Hyperbaric Oxygen Therapy in Orthopaedics – Principles, Indications and Clinical Applications

Hyperbaric oxygen therapy (HBOT) is a medical treatment in which a patient breathes nearly 100% oxygen inside a chamber pressurised above normal atmospheric pressure.

Increasing ambient pressure markedly increases the amount of oxygen dissolved in plasma and consequently increases the oxygen tension within tissues.

In Trauma and Orthopaedics, HBOT is used primarily as an adjunctive treatment in conditions characterised by tissue hypoxia, infection, impaired wound healing or ischaemia-reperfusion injury.

Hyperbaric oxygen therapy does not replace surgical debridement, fracture stabilisation, vascular repair, fasciotomy or appropriate antimicrobial therapy.

HBOT involves intermittent administration of oxygen at a pressure greater than normal sea-level atmospheric pressure.

Clinical treatments are commonly delivered at approximately 2.0–3.0 atmospheres absolute (ATA), depending on the indication and protocol.

Treatment sessions commonly last approximately 60–120 minutes and may be repeated over several days or weeks.

The exact pressure, treatment duration and number of sessions depend on the pathology, response to treatment and hyperbaric medicine protocol.

Monoplace Chamber

Designed for a single patient. The chamber itself is usually pressurised while the patient receives oxygen.

Multiplace Chamber

Accommodates several patients and healthcare personnel. The chamber is commonly pressurised with air while patients breathe oxygen through masks, hoods or specialised breathing systems.

Several physical laws help explain hyperbaric oxygen therapy.

Henry's Law

The amount of gas dissolved in a liquid is proportional to the partial pressure of that gas above the liquid.

Therefore, increasing oxygen pressure markedly increases the quantity of oxygen dissolved directly in plasma.

Boyle's Law

At constant temperature, the volume of a gas is inversely proportional to its pressure.

This principle is particularly important in conditions containing gas bubbles such as decompression sickness or arterial gas embolism.

Under normal conditions, most oxygen is transported bound to haemoglobin, with only a small quantity dissolved in plasma.

During HBOT, the marked increase in inspired oxygen partial pressure causes a substantial rise in plasma-dissolved oxygen.

This allows oxygen to diffuse farther from functioning capillaries into relatively hypoxic tissue, which may be particularly important in traumatised or oedematous tissue.

• Markedly increases tissue oxygen tension.
• Improves oxygen delivery to relatively ischaemic tissues.
• Reduces tissue oedema through oxygen-induced vasoconstriction.
• Supports leukocyte oxidative killing of bacteria.
• Promotes fibroblast activity.
• Supports collagen synthesis.
• Promotes angiogenesis and neovascularisation.
• May reduce components of ischaemia-reperfusion injury.
• Supports wound healing in selected hypoxic tissues.
• May enhance activity of selected antimicrobial agents.

Hyperoxia causes vasoconstriction in relatively normal vascular beds.

Normally, vasoconstriction might be expected to reduce tissue oxygenation. During HBOT, however, the marked increase in plasma oxygen content helps maintain high tissue oxygen tension despite reduced blood flow.

The reduction in microvascular blood flow decreases capillary filtration and may therefore reduce tissue oedema.

This mechanism is particularly relevant in crush injury and acute traumatic ischaemia.

Severe soft-tissue trauma can create a self-perpetuating cycle:

HBOT attempts to interrupt this cycle by increasing tissue oxygen availability and reducing oedema.

Chronic refractory osteomyelitis is one of the most important orthopaedic indications for HBOT.

It generally refers to bone infection that persists or recurs despite appropriate conventional treatment, including surgical and antimicrobial management.

The infected bone environment may be characterised by:

• Reduced vascularity.
• Scarred soft tissue.
• Sequestrum formation.
• Local tissue hypoxia.
• Biofilm-associated infection.
• Reduced antibiotic delivery.
• Impaired immune-cell function.

HBOT aims to improve local oxygen availability and enhance host defence and tissue repair.

