NSAIDs part 2: The Ceiling Effect

Sorry readers.  I've been slacking off on vacation in NYC, eating too much and blogging about food more than medicine.  Tonight at dinner with Mr. EMCrit, Scott called me out a bit for insufficient content.  Also, one of my readers has some rounds coming up soon, and needs to talk NSAIDs.  With that in mind, here's part 2 of the NSAID saga.

In part 1 on NSAIDs, we looked at NSAID equivalency for analgesia and the myth that is  ketorolac (Toradol).  

Hat tip to readers Moshe and Elisha (@ETtube on twitter) for pointing out the concept of the ceiling effect with NSAIDs.  I did not mention this in part 1, and will discuss it today.
There's a great talk by Larry Raney on the Free Emergency Talks website that discusses NSAIDs and the ceiling effect.  You can find it here.  As an aside, the Free Emergency Talks website is run by Joe Lex, one of the great EM educators, and has a thousands of talks from any conference you can think of. 

What is the ceiling effect?

* Free sammich to the first reader who tells me where this ceiling is. (Sammich will be good when it goes in the mail, but I can't guarantee quality on arrival.  Might make it a cockroach and twinkie sammich to prevent spoilage.)

The ceiling effect is the concept that there is a maximum level of analgesia that can be reached with a dose of medication, and beyond that dose, you get no more analgesia.  

In addition, you continue to get more side effects.  That double sucks!

Tylenol and NSAIDs classically fall into the category of analgesics with a ceiling, while opiates have no ceiling.  This is why we can bomb in loads of fentanyl or morphine, but you don't see us pounding patients with ibuprofen.

If you look at the doses of NSAIDs listed in part 1, you'll see some pretty whopping doses.  
Aside from the ceiling of anti-inflammatory dosing, there is also the concept of a second ceiling for acute pain?

Two ceilings?  Yup, two ceilings.

The ceiling dose for acute pain with ibuprofen is 400 mg po.

The higher ibuprofen dose ceiling of 800 mg I mentioned in part 1 is the anti-inflammatory ceiling of the NSAID and comes from the rheumatology literature.   I apologize if I confused anyone with this.  One key to understanding the NSAID literature is that it generally comes from 3 patient groups: rheumatologic disease, post-operative pain and dental pain.  The latter two are probably both representative of pain we see in ED patients, ie: acute, non-inflammatory pain.

This is the reason why meta-analyses of NSAID efficacy are a challenge; the indications, duration of therapy, dose, etc. are completely different.   In some studies, you are looking at patients with chronic inflammatory conditions on long term therapy.  These patients may need higher dose NSAIDs for their anti-inflammatory effects.  In other studies, it is single dose or short-term NSAIDs where analgesic ceiling will be 400 mg.

You can see how lumping all of these studies together in a review would misconstrue pretty much any endpoint.

Let's now look at the two main studies supporting the 400 mg ceiling dose of ibuprofen and 10 mg ceiling dose of ketorolac.

In contrast to the usual scenario in which old research = bad research (or a HSSP: High School Science Project), there are papers from 1978 and 1986 looking at the ibuprofen ceiling effect.  

The first, by Winter et al. in 1978 looked at 510 post oral surgery patients who had 1 or more extractions, impactions and even a few with alveolectomies. That all sounds pretty painful!  They compared five treatments: ibuprofen 400 mg, ibuprofen 800 mg, ASA 650 mg, Darvon 65 mg and placebo.  Both ibuprofen groups had similar reduction in pain scores and were better than the other 3 treatment arms.  The study was done with pooled data from two separate dentists; in one group 400 mg ibuprofen seemed slightly more effective, while 800 mg seemed slightly more effective in the other.  However, there are no data to support any statistically significant difference between ibuprofen groups in the article.

The second article, by Laska et al. in 1986 was a double blind parallel group study with 200 patients post oral surgery compared doses of 400 mg , 600 mg and 800 mg of ibuprofen.  There was no evidence of a dose response efficacy difference between 400, 600 and 800 mg.

Considering that dental pain hurts like hell, I'm inclined to believe these studies are sufficiently representative of ED patients with most injuries.  *As an aside, learn to do dental blocks, they are invaluable to patients.

With regards to ketorolac, this double blind RCT from Staquet in 1989 compared 10 mg, 30 mg and 90 mg IM ketorolac with placebo in 128 patients with cancer pain.  Again, no difference was found between the 3 ketorolac dosing regimens, with all being much superior to placebo.

