WITHDRAWN: Haemostatic drugs for traumatic brain injury

I wonder if this applies to hemorrhages also. If we had publicly available stroke protocols maintained by our stroke associations we could look it up. But we have jackshit. Stroke survivors are just all around screwed.
http://europepmc.org/abstract/med/25970597
Perel P, Roberts I, Shakur H, Thinkhamrop B, Phuenpathom N, Yutthakasemsunt S

Department of Population Health, London School of Hygiene & Tropical Medicine, Room 134b Keppel Street, London, UK, WC1E 7HT.

The Cochrane Database of Systematic Reviews [2015, 5:CD007877]

Type: Journal Article
DOI: 10.1002/14651858.CD007877.pub3

Abstract

Highlight Terms Gene Ontology(1) Genes/Proteins(1) Chemicals(3)

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 SELECTION CRITERIA: We included published and unpublished randomised controlled trials comparing haemostatic drugs (antifibrinolytics: aprotinin, tranexamic acid (TXA), aminocaproic acid or recombined activated factor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.