National Disaster Medical System

Transcription

1 Tuesday, October 1, 2013, Aerospace Day National Disaster Medical System Preventive /Aerospace/Occupational Medicine Role Disclosure Information American OsteopathicCollegeof Occupational & Preventive MedicineOMED-Las Vegas, NV-October1, 2013 Allen J. Parmet, MD I have no financial relationships to disclose. I will not discuss off-label use and/or investigational use in my presentations Allen J. Parmet, MD, MPH, FACPM, FASMA, FACOEM, AIAASM MO1-DMAT drparmet@kc.rr.com National Disaster Medical System United States Department of Health and Human Services (HHS) responsible for managing Federal government's medical response to major emergencies and disasters NDMS was returned to DHHS (US Department of Health and Human Services) on January 1, 2007 by an Act of Congress). Federal Partners: FEMA, DoD, DVA National Disaster Medical System (NDMS) Response Teams Disaster Medical Assistance Team (DMAT) (55) Disaster Mortuary Operational Response Teams (DMORT) (10) International Medical Surgical Response Team (IMSURT) (4) National Veterinary Response Team (NVRT) (10) National Disaster Medical System Disaster Medical Assistance Team (DMAT) Disaster Mortuary Operational Response Team (DMORT) International Medical Surgical Response Team (IMSuRT) A-1

2 Tuesday, October 1, 2013, Aerospace Day Disaster Medical Assistance Team (DMAT) A DMAT is a group of professional and para-professional medical personnel (supported by a cadre of logistical and administrative staff) designed to provide medical careduring a disaster or other event. NDMS recruits personnel for specific vacancies, plans for training opportunities, and coordinates the deployment of the teams. DMATs are designed to be a rapid-response element to supplement local medical care until other Federal or contract resources can be mobilized, or the situation is resolved. DMATs deploy to disaster sites with sufficient supplies and equipment to sustain themselves for a period of 72 hours while providing medical careat a fixed or temporary medical care site. The personnel are activatedfor a period of two weeks. State Disaster Medical Assistance Team (DMAT) MO1-DMAT/MoDRS The DMAT as a state organization is a 501.3ctaxexemptentity which can be activatedbythe state disasterresponse system and respond to the governor s requeststo supportmedical needsin anyemergency. Examples in tornados,floods,ice storms augmenting orreplacing local medical resources, sheltering special needsand institutionalized persons. Aerospace Medicine in DMAT Team Occupational Medicine Fitness For Duty Pre-deployment vaccinations, respirator fits Deployment injuries, illness and follow-up Deployed Public Health Aeromedical Evacuation MODRS Information: Personnel should check their go kits Monitor your closely for any MODRS related information Check your personaland family preparedness plans andchangethebatteries inyour All Hazards Weather Radio THIS DOCUMENTIS FOR OFFICIALUSE AND INFORMATIONAL PURPOSESONLY AND IS NOTINTENDED TOBE AN OPERATIONS ORDER OR MISSIONASSIGNMENT. ADDITIONALUPDATESWILLBE SENTAS WARRANTED. ### DMATs around the USA Strike Team-Rapid Response Unit 4 hours, 5 people, 4 Beds A-2

3 Tuesday, October 1, 2013, Aerospace Day Full Team-Mobil Medical Unit 24 hours, 50 people, 50 Beds Tornado Response-Joplin, MO May 22, Hurricane Charlie-Punta Gorda, FL Tornado Response-Joplin, MO May 22, 2011 Tornado Response-Joplin, MO May 22, 2011 Casualties 158 Dead 1,150 Injured 450Patients inst. John s Hospital $3 Billion damages Timeline: May 22 5:34-6:12PMCDT-TornadoinJoplin 6:25-Governordeclares disaster 6:40-MO1-DMAT Activated 8:30 FirstStrikeTeamArrives May 23 2:30AM-ThirdStrikeTeam Arrives 2:00PM-Mobil MedicalUnitsets up 4:00PM-Patients transferredfrom St. Johns May 25 StrikeTeams close May 29 MobilMedicalUnitturned over to St. John s staff andis designated St. John s/mercy FieldHospital June 1 DMORT7completes casualty IDs Disaster Mortuary Operational Response Teams (DMORTs) The National Response Framework (NRF) utilizes the National Disaster Medical System (NDMS), as part of the Department of Health & Human Services, Assistant Secretaryfor Preparedness and Response (ASPR), Office of Preparedness and Operations (OPEO), under Emergency Support Function #8 (ESF #8), Healthand Medical Care, to provide victim identification and mortuary services. These responsibilities include: temporary morgue facilities victim identification forensic dental pathology forensic anthropology methods processing preparation disposition of remains A-3

4 Tuesday, October 1, 2013, Aerospace Day DMORT Teams REGION I (ME, NH, VT, MA, CT, RI) REGION II (NY, NJ, PR, VI) REGION III (PA, MD, DC, DE, VA, WV) REGION IV (AL, KY, TN, NC, SC, GA, MS, FL) REGION V (MN, WI, IL, IN, MI, OH) REGION VI (NM, TX, OK, AR, LA) REGION VII (NE, IA, KS, MO) REGION VIII (MT, ND, SD, WY, UT, CO) REGION IX (AZ, NV, CA, HI) REGION X (WA, AK, OR, ID) International Medical Surgical Response Team (IMSURT) The International Medical Surgical Response Team (IMSURT) is a National Disaster Medical System (NDMS) team of medical specialists who provide surgical and critical care during a disaster or public health emergency. Originally conceived to address the needs of U.S. citizens injured overseas, the IMSURT role has expanded over the years to include both domestic deployments, including the World Trade Center Bombings and Hurricane Katrina, and international deployments, including the earthquakes in Bam, Iran, and Port au Prince, Haiti. IMSURT personnel are Federal employees used on an intermittent basis to deploy to the site of a disaster or public health emergency and provide high quality, life saving surgical and critical care. National Veterinary Response Team (NVRT) IMSURT The National Veterinary Response Team (NVRT) is a cadre of individuals within the NDMS systemwho have professional expertise in areas of veterinary medicine, public health and research. Assessing the Veterinary Medical Needs of the Community Medical Treatment and Stabilization of Animals Animal Disease Surveillance Zoonotic Disease Surveillance and Public Health Assessments Technical Assistance to Assure Food Safety and Water Quality Hazard Mitigation Care and Support of Animals Certified as Official Responders to a Disaster or Emergency National Veterinary Response Team (NVRT) Strategic National Stockpile (SNS) CDC's Strategic National Stockpile (SNS) has large quantities of medicine and medical supplies to protect the American public if there is a public health emergency (terrorist attack, flu outbreak, earthquake) severe enough to cause local supplies to run out. Once Federal and local authorities agree that the SNS is needed, medicines will be delivered to any state in the U.S. in time for them to be effective. Each state has plans to receive and distribute SNS medicine and medical supplies to local communities as quickly as possible. A-4

5 American Osteopathic College of Occupational and Preventive Medicine Tuesday, October 1, 2013, Aerospace Day Join NDMS! Recruitment Information Emergency System for Advance Registration of Volunteer Health Professionals (ESAR-VHP) The Emergency System for Advance Registration of Volunteer Health Professionals (ESAR-VHP) is a federal program created to support states and territories in establishing standardized volunteer registration programs for disasters and public health and medical emergencies. The program, administered on the state level, verifies health professionals' identification and credentials so that they can respond more quickly when disaster strikes. By registering through ESAR-VHP, volunteers' identities, licenses, credentials, accreditations, and hospital privileges are all verified in advance, saving valuable time in emergency situations. s/ndms/teams/pages/recruitment.aspx References Department of Health and Human Services, Centers for Disease Control, Emergency Preparedness and Response: Department of Health and Human Services, National Disaster Medical System: ers/ndms/pages/default.aspx A-5