• Raises oxygen tension within hypoxic infected tissue.
• Supports oxygen-dependent neutrophil bacterial killing.
• Enhances fibroblast activity and collagen formation.
• Promotes angiogenesis in poorly vascularised tissue.
• May improve the activity of selected antibiotics.
• May improve bone-remodelling biology.

Evidence is mostly derived from observational studies and case series rather than large randomised controlled trials.

HBOT for refractory osteomyelitis is an adjunct to adequate debridement and culture-directed antibiotics – not an alternative to them.

1. Confirm the diagnosis and determine the anatomical extent of infection.
2. Obtain appropriate deep tissue and bone cultures.
3. Perform adequate debridement of necrotic bone and soft tissue where indicated.
4. Restore mechanical stability if fracture or nonunion is present.
5. Give culture-directed systemic antimicrobial therapy.
6. Optimise host factors including glycaemic control, nutrition and smoking cessation.
7. Consider HBOT when infection remains refractory or when the biological environment is severely compromised.
8. Provide appropriate soft-tissue reconstruction.

Severe crush injuries involve a combination of direct tissue destruction, microvascular damage, swelling, ischaemia and reperfusion injury.

Muscles may exist within a zone of injury ranging from normal tissue to irreversibly necrotic tissue. Between these extremes may be hypoxic but potentially salvageable tissue.

HBOT may help selected patients by:

• Increasing oxygen diffusion into hypoxic muscle.
• Reducing tissue oedema.
• Limiting components of reperfusion injury.
• Supporting host defence against infection.
• Supporting tissue repair.

Acute compartment syndrome results when increasing tissue pressure within a closed osteofascial compartment compromises microvascular perfusion and produces progressive muscle and nerve ischaemia.

HBOT has been investigated as an adjunct in acute traumatic ischaemia and selected compartment-related injuries.

However:

Established acute compartment syndrome requires urgent surgical fasciotomy. HBOT must never delay decompression.

HBOT may have an adjunctive role after decompression or in selected traumatic ischaemic situations where salvageable hypoxic tissue remains.

Acute traumatic ischaemia represents a group of conditions in which trauma and inadequate tissue perfusion occur simultaneously.

Examples include:

• Severe crush injury.
• Compartment-related muscle ischaemia.
• Replantation injuries.
• Reperfusion injury following vascular repair.
• Severely compromised soft-tissue trauma.

Hyperbaric oxygen should be considered an adjunct to restoration of perfusion and appropriate surgical management rather than a substitute for revascularisation.

Restoration of blood flow to previously ischaemic tissue is essential, but reperfusion itself can initiate additional inflammatory injury.

Mechanisms include:

• Endothelial activation.
• Neutrophil adhesion.
• Reactive oxygen species generation.
• Microvascular dysfunction.
• Capillary leakage.
• Progressive oedema.

HBOT may modify some components of this inflammatory and microvascular response.

Soft-tissue reconstruction is central to orthopaedic trauma, chronic infection and limb salvage.

HBOT is not routinely indicated for a normal healthy flap or graft.

It may be useful when a graft or flap becomes compromised by:

• Arterial insufficiency.
• Venous congestion after appropriate surgical assessment.
• Hypoxic wound bed.
• Previous irradiation.
• Severe traumatic soft-tissue injury.
• Ischaemia-reperfusion injury.

HBOT may increase oxygen delivery, improve fibroblast activity, support angiogenesis and improve survival of marginally perfused tissue.

HBOT should never substitute for correction of a surgically treatable cause of flap failure.

Examples requiring immediate surgical evaluation include:

• Arterial thrombosis.
• Venous thrombosis.
• Kinking of the vascular pedicle.
• Haematoma compressing the pedicle.
• Mechanical tension or compression.

First correct the mechanical or vascular cause of flap compromise; use HBOT to support salvageable hypoxic tissue.

Hyperbaric oxygen has been investigated in early-stage osteonecrosis of the femoral head.

Proposed mechanisms include:

• Improved oxygenation of ischaemic bone.
• Reduction in bone-marrow oedema.
• Promotion of angiogenesis.
• Support of bone repair and remodelling.

The potential role is greatest in pre-collapse or early-stage disease.

