But we haven't already created protocols on this from years of research? No? Then everyone involved is incompetent.
tranexamic acid (13 posts to March 2013)
Tranexamic Acid for Acute Spontaneous Intracerebral Hemorrhage: A Meta-Analysis of Randomized Controlled Trials
Yu Guo1†, Xin-Mei Guo2†, Rui-Li Li3†, Kai Zhao1, Qiang-Ji Bao1, Jin-Cai Yang1, Qiang Zhang4 and 
Ming-Fei Yang4*- 1Graduate School, Qinghai University, Xining, China
- 2Biomedical Engineering Research Center, Kunming Medical University, Kunming, China
- 3Neurological Intensive Care Department, Shengli Oilfield Central Hospital, Dongying, China
- 4Department of Neurosurgery, Qinghai Provincial People's Hospital, Xining, China
Background: The role of tranexamic acid (TXA) in preventing hematoma expansion (HE) in patients with acute spontaneous intracerebral hemorrhage (ICH) remains unclear. We aim to investigate the efficacy and safety of TXA in acute spontaneous ICH with a particular focus on subgroups.
Methods: Randomized controlled trials (RCTs) were retrieved from CENTRAL, Clinicaltrials.gov, EMBASE, PubMed, and WHO ICTRP. The primary outcome measurement was HE. The secondary outcome measurements included 3-month poor functional outcome (PFO), 3-month mortality, and major thromboembolic events (MTE). We conducted subgroup analysis according to the CT markers of HE (standard-risk population and high-risk population) and the time from onset to randomization (>4.5 and ≤4.5 h).
Results: We identified seven studies (representing five RCTs) involving 2,650 participants. Compared with placebo, TXA may reduce HE on subsequent imaging (odd ratio [OR] 0.825; 95% confidence interval [CI] 0.692–0.984; p = 0.033; I2 = 0%; GRADE: moderate certainty). TXA and placebo arms did not differ in the rates of 3-month PFO, 3-month mortality, and MTE. Subgroup analysis indicated that TXA reduced the risk of HE in the high-risk population with CT markers of HE (OR 0.646; 95% CI 0.503–0.829; p = 0.001; I2 = 0 %) and in patients who were treated within 4.5 h of symptom onset (OR 0.823; 95% CI 0.690–0.980; p = 0.029; I2 = 0%), but this protective effect was not observed in the standard-risk population and patients who were treated over 4.5 h of symptom onset.
Conclusions: Tranexamic acid (TXA) may decrease the risk of HE in patients with acute spontaneous ICH. Importantly, the decreased risk was observed in patients who were treatable within 4.5 h and with a high risk of HE, but not in those who were treatable over 4.5 h and in standard-risk population. However, PFO or mortality at 3 months did not significantly differ between patients who received TXA and those who received placebo. TXA is safe for acute spontaneous ICH without increasing MTE.
Introduction
Spontaneous intracerebral hemorrhage (ICH) is one of the leading causes of disability and death worldwide, and is one of the serious global public health and socioeconomic burdens. Globally, up to 3 million people die from ICH each year, accounting for 5% of all human deaths, while an estimated 18 million people suffer from the sequelae of ICH (1, 2). Although an organized in-patient (stroke unit) care has been shown to contribute in reducing disability and mortality, there is no strong evidence-based acute therapy that is specific to acute spontaneous ICH (3, 4).
Age, neurological deficit, hemorrhage cause, location, and hematoma volume are the main determinants of clinical outcomes in patients with ICH (5, 6). Among them, hematoma volume is the most important factor. Roughly one-third of acute spontaneous ICH are complicated by hematoma expansion (HE), which most often occurs within the first few hours, but could also occur at up to 24 h, presenting a target window for intervention (7, 8). Emergency medical services are traditionally established to bring in patients with acute stroke with haste for diagnosis and treatment within 4.5 h of symptom onset. In addition, tranexamic acid (TXA) therapy is theoretically more suitable for patients with high-risk for ICH growth, such as patients with early computed tomography (CT) markers of HE. CT markers, including black hole sign, blend sign, island sign, and spot sign, have been used as reliable predictors for early HE in patients with acute spontaneous ICH (9–14). Therefore, it seems feasible to identify patients at high risk for HE early, and then for early therapeutic intervention to improve the clinical outcomes of patients with acute spontaneous ICH.
The researchers are looking for a safe acute therapy to reduce the risk of HE and improve the outcome for acute spontaneous ICH patients. TXA is an antifibrinolytic agent that reduces bleeding by inhibiting plasminogen activation and fibrinolysis. It has been shown that it can reduce perioperative blood loss and risk of blood transfusion (15, 16). In addition, trauma guidelines have recommended the early use of TXA in patients with traumatic ICH, as TXA can provide a survival benefit without increasing its adverse events (17, 18). However, the role of TXA in preventing HE and in improving outcome in patients with acute spontaneous ICH remains unclear.
Several randomized controlled trials (RCTs) evaluating the efficacy and safety of TXA in patients with acute spontaneous ICH have been performed in recent years. However, the existing RCTs and previously published systematic reviews have reported fragmentary and conflicting results. Some studies have shown a protective association between TXA use and ICH growth. Other studies have found no such relationship. These studies differed in their study populations. Herein, we performed meta-analysis on the available RCTs to determine the following: (1) the effectiveness and safety of TXA administration, compared against placebo or open control, in adults with acute spontaneous ICH; (2) how this differs between the standard-risk population and the high-risk population (those with ICH with CT markers of HE); and (3) how this differs between the range within 4.5 h and over 4.5 h of the time from onset to randomization.
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