Other similar studies have been done and show 10 mg is probably the ceiling dose of ketorolac both orally and parenterally.  

In the next parts of the NSAID saga, we'll discuss side effects profiles of various NSAIDs, and NSAID hodgepodge such as effect on fracture healing, use in renal colic and more.

Cheers,

SOCMOBEM  


References:

Winter et al. Oral Surg Oral Med Oral Pathol. 1978 Feb;45(2):159-66.
 
Laska et al. Clin Pharmacol Ther. 1986 Jul;40(1):1-7.

Staquet MJ J Clin Pharmacol. 1989 Nov;29(11):1031-6.

NSAIDs Part 1: Which one is best?

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I love NSAIDs!  Yup, love ‘em!

NSAIDs (Non-steroidal anti-inflammatory drugs) are some of the best analgesics available, plus they’re generally over the counter.  Despite their daily use for decades, NSAIDs remain sorely misunderstood.  I know they’re not a panacea, and they have some serious side effects in certain populations.   But for healthy patients without co-morbidities, they are pretty awesome painkillers, with no addictive potential (that I’m aware of).

Before we start, perform a Gedanken experiment if you will.  Not a true Gedanken Schrodinger’s Cat type experiment, but answer the following questions in your mind.

1) What is the best NSAID for analgesia?

2) Do oral or parenteral NSAIDs provide better pain relief?

Got your answers? Good.

Based on the conversations among staff, residents and nurses in the ED, oral or parenteral ketorolac (AKA: IM Toradol) is the strongest/bestest/most fantastic/awesome NSAID out there. 

WRONG!

I know that regardless of what I say from here on, some of you will stand by IM Toradol like a dying loved one. That’s okay, I understand.  It’s not your fault that you’ve been brainwashed into thinking this way.  Or maybe it’s anecdotal experience from years of practice, and I’m just a young pup who doesn’t know anything.

Just hear me out. 

What is the best NSAID for analgesia?

There isn’t one. 

They’re all the same when dosed appropriately. I cannot say it better than Grant Innes did in this 2005 review of ED pain medications.

“Although some agents have been advocated for specific indications (eg, indomethacin for gout), there is no compelling evidence that any one NSAID is superior to any other—for any indication. Consequently, NSAIDS should be selected based on convenience, cost, and availability rather than on theoretical efficacy advantages.”

Important to note are the dosing regimes for each NSAID, as they are more than often used in the ED:

Ibuprofen up to 800 mg QID

Naproxen up to 500 mg TID

Ketorolac up to 10 mg QID

Indomethacin up to 50 mg QID

*Edit: There is an important concept of ceiling effect with NSAIDs.  I left this out here, and it is very important so we'll discuss it in part two of the NSAID saga.  Thanks to reader @ETtube for pointing this out.

Other NSAID regimes are also found in this paper, but these are the most common ones in North America.

 

But what about IM toradol?  It always works for my patients.

I don't know but maybe these these guys know the answer.

That's right, Sanjay Arora and Mel Herbert from EM:RAP actually wrote a paper on this.  6 years ago!

I highly suggest you take 10 minutes of your day to read this great article in CJEM in 2007. The full text version is free as well.

Alternatively, I'll summarize it here.

1994 Wright et al.– Retrospective analysis of data that was collected by prior prospective survey. 

800 mg ibuprofen po vs. 60 mg ketorolac IM - NO DIFFERENCE in pain as rated by visual analogue scale (VAS)

1995 Turturro et al. – Prospective DBRCT (Double blind randomized controlled trial). 

800 mg ibuprofen vs. 60 mg ketorolac IM  - NO DIFFERENCE

1998 Neighbor and Puntillo – Prospective DBRCT. 800 mg ibuprofen vs. 60 mg ketorolac IM.  All patients had self-assessed pain between 5-8/10 on VAS. 

NO DIFFERENCE

*Funny thing about this study is the author’s name is spelled as Neighbour with a “U” in the text, but not in the references.  Funny because the Canadian CJEM autocorrect probably added the “U”.  Maybe funny just to me.*

They also cite two more trials comparing post-op pain with the same ibuprofen vs. ketorolac dosing, but at this point, you get the picture.

Finally, all of these studies compared 60 mg of ketorolac IM to 800 mg of ibuprofen.  Who actually gives 60 mg?  I've never seen it where I work, where 30 mg is the standard dose.  So, maybe ibuprofen is actually better than the 30 mg of IM ketorolac that we give.

