Non-diving related hyperbaric treatment

CARAT 2014

LTJG Chamchan Chanchang

∗ A period of breathing high percentage oxygen for therapeutic purposes at the pressure greater than 1

Hyperbaric Oxygen Therapy (HBOT)

therapeutic purposes at the pressure greater than 1 ATA (>1.4 ata)

∗ HBO Mechanisms

∗ Bubble crunching : Pressure effect

∗ Increase oxygenation to the tissue : O2 as a drug

∗ Bubble related disease : Diving accident

∗ AGE/DCS

Bubble Crunching

∗ AGE/DCS

Hyperoxygenation of tissueNormalization of the pO2 in hypoxic area

• 14-20 times more O2 in plasma

• 4 times into the surrounding tissue

∗ Arterial blood contains 20 Vol% of oxygen

∗ Venous blood contains 14 Vol% of oxygen

∗ 6 Vol% of O2 is tissue respiration need

∗ Breathing 100% O2 at these absolute pressures, sufficient oxygen is dissolved in plasma to supply the body’s requirement

∗ Vasoconstriction

∗ Decrease edema

HBOT Physiologic effects

∗ Decrease edema

∗ Stimulate capillary growth

∗ Improve body defence against infection

∗ Enhance wound healing

∗ Elimination of carbon monoxide

UHMS 2012

3. CO poisoning +/- CN 9. Clostridia myositis and myonecrosis

1. Air or gas embolism

2. Decompression sicknessDiving related

Non Diving related

3. CO poisoning +/- CN

4. Acute thermal injury

5. Acute traumatic ischemia

6. Arterial insufficiency

- CRAO

- Problem wounds

7. Compromised Grafts or flaps

8. Delayed radiation injury

9. Clostridia myositis and myonecrosis

10. Necrotizing soft tissue infection

11. Osteomyelitis (Refractory)

12. Intracranial abscess

13. Severe anemia

14. Idiopathic Sudden Sensorineural

Hearing loss

∗ DCI. 17∗ Delayed radiation injury 200∗ ORN. 139∗ Radiation cystitis 53∗ Radiation soft tissue 9

∗ DM Ulcer and Problem wound 23

Underwater Medicine department Number of treatments 2o13

∗ DM Ulcer and Problem wound 23∗ SSNHL 23∗ Osteomyelitis 7∗ Crush injury 5∗ Necrotizing soft tissue 5 ∗ Compromised flap 3∗ CRAO 2

∗ Other 15∗ Total 299

Underwater Medicine department Number of treatments 2o14

Multiplace chamber

Monoplace chamber

3 compartments multiplace

Clinical HBO

Carbon monoxide and cyanide poisoning

Carbon monoxide poisoning

∗ Most benefit when treatment less than 6 hr

∗ Maintains tissue oxygenation

HBO Benefits

Maintains tissue oxygenation

∗ Speed COHb dissociation

– Half-life of CO 320 min on room air

90 min on 100% O2

23 min on HBO (3 ATA)

∗ Prevent delayed neurological sequelae (DNS) following acute severe CO poisoning if treatment begins < 6 hr or exposure (Incidence of DNS in pt. treated with HBO 0-4% : 10-20% not treated)

Carbon monoxide and cyanide poisoning

∗ Recommend of U.S. Navy Diving Manual Revision 6

• Treatment Table 5

Treatment Protocol

• Treatment Table 5

– Carbon monoxide poisoning

• Treatment Table 6

– Severe carbon monoxide poisoning, cyanide poisoning or smoking inhalation (i.e. severe headache,

mental status changes, any neurological symptoms, rapid heart rate)

∗ A burn is a type of injury to flesh or skin caused by heat, electricity, chemicals, friction, or radiation.

∗ At temperatures greater than 44 °C (111 °F),

Acute Thermal Burn

∗ At temperatures greater than 44 °C (111 °F), proteins begin losing their three-dimensional shape and start breaking down

∗ Many of the direct health effects

Pathology

∗ directed toward minimizing edema

∗ preserving marginally viable tissue

HBO Benefit

∗ preserving marginally viable tissue

∗ protecting the microvasculature

∗ enhancing host defenses

∗ promoting wound closure

Guideline therapy

∗ US Navy Treatment table 9

∗ TID x 1 day

∗ Then OD∗ Then OD

Minimum treatment 5

Maximum treatment 45

∗ Crush Injury and Acute traumatic ischemia

∗ Compromised Grafts or flaps

Ischemic/Hypoxic Tissue Conditions

∗ Compromised Grafts or flaps

∗ Delayed radiation injury

∗ Arterial insufficiency

- CRAO

- Problem wounds

∗ Compartment Syndrome

Crush Injury and Acute traumatic ischemia

∗ Threatened Flaps

∗ Burns

∗ Frostbite

NON – VIABLE DEAD TISSUET

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NORMAL VIABLE TISSUE

INFECTION

RECOVERYRECOVERY

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LOSS OFLOSS OF

FUNCTIONFUNCTION

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: Pathophysiology of : Pathophysiology of crush crush injury injury

