Tag Archives: pneumothorax

The Deal with Seals

Greg Brown returns to look at an important thing relevant to first responders (and lots of other people really) – the sucking chest wound. 

We’ve all been there – sitting through some kind of “first aid” training and having some kind of “first aid trainer” speaking authoritatively on some kind of “first aid style” topic. If you are like me you’ve used your time productively over the years and perfected what my wife refers to as “screen-saver mode” – it’s that look on your face that tells the instructor that you are listening intently, often supplemented by the insertion of “knowing nods” or head-tilts, but in actual fact you are asking yourself “if I was able to collect all of my belly button lint over a 12 month period and spin it into yarn, I wonder if I could make enough to abseil off London Bridge?”

Don’t get me wrong – I reckon effective and accurate first aid training should be a mandatory part of having a car / bike / truck / bus licence. More appropriately trained people should mean faster recovery rates for most injured people (and less work for overstretched first responders).

It’s just that sometimes first aid trainers teach stuff based on ‘we reckon’ or ‘that’s how we’ve always done it’ rather than evidence or knowing it works in the real world. This post is about one of those things.

“What is a sucking chest wound?”

In the Army questions come in a few different shapes and sizes. A popular one is “there is only one obscure answer you should have guessed I wanted”. Trust me, the muzzle velocity of your primary weapon is 970 metres per second.

Another popular one is “the question that should be about one thing, but is actually to demonstrate a quite tangential point”.  Like,

“What is a sucking chest wound?”

For an army instructor the answer is not what you are thinking right now. It is “Nature’s way of telling you that your field craft sucks and everyone can see you and now you got shot”.

Let’s Go With the Medical One

We’re going to go with the alternative, more medical one. A sucking chest wound is defined as air entering the thorax via a communicating wound that entrains air into the space between the lungs and ribs more readily than the lungs can expand via inspiration through the trachea.

This is about pressure differentials – in order to inhale, the lungs must generate a relative negative pressure such that air can be sucked into them via the trachea. But if you make a big communicating hole in the trachea, that might become a pretty big highway for air to enter the space with the negative pressure.

The communicating hole does need to be pretty big. Depending upon which textbook you read, this hole needs to be a minimum of a half to three quarters the diameter of the trachea. Also, the patient needs to be undergoing relative negative pressure ventilation (or, in simple terms, breathing spontaneously). If they are being artificially ventilated (which requires positive pressure) then the pressure inside the lungs will be higher than the pressure on the outside of the body; the result is that air will be forced out of the intra-pleural space (or thorax) by the expanding lung (as opposed to being entrained into the thorax via the hole in the chest).

Are sucking chest wounds really that bad?

Well, yes. They suck in fact.

A sucking chest wound creates what is known as an open pneumothorax. Let’s consider the option where that hole does not seal on expiration. We’ll get onto the also very annoying sealing with a flap version in a bit.

In this slightly not so annoying case, the patient will have a ‘tidalling’ of air in and out of this communicating hole. The effect? Respiratory compromise, increased cardiovascular effort and reduced oxygen saturations. Patient satisfaction? No, not really. Death? Maybe – depends on what other injuries exist and the ability of the individual to compensate. See Arnaud et al (2016) for more details.

But if this communicating hole were to seal itself on expiration then you now have an open tension pneumothorax. Sounds bad; IS bad.

In such a case, each time the patient breathes in they will entrain air through the communicating hole in the chest wall (that whole “negative pressure” thing in action). But when they breathe out, instead of having that additional intra-pleural air tidal outwards, the flap will seal it in place; each time they breathe in, the volume of trapped air will increase and you’ll end up with the tension bit.

How much air is required? Well a randomised, prospective, unblinded laboratory animal (porcine) trial conducted by Kotora et al (2013) found that as little as 17.5mL/kg of air injected into the intra pleural space resulted in a life-threatening tension effect.

Actually, that’s a fair bit of air…for those of you who are lazy and don’t want to do the math, that’s 1400mL for an 80kg person. But remember, any tension pneumothorax (open or closed) is progressive – each time you breathe, more air is trapped; therefore, it doesn’t take long to reach crisis levels.

“But are they common enough for us to be worried about?”, I hear you asking. The short answer is yes – in fact, the long answer is also yes.

Kotora et al (2013) reviewed the statistics from the Joint Theater Trauma Registry regarding contemporary combat casualties with tension pneumothorax and found that they accounted for 3 – 4% of all casualties, but 5 – 7% as the cause of lethal injury.

