Non-diving related hyperbaric treatment. CARAT 2014 LTJG Chamchan Chanchang

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1 Non-diving related hyperbaric treatment CARAT 2014 LTJG Chamchan Chanchang

2 Hyperbaric Oxygen Therapy (HBOT) A period of breathing high percentage oxygen for 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

3 Bubble Crunching Bubble related disease : Diving accident AGE/DCS

4 Hyperoxygenation of tissue Normalization of the po2 in hypoxic area times more O2 in plasma 4 times into the surrounding tissue

5 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

6 HBOT Physiologic effects Vasoconstriction Decrease edema Stimulate capillary growth Improve body defence against infection Enhance wound healing Elimination of carbon monoxide

7 UHMS Air or gas embolism 2. Decompression sickness Diving related Non Diving related 3. CO poisoning +/- CN 9. Clostridia myositis and myonecrosis 4. Acute thermal injury 10. Necrotizing soft tissue infection 5. Acute traumatic ischemia 11. Osteomyelitis (Refractory) 6. Arterial insufficiency 12. Intracranial abscess - CRAO 13. Severe anemia - Problem wounds 14. Idiopathic Sudden Sensorineural 7. Compromised Grafts or flaps Hearing loss 8. Delayed radiation injury

8 Underwater Medicine department Number of treatments 2o13 DCI. 17 Delayed radiation injury 200 ORN. 139 Radiation cystitis 53 Radiation soft tissue 9 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

9 Underwater Medicine department Number of treatments 2o14

10 Multiplace chamber

11 Monoplace chamber

12 3 compartments multiplace

13 Clinical HBO

14 Carbon monoxide and cyanide poisoning

16 Carbon monoxide poisoning

17 HBO Benefits Most benefit when treatment less than 6 hr 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)

18 Carbon monoxide and cyanide poisoning

19 Treatment Protocol Recommend of U.S. Navy Diving Manual Revision 6 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)

20 Acute Thermal Burn 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), proteins begin losing their three-dimensional shape and start breaking down Many of the direct health effects

21 Pathology

22 HBO Benefit directed toward minimizing edema preserving marginally viable tissue protecting the microvasculature enhancing host defenses promoting wound closure

23 Guideline therapy US Navy Treatment table 9 TID x 1 day Then OD Minimum treatment 5 Maximum treatment 45

24 Ischemic/Hypoxic Tissue Conditions Crush Injury and Acute traumatic ischemia Compromised Grafts or flaps Delayed radiation injury Arterial insufficiency - CRAO - Problem wounds

25 Crush Injury and Acute traumatic ischemia Compartment Syndrome Threatened Flaps Burns Frostbite

26 TRAUMA PARTIALL LY VIABLE TISSUE NON VIABLE DEAD TISSUE ISCHEMIA HYPOXIA EDEMA NORMAL INFECTION VIABLE TISSUE : Pathophysiology of crush injury RECOVERY OR LOSS OF FUNCTION

27 Effects of HBOT In Crush Injuries 1. Hyperoxygenation 2. Vasoconstriction 3. 20% decrease in edema 4. Host factors 5. Red Blood Cell Deformability

28 Hyperbaric oxygen therapy in no way supercedes the surgical principles for management of crush injuries / ATPIs HOWEVER, if surgical intervention is going to be delayed, there may be benefit (in theory at least) to treatment with HBO while awaiting surgery

29 HBOT Protocols Crush Injuries / ATPIs HBO Committee Report ATA ; min TID (2d), BID (2d), Daily (2d)

30 Compromised Grafts or flaps

31 Compromised Grafts or flaps Grafts previous radiation to the wound area diabetes mellitus Infections Flaps age nutritional status smoking previous radiation

32 HBOT Benefits Stimulate fibroblast and enhancing collagen synthesis Neovascularization Hyperoxygenation Edema reduction

33 HBOT Protocols Pressure ata min Initial treatment should be twice daily once a day when flap or graft appear more viable and stable

34 Delayed radiation injury Osteoradionecrosis Mandible or other bones Soft tissue Radionecrosis Radiation cystitis, proctitis, enteritis, etc.

