Journal Club: Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. Morrison et al

The study: This was a retrospective, observational, cohort study enrolling 896 trauma patients who had received at least 1 unit of packed red blood cells after admission to a single surgical hospital at Camp Bastion in Southern Afghanistan following a combat related injury. They compared the group of patients who had received tranexamic acid to those who had not received it.


Primary outcomes:

-Mortality at 24hrs, 48 hrs, & 30 days


Secondary outcomes:

-Transfusion requirements

-Coagulation parameters (prothrombin time & activated partial thromboplastin time): measured at 2 points: (1) admission to the ED of the surgical hospital & (2) admission to the ICU following OT

-Incidence of thrombotic events such as DVT or PE



-There was no statistically significant survival benefit using TXA within 24 hrs in either the overall group or the massive transfusion group.

-There was an overall mortality reduction in the TXA group within 48 hrs (11.3% vs 18.9% p value 0.004) & In-hospital mortality (17.4% vs 23.9% p value 0.03).

-There was a significant mortality reduction in the TXA arm of the massive transfusion group within 48hrs (10.4% vs 23.5% p value 0.003) & in-hospital mortality (14.4% vs 28.1% p value 0.004)

-In the overall group there was a statistically significant increase in the amount of all blood products (PRBC, FFP, Platelets & cryoprecipitate) used in the TXA group. This may reflect the increased severity in this group.

 -In both the overall & massive transfusion cohorts there was a statistically significant reduction in hypocoagulation in the TXA groups when comparing the patients bloods taken in emergency to their bloods taken in ICU following OT.

-In the TXA group there was a statistically significant increase in the number of pulmonary embolisms (2.7% vs 0.3% p value .001) & deep vein thrombosis (2.4% vs 0.2% p value .001). The number of venous thrombotic events in this study is too small to assess any independent risk of TXA. Due to the reduction in hypocoagulation it is plausible that the higher rates of thrombotic events relate to the TXA.



-This study suggests a survival benefit to giving tranexamic acid to bleeding trauma patients. This article suggests that this may be linked to clot stabilisation & reduction in inflammation.

-We should be considering tranexamic acid in bleeding trauma patients, particularly if they are haemodynamically unstable.

-TXA is included in our massive transfusion protocol.


Link to the article


Link to the full appraisal


Link to our massive transfusion protocol

Journal Club: Effects of tranexamic acid on death, vascular occlusive events, & blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial.

The study:  20 211 trauma patients with or at risk of significant bleeding over 40 countries & 274 hospitals were randomised to receive tranexamic acid or placebo.


Primary outcome:

-All-cause mortality within 4 weeks of injury


Secondary outcomes:

-Vascular occlusive events (MI, CVA, PE, DVT)

-Surgical intervention (neurosurgery, thoracic, abdominal, pelvic)

-Receipt of blood transfusion, units of blood transfused

-Degree of dependency

-FVIIa use

-GI bleeding



-All cause mortality at 4 weeks was significantly lower in the TXA group compared to placebo: 14.5% (1463) vs 16% (1613) (Relative risk 0.91 confidence interval (0.85-0.97) p value 0.0035

-The risk of death due to bleeding was significantly reduced 4.9% (489) vs 5.7% (574) RR 0.85, 95% CI (0.76-0.96) p value 0.0077

-Trend towards more vascular occlusive events in the placebo group

-No difference in transfusion & need for surgery

-Trend towards early treatment being more effective

-No statistical difference in FVIIa use or GI bleeding (secondary to small numbers)

-Degree of dependency: statistically significant improvement in the number of patients with no symptoms within the tranexamic acid group (14.7% vs 13.3%) however, in the other degrees of dependency there was no statistically significant difference.



-This study suggests that the early administration (within 3 hrs) of tranexamic acid to trauma patients with, or at risk of, significant bleeding reduces the risk of death from haemorrhage with no apparent increase in vascular occlusive events.


Link to article


Link to full appraisal

Journal club: Canadian C-spine and NEXUS rules


Neck pain post blunt trauma is a very common ED problem.

This review looks very briefly at the two main clinical decision rules used in these patients: NEXUS and CCR.

The link to the NEXUS and CCR article is here.

The link to the NEXUS and CCR analysis, and the CASP guidelines used are here.

One interesting feature that comes up going through the literature is that these decision rules were made with XR as the gold standard of imaging, something which has changed in the last few decades due to publications of papers showing XR having a sensitivity of roughly 50%[1].

However, both of these decision rules had very good follow up (telephone questionnaires in CCR and review of local neurosurgical records and quality assurance logs in NEXUS) without missed injuries being identified.  Not sure what to do with that!

Personally, when possible I prefer to use the CCR rule due to the higher specificity, addition of ROM and a study[2] which compared CCR to CT which showed no missed injuries (Population 3,200 with 192 fractures).

This article was interesting in that it’s results suggested that the CCR rule had a specificity of only .6% for C-spine fractures…which again I’m not sure how to interpret.

 It’s reassuring to know that none were missed however.       

Would be very keen to hear how other people approach this problem.



