile range : 25 - 52 ) with a 79 % male predominance and 88 % blunt trauma . Eight percent ( 95 % CI , 5 - 12 % ) of patients had coagulopathy . The rate of coagulopathy in TBI patients ( 17 % ) was significantly higher than non-TBI patients ( 6 % ) ( 11 % difference , 95 % CI , 3 - 20 % ] . The relative risk of coagulopathy in TBI patients was 2.9 ( 95 % CI , 1.3 - 6.6 ) . CONCLUSION Coagulopathy as defined by elevated INR and /or PTT is associated with TBI after isolated head injury BACKGROUND Severe bleeding accounts for about one-third of in-hospital trauma deaths . Patients with a high baseline risk of death have the most to gain from the use of life-saving treatments . An accurate and user-friendly prognostic model to predict mortality in bleeding trauma patients could assist doctors and paramedics in pre-hospital triage and could shorten the time to diagnostic and life-saving procedures such as surgery and tranexamic acid ( TXA ) . OBJECTIVES The aim of the study was to develop and vali date a prognostic model for early mortality in patients with traumatic bleeding and to examine whether or not the effect of TXA on the risk of death and thrombotic events in bleeding adult trauma patients varies according to baseline risk . DESIGN Multivariable logistic regression and risk-stratified analysis of a large international cohort of trauma patients . SETTING Two hundred and seventy-four hospitals in 40 high- , medium- and low-income countries . PARTICIPANTS We derived prognostic models in a large placebo-controlled trial of the effects of early administration of a short course of TXA [ Clinical R and omisation of an Antiﬁbrinolytic in Signiﬁcant Haemorrhage ( CRASH-2 ) trial ] . The trial included 20,127 trauma patients with , or at risk of , significant bleeding , within 8 hours of injury . We externally vali date d the model on 14,220 selected trauma patients from the Trauma Audit and Research Network ( TARN ) , which included mainly patients from the UK . We examined the effect of TXA on all-cause mortality , death due to bleeding and thrombotic events ( fatal and non-fatal myocardial infa rct ion , stroke , deep-vein thrombosis and pulmonary embolism ) within risk strata in the CRASH-2 trial data set and we estimated the proportion of premature deaths averted by applying the odds ratio ( OR ) from the CRASH-2 trial to each of the risk strata in TARN . INTERVENTIONS For the stratified analysis according baseline risk we considered the intervention TXA ( 1 g over 10 minutes followed by 1 g over 8 hours ) or matching placebo . MAIN OUTCOME MEASURES For the prognostic models we included predictors for death in hospital within 4 weeks of injury . For the stratified analysis we reported ORs for all causes of death , death due to bleeding , and fatal and non-fatal thrombotic events associated with the use of TXA according to baseline risk . RESULTS A total of 3076 ( 15 % ) patients died in the CRASH-2 trial and 1705 ( 12 % ) in the TARN data set . Glasgow Coma Scale score , age and systolic blood pressure were the 
    Output:
    
Subgroup analysis on RCTs with low risk of bias showed that TXA was associated with reduced mortality and hemorrhagic expansion .
GRADE was performed for the RCT with low risk of bias subgroup , it showed a high certainty of evidence for lower mortality , less hemorrhage expansion , and similar need for neurosurgical intervention in TXA group compared to placebo group .
TXA was associated with reduced mortality and hemorrhagic expansion but similar need for neurosurgical intervention and unfavorable GOS .