Suspension Trauma

Suspension trauma - also known as, harness-induced pathology (1), orthostatic shock while suspended (2), harness suspension (3), suspension trauma cascade (4) and orthostatic intolerance (5) has been a topic of debate in the mountaineering and industrial community for decades.   What is it?   What isn’t it?  And what do we do about it?


A Historical Perspective

The concept of mortality and morbidity from being suspended motionless has been around for a long time; indeed, it is theorised that this may be one of the causes of death in crucifixion (6). 

Early work on the physiological response to suspension and orthostatic intolerance was conducted in 1968 at the Harry G Armstrong Aerospace Medical Research Laboratory including five volunteer subjects who were suspended in a parachute harness, one of whom lost consciousness at 27 minutes.   His unconsciousness was attributed to “venous pooling caused by forward body positioning and an inadequate pre-test diet.” (7)

Madsen et al (8) reported a case where a soldier was instructed to mimic being unconscious while on a rope and was subsequently found dead only 6 minutes later.

The impetus in the mountaineering world came in 1972 at the Second International Conference of Mountain Rescue Doctors;  Scharfetter and Flora presented research papers pertaining to 10 climbers who became trapped in a suspended position before rescue for durations ranging from 30 minutes to eight hours.  Two died pre-rescue, three died almost immediately after rescue and five died over the course of the ensuing 11 days. (9, 10)

None of these victims had any other injury commensurate with death raising the question ‘why did they die?’   

Notable cases included a 23-year-old female who died within minutes of being rescued. Her autopsy revealed no significant trauma. (11)

A second concerning case comes from American Caving Accidents of a male caver who became stuck on rope who died suddenly when released from his harness. (12)

The sudden death of these casualties post-rescue raised concerns of “rescue death

Theories evolved around the tourniquet effect of constricting harnesses similar to the effects seen in crush injury as late as 2007 (2).  These include the volume of hypoxic blood pooled in the legs returning to the heart suddenly causing an ischaemic heart failure; overloading of the right ventricle on horizontal positioning; a reperfusion injury of the vital organs that had become hypoxic during vertical immobility; and a crush-type injury from toxins produced by the accumulated blood in the legs.

As such guidance on the management of suspension trauma casualties was in debate about whether or not to lay the rescued casualty flat or not (2).


Current thinking

Recent work, including the seminal article from Mortimer (13) questioned these hypotheses and the theory behind them.  What had been excluded from previous meta-reviews was that in the 1960s and 70s sit-harnesses were not routinely used by climbers and cavers, rather, simply tying the rope directly around the chest, so the theory of harnesses causing toxins to develop through the constriction of leg loops are largely supposition.

Furthermore, recent ultrasound research has not demonstrated significant impedance on venous flow due to prolonged exposure in a suspended sit-harness (14, 15).  The superficial femoral artery, which may be compressed by the harness straps, is only responsible for 15-20% of the flow.  The deep femoral artery that provides most of the flow is protected by its extreme internal situation.
In both of the highlighted cases of “rescue death” the fatalities occurred after 4 hours of suspension suggesting it was the prolonged suspension which eventually killed them (as it did with all of the other cases) rather than the rescue.

As to suspension trauma being attributable to the accumulation of toxins (and the subsequent release upon rescue) current research around crush and reperfusion injury shows issues as taking hours to develop rather than the minutes which appear to strike suspension trauma casualties.


The Cascade

Current thinking surrounding suspension trauma is no longer around the harness but the pathophysiological response to prolonged suspension.  Furthermore, suspension injury and death from suspension trauma appears to be a cascade of several events rather than a singular issue.


One thing is clear; the morbidity and potential mortality of prolonged suspension must start with the suspension – it has long been accepted that prolonged immobility under the influence of gravity reduces venous return due to pooling in the lower limbs (16) which in turn leads to reduced thoracic blood pressure, reduced cerebral perfusion and eventual unconsciousness.   This mechanism is rarely seen in isolation as a number of physiological responses exit to prevent individuals from losing consciousness simply by ‘being still’.  Rare, but not impossible as evidenced at many ceremonial guard duties.

Suspension trauma is accelerated or accentuated by a cascade of contributing factors.



In ordinary situations, antigravity muscles which humans use to maintain balance (namely the soleus muscles, the extensors of the leg, the gluteus maximus, the quadriceps femoris and the muscles of the back) activate a neuro-sympathetic reflex called “muscle sympathetic nerve activity” (MSNA) which maintains systemic arterial pressure to provide minimal cerebral blood flow.  This is can be delayed briefly if one is to stand up too quickly leading to a feeling of ‘light headedness’.   In the absence of movement – and therefore absence  of this reflex – such as prolonged suspension, the ability to maintain cerebral blood flow may be compromised. (17)   This may be due to unconsciousness following a fall, hypothermia, exhaustion or some other co-morbidity.



Another contributing factor may be pain – borne from an originating injury, a fall or simply the prolonged suspension in an ill-fitting harness.  Pain appears to increase MSNA and diastolic blood pressure (18) through activation of the sympathetic nervous system but can also trigger two paradoxical responses.