[1]Mathen R, Prospective evaluation of multi-slice computed tomography versus plain radiographic cervical spine clearance in trauma patients, Journal of trauma, 2007, 62(6) 1427

[2]Duane T, Canadian Cervical Spine rule compared with computed tomography: a prospective analysis, Journal of Trauma, 2011, 71(2), 352-355.

3AM Rundown: Sympathetic acute crashing pulmonary oedema

Those that listen to Scott Weingart on EmCrit will recognise that this is basically taken from his podcast on SCAPE.

I’ve used the management plan on a number of patients’ now and find it really effective.

Saved me a couple of intubations.

If you want some more information or a more entertaining presentation I would recommend checking out podcast 1.

Should emphasise that this algorithm is geared towards the typical 6am patient presenting with marked sympathetic overload (diaphoretic/hypertensive) and signs of acute pulmonary oedema as compared to the patient with a bit of fluid in their lungs secondary to CCF

Run down:

  1. Pathophysiology: Afterload mediated heart failure.

- Aim of treatment is to decrease SBP rapidly and remove the oedema from the lungs with PPV

    2.   Treatment:

- PEEP: Start at 6-8 and titrate up to 10-12 as tolerated

- GTN Infusion: Loading dose of 400mcg/min for 1-2 minutes (or until lose radial pulse) and then decrease to 60mcg/min.

- Dosing using our infusion concentrations: 50mg in 500mls = 100mcg/mL

- Would start the infusion at 240mls/hr and decrease to 60mls/hr after any of the endpoints below:

  •          SBP normalising
  •          Infusion lasting 2 minutes
  •          Losing radial pulse (it comes back quickly!)

Titrate to blood pressure: Goal roughly SBP of 120mmHg

- Can use low dose captopril once patients stabilised to facilitate weaning of GTN drip (3.125mg-6.25mg)

- Don’t waste your time with frusemide: GTN more effective and patients with SCAPE can often be volume deplete.

If you have any thoughts/criticisms about this protocol feel free to post in the comments.


3AM Rundown: Automonic dysreflexia

The idea for these posts are to have some brief rundowns/management plans for critical pathologies that may come in overnight when you don’t have the time/head space to review the correct management.

If you had any additional thoughts/tips for the topics covered then please feel free to add those in the comments…any suggestions would help make this resource much better.

The first post is on autonomic dysreflexia.

I’ve only seen two patients with this, and the algorithm listed was incredibly helpful in working through the issues.

Algorithm listed here.

The Rundown:

1. Pathophysiology: Loss of coordinated autonomic responses to stimuli due to spinal cord damage above T6

2. Important tip: Normal blood pressures concerning in spinal patient.

- If SBP > 20mmHG above resting BP = Autonomic dysreflexia till proven otherwise

3. Symptoms: Headache/flushing are concerning

4. Causes: Retention and constipation big two.

- If not these then a head to toe exam for other painful stimuli required.

5. Why concern?: Hypertensive crisis. Seizures/Cardiac arrests/ICH

6. Treatment: As per algorithm.

7. Who to call for help: Rehab physician unless at large centre (Spinal Consultant)

Could this be Necrotising Fasciitis: The LRINEC study

I recently undertook a literature search surrounding this, after I was asked the question on a shift and found out that I really had no idea how to distinguish between necrotising fasciitis (NF) and severe cellulitis.

Unfortunately, it appears that this is a common issue, with the largest trial showing that only 15% of patients with NF were diagnosed on admission.

Which is a problem, seeing as the main predictor of mortality is time to surgical debridement.

Thankfully there are some tools to help us with this, in particular a clinical decision rule (LRINEC), bedside US, and the “finger test”.

The link to the LRINEC study is here

This was analysed using the CASP questions on clinical prediction rules: Analysis.

- For Questions please reference CASP UK website

The link to the finger test description is here.

- Page 1027 of this article or 1539 of the LRINEC study.

The link to the US study is here.

- Videos of normal and positive US are listed as well.

Bottom line:

1. Pathophysiology: Rapidly progressive infection involving the fascia and subcutaneous tissue with thrombosis of the cutaneous microcirculation.

- Moves from horizontal to vertical plane of spread.

2. Mortality rate = 34%. 

- Early operative debridement key to decreasing mortality.

- Appearance early difficult to distinguish from cellulitis or abscess

3. Clinical triad: Exquisite pain (98%)/swelling (92%) and fevers (80%)

4. Appearance: Initial = Redness with ill-defined borders.

 - Horizontal plane: Rapidly progressing with severe pain and tenderness beyond apparent area of involvement

- Vertical plane: Bullae →Gangrene (Necrosis/ulceration/crepitus and SC emphysema)

5. Investigations:

- Bedside US = STAFF examination:  Subcutaneous thickening, air, fascial fluid = 93% Specific

- LRNIEC scoring system: Score ≥ 6 requires further investigations

- Finger test: ↓Bleeding/”dishwater pus”/lack of resistance to blunt dissection post 2cm incision positive findings

- CT/ MRI helpful in ambiguous cases

6. Any patient with a LRINEC score of 6 requires further investigations for NF

- Quick algorithm listed here