Once substantial structural collapse and secondary arthritis have developed, HBOT cannot mechanically restore the architecture of the femoral head.

Treatment decisions in osteonecrosis should still consider:

• Stage.
• Size of the necrotic lesion.
• Location of the lesion.
• Presence of subchondral fracture.
• Femoral-head collapse.
• Patient age and activity level.
• Underlying cause.

Joint-preserving surgery or arthroplasty remains necessary when structurally indicated.

Clostridial myonecrosis is a rapidly progressive, life-threatening infection associated with muscle necrosis, toxin production and systemic toxicity.

Management requires:

1. Immediate resuscitation.
2. Urgent and aggressive surgical debridement.
3. Appropriate intravenous antibiotics.
4. Critical-care support.
5. Adjunctive HBOT when available and appropriate.

High tissue oxygen tensions inhibit the growth and toxin production of susceptible anaerobic organisms and improve host leukocyte function.

HBOT must never delay surgical debridement of gas gangrene.

HBOT has also been used as an adjunct in selected necrotising soft-tissue infections.

Potential effects include improved tissue oxygenation, enhanced leukocyte function and inhibition of selected anaerobic organisms.

However, definitive management remains:

• Urgent surgical debridement.
• Broad-spectrum intravenous antimicrobial therapy followed by targeted treatment.
• Haemodynamic and intensive-care support.
• Repeated debridement when necessary.

Selected diabetic foot wounds represent another important interface between hyperbaric medicine and orthopaedic practice.

Patients may present with:

• Deep ulceration.
• Exposed bone.
• Osteomyelitis.
• Peripheral arterial disease.
• Neuropathy.
• Charcot-related deformity.

HBOT is not indicated for every diabetic foot ulcer and should be considered within a comprehensive limb-salvage programme involving vascular assessment, pressure off-loading, wound care, infection control and glycaemic optimisation.

Radiation can produce progressive hypovascular, hypocellular and hypoxic tissue damage long after radiotherapy has been completed.

Delayed radiation injury may affect:

• Bone.
• Skin.
• Subcutaneous tissue.
• Muscle.

HBOT may stimulate angiogenesis and improve oxygenation within the chronically hypovascular tissue bed.

Osteoradionecrosis refers to devitalised irradiated bone that fails to heal appropriately in the absence of persistent or recurrent malignancy.

Although classically described in the mandible, radiation-associated bone necrosis can also be relevant to orthopaedic oncological reconstruction.

HBOT may be incorporated into multidisciplinary management in selected cases.

Hyperbaric oxygen has biological effects that could theoretically support bone healing, including increased oxygenation and angiogenesis.

However, HBOT is not a standard routine treatment for uncomplicated fractures.

Routine use solely to accelerate union of an otherwise normally healing fracture is not established.

Its orthopaedic role is more relevant when fracture healing is threatened by severe soft-tissue ischaemia, refractory infection or other recognised hyperbaric indications.

HBOT should not be viewed as a general treatment for all nonunions.

When nonunion is present, evaluate:

• Mechanical stability.
• Fracture gap.
• Alignment.
• Infection.
• Bone loss.
• Vascularity.
• Smoking and host factors.

HBOT may be considered when a nonunion occurs in the setting of chronic refractory osteomyelitis or severe tissue hypoxia, but correction of mechanical and biological causes remains essential.

Hyperbaric protocols are disease-specific and should be prescribed by an appropriately trained hyperbaric physician.

Broadly, many orthopaedic-related protocols use:

• 100% oxygen.
• Approximately 2.0–3.0 ATA.
• Approximately 60–120 minutes per session.
• Daily or near-daily treatments.
• Multiple sessions depending on the indication.

Acute traumatic ischaemia may require treatment very early after injury, whereas chronic osteomyelitis may require several weeks of therapy.

Commonly described regimens involve approximately:

• 2.0–3.0 ATA.
• 90–120 minutes per treatment.
• Daily treatment on most weekdays.
• Approximately 20–40 or more treatments depending on response and protocol.

Treatment response should be reassessed rather than automatically extending HBOT indefinitely when infection fails to improve.

