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1 Role of Hyperbaric Oxygen Therapy in Complex Wounds and Infections Raj Adurty MD, FCCP,FACP Director Medical Intensive Care Unit Division of Pulmonary & Critical Care Medicine ALLEGHENY GENERAL HOSPITAL WEST PENN ALLEGHENY HEALTH SYSTEM Disclosure Information I have no conflicts of interest with the topics that I am going to discuss. Raj Adurty, MD, FCCP, FACP Objectives Introduction to Hyperbaric Medicine Physiological principles Review of current indications of HBOT Contraindications and side effects 1

2 Wound Healing Hemostasis Inflammation Proliferation Remodeling Factors Influencing Healing Local Oxygenation Infection Foreign Bodies Systemic Age Comorbid conditions Nutrition Immune compromise Smoking Hyperbaric Oxygen (HBO) Definition Breathing 100% oxygen, delivered in a chamber, pressurized at more than 1atmospheric pressure(ata) Typically pressures must equal or exceed 1.4ATA 2

3 Gas laws Dalton s Law Henry s Law Fick s Law Dalton s Law In a gas mixture, the total pressure exerted is equal to the sum of partial pressures. Partial pressure = Pressure x Fraction of gas PO2 =760x0.21=160mmHg PO2 in HBO chamber with 3 ATA =760x3x0.21=479mmHg Henry s Law At a constant temperature, the amount of gas that dissolves in a liquid is proportional to the partial pressure of that gas 1ATA 3ATA 3

4 Fick s Law Rate of diffusion of a gas is = K x A x ΔP D Where K is a constant A= surface area P= pressure gradient D= distance of diffusion (thickness) Physiology Arterial Oxygen Content CaO2 = Hemoglobin binding oxygen + Dissolved oxygen in Plasma 1.34 x Hb x %Saturation x PaO x 15 x 0.95 = 20vol % In Hyperbaric condition of 100%O2 and 3 Atm press, PaO 2 = 2183 Dissolved Oxygen =0.0031x2183=7vol% Physiologic Effects Cardiac Other Bradycardia CO decreased SV unchanged ICP decreased initially and then increased Hypoglycemia SVR increased 4

5 Mechanism of Action Primary effects Hyperoxygenation and Diffusion Bubble size reduction Secondary effects Vasoconstriction Fibroblast proliferation Collagen synthesis Neovascularization Leucocyte oxidative killing Clostridial alpha toxin inhibition Aminoglycoside synergism Hyperbaric Chamber Indications of Hyperbaric Oxygen Therapy HBOT UHMS 13 th ed Air embolism Carbon Monoxide poisoning Decompression sickness Clostridial myonecrosis Crush injury, Compartment syndrome Compromised Graft Arterial Insufficiency Intracranial abscess Necrotizing soft tissue infections Refractory Osteomyelitis Severe Anemia Delayed radiation injury 5

6 Recommendations Tenth European Consensus Conference on Hyperbaric Medicine Div Hyperb Med Mar,47(1):24-32 Level B CO Poisoning Open Fractures with Crush Injury Prevention of Osteoradionecrosis(mandi ble) after Dental extraction Soft Tissue Radionecrosis (cystitis, proctitis) Diabetic Foot Lesions Level C Anaerobic or mixed bacterial infections Compromised skin grafts and musculo-cutaneous flaps Refractory Chronic Osteomyelitis Treatment principles Pressure Decompression/Air embolism Neovascularization Radiation necrosis Wound healing Antimicrobial Gas gangrene/necrotizing infections/osteomyeliti s Hyperoxia CO poisoning Crush injuries Anemia Vasoconstriction Compartment syndrome Compromised grafts Lower extremity Wounds Diabetic foot ulcers Arterial insufficiency ulcers Venous stasis ulcers Marginal flaps/graft 6

7 Diabetic Foot CDC estimates 25.8 million (8.3%) of US population have Diabetes 60% of non traumatic amputations 85% of amputations are preceded by a foot ulcer $1.5Billion/year due to amputations Goals of therapy in Diabetic Ulcers International Working Group on the Diabetic Foot Guidelines IWGDF Treat underlying infection Revascularize if appropriate Offloading to minimize trauma to ulcer Manage wound bed to promote healing Peripheral neuropathy, Ischemia and Infection are the dominant causes of Diabetic foot ulcers Tissue Cutaneous Oximetry(TcPO2) has been shown to be an independent predictor of healing TcPO2 >200mmHg under hyperbaric conditions predicted wound healing with 75-80% accuracy 7

8 Wagner s Classification - Ulcers Grade 0 Grade 1 Grade 2 Grade 3 Grade 4 Grade 5 Intact Skin Superficial Ulcer of Skin or SC tissue Deep Ulcer extending into tendon, bone or capsule Deep Ulcer with Osteomyelitis or Abscess Gangrene of toes or forefoot Gangrene of whole foot/hind foot Recommendations In Patients with Wagner Grade 2 or lower Diabetic Foot Ulcers (DFU)- No Role of adding HBOT to prevent amputation and promote healing In patients with Wagner Grade 3 or higher who have not shown improvement after 30days, adding HBOT is recommended Huang ET,UHM 2015; 42: 3 CLINICAL PRACTICE GUIDELINE FOR HBO2 TO TREAT DFU Recommendations Treatment with ATA for min for 30 sessions is recommended. Additional sessions if improvement in wound is noted but ongoing issues of infection, ischemia & necrotic tissue are still present 8

