It's interesting how things sometimes seem to come together at the same time for different reasons. I've been thinking about extrication recently in the setting of a competitor trapped by compression. That got me thinking about a talk given by Sydney HEMS doctor, Cliff Reid, titled "The wrong stuff" during which he went through some pre-hospital dogma bug-bears (bug-dogs?), including the management of crush injury/syndrome. At the same time of my pondering a tweet went out for a doctor in Italy looking for any updated information on crush injury management as he had become involved with the medical provision for the awful recent earthquake there. And then there is the ongoing rubble that are bombed Syrian cities with survivors trapped beneath.

Crush injury management is one of those areas where management algorithms appear to be driven by a mixture of reasonable physiological assumptions and strong faith. Perusing the literature unearths more reviews and consensus statements than actual data. The data that does exist is either retrospective cohort audits or lab-based animal studies. Probably understandable as prehospital research is fairly challenging in general and the effort required to generate the numbers for a rigorous RCT for this subject would most likely be considerable.

I have to admit that I have been sucked into the riptide of extrapolation here. Having been taught the value of pre-release bicarbonate to prevent the imminent hyperkalemia-driven fatal arrythmia, I merrily applied it to any and all compression scenarios in the firm contentment of therapeutic righteousness. I've been less enthusiastic about the role of tourniquet application to slow the hyperkalaemic tsunami but I could be persuaded.

So, what do you do when you discover that your current practice might actually be based on well intended dogma? You go looking.


The current state of knowledge

Crush injury is an injury to a focal region of a person's body caused by a compressive force that results in direct cell damage. Crush syndrome is the systemic effects of that crush injury; typically a hypovolaemic shock, hyperlactataemia, a metabolic acidosis, hyperkalaemia, hypocalcaemia along with other metabolic disturbances and subsequent acute kidney injury or failure. Related to these two entities though somewhat different in pathogenesis is compartment syndrome, where instead of an external compressive force there is swelling contained within a restricted compartment that exceeds venous drainage and in the late stages, arteriolar perfusion, resulting in ischaemic injury.

The mechanism of crush syndrome is a combination of direct cell damage, ischaemic cell damage and, upon release of the compression, reperfusion injury. The concern is the sudden release of a combination of myoglobin (nephrotoxin), potassium (asystole), lactate (ultimately a heart and brain fuel but also a marker of badness during illness), uric acid and purines (nephrotoxins) when the compression is relieved causing a sudden and catastrophic deterioration in a previously trapped but up to that point systemically well person.

So, the commonly recommended pre-release management includes:

But let's slow down a moment and look at what is really going on before rigidly applying this to the very next competitor who needs to be cut out of their wrecked race car.



Is it a problem in motorsport?

There are a few requirements to be at risk of a crush syndrome. First, the crushed area needs to involve a reasonable bulk of muscle. So this means thigh, calf, buttock, back (the paravertebral muscles), arm and forearm. Compression of the feet, hands, ankles or wrists will not affect enough muscle to risk a crush syndrome, though skin compromise can still be a major problem with regard to infection later on. Chest wall and abdominal  compression might, but is more likely to result in a ventilation/breathing emergency before crush syndrome becomes a problem.


This segues nicely to the second requirement for crush syndrome; that of sufficient compressive pressure for a prolonged time. The whole issue of crush syndrome dates back to a World War II period BMJ article that describes the occurrence of renal failure and death associated with elevated serum potassium in patients within a week of being pulled from the rubble of bombed buildings. Within a week, not minutes. The hyperkalaemia described in this paper probably resulted from a combination of hypovolaemic ATN and the myoglobin and other nephrotoxin induced renal failure and does not form a picture of sudden arrythmic death within seconds of removing  the compression. It is now generally recognised that compression for a "prolonged time" means about four to six hours of compression.


Why does this matter? Not many of our competitors are trapped by compression for 4-6 hours. Maybe on long distance endurance Dakar style safari events, but not circuits and probably not rallies or off-road sprint events.

That is not to say that there is no muscle damage nor that we can take our sweet time over the disincarceration and extrication. It's that the roll cage element compression of a competitor's leg for 20 - 40 minutes is not going to lead to a crush syndrome.

If there is a sudden post release deterioration, it probably isn't due a sudden surge of potassium and lactate; it is probably hypovolaemic shock from the haemorrhage that hasn't yet been addressed, or perhaps the expanding intracranial haematoma or maybe even the cumulative dosing of sedative analgesia used during the disincarceration process. Remember that motorsport medical response teams are usually on scene very soon after the incident, especially on circuits, and the injury mechanism is in the early stages of evolution such that an initially apparently well patient can deteriorate during the subsequent scene time.