Some of you may say, “I use the toradol for the placebo effect of an injection.  You can’t argue with that.” 

Sorry, someone studied that too.

This study by Schwartz et al. was a prospective DBRCT in which patients “were unknowingly given 800 mg oral ibuprofen in a flavoured drink and then given either a placebo IM injection or a placebo pill.”  No patient really received any IM medication in either group, and there was similarly no difference in the VAS between the two groups.  So IM for placebo effect only also appears unwarranted.  

Also, that study design is kick ass!

Treatment bottom line: 

There is no difference between NSAIDs when it comes to pain control.  Just use an adequate dose of whichever you choose.   

IM ketorolac still has a role in vomiting patients or those unable to take po meds, but don’t kid yourself that it’s a “stronger” medication.  It’s not.

Despite all of this, I agree that some NSAIDs work better for certain people?  Why is this?

Watch for parts 2 and 3 of the NSAID discussion, where we'll talk about this and much more.  

*Personal disclosure: I use ibuprofen almost exclusively, but also use Naproxen, as the BID (can go TID) dosing regimen generally means patients will be more compliant and hopefully have better pain control for a greater duration.  When we discuss side effect profiles in the coming weeks, you'll see why I don't use ketorolac.

Cheers,

SOCMOBEM

References:

Innes GD, Zed PJ, Emerg Med Clin North Am. 2005 May;23(2):433-65, ix-x. 

Arora S, Wagner JG, Herbert M. CJEM. 2007 Jan;9(1):30-2. 

Schwartz NA, et al. Acad Emerg Med. 2000 Aug;7(8):857-61. 

Drinking the PPI Hate-O-Rade

Hi all, sorry about the extended hiatus.  I was away after Christmas for about 12 days and have been getting back in the swing of things over the past week.  

Since the break, one great new blog that has popped up on the FOAMed landscape is the boringem blog, started by Brent Thoma, one of the other ER residents in Saskatoon.  You can check it out here.

Also, look for a new blog section for med ed. videos in the near future.  I'll start it out with a cardiology parody I made back as a med student.  Watch for a How To video on making a homemade cricothyrotomy trainer soon.

Onto the blog.

Proton pump inhibitors (PPIs) have been taking a beating in the FOAM arena lately, with a large portion of the credit going to David Newman of SmartEM and theNNT.  Just before Christmas, theSGEM blog did an excellent blog post and podcast on this topic as well.  The links above will allow you to review the common misconceptions surrounding PPIs, as well as the evidence to support this. 

Briefly, PPIs have been thought of as a panacea over the past decade, with the 80 and 8 bolus + infusion protocol thought of as the cure for all UGIBs.  Unfortunately, this 2010 Cochrane systematic review on PPIs for UGIB showed no reduction in mortality at 30 days, nor did it show any reduction in rebleed rates or requirement for surgery at 30 days.  Transfusion requirements and hospital LOS could not be analyzed, but there is no good, reproducible evidence that these outcomes are improved either. 

At this point, it seems pretty obvious that I'm not too keen on the empiric use of PPIs for UGIB.  Unfortunately, there's one reason we will not win this battle with gastroenterologists any time soon.  Need for endoscopic intervention.  This RCT by Lau et al. showed that despite no reduction in other significant outcomes, there was a decreased need for endoscopic therapy (28% vs. 19%, p <0.007).

As ER physicians, we do not admit or scope our UGIB patients.  We resuscitate, stabilize and refer for endoscopy.  Despite the fact that there is no change in major outcomes (eg. mortality, rebleeding and surgery), a faster endoscopy requiring less intervention remains a significant outcome for the physician performing it.  For that reason, I find it difficult to believe this battle will be won by ER physicians any time in the near future.  I would love to be proven wrong.

My question to readers is if you have discussed this with your GI docs, and what reasoning they are using for the PPI infusions?  Please post in the comments if you have.

However, I think it remains important for med students, residents and nurses to understand that the PPI infusion is not the most critical intervention in the course of the UGIB patient. 

Bottom Line: PPIs do not reduce 30 day mortality, rebleed rates or surgery requirements at 30 days.  However, because of reduced need for endoscopic intervention and the prolonged period required for knowledge translation, their empiric use will continue for the foreseeable future.