6 Tuesday, October 1, 2013, Aerospace Day 2010 Haiti Earthquake NDMS, DMAT and the Aerospace Medicine Physician Disclosure Information American OsteopathicCollegeof Occupational & Preventive MedicineOMED-Las Vegas, NV-October1, 2013 Allen J. Parmet, MD I have no financial relationships to disclose. I will not discuss off-label use and/or investigational use in my presentations Allen J. Parmet, MD, MPH MO1-DMAT drparmet@kc.rr.com Haiti in History Historical Earthquakes 1790-Richest French colony, population 30, Slave Revolt and Yellow Fever Epidemic-becomes second independent country in the Americas-Napoleon sells Louisiana to US 1815-Haiti sponsors Bolivar s revolt in South America 1820-Richest country in the world, per capita, series of 32 coups follows U.S. Military occupation, building most roads and infrastructure Duvalier dictatorships Location/Intensity Chile, Indonesia, Alaska, Chile, New Madrid, Tokyo, San Francisco, China, Haiti, Mexicali, San Francisco, Casualties 6, , ? 143,000 3, , , January 12, 2010 Chile was ready for earthquake, Haiti wasn't Chile has history of dealing with temblors; Haiti's was first in living memory January 2010 February 2010 Damagefrom Haiti's magnitude-7earthquake. Chile's magnitude-8.8earthquake. B-1

7 American Osteopathic College of Occupational and Preventive Medicine Tuesday, October 1, 2013, Aerospace Day Images of Destruction Port-au-Prince Hotel Montana-200 dead, including about 100 Americans International Response B-2

8 American Osteopathic College of Occupational and Preventive Medicine Tuesday, October 1, 2013, Aerospace Day Search and Rescue National Disaster Medical System Disaster Medical Assistance Team (DMAT) Disaster Mortuary Operational Response Team (DMORT) International Medical Surgical Response Team (IMSuRT) MO-1 DMAT * Pre-Deployment Pre-Deployment B-3

9 American Osteopathic College of Occupational and Preventive Medicine Tuesday, October 1, 2013, Aerospace Day The Scenes on Arrival Toussaint L Overture International Airport Arrival LZ GHESKIO Field Hospital GHESKIO Clinic Patients B-4

10 American Osteopathic College of Occupational and Preventive Medicine Tuesday, October 1, 2013, Aerospace Day Infectious Disease B-5

11 American Osteopathic College of Occupational and Preventive Medicine Tuesday, October 1, 2013, Aerospace Day Surgery Facilities Prevention/Occupational B-6

12 American Osteopathic College of Occupational and Preventive Medicine Tuesday, October 1, 2013, Aerospace Day Patient Movement U.S. HEALTH AND HUMAN SERVICES: MEDICAL MOVEMENT OF EVACUEES Patient Evacuation Patient Tracking Patient Movement En-Route Medical Care USNS Comfort NATIONAL GUARD OR DOD ASSETS (GPMRC) Aeromedical Evacuation US Military & Civilian Non-US Medical Regulating GHESKIO Field Hospital NDMS: IMSURT-W + MO-1 DMAT Patient Re-Entry NGOs OPEO C: ESF#8 B-7 Walk-Ins NDMS Strike Teams: OH-5, SC-1, FL-7 DMATs

13 U-2 DCS Update Leonardo C. Profenna, MD, MPH, Col (ret) Medical Director, Wound Care Center Connally Memorial Medical Center Floresville, TX Thanks to: Steve McGuire, MD Lt Col Sean Jersey, MD Lt Col Alan Flower, DO Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013 $61 billion impact (2012), 116,000 jobs Production barrels/day 26 permits ,000 barrels/day 4,143 permits Projected to barrels/day Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013 Background Information Original Review of Problem U-2 Mission High altitude (+60,000 ft) reconnaissance High risk of DCS without prevention measures Standard DCS Prevention Measures Full pressure suit, 1-hour resting pre-breathe, 100% O2 Low Historical Incidence of U-2 DCS 90 incidents of joint pain reported in the literature as of 2000 Many unreported cases of joint/skin DCS No recorded cases of CNS DCS or permanent damage Number of U-2 DCS Incidents incidents of all types with 37 pilots Retrospective Review of U-2 DCS Incidents Before Dec 09 DGMC Travis AFB IRB Approval (FDG H) Series of CNS DCS Incidents Jan 02-Dec 09 Confirmed cases (16): documented in medical records Probable cases (4): reported but insufficient documentation Possible cases (0): retrospective reports (unofficial) by pilots Research Limited to Existing Sources: Medical & physiological support records Flight, maintenance, & safety records Many Severe Neurological Cases with Unusual Clinical Symptoms Jersey SL, Hundemer GL, Stuart RP, West KN, Michaelson RS, Pilmanis AA. Neurological decompression sickness among U-2 pilots: Aviat Space Environ Med 2011; 82:1-10 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep C-1

14 Patient Characteristics 20 Total Cases 16 Confirmed, 4 Probable Incidents 12 pilots with one incident each 4 pilots with two incidents each Pilot Ages: 30 to 48 yo Gender: 15 men, 1 woman BMI: 21 to 32 Prior Medical History: All non-smokers 2 pilots had prior history of rhino-septoplasty for sinus disease o/w negative No routine medical use prior to incidents No medications taken prior to flight 3 of 16 pilots used dexamphetamine during flight Initial Treatment Standard of Care Aircrew: descend & return ASAP after symptom onset Flight Docs: must TREAT if DCS is considered (diagnosis of exclusion) ABCs, O2, & transport to nearest hyperbaric chamber USN Treatment Table 6; keep treating until symptoms resolve/plateau Most Cases Received Appropriate Treatment 19 of 20 cases received prompt hyperbaric oxygen (HBO) treatment Responses varied by case (see following slides) Treatment delayed in some cases Some patients required multiple HBO treatments Treatment Delayed Inappropriately 1 Case Combination of factors contributed to delay Symptoms resolved after HBO treatment 11 days later Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Expected Clinical Response Good Clinical Outcome Despite Treatment Delay Recurrent Symptoms After Treatment Persistent or Permanent Symptoms Despite Adequate Treatment Spectrum of Clinical Outcomes In 5/20 (25%) cases, pilots reported DCS symptoms immediately Prompt HBO treatment administered Full resolution of symptoms with no recurrence or persistence 4/20 (20%) cases: delayed symptom recognition, reporting, or treatment Treatment delayed by hours up to 11 days Symptoms resolved with no recurrence or persistence 19/20 (95%) cases received appropriate HBO treatment in theater 2/20 (10%) cases had recurrent symptoms during commercial flights Symptoms recurred in2 more (10%) after elevation changes while driving 10/16 (62.5%) pilots reported persistent symptoms for 3 months to 9 years+ Similar constellation of symptoms (headache, fatigue, irritability, etc.) Considered permanent in 2/16 (12.5%) pilots lasting > 6 & 9 years, respectively **NO FATALITIES** Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013 Clinical Course The Good 9/20 cases with no adverse clinical outcomes 5/20 (25%) reported promptly (in-flight) 4/20 (20%) delayed, but no problems after HBO Delays in treatment varied from a few hours up to 11 days: Situational: can t teleport to a chamber Pilots: hard to recognize vague symptoms in operational environment Docs: some didn t recognize or know how to treat DCS Both(?): some pilots still didn t trust docs (fear of grounding) Symptoms resolved completely with HBO treatment No reported recurrent orpersistent symptoms Returned to flying status after normal exam 6/9 (67%) of these pilots voluntarily left U-2 program after incidents Are historical outcomes as rosy as we think? Reported permanent symptoms extremely rare No long-term follow-up in recorded DCS cases in literature 9 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Most Common Symptoms Time Course of Presentation 1-h resting pre-breathe Variable recognition of symptom onset ( h) Landing HBO treatment Return home on commercial flight (48-72 h later) Further treatment & evaluation? Return to flying status 1-h resting pre-breathe Variable recognition of symptom onset ( h) Landing HBO treatment Return home on commercial flight (48-72 h later) Further treatment & evaluation? Return to flying status Presenting Symptoms Headache (10/20 cases) Fatigue (7/20) Confusion/memory lapses (7/20) Impaired mentation (5/20) Paresthesias (5/20) Vision problems (3/20) Nausea (3/20) Dizziness (2/20) Loss of consciousness (2/20) Disorientation (2/20) Weakness (2/20) CNS DCS symptomsareoftennon-specific Focal neurological symptomsare rare Requires highindex of suspicion If in doubt TREAT! Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013 MP16 MP14 MP15 MP14 MP13 MP12 MP11 MP10 MP6 MP8 MP9 MP8 MP7 MP7 MP6 MP5 MP4 MP3 MP2 MP1 Unreported time during flight Unreported time during flight Time of Recognized Symptom Onset (h) Unknown inflight 10% Onset postflight 40% Onset h inflight 15% 11 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013 Onset 0-4 h inflight 35% Take-Home Points: DCSsymptoms vary markedly Delays in symptom recognitionare common Operational concerns also cause delays 12 C-2