9 Recommendations In Patients with Wagner Grade 3 or higher that require immediate surgery, adding inpatient HBOT is recommended ATA for min x 30 sessions but is modified based on goals (survival of flap 7days, angiogenesis-2weeks, refractory osteomyelitis treatments) Further Research Patient selection based on TcPO2 proposed but not prospectively evaluated Algorithm for TcPO2 use TcPO2 Wound Hypoxia with <40mmHg No HBO is not indicated YES Normobaric Oxygen Challenge TcPO2 >100mm Hg TcPO Vascular Surgery TcPO2<50 Adequate reversal. HBO indicated Can consider in chamber TcPO2 and trial of HBO if >200 Not a HBO candidate 9

10 Venous Leg Ulcers Associated with venous disease (varicose veins, DVT)that causes sustained venous hypertension Inflammation with leucocyte activation, endothelial damage, and edema Obesity,trauma,immobility,old age, DM and PAD may be present Kimmel HM Wounds,2013;25(9):242An EvidenceBasedAlgorithm for Treating Venous Leg Ulcers Venous Ulcers Generally HBOT not indicated for venous ulcers unless in preparation for graft or limb threatening Only 1 RCT with HBO that showed decrease in wound size at end of 6weeks with 2.5ATA x90min every day Hammarlund C, Plast Reconstr Surg;1994;93(4):829HBO reduced size of chronic leg ulcers: a randomized doubleblind study.. Arterial Ulcers Not indicated unless ulcer persists after vascularization or revasculization is not possible. No good RCT to support 10

11 Crush Injuries Crush injuries, Traumatic ischemias, Compartment syndromes, Burns and Threatened flaps have common pathophysiology Ischemia, Tissue hypoxia, Edema, Disturbed microcirculation and reperfusion injury contribute Garcia-CovarrubiasL,Am Surg Feb;71(2):144 Adjuvant hyperbaric oxygen therapy in the management of crush injury and traumatic ischemia: an evidence-based approach. HBOT improves tissue hypoxia by a ten fold increase in O2 dissolved in plasma Threefold increase in O2 diffusion distance-diffusion =Fick s law Vasoconstriction leads to 20% decrease in blood flow and hence edema Compartment Syndrome Compartment syndrome diagnosed by pain,paresthesia,pulselessness,pallor, and progression of symptoms Normal perfusion pressure of capillaries is 30-35mmHg, the critical compartment pressure of >30mmHg for 6hrs or longer results in above 11

12 Gustilo Classification for Crush Injuries Manual of Hyperbaric Medicine Gustilo classification and HBO Indications Crush Injuries HBOT Start HBO ideally within 4-6hrs of injury 2-2.5ATA, min TID x2-3days, then Bid x2-3days then QDx2-3days 12

13 Anaerobic and Soft Tissue Infections Clostridial infections Necrotizing fasciitis Fournier's gangrene Non Clostridial myonecrosis Classification Handbook on Hyperbaric Medicine Common to all infections is presence of cloudy exudate, pale necrotic tissue and minimal bleeding. Wide spread thrombosis of small vessels and edema are noted. Bacterial invasion, toxin production and host factors facilitate infection 13

14 Role of HBOT is to provide a hyperoxic environment to anaerobic bacteria, improve leucocyte function, reduce tissue loss and improve demarcation. Neutralizing alpha toxin and facilitating antibiotic action may also play a role Anaerobic & Soft Tissue Infections HBOT Non Clostridial necrotizing fasciitis HBOT 2.5ATA x 90min BID till clinical improvement. Usually about 3-5days of treatment Clostridial myonecrosis HBOT 3ATA x 90min TID on day 1 and then BID for next 3-5days or clinical improvement Refractory Osteomyelitis Persistent inflammation of bone with secondary infection leading to non healing wound HBOT improves tissue hypoxia, leucocyte function and osteoclastic activity 14

15 Refractory Osteomyelitis HBOT 2-2.5ATA x90min BID if inpatient or QD as outpatient for treatments Exceptional Blood Loss Anemia Due to low hemoglobin, arterial oxygen content and O2 delivery is decreased Using HBO, Oxygen dissolution in plasma is improved, RBC elasticity and flow improved Blood Loss Anemia HBOT HBOT 2-3 ATAx90min every 4-6hrs until O2 delivery is improved and no signs of end organ ischemia 15

16 Radiation Tissue Injury Delayed injuries seen after minimum dose of 6000cGY Tissue hypoxia, obliterative endarteritis, and periarteritis contribute to secondary fibrosis Prophylactic HBOT before Surgery in Osteoradionecrosis 2.4ATA for 90min once a day x20 sessions before surgery and 10 sessions post operatively Osteoradionecrosis Marx Protocol Stage I small exposed alveolar bone HBOTx30 treatments and if favorable response,10 additional Stage II (Non responder of stage I)-perform sequestrectomy/wound closure and 10 additional treatments Stage III(Failed stage II) or has fistula,fracture- 30treatments followed by resection/fixation and 10 additional treatments Stage IIIR Mandibular reconstruction after successful treatment and 10 HBO sessions 16

17 Side Effects of HBOT Oxygen toxicity Barotrauma middle ear, sinus squeeze, pneumothorax Lowering Seizure threshold Claustrophobia Summary HBOT is utilized in a multitude of situations including poisoning, infections, problem wounds & air bubble disease Improving oxygen delivery, reducing bubble size and promoting angiogenesis play key roles in treatment Thank You 17