What is Osteonecrosis (Avascular Necrosis)?
Painful condition caused by the death of bone tissue due to a lack of blood supply
The condition usually takes months to years to appear
Causes of Osteonecrosis (Avascular Necrosis) may include:
This condition may occur without any clear reason
Risk factors include bone fractures, joint dislocations, alcoholism, the use of high-dose steroids, organ transplantation, cancer, lupus, sickle cell disease, HIV infection, Gaucher's disease, and Caisson disease (dysbaric osteonecrosis)
Commonly diagnosed Osteonecrosis (Avascular Necrosis) include:
Commonly affected sites include the femoral head, knee, talus, and humeral head, but may affect other regions of the body
Diagnosed through medical imaging such as X-ray, MRI, or bone scintigraphy
HBOT is an adjunctive treatment for Osteonecrosis (Avascular Necrosis):
Highly effective beneficial effects of HBOT include:
Reduces bone-marrow pressure/edema increasing oxygen delivery preventing further bone necrosis
Stimulates angiogenesis and mobilization of cells involved in bone remodeling:
Osteoblasts responsible for bone deposition
Osteoclasts responsible for bone resorption
Leads to significant pain relief and better range of motion
Complete healing or resolution of the lesion can be obtained in the early stages of the disease
Standard HBOT protocol for Osteonecrosis (Avascular Necrosis):
HBOT treatment @ 2.0 - 2.4 atmospheres daily
Each HBOT treatment is approximately 2 hours long
HBOT regimen ranges between 40 to 60 treatments
What is delayed radiation injury?
Tissue insult following radiation therapy
Often seen after a latent period of six months or more
Causes of radiation injury may include:
Inflammation/occlusion of the arterial lining
Fibro-atrophic effects
Commonly diagnosed delayed radiation injuries include:
Osteoradionecrosis of bone:
Mandibular complications
Other bone radionecrotic complications
Soft tissue radionecrosis:
Head/neck/laryngeal necrosis
Chest wall non-healing wounds
Pelvic hemorrhagic cystitis and/or rectal bleeding
Neurologic injury secondary to radiation therapy
HBOT is a adjunctive treatment for delayed radiation injury:
Highly effective beneficial effects of HBOT include:
Neovascularization and angiogenesis
Improved tissue oxygenation
Reduces fibrosis within radiation field
Induces and mobilizes increased stem cell activity
Standard HBOT protocol for delayed radiation injuries:
HBOT treatment @ 2.0 - 2.4 atmospheres daily
Each HBOT treatment is approximately 2 hours long
Typical HBOT regimen ranges between 30 to 60 treatments
What are compromised skin grafts/flaps?
Grafts/flaps with poorly perfused wound beds
Leads to compromise of the transferred tissue
Causes of compromised skin grafts/flaps may include:
Irradiation
Ischemic reperfusion injury
Significant scar tissue following multiple surgeries or burns
Clinical management of compromised skin grafts/flaps includes:
Surgical correction of mechanical issues prior to HBOT
Consult for emergent HBOT treatment as soon as possible
HBOT as adjunctive treatment for compromised skin grafts/flaps:
Highly effective beneficial effects of HBOT include:
Hyperoxygenation of plasma and tissue
Mitigation of ischemia and reperfusion injury
Edema reduction
Increased stem cell and macrophage activity
Neovascularization and angiogenesis
Standard HBOT protocol for compromised skin grafts/flaps:
HBOT started as soon as graft/flap shows compromise
HBOT treatment @ 2.0 - 2.4 atmospheres
Initial HBOT treatments twice daily until graft/flap stabilizes
Daily HBOT treatments thereafter
Each HBOT treatment is approximately 2 hours long
Typical HBOT regimen is 20 treatments
What type of diabetic foot ulcer will benefit from HBOT?