15 Clinical Course The Bad Re-Injury After Treatment 1-hr resting pre-breathe Variable recognition of symptom onset ( h) Landing HBO treatment Return home on commercial flight (48-72 h later) Further treatment & evaluation? Return to flying status Pathophysiological Process Proposed by Goodman, et al. Based on animal (mice) model of traumatic brain injury Studies evaluating optimum time to fly following battlefield traumatic brain injury (TBI) Mild hypoxia of commercial flight altitudes can exacerbate brain injury 4/20 (20%) cases had recurrent symptoms after HBO Rx 2 cases (2 pilots) occurred during commercial flights home Both pilots received repeat HBO treatment with resolution of symptoms Both pilots had persistent symptoms of fatigue, HA, & memory problems 2 cases (2 other pilots) occurred after elevation changes while driving home Both pilots experienced recurrent symptoms driving home after HBO Rx Both lived in same community, approximately 2,400 ft elevation Neither reported recurrence so did not receive repeat HBO treatment Both have symptoms persisting for years (likely permanent) & disqualified from flying Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013 So-Called Second Hit Phenomenon Initial CNS DCS injury damages neurons, initiates inflammatory cascade Symptoms resolve with treatment, but neurons incompletely recovered Subsequent hypoxia re-stresses damaged neurons & exacerbates inflammatory cascade recurrence of symptoms May Explain Unusual Symptoms in Some U-2 DCS Cases Recurrence of symptoms during commercial flights (2 cases) Recurrence of symptoms after elevation changes while driving (2 cases) Reported cases responded to repeat treatment with hyperbaric oxygen 13 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Clinical Course The Ugly 10/16 (62.5%) pilots with persistent symptoms Ranged from 3 months up to 9+ years Considered permanent in at least 2 cases 5 life-threatening cases* (4/5 cases at same location) 3 cases of severe neurological/pulmonary symptoms 2 cases of abrupt onset severe neurological symptoms in flight No fatalities all 5 pilots recovered & treated with HBO Good initial response to HBO treatment in all Appropriate HBO treatment in all cases (life saving in 5) Symptoms plateaued after repeat HBO treatments Common constellation of physical symptoms in 7/9 Symptoms similar to those seen after mild TBI *See published case reports fortwo life-threatening incidents: 1. Pickard BJ. Altitude decompression sickness in a pilot wearing a pressure suit above 70,000 ft. Aviat Space Environ Med 2003; 74: Jersey SL, Baril RT, McCarty RM, Millhouse CM. Severe neurological decompression sickness in a U-2 pilot. Aviat Space Environ Med 2010; 81:64-8. Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep h resting pre-breathe Persistent and/or Permanent Symptoms Variable recognition of symptom onset ( h) Landing Presenting Symptoms Headache (10/20 cases) Fatigue (7/20) Confusion/memory lapses (7/20) Impaired mentation (5/20) Paresthesias (5/20) Vision problems (3/20) Nausea (3/20) Dizziness (2/20) HBO treatment Loss of consciousness (2/20) Disorientation (2/20) Weakness (2/20) Return home on commercial flight (48-72 h later) Further treatment & evaluation Persistent Symptoms Inappropriate fatigue (9/20) Headaches (7/20) Personality changes (5/20) Memory problems (5/20) Difficultyconcentrating (2/20) Difficultysleeping (2/20) 10 of 16 pilots (62.5%) Duration: 3 months to 9+ years Considered permanent in at least 2 cases 15 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013? Return to flying status Foggy thinking 16 Clinical Course The Ugly Typical clinical course in each case: Good initial response to HBO treatment 2-4 days later: fatigue, headaches, etc. 3 of 4 treated with repeat HBO (partial relief) Medication for symptomatic relief problematic in one case Including: steroids, NSAIDs, ergot, sleep, anti-depressants Little relief with adverse clinical & occupational impacts Attempted repeat HBO months after incident no relief Pilot eventually permanently disqualified from all flying Minimized medication use in remaining pilots NSAIDs used as needed for headache Partial improvement with increased rest, duty restrictions Limited success only one pilot returned to unrestricted U-2 duties Heavy psychological sx (anxiety, depression, PTSD) in all Permanent flying restrictions (7) and/or DQ (2) Return to Flying Status No Previous History of Long-Term Effects Fewcase reports oflasting effects after HBOtreatment Altitude DCSconsidered less severe than divingdcs Operational Incentives to Return Pilots to Flying EachnewU-2 pilot costs ~$2.5 million to train Limited poolofpilots to man deployment slots Limited housing& personnel slots at deployed locations Medical Consequences: Pilots flewhome from deployment ASAP (<72 h) after DCS Pilots attempted return to flyingstatus soon after DCS Waiver guide: returnafter resolutionofsymptoms,normal exam Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep C-3