“Yes, but I don’t live in a combat zone…”, I hear you say. I have two responses:

  1. Good for you; but also,
  2. According to Littlejohn (2017), thoracic injury accounts for 25% of all trauma mortality. And sure that stat is for all forms of thoracic injury and a sucking chest wound is but one of those but there’s a neat article by Shahani which sums up the incidence nicely and it turns out you should give this some thought.
The Table
We even saved you some time by grabbing the relevant image.

So, your field craft sucks – now what?

Now that we know that sucking chest wounds are both possible and bad, we should probably discuss treatment.

Some History

Back in the mid 1990’s, Army instructors were very big on rigging up a three-sided dressing. Unwrap a shell dressing, turn the rubbery-plastic wrapper into a sheet and tape three sides down with the open bit facing the feet to allow blood drainage.

And, in an astonishing turn of events, everyone I’ve met who tried this confirmed it didn’t really work that well.

In that Littlejohn paper they make reference to the fact that by the 2004 ATLS guidelines (which are not usually that quick moving), it was being written unblock and white that there was no evidence for or against the three-sided dressing option. It was done because it sounded good in theory, but the evidence wasn’t there.

Now to the New

Actually, not that new. Chest seals already existed.

These chest seals (at that time the Bolin produced by H & H Medical, and the Asherman produced by Teleflex medical) included one-way valves to allow for the forced escape of trapped intrathoracic air and blood. basically they took the impromptu three-sided dressing and made it a ready-made device in the form of an occlusive dressing with an integral vent.

But did they work?

Yes and no.

On a perfectly healthy (albeit with a surgically created open pneumothorax) porcine model with cleaned, shaved, dry skin they sealed well and vented air adequately.

However, once the skin was contaminated (dry blood, dirt, hair etc) the Bolin sealed much better than the Asherman. And if there was active blood drainage too (such as in an open haemo-pneumothorax) then all bets were off. Both vents clogged with blood and ceased to work. Sure, you could manually peel the seal back and physically burp the chest but if you did so the Bolin became an un-vented seal and the Asherman was as good as finished (i.e. it wouldn’t reseal). But hey, at least you had sealed the communicating hole and in doing so stopped entraining air.

“Is this the best you can do?” you may be asking. Well to be honest, since the vents didn’t work for more than a breath or two most people decided that the vents were pointless. The outcome was that we all decided to forget about the vents and just seal the wound. That way, assuming that there was no perforation to the lung, this open tension pneumothorax (aka sucking chest wound) became a routine, run of the mill, plain old pneumothorax. And if there were signs of tensioning (e.g. increasing respiratory distress, hypotension, tachycardia….) one just needed to peel back the seal and manually burp the communicating hole thus relieving the pressure. Use a defib pad – those bad boys stick to anything! Problem solved….

Or how about a newer idea + research?

In 2012 the Committee on Tactical Combat Casualty Care (CoTCCC) started questioning the efficacy of contemporary practices regarding the placement of chest seals on sucking chest wounds. It had already been accepted that the current vented chest seals had ineffective vents, so practice had changed from using a chest seal with an ineffective vent to simple, “soldier proof” unvented seals and burping them as required. Surely there had to be a better way…?

Kotora et al (2013) decided to test three of the most readily available vented chest seals in their aforementioned randomised, prospective, un-blinded laboratory animal (porcine) trial: enter the Hyfin, Sentinal and SAM vented chest seals.

What they found was that all three were effective in sealing around the surgically inflicted wounds and in evacuating both air and blood. Thus, in 2013, CoTCCC changed their recommendations back to the use of vented chest seals.

But there were still some questions:

  1. Once life gets in its messy way, do they seal (or at least stick to skin)?
  2. Are all vent designs equal?

To answer question 1, Arnaud et al (2016) decided to evaluate the adhesiveness of the 5 most common chest seals used in the US military using porcine models. What they found was that the Russell, Fast Breathe, Hyfin and SAM all had similar adherence scores for peeling (> 90%) and detachment (< 25%) when tested at ambient temperatures and after storage in high temperature areas when compared to the Bolin. The researchers admitted, though, that further testing was required to assess the efficiency of the seals in the presence of an open tension haemo-pneumothorax.

