The Bind About Pelvic Binders – Part 4

Is this the last bit for now? Dr Alan Garner following up on pelvic binders after all the stimulating comments. If you haven’t already, check out part 1, part 2 and part 3.

During the writing of part three of this series on pelvic fractures and particularly after reading Julian Cooper’s comments (thank you Julian) I realised that the observational data around pelvic binders does not entirely fit with the theories. Let’s start with the theory and I might directly borrow Julian’s comments from Part 2 as he says it better than I could:

“In any type of pelvic injury. the bleeding will be either:

  1. Venous or bone ends: in which case keeping things still with a binder is likely to allow clot formation (low pressure bleeding, low or high flow).
  2. “Slow” arterial (the sort of thing seen as a blush on contrast CT) which will probably trickle on even with a binder but at a rate which is compatible with survival to hospital and (ideally) interventional radiology if they don’t stabilise spontaneously (high pressure, low flow bleeding).
  3. “Fast” arterial (e.g. free iliac rupture) which is likely to be fatal whatever one does, binder or not (high pressure, high flow bleeding).”

I need to state right up front that I agree with all of this. It all seems entirely reasonable and there is some cadaver evidence that movement of fractures associated with patient movement (e.g. sliding a patient from stretcher to a bed) is reduced when a binder is applied. It seems reasonable that a binder might slow, or at least reduce aggravation of venous and bone end bleeding with movement. It might even help the “slow” arterial bleeders too.

So what is my issue with all this? Studies like the Tan paper (15 patients) describe a dramatic and immediate increase in blood pressure associated with applying a binder to an “open book” style fracture and reducing it. Mean arterial pressure increased from 65mmHg to 81 and HR fell from 107 to 94 per min 2 minutes after application. The effect was associated with (although of course not necessarily caused by) reduction of the fracture. Nunn’s series of 7 patients showed even more dramatic changes in blood pressure measured at 15 minutes post binder application although they do not report the degree of fracture reduction achieved. Again we are dealing with tiny numbers of patients but the effect seems consistent – in shocked patients with anteroposterior compression or mixed type injuries who have a binder applied the blood pressure usually immediately rises (note one patient in Tan series who significantly deteriorated). In Nunn’s series with BP reported at 15 mins post application it is possible that the pelvis was “stabilised” and then a big fluid bolus was given but this cannot be the case in the Tan series where the effect is seen immediately.

Stabilising the pelvis against further movement and stopping venous and bone end bleeding cannot be the mechanism for this sudden rise in BP. Even stopping the “slow” arterial bleeders could not create such an immediate effect.

So what is going on? Warning – brainstorming not supported by any evidence following:

  • Compression of arteries in the pelvis resulting in increased systemic vascular resistance? (warned you about the brain storming – this seems pretty unlikely to me)
  • Compression of distended venous spaces causing a fluid shift back into the central circulation and increased BP. If this is the case then what you are seeing is a MAST suit effect and this has been shown to not necessarily be a good thing if you don’t also stop the bleeding.
  • One of my colleagues suggested it is pain associated with binder application that is causing the BP rise? Again doubt this is the case. Also not sure this is helpful if you are not also stopping the bleeding (as per MAST suit issues)

I don’t actually have a good theory for what is going on here but the effect is very clearly described in the literature. It seems to be a good thing although the Nunn paper in particular notes that ongoing volume resuscitation and other measures to stop the bleeding are usually then required. If anyone has any theories on what is happening here then please share with the rest of us.

A Recap

I might summarise the literature on pelvic binders as:

  • No study has yet demonstrated a significant decrease in mortality associated with binders
  • Increased fragment displacement, haemodynamic deterioration and some really ugly pressure injures (have a look at the case report by Mason for an absolute shocker) have been described with their use i.e. they are not benign.
  • They might decrease venous and bone end bleeding by preventing movement but we currently have no direct evidence to support this. Agree that this seems reasonable though.
  • An improvement in haemodynamics is often seen immediately at the time of application of a binder in shocked patients with an open pubic symphysis. Mechanism for this is currently unknown and we don’t have enough evidence to know whether this is actually a good thing or not. Going right back to part 1 of this series we should be very cautious about using surrogates such as improved BP as measures of outcome or binders may turn out to be MAST suit Mark 2.

I don’t want to be a wet blanket but I do believe that this is a realistic evaluation of the current evidence.

The Bottom Line on What I Do

Do I personally use binders prehospital?

Yes I do unless the injury is clearly lateral compression. I also am not afraid to loosen it again if the patient deteriorates. I think they are helpful for the open symphysis patients based on the documented haemodynamic improvement often seen in these patients but I acknowledge that I am hoping that this BP rise translates into lower mortality but I don’t have evidence to support this. I definitely will never criticise someone who has not put one on as there is just not enough evidence one way or the other.

Time for a segue – and perhaps a paradigm shift.