16 Persistent DCS Symptoms Aviation DCS is Rare, Particularly CNS Manifestations Overall incidence less than 1% (Butler et al. USAF, Bason et al. USN) Only 10-20% of these cases involved CNS symptoms Recurrent symptoms after treatment extremely rare (38 USAF, 6 USN cases) No reported incidents of CNS DCS in U-2 operations before 1991 Persistent CNS Symptoms Extremely Rare in Modern Aviation DCS Butler et al.: 95-98% treatment success with 1153 USAF cases ( ) Wirjosemito: 97.7% treatment success in 133 CNS DCS cases ( ) Fryer (1969): 6 CNS cases of persistent symptoms (all eventually cleared) No series we reviewed had any significant follow-up Persistent DCS Symptoms Permanent Neurological Sequelae Common with Diving-Related DCS 7/16 (44%) Pilots had Similar Constellation of Long-Term Symptoms Headaches, central fatigue, sleep disturbance, irritability, memory deficits Similar symptoms reported after TBI, concussions Is there a common final pathway for brain injury? Have we overlooked significant long-term effects from altitude DCS? Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Lessons Learned Lessons Learned 1-h resting pre-breathe Variable recognition of symptom onset ( h) Landing HBO treatment Return home on commercial flight (48-72 h later) Further treatment & evaluation Changes made as a result of these cases: Reinforced preexisting procedures (maintain hydration, descend, etc.) Encouraged pilots to report suspected symptoms Operational decision trial of exercise-enhanced pre-breathe Increased recovery time between flights Increased number of pilots in training (reduce operational burden) CNS DCS cases treated with USN TT6 with 2 extensions at baseline Results: Cultural resistance to some changes initially, eased with time Subjectively greater willingness to report symptoms Impact of pre-breathe changes positive Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013? Return to flying status 1-hr resting pre-breathe Variable recognition of symptom onset ( h) Landing HBO treatment Return home on commercial flight (48-72 h later) Further treatment & evaluation 4/20 (20%) cases had recurrent symptoms after indicated HBO treatment Possible explanations for recurrent symptoms: Mild hypoxia known to occur during commercial flights Damaged neurons susceptible to further injury during flight Changes made as a result of these cases: Pilots must wait at least 7 days before flying home after HBO treatment; pilots flying home must use supplemental oxygen Pilots at Travis AFB admitted or remain on base 72 hours after HBO No new cases of recurrent symptoms since changes implemented (Aug 09) 21 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013? Return to flying status 22 1-h resting pre-breathe Lessons Learned Variable recognition of symptom onset ( h) Landing HBO treatment Return home on commercial flight (48-72 h later) Further treatment & evaluation 10/16 (62.5%) pilots had persistent/permanent symptoms One pilot with medical course complicated by medication use At least 4/16 (25%) pilots reported clinically significant mental health problems Only 3/16 (19%) case pilots returned to unrestricted U-2 duty Lessons learned: Minimize use of medication (esp. narcotic/sedating meds) Provide proactive, persistent mental health support to pilots/family Flight surgeon & flying squadron manage work schedules Cooling off period of 6 months of no flying activities? Return to flying status ACS Evaluation Six incident U-2 pilots underwent a directed evaluation 10/2010 1/2011 Comprehensive medical and neurological exam Cardiac exam to include ECHO (PFO in 1 of 6) Neurophysiological exam (EEG, VEP normal) Neurocognitive exam (no deficits) Comprehensive brain imaging MRI, MRS, DTI, PET Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep C-4

17 MRI (pilot A ) 49 lesions (39 WMH/10 ependymal) cm 3 volume loss 158 clean controls age Population-based, Hispanic Avg 6.18 lesions cm 3 volume loss MRI (pilot B ) Necrotic appearing lesion at gray-white junction 1 WMH Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep MRI Transformation Process Nonbrain removed from FLAIR image FLAIR registered to T1-weighted image Registered to Talairach-atlas-based stereotactic frame Lesions analyzed using Talairach-based boundaries Transformed MRI (pilot A ) Transformed FLAIR images Lesions better defined Normalized brain size Permits crosssubject comparison Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Total Lesion Number/Volume ACS Assessment Subject ID Total Subcortical Lesions Total Ependymal Lesions Total Lesions Total FLAIR Volume (cm 3 ) Total Subcortical Volume (cm 3 ) Total Ependymal Volume (cm 3 ) C C C1 * C2 * C C Mean Controls Subcortical injury occurring Unusual in pattern of distribution Single subject with an apparent embolic lesion U-2 population concerned Unknowns: Prevalence of injury in entire U-2 population Proximate precipitating factors for NDCS Possibly ops tempo related Neurocognitive impairment (now & long term) Mission impact * Does not include necrotic lesions Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep C-5

18 Research Options 9/2011 Decision brief to AF/SG2 re: primate model Limited (nonsignificant p-value) data on 24 subjects Extremely high uncertainty re: primate protocol success Questions on validity of normative data and on new technology Research re-scoped to obtain true normative data Similar age range FC-II neurological standards Similar neurocognitive performance skills Normative Study Age active duty FC-II neurological standards Exclusionary criteria: Significant head trauma/surgery Significant headache/migraine history Significant psychiatric history Family history of degenerative neurological disease History of seizure after age 6 History of DCS Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Normative Study Doctorate limb (n=212) Flight Surgeon limb (n=82) 1 operational tour Altitude Exposure limb (n=82) > 50 exposures > 20,000 ft Calibration limb (n=20) Image at WHASC Cortical Thickness (n= 99 DCS; 75 DOC+FSG) Blue shaded regions represent areas of relative thinning of cortex compared to normative controls Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep WMH Comparison U-2 Pilots 11/9/2012 Hypothesis Significant difference between control (DOC + FSG) and all U-2 (scaled and unscaled) irrespective of clinical NDCS symptoms Among only U-2 pilots significant difference between clinical NDCS vs. no clinical NDCS (p=0.026) whataboutthese folks? DC S (n=105) U-2 pilots DOC+FSG (n=82) p-value (2-tailed Wilcoxon Rank) Subcortical WMH vol(scaled) 0.15±0.30 cm ±0.07 cm Subcortical WMH vol(unscaled) 0.13±0.27 cm ±0.07 cm Subcortical WMH count (scaled) 9.67± ±4.49 <0.001 Subcortical WMH count (unscaled) 7.57± ± If pilots exposedtohigh altitudes demonstrate changes onmri McGuire et al. Neurol 2013 (submitted) Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep C-6

19 Typical Altitude Chamber Exposure MRI Abnormalities in Altitude Chamber Technicians 25K ft 18K ft 5K ftear/sinus check 30 min denitrogenation Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep MRI Abnormalities in Altitude Chamber Technicians WMH Comparison Chamber 12/31/2012 PHY (n=57) DOC+FSG (n=102) p-value (2-tailed Mann-Whitney) Subcortical WMH vol Subcortical WMH count 0.157±0.481 cm ±0.076 cm 3 p= ± ±5.6 p=0.022 Significant difference between control (DOC+FSG) and PHY (hypobaric physiology personnel) WMH distribution similar in pattern to DCS (U-2 pilots) Unrelated to clinical episodes of NDCS Correlation with exposure hours not yet performed Difference noted for cortical thickness as well Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Cortical Thickness (n= 52 PHY; 75 DOC+FSG) Blue-shaded regions represent areas of relative thinning of cortex compared to normative controls Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep 2013 WMH in Other Populations WMH nonspecific seen in a variety of neurological conditions as well as a consequence of aging WMH reported in high-altitude mountain climbers, even in the absence of clinical symptoms of mountain sickness attributed to a combination of hypoxia and hypobaria WMH change present in 23% (26/113) of Turkish military divers with no history of DCS compared with 11% (7/65) of controls WMH change was found in 43.7% of French military divers with no history of DCS compared with 21.8% of controls Fayed et al.amj Med 2006; 119(2):168.e1-6 Erdem et al. Aviat SpaceEnvironMed 2009;80:2-4 Gempp et al.aviatspaceenvironmed 2010; 81: Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep C-7