Chronic refractory diabetic foot ulcers (CRDFU)
Approximately 15% of diabetic patients affected
Causes of chronic diabetic foot ulcers may include:
Progressive sensory, motor, & autonomic neuropathy
Deformity induced increasing plantar foot & toe pressures
Alterations in dermal blood flow autoregulation
Resultant tissue hypoxia within affected areas
Considerations for hyperbaric management of CRDFU:
DFU Wagner grade 3 or higher
Deep ulcer with osteomyelitis and/or abscess
Partial or whole foot gangrene
Unresponsive after 30 days of standard wound care
Ankle brachial index ≥ 0.6
HBOT is not a substitute for revascularization
HBOT as adjunctive treatment for CRDFU:
Highly effective beneficial effects of HBOT include:
Improved tissue oxygenation and collagen production
Induces and mobilizes increased stem cell activity
Neovascularization and angiogenesis
Reduces bacterial growth and/or gangrene
Standard HBOT protocol for CRDFU:
Hyperbaric oxygen treatment @ 2.0 - 2.4 atmospheres daily
Each HBOT treatment is approximately 2 hours long
Typical HBOT regimen ranges between 20 to 40 treatments
What is chronic refractory osteomyelitis?
Chronic pyogenic or mycogenic infection of bone or marrow
Persistent/recurrent followingstandard interventions
Often results in non-healing ulcers and/or sinus tracts
Immunocompromised patients at high risk
Clinical management for chronic refractory osteomyelitis includes:
Concurrent HBO therapy
Concurrent surgical debridement
Concurrent antibiotic therapy
HBOT as adjunctive treatment for chronic refractory osteomyelitis:
Highly effective beneficial effects of HBOT include:
Restoration of normal/elevated oxygen tension in bone
Osteogenesis, neovascularization, and angiogenesis
HBOT augments active cell wall transport of antibiotics
Enhances leukocyte and stem cell activity
Standard HBOT protocol for chronic refractory osteomyelitis:
HBOT treatment @ 2.0 - 2.4 atmospheres
Initial HBOT treatments may be BID for up to 3 days
Each HBOT treatment is approximately 2 hours long
Typical HBOT regimen ranges between 20 to 40 treatments
What is necrotizing fasciitis?
An acute and potentially fatal polymicrobial infection
Also known as “flesh-eating bacteria” infection
Involves superficial/deep fascia and soft tissue
Progresses to soft tissue necrosis
Both gas and fluid producing
Risk factors associated with necrotizing fasciitis include:
Trauma and/or surgery
Immunodeficiency, diabetes, peripheral vascular disease
Alcoholism, obesity, smoking, IV drug abuse
Clinical management of necrotizing fasciitis includes:
Treatment as early as possible:
Emergent surgical management
Emergent HBOT treatment
Emergent IV antibiotic therapy
All three interventions concurrent until patient stabilizes
HBOT as adjunctive treatment for necrotizing fasciitis:
Highly effective beneficial effects of HBOT include:
HBOT stops toxin production
HBOT is bacteriostatic
HBOT increases formation of oxygen-free radicals
Improved tissue oxygenation
Standard HBOT protocol for necrotizing fasciitis:
HBOT treatment @ 2.4 atmospheres
Initial HBOT treatments twice daily until patient stabilizes
Each HBOT treatment is approximately 2 hours long
Continue single HBOT treatments daily thereafter
Number of HBOT sessions is patient response dependent
What is gas gangrene?
Life threatening clostridial infection of the muscle tissues
Acute and progressive non-pyogenic invasive infection
Produces toxemia, edema, tissue death, & gas production
Causes of gas gangrene may include:
Endogenous infection from clostridial contamination
Exogenous infection of complex fractures and/or soft tissue
Clinical management of gas gangrene includes:
Emergent surgical management of the affected area
Emergent HBOT treatment as soon as possible
Emergent IV antibiotic therapy
Continue all concurrently until patient condition stabilizes
HBOT as adjunctive treatment for gas gangrene:
Highly effective beneficial effects of HBOT include:
HBOT stops alpha toxin production
HBOT is bacteriostatic
HBOT increases formation of oxygen-free radicals
Improved tissue oxygenation
Standard HBOT protocol for gas gangrene injuries:
Emergent HBOT treatment within 24 hours of diagnosis
HBOT treatment @ 2.8 atmospheres
Three HBOT treatments within 24 hours of diagnosis
HBOT twice daily until patient condition improves
Each HBOT treatment is approximately 2 hours long
Typical HBOT regimen completed within 3 to 5 days
What is intracranial necrosis?