• Chronic osteomyelitis persisting despite appropriate debridement and antibiotics.
• Severe crush injury with threatened but potentially viable tissue.
• Complex acute traumatic ischaemia.
• Compromised reconstructive flap or graft after surgically correctable causes have been addressed.
• Selected early osteonecrosis cases within an appropriate multidisciplinary protocol.
• Gas gangrene.
• Selected necrotising soft-tissue infections.
• Selected severe diabetic foot wounds.
• Delayed radiation-induced bone or soft-tissue injury.

Important Absolute Contraindication

Untreated pneumothorax is the classic major absolute contraindication to HBOT.

Pressure changes can cause expansion of trapped intrathoracic gas during decompression, potentially resulting in tension pneumothorax.

Relative Contraindications / Precautions

• Severe obstructive lung disease with air trapping.
• Pulmonary bullae or blebs in selected patients.
• Upper respiratory tract infection.
• Difficulty equalising middle-ear pressure.
• History of seizure disorder.
• Uncontrolled fever.
• Severe claustrophobia.
• Selected medications that increase toxicity risk or interact with hyperoxia.
• Unstable medical conditions requiring careful assessment.

The risk-benefit assessment should be performed by the treating hyperbaric medicine team.

HBOT is generally well tolerated when appropriately supervised, but complications can occur.

• Middle-ear barotrauma.
• Sinus barotrauma.
• Pulmonary barotrauma.
• Oxygen-toxicity seizure.
• Temporary myopic visual change.
• Pulmonary oxygen toxicity with prolonged exposure.
• Hypoglycaemia in susceptible diabetic patients.
• Claustrophobia.
• Rare decompression-related pulmonary complications.

Changes in ambient pressure affect gas-containing spaces.

Middle-ear discomfort and barotrauma are among the most frequent adverse effects.

Patients are taught pressure-equalisation techniques during chamber compression and decompression.

Very high oxygen partial pressures can produce toxicity, particularly in the central nervous system and lungs.

Central Nervous System Oxygen Toxicity

The most dramatic manifestation is an oxygen-toxicity seizure.

These events are uncommon and are generally self-limited when oxygen exposure is discontinued.

Treatment protocols may incorporate air breaks to reduce oxygen exposure.

• Improved oxygen delivery to compromised tissues.
• Reduction of oedema in selected acute injuries.
• Potential enhancement of infection control.
• Promotion of angiogenesis.
• Support of fibroblast and collagen activity.
• Potential improvement in salvage of selected flaps and grafts.
• Adjunctive benefit in difficult refractory osteomyelitis.

• Limited availability of hyperbaric chambers.
• Need for repeated treatment sessions.
• Cost and logistical burden.
• Transport difficulties in critically injured patients.
• Potential complications of pressure and oxygen exposure.
• Variable quality of evidence between indications.
• Difficulty performing some intensive-care interventions inside certain chambers.
• Risk of inappropriate use for poorly supported indications.

The strength of evidence supporting HBOT differs considerably between conditions.

Chronic refractory osteomyelitis is a recognised indication, but the evidence base consists largely of observational series and non-randomised studies rather than high-quality randomised controlled trials.

Similarly, evidence for acute traumatic ischaemia and compromised flaps is supported by physiological rationale, experimental work and clinical studies, but patient selection remains important.

A recognised indication for HBOT does not mean that every patient with that diagnosis automatically requires HBOT.

Consider a patient with a previously open tibial fracture who develops chronic infection with draining sinus formation despite previous surgery and appropriate antimicrobial treatment.

Management should include:

1. Define infection extent and assess fracture stability.
2. Obtain multiple deep cultures.
3. Perform radical debridement of infected and devitalised tissue.
4. Provide stable fixation when required.
5. Administer culture-directed antibiotics.
6. Address dead space and soft-tissue coverage.
7. Optimise patient-related risk factors.
8. Consider adjunctive HBOT when disease remains refractory or the local biological environment is severely compromised.

Consider a patient with a severely crushed leg after high-energy trauma.

