Suspension Trauma

Date: 04/12/2014



Suspension trauma (also known as ‘‘harness-induced pathology’’ or ‘‘orthostatic shock while suspended’’) is the development of presyncopal symptoms and loss of consciousness if the human body is held motionless in a vertical position for a period of time. It has been described in experiments of personal fall protection, and has been implicated in causes of death in mountaineering accidents, but it seems neither to be widely known about nor to have been presented to the medical profession.
(Suspension trauma, 2007)


Suspension trauma can occur in any activity that uses a body harness system. This includes sports such as mountaineering, rock climbing, parachuting, paragliding, via ferrata, canyoneering, BASE jumping, and spelunking.
Occupational activities include work on high wires or rescue operations in hostile environments (mountainous or other difficult terrain, helicopter winching in rescues at sea, etc). There aren't precise data on the prevalence of suspension trauma and the currently available literature describes only cases from sports accidents or healthy volunteer studies.
The pathology caused by safety harnesses is applicable only in the context of a person hanging vertically suspended and motionless.
(Clinical update: suspension trauma, 2011)


In the normal person, venous return happens through muscular contractions forcing blood through the one-way valves of the lower extremity veins.
This venous pump is disabled in the motionless patient while arterial flow continues; suspension leads to decreased involuntary small muscle contractions normally used to maintain blood pressure when upright. Failure of the venous pump leads to pooling of blood in the legs with decreasing central volume as demonstrated by enlarging thighs, decreasing heart size, decreasing stroke volume, decreasing glomerular filtration rate, and increasing transthoracic impedance. Once capillary pressures rise, significant fluid can leak into interstitial spaces, decreasing total intravascular volume.
With decreasing stroke volume in a hyperautonomic state, the person becomes subject to the Bezold-Jarisch reflex, which triggers decreased heart rate and blood pressure.
Adaptive reflexes can be pathological in the artificial situation of hanging motionless. In normal circumstances, acidosis from anaerobic metabolism decreases vascular resistance. Decreased resistance usually leads to increased blood flow with concomitant increases in available oxygen and nutrients along with removal of waste products. In the motionless hang situation, increased flow sequesters even more blood in the periphery.
Central hypovolemia eventually leads to fainting. The vasovagal response to poor circulation normally returns one to a horizontal position, which improves blood flow. to the brain. Soldiers at attention fainting on the parade ground are classic examples of this—once they are down they rapidly regain consciousness. The suspended person, however, can fall no farther—decreased heart rate and blood pressure from increased vagal tone simply results in yet more catastrophic flow reduction.
In the experimental setting, one sees evidence of increasing sympathetic tone followed by a parasympathetic response. Increased sympathetic tone leads to increased heart rate to compensate for decreasing volume. Pulse pressure narrows. Finally, blood pressure decreases either as a result of the decreased available volume, or more catastrophically from a vasovagal response including bradycardia. Symptomatically, patients report nausea, lightheadedness, and flushing. While likely multifactorial, the fainting response may be partly due to the Bezold-Jarisch reflex. This reflex is mediated by receptors in the posterior left ventricle that sense volume. At normal volume, they fire tonically to control blood pressure. As volume decreases, they fire less to allow vasoconstriction. When stroke volume decreases dramatically, they fire more resulting in bradycardia, vasodilation, and hypotension. This reflex has been blamed for bouts of hypotension and bradycardia and even asystole in patients having shoulder surgery in a sitting position, not that far removed from the tilt-table experience. The reflex can be demonstrated in an animal model by ligating the inferior vena cava. Once volume is sequestered peripherally, receptor cells abruptly fire more and blood pressure and heart rate drop. When the occlusion is released and volume returns, the receptors fire less, and vital signs return towards normal.
In the human subjects, once off rope, several outcomes can be observed: most recover uneventfully, some have had sub-acute sequelae like rhabdomyolysis, renal failure or hematuria. Long-term stasis eventually leads to muscle cell necrosis with release of myoglobin, in turn leading to renal failure by a variety of mechanisms.
There may be some overlap of suspension trauma with compression asphyxia in which death is caused by inadequate ventilation from outside constriction. Suspension in a chest harness alone does lead to decreases in forced vital capacity, heart rate, blood pressure, and cardiac output. These changes are not observed in people wearing a sit harness; a chest harness alone may include a degree of compression asphyxia.
Airway constriction itself is unlikely given the hyperextended position of the neck in passive hanging in a harness. So restricted breathing may play a part in deaths on rope, but is unlikely to contribute much to those cases in sit harnesses. Some have suggested that the sequestration of blood is due to a tourniquet effect from the harness.
This seems unlikely for several reasons, in fact climbers routinely spend an entire day in a harness and can be suspended for hours at a time. Although this can be very uncomfortable, it has not proved dangerous while the climber is conscious, despite the same constriction of the harness around the leg, maybe because in alpine style harnesses with front attachments there is no compression of the anterior thighs where the femoral veins return blood to the core circulation. The pathology of suspension trauma is not absolutely clear. Other factors that can help precipitate an accident, such as drugs and alcohol, can worsen maladaptive responses. Especially in the early cases where no sit harness was used, respiratory function can also be compromised in the unconscious person on rope. What does seem clear is that passive suspension does lead to sequestering of volume in the periphery, hypotension, bradycardia, and, in the worst cases, death. Survivors are at risk for rhabdomyolysis and renal failure.
(Risks and management of prolonged suspension in an Alpine harness, 2011)


