This question was asked by a student who is now a contractor teaching TCCC in the Middle East.

I have been asking around but nobody seems to know so far. So, in TCCC the guidelines for TXA is 1g in 100cc NS or LR over 10 min. Check. However. in remote areas (like the one I am working in) do not always have 100cc bags available. Most of the time they are 500cc bags or bottles. Due to supplies being very limited at times, I hate to waste 400cc of fluid every time I need TXA. Do you have any idea about the supporting evidence for 1g in 100cc? Am I able to mix a higher dose and give partial? I am just trying to think outside the box. Any thoughts?

Doc's Reply via Pharmacist consultation: 
​​So really the bottom line is the concentration doesn’t matter. It can be given undiluted it can be given in a 100ml bag it can be given in a 1000ml bag. What matters is the total dose and the time. So whatever way you can get 1g in over ~10min in whatever way works the best for the particular crew, that’s what you should do.

Things to consider:
Why do we usually give TXA? We want to stop the body's process to breakdown the clots in the black box area in order to evacuate them to the most appropriate trauma center. We strive for permissive hypotension with these injury patterns. Would administering 1000ml of NS which has your TXA in it benefit the patient? Probably not. We are trying limit the amount of fluid we are giving the patient. I bring this up because we want you to think outside the box when you do not have 100cc piggyback bags for the TXA infusion. The point being made is that it does not matter what the concentration is, just that 1 gram is infused over 10 minutes but don't run with utilizing the 1,000ml bag for convenience of not carrying the 100cc bags. Be a thinking medic!

Student Questions:

1. I discussed Mobic or Meloxicam with our ER pharmacist and she said that Mobic still causes platelet inhibition, just less than all the other NSAIDS but more than Tylenol
2. Why does TCCC use Moxifloxacin vs a 3rd generation cephalosporin like Suprex or clindamycin? Both those meds has better coverage, less resistance patterns and they do not cause tendon rupture like the Moxifloxacin, also cheaper?

Doc's response.
​
​Good questions.  The answer is moxifloxacin appears to be a compromise choice, not a perfect choice.  I have attached the 2011 IDSA guidelines for combat wound which goes into more detail on what to use when.  I think moxi is a reasonable choice (I cant speak for the committee here but...)

1) moxi will cover for staph (MSSA) and coag neg staph, strep, Aeromonas spp (water contaminate), Acinetobacter and coliforms.  Clinda does offer better MRSA (Moxi and cefixime do not), but neither clinda nor cefixime will cover Aeromonas or Acinetobacter.  Clinda does not cover coliforms.

2) IDSA recommends narrow spectrum (gen 1 ceph) as base for combat injuries with exception of occular injury.  (they do recommend addition of flagyl in some circumstances such as abd wounds).  By using moxi you are meeting the abx within 3 hours guideline and you cover injury to almost all body areas with 1 pill.

3)  Overall risk of tendonopathy with a single dose in an otherwise healthy young pt is actually pretty low.  Check out this paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921747 which sites risk of tendonopathy at 3.8 fold increase compared to other abx with avg age of incidence at 64 y/o.

4) Finally, you are correct.  Meloxicam has a comparatively lower antiplatelet effect compared to other NSAIDs, not a zero effect.  It is a choice of lesser evils.  You get an additiive effect with the tylenol and meloxicam, might be able to avoid narcs or ketamine and so the payoff may be worth it.

This is just a quick answer, but I hope it helps.  If not please let me know and I'll keep looking for you!

   So recently asked why TCCC still recommends 14 gauge vs 10 gauge.  Or for that matter why not some other device?  A brief scan of literature didn't readily yield and back to back comparison of needle gauges.  Anecdotally some say the 10 gauge is less likely to kink.  

Additionally, there are now several new products which might be used. 
    1) ThoraQuick  from Medical Tree (UK) - slick product with spring loaded blunt tip that allows penetration of skin whilst reducing risk of injury to underlying structures once in the thoracic cavity.  It is essentially an improvement on the Turkel needle (see below) with an improved hub that allows for easy adhesion to the pt's chest wall.  2 ports on side of catheter as additional protection against occlusion.  Length of catheter: 10cm, Size: 3mm ID (approx. 8 ga).  Cost: 33.95 sterling or $47.96? (Not sold in US yet)
   
    2) Turkel Needle: Also from Medical Tree.  Spring loaded blunt tip.  Catheter length: 3.5" (88.9cm), Size: 8 Fr (11.5 ga).  Cost $60.99. (Available now)

   3) 10 Fr (10 ga) Thoracotomy Tube with trocar.  The IDF has been using a Vygon 10 Fr trocar with drain.  This was originally designed for tube thorocostomy in neonates.  The tube material is stiffer than the usual polyurethane in the 14 ga needle.  The argument being it further helps prevent kinking and thus failures.  A recent article (see below) discussed this but failed to directly compare the two devices and was limited by small sample size. 

