WHOM is going to look into this as a possible intervention for certain types of hemorrhages? Specific names only.
But what about this research?
Tranexamic Acid Shows No Symptom Benefit for Traumatic Brain Injuries
September 2020
And earlier research for hemorrhages:
Predictors and Outcomes of Neurological Deterioration in Intracerebral Hemorrhage: Results from the TICH-2 Randomized Controlled Trial
September 2020
A paragraph from there:
Tranexamic acid reduced the risk of early (aOR 0.79, 0.63–0.99; p = 0.041) but not late neurological deterioration (aOR 0.76, 0.52–1.11; p = 0.15). Larger hematoma size, intraventricular and subarachnoid extension increased the risk of neurological deterioration. Neurological deterioration increased the risk of death and dependency at day 90. Tranexamic acid reduced the risk of early neurological deterioration and warrants further investigation in ICH. URL:https://www.isrctn.com Unique identifier: ISRCTN93732214
I expect your doctor to know everything about this.
The latest here:
Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3): a randomised, placebo-controlled trial
Summary
Background
Tranexamic
acid reduces surgical bleeding and decreases mortality in patients with
traumatic extracranial bleeding. Intracranial bleeding is common after
traumatic brain injury (TBI) and can cause brain herniation and death.
We aimed to assess the effects of tranexamic acid in patients with TBI.
Methods
This
randomised, placebo-controlled trial was done in 175 hospitals in 29
countries. Adults with TBI who were within 3 h of injury, had a Glasgow
Coma Scale (GCS) score of 12 or lower or any intracranial bleeding on CT
scan, and no major extracranial bleeding were eligible. The time window
for eligibility was originally 8 h but in 2016 the protocol was changed
to limit recruitment to patients within 3 h of injury. This change was
made blind to the trial data, in response to external evidence
suggesting that delayed treatment is unlikely to be effective. We
randomly assigned (1:1) patients to receive tranexamic acid (loading
dose 1 g over 10 min then infusion of 1 g over 8 h) or matching placebo.
Patients were assigned by selecting a numbered treatment pack from a
box containing eight packs that were identical apart from the pack
number. Patients, caregivers, and those assessing outcomes were masked
to allocation. The primary outcome was head injury-related death in
hospital within 28 days of injury in patients treated within 3 h of
injury. We prespecified a sensitivity analysis that excluded patients
with a GCS score of 3 and those with bilateral unreactive pupils at
baseline. All analyses were done by intention to treat. This trial was
registered with ISRCTN (ISRCTN15088122), ClinicalTrials.gov (NCT01402882), EudraCT (2011-003669-14), and the Pan African Clinical Trial Registry (PACTR20121000441277).
Results
Between
July 20, 2012, and Jan 31, 2019, we randomly allocated 12 737 patients
with TBI to receive tranexamic acid (6406 [50·3%] or placebo [6331
[49·7%], of whom 9202 (72·2%) patients were treated within 3 h of
injury. Among patients treated within 3 h of injury, the risk of head
injury-related death was 18·5% in the tranexamic acid group versus 19·8%
in the placebo group (855 vs 892 events; risk ratio [RR] 0·94
[95% CI 0·86–1·02]). In the prespecified sensitivity analysis that
excluded patients with a GCS score of 3 or bilateral unreactive pupils
at baseline, the risk of head injury-related death was 12·5% in the
tranexamic acid group versus 14·0% in the placebo group (485 vs
525 events; RR 0·89 [95% CI 0·80–1·00]). The risk of head
injury-related death reduced with tranexamic acid in patients with
mild-to-moderate head injury (RR 0·78 [95% CI 0·64–0·95]) but not in
patients with severe head injury (0·99 [95% CI 0·91–1·07]; p value for
heterogeneity 0·030). Early treatment was more effective than was later
treatment in patients with mild and moderate head injury (p=0·005) but
time to treatment had no obvious effect in patients with severe head
injury (p=0·73). The risk of vascular occlusive events was similar in
the tranexamic acid and placebo groups (RR 0·98 (0·74–1·28). The risk of
seizures was also similar between groups (1·09 [95% CI 0·90–1·33]).
Interpretation
Our
results show that tranexamic acid is safe in patients with TBI and that
treatment within 3 h of injury reduces head injury-related death.
Patients should be treated as soon as possible after injury.
Funding
National
Institute for Health Research Health Technology Assessment, JP Moulton
Charitable Trust, Department of Health and Social Care, Department for
International Development, Global Challenges Research Fund, Medical
Research Council, and Wellcome Trust (Joint Global Health Trials
scheme).
Translations
For the Arabic, Chinese, French, Hindi, Japanese, Spanish and Urdu translations of the abstract see Supplementary Material section.
Introduction
Each year, worldwide, there are more than 60 million new cases of traumatic brain injury (TBI). Road traffic crashes and falls are the main causes and the incidence is increasing. Intracranial bleeding is a common complication of TBI and increases the risk of death and disability. Although bleeding can start from the moment of impact, it often continues for several hours after injury.,
Ongoing intracranial bleeding can lead to raised intracranial pressure,
brain herniation, and death. Tranexamic acid reduces bleeding by
inhibiting the enzymatic breakdown of fibrin blood clots (fibrinolysis).
The CRASH-2 trial,
showed that in patients with trauma with major extracranial bleeding,
early administration (within 3 h of injury) of tranexamic acid reduces
bleeding deaths by a third. Subsequent analyses showed that even a short
delay in treatment reduces the benefit of tranexamic acid
administration.
On the basis of these results, tranexamic acid was included in
guidelines for the pre-hospital care of patients with trauma, although
patients with isolated TBI were specifically excluded. However,
increased fibrinolysis, as indicated by increased concentrations of
fibrinogen degradation products, is often seen in patients with TBI and
predicts intracranial haemorrhage expansion.
Therefore, early administration of tranexamic acid in patients with TBI
might prevent or reduce intracranial haemorrhage expansion and thus
avert brain herniation and death.
No comments:
Post a Comment