20 Pathophysiology of NDCS (Classic View) Believed to be secondaryto nitrogen gas bubble formation Subsequent application of direct pressure on nerves and other tissues, blockage of small arteriolar vessels, and interaction with proteins in the blood Venous bubble formation occurs in 47%-66% of subjects exposed to chamber altitudes of 8992 m (29,500 ft) In lab clinical symptoms of DCS occur in 40%-42% CNS involvement (NDCS) is infrequent 49/1108 (4%) of lab DCS events Standard DCS therapy is U.S. Navy Treatment Table 6 (100% FIO 2; 2.8 atmospheres absolute) Based on empirical experience not laboratory studies Pilmanis et al. Aviat Space Environ Med 1999;70:22-9. Webb et al. Aviat SpaceEnviron Med 2002;73: Balldin et al. Aviat Space Environ Med 2004;75: Bennett et al. Cochrane Database of Systematic Reviews 2007 (2) DOI: / CD pub2 Pathophysiology (Alternative Mechanism) Lesion distribution pattern suggests simple compression of white matter by arteriolar gas bubble not complete explanation Microbubble (<30 μm) shower Accelerated coagulation of human whole blood and cell-free plasma with in vitro bubbles In rabbits, platelet thrombi found in pulm art In SCUBA platelet count decreased with venous bubbles In SCUBA microparticle production & neutrophil activation In cerebrovascular disease, early platelet adhesion and activation orchestrates a thrombo-inflammatory cascade not dependent upon platelet aggregation and thrombus formation Pontier et al. Aviat Space Environ Med 2008;79(12): Nieswandt et al. J Thromb Haemost 2011;9(suppl. 1): Thomet al. J Appl Physiol 2012;112: Pontier et al. J Appl Physiol 2011;110: Hallenbeck et al. Aerospace Med 1973;44: Tanoue et al. J Appl Physiolo 1987;62(5): Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Implications? WMH associated with impairment of executive processing in other neurological diseases Statistical but not clinical deficits noted in U-2 pilots Is there a threshold effect? Presumably a static process Standard treatment for NDCS is hyperbaria Should this be augmented by anti-thrombotic or anti-inflammatory treatment? Is there a dose:effect relationship to exposure? Questions? Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC , 3 Sep C-8

21 American Osteopathic College of Occupational and Preventive Medicine Tuesday, October 1, 2013, Aerospace Day JOIN NDMS/DMAT How goodly are your tents, O Jacob, and your dwelling places O Israel! ndms@hhs.gov Num 24:5 Your own state! BON KOURAJ References Department of Health and Human Services, Centers for Disease Control, Emergency Preparedness and Response: U.S. Government Response to the Haiti Earthquake: htm MO1-DMAT, IMSURT-W, 82nd ABN AT GHESIKO FIELD HOSPITAL, HAITI: JANUARY-FEBRUARY 2010 B-8

22 Tuesday, October 1, 2013, Medicine Aerospace Day Hyperbaric Oxygen for Idiopathic Sudden Sensorineural Hearing Loss Leonardo Profenna, MD, MPH Medical Director of Wound Care and Hyperbaric Medicine Connally Memorial Medical Center Introduction - ISSHL Introduction - ISSHL US Incidence 5-20 cases/100,000/year ~4000 cases annually Many cases unreported Heavy social and economic burden Difficult to obtain, keep jobs Stigmatization and isolation Special educational needs Most common cause of disability globally 15 th leading cause of burden of disease Definition Per ceptivehearing loss Hearing loss occurredwithin 72 hours Severityofthe hearing loss averages at least 30 dbhl for three subsequent one octave steps in frequency as shown in the standardpure-tone audiogram Hearing loss is nonfluctuating Etiology remainsunknown after clinical, laboratory andimaging studies Blank otologicalhistory in an otherwise healthy individual Unilateralin >97% ofcases Common presentation Sudden unilateralhearingloss Tinnitus (70%-90%) Sensation ofauralfullness (blocked or full ear ) Dizziness Ver tigo(20-60%) Diagnosis Differential Diagnosis Symptom complex On phone ask ptto hum if sound lateralizes to sideof hearingloss suspect conductive (non-urgent) If doesn t lateralize or lateralizes to opposite ear, urgenteval History: trauma, pain, drainage,fever, FNS, HA, diplopia,eyepain, prior history of hearingloss Otoscopic exam (OM, foreign body, perforation, OE, cholesteatoma Neuroexam exclude stroke Acute stroke Anterior inferior cerebellar artery Ipsilateral Horner syndrome, diplopia, nystagmus, facial weakness, limb sx, ataxia, contralateral pain or temp sensation loss MS, meningitis, schwannoma, migrainous infarction Rinne/Weber Audiometric exam MRI withcontrast ( %) normalinisshl r/oacousticneuroma, perilymph fistula, Meniere s, vascular, MS D-1

23 Tuesday, October 1, 2013, Medicine Aerospace Day Ear anatomy Blood supply to Ear Etiology of ISSHL Unclear! Vascular occlusion Viral infections Labyrinthine membrane breaks Immune associated disease Abnormal cochlear stress response Abnormal tissue growth Toxins Cochlear membrane damage Natural History of ISSHL Often quoted recovery rate of 65% Lamm et al % spontaneous full remissions and 47 89% partial remissions Costs Hearing aids $1,500 3,000 per pair Replace 3-5 years Cost of ten HBO2 treatments $2,000 5,000 Difficult to judge efficacy of therapy given high remission rate and low incidence D-2

24 Tuesday, October 1, 2013, Medicine Aerospace Day Corticosteroids and ISSHL Rationale Decrease inflammation and edema Scant data Cochrane review two randomized, controlled trials Results conflicting one no difference, one statistically better outcome with steroids pts with SSHLwithin 10 days (poor study) Glucocorticoid (varying dose) vs. Placebo overall 61% vs. 32% recovery, RR 1.3, 95% CI Pts with mild loss recovered regardless Profound hearing loss no benefit Moderate loss GC 78% vs. placebo 38%, RR 1.74, CI Corticosteroids, cont randomized trial, 41 patients 4 treatment groups glucocorticoids, carbogen inhalation, placebo, combined No difference Multiple retrospective studies equivocal AmericanAcademy of Otolaryngology - Head and Neck Surgery Recommend treatment with oral glucocorticoids Most likely to help if early in course 1mg/kg/day (max 60 mg) x days Can give intratympanic glucocorticoids recommended if no improvement with oral or oral contraindicated Antivirals and ISSHL Not recommended by AAO-HNS due to lack of evidence of efficacy and risk of side effects Rationale for HBO 2 use High metabolism and scant vascularity to cochlea Cochlea and inner structures require a high O 2 supply Oxygen to supply to inner cochlea is via oxygen diffusion through perilymph Studies of perilymph po 2 showed trend toward low O 2 in ISSHL Normobaric O 2 (3.4 X) and HBO 2 (9.4 X) raise perilymph O 2 compared to room air HBO 2 also is anti-inflammatory, reduces edema and blunts ischemia-reperfusion injury Cochrane reviews 2005, 2007, 2009, 2010, 2012 reviewed corticosteroids, vasodilators and HBO 2 Only HBO 2 received conservatively favorable review 2007 and 2010 For people with acute ISSHL, the application of HBO 2 significantly improved hearing, but the clinical significance remains unclear. Average hearing gains of 19.3 db for moderate loss and 37.7 db for severe Cochrane Review studies, 392 participants form 1985 to received HBOT and 185 control Dosages from 1.5 ATA for 45 minutes daily X 15 days to 2.5 ATA for 90 minutes daily X 25 days Exclusions and comparator regimens were different some to no treatment, some to pharmacologic treatment, some to sham. F/U periods varied 10 days to 3 months Entry criteria also different (time, db loss, pharmacologic failure, etc) Overall blinding and randomization procedures were poor D-3

