Crush injuries and other forms of acute traumatic ischemia can produce extensive damage to muscle, soft tissue, bone, nerves, and blood vessels. Even after initial stabilization and restoration of circulation, progressive edema, tissue hypoxia, microvascular dysfunction, and ischemia-reperfusion injury may continue to threaten tissue viability.
Hyperbaric Oxygen Therapy (HBOT) is recognized by the Undersea & Hyperbaric Medical Society (UHMS) as an accepted adjunctive treatment for crush injury, compartment syndrome, and other acute traumatic ischemias.
When appropriately integrated into trauma care, HBOT may improve oxygen delivery to injured tissue, reduce edema, modulate ischemia-reperfusion injury, support host defenses, and help preserve threatened but potentially viable tissue.
HBOT does not replace surgical decompression, revascularization, fracture stabilization, debridement, hemorrhage control, or other definitive trauma management.
The period immediately following severe extremity trauma is critical.
Tissue that is clearly necrotic cannot be salvaged by HBOT. The potential role of hyperbaric treatment is greatest in tissue that remains viable but is threatened by hypoxia, edema, impaired microcirculation, and reperfusion injury.
Early communication between the trauma, orthopedic, vascular, and hyperbaric medicine teams may therefore be appropriate when a patient has a severe crush injury or traumatic ischemic injury in which loss of tissue, function, or limb is a concern.
Hyperbaric evaluation should occur in parallel with definitive trauma management and should never delay:
A crush injury results from substantial compressive force applied to a body part, frequently affecting several tissue layers simultaneously.
Depending on the severity of injury, damage may involve:
Crush injuries can result from:
The initial mechanical injury may be only part of the problem.
Tissue edema, vascular disruption, thrombosis, inflammation, impaired microcirculation, and reperfusion injury can expand the zone of damage after the original traumatic event.
Severe crush injuries may also be associated with rhabdomyolysis, hyperkalemia, acute kidney injury, shock, and other systemic consequences requiring aggressive medical management.
Acute traumatic ischemia occurs when trauma significantly compromises blood flow and oxygen delivery to injured tissue.
This may result from:
Although restoration of major arterial blood flow is essential when a correctable vascular injury is present, normal macroscopic blood flow does not necessarily mean that tissue oxygenation has returned to normal.
Microvascular obstruction, edema, endothelial injury, and reperfusion-associated inflammation may continue to compromise tissue after vascular repair.
Acute compartment syndrome occurs when pressure increases within a closed fascial compartment to the point that tissue perfusion becomes inadequate.
Bleeding and edema within a relatively noncompliant fascial envelope can progressively reduce capillary blood flow to muscle and nerve.
Without timely treatment, sustained ischemia may result in:
Acute compartment syndrome is a surgical emergency.
When compartment syndrome is established and decompression is indicated, urgent fasciotomy remains the definitive treatment. HBOT must not be used as an alternative to or reason to delay surgical decompression.
Hyperbaric therapy may have a role as an adjunct in selected patients with severe traumatic injury, including after decompression or in carefully monitored injuries where tissue viability remains threatened.
Severe extremity trauma often creates a self-perpetuating cycle of tissue injury. Mechanical trauma damages cells and blood vessels. This leads to bleeding, inflammation, and edema. Increasing edema raises tissue pressure and increases the distance through which oxygen must diffuse from functioning capillaries. Reduced microvascular perfusion then produces additional hypoxia. Hypoxic tissue becomes increasingly dysfunctional, which contributes to further edema and cellular injury. This creates an edema-ischemia cycle in which:
Trauma → edema → impaired perfusion → tissue hypoxia → cellular injury → additional edema and ischemia
Restoring blood flow is essential, but reperfusion itself may also contribute to secondary injury. Following a period of ischemia, restoration of circulation can activate neutrophils, endothelial adhesion mechanisms, inflammatory mediators, and reactive oxygen species. These processes may further damage the microcirculation and contribute to the phenomenon sometimes described as “no-reflow,” in which adequate tissue perfusion does not immediately return despite restoration of larger-vessel circulation. HBOT is used in this setting primarily to support threatened tissue while these secondary pathophysiologic processes are occurring.