Cerebral necrotic abscess
Subdural empyema and/or epidural empyema
Localized brain necrosis
Causes of intracranial necrosis may include:
Pyogenic microaerophilic and/or anaerobic bacteria
Septic arteritis and thrombophlebitis due to fungal infection
Neurologic injury secondary to radiation therapy
Clinical management of intracranial necrosis include:
Consider adjunctive HBOT if patient displays:
Multiple abscesses
Abscesses deep or dominantly located
Poor or contraindicated surgical risk
No response to surgery and/or antibiotics
HBOT as adjunctive treatment for intracranial necrosis:
Highly effective beneficial effects of HBOT include:
Inhibits growth of anaerobic oganisms
Reduces perifocal brain edema
Enhances neutrophil-mediated phagocytosis
Improves metabolic acidosis and low oxidation-reduction potential due to angioinvasive fungi
Standard HBOT protocol for intracranial necrosis:
HBOT treatment @ 2.0 - 2.4 atmospheres daily
Initial HBOT treatments twice daily until patient stabilizes
Daily HBOT treatments thereafter
Each HBOT treatment is approximately 2 hours long
Typical HBOT regimen ranges between 20 to 30 treatments
What are acute traumatic ischemias?
They are a constellation of disorders that range front crush injuries to compartment syndromes, from burns to frostbite, and from threatened flaps to compromised re-implantations.
Severe traumatic injuries producing:
Questionable tissue viability (trauma plus ischemia/necrosis)
Potential functional deficit
Clinical management of acute traumatic ischemias includes:
Concurrent emergent surgical intervention (revascularization/restoration of perfusion, fasciotomy/debridement, etc.)
Surgical delays increase probability of severe infection and tissue death.
Concurrent emergent HBOT treatment (as close to the time of injury as possible)
HBOT benefit drastically reduced if treatment delayed.
Concurrent antibiotic therapy
HBOT as adjunctive emergent treatment for acute ischemia:
Highly effective beneficial effects of HBOT include:
Hyper-oxygenation of plasma and hypoxic tissues. HBOT increases oxygen diffusion distance from the capillaries to the traumatized tissues.
HBOT-induced vasoconstriction and edema reduction
Mitigation of ischemia and reperfusion injury
Mobilization and activation of precursors necessary to initiate healing such as growth factors.
Enhances leukocyte and stem cell activity.
Neovascularization and angiogenesis
With HBO, oxygen becomes no more flow dependent than the other dissolved substances in the plasma. This allows oxygen to be available to tissues when normal perfusion is impeded.
Standard HBOT protocol for acute ischemia:
HBOT treatment @ 2.0 - 2.4 atmospheres
Initial HBOT treatments may be twice a day for 2-3 days.
Each HBOT treatment is approximately 2 hours long
Typical HBOT regimen ranges between 4 – 20 treatments
Total number of HBOTs should be a joint decision between the referring physician and the hyperbaric physician.
What is crush injury (CI)?
Severe traumatic injuries producing:
Questionable tissue viability
Potential functional deficit
What is skeletal muscle compartment syndrome (SMCS)?
Trauma induced fluid /swelling within the skeletal muscle compartment causing ischemia in muscle and nerve tissues
Clinical management of CI & SMCS includes:
Concurrent emergent surgical fasciotomy and debridement
Surgical intervention as soon as possible
Surgical delays increase probability of severe infection
Concurrent emergent HBOT treatment
Early emergent application of HBOT
HBOT benefit drastically reduced if treatment delayed
Concurrent antibiotic therapy
HBOT as adjunctive emergent treatment for CI & SMCS:
Highly effective beneficial effects of HBOT include:
Hyper-oxygenation of plasma and hypoxic tissues
HBOT-induced vasoconstriction and edema reduction
Mitigation of ischemia and reperfusion injury
Neovascularization and angiogenesis
Enhances leukocyte and stem cell activity
Standard HBOT protocol for CI & SMCS:
HBOT treatment @ 2.0 - 2.4 atmospheres
Initial HBOT treatments may be TID or BID for 2-3 days
Each HBOT treatment is approximately 2 hours long
Typical HBOT regimen ranges between 3 - 21 treatments
What causes decompression sickness (DCS)?