Cheers,

SOCMOBEM

References:

Cochrane Database Syst Rev. 2010 Jul 7;7:CD005415. Review. PubMed PMID: 20614440

N Engl J Med. 2007 Apr 19;356(16):1631-40.

Evidence Based Laceration Repair

First, a huge thanks to everyone who has been visiting the site, tweeting and spreading the #FOAMed love.  FOAM is all about word of mouth, and having others spread the word drives me to put up more posts.  Second, if you have comments or suggestions to improve the blog, questions for me, or myths you'd like to see busted, please tweet or email.  I'm always looking for new ideas.

Also, a shout out to a new podcast I've found recently.  The SGEM (Skeptics Guide to Emergency Medicine) podcast is based out of Ontario, Canada, and takes a similar approach to topics as I do.  Episode 9 covers some of the wound management myths I'm about to deal with, and a few others I've left out.  It can be found on iTunes or on their website http://thesgem.com/

Onto the blog.

Case: A 25 year old female presents to the ED with a 3 cm laceration to the dorsum of her forearm.  It is superficial, entering only the hypodermis.  It is easily approximated, not over a joint, and under no tension.  Before reading on, mentally go through the steps of how you would manage this wound. (eg. cleaning, prepping, suture material, dressing) Got it?  Read on.

No procedure in medicine contains as many ancient, dogmatic teachings as laceration repair.  Considering this is something we do and teach every day, it's critical that we have an evidence based approach.

In this post, I will present the thinking that goes through my head as I prepare to close a wound.

NB. Throughout this post, we are talking about uncomplicated lacerations/wounds ie: no fracture, foreign body, tendon injury, bone injury, joint injury, immunosuppression, anti-coagulation, etc.

The reason behind all of the laceration repair dogma can be summarized in one word, infection.  

We've all seen someone prepare a simple cut as if it were an open abdomen in the OR.  Why?  Not so long ago, surgeons began using sterile technique in the OR; this was critical for reducing post-op infection rates.  Naturally, that meticulous preparation was then passed down to ED physicians as lore.  

But lets think about this for a minute.  There are millions of lacerations every year, and we see a miniscule number of them in the ED.  The rest are managed at home with water, some paper towel and maybe a band-aid.  That's certainly not sterile technique.  So why aren't our departments overrun with wound infections from people who cut themselves and didn't waste 4 green huck towels, a bottle of chlorhexidine, a sterile kidney basin, and countless other tools?  Because clean wounds rarely get infected. 

Preparing wounds with sterile technique and meticulous detail is not only unnecessary from an infectious standpoint, it's time consuming.  As a medical student and resident, laceration repair is great.  It's fun, you get to work with your hands, sit down, take a mental break.  Overall, as a presenting complaint, laceration is about as good as it gets.  As I get closer to the realm of being a staff physician, I view lacerations differently, in much the same way as I look at insertion of lines and tubes (see previous blogs).  Properly repairing a laceration remains the most important element, but efficiency and managing department flow are also critical.  Furthermore, I don't want to waste my patient's time by having them unnecessarily return to the ED for follow-up, suture removal, or complications of the procedure.

Onto the pseudoaxioms.

1)Wounds must be cleaned with fancy solutions.      NO!

    VS.     


We usually clean lacerations with tap water at home, so why do we need sterile water/saline or chlorhexidine in the ED? 

Thankfully, this has been studied.

First, forget antiseptics.  There is little, if any evidence that chlorhexidine or other antiseptics reduce rates of infection.  Conversely, chlorhexidine and povidone-iodine solutions are more likely damage normal cells and slow healing.  These are skin cleansers, for external use only.

So the real choice is between tap water and sterile saline/water.

This Cochrane Review last updated in 2010 included 11 quasi-randomized studies, 3 of which were RCTs.  In adults, tap water is at least as good, if not better, than sterile saline for preventing infectious complications.  In children, there was similarly no difference between tap water and sterile saline. 

I think my favorite part of this review is the authors conclusion that there is no evidence that cleansing a wound is better than not cleansing it.  Now that would be a kick ass RCT!  Even if it passed ethics, I think you'd need a used car salesman to consent the patients for the no cleansing group.

This prospective RCT done in 2007 also compared sterile saline with tap water.  Though the study had several problems, one thing it made clear was the cost savings of using tap water in place of sterile saline, a syringe and splash guard would be ~$65.6 million annually in the U.S.  That's huge!