Come this way for other new thoughts but no more bad visual puns, people of the future. [Via Alan Kotok on flickr under CC 2.0]
Come this way for other new thoughts but no more bad visual puns, people of the future. [Via Alan Kotok on flickr under CC 2.0]
The Ones Who Need More

Let’s look at Julian’s group 3: – ”Fast” arterial (e.g. free iliac rupture) which is likely to be fatal whatever one does, binder or not (high pressure, high flow bleeding). Again I agree with Julian here. These patients can die in minutes as is usually the case if you lacerate a vessel the size of the iliac artery, and there is absolutely nothing you can do about it prehospital.

Or is there?

Another thing I was taught as a boy is that if you can’t control arterial bleeding at the haemorrhage site then get proximal control. So how can you get proximal control for a punctured iliac artery? Clearly we are talking about occluding the aorta here but how do you achieve this prehospital?

The idea of REBOA (resuscitative endovascular balloon occlusion of the aorta) in the prehospital context has been getting a bit of attention with London HEMS recently introducing it. Now this sounds really sexy but it requires a skilled doctor with an ultrasound machine, time and good access to the patient. What I am proposing is the much simpler version of REBOA where the E stands for “External”.

Conflict of interest statement: Neither I nor either of my employers have a financial interest in the manufacture or distribution of the device I am about to mention – I just think it is a really cool idea.

AAJT copy

The device is the Abdominal Aortic and Junctional Tourniquet (AAJT) (here’s the link to the manufacturer’s website for their obviously positive coverage). A reasoned discussion on the relative merits of AAJT over traditional endovascular REBOA and some of the literature on both approaches can be found here.

The nice thing is that it sits around the waist and does not limit access to groins so that endovascular REBOA remains an option when you hit the trauma centre. If you can get one of these things on fast enough then even free rupture of an iliac vessel will potentially be controllable.

There are no reports yet of this device being used in catastrophic pelvic fracture haemorrhage but there are lots of reports of manual compression of the aorta being used in other causes of massive pelvic haemorrhage such as penetrating trauma, post partum haemorrhage and pelvic surgery. There are reports of the device being successfully used for massive bilateral lower limb injury in the military context. It should work in pelvic fracture too if proximal control is the key (famous last words).

The AAJT seems like the ideal prehospital device as you can place it in about 45 secs, in some situations you may be able to place it in a patient who is still trapped or whilst in transit to the hospital. That is just not going to happen with endovascular REBOA. And of course you don’t need a highly skilled physician with an ultrasound machine. Might have lower sex appeal factor but if occluding the aorta saves lives, this device is going to save far more lives than endovascular REBOA as it can be applied by a lot more people in a wider variety of situations. It is possible to put on an AAJT as well as a Pelvic binder as the binder sits around the greater trochanters and the AAJT is positioned over the umbilicus.

My own service has now acquired some AAJTs and we are about to introduce them to service. We will try and update you on our experience as it is early days yet for this device.

Lastly apologies to Julian if I have in any way misrepresented his opinions or taken his comments out of context. His comments certainly got me thinking however and that is what the Collective is supposed to be about so thanks Julian for contributing.

References:

Mason LW, Boyce DE, Pallister I.   Catastrophic myonecrosis following circumferential pelvic binding after massive crush injury: A case report doi:10.1016/j.injury.2009.01.101

Revisiting Old Stories About Little Airways

Dr Andrew Weatherall returns to stuff about paediatric airways, a bit of a companion to an earlier post with some practical tips. 

There are some things you’re taught from a very young age to believe in. Then it turns out it’s just plain wrong. Santa Claus. The Tooth Fairy. The Public Holiday Numbat. (Well, the last one might be specific to my upbringing.)

And in medicine there are plenty of examples those too. Oxygen is always good. You can’t manage trauma without a cervical collar. Then of course there’s pretty much everything about the paediatric airway. As if managing kids didn’t come with challenges anyway, we all get to work with information that is just plain wrong.

And there’s no mistaking that clinicians find paediatric airways difficult. The staff from Royal Children’s Hospital Melbourne have recently published a sizeable prospective study of emergency department intubations. This is from a big, clinically excellent tertiary kids’ hospital receiving 82000 patients in their ED every year. In 71 intubations across a year (only 71!), 39% had adverse events (most commonly hypotension in 21% and desaturation in 14%) and the first pass success rate was 78% (only 49% had a first pass intubation with no complications).

Now lots of things will contribute to those figures. But at least part of pondering that has to be making sure we understand what we’re dealing with.

"Please, go on" says Public Holiday Numbat [unchanged via quollism on flickr under CC]
“Please, go on” says Public Holiday Numbat [unchanged via quollism on flickr under CC]

Old Truths

Some old historical truths are harder to pull away than a spider web stuck to a bear with superglue. There’s a recent review that appeared in Pediatric Anesthesia written by Dr J Tobias  which steps through some of this dogma.

It points out that some of the classic teaching on the paediatric airway come out of a 1951 report by a Dr Eckenhoff. This includes the issues of the position of the larynx, the shape of the epiglottis and the funnel-shaped airway. Actually, to really trace the story, you have to start a little earlier.

