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

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
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