National DisasterMedical American OsteopathicCollegeof … · 2013-09-27 · B-1 American...

American Osteopathic College of Occupational and Preventive MedicineOMED 2013, Mandalay Bay Convention Center, Las Vegas

Tuesday, October 1, 2013, Aerospace Day

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National Disaster MedicalSystem

Preventive /Aerospace/OccupationalMedicine Role

Allen J. Parmet, MD, MPH, FACPM,FASMA, FACOEM, AIAASM

MO1-DMAT

[email protected]

Disclosure InformationAmerican Osteopathic College of Occupational & Preventive

Medicine OMED-Las Vegas, NV-October 1, 2013

Allen J. Parmet, MD

I have no financial relationships to disclose.

I will not discuss off-label use and/or investigational usein my presentations

National DisasterMedical System

• United States Department of Health andHuman Services (HHS) responsible formanaging Federal government's medicalresponse to major emergencies and disasters

• NDMS was returned to DHHS (US Departmentof Health and Human Services) on January 1,2007 by an Act of Congress).

• Federal Partners: FEMA, DoD, DVA

National Disaster MedicalSystem (NDMS) Response

Teams

• Disaster Medical Assistance Team (DMAT) (55)

• Disaster Mortuary Operational ResponseTeams (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)



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Disaster Medical Assistance Team(DMAT)

A DMAT is a group of professional and para-professional medicalpersonnel (supported by a cadre of logistical and administrativestaff) designed to provide medical care during a disaster or otherevent. NDMS recruits personnel for specific vacancies, plans fortraining opportunities, and coordinates the deployment of theteams.

DMATs are designed to be a rapid-response element to supplementlocal medical care until other Federal or contract resources can bemobilized, or the situation is resolved. DMATs deploy to disastersites with sufficient supplies and equipment to sustain themselvesfor a period of 72 hours while providing medical care at a fixed ortemporary medical care site. The personnel are activated for aperiod of two weeks.

State Disaster Medical AssistanceTeam (DMAT)

MO1-DMAT/MoDRS

The DMAT as a state organizationis a 501.3c taxexemptentitywhich can be activatedbythestate disaster response systemand respond to the governor’srequests to supportmedicalneeds in anyemergency.

Examples in tornados, floods, icestorms augmenting or replacinglocal medical resources,sheltering special needs andinstitutionalized 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 email closely for any MODRSrelated information Check your personaland family preparednessplans and change the batteries in yourAl l ‐Hazards Weather RadioTHIS DOCUMENT IS FOR OFFICIAL USE ANDINFORMATIONAL PURPOSESONLYAND IS NOT INTENDED TOBE AN OPERATIONSORDER OR MISSIONASSIGNMENT.ADDITIONAL UPDATESWILL BE SENT ASWARRANTED.###

DMATs around the USA Strike Team-Rapid Response Unit4 hours, 5 people, 4 Beds



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Full Team-Mobil Medical Unit24 hours, 50 people, 50 Beds

• 2006-Hurricane Charlie-Punta Gorda, FL

Tornado Response-Joplin, MOMay 22, 2011


Casualties158 Dead1,150 Injured450 Patients in St. John’s Hospital$3 Billion damages


Timeline:May 22 5:34-6:12 PM CDT-Tornado in Joplin

6:25-Governor declares disaster6:40-MO1-DMAT Activated8:30 First Strike TeamArrives

May 23 2:30 AM-Third Strike Team Arrives2:00 PM-Mobil Medical Unit sets up4:00 PM-Patients transferred from

St. JohnsMay 25 Strike Teams closeMay 29 Mobil Medical Unit turned over

to St. John’s staff and is designatedSt. John’s/Mercy Field Hospital

June 1 DMORT 7 completes casualty IDs

Disaster Mortuary OperationalResponse Teams (DMORTs)

• The National Response Framework (NRF) utilizes the NationalDisaster Medical System (NDMS), as part of the Department ofHealth & Human Services, Assistant Secretary for Preparedness andResponse (ASPR), Office of Preparedness and Operations (OPEO),under Emergency Support Function #8 (ESF #8), Health and MedicalCare, to provide victim identification and mortuary services. Theseresponsibilities include:

• temporary morgue facilities• victim identification• forensic dental pathology• forensic anthropology methods• processing• preparation• disposition of remains



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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 SurgicalResponse Team (IMSURT)

• The International Medical Surgical Response Team(IMSURT) is a National Disaster Medical System (NDMS)team of medical specialists who provide surgical and criticalcare during a disaster or public health emergency.Originally conceived to address the needs of U.S. citizensinjured overseas, the IMSURT role has expanded over theyears to include both domestic deployments, including theWorld Trade Center Bombings and Hurricane Katrina, andinternational deployments, including the earthquakes inBam, Iran, and Port au Prince, Haiti.

• IMSURT personnel are Federal employees used on anintermittent basis to deploy to the site of a disaster orpublic health emergency and provide high quality, lifesaving surgical and critical care.

IMSURT

National Veterinary Response Team(NVRT)

• The National Veterinary Response Team (NVRT) is a cadre ofindividuals within the NDMS system who have professionalexpertise in areas of veterinary medicine, public health andresearch.

• 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 largequantities of medicine and medical supplies to protectthe American public if there is a public healthemergency (terrorist attack, flu outbreak, earthquake)severe enough to cause local supplies to run out. OnceFederal and local authorities agree that the SNS isneeded, medicines will be delivered to any state in theU.S. in time for them to be effective. Each state hasplans to receive and distribute SNS medicine andmedical supplies to local communities as quickly aspossible.



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Emergency System for Advance Registration

of Volunteer Health Professionals (ESAR-VHP)

• The Emergency System for Advance Registration ofVolunteer Health Professionals (ESAR-VHP) is a federalprogram created to support states and territories inestablishing standardized volunteer registrationprograms for disasters and public health and medicalemergencies.

• The program, administered on the state level, verifieshealth professionals' identification and credentials sothat they can respond more quickly when disasterstrikes. By registering through ESAR-VHP, volunteers'identities, licenses, credentials, accreditations, andhospital privileges are all verified in advance, savingvaluable time in emergency situations.

Join NDMS!Recruitment Information

• http://www.phe.gov/Preparedness/responders/ndms/teams/Pages/recruitment.aspx

References

• Department of Health and Human Services,Centers for Disease Control, EmergencyPreparedness and Response:http://emergency.cdc.gov/

• Department of Health and Human Services,National Disaster Medical System:http://www.phe.gov/preparedness/responders/ndms/Pages/default.aspx

B-1



2010 Haiti EarthquakeNDMS, DMAT and theAerospace Medicine

Physician

Allen J. Parmet, MD, MPH

MO1-DMAT

[email protected]

Disclosure InformationAmerican Osteopathic College of Occupational & Preventive

Medicine OMED-Las Vegas, NV-October 1, 2013

Allen J. Parmet, MD

I have no financial relationships to disclose.

I will not discuss off-label use and/or investigational usein my presentations

Haiti in History

• 1790-Richest French colony, population 30,000

• 1803-Slave Revolt and Yellow Fever Epidemic-becomessecond independent country in the Americas-Napoleonsells Louisiana to US

• 1815-Haiti sponsors Bolivar’s revolt in South America

• 1820-Richest country in the world, per capita, series of32 coups follows.

• 1915-1935-U.S. Military occupation, building mostroads and infrastructure.

• 1957-1981-Duvalier dictatorships

HistoricalEarthquakes

Location/Intensity

• Chile, 1960- 9.5

• Indonesia, 2004- 9.3

• Alaska, 1964- 9.2

• Chile, 2-27-2010- 8.8

• New Madrid, 1811- 8.1

• Tokyo, 1923 7.9

• San Francisco, 1909- 7.9

• China, 1976- 7.5

• Haiti, 1-12-2010 7.3

• Mexicali, 4-6-2010 7.2

• San Francisco, 1989- 7.1

Casualties

• 6,000

• 230,000

• 131

• 700

• ?

• 143,000

• 3,000

• 655,000

• 230,000

• 2

• 63

January 12, 2010Chile was ready for earthquake, Haiti wasn'tChile has history of dealing with temblors;

Haiti's was first in living memory

January 2010 February 2010

Damage from Haiti's magnitude-7 earthquake. Chile's magnitude-8.8 earthquake.