Stepping Back

It’s 1897. Waistcoats aren’t ironic yet. Pipes aren’t an affectation they’re an expectation. Jack the Ripper is part of shared memory, not fevered historical narratives. And Bayeux was making casts of the airways of dead children. 15 casts actually in kids aged 4 months to 14 years.

Taking measurements of the circumference of the airway at the glottis, cricoid level and trachea, the cricoid ring was noted to be narrower than other parts of the airway (the topic of the shape of the airway wasn’t mentioned). This is the work that led to the idea that kids under the age of 8 had a conical larynx, with the cricoid ring as the narrowest point.

Consider for a second the qualities of plaster poured into a distensible tube. Wait, it’s not entirely distensible because the cricoid can’t distend. Is it maybe possible that the plaster may have distorted the anatomy? I’ll leave that with you for a bit.

This suggestion of the conical airway made its way into Eckenhoff’s later paper (though with a specific note that cadavers may not represent the living accurately). There were also some descriptive points raised:

  • The larynx moves down from the C3-4 level in the neonate to C4-5 in the adult (I’ve always been under the impression this move is brought about both by the need to phonate properly for speech and the loss of the need to breathe and breastfeed at the same time, but this point doesn’t feature in airway descriptions and I’m happy to be corrected).
  • A stiffer and more “U” or “V”-shaped epiglottis with an angle to the anterior pharyngeal wall of around 45 0 rather than lying close to the base of the tongue.
  • A case report of a 2 year old with airway complications thought to be related to an inappropriately sized tube, feeding the idea of uncuffed endotracheal tubes in kids under the age of 8.

All these points that form part of so much teaching lead to another question – would such a descriptive effort get a run in modern publishing?

 

Newer Tools Means Better Understanding

The answer of course is probably not. Of course you can only use what you have and it’s absurd to judge Eckenhoff (or Bayeux) for their accuracy against modern modalities. All we can do is revisit our thinking when new information becomes available.

We now have the significant advantage of radiological techniques (CT or MRI) and bronchoscopy to evaluate airways in children who aren’t dead. Again the Tobias article goes into more details but there are some key things to take from this modern literature:

  • In spontaneously breathing and muscle relaxed patients, the cricoid was not the narrowest part of the airway. That honour belongs to the vocal cords.
  • There is no change in the ratios of the cross sections over age – the cricoid doesn’t start relatively smaller and enlarge by the time you hit 8.
  • The cross-section looks like an ellipse (there’s more distance between the anterior and posterior bits than the two side bits).

 What should we do then?

Well for starters we should probably settle the tube choice thing. This is just more support for the argument to use a cuffed tube. For starters, the old “leak” test seems pretty dubious when you could be snug against the lateral walls but still leaking around the anterior or posterior areas. And I’m guessing no one has had their “leak accuracy assessment” externally audited.

It makes more sense to use an appropriately sized cuffed tube with the cuff pressure kept < 20 cm H2O. There’s now fairly convincing evidence that appropriately used cuffed tubes don’t cause big issues in recovery. Better ventilation, better monitoring, less flows and gentler tube material in contact with the mucosal wall. Makes sense.

What you can’t do is ignore the cricoid. It is still an unyielding bit of the anatomy and anyone can turn a high volume-low pressure cuff into a high volume-high pressure cuff – the difference is a couple of mL. And swelling in an airway that starts with a much smaller cross-sectional airway still means less margin for flow obstruction.

So choose the right tube, use it safely and you can get on with things.

 

While We’re At It, Let’s Forget One Blade to Rule Them All

Seeing as we’re talking about things that aren’t things, you may have also come across the idea that you should use a straight blade for the smaller kids (say, kids under 2). I’ve mentioned elsewhere that I think this is baloney but here’s a little bit of evidence.

Varghese and Kundu have published something on exactly this issue. 120 kids aged from 1-24 months had laryngoscopy (once anaesthetised and given muscle relaxation) with either a Miller or Macintosh blade, and then crossed over to the other type of blade. (Note they used both with the tip in the vallecula.)

The findings? The views were pretty much the same. The rates of difficulty were about the same. In fact, it’s a pretty beige set of numbers where being beige is actually as cool as things could be.

Some where the view wasn’t so great with a Macintosh had a better view with the Miller blade. Some went in reverse. The message though is a pretty resounding “same, same”.

 

So there’s just some truths that needed revisiting. There are no funnel-shaped airways. The airway isn’t round. There’s not one correct blade for the under 2s.

I still resent having to give up on the Public Holiday Numbat though.

References:

Here are the PubMed links for those mentioned in this post.

Long E, Sabato S, Babl FE. Endotracheal intubation in the pediatric emergency department. Pediatric Anesthesia 2014;24:1204-11. doi: 10.1111/pan.12490

Tobias JD. Pediatric airway anatomy may not be what we thought: implications for clinical practice and the use of cuffed endotracheal tubes. Pediatric Anesthesia 2015;25:9-19. doi: 10.1111/pan.12528

Varghese E and Kundu R. Does the Miller blade truly provide a better laryngoscopic view and intubating conditions than the Macintosh blade in small children? Pediatric Anesthesia 2014;24:825-9. doi: 10.1111/pan.12394