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.

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.

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