In response to question 2, Kheirabadi et al (2017) tested the effectiveness of 5 common chest seals in the presence of an open tension haemo-pneumothorax (again, on porcine models). Essentially, there are two types of vent: (i) ones with one-way valves (like in the Bolin and Sam Chest Seals), and (ii) ones with laminar valves (like in the Russell and Hyfin Chest Seals). Their question was: do they both work the same?

What they found was that when the wound is oozing blood and air then seal design mattered. They found that the seals with one-way valves (specifically the SAM and Bolin) had unacceptably low success rates (25% and 0% respectively) because the build-up of blood either clogged the valve or detached the seal. By contrast, seals with laminar venting channels had much higher success rates – 100% for the Sentinel and Russell, and 67% for the Hyfin.

The Summary


  1. Sucking chest wounds are bad for your health.
  2. Sealing the wound is good.
  3. If the seal consistently allows for the outflow of accumulated air and blood, then that’s even better.

Therefore, now that we know all of this, one’s choice of chest seal is important. At CareFlight we use the Russell Chest Seal by Prometheus Medical (and no, we’re not paid to mention them we’re just sharing what we do). Why? Because it works – consistently. Both for us and in all the aforementioned trials.


The premise of this addition to the Collective is that you’re a first responder. That being the case, use an appropriate vented chest seal on a sucking chest wound.

However, you still need to recognise that the placement of the seal does not automatically qualify you for flowers and chocolates at each anniversary of the patient’s survival – you still need to monitor for and treat deterioration. Such deterioration is likely to include a tension pneumothorax for which the treatment is outside of the scope of most first responders (other than burping the wound).

If you are a more advanced provider then your treatments might include the performance of a needle thoracocentesis, or perhaps intubation with positive pressure ventilation and a thoracostomy (finger or tube).

In essence, know the signs and symptoms then master the treatments that are inside your scope of practice. (Or you could enrol in a course…such as CareFlight’s Pre-Hospital Trauma Course or even THREAT… OK that was pretty shameless.)

Meanwhile we’d love to hear:

  1. What chest seal do you use?
  2. Why?
  3. How does it go?

Or you could just tell us what other things you think suck.

Could be the leafy green thing. Could be a person maybe.


We’re not kidding about hearing back from you. Chip in. It only helps to hear other takes.

You could also consider sharing this around. Or even following along. The signup email thing is around here somewhere.

That image disparaging all things Kale (or kale) is off the Creative Commons-type site unsplash.com and comes via Charles Deluvio without any alterations.

Now, here are the articles for your own leisurely interrogation.

If you’re time poor and will only read one, make it this one by Littlejohn, L (2017). It’s “Treatment of Thoracic Trauma: Lessons from the Battlefield Adapted to all Austere Environments”. 

Another great one (albeit somewhat longer) is by Kheirabadi, B; Terrazas, I; Miranda, N; Voelker, A; Arnaud, F; Klemcke, H; Butler, F; and Dubick, A (2017). It’s “Do vented chest seals differ in efficacy? An experimental evaluation using a swine hemopneumothorax model”.

An oldie but a goodie is this one by Kotora, J; Henao, J; Littlejohn, L; and Kircher, S (2013). It’s “Vented chest seals for prevention of tension pneumothorax in a communicating pneumothorax”.

To round it out, take a squiz at Arnaud, F; Maudlin-Jeronimo, E; Higgins, A; Kheirabadi, B; McCarron, R; Kennedy, D; and Housler, G (2016) titled “Adherence evaluation of vented chest seals in a swine skin model”.

Sucking or Blowing – What’s the Difference?

Sometimes it’s worth wondering if the things we hear, see and feel are quite as we thought they were. Dr Alan Garner has a look at your senses when you get into the chest and wonders whether it’s all as straight forward as we like to think? 

Let’s start this post by stating right upfront that this is about chest wounds.  If that is not what you were thinking then time to look elsewhere.

What I want to discuss is the clinical diagnosis of tension pneumothorax in the field.  The reason for the discussion is that I believe it is way over-diagnosed.  When I worked in the UK 6 years ago it seemed tension was being diagnosed frequently and the reason given was the sound as they breached the pleura with the forceps.  As the patient was positive pressure ventilated at the time then the sound must have been air rushing out of the pleural space as their intrathoracic pressure was positive throughout the respiratory cycle right?