In the case of passive orthostasis, the appearance of presyncopal symptoms is the rule and these can develop very quickly. Eight percent of volunteers subjected to a passive head-up tilt of 50° experienced such symptoms after only 5 minutes, and 50% were symptomatic after 27 minutes. These time periods are even shorter when one is suspended in a harness, and depend on the type of harness used. The tolerance for motionless suspension was shown to be greater in a whole body harness (14.38min) than in a body belt (1.63 min) or a simple chest harness (6.08 min). Under normal conditions, a return to the horizontal position typically allows restoration of adequate cerebral blood flow to prevent syncope. However, when a subject is suspended in a harness, the orthostatic position together with reduced leg movement can lead to a loss of consciousness. The time between the appearance of symptoms and syncope itself during suspension is not known, as the first symptoms of presyncope come exclusively from prospective human studies. The lead time from symptoms to syncope can therefore be as short as a few seconds.
(Clinical update: suspension trauma, 2011)


Although a risk of death from suspension trauma does exist, it is likely very small. Whereas there are reported cases of deaths involving suspension, the cause of death in these cases was inconclusive. These reports involved either prolonged suspension times of several hours or did not have sufficient data to unequivocally attribute the death to suspension trauma alone. Depending on the type of harness used, a reduction in cardiac output or a compromised respiratory system are the most likely mechanisms leading to nontraumatic death during motionless suspension.
(Clinical update: suspension trauma, 2011)


Suspension trauma is probably an unrecognised condition in modern medical practice, as in the majority of cases where an individual is suspended vertically the workers or climbers can keep themselves moving using their legs as muscle pumps, and additionally are rescued relatively quickly. In those who are stranded, for example, on the side of a mountain, other factors probably account for their collapse, including traumatic injury and environmental conditions.
Modern harnesses now use a sitting position with a waist strap and sub-pelvic leg straps for support, which means a shorter vertical distance for blood to be pumped back from the legs. People using this equipment are also taught that if they find themselves suspended vertically, they need to do any of the following: adopt a sitting position, move themselves into a horizontal position or push their legs off from a hard surface to keep their muscle pumps active. Some harnesses also have foot straps to keep the legs mobile for the same reason.
Workers using safety harnesses are not permitted to work alone at height so that a rescue plan can be activated promptly if they come into any difficulty, and so that they will therefore not be suspended for very long. These guidelines are emphasised in the Health and Safety Executive’s Work at Height Regulations 2005.
(Suspension trauma, 2007)


In addition to the basic ABC management of a patient who has been involved in a suspended fall, there seems to be controversy regarding the positioning of a casualty after rescue. Authors of several articles on suspension trauma advise that if a person has been suspended in a vertical position motionless for longer than 30 min, then he or she should not be laid in a horizontal position on his or her rescue as this may cause ‘‘rescue death’’.
The aetiology of this has been contributed to a number of suggested factors. These include the hypoxic volume of 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.
For this reason, some authors suggest that the casualty should be positioned in a sitting position with the upper body supported for at least 30 min before being allowed to lie horizontal. Other authors recommend immediate supine positioning, in particular when there are other injuries. There is no consensus opinion regarding this issue.
(Suspension trauma, 2007)


Suspension trauma is the result of the normal response of the human body to motionless suspension in an orthostatic position. Its identification is crucial for those participating in certain sports, and occupations, as well as in rescue organizations, because of the possible medical risks and complications associated with suspension trauma. Typically, the natural course of immobilized suspension will lead to syncope, which can occur within minutes. A symptomatic victim should therefore be released from suspension as soon as possible. If a victim is conscious, moving the legs and placing them in a horizontal
position will delay the onset of presyncopal symptoms. There is currently insufficient scientific evidence to
support the concept of immediate rescue death or to therefore justify changing the current treatment recommendations for these victims once they have been released from suspension. Therefore, once a victim has been brought to the ground, rescue professionals should follow the current international prehospital and advanced life support guidelines without modifications.
(Clinical update: suspension trauma, 2011)


1. Pasquier M. et al. Clinical Update: Suspension Trauma. Wilderness Environ Med. 2011 Jun;22(2):167-71

2. Mortimer R.B. Risks and management of prolonged suspension in an Alpine harness. Wilderness Environ Med. 2011 Mar;22(1):77-86

3. Lee C. et al. Suspension trauma. Emerg Med J. 2007 Apr;24(4):237-8

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