35 Radiation Effect on tissue Bone; Periosteum; necrosis of osteoblast & osteocyte, fibrosis of marrow spaces fibrosis Blood vessel; endothelial death, hyalinization & thrombosis Mucosa & Skin; diminished cellularity, fibrosis

36 Osteoradionecrosis Any exposed bone in a field of irradiation (> 50 Gy), resist to conservative treatment and fail to heal within 3 months

37 Osteoradionecrosis Hypoxia Hypovascular Hypocellular + surgical truama +/- secondary infection

38 HBO 2.4 ATA for 90 min The 20/10 protocol - Elective surgery or wounding within radiated tissues *Bone graft reconstruction *Soft tissue vascular flaps *Tooth removal

39 Soft tissue Radionecrosis Radiation cystitis Hematuria HBO Protocol TT9 for 40 dives

40 Arterial Insufficiency Central Retinal Arterial Occlusion (CRAO)

41 Central Retinal Arterial Occlusion (CRAO) Sudden painless vision loss, which is usually dramatic 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

42 Role of Oxygen Treatment should be aimed at promptly supplying oxygen to the ischemic retina at a partial pressure 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

43 HBOT Protocol 2.8 ATA 90 min Bid, OD TT5 OD HBOT Acceptable, safe, considered efficacious No evidence of harm No alternative therapies with similar outcomes

44 Problem Wounds Microvascular chronic ischemic wound; Diabetic wound Problem wounds are usually hypoxic elevation of wound oxygen tension to normal enhanced wound healing Transcutaneous oximetry HBO

45 Transcutaneous oximetry TcpO2 < 40 mm Hg : Hypoxic wound THEN test100 % O2 breathing at 1 ATA. IF TcpO2 rise > 50 % THEN HBO

46 HBO 2.4 ATA 90 min x times Related to clinical Patient must have adequate debridement and/or ATB

47 ก อน HBO 4 คร ง 16 คร ง 23 คร ง

48 Infectious Condition Clostridia myositis and myonecrosis (Gas gangrene) Intracranial abscess Osteomyelitis (Refractory) Necrotizing soft tissue infection

51 1. Increase O2 tension in infected tissues including bone 2. 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

52 5. Produce neovascularization and osteogenesis 6. Increase tissue and bone healing 7. Augment the effect of antibiotics (aminoglycosides etc.)

53 HBO Protocol Clostidial Myositis (Gas gangrene) 3.0 ATA, 90 min, tid in first 24 hr, then Bid-OD according to clinical response Necrotising soft tissue infection ATA, 90 min Bid-OD according to clinical response

54 HBO Protocol Intracranial abscess 2.5 ATA, min., OD/bid, total number of treatment- clinical response, radiological findings Refractory osteomyelitis ATA, 90 min OD treatments

55 Miscellaneous Severe anemia Idiopathic Sudden Sensorineural Hearing loss

56 Severe Anemia & HBO 1. Increases O2 supply reserve by increasing plasma po2 2. Increases RBC elasticity and improves flow through the 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

57 Idiopathic Sudden Sensorineural Hearing loss New approved indication by October 8, 2011 Sensorineuralhearing loss of a minimum of 30 db in at least three frequencies occuringwithin a period of 3 days 80% Unclear cause Several Mechanisms that lead to hypoxia

58 Mechanism of Sudden Deaf 1. Vascular any thrombosis or embolus of the arteria labyrinthi 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

59 HBOT 11 th International Congress of Hyperbaric Medicine 1993 Most of Otolaryngologist HBOT + Vaso active+ Hemodilution Within 48 h. of onset hearing loss

60 Off lebel Indications Acute coronary syndrome Truamatic brain injury Stroke Cerebral palsy/ Autism Multiple sclerosis AVN of femur Sport injury Tumor sensitization for radiotherapy

62 Thank you

Hyperbaric Oxygen Therapy

Hyperbaric Oxygen Therapy 1 RSPT 1410 Medical Gas Therapy Part 2: Wilkins: Chapter 38; p. 891-894 Cairo: Chapter 3, p. 78-81 2 Definitions Hyperbaric oxygen (HBO) therapy is the therapeutic use of oxygen at pressures greater than