Remember how we can’t rely on the sounds involved in clinical examination in the prehospital environment because they’re too unreliable? Well I was being told this one was always right. ‘Always’ is a big word in medicine

I’m also aware of at least one case where a patient with a single epigastric gunshot wound from a low velocity weapon had intubation and then bilateral finger thoracostomies.  The comment at the time was that the prehospital doctor, who no doubt went into it all in good faith, stated that at the time of the thoracostomies they found a pneumothorax on one side and a tension on the other.

However on imaging and surgery the projectile went straight back into the pancreas and nowhere near either hemithorax or the diaphragm.  Indeed the only injuries identified to any part of the chest were the thoracostomy wounds themselves.  Again an intubated patient so the intrathoracic pressure must have been positive right?  If the lung felt down then it had to be a pneumothorax?  And if there was a sound on breaching pleura it must have been a tension?

Clearly in the second case the signs were misleading so what is happening here? Let’s put aside for a second the challenges of the initial diagnosis of pneumothorax and focus on the feel with the finger and the sound to the ears. Could it be that some of the evidence we’ve been lead to believe tells us we’re dealing with a pneumothorax can mislead experienced, well trained clinicians?

Diving In

Perhaps I have done a few more chest drains than most.  Partly that is due to more than 20 years in the prehospital space but I probably did even more when I was a registrar 25 year ago.  I spent 6 months working for a couple of respiratory physicians and I put lots of drains (mainly for malignant effusions) in patients who certainly did not have a pneumothorax before I started.  It was common to hear a noise as the pleura was breached as the air rushed in.  But this of course was in spontaneously ventilating patients and that is different right?

Obviously we need to go back to the physiology to see what is driving the movement of air either into or out of the hole we have made to determine whether the sound we are hearing is air going in, or air going out.

Back to Basics

Transpulmonary pressure is the pressure gradient that drives normal ventilation.  It is the difference between the alveolar pressure and the intrapleural pressure in the lungs.

Ptp = Palv – Pip. Where Ptp is transpulmonary pressure, Palv is alveolar pressure, and Pip is intrapleural pressure.

(If you’d like a little more on this the excellent Life in the Fast Lane has a bit on transpulmonary pressure here.)

Also it turns out that you can get a google preview of John West’s classic textbook on respiratory physiology. Take a moment to go and enjoy Figure 4-9 on page 59. 

You can see from panel B (I meant it, go and have a look) that intrapleural pressure varies between about -5 and -8 cmH2O at the mid-lung level during normal respiration. It is always negative and that’s due to elastic recoil of the lung which is being opposed by the chest wall. It is less negative at the dependent regions of the lung (reducing alveolar size) and more negative at the apex (increasing alveolar size).

Let’s Add Air

In the situation of a small pneumothorax the air in the pleural space makes the intrapleural pressure less negative and the driving pressure difference for ventilation is therefore reduced.  If the pneumothorax is completely open to the air such as with an open thoracostomy wound the intrapleural pressure is equal to atmospheric pressure, the elastic recoil of the lung causes complete collapse and ventilation by chest expansion is impossible – positive airway pressure has to be applied.

It is not the situation of the pneumothorax that particularly concerns me.  If they are hypoxic or hypotensive and the patient has a pneumothorax the chest should be decompressed – a complete no-brainer.  The question is why are good clinicians decompressing normal chests and thinking there was a pneumothorax or even a tension when there was not? Does the physiology lead us there?

Patient One

First let’s consider the non-intubated patient with normal respiration and no pneumothorax.  This is the situation with the patients with malignant effusions I was putting drains in years ago.  Here the alveolar pressure is never more than a cmH2O or two positive or negative.  The intrapleural pressure however is -5 to -8 cmH2O.  Therefore it does not matter what phase of respiration you breach the pleura, the pressure gradient between the pleural space and atmosphere is negative and air will rush in.

The gradient is bigger in inspiration when alveolar pressure is negative (and therefore the total pressure is around -8 cmH2O) and less negative during expiration when it is more like -5 cmH2O.  It is however always negative.  It does not matter which part of the respiratory cycle you breach the pleura, air is going to flow into the pleural space and the elastic recoil of the lung will drive it to collapse.  If you hear a noise as I often did, it is air rushing in, the classic sucking chest wound. An iatrogenic one.

Patient Two

I don’t think anyone would have an issue with things so far.  So let’s move on to the intubated patient who does not have a pneumothorax.  I am going to assume here that there is not a lot of airway resistance in our trauma patient (which is not to say they don’t have underlying obstructive pulmonary disease, anaphylaxis to the induction drugs you gave or a clot sitting in a big bronchus/ETT) as it makes the discussion a bit easier to assume that resistance is minimal (futile according to the Daleks) and the pressure you are seeing on your ventilator gauge is largely transmitted directly to the alveoli.

