I was recently asked why TXA should not be used in subarachnoid hemorrhage.  A recent cochrane review (one of the most respected sources of review articles) discussed a search of 10 trials invovling 1904  patients.  A SAH commonly occurs as a result of an aneurysm or weak spot in the brain rupturing and leaking blood into the space immediately around the brain.  Two common consequences of this are devastating rebleeding (about 30% will die!) and hydrocephalus (clotted blood blocks the openings that allow the CSF to drain out of the brain and around the spinal cord - it occurs in as much as 20-30% for all SAH cases). 

Treatment with TXA ranged from < 72 hours to 6 weeks.

It was theorized that TXA would decrease the rebleed rate by preventing breakdown of the clot in the damaged vessel.  In fact it did reduce rebleeding rates by 35%.  However, TXA also increased the rate of cerebral ischemia and completely offset any benefit of preventing rebleeding.  It is likely that the reason for worsening ischemi is prevention of recanalization of blocked blood vessels and the restoration of blood flow to surviving brain tissue.

There was no effect on rates of hydrocephalus.

Bottom line: This has little impact on TXA use for bleeding in trauma in a tactical environment- but if you should be asked, now you know why TXA is contraindicated in SAH.

M. Baharoglu, M Germans, G Rinkel, A Algra, M Vermeulen, J van Gijn, Y Roos, "Antifibrinolytic therapy for aneurysmal suabarachnoid haemorrhage." Cochrane Database Systematic Review, 30 Aug 2013.

see also:
T Eastin, C Snipes, R Seupaul, "Are antifibrinolytic agents effective in the treatment of aneurysmal subarachnoid hemorrhage?". Annals of Emergency Medicine V 64: 6, pp 658-659. 01 Dec 2014.

CRASH II was a massive trial held in over 49 countries enrolling over 20,000 patients.  They looked at blunt and penetrating trauma in adults of all ages and compared to TXA to placebo for patients in all shock categories (GCS, SBP, RR).   The dose given was 1g over 10 minutes followed by 1 g over 8 hours.
  The results showed that TXA improved survival at 28 days from injury with an absolute risk reduction (death) of 1.5%.  This may not seem like much but consider that there was no increased rate of death or serious side effects associated with the drug.  This includes no increased risk of thromboembolic events (stroke, MI, PE, DVT).
   There was no change in the rate or amount of blood transfusions required either, highlighting the importance of the drug as an adjunct and the continued need to get blood on board quickly.

This paper was donated to the public as an open document in an attempt to widen it's use and can be obtained at: ​http://www.journalslibrary.nihr.ac.uk/hta/volume-17/issue-10#abstract