Disclaimer: If you don't have a clean tap water source, this likely doesn't apply, but you could still be using boiled and cooled distilled water in place of the more expensive alternatives.  

When I clean a wound in the ED, especially if it's an upper extremitiy, I will anesthetize, walk the patient over to the sink, and wash their hand under running water for a few minutes. The volume difference is huge, and it takes virtually no time at all.

Bottom line: Tap water is just as good, if not better than sterile saline for irrigating simple wounds in the ED.

2)Glove selection



After I've cleaned my patient's hand in tap water, should I grab some sterile gloves to sew them up?  Maybe the patients love to see me snap on those fancy gloves that come from their own, individually sealed bag.

Bottom Line: Clean gloves are just fine.  
The best data on this comes from a 2004 study by Perelman et al. in Annals of EM.  This Canadian study was a prospective RCT, and looked at 816 patients over the age of 1 year with simple lacerations.  They found the infection rate for sterile vs non-sterile gloves was 6.1% and 4.4%, respectively with no significant statistical difference.  

Again, the cost difference between using sterile and non-sterile gloves is massive when we consider how often they are used on a daily basis.  

I will admit that in cases that require a significant amount of suturing or I want an optimal cosmetic result, (eg. facial lacs) I will use sterile gloves because they provide a much better feel than the non-sterile ones.  Go ahead and call me a hypocrite.  

3)All lacerations must be sutured using non-absorbable suture.

First, there is evidence that not all lacerations < 2 cm even require suturing in the first place.  But let's say that we do decide to close this laceration, how will we do it?

Who asks for prolene, ethilon or another non-absorbable suture when they repair lacerations?  What about vicryl rapide, fast chromic gut or another absorbable suture?  Does anyone ask for glue?

Has anyone heard this: Don't use absorbable sutures or glue, they'll get a nasty scar! 

Let's look at the evidence.

First let's take the scenario of the 3 year old child with a non-gaping facial laceration after running into a coffee table.  I'm sure many of us have gone through the joy of anesthetizing this child and suturing them while a nurse holds them in a death grip.  All the while, the parents are looking on horrified and never wanting to return to the hospital.  

 

While rotating through the Alberta Children's Hospital (AKA Lego-land with an ICU), I was exposed to all the awesome ways of repairing lacs in kids.  The children would have topical maxilene or lidocaine applied at triage and we would sometimes give intranasal midazolam as well.  Suffice it to say, this place is pretty much heaven as far as peds EM is concerned, and laceration repair was all happiness and roses.  Unfortunately, most of our EDs do not have these luxuries, but we do have one awesome thing.  Glue!

Again we have some Canadians to thank for this Cochrane Review looking at tissue adhesives vs. standard wound closure for laceration repair.  Eleven studies compared a tissue adhesive with standard wound closure. No significant difference was found for cosmesis at any time point examined. As would be expected, pain scores and procedure time significantly favoured tissue adhesives.  However, there was a statistically significant increased rate of wound dehiscence favouring standard wound care, with a NNH of 40.   

But what about gaping lacerations where glue won't work?

Traditionally we are taught to always use non-absorbable sutures, as they are stronger, less prone to infection, etc.  Having been sutured up several times as a child, I recall fearing the return visit for suture removal even more than the initial visit to get sewn up.  When a child is bleeding everywhere, the pain is bearable, but pulling out the scissors and forceps in front of a completely well child creates unnecessary fear.

Can we avoid this return visit without compromising cosmesis?  Yes.

This 2004 paper by Karounis et al. looked at pediatric patients (0 to 18 years) with traumatic lacerations.  It showed no differences in early or late cosmesis, wound dehiscence or need for scar revision when comparing absorbable and non-absorbable suture.  In fact, all of the outcomes showed a trend toward benefit in the absorbable suture group.  (I know, trends don't mean squat in EBM)
The main weakness of this study was the extremely high loss to follow-up of 34%.  However, this is a very common weakness of laceration repair studies, and getting good follow-up in these types of studies seems impossible.

Another study from 2008 looked at fast absorbing catgut suture vs. nylon in 88 pediatric patients.  Again there were no differences in cosmesis, infection rate, dehiscence, keloid formation or parental satisfaction.  This paper also suffered from a lack of follow-up (though it was equal in both groups).

Bottom Line: For non-gaping lacerations, glue is where it's at.  For gaping lacerations in children, absorbable suture is at least as good as non-absorbable. 
The savings on patient/parental trauma and time are huge. 