Looking at our transpulmonary pressure equation, unless the airway pressure and hence alveolar pressure is higher than about 5 cmH2O then the gradient at the time you open the pleura means air is going to enter the pleural cavity.  (If they have significant airway resistance this could happen with much higher airway pressures).

Just have a quick eyeball of this time pressure chart of a standard volume cycled ventilator with no PEEP (and a self-inflating bag will provide a similar though more variable trace).  And I deliberately have no PEEP in this chart.  PEEP is not likely to be the first thing we reach for in the hypotensive trauma patient we have just intubated where we are concerned about the possibility of a pneumothorax.


With normal lungs the peak pressure here is probably about 20 cmH2O.  What proportion of the total respiratory cycle is the airway pressure (and hence the alveolar pressure in our patient with low airway resistance) likely to be below 5 cmH2O?  If your little prehospital ventilator has a roughly 1:2 I:E ratio as most do, then the answer is most of it.

In other words unless you have PEEP of at least 5 cmH2O even in your intubated patient the transpulmonary pressure is negative for a good half of the respiratory cycle.  During at least half the respiratory cycle, if you hear a noise as you breach the pleura you are hearing air rushing IN.

The elastic recoil of the lung is the reason that you feel the lung has collapsed by the time you pull the forceps out and put your finger in unless you have some PEEP in play.

Now I’m not saying there has never been a time when the air wasn’t rushing in. I don’t think much of the word “always” in medicine, remember? I’m just suggesting that what we know of physiology would argue that there is at least a solid proportion of the time where that transpulmonary pressure gradient is negative when you breach the pleura, which means that there’s likely to be a good proportion of cases where those “certain” clinical signs become less reliable.

For a demonstration of this with the mother of all open thoracotomies (in a cadaver) check out this video.

The cadaver is intubated, a “generous” pleural decompression wound has been created, and on each expiration the lung collapses right down unless PEEP is applied.  And note the collapse is complete on each expiration.

As long as the thoracostomy is big enough to freely communicate with the air (and if you are relying on the open “finger” technique rather than putting in a drain it needs to be large or they may re-tension), when you put your finger in during expiration the lung will be collapsed unless there is a reasonable amount of PEEP splinting things open pretty impressively.

It will be collapsed whether it already was before you made the wound or whether it happened as you spread the forceps and made the communicating hole.  The time between making the hole and getting that sense of lung up or lung down with the finger is ample time for the lung to collapse down. It seems like this particular clinical sign probably tells you nothing about the state of play prior to the wound being made.

So noises can be deceptive and feeling a collapsed lung just means that the lung recoiled as the pleura was opened.  Can you even guarantee which phase of the respiratory cycle the patient was in when you made that hole? Unless you had at least 5 cmH2O (and maybe more) PEEP on at the time you breached the pleura neither of these signs necessarily means anything.

Maybe none of us can trust our big ears?

Now, what?

Again, I’m not really into saying things like “always” or “never”. What I’m suggesting is that there might be a lot more grey around these clinical signs than might first seem to be the case.

So how do you know if they had a pneumothorax? For me that is almost always by ultrasound now.  I don’t know how I managed for 15 of those 20+ years of prehospital care without one.  Sometimes of course the scan is equivocal and you need to make a call based on the signs you see and the condition of the patient but I find this to be very infrequent with a good high frequency linear probe.

And as for tension the hallmark is abnormal physiology, particularly blood pressure.  If decompressing the chest fixes the physiology then they had a tension.  If it does not then they had a simple pneumothorax – or none at all.  Because the noise you heard as you breached the pleura may have been air either entering or leaving the building, hearing a noise does not help you either way.  Was Elvis ever in the building at all?



I had the brilliant Dr Blair Munford review a heap of the physiology here to make sure it matched up.

After that link to the LITFL bit on transpulmonary pressure again? Then go right here.

And John West’s masterpiece (well at least the page mentioned) is here.

That image of Nahni with the big ears was posted to the Creative Commons part of flickr by Allan Henderson and is unaltered here.

Oh, and in case you didn’t know the truly amazing John West, Adelaide boy made good, has recorded his whole lecture series for you to go and watch. Because when you’re in your 80s you’ll probably be contributing to medical education like that too, right?