So we could stop right here. Crush syndrome: definitely an issue for rescuers dealing with prolonged compression at disaster scenes (earthquakes, building collapses, landslides) and construction sites (trench collapses, industrial machinery accidents). Not really a common risk at motorsport events.

However, for interest sake, let's say a call has come in to respond to a Dakar competitor who has been missing for 4 hours and has been located, pinned by his legs under his truck. His co-driver and engineer, who are uninjured, couldn't make contact until now as their comms gear was inoperative. It will take an hour to get to him. How might this play out and what management should be undertaken?


What is the recommended approach to managing a crush injury?

Here are the potential issues:

1) Establishing secure IV (or IO) access.

Yep, no questions about this. He's going to need some IV fluids and analgesia at least. Possibly blood products if available.

2) Pre-loading the person with IV fluid volume.

The reasoning here, other than blood pressure support as part of prehospital trauma management (This is a different conversation), is twofold.

3) Getting bicarbonate into them

Things get pretty sketchy here. There are two plausible roles for bicarbonate. One is to counter the acidosis which could potentiate hyperkalaemia and increase the tendency of myoglobin to precipitate out in the renal tubules (one of the three suggested mechanisms of myoglobin induced renal failure). The second is to shift the surging serum hyperkalaemia into the cells and dampen its arrythmogenic potential.

There is some physiological doubt about these benefits. Crush syndrome is often also accompanied by hypocalcaemia, which can potentiate hyperkalaemic cardiotoxicity. And adding bicarbonate can drive the calcium lower still - Think about why we get hyperventilating  people with carpopedal spasm to rebreathe CO2. An alkalosis won't drop your total calcium but it will shift the free and bound calcium eqilibrium towards a functional hypocalcaemia.

In the latest version of the ILCOR resuscitation guidelines (2015) bicarbonate therapy features much less prominently in the management of hyperkalaemic cardiac arrest. It doesn't appear in the European Resuscitation Council ALS agorithm, although it is mentioned as an option in the text. The American interpretation has kept it as an option in the AHA guidelines. The Australian and New Zealand guidelines keep it as a consideration (Class A, expert opinion).

So bicarbonate still has a role in the event of a hyperkalaemic cardiac arrest, but prophylactic administration in advance of compression release has the potential to make no difference or possibly even cause harm.

4) Having a tourniquet in place proximal to the crush region

Like I said earlier, I've never been totally convinced by this. For distal limb uncontrolled bleeding, sure. But as a crush injury release prevention strategy, not so much.

And thankfully, I'm not alone.

UK guidelines say to reserve the tourniquet for uncontrolled haemorrhage, which suits my bias so I'm happy.
US guidelines recommend considering a tourniquet to manage crush syndrome hyperkalaemia if IV fluids cannot be given. Huh!
Australian guidelines (which are of course without fault) state "DO NOT use a tourniquet for the first aid management of a crush injury". Instead they advise to be aware of the possibility and to continually reassess for evolving deterioration.

Three national guidelines. Two different recommendations.

5) Monitoring with continuous ECG leads for hyperkalaemia

Sounds fair enough and we've all learned the progressive ECG changes associated with rising levels of serum potassium, from the peaked T waves through to sine waves and asystole. The problem is that asystole can occur at pretty much any level of hyperkalaemia. In addition, there's a paper demonstrating that physician diagnosis of hyperkalaemia based on ECGs had a sensitivity of 45% and a specificity of 82%. That's rubbish by any standards.

Admittedly the interpretation was performed by only two physicians, so maybe it does not reflect general ability. I'm still putting the leads on, but I'll be looking for the hypovolaemic cause of the PEA/Asystole in this trauma patient ahead of any hyperkalaemia.

6) Analgesia

Totally fair. No argument from me.


Summary

For most motorsport incidents a crush injury is unlikely to be of sufficient duration or extent to result in the complications of crush syndrome. Management should be along standard trauma pathways.

An IV or IO cannula is probably going to be needed for the analgesia and fluid management anyway, depending upon the situation, though intranasal fentanyl and IM ketamine work just great for providing analgesia without the need for cannulation.

I still think placing ECG monitoring is reasonable, as much for reasons other than hyperkalaemia and it would be part of prolonged trackside trauma management at motorsport events anyway.

Bicarbonate is a part of the pharmacy of any of the medical packs that I have worked with at motorsport events, but I won't be breaking it out prior to releasing the compression mechanism.

And the tourniquet remains a strategy for uncontrolled distal limb haemorrhage, not crush injury management.

As always, your thoughts, opinions, criticisms and replies are welcome below.