Note: Although I didn't cover staples, they are likely as good as sutures for repairing scalp lacerations.  There are small studies comparing them, but no large RCTs.

4)After closing the wound you should apply a topical antibiotic such as polysporin/neosporin.

This one may be my biggest peeve of all, as somehow the marketing of topical antibiotics that are primarily effective against Gram -ve bacteria has resulted in physicians regularly recommending these to patients.  For this, we have to go to the Dermatology literature.  This peeve comes from doing 6 weeks of dermatology electives, several of which were spent with someone who only did patch testing for contact dermatitis.

It is true that a clean, moist, covered wound will heal faster than an uncovered, dirty wound.  However, all of the dermatology literature points toward non-antibiotic containing petroleum based lubricants being equally efficacious to neomycin (Neosporin), bacitracin and polymixin B (both in Polysporin) containing ones.  Furthermore, neomycin is the number one contact allergen in patch testing at a whopping 11% of the U.S. population.  Bacitracin is not far behind at 8% of the population.
Fortunately Neosporin is no longer sold in Canada, but it is the bane of American dermatologists.

Bottom Line: Use Vaseline, Aquaphor or other petrolatum based gel for wounds, and stop creating allergies.


Summary:

1)Tap water is as good as sterile saline

2)Clean gloves are fine

3)Glue and absorbable sutures provide the same cosmetic results as non-absorbable ones, particularly for facial lacerations.

4)Use non-antibiotic, petrolatum based gels to cover wounds, not poly/neosporin.

You now have all the evidence you need to manage simple lacerations in 5-10 minutes, without putting your patients at increased risk of infection, giving them an ugly scar, or causing a contact dermatitis.

Until next time, I'll be getting up in people's faces, not minding my own business.  I'm way less likely to get stabbed that way.  

Happy sewing.

SOCMOBEM


References:

Cleaning Wounds:

Fernandez R, Griffiths R. Water for wound cleansing. Cochrane Database of Systematic Reviews 2008, Issue 1. Art. No.: CD003861. DOI: 10.1002/14651858.CD003861.pub2. 

Moscati RM et al. Acad Emerg Med 2007; 14:404–410

Gloves:

Perelman VS et al. Ann Emerg Med. 2004 Mar;43(3):362-70.

Suture and glue:

Farion KJ, Russell KF, Osmond MH, Hartling L, Klassen TP, Durec T, Vandermeer B. Tissue adhesives for traumatic lacerations in children and adults. Cochrane Database of Systematic Reviews 2002, Issue 3. Art. No.: CD003326. DOI: 10.1002/14651858.CD003326. 

Karounis H et al. A Randomized, Controlled Trial Comparing Long-term Cosmetic Outcomes of Traumatic Pediatric Lacerations Repaired with Absorbable Plain Gut Versus Nonabsorbable Nylon Sutures Acad Emerg Med July 2004; 730-735

Luck RP et al. Pediatr Emerg Care. 2008 Mar;24(3):137-42.

 

All about chest tubes

Of all the interventions we perform, chest tube insertion is one of the most dangerous, complicated and misunderstood.  Today I'll discuss not only the myths, but also some unfortunate realities that we must understand when we undertake this procedure.

Myth # 1

Bigger is better

I'm pretty sure we've all been told, partially thanks to ATLS, that we better put a 36 or 40 French chest tube in during trauma, otherwise the blood will clog up the tube and drainage will cease.  Wrong, wrong, wrong!

This prospective, non randomized trial of trauma patients over a 3 year period from 2007-2010 compared small (28-32 French) with large (36-40 French) chest tubes.  The operator chose tube size, and sicker patients got bigger tubes (More ISS >25, GCS <8, sBP <90, (all p<0.01) for large chest tube group)  However, there was no difference in thoracic trauma pathology between the two groups (eg. flail chest, pulmonary contusions, PTX, pneumomediastinum, etc.)

Overall, there was no difference in the rate of complications between the two groups.  This includes pneumonia, empyema and retained hemothorax.  Further, there was no difference in interventions required for retained hemothorax (Additional chest tube insertion, intrapleural throombolysis, IR guided catheter insertion, VATS and thoracotomy)
When adjusted for ISS, GCS and sBP, there was still no difference between the two groups, with respect to complication rates or interventions for retained hemothorax. 

When pneumothoraces were analyzed separately, there was no difference in rate of complications or requirement for further intervention in this group either.

