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Info for Patients

A crush injury can cause bleeding, bruising, fractured bones, open wound, nerve injury, infection or compartment syndrome.

Compartment syndrome is caused following the initial crush injury and bleeding occurs into the muscle compartment. Thick layers of fascia separate groups of muscles to the arms and legs, inside this facia is a space called the compartment which includes muscle tissue, nerves and blood vessels.

The fascia does not expand, therefore any bleeding into the space will cause the compartment to be blocked, if the pressure is high enough it can cause permanent damage to the muscles and nerves, if the pressure continues long enough the muscle can die causing the arm or leg to no longer work. Surgery is often the immediate treatment which can be coincided with hyperbaric oxygen therapy as it improves the circulation of oxygenated blood to wounds to help fight infection, reduce swelling, and promote healing.

Info for Professionals

Crush Injury, Compartment Syndrome and Acute Traumatic Ischaemias

Acute Traumatic Ischaemias, of which Crush Injury and Compartment Syndrome (below) are examples, share a common pathophysiology. Direct trauma to blood and lymphatic channels causes fluid accumulation in the interstitium. Inflammatory pathways additionally increase capillary permeability, resulting in oedema of the interstitial space (Buettner MF).

Interstitial pressure rises in response and there is compression of the thin-walled venous outflow, favouring further fluid accumulation. The distance across which oxygen must diffuse from cells to capillaries thus increases. This further compromises perfusion to tissues which may already be hypoxic following capillary damage and consequent blockage to the circulation of erythrocytes.
In the face of significant hypoxia, intracellular supplies of ATP are eventually exhausted. This leads to failure of the sodium pump responsible for active transport of sodium from intracellular fluid. The rise in intracellular sodium concentration is accompanied by an influx of chloride; intracellular osmotic pressure rises and prompts an influx of water and cytogenic oedema (Bao JYS).

A vicious cycle develops, involving ischaemia, hypoxia and oedema. Injured, ischaemic tissue becomes oedematous at both intracellular and extracellular levels, so increasing the likelihood of further hypoxia and so creating a situation whereby traumatised tissue tends to be progressively more hypoxic at the centre, (Malerba F).

At the point of injury, damaged tissues are devitalised and non-viable. Intervention here should be surgical, aimed at adequate removal of necrotic tissue. Between this zone of tissue destruction, and the healthy tissues at the rim of the wounded area, lie tissues which have suffered varying degrees of damage and which may be prone to secondary ischaemic insult in the aftermath of the initial injury. This may arise from large vessel thrombosis, but is more often due to microvascular ischaemia prompted by the vicious cycle above. The development of compartment syndrome is an extreme example of this phenomenon. HBO treatment is directed at this middle zone of variably injured tissue with the aim of minimising secondary insult and maximising the preservation of healthy tissue.

Crush Injuries

The value of this approach is well illustrated in crush injuries which, in addition to soft tissue trauma, may also feature broken bones, neurological injury, and vascular damage. Surgery can be employed to stabilise fractures and to repair nerves and vessels, but there are no surgical interventions that address tissue damage at the microvascular level.

The best evidence for the use of HBO therapy comes from a controlled trial performed by Bouachour, Cronier et al. Following initial surgery within six hours, 36 cases of Gustilo and Anderson grade two or three crush injury were randomised within 24 hours of surgery to either treatment with HBO (100% O2 at 2.5 ATA for 90 minutes, twice daily for six days), or sham hyperbaric treatment (21% O2 at 1.1 ATA, identical treatment schedule). The two groups were similarly treated with antibiotics, anticoagulants and wound dressings and were similar in respect of age, co-morbidities and injury patterns. Results showed that 17 patients achieved complete healing in the HBO group, compared to ten in the sham group (p<0.01). Following blind reassessment, six patients in the sham group, but only one patient in the treatment group required a second surgical intervention (p<0.05). Sub-group analysis revealed that the addition of HBO had been especially effective in patients aged over 40 with grade three injuries. In this sub-group, there were seven successes and one failure in the HBO group, but three successes and seven failures in similarly aged patients treated with sham therapy (p<0.005).

Compartment Syndrome

In compartment syndrome, pressures in skeletal muscle compartments are sufficiently raised to reduce or halt vascular flow and for this reason, prompt surgical decompression is the accepted first treatment to restore tissue perfusion. Fasciotomy may be performed entirely on clinical grounds, or proposed when measured compartmental interstitial pressures exceed 30mmHg. Yet following inadvertent calf compression and intra-operative hypotension, intra-compartmental calf pressures in excess of 35mmHg have been controlled by prompt HBO treatment without the need for fasciotomy (Van Poucke S).

In another series, ten symptomatic patients were treated with HBO when compartment pressures were elevated between 15 and 48mmHg, but before surgery was indicated. All recovered without the need for surgery (Strauss MB). It is not suggested that HBO therapy should replace fasciotomy in established cases. Yet in presentations where compartment syndrome is a risk, the early addition of HBO into the standard care of repeated examination and pressure readings may prevent progression. No randomised trials have been performed into this pre-operative indication. In the post-operative phase following fasciotomy, the potential for preservation of marginally ischaemic tissue provide good reason for considering adjunctive treatment with HBO (Greensmith JE).

Treatment is decided on a case by case basis.


Buettner MF (2007)
Buettner MF, Wolkenhauer D. Hyperbaric oxygen therapy in the treatment of open fractures and crush injuries.
Emerg Med Clin N Am
25: 177-188


Bao JYS (1987)
Bao JYS. Hyperbaric oxygen therapy in reimplantation of severed limbs: A report of 34 cases. In: Kindwall EP ed. Proceedings of the Eighth International Conference on Hyperbaric Medicine. San Pedro California: Best Publishing, 182-186


Malerba F (1996)
Malerba F, Oriani G, Farnetti A.
HBO in orthopaedic disorders. In: Oriani G, Marroni A, Wattel F eds. Handbook on Hyperbaric Medicine. Milano: Springer Verlag, 409-427; Myers RA.
Hyperbaric oxygen therapy for trauma: crush injury, compartment syndrome, and other acute traumatic peripheral ischemias.
Int Anesthesiol Clin,


Bouachour G(1996)
Bouachour G, Cronier P, Gouello JP, Toulemonde JL, Talha A, Alquier P.. Hyperbaric oxygen therapy in the management of crush injuries: a randomised, double-blind, placebo-controlled clinical trial. J Trauma, Injury, Infection and Clin Care, 41: 333-339


Van Poucke S (2001)
Van Poucke S, Leenders T, Saldien V, Verstreken J, Beaucourt L, Adriaensen H. Hyperbaric oxygen (HBO) as useful, adjunctive therapeutic modality in compartment syndrome.
Acta Chir Belg,
101: 73-74


Strauss MB(1989)
Strauss MB, Hart GB.
Hyperbaric oxygen and the skeletal muscle compartment syndrome.
Contemp Orthop,
18: 167-174


Greensmith JE. (2004)
Hyperbaric oxygen therapy in extremity trauma.
J Am Acad Orthop Surg,
12: 376-384