It is my opinion that the real reason CoTCCC may still be recommending the 14 gauge catheter may have a lot to do with cost.  A 14 gauge needle/cath with hard case cost $9.99 from NAR.  Even if you have to use multiple per pt, it's still cheaper, and it's a well established item in the supply chain.  Add to that the lack of hard data showing superiority of other devices and it may be that a good solution now is better than a perfect solution later. 

Beyond which is better there is some argument that perhaps we should abandon the needle altogether and go to finger thoracotomies both in the ED and in the field.  See Scott Weingart's post about this as well as an article in JEMS below.

In the meantime I would say if you want to carry a 10 gauge, Turkel needle or the hot new ThoraQuick - go for it!  There certainly is no data so suggest any of these options in inferior.  And in the meantime if all you can get is a 14 gauge angiocath - do sweat it.  Know the problems that may arise (kinking, clotting, risk of injury to intrathoracic structure) and anticipate the problems and have a plan.

Emerg Med J 2011;28:750-753

J. Chen et. al. " Needle thoracostomy for tension pneumothorax: the Israeli Defense Forces experience", Canadian Journal of Surgery, Vol 58 (3) Supplement 3, June 2015.

M Escott, et al. "Simple Thoracostomy: Moving Beyond Needle Decompression in Traumatic Cardiac Arrest"  JEMS 39(4), MAR 2014.

There has been some recent debate on the merits of using occlusive dressings on chest wounds.   Current TCCC guidelines recommend that all 'open and/or sucking chest wounds should be treated by immediately applying a vented chest seal to cover the defect."  The guidelines then go on to state that if no vented seal is available a non vented dressing should be applied and the patient monitored for development of a tension pneumothorax. 

The question has been raised (and at least conceptually proven) why should we treat an open pneumothorax with an occlusive dressing potentially converting it to a leathal tension pneumothorax?  Why not just leave it alone? (1)

Before continuing a brief overview of physiology may be helpful here.  First, the muscles of respiration and the chest wall do not directly pull on the lungs.  Rather they expand and create negative pressure (-5mm Hg) (7) in the intrapleural space between the lining of the chest wall (parietal pleura) and the lung (visceral pleura).  When an injury allows open communication between atmospheric air and the intrapleural space, that negative pressure which expands the lungs is either diminished or lost.  The degree of impact depends on the size of the hole and how much time during the respiratory phase the hole remains patent to the outside.   The concern here is that if there is complete loss of the negative pressure in the pleural space for the entire inspiratory phase then that lung will not be ventilated.  If it is only open for part of the inspiratory phase (imagine that the lung itself blocks the hole for the first half of the respiratory phase) then partial filling of the lung may occur.  In either case this may result in respiratory compromise of the patient.

Any communication with atomospheric pressure and the intrapleural space can create a pneumothorax.  There are 3 types of pneumothoraces. 

1) Open pneumothorax: injury through the chestwall that extends to the intrapleural space. This is what we classically think of with penetrating trauma.

2) Closed pneumothorax:  With no hole in the chest wall it is considered a closed pneumothorax, for example a primary blast injury to the lung or even underlying COPD with ruptured bleb.  

3) Tension pneumothorax: A tension pneumothroax develops when the wound remains open longer in the inspiratory phase (allowing air into the chest cavity) than it is open in the expiratory phase (preventing air from escaping the chest cavity).  When the pressure in the chest cavity around the lung is greater than the the air pressure in the lung- it collapses and eventually the pressure builds enough to push the heart to the side and slowing blood return to the heart (a mix of physical kinking of the vessels with blood backing up -seen as JVD- and increased intrathoracic pressure which prevents blood returning into the chest to get to the heart) somewhere around 15-20 mmHg intrathoracic pressure.(7)  This will be seen as a drop in blood pressure, increased heart rate, drop in O2 sats and classically the deviated trachea and JVD.

A little physics here helps explain that in general air will still prefer to enter the trachea over the wound in the intrapleural space until the trachea is no longer the path of least resistance.  This tipping point happens when the hole in the chest wall approaches 1/2 size (area) of the trachea.  Poiseuille's Law - look it up, you know you want to....