25 Tuesday, October 1, 2013, Medicine Aerospace Day Cochrane Review 2012 Results Cochrane Review 2012 Results Proportion of participants with > 50% return of hearing 2 trials, 114 patients RR of improvement with HBOT 1.53, p=0.16, 95% CI 0.85 to Proportion of participants with > 25% return of hearing 2 trials, 114 patients RR of improvement with HBOT 1.39, p=0.02, 95% CI 1.05 to 1.84, NNT 5 for improvement in 1 Mean improvement in hearing over all frequencies 4 trials (169 participants), 2 dropped due to lack of standard deviations (both were positive), so 91 participants HBOT 15.6 db improvement over controls, p=0.03, CI 1.5 to 29.8 Severe and moderate did better than mild Mean improvement in pure tone average as percentage of baseline 1 trial, 50 participants, with HBOT 61%, without 24%, so 37% better with HBOT, statistically significant Cochrane 2012 Review Conclusions Impairment ranges Limited evidence from poor studies HBOT improves hearing in pts with ISSHL Within 2 weeks Might improve tinnitis No evidence that improvement is functionally significant Routine use cannot be justified Slight db hear and repeat spoken words at 1 meter Moderate db hearing aids Severe >61 db hearing aids, lip-reading, sign language training Additional data UHMS conclusion 12 retrospective and prospective case-controlled studies >1650 patients All but 2 studies positive, none negative Six of the studies combined HBOT with oral steroids Of randomized controlled studies, none negative Given the large amount of positive data - recommend treatment as an adjunct with corticosteroid treatment Patient selection Moderate to profound hearing loss Early in course of disease (< 14 days) Use as adjunct to corticosteroids < 60 years old Dosage 100% O 2 at 2 to 2.5 ATA for 90 minutes daily X treatments D-4

26 Tuesday, October 1, 2013, Medicine Aerospace Day AAO-HNS Clinical Practice Guideline Although hyperbaric oxygen therapy (HBOT) is not widely available in the United States and is not recognized by many US clinicians as an intervention for ISSNHL, the panel felt that the level of evidence for hearing improvement, albeit modest and imprecise, was sufficient to promote greater awareness of HBOT as an intervention for ISSNHL. Questions? D-5

27 Hypoxia Office COL Brian W. Smalley DO, MSPH, CPE Or this Or even this Hypoxia State of oxygen deficiency in the blood cells and tissues sufficient to cause impairment of function 4 Types Hypoxic Hypemic Stagnant Histotoxic E-1

28 TYPES OF HYPOXIA Hypoxic Hypoxia HYPOXIC (ALTITUDE) HISTOTOXIC (POISONING) Reduced po 2 in the lungs (high altitude) O2 O2 HYPEMIC O2 (BLOOD) O2 STAGNANT (POOLING) Body tissue Red blood cells ALVEOLAR PO2 AIR Po2 = 152 mm Hg Pco2 = 0.3 mm Hg Oxyhemoglobin Dissociation Curve Po2 = 103 mm Hg P H2O = 47 mmhg Pco2 = 40 mm Hg ALVEOLI increasedtemp,pco2,or decreasedphshift curve to the right ARTERIES Po2 = 40 mm Hg Pco2 = 46 mm Hg LUNGCAPILLARIES Po2 = 100 mm Hg Pco2 = 40 mm Hg VEINS RIGHT HEART LEFT HEART ALVEOLAR AIR AT SEA LEVEL ALVEOLAR AIR AT 10,000 FT GAS mmhg N O CO 2 40 H 2 O 47 TOTAL 760 GAS mmhg N O 2 61 CO 2 35 H 2 O 47 TOTAL 522 O 2 Hb SAT = 98% O 2 Hb SAT = 87% E-2

29 ALVEOLAR AIR AT 25,000 FT ALVEOLAR AIR AT 34,000 FT GAS mmhg N O 2 30 CO 2 27 H 2 O 47 TOTAL 283 GAS mmhg N 2 90 O 2 26 CO 2 24 H 2 O 47 TOTAL 187 O 2 Hb SAT = 55% O 2 Hb SAT = 42% ALVEOLAR AIR AT 34,000 FT ON 100% OXYGEN GAS mmhg N 2 0 O CO 2 40 H 2 O 47 TOTAL 187 OTHER CAUSES: Hypoventilation Airway obstruction Reduction in gas exchange area Impairment of gas exchange O 2 Hb SAT = 98% + + Hypemic Hypoxia Inability of the blood to accept oxygen in adequate amounts + + Reduced RBC count CAUSES blood donation hemorrhage Carbon Monoxide (CO) incomplete combustion forms carboxyhemoglobin Sulfa drugs/ferricyanide forms methemoglobin E-3

30 Adequate oxygen Blood moving slowly Stagnant Hypoxia Reduced blood flow Red blood cells not replenishing tissue needs fast enough CAUSES SYSTEMIC Sustained high G Sustained PPB Shock Reduced cardiac output LOCAL Body posture Hyperventilation Emboli Extreme temperatures Histotoxic Hypoxia Adequate Oxygen Inability of the cell to accept or use oxygen Red blood cells retain oxygen Poisoned tissue HISTOTOXIC HYPOXIA Inability of tissues to accept and/or utilize oxygen Causes: Carbon monoxide Alcohol Cyanide Hydrogen sulfide REMEMBER: Can occur at any altitude Different types are additive Individual and daily variability E-4

31 Hypoxic Hypoxia Reduced po 2 in the lungs (high altitude) PHYSIOLOGICAL RESPONSES TO HYPOXIC HYPOXIA RESPIRATORY CARDIOVASCULAR Red blood cells Body tissue RESPIRATORY RESPONSE TO HYPOXIA Decreased arterial PO2 Stimulate ventilation (8-10K feet) Decrease PACO2 CARDIOVASCULAR RESPONSE TO HYPOXIA Increase in cardiac output (6-8 K Feet) Increase in rate; no change in stroke volume No change in mean arterial pressure Decreased peripheral resistance Redistribution of blood flow Less Reduction in PAO2 CEREBRAL CIRCULATION Below 15,000 ft Decrease PCO2 predominates Reduced blood flow Above 16,000 ft Decreased PO2 predominates Increased blood flow CARDIOVASCULAR RESPONSE Increased heart rate Decreased peripheral resistance Redistribution of cardiac output increase coronary and cerebral decrease renal and skin Normally, no change in skeletal muscle resistance E-5

32 SYMPTOMS (subjective ) SYMPTOMS (objective) apprehension euphoria tingling dizziness blurred vision tunnel vision headache hot/cold flashes nausea numbness belligerence fatigue hyperventilation cyanosis poor judgment mental confusion loss of muscle coordination unconsciousness STAGES OF HYPOXIA STAGES OF HYPOXIA INDIFFERENT COMPENSATORY DISTURBANCE CRITICAL Indifferent Stage Altitudes: Sea Level - 10,000 feet Symptoms: decrease in night 4000 feet acuity color perception Compensatory Stage Altitudes: 10,000-15,000 feet Symptoms: impaired efficiency, drowsiness, poor judgment and decreased coordination E-6

33 Disturbance Stage Altitudes: 15,000-20,000 feet Symptoms: Decreased memory, impaired judgment, decreased reliability, poor understanding Personality: happy drunk versus the mean drunk Blurred vision, increased sense of touch & pain, impaired hearing Poor coordination, erratic flight control, slurred speech, illegible handwriting Critical Stage Altitudes: 20,000 feet and above Signs: loss of consciousness, convulsions and death WARNING! When hemoglobin saturation fallsbelow 65% serious cellulardysfunctionoccurs; andif prolonged, cancausedeath! TUC (time of useful consciousness) Altitude TUC TUC The time from an interruption of an adequate oxygen supply to the time useful function is lost. FL 430 & up FL 400 FL 350 FL 300 FL 280 FL 250 FL sec sec sec 1-2 min 2-3 min 3-5 min min Signs of Hypoxia (what you might see) Mental Disturbance Hyperventilation Cyanosis Mental confusion Poor judgment Lack of muscle coordination E-7