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Images of DestructionPort-au-Prince

Hotel Montana-200 dead,including about 100

Americans

International Response

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Search and RescueNational 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

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The Scenes on Arrival

Toussaint L’Overture International Airport

ArrivalGHESKIO Field Hospital

GHESKIO Clinic

LZ

Patients

B-5



Infectious Disease

B-6



Surgery

Facilities

Prevention/Occupational

B-7



PatientMovement

U.S. HEALTH AND HUMAN SERVICES:MEDICAL MOVEMENT OF EVACUEES

Patient

Movement

MedicalRegulating

PatientEvacuation

PatientTracking

En-RouteMedical Care

PatientRe-Entry

NATIONAL GUARD ORDOD ASSETS

(GPMRC)

OPEO 2011-01C: ESF#8

GHESKIO Field Hospital

NDMS: IMSURT-W + MO-1 DMAT

Walk-Ins

NDMS StrikeTeams: OH-5, SC-1,

FL-7 DMATsNGOs

USNS Comfort

Aeromedical Evacuation

US Military & CivilianNon-US

C-1


Tuesday, October 1, 2013, Aerospace Medicine Day

Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC-2013-0137, 3 Sep 2013

U-2 DCS Update

Leonardo C. Profenna, MD, MPH, Col (ret)

Medical Director, Wound Care CenterConnally Memorial Medical Center

Floresville, TX Thanks to:Steve McGuire, MD

Lt Col Sean Jersey, MDLt Col Alan Flower, DO



$61 billion impact (2012), 116,000 jobsProduction 2008 – 358 barrels/day 26 permits

2012 – 352,000 barrels/day – 4,143 permits2016 - Projected to 900.000 barrels/day



Background Information

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 2002-09• 45 incidents of all types with 37 pilots

Many Severe Neurological Cases with Unusual Clinical Symptoms

5 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC-2013-0137, 3 Sep 2013

Original Review of Problem

Retrospective Review of U-2 DCS Incidents BeforeDec 09• DGMC Travis AFB IRB Approval (FDG2010012H)

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

Jersey SL, Hundemer GL, Stuart RP, West KN, Michaelson RS, Pilmanis AA. Neurological

decompression sickness among U-2 pilots: 2002-2009. Aviat Space Environ Med 2011; 82:1-10

6

C-2




Patient Characteristics

20 Total Cases – 16 Confirmed, 4 ProbableIncidents• 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

8


Spectrum of ClinicalOutcomes

•In 5/20 (25%) cases, pilots reported DCS symptoms immediately

•Prompt HBO treatment administered

•Full resolution of symptoms with no recurrence or persistence

•In 5/20 (25%) cases, pilots reported DCS symptoms immediately

•Prompt HBO treatment administered

•Full resolution of symptoms with no recurrence or persistence

Expected ClinicalResponse

•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

•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

Good ClinicalOutcome DespiteTreatment Delay

•19/20 (95%) cases received appropriate HBO treatment in theater

•2/20 (10%) cases had recurrent symptoms during commercial flights

•Symptoms recurred in 2 more (10%) after elevation changes while driving

•19/20 (95%) cases received appropriate HBO treatment in theater

•2/20 (10%) cases had recurrent symptoms during commercial flights

•Symptoms recurred in 2 more (10%) after elevation changes while driving

Recurrent SymptomsAfter Treatment

•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

•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

Persistent orPermanent

Symptoms DespiteAdequate Treatment

**NO FATALITIES**9 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC-2013-0137, 3 Sep 2013

Clinical CourseThe 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 hoursup 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

10


Most Common Symptoms

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)

?

Variable recognitionof symptom onset

(2.5 – 36 h)Return home on

commercial flight

(48-72 h later)

Further treatment& evaluation

Return toflying status

Landing HBO treatment

1-h restingpre-breathe

• CNS DCS symptomsare often non-specific• Focal neurological symptomsare rare• Requires high index of suspicion• If in doubt – TREAT!