So in either case - an open pneumothorax that causes oxygen desaturation because of failed oxygenation and ventilation, loss of negative pressure also decreases the amount of blood that returns to the chest and subsquently the heart,  or a tension pneumothorax which further decreases cardiac output - and our patient suffers.  Add to that hypovolemic shock with already compromised tissue perfusion or a TBI and you have a recipe for disaster.

So why not ignore the open pneumothorax and simply transport?  In a system the provides rapid transit to definitive (surgical) repair like civilian EMS, this might be acceptable.  With only one pt to worry about you can simply overcome the failure to oxygenate with increased supplemental O2.  If a tension pneumorthorax develops, then the standard NCD can be performed.  Once a chest tube has been placed, positive pressure ventilation will allow for expansion of the lungs regardless of loss of negative pressure in the intrapleural space.

The paper from the CoTCCC points out that in austure or tactical environments this level of one on one care might not always be possible.  Especially in an MCI where your ability to monitor patients will be strained and the ability to provide PPV potentially unrealistic.  It is in these settings that the occlusive dressing might be of greatest benefit.  A study by Kheirabadi demonstrated in animal models that a vented chest seal could in fact prevent conversion of an open pneumothorax to a tension pneumothorax.(2)

Manufacturers differ in the type of venting system they provide.  A study by J Kotora evaluated three vented chest seals: Hyfin by North American Rescue, SAM (SAM Medical Products) and the Sentinel Battle Seal (Combat Medical Systems) all performed equally well in preventing accumulation of a tension pneumothorax in their animal models. (3)  While the authors did inject blood into the chest cavity, it was unclear if blood ever came in contact with the vents of the chest seal and if so what the effect was.   Nor were there recommendations on what to do if blood was seen at the vents.  It seems reasonable that if there is concern you could either burp the chest seal, perform NCD, or replace it.  Pt positioning may also be helpful here when circumstances allow it.  This is a frequently misunderstood point with medics who confuse which way to place the injured side with the pt in the recovery position.  The chest seal should be up allow air to reach the vent and hopefully minimizing risk of blood pooling around the vent.  Alternatively, a patient could be left sitting up or reclined if risk of vomiting/aspiration not a concern.

The Asherman chest seal was one of the first vented chest seals in use, but experience and eventually a study showed it failed to adhere sufficiently to bloody or dirty skin (4) compared to the Bolin chest seal.  The focus article cites a pending publication that comparing the Bolin, Halo, Sherman, H&H, Hyfin, Russell, SAM-valved, and Sentinel chest seals on volunteers who were sprayed with evaporated or canned milk.  The results suggested that the SAM-valved and Bolin chest seals adhered the best.(5)

The article also reminds readers that previous a 2008 CoTCCC review of hasty dressings made of any readily available impermeable material and taped on three sides failed to show any proof that they reliably prevented development of a tension pneumothorax. (5)  That said if it's all you have, it might be considered with the understanding that it is no better than a completely occlusive dressing and will necessitate close monitoring of the pt, vs not treating the open thorax.

Of note Kotora did an excellent job pointing out that no chest seal was designed for prevention of accumulation of pneumothorax in a patient on positive pressure ventilation (BIPAP, BVM, ETT on vent, etc).(3)  While PPV will allow you to restore adequate expansion of the lung despite loss of intrapleural negative pressure- these patients require a chest tube first.

Bottom Line:
Great article and well worth the read.  I believe it absolutely justifies the use of vented chest seals for treatment of open pneumothoraces in a tactical environment.  Within the civilian sector, if rapid transport is available or if close monitoring of the patient is practical, it may be acceptable to not occlude the open pneumothorax and simply transport.  The debate regarding not treating may more appropriately reflect the importance of choosing the right tool for the right job and highlight the critical need for thinking providers.  Know what you're treating, know the complications and be prepared to intervene.  

Understand the different types of pneumothraces (closed, open, tension).  Know that an occlusive dressing is applied to an open chest wound with the intent of allowing at least partial restoration of lung ventilation and oxygenation.  The risk of any occlusive dressing is the potential conversion of an open pneumothorax to a tension pneumothorax.  Using a vented chest seal decreases that risk.  If a tension pneumothorax develops either burp the chest seal, place an NCD or replace the chest seal (if vents become clogged).