34 Performance Disturbance Handwriting at 25K Time offoxygen 1 minute 2 minutes 3 minutes 4 minutes 5 minutes 6 minutes Backon oxygen CAUTION! Failureto recognizeyoursignsand symptomsby the disturbancestagemay result in an aircraft mishap Altitude (cabin) Rate of Ascent Factors Influencing Hypoxia and TUC Duration of Exposure Fitness Level Activity at Altitude Temperature Self-imposed stress Prevention Limit time at altitude Know your symptoms Pressurized cabin Minimize self imposed stressors 100% O 2 Hypoxia Treatment Descend to a safe altitude 100% O 2 RECOVERY FROM HYPOXIA RAPID AND COMPLETE O2 PARADOX DECREASE IN PCO2 INTRODUCTION OF HIGH FIO2 QUESTIONS? E-8

35 Lectures References Link Hyperbaric Medicine 2013 Best Evidence and Practice Standards American Osteopathic College of Occupational and Preventive Medicine Las Vegas, Nevada Approved Indications for Hyperbaric Oxygen Therapy FDA on label standard UHMS leading scientific resource Published evidence EBM hierarchy CMS/Medicare leading health care purchaser Commercial insurers largely guided by CMS Cerebral Arterial Gas Embolism Pathophysiology I/R injury clarifies earlier relapse issues Essential elimination of USN TT 6A Hyperbaric dosing: USNTT 6; Comex Cx 30 Differential diagnosis CAGE vs. DCS unnecessary Iatrogenic prevalence The monoplace chamber Cerebral Arterial Gas Embolism Pathophysiology I/R injury clarifies earlier relapse issues Essential elimination of USN TT 6A Hyperbaric dosing: USNTT 6; Comex Cx 30 Differential diagnosis CAGE vs. DCS unnecessary Iatrogenic prevalence The monoplace chamber F-1

36 National Board of Diving & Hyperbaric Medical Technology Position Statement ( ) Intermittent Air Breathing It is the position of the National Board of Diving & Hyperbaric Medical Technology that every recompression treatment facility and every clinical hyperbaric oxygen chamber, regardless of type or class, be equipped to provide intermittent air breathing.intermittentairbreathing, commonly referred to as an airbreak, serves to prophylax against and lower the incidence of central nervous system oxygen toxicity. Intermittent air breathing also serves to treat premonitory signs and symptoms of oxygen toxicity, thereby reducing the potential for symptom progression to overtseizure. The application and sequencing of intermittent air breathing will be at the discretion of the hyperbaric physician. However, intermittent air breathing should be immediately instituted (by either multiplacechamber tender or monoplace chamber operator) whenever an acutechangein patientstatusoccursand is consistentwith, or suggestiveof, CNSoxygen toxicity. Decompression Sickness Cochrane: recompression universally accepted standard US Navy Diving Manual Rev. 6; 2005 TT6 (Comex Cx 30) Serial dosing protocol Basic science advances Effects of treatment delay; current controversy Monoplace aspects Clinical Outcome as a Function of Treatment Delay ~ 5,278 consecutive cases Delay(h) N CR IR Effectiveness 1 6 2,559 2,401 (94%) 135 (5%) 2,536 (99%) ,802 1,579 (88%) 216 (12%) 1,795 (97%) (85%) 80 (14%) 553 (100%) (81%) 43 (18%) 232 (99%) > (76%) 29 (24%) 119 (99%) Xu W, et al. PLoS One2012;7(11):e50079 Decompression Sickness Cochrane: recompression universally accepted standard US Navy Diving Manual Rev. 6; 2005 TT6 (Comex Cx 30) Serial dosing protocol Basic science advances Effects of treatment delay; current controversy Monoplace aspects F-2

37 Oxygen is the antidote Carbon Monoxide Poisoning Cochrane: Existing RCT s do not establish whether HBO reduces incidence of adverse neurologic outcomes RCT trial design & interpretation issues: O2 dosing; serious vs. mild cases; blinding/shams; f/u periods and screening tools Raphael, etal.1989 Ducasse, etal.1995 Thom, et al.1995 Scheinkestel, et al Weaver, et al Annane, et al Garrabou, etal Carbon Monoxide Poisoning 1. Lab studies uniformly (less 1) support HBO demonstrate HBO mechanisms; superiority of HBO at 3 ATA oxygen 2. Pregnant pts. not studied lab, retrospective and prospective (Elkharrat, et al. 1991) data produce an essential hyperbaric consensus; no contrarian views trans-placental physiology fetus as a sponge 3. Pediatric pts. not studied softer consensus; no published debates pro and con 4. Severe* cases, preponderance of evidence supports HBO * arguably: significant CNS manifestations: LOC: coma: profound cognitive, visual or auditory changes Annane group treat pregnant pts. 5. Less severe* cases, no compelling data HBO vs. NBO * arguably: headache; nausea; vomiting; dizziness; fatigue; malaise; syncope; confusion; subtle cognitive, visual or auditory changes; tachycardia; tachypnea 6. Data argues for high (3 ATA) initial tx. pressure precise dosing course not reconciled 7. HBO harms ; good patient safety profile 8. HBO economics arguably favorable Problem Wound Healing: Diabetic Foot Ulcers Basic science advances Controlled trials Cochrane Meta-analysis update Efficacy vs. effectiveness Tissue oximetry case management Modern dosing F-3

38 HBO Cell Signaling Mechanisms in Wound Repair Enhanced VEGF expression, Feng J, et al A HBO induced VEGF per c-jun/ap-1 activation, Lee C-C, et al Simultaneous activation of ERK and JNK pathways, Lee C-C, et al Enhanced SPC mobilization via NO elevation, ThomSR, et al NO (nm) NO mediated inhibition of neutrophil adhesion, Thom SR, SNP NO mediated reversal of impaired EPC mobilization, Gallagher KA, mg/kg HBO NO mediated enhancement of Ang2 gene expression, Lin S, et al Time (min) Thom SR, et al Am J Physiol. Heart Circ;290C Problem Wounds Healing: Diabetic Foot Ulcers Basic science advances Controlled trials Cochrane Meta-analysis update Efficacy vs. effectiveness Tissue oximetry case management Modern dosing Cochrane (2012) HBO seems to improve chances of healing in pts. with DFU s and may reduce the number of major amputations F-4

39 Problem Wounds Healing: Diabetic Foot Ulcers Basic science advances Controlled trials Cochrane Meta-analysis update Efficacy vs. effectiveness Tissue oximetry case management Modern dosing Problem Wounds Healing: Diabetic Foot Ulcers Basic science advances Controlled trials Cochrane Meta-analysis updates Efficacy vs. effectiveness Tissue oximetry case management Modern dosing F-5

40 Crush Injury, Compartment Syndrome, Acute Traumatic Peripheral Ischemia Basic science Dosing protocol Controlled clinical trial Evidence-based appraisal Hyperbaric Mechanisms Immediate support of hypoxic tissues Edema reduction Mitigation of reperfusion injury Generation of oxygen free radical scavengers Dosing protocol Complete vs. partial perfusion compromise Pre-op in intermediate compartment pressures Well spaced BID post-op C. Perfringens Infections/Gas Gangrene Basic mechanisms Clinical evidence Timing of HBO re surgery Confusion; gas gangrene vs. nec. fasciitis F-6

41 Basic Mechanisms Inhibition alpha toxin production: Van Unnik AJM, 1965 Bactericidal (stops clostridia) at 1,400 mmhg O2:Kaye D, 1967 Bacteriostasis (stops a toxin production) at 250 mmhg Other Benefits Reduced mortality (when combined with surgery & antibiotics) Vasoconstriction; edema reduction & improved perfusion Tighter demarcation for ablation Advantages of Early HBO It is life-savingbecause less heroic surgery needs to be performed in very ill pts. and cessation of alpha-toxin production is rapid It is limb and tissue sparing because no major amputations or excisions are done in advance and until demarcation becomes clear It clarifies demarcation, so that there is a clear distinction between obviously lost and still viable tissue Bakker DJ, 1988 C. Perfringens Infections/Gas Gangrene Basic mechanisms Clinical evidence Timing of HBO re surgery Confusion; gas gangrene vs. nec. fasciitis Late Radiation Tissue Injury Mandibular osteoradionecrosis Soft tissues; pelvic, larynx, colon, skin, etc ~ little evidence supporting radiation myelitis Radiation tissue injury prophylaxis Mandibular Osteoradionecrosis Marx Protocol ; treatment pressure issues Annane et al. RCT issues XRT portal issues; IMRT and IGRT Decreasing ORN incidence-conformal XRT F-7