Time Course ofPresentation

Time of Recognized Symptom Onset (h)

0.0 4.0 8.0 12.0 16.0 20.0 24.0 28.0 32.0 36.0 40.0

MP1MP2MP3MP4MP5MP6MP7MP7MP8MP9MP8MP6

MP10MP11MP12MP13MP14MP15MP14MP16

Onset0-4 h

in-

flight35%

Onset4.1-8 h

in-

flight15%

Un-known

in-

flight10%

Onsetpost-flight

40%

?

Unreported time during flight

Unreported time during flight



commercial flight

(48-72 h later)




Take-Home Points:• DC S symptoms vary markedly• Delays in symptom recognitionare

common• O perational concerns also cause

delays


12

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Clinical Course – TheBad

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 whiledriving 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

?



commercial flight

(48-72 h later)




1-hr restingpre-breathe


Re-Injury AfterTreatment

Pathophysiological Process Proposed by Goodman,et al.

• Based on animal (mice) model of traumatic brain injury

• Studies evaluating optimum time to fly following battlefield traumaticbrain injury (TBI)

• Mild hypoxia of commercial flight altitudes can exacerbate brain injury

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 & exacerbatesinflammatory cascade recurrence of symptoms

May Explain Unusual Symptoms in Some U-2 DCSCases

• 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

14


Clinical CourseThe 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 for two 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;

74:357-9.

2. 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.


Persistent and/or PermanentSymptoms

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)

Persistent Symptoms

Inappropriate fatigue (9/20)

Headaches (7/20)

Personality changes (5/20)

Memory problems (5/20)

Difficulty concentrating (2/20)

Difficulty sleeping (2/20)

• 10 of 16 pilots (62.5%)• Duration: 3 months to 9+ years• Considered permanent in at least 2 cases

?



commercial flight

(48-72 h later)





Foggythinking

16


Clinical CourseThe 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

•Few case reports of lasting effects after HBO treatment

•A ltitude DCS considered less severe than divingDCS

Operational Incentives to Return Pilots toFlying

•Eachnew U-2 pilot costs ~$2.5 million to train•Limited pool of pilots to man deployment s lots

•Limited housing& personnel s lots at deployed locations

Medical Consequences:

•P ilots flew home from deployment ASAP (< 72 h) after DCS

•P ilots attempted return to flyings tatus soon after DCS•Waiver guide: returnafter resolutionof symptoms, normalexam

18

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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 (1941-99)• Wirjosemito: 97.7% treatment success in 133 CNS DCS

cases (1960-86)• 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 withDiving-Related DCS

7/16 (44%) Pilots had Similar Constellation ofLong-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?

20


Lessons Learned

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

?



commercial flight

(48-72 h later)


Return toflying statusLanding HBO treatment



Lessons Learned

4/20 (20%) cases had recurrent symptoms after indicatedHBO 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 changesimplemented (Aug 09)

?



commercial flight

(48-72 h later)



1-hr restingpre-breathe

22


Lessons Learned

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 mentalhealth 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

?



commercial flight

(48-72 h later)





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

24

C-5




MRI (pilot “A”) 49 lesions (39 WMH/10 ependymal)

0.425 cm3 volume loss

158 “clean” controls age 30-40

• Population-based, Hispanic

• Avg 6.18 lesions

• 0.094 cm3 volume loss


MRI (pilot “B”) Necrotic appearing

lesion at gray-whitejunction

1 WMH

26


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 cross-subject comparison

28


SubjectID

TotalSubcortical

Lesions

TotalEpendymal

Lesions

TotalLesions

TotalFLAIR

Volume(cm3)

TotalSubcortical

Volume(cm3)

TotalEpendymal

Volume(cm3)

C5 39 10 49 1.068 0.425 0.643

C6 18 6 24 0.928 0.417 0.5103

C1* 1 6 7 1.395 0.023 1.3732

C2* 2 4 6 3.271 0.060 3.211

C3 1 8 9 1.615 0.011 1.6052

C4 3 6 9 2.446 0.115 2.332

Mean 10.67 6.67 17.33 1.787 0.175 1.612

Controls 6.18 0.094

* Does not include necrotic lesions

Total Lesion Number/Volume


ACS Assessment

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

30

C-6




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