Non-diving related hyperbaric...
Transcript of Non-diving related hyperbaric...
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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RECOVERYRECOVERY
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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
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