42 Mandibular Osteoradionecrosis Annane et al. RCT issues Marx Protocol ; treatment pressure issues XRT portal issues; IMRT and IGRT Decreasing ORN incidence-conformal XRT Mandibular Osteoradionecrosis mmhg Annane et al. RCT issues Marx Protocol ; treatment pressure issues XRT portal issues; IMRT and IGRT Decreasing ORN incidence-conformal XRT Soft Tissue Radiation Injury XRT late effects not anatomic specific assumption Radiation proctitis XRT results: Level 1 evidence Disease modifying vs. supportive care alternative Dosing issues; chamber pressure vs. oxygen pressure F-8

43 Soft Tissue Radiation Injury XRT late effects not anatomic specific assumption Radiation proctitis XRT results: Level 1 evidence Disease modifying vs. supportive care alternative Dosing issues; chamber pressure vs. oxygen pressure Radiation Tissue Injury Prophylaxis National Cancer Institute Consensus; 1990 High risk-lifetime risk definitions Small vintage 1985 RCT as the basis Dosing protocol; 20/10 vs. 30/10 confusion Radiation Tissue Injury Prophylaxis National Cancer Institute Consensus; 1990 High risk-lifetime risk definitions Small 1985 RCT as the basis Dosing protocol; 20/10 vs. 30/10 confusion pre and post-op timing issues Skin Flaps-Skin Grafts Compromised Skin Flaps Surgical exploration vs. immediate hyperbaric referral Tissue oxygen tension screening Dosing protocol Evidence-based appraisal F-9

44 Skin Flaps-Skin Grafts Compromised Skin Grafts Preparation vs. preservation Tissue oxygen tension screening Autologous vs. bioengineered Medicare Hyperbaric LCD s: Clearly meeting the intent of this policy limitation Preparation/preservation of Compromised Skin Grafts excludes artificial skin Autografts (autologous, patient s skin) Allografts (allogenic, genetically non-identical; cadaver sourced) Isografts (genetically identical; patient s twin) Arguably meeting intent Alloderm donated human skin * Graftjacket donated human skin * Epicel epidermal autograft cultivated from the patient Laserskin epidermal autograft cultivated from the patient * FDA approved as banked human tissue Products arguably not meeting intent no human elements Biobrane silicone, collagen, nylon mesh EZ-derm porcine-derived xenograft Integra fully artificial product Oasis porcine-derived extracellular matrix Permacol porcine-derived collagen based Strattice porcine-derived dermal graft Suprathel fully synthetic monolayer dressing F-10

45 Exceptional Blood Loss Anemia Challenging cases multidisciplinary management HBO best guided by pt s calculated accumulating O2 debt HBO tapered with increasing RBC mass Dosing protocol Necrotizing Soft Tissue Infections Softer evidence support than gas gangrene Confusion re mixing this condition with gas gangrene Dosing issues Basis for HBO Therapy Improve leukocyte function in hypoxic tissues Bacteriostatic for some organisms Reduces amount/number of debridements Earlier opportunities for skin grafting Study N Overall Rate HBORate Non-HBO Mortality (%) Mortality (%) Mortality (%) P Value Gibson /29 (31) 7/12 (58) <0.05 Riseman /17 (23) 8/12 (67) <0.02 Brown (1994) /30 (30) 10/24 (42) 0.40 Shupak (1995) /25 (36) 3/12 (25) 0.71 Holllabaugh (1998) /14 (7) 5/12 (42) 0.5 Wilkinson (2004) /33 (6) 4/11 (36) 0.03 Necrotizing Soft Tissue Infections Softer evidence support than gas gangrene Confusion re mixing this condition with gas gangrene Dosing issues Mindrup (2005) /16 (13) 7/26 (27) 0.44 George (2009) /48 (8) 4/30 (13) 0.48 Hassan (2010) /29 (17) 10/38 (26) 0.37 TOTALS /241 (19) 58/177 (33) F-11

46 Refractory Osteomyelitis Scientific and laboratory basis Limited and poorly clinical data Abuse issues Basis for HBO Therapy Bone po2 (mmhg) Healthy bone ~ 45 mmhg Infected bone ~ mmhg Infected bone & HBO ~ 109mmHg Bacteriostatic (anaerobes); Enhances PMNL function Enhances aminoglycoside transport across cell wall Stimulates osteoclasts, fibroblasts and angiogeneis Refractory Osteomyelitis Scientific and laboratory basis Limited and poorly clinical data Abuse issues Acute Thermal Burn Injury Hyperbaric medicine s basis Cochrane position re clinical data Clinical practice; dosing protocol Basis for HBO Therapy Reduced edema Enhanced collagen synthesis Cochrane 2005) Insufficient evidence to support-refute HBO effectiveness Evidence from two RCT s don t produce clear guidelines Improved dermal elementpreservation Better preservation of ATP levels Improved infection control Improved microcirculation F-12

47 Clinical Practice and Hyperbaric Dosing F-13

48 The Disappearing 24/7 Hyperbaric Medicine Service A National Crisis Long appreciated that the immediate availability of HBO therapy is imperative Can prove life-saving Is central nervous system sparing Optimizes care of C. perfringens infections American Osteopathic College of Occupational and Preventative Medicine Enhances extent of skin flap survival Improves limb-salvage rates in traumatic ischemia Historic basis for hyperbaric oxygen therapy has been a 24/7 treatment capability Early hyperbaric chambers not hospital-based Dominating today s practice is a model designed to eliminate from contention those in immediate need This model and the loss of 24/7 care at established facilities serves to critically compromise patient access Late 1950 s: First employment of hospital-based facilities 1960 s: Growing list of acute indications Cardiac surgery; cardiac ischemia Cerebral arterial gas embolism Gas gangrene Necrotizing infections Acute peripheral insufficiency Acute traumatic ischemia CO poisoning G-1

49 1970 s: Increasing availability of hyperbaric medicine All such facilities operated with a 24/7 call response; early outpatient element to the service evolves 1980 s: Outpatient application dominates Monoplace chambers widely adopted; increased geographic access ~ ancillary equipmentadvancesfor critical patients ~ continuesto ensurethat allfacilities are 24/7 Refractory bone infections Lower extremity chronic wounds Late radiation tissue injury Mid-1990 s: Unique business model introduced; now dominates The Comprehensive Wound Healing Center ~ hospital affiliated but not hospital-based ~ outpatients only ~ no ancillary support for sicker patients ~ absolutely no 24/7 call availability ~ erosion of hyperbaric physician expertise Majority of new programs in past decade fitthis model ~ increasing geographicavailability comesata price By design, access fails those who might benefitmost Competitive & financial pressure on 24/7 services began to losemarket share usually theless clinically demanding cases/skills invariably thosewith better reimbursement burdened with costs ofhigherclinicalskills & 24/7 staffing The net effect of all of this By-product of this dilemma: loss of key ancillary equipment Increasing number of otherwise 24/7 programs reconsidering this service level in the face of increasing costs and falling revenues Some discontinued 24/7 availability, others have closed the service altogether A steady and critical decline in a vital standard of care as the cost argument wins out over best practice standards G-2