Initial management should focus on:

1. Trauma resuscitation.
2. Vascular assessment and revascularisation where required.
3. Recognition and urgent fasciotomy of compartment syndrome.
4. Debridement of nonviable tissue.
5. Fracture stabilisation.
6. Antimicrobial and tetanus prophylaxis as appropriate.
7. Early reconstructive planning.

HBOT may subsequently be added in selected patients to support marginally viable, hypoxic tissue and reduce the consequences of acute traumatic ischaemia.

“HBOT can cure osteomyelitis without surgery.”

Incorrect. Necrotic infected bone may require surgical removal, and appropriate antibiotics remain essential.

“HBOT can prevent fasciotomy in established compartment syndrome.”

Incorrect. Established acute compartment syndrome requires urgent decompression.

“HBOT makes every fracture heal faster.”

Routine uncomplicated fracture healing is not an established indication.

“HBOT can regenerate a collapsed femoral head.”

No. Its proposed role is primarily in selected early-stage osteonecrosis; established collapse is a structural problem.

“A failing flap should be sent directly for HBOT.”

A surgically correctable vascular or mechanical cause should first be urgently identified and corrected.

• HBOT involves breathing nearly 100% oxygen at a pressure above normal atmospheric pressure.
• Clinical HBOT is commonly administered at approximately 2–3 ATA.
• Henry's law explains the marked increase in dissolved plasma oxygen during HBOT.
• HBOT greatly increases oxygen dissolved directly in plasma.
• Hyperoxia-induced vasoconstriction may decrease tissue oedema while high oxygen tensions maintain tissue oxygen delivery.
• HBOT supports leukocyte oxidative bacterial killing.
• HBOT can support fibroblast activity, collagen synthesis and angiogenesis.
• Chronic refractory osteomyelitis is an important recognised orthopaedic indication.
• HBOT in refractory osteomyelitis is an adjunct to surgical debridement and culture-directed antibiotic therapy.
• Crush injury and other acute traumatic ischaemias are recognised indications for adjunctive HBOT in selected patients.
• HBOT must never delay fasciotomy in acute compartment syndrome.
• Compromised flaps may benefit from HBOT after a surgically correctable cause of vascular compromise has been addressed.
• HBOT is not required for healthy, uncompromised grafts and flaps.
• Selected early-stage osteonecrosis of the femoral head has been investigated as an HBOT indication.
• Advanced structural collapse from osteonecrosis cannot be reversed simply by increasing tissue oxygenation.
• Gas gangrene requires urgent debridement and antibiotics; HBOT is an adjunct.
• Routine uncomplicated fractures are not a standard indication for HBOT.
• Untreated pneumothorax is the classic major absolute contraindication.
• Middle-ear barotrauma is one of the common adverse effects.
• Oxygen-toxicity seizures are a recognised but uncommon complication.
• The key word in orthopaedic HBOT is “adjunct.”

1. Understand the principle: HBOT substantially increases dissolved plasma oxygen and tissue oxygen tension.
2. Think hypoxia: its greatest orthopaedic value is in selected tissues where oxygen delivery is severely compromised.
3. Think refractory infection: chronic refractory osteomyelitis is one of the key orthopaedic indications.
4. Think acute traumatic ischaemia: crush injuries may benefit when viable but hypoxic tissue remains.
5. Never delay definitive surgery: compartment syndrome needs fasciotomy, vascular occlusion needs revascularisation and necrotic infection needs debridement.
6. Think reconstruction: HBOT may support threatened grafts and flaps but cannot correct pedicle thrombosis or mechanical obstruction.
7. Use caution with AVN: potential benefit is predominantly in selected early disease rather than established collapse.
8. Know the contraindication: untreated pneumothorax is the classic absolute contraindication.
9. Know the complications: barotrauma and oxygen toxicity are the major physiological concerns.
10. Use HBOT selectively: it should be integrated into multidisciplinary orthopaedic care rather than used as a stand-alone treatment.

In orthopaedics, hyperbaric oxygen is best understood as a biological adjunct that improves oxygen delivery to threatened tissue while the surgeon corrects the underlying mechanical, infectious, vascular or reconstructive problem.