Effects of HBOT In Crush InjuriesEffects of HBOT In Crush Injuries

11. . HyperoxygenationHyperoxygenation

22.. VasoconstrictionVasoconstriction22.. VasoconstrictionVasoconstriction

33.. 2020% decrease in edema % decrease in edema

44.. Host factorsHost factors

55.. Red Blood Cell DeformabilityRed Blood Cell Deformability

Hyperbaric oxygen therapy in no wayHyperbaric oxygen therapy in no way

supercedessupercedes the surgical principles for the surgical principles for

management of crush management of crush injuries / ATPIsinjuries / ATPIs

HOWEVER , if surgical intervention is HOWEVER , if surgical intervention is HOWEVER , if surgical intervention is HOWEVER , if surgical intervention is

going to be delayed , there may be going to be delayed , there may be

benefit (in theory at least) to treatment benefit (in theory at least) to treatment

with HBO while awaiting surgerywith HBO while awaiting surgery

HBOT ProtocolsHBOT Protocols

Crush Crush Injuries / ATPIsInjuries / ATPIs

HBO Committee ReportHBO Committee Report

22..0 0 –– 22..5 5 ATA ; ATA ; 90 90 –– 120 120 minmin

TID (TID (22d) , BID (d) , BID (22d) , Daily (d) , Daily (22d)d)

Compromised Grafts or flaps

Compromised Grafts or flaps

Grafts Flaps

∗ previous radiation to the wound area

∗ diabetes mellitus

∗ Infections

∗ age

∗ nutritional status

∗ smoking

∗ previous radiation

HBOT Benefits

∗ Stimulate fibroblast and enhancing collagen synthesissynthesis

∗ Neovascularization

∗ Hyperoxygenation

∗ Edema reduction

HBOT Protocols

∗ Pressure 2.0-2.4 ata 90-120 min

∗ Initial treatment should be twice daily

∗ once a day when flap or graft appear more viable and stable

∗ Osteoradionecrosis

∗ Mandible or other bones

Delayed radiation injury

∗ Mandible or other bones

∗ Soft tissue Radionecrosis

∗ Radiation cystitis, proctitis, enteritis, etc.

• Bone; necrosis of osteoblast & osteocyte,

fibrosis of marrow spaces

Radiation Effect on tissue

fibrosis of marrow spaces

• Periosteum; fibrosis

• Blood vessel; endothelial death ,

hyalinization & thrombosis

• Mucosa & Skin; diminished cellularity, fibrosis

∗ Any exposed bone in a field of irradiation (> 50 Gy), resist to conservative treatment and fail to heal

Osteoradionecrosis

resist to conservative treatment and fail to heal within 3 months

∗ Hypoxia

∗ Hypovascular

∗ Hypocellular

Osteoradionecrosis

+ surgical truama

+/- secondary infection∗ Hypocellular

∗ 2.4 ATA for 90 min

∗ The 20/10 protocol - Elective surgery or wounding

HBO

∗ The 20/10 protocol - Elective surgery or wounding within radiated tissues

*Bone graft reconstruction

*Soft tissue vascular flaps

*Tooth removal

∗ Radiation cystitis

∗ Hematuria

Soft tissue Radionecrosis

∗ Hematuria

∗ HBO Protocol

∗ TT9 for 40 dives

∗ Central Retinal Arterial Occlusion (CRAO)

Arterial Insufficiency

∗ Sudden painless vision loss, which is usually dramatic and permanent

Central Retinal Arterial Occlusion (CRAO)

and permanent

∗ Management

∗ Ocular massage, Anterior chamber paracentesis, Intraocular pressure lowering medication, Vasodilators, Oral diuretics

∗ Thrombolytic agents

∗ Surgical removal of embolus or thrombus

∗ Supplemental oxygen therapy

∗ Treatment should be aimed at promptly supplying

oxygen to the ischemic retina at a partial pressure

sufficient to maintain viability while medically assisted or

Role of Oxygen

sufficient to maintain viability while medically assisted or spontaneous restoration of central retinal artery blood flow occurs