1)  Frank K. Butler, MD; Joseph J. Dubose, MD; Edward J. Otten, MD; Donald R. Bennett, MD; Robert T. Gerhardt, MD; Bijan S. Kheirabadi, PhD; Kirby R. Gross, MD; Andrew P. Cap, MD; Lanny F. Littlejohn, MD; Erin P. Edgar, MD; Stacy A. Shackelford, MD; Lorne H. Blackbourne, MD; Russ S. Kotwal, MD; John B. Holcomb, MD; Jeffrey A. Bailey, MD. "Management of Open Pneumothorax in Tactical Combat Casualty Care: TCCC Guideline Change 13-02", Journal of Special Operations Medicine, Fall 2013; 13(3)  PMID: 24048995

2)  B Kheirabadi, et al.  "Vented versus unvented chest seals for the treatment of pneumothorax and prevention of tension pneumothorax in a swine model." Journal of Trauma Acute Care Surgery, Jul 2013; 75(1):150-6. PMID 23940861

3) J Kotora, J Henao, L Littlejohn, S. Kircher.  "Vented chest seals for prevention of tension pneumothorax in a communicating pneumothorax". The Journal of Emergency Medicine, 2013; 45 (5) 686-694. PMID: 23921173

4) F Arnaud, T Tomori, J Yun, R McCarron, R Mahon. "Evaluation of chest seal performance in a swine model: comparison of Asherman vs. Bolin seal." Injury, 2008 SEP; 39(9): 1082-8.  PMID:18589420

5) Supinski DP, Nesbitt ME, Gerhardt RT: Chest seal adherence on human test subjects: a prospective study. Manuscript in preparation. - as cited in the title article.

6) CoTCCC minutes July 2008

7) BA Nicks, D Manthey: Ch 68: Pneumothorax, Tintinalli's Emergency Medicine, A Comprehensive Study Guide, Eighth Edition, 2016.

Current TCCC guidelines advocate the use of 14g, 3.25" (80mm) needle.  This recommendation evolved after studies looking at chest wall length demonstrated that the average size angiocath (1.77") would fail in as many as 50% of patients on the battlefield (1). 

A newer study by the UK military revisited not just chest wall thickness, but also distance to vital structures from the 2 recommended needle thoracostomy sites- 2nd intercostal space MCL and 5th intercostal space mid axillary line.  Several interesting points were made.  First, was that chest wall thickness averaged about 37mm at 2ICS MCL and 34.5mm at 5ICS MAL.  Second, that if the standard 3.25 in (80mm) needle decompression device was placed in the chest wall to the hub, injury to underlying vital structures (diaphragm, heart, aorta, pulmonary arteries) would occur in 21% of patients. (3)

It should be noted that there are several limitations to this paper.  It was retrospective, involved only 63 patients, of which all were young healthy males.  The UK averages for chest wall thickness were smaller than US studies for chest wall thickness.  US chest wall averages published were 48.6-53.6 mm depending on angle of needle through chest wall. (2)  The Harke paper noted that chest wall thickness increased with age and in females, but the majority of those studied can still be treated with the 3.25" needle.

Bottom line:
1) Current needle decompression needle length of 3.25" (80 mm) should be long enough for 99% of the studied population.
2) DO NOT HUB the needle.  Going too far can be just as bad as not going far enough.
3) Parallel to chest wall has shorter distance than parallel to floor/litter.

1. Stevens RL, Rochester AA, Busko J, et al.  Needle thoracostomy for tension pneumothorax: failure predicted by chest computed tomography.  Prehospital Emergency Care 2009;13:14-17.
2. Harke HT, Pearse LA, Levy AD, et al. Chest wall thickness in military personnnel: implications for needle thoracentesis in tension pneumothorax. Military Medicine. 2007; 172:1260-1263.
3. J Chen, R Nadler, D Schwartz, H Tein, A Cap, E Glassberg.  What is the optimal device length and insertion site for needle thoracostomy in UK military casualties?  Can J Surg. 2015 Jun;58(3 Suppl 3):S118-24.  PMID:
26100771​.

Question: Does high cholesterol affect the clotting cascade? 

There is not much I could find on a brief search.  The papers I found seem to support the established teaching that elevated triglycerides or cholesterol seem to promote inappropriate clotting increasing the risk of cardiovascular disease.  The effect this has in trauma does not seem to be as well defined.  Though there may be some effect on long term healing (not well studied) - the immediate problem and treatment of injury appears to be unchanged.

Papers included as matter of interest only- not great data....

R Krysiak, B Okopein, "Effect of simvastatin on hemostasis in patients with isolated hypertriglyceridemia". Pharmacology 92|(3-4):187-90. 2013.
                           - statin prolonged PT/PTT

W Chung, et. al. "Hyperlipidemia and statins affect neurological outcome in lumbar spine surgery." Int Journal of Environmental Research and Public Health". 12(1):402-13. 05 Jan 15.

You may need to up your dose of ritalin....but here is a link to a site with a decent explaination of the clotting cascade for those of you looking to geek out for a mo'.

http://themedicalbiochemistrypage.org/blood-coagulation.php