Delayed Radiation Injury
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
Compromised Skin Grafts
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
Chronic Diabetic Foot Ulcers
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
Chronic Refractory Osteomyelitis
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
Necrotizing Soft Tissue Infections
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
Gas Gangrene
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
Intracranial Necrosis
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
Crush Injury (CI) & Skeletal Muscle Compartment Syndrome (SMCS)
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
Decompression Sickness
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
Carbon Monoxide Poisoning
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
Gas Embolisms
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
Sudden Blindness: Central Retinal Artery Occlusion (CRAO)
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
Idiopathic Sudden Sensorineural Hearing Loss (ISSHL)
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
