BackgroundTraumatic 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 aimed to determine the effectiveness and safety of TXA in preventing progressive intracranial haemorrhage in TBI.MethodsThis is a double blinded, placebo controlled randomized 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 standard 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 expanded by 25% or more on any dimension (height, length, or width) on the second scan.ResultsProgressive 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.ConclusionsTXA 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.

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Background Traumatic brain injury (TBI) is a leading cause of death and disability. Intracranial bleeding is a common complication of TBI, and intracranial bleeding can develop or worsen after hospital admission. Haemostatic drugs may reduce the occurrence or size of intracranial bleeds and consequently lower the morbidity and mortality associated with TBI. Objectives To assess the effects of haemostatic drugs on mortality, disability and thrombotic complications in patients with traumatic brain injury. Search methods We searched the electronic databases: Cochrane Injuries Group Specialised Register (3 February 2009), CENTRAL (The Cochrane Library 2009, Issue 1), MEDLINE (1950 to Week 3 2009), PubMed (searched 3 February 2009 (last 180 days)), EMBASE (1980 to Week 4 2009), CINAHL (1982 to January 2009), ISI Web of Science: Science Citation Index Expanded (SCI-EXPANDED) (1970 to January 2009), ISI Web of Science: Conference Proceedings Citation Index - Science (CPCI-S) (1990 to January 2009). Selection criteria We included published and unpublished randomised controlled trials comparing haemostatic drugs (antifibrinolytics: aprotinin, tranexamic acid (TXA), aminocaproic acid or recombined activated factor VIIa (rFVIIa)) with placebo, no treatment, or other treatment in patients with acute traumatic brain injury. Data collection and analysis Two review authors independently examined all electronic records, and extracted the data. We judged that there was clinical heterogeneity between trials so we did not attempt to pool the results of the included trials. The results are reported separately. Main results We included two trials. One was a post-hoc analysis of 30 TBI patients from a randomised controlled trial of rFVIIa in blunt trauma patients. The risk ratio for mortality at 30 days was 0.64 (95% CI 0.25 to 1.63) for rFVIIa compared to placebo. This result should be considered with caution as the subgroup analysis was not pre-specified for the trial. The other trial evaluated the effect of rFVIIa in 97 TBI patients with evidence of intracerebral bleeding in a computed tomography (CT) scan. The corresponding risk ratio for mortality at the last follow up was 1.08 (95% CI 0.44 to 2.68). The quality of the reporting of both trials was poor so it was difficult to assess the risk of bias. Authors’ conclusions There is no reliable evidence from randomised controlled trials to support the effectiveness of haemostatic drugs in reducing mortality or disability in patients with TBI. New randomised controlled trials assessing the effects of haemostatic drugs in TBI patients should be conducted. These trials should be large enough to detect clinically plausible treatment effects.

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Introduction:The authors aimed to estimate the prevalence of pressure ulcers and to explore the nutritional effects of the prognostic factors on successful pressure ulcer closure in a public tertiary care hospital in Thailand.Patients and Methods:The study was a retrospective cohort analysis of seven-year census (2008 - 2014) at Surin hospital in Thailand. There were 424 of total 240,826 patients aged over than 15 years admitted to surgery, orthopedics and medicine wards during the study period with documented pressure ulcers (ICD 10TM). We analyzed four hundred and ten patients after excluding 14 patients with non-pressure ulcers (due to burning/ diabetic/ ischemic neuropathic ulcers, and less than 24 hours of admission) and loss medical record. We selected independent factors from demographic data, nutritional factors, pressure ulcer characteristics, and management data. The outcome of interest was successful pressure ulcer closure. The analysis method was the semi-parametric Cox regression model and reported as Hazard Ratios (HR) with 95% confidence interval (95% CI).Results:The total hospital admission was 240,826 patients between 2008 - 2014. 410 patients were developing pressure ulcers, of these, 7% (28/410) success in ulcer closure, and 77% (314/410) failure in closure requiring for additional procedures (excisional debridement). The rest of patients (16%, 68/410) was non-operative care. The prevalence of pressure ulcers was 1.7 per 1,000 person-year. The multivariable model found that only the Nottingham Hospital Screening Tool (NS) score was a statistically significant nutritional variable, and additional subgroup analysis of two models of sepsis and spinal cord co-morbidities was also significant. Adjusted hazard ratios (HR) for NS score = 0.355 (95% CI: 0.187, 0.674), p=0.002), for sepsis = 0.312 (95% CI: 0.140, 0.695), p=0.004), and for spinal cord co-morbidity = 0.420 (95% CI: 0.184, 0.958), p=0.039).Conclusions:The annual prevalence was 1.7 per 1,000 persons. NS score was strongly associated with ulcer closure success.