∗ Outcome depends on– Vessel occluded

– Degree of occlusion

– Time interval until therapy is initiated

– Presence of alternate sources of oxygen to the ocular tissues

∗ 2.8 ATA 90 min Bid, OD

∗ TT5 OD

HBOT Protocol

∗ TT5 OD

• HBOT

– Acceptable, safe, considered efficacious

– No evidence of harm

– No alternative therapies with similar outcomes

∗ Microvascular chronic ischemic wound;

Diabetic wound

Problem Wounds

Diabetic wound

∗ Problem wounds are usually hypoxic

∗ elevation of wound oxygen tension to normal enhanced wound healing

∗ Transcutaneous oximetry

HBO

∗ TcpO2 < 40 mm Hg : Hypoxic wound

Transcutaneous oximetry

∗ THEN test 100 % O2 breathing at 1 ATA.

IF TcpO2 rise > 50 %

THEN HBO

∗ 2.4 ATA 90 min x 20-40 times

∗ Related to clinical

HBO

∗ Related to clinical

∗ Patient must have adequate debridement and/or ATB

ก่อน HBO 4 ครั งก่อน HBO 4 ครั ง

16 ครั ง 23 ครั ง

∗ Clostridia myositis and myonecrosis (Gas gangrene)

∗ Intracranial abscess

Infectious Condition

∗ Intracranial abscess

∗ Osteomyelitis (Refractory)

∗ Necrotizing soft tissue infection

1. Increase O2 tension in infected tissues including bone

2. Enhance the leukocytes killing mechanism2. Enhance the leukocytes killing mechanism

3. Has a direct suppression effect on anaerobic organisms (Inhibit alpha toxin production)

4. reducing tissue edema , decrease intra-compartmental pressure

5. Produce neovascularization and osteogenesisosteogenesis

6. Increase tissue and bone healing

7. Augment the effect of antibiotics (aminoglycosides etc.)

HBO Protocol

∗ Clostidial Myositis (Gas gangrene)

∗ 3.0 ATA, 90 min, tid in first 24 hr, then∗ 3.0 ATA, 90 min, tid in first 24 hr, then

∗ Bid-OD according to clinical response

∗ Necrotising soft tissue infection

∗ 2.0-2.5 ATA, 90 min Bid-OD

∗ according to clinical response

HBO Protocol

∗ Intracranial abscess

∗ 2.5 ATA, 60-90 min., OD/bid,∗ 2.5 ATA, 60-90 min., OD/bid,

∗ total number of treatment- clinical response, radiological findings

∗ Refractory osteomyelitis

∗ 2.0-2.5 ATA, 90 min OD

∗ 30-40 treatments

Miscellaneous

∗ Severe anemia

∗ Idiopathic Sudden Sensorineural Hearing loss∗ Idiopathic Sudden Sensorineural Hearing loss

1. Increases O2 supply reserve by increasing plasma pO2

2. Increases RBC elasticity and improves flow through the microcirculation

Severe Anemia & HBO

microcirculation

3. Protects against oxygen free radicals during reperfusion

Protocol∗ as minimal as possible to avoid side effects

∗ Continue treatment until hematocrit rises to about 20 or better

∗ New approved indication by October 8, 2011

∗ Sensorineural hearing loss of a minimum of 30 dB in at

Idiopathic Sudden SensorineuralHearing loss

∗ Sensorineural hearing loss of a minimum of 30 dB in at

least three frequencies occuring within a period of 3

days

∗ 80% Unclear cause

∗ Several Mechanisms that lead to hypoxia

∗1. Vascular

any thrombosis or embolus of the arteria labyrinthi

∗2.Viral :mumps, cytomegalovius, rubeola, varicella

Mechanism of Sudden Deaf

∗2.Viral :mumps, cytomegalovius, rubeola, varicella

Viremia itself leads to a disturbance in the circulation and the formation of edema in

the intima of the inner ear blood vessels

∗3. Auto-immune disorder

Hypoxia

11 th International Congress of Hyperbaric Medicine 1993

Most of Otolaryngologist

HBOT

Most of Otolaryngologist

HBOT + Vaso active+ Hemodilution

Within 48 h. of onset hearing loss

∗ Acute coronary syndrome

∗ Truamatic brain injury

Off lebel Indications

∗ Truamatic brain injury

∗ Stroke

∗ Cerebral palsy/ Autism

∗ Multiple sclerosis

∗ AVN of femur

∗ Sport injury

∗ Tumor sensitization for radiotherapy

Thank you