Decompression sickness is due to gas bubble formation
Caused by ambient pressure reduction
Examples of possible DCS injury mechanisms:
Diving ascent(s)
Aircraft decompression
Diagnosis is based on symptoms and onset relation to decompression
HBOT should initiated quickly following injury
Standard HBOT protocol for decompression sickness:
HBOT treatment @ 2.8 atmospheres
Based on US Navy Treatment Tables 5 and/or 6
HBOT treatment protocols range from 2.5 – 5 hours long
One HBOT session may be enough
Repetitive HBOT treatments daily until improvement ceases
What causes carbon monoxide poisoning?
Carbon monoxide (CO) is a gaseous byproduct of incomplete combustion
CO poisoning is caused by inhalation of carbon monoxide
Elevated CO levels cause hypoxia
Diagnosis of carbon monoxide poisoning combines:
CO exposure history
Abnormal neurological/cardiac evaluation(s)
Severe CO poisoning should be immediately referred for HBOT
Standard HBOT protocol for carbon monoxide poisoning:
HBOT treatment @ 2.8 atmospheres
Based on US Navy Treatment Tables 5 and/or 6
HBOT treatment protocols range from 2.5 – 5 hours long
One HBOT session may be enough
Repetitive HBOT treatments daily until improvement ceases
What are gas embolisms?
Gas embolism occurs when gas bubbles enter arteries or veins
Arterial gas embolism (AGE) clinical management:
Urgent (ASAP) HBOT indicated when brain symptoms present
Diagnosis of AGE is clinical
Based on history and symptoms
Head CT & MRI have low diagnostic sensitivity
Venous gas embolism (VGE) clinical management:
HBOT rarely indicated unless brain symptoms present
Standard HBOT protocol for gas embolisms:
HBOT treatment @ 2.8 atmospheres
Based on US Navy Treatment Tables 5 and/or 6
HBOT treatment protocols range from 2.5 – 5 hours long
One HBOT session may be enough
Repetitive HBOT treatments daily until improvement ceases
What is central retinal artery occlusion (CRAO)?
Emergent sudden painless vision loss
Left untreated, vision loss may be permanent
Patients at risk for CRAO may include those with:
Giant cell arteritis
Thromboembolic disease
Clinical management for sudden painless CRAO:
Rule out recent trauma and/or pain
Documentation of decreased visual acuity
Consult for emergent HBO treatment as soon as possible
Intraocular pressure measured/treated post HBO
Ophthalmology consult post HBO
HBOT as emergent treatment for CRAO:
Highly effective beneficial effects of HBOT include:
Reduction of ischemic reperfusion injury
Improved retinal tissue oxygenation
Neovascularization and angiogenesis
Induces and mobilizes increased stem cell activity
Standard HBOT protocol for CRAO:
Emergent HBOT treatment within 24 hours of injury onset
Hyperbaric oxygen therapy @ 2.0 – 2.8 atmospheres daily
Type and length of HBOT is patient response dependent
Repetitive HBOT treatments daily until improvement ceases
What is idiopathic sudden sensorineural hearing loss (ISSHL)?
Hearing loss of at least 30 dB occurring within three days over at least three contiguous frequencies
Typical symptoms include sudden unilateral hearing loss, tinnitus, aural fullness, and vertigo
Causes of ISSHL may include:
Vascular occlusion, ischemia, and/or trauma
Labyrinthine membrane breaks
Cochlear membrane damage
Abnormal cochlear stress response
Abnormal tissue growth
Toxins and/or ototoxic drugs
Viral infection and/or immune associated disease
Clinical management of ISSHL includes:
Audiology and otolaryngology evaluations
HBOT treatments within 14 days of hearing loss (ideally)
Concurrent corticosteroid therapy
HBOT as adjunctive treatment for ISSHL:
Highly effective beneficial effects of HBOT include:
Very high arterial peri-lymphatic oxygen levels
Blunting of ischemia/reperfusion injury
Anti-inflammatory effects & edema reduction
Neovascularization and angiogenesis
Standard HBOT protocol for ISSHL:
HBOT treatment @ 2.0 - 2.4 atmospheres daily
Each HBOT treatment is approximately 2 hours long
Typical HBOT regimen ranges between 10 - 20 treatments
