By Raphael Dworkin, HEMS registrar.

Every morning our team discusses cases over coffee. Here is a useful snippet…

Fictional Vignette
– 52M rally car driver accidentally clips a tyre wall causing his car to flip upside down at low speed. It takes approx. 30 mins for scene to be cleared and ambulance teams to arrive. Patient is suspended vertically by safety harness throughout this time.
– Prior to extraction, he was GCS 15 and talking. Soon after HEMS attendance he became acutely confused and subsequently arrested, with ROSC several minutes later.
– Eventual hospital assessment demonstrated no traumatic injuries. Was ‘Suspension Trauma’ a factor in precipitating his arrest?

What do suspension trauma (ST) and the Yeti have in common?
I thought you’d never ask. Both the stuff of legend and go by multiple names including harness hang syndrome and orthostatic intolerance, as well as bigfoot and the abominable snowman, respectively.

That’s it?
I haven’t finished. Despite both phenomena being widely appreciated throughout the adventurer and wilderness communities, they are but poorly understood folklore to medical science.

A literature search on ST as recently as 2009 yielded only 5 articles, as compared to thousands of non-medical commentaries. Thus, ST management has been heavily based on lay opinion, and until recently, lightly on peer-reviewed research.

Erm doesn’t sound real to me…what is ST supposed to be?
A maladaptive, and potentially life-threatening, physiological response to prolonged motionless suspension^(1).

Is it pretty much the same thing as crush injury…?
Nope they’re different. In crush, the main aetiology of end organ damage is rhabdomyolysis, something that usually requires direct trauma and takes several hours to cook.

In contrast, shock (leading to syncope and rarely cardiac arrest) from ST can occur well before mechanisms of crush injury come into play, with low-flow states described as early as within 6 minutes ⁽²⁾. 

Ok now I’m listening. Clear it up for us – who’s at risk of getting ST?
Think anyone working on rope in a harness e.g. climbers, rescuers, or construction employees.

Modern harnesses are typically worn across the shoulders and upper thighs which, following a fall, more safely protect against visceral organ or thoracic injury via energy redistribution. However, prolonged passive suspension within these harnesses can provoke suspension trauma.

Got it – bore me with the actual science then:
We are still largely in the dark unfortunately. Whilst there are numerous proposed pathophysiological mechanisms, the true cause is likely multifactorial:
– Significant venous pooling (potentially >20% of blood volume) from loss of the lower limb muscle pump and femoral vein compression can lead to reduction in preload and a subsequent decrease in cardiac output, in theory leading to LOC and arrest if unresolved ⁽³⁾. However, ST can occur even without thigh compression harnesses⁽⁴⁾.
– Vagally-mediated bradycardia/hypotension, precipitating syncope and ultimately circulatory collapse. May be exacerbated by preceding exertion ⁽⁵⁾.   
– Concurrent traumatic injuries, along with hypothermia, hypoglycaemia, pain and fear can all stimulate maladaptive compensation, potentiating the above mechanisms.

So prolonged passive harness suspension = bad. Get them down, right?
Yes.

Despite historical controversy surrounding ‘rescue death’,  actual evidence is aligning with expert consensus that these patients should be immediate rescued to ground and placed in the supine position for A-E primary survey.

If immediate descent is not possible, rescuers should stimulate leg movements, ideally with pushing the patient’s feet against a flat surface⁽⁶⁾.

‘Rescue death’!? That sounds like an IIMS waiting to happen…why the controversy?  
It was previously hypothesised from rescuers (in the 1970’s) that too rapid a change from vertical to supine was deleterious. In fact as recently as 2002 a UK Health and Safety Executive report recommended that suspended patients ‘must never be laid down’, rather gradually transferred via a number of intermediate seated positions⁽¹⁾.

Proposed mechanisms of this ‘re-flow’ syndrome included:  
– RV overload from the rapid return of the pooled blood volume.
– Cardiac ischaemia following return of accumulated deoxygenated blood replete with toxic metabolites.
– Non-cardiac end organ dysfunction secondary to rhabdomyolysis.

Evidence has now aligned with expert opinion that this is outdated guidance.

Yikes. So what is the recent evidence that disproves these theories?
In 2019 the first experimental randomised crossover trial⁽⁷⁾ into ST found:
– Of the suspended trial participants that developed pre-syncope, all showed rapid recovery following immediate rescue to supine position.
– No ventricular overdistension occurred following immediate rescue to supine position in pre-syncopal suspended participants.
– Pre-syncopal events in participants were preceded by decrease in HR and BP – suggesting vagally-mediated mechanisms.
– Despite demonstrable lower limb blood pooling there was no relevant impact on macro-haemodynamics.

Organ failure from rhabdo? See I told you this sounded a lot like crush injury…
Let me put it another way: ST is a state of shock that can be rapidly induced by passive hanging.

The survivors of these ST mechanisms, if suspended motionless for hours, are then at theoretical risk of later developing rhabdo. This occurs via inadequate muscle perfusion. Thus, ST-induced rhabdo is secondary to stasis rather than direct physical trauma (as seen in crush injury).

Although remember, as is observed intra-operatively from tourniquet application, muscle can tolerate hours of hypoxia. Even in earthquake victims, crush syndrome is not commonly observed prior to 3 hours of entrapment. ST mechanisms can occur before then.

Take homes?
– ST and crush injury are NOT the same thing.
– Passive suspension for a short time can lead to arrest.
– Immediately get the patient to flat ground. This will reverse suspension trauma mechanisms, and allow you to proceed with the primary survey.

References
1. Seddon P: Harness suspension: review and evaluation of existing information . Health and Safety Executive Research Report 451. UK Health and Safety Executive, London; 2002.

2. Mortimer RB: Risks and management of prolonged suspension in an alpine harness . Wilderness Environ Med. 2011, 22:77-86. 10.1016/j.wem.2010.10.008

3. Lee C, Porter KM (2007) Suspension trauma. Emerg Med J 24:237– 238. https://doi.org/10.1136/emj.2007.046391

4. Merchant D. Suspension trauma can be unrelated to harness use. Emerg Med J, eLetters. January 30, 2008;24:237-238

5. Halliwill JR, Sieck DC, Romero SA, Buck TM, Ely MR (2014) Blood pressure regulation X: what happens when the muscle pump is lost? Post-exercise hypotension and syncope. Eur J Appl Physiol 114:561–578. https://doi.org/10.1007/s00421-013-2761-1

6. Weber SA, McGahan MM, Kaufmann C, Biswas S. Suspension Trauma: A Clinical Review. Cureus. 2020 Jun 8;12(6):e8514. doi: 10.7759/cureus.8514. PMID: 32656030; PMCID: PMC7346344.

7. Rauch S, Schenk K, Strapazzon G, et al.: Suspension syndrome: a potentially fatal vagally mediated circulatory collapse—an experimental randomized crossover trial. Eur J Appl Physiol. 2019, 119:1353-1365. 10.1007/s00421-019-04126-5

Best recent review
Weber SA, McGahan MM, Kaufmann C, Biswas S. Suspension Trauma: A Clinical Review. Cureus. 2020 Jun 8;12(6):e8514. doi: 10.7759/cureus.8514. PMID: 32656030; PMCID: PMC7346344.