The second hypothesis of this study was that bigger tubes are more painful, and a visual analogue scale was used to rate patient pain.  There was no difference in VAS scores between the small and large chest tube groups.

Bottom Line: Any tube that is at least 28 French is suitable for draining a chest.  

Although it might not hurt less than a larger tube, it may still pass through the intercostal space a little more easily, so go ahead with those smaller tubes.  The logical next question is: Are tubes smaller than 28 French adequate?  That remains to be studied.

Myth #2

Directing the chest tube.  ie: Up for air, down for blood.

Every medical student/resident is asked this question repeatedly throughout their training.  "Where would you put the tube for a hemothorax?  What about a pneumothorax?"  The answers is always posterobasal for fluid and apical for air, right? 

2 things about this myth.  First, once the tube gets inside the chest, our ability to direct it is poor.  Second, as long as you are in the pleural space, you'll be fine.  It is a closed system and you have suction.  The fluid will drain regardless.  You may still have complications, but it's not because you put the tube in the apex of a hemothorax.

More important than directing the chest tube is ensuring it's in the pleural space, not advancing when you meet resistance and not causing any other complications.

There is a BestBets on this topic which can be found here.  There really isn't great data on this, so it is more of a physics myth than anything else.

Truth #1

Complications of chest tubes - This is not a myth, this is for real.

This is one critical point for all of us, but especially for residents inserting chest tubes.

The morbidity associated with chest tube insertions is astronomical!  About 25-30% of chest tube insertions have a complication, regardless of who inserts them.  A 2012 AAST study looking at post-traumatic empyema rates in major trauma centers is 27%.  That is crazy.
However, as an EM resident, I was disappointed to read this article that suggests EM residents may be the worst of all.  Really it's only a trend toward significance, and a retrospective study, but I'm still a bit sad to read it.  

We have to do something to get these rates of complications down.  

Use of antibiotic prophylaxis when inserting chest tubes is a topic of controversy.  EAST (The Eastern Association for the Surgery of Trauma) published a guideline in 2000 suggesting antibiotic prophylaxis for chest tube insertion.  More recently, this meta-analysis reviewing antibiotic prophylaxis was published in 2012.

For penetrating trauma, I would say that at least a single dose of antibiotic (1st gen cephalosporin) should be given at the time of insertion, if time and resources allow. This results in reduced rates of empyema and pneumonia, which in turn affects hospital and ICU LOS. 

For blunt trauma, which is the majority of what we see in Canada, no statistically significant reduction in infectious complications was found, and you may choose to withhold antibiotics in this group.

In all cases, duration of therapy is controversial.  It appears that short term (single dose or 24 hours) is equally effective as prolonged antibiotics (until time of chest tube removal).

Bottom line: Our rates of post-chest tube complications (empyema and pneumonia) are ridiculously high, even in major trauma centers.  A single dose of cefazolin at the time of chest tube insertion is a pretty benign intervention, and in my opinion warranted, particularly in penetrating trauma.

I'm curious who is giving antibiotics and if so, is it single dose, 24 hours, or longer?

Summary:

1)Any chest tube at least 28 French is suitable for traumatic hemo/pneumothorax.

2)Get the tube in the pleural space but direction doesn't matter.

3)Complications of chest tubes are exceedingly high.  Give a single dose of peri-procedure antibiotics (particularly in penetrating trauma) and use sterile technique.

Until next time, I'll be standing on the corner, mindin' my own business. 

Cheers,

@SOCMOBEM

References and some chest tube links from people much more intelligent than me:

Own the chest tube with Chris Nickson at Life in the Fast Lane

Michael McGonigal's Trauma Professionals Blog has some great videos and posts about chest tubes as well.

Eastern Association of Surgeons for Trauma (EAST) Guidelines for Hemothorax and Occult PTX can be found here.

EAST Guideline on antibiotic prophylaxis for tube thoracostomy can be found for free here.
This is the reference. J Trauma. 48(4): 758-759, April 2000.

2012 Meta-analysis for antibiotic prophylaxis
Bosman A, de Jong MB, Debeij J, van den Broek PJ, Schipper IB.  Br J Surg. 2012 Apr;99(4):506-13

Chest tubes: Does Size Matter
Inaba, K et al. J Trauma 72(2):422-427, 2012.





Post-traumatic chest tube empyema rates
J Trauma 73(3):752-757, 2012.