The clinical presentation varies substantially according to the mechanism and severity of injury.
Evaluation begins with the mechanism of injury and repeated clinical examination.
Important factors include:
Compartment pressure measurement may be useful when acute compartment syndrome is suspected but the clinical examination is unreliable or equivocal.
Vascular studies, laboratory testing, imaging, transcutaneous oxygen measurement, and other assessments may also be used according to the clinical situation.
No diagnostic test used to evaluate eligibility for HBOT should delay emergency decompression or revascularization when definitive intervention is clearly indicated.
HBOT targets several mechanisms involved in acute traumatic ischemic injury.
Under hyperbaric conditions, substantially more oxygen dissolves directly into plasma. This increases the diffusion distance of oxygen and can improve oxygen availability in injured tissue even when local microvascular perfusion is impaired. The goal is to support tissue that is hypoxic but not yet irreversibly damaged.
Hyperbaric oxygen produces vasoconstriction in normally responsive vessels while maintaining high levels of tissue oxygenation. In injured tissue, this can help decrease edema without producing the reduction in tissue oxygen delivery that would normally accompany vasoconstriction. Reducing edema may improve the relationship between tissue pressure and microvascular perfusion and help interrupt the edema-ischemia cycle.
Restoration of blood flow after an ischemic period can initiate inflammatory injury involving activated neutrophils, endothelial dysfunction, reactive oxygen species, and impaired microvascular flow. HBOT has demonstrated effects on several components of this ischemia-reperfusion cascade. This mechanism is one reason hyperbaric therapy may remain relevant even after major blood flow has been surgically restored.
Adequate tissue oxygen tension is important for leukocyte antimicrobial activity, collagen synthesis, fibroblast function, angiogenesis, and other components of wound repair. Severe traumatic injury can leave surrounding tissue profoundly hypoxic. Improving tissue oxygenation may help support these oxygen-dependent healing and host-defense processes during the acute post-injury period.
A major objective of adjunctive HBOT is preservation of tissue that is injured and ischemic but potentially salvageable. Reducing secondary tissue loss may ultimately decrease the extent of necrosis, repeated debridement, reconstructive requirements, infection, and amputation in selected severe injuries.
Early hyperbaric consultation may be appropriate in severe traumatic injuries where tissue viability remains threatened despite appropriate initial trauma management.
Examples include:
The European Consensus Conference on Hyperbaric Medicine specifically recommends HBOT for severe open fractures with crush injury and identifies Gustilo grade IIIB and IIIC injuries as particularly appropriate for consideration.
Less severe injuries may also warrant evaluation when injury-related or patient-related risk factors substantially increase the likelihood of tissue loss, infection, or impaired healing.
The relationship between HBOT and compartment syndrome requires careful distinction.
When acute compartment syndrome requiring decompression is established, fasciotomy should proceed without delay.
HBOT does not replace fasciotomy.
Hyperbaric treatment may be considered as an adjunct:
Any use of HBOT in a patient at risk for compartment syndrome requires continued clinical surveillance. Hyperbaric treatment must not obscure, postpone, or substitute for recognition of a compartment requiring surgical decompression.
When HBOT is selected, treatment is generally most relevant during the early phase of traumatic ischemic injury.
This corresponds to the period during which edema, tissue hypoxia, microvascular dysfunction, and reperfusion injury are actively evolving and potentially salvageable tissue remains at risk.
The optimal treatment course depends on:
Treatment frequency and duration are determined by the hyperbaric physician in coordination with the trauma and surgical teams.
HBOT should fit around essential surgical procedures rather than determine their timing.
Severe crush injury and acute traumatic ischemia frequently require coordinated care across multiple specialties.