The von Bezold–Jarisch reflex

The von Bezold–Jarisch reflex is a paradoxical triad of hypopnea (shallow breathing), hypotension (low blood pressure and bradycardia (slow pulse) at a time of increased need for oxygen (19) and may be present in suspension trauma triggered by extremely low blood pressure (20).


Vasovagal Reflex

Pain (as well as other psychological triggers such as the sight of blood or an extreme emotion) can trigger the nucleus tractus solitarii of the brain stem.   The result is innervation of the vagus nerve which is a principle messenger to the heart and diaphragm. 


Both of these reflexes suppress the sympathetic response, causing vasodilation, reducing blood pressure and increasing the parasympathetic response; reducing heart rate and cardiac output.   These factors accelerate the cycle of hypotension, decreased cerebral perfusion and unconsciousness.


Endogenous opioids

Pain may also trigger the sympathetic release of endogenous opioids (respiratory depressants) (21).   The triggering of this reflex by pain but it is not yet fully understood whether this may have an effect on respiration.

What is known is that pain tolerance is a) subjective and b) dependant on the design and fit of the harness and the preceding incident (the height of the fall, for example) which may account for the variations on time tolerances between individuals and specific cases.


Chest Harness

The addition of a chest harness, intended to prevent the fallen casualty from inverting may apply enough constriction around the chest to decrease respiratory efficacy, further reducing cerebral perfusion. (22, 23)


Type of harness

For fall arrest devises the HSE dictate full body harnesses with a sternal or dorsal attachment point are used under EN 361:2002 (24) although arboriculturalists who perform tree climbing are allowed sit harnesses (25) as are operators of Mobile Elevated Work Platforms (26).

All harnesses have pros and cons:

Harness choices.png


If suspended unconscious from a dorsal attachment point on the harness, the head and neck may fall forward causing a potential airway obstruction.   Airway obstruction alone may lead to cardiac arrest in as little as 7 minutes  (27).  Death is imminent.

If suspended unconscious from a ventral (waist) or sternal attachment point on the harness, hyperextension of the cervical spline could exacerbate the vasovagal response above (28).  The inverted suspended casualty in the sit harness is likely to hang cruciform with outstretched arms further compromising breathing efficacy.



There is no specific treatment for suspension trauma – the suspension and cascade of contributory cascade is killing the casualty.

If it is not possible to get the casualty to the ground try to position the casualty horizontally to restore cerebral perfusion.

As with the traditional treatment of crush injury, the myth of ‘poisonous blood’ returning to heart should be buried in the annals of time.  Should crush injury become a factor from extremely prolonged suspension, there is still only one treatment.   Get them down!  

So…if there is no special treatment for this casualty, why the lengthy article?



A suspended casualty is a unique casualty and it is the issue of suspension which needs addressing, not because it warrants specific treatment but because it warrant better understanding.

The fallen and suspended casualty is going to deteriorate quicker and in less predictable ways than an unsuspended casualty.   The best we can do is recognise the dangers and prevent suspension trauma through education.

The onset of suspension trauma maybe predictable.

Any unconscious, hypothermic, injured or immobile casualty is at risk.

Gradual onset may occur without a fall or preceding injury due to prolonged period of immobility alone (exacerbated by hypothermia, heat illness, dehydration or exhaustion).

Early warning signs of suspension trauma include (29):

  • experiencing hot flashes

  • sweating

  • numbness in the legs

  • nausea

  • dizziness

  • confusion

These signs may appear in one in five victims within 10 minutes (but typically after being suspended for an hour) (29).  This presents an opportunity to call for help and lay down or re-position oneself horizontally.

In addition to getting the casualty down or if this is not possible:

  • Encourage the casualty to move their legs to promote venous return.

  • A chest strap should be placed if the victim is injured or hanging more than a few minutes in a sit harness.

  • An etrier can be sent down the rope to be deployed as a leg rest – even static muscle tone can aid venous return.



  1. The key to managing suspension trauma is to avoid it through education.

  2. If a casualty is suspended, get them down as quickly as possible

  3. Practice rope rescue techniques to facilitate an effective, safe and prompt recovery of the casualty.



  1. Seddon, Paul. (2001) “Harness Suspension: Review and evaluation of existing information”. Health and Safety Executive. Research Report 451/2002. 104 pp.

  2. Lee C, Porter KM. (2007) “Suspension trauma”. Emergency Medicine Journal. 24(4),237–238.

  3. Adisesh A, Lee C, Porter K. (2011) “Harness suspension and first aid management: Development of an evidence-based guideline”. Emergency Medicine Journal. 28(4),265–268.

  4. Wood N. (2012.) “Suspension trauma: A lethal cascade of events”. Ellis Fall Safety Solutions. Retrieved March 29, 2015, from NormanWoodsSuspensionTraumaALethalCascadeOfEvents.pdf.

  5. U.S. Department of Labor Occupational Safety and Health Administration. (2011.) “Suspension trauma/orthostatic intolerance”. Safety and health information bulletins. Retrieved March 29, 2015, from

  6. Maslen M, Mitchell PD (2006). “Medical theories on the cause of death in crucifixion”. Journal of the Royal Society of Medicine. 99 (4): 185–188.

  7. Orzech M A, Goodwin M D, Brinkley J W, Salerno M D, Seaworth J (1987) “Test program to evaluate human response to prolonged motionless suspension in three types of fall protection harnesses”. Harry G Armstrong Aerospace Medical Research Laboratory, Wright Patterson Air Force Base, Ohio, USA.

  8. Madsen P, Svendsen LB, Jørgensen LG, et al. (1998) “Tolerance to head-up tilt and suspension with elevated legs”. Aviation Space and Environmental Medicine. 69(8):781–784.

  9. Various (1972) “Falls into the rope: skull injuries in alpine regions” Papers of the Second International Conference of Mountain Rescue Doctors, Austria. [German to English translation by HSE Language Services Transl. No. 16372(I)]

  10. Flora G, Holzl HR. (1972) “Fatal and non-fatal accidents involving falls into the rope”. Paper presented at: 2nd International Conference of Mountain Rescue Doctors [German to English translation by HSE Language Services Transl. No. 16372(1)]; November 18, 1972; Innsbruck, Austria

  11. Fodisch HJ. (1972) “Morphological findings in the case of death after hanging on a rope for four hours”. Paper presented at: 2nd International Conference of Mountain Rescue Doctors. [German to English translation by HSE Language Services Transl. No. 16372(1)]; November 18, 1972; Innsbruck, Austria.

  12. Knutson S. (1993) “American caving accidents”. NSS News. 51(12, part 2):366–367.

  13. Mortimer RB. (2011) “Risks and management of prolonged suspension in an Alpine harness”. Wilderness and Environmental Medicine. 22(1):77–86.

  14. Bariod J. (1994) “Update on the harness induced pathology”. Spelunca 55: 39-42.

  15. Mattern R. (1991) “Optimisation of intercepting devices, Biomecanichal stress limits of humans. Investigations of personal safety equipment against falls”. Deutsch montantechnologie (DMT).

  16. Mayerson, HS, Burch GE. (1940) “Relationships of tissue (subcutaneous and intramuscular) and venous pressure to syncope induced in man by gravity”. American Journal of Physiology. 128; 258-69

  17. Fu Q. et al (2001) “Effects of lower body positive pressure on muscle sympathetic nerve activity response to head-up tilt”. American Journal of physiology. Regulatory, integrative and comparative physiology. Sep;281(3):R778-85.

  18. Lautenschläger G1, Habig K1, Best C2, Kaps M1, Elam M3, Birklein F4, Krämer HH (2015) “The impact of baroreflex function on endogenous pain control: a microneurography study”. European Journal of Neuroscience. 42(11):2996-3003.

  19. Mark AL (1983) “The Bezold Jarisch reflex revisited: clinical implication of inhibitory reflexes originating in the heart”. Journal of the American College of Cardiology. 1,90-102.

  20. Crystal GJ, Heerdt PM (2013) “Cardiovascular Physiology” in Pharmacology and Physiology for Anesthesia, 2013

  21. Schlereth T, Birklein B. (2008) “The Sympathetic Nervous System and Pain”. NeuroMolecular Medicine. 10:141–147

  22. Roeggla M, Brunner M, Michalek A, Gamper G, Marschall I, et al. (1996) “Cardiorespiratory response to free suspension simulating the situation between fall and rescue in a rock climbing accident”. Wilderness and Environmental Medicine. 7: 109-114.

  23. Murphy D, Garner A, and Bishop R. (2011) “Respiratory Function in Hoist Rescue: Comparing Slings, Stretcher, and Rescue Basket”. Aviation, Space, and Environmental Medicine. 82;2. 123-127

  24. British Standards Institute (2002) BS EN 361:2002 Personal protective equipment against falls from a height. Full body harnesses.

  25. Health & Safety Executive (2009) AFAG401 Tree-climbing operations. Accessed 26th October 2017

  26. Health & Safety Executive (2004) AFAG403 Aboriculture & Forestry Advisory Group (AFAG) Guide 403. accessed 26th October 2017

  27. Berg RA, Hilwig RW, Kern KB, Babar I, Ewy GA (1999) “Simulated mouth-to-mouth ventilation and chest compressions (bystander cardiopulmonary resuscitation) improves outcome in a swine model of prehospital pediatric asphyxial cardiac arrest”. Critical Care Medicine. Sep;27(9):1893-9.

  28. Leal S, Becker F, Nespoulet H, Zellner P and Cauchy E (2016) “Proposal of an Effective Algorithm to Manage Suspension Trauma in the Field”. Trauma and Acute Care 1:15.

  29. Raynovich B, Rwaili FT, Bishop P. (2009) “Dangerous suspension trauma: Understanding suspension syndrome and prehospital treatment for those at risk”. Journal of Emergency Medical Services. 34(8):44–51, 53.