Management may involve:
Standard treatment may include:
HBOT should be integrated into this treatment pathway as an adjunct when the anticipated benefit to threatened tissue outweighs the risks and logistical requirements of hyperbaric treatment.
Crush injury, compartment syndrome, and other acute traumatic ischemias are recognized by the Undersea & Hyperbaric Medical Society as accepted indications for Hyperbaric Oxygen Therapy.
The clinical evidence base is smaller than that for many more common medical interventions because severe crush injuries are heterogeneous, time-sensitive, and difficult to study in randomized trials.
One frequently cited randomized, double-blind, placebo-controlled trial evaluated 36 patients with severe limb crush injuries who received either HBOT or sham treatment in addition to standard surgical and medical management.
Complete healing occurred more frequently in the HBOT group, and patients receiving HBOT required fewer additional surgical procedures. The investigators concluded that HBOT was a useful adjunct in selected severe crush injuries.
A 2024 systematic review examining adjunctive HBOT for severe lower-extremity soft-tissue trauma identified seven studies involving 229 patients. The authors reported that available studies generally suggested improved wound healing and reductions in tissue necrosis, infection, or additional surgical intervention when HBOT was added to standard trauma care.
However, the evidence remains limited by small patient populations, heterogeneous injuries, differing treatment protocols, and relatively few randomized clinical trials.
An earlier Cochrane review similarly concluded that the available crush-injury trial suggested improved healing and less tissue necrosis but emphasized that the overall body of evidence for acute traumatic wounds was limited and at risk of bias.
Accordingly, HBOT should not be viewed as a replacement for established trauma management. Its role is best considered as an adjunct for carefully selected patients with significant tissue ischemia and a meaningful risk of loss of function, tissue, or limb.
European hyperbaric consensus recommendations support early HBOT for severe open fractures with crush injury and suggest consideration in selected crush injuries where tissue viability is threatened.
The Centers for Medicare & Medicaid Services National Coverage Determination for Hyperbaric Oxygen Therapy (NCD 20.29) specifically includes:
Acute traumatic peripheral ischemia, when HBOT is used as an adjunct to accepted standard treatment and loss of function, limb, or life is threatened.
CMS also specifically covers:
Crush injuries and suturing of severed limbs, again as adjunctive treatment when loss of function, limb, or life is threatened.
Coverage recognition does not mean that every traumatic injury qualifies for HBOT or guarantees payment for an individual treatment.
Documentation should clearly establish the severity of injury, the threatened tissue or function, standard treatments being provided, medical necessity for adjunctive HBOT, and applicable payer requirements.
Consider early consultation with a hyperbaric medicine specialist when a patient has a severe crush injury or other acute traumatic ischemic injury and there is concern for threatened tissue, loss of function, or limb loss despite appropriate trauma management.
Situations that should prompt consideration include:
HBOT should never delay fasciotomy, revascularization, hemorrhage control, debridement, fracture stabilization, or other immediately necessary surgical treatment.
When possible, early communication between the treating trauma team and an experienced hyperbaric center allows HBOT logistics to be coordinated alongside definitive care rather than after tissue deterioration has already occurred.
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Undersea & Hyperbaric Medical Society. Hyperbaric Oxygen Therapy Indications: Crush Injury, Compartment Syndrome and Other Acute Traumatic Ischemias.
Strauss MB. The role of hyperbaric oxygen for acute traumatic ischemias. Undersea & Hyperbaric Medicine. 2022;49(2).
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Kwee E, Borgdorff M, Schepers T, et al. Adjunctive hyperbaric oxygen therapy in the management of severe lower limb soft tissue injuries: a systematic review. European Journal of Trauma and Emergency Surgery. 2024;50:1093–1100.
Eskes A, Vermeulen H, Lucas C, Ubbink DT. Hyperbaric oxygen therapy for treating acute surgical and traumatic wounds. Cochrane Database of Systematic Reviews. 2013;12.
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Centers for Medicare & Medicaid Services. National Coverage Determination 20.29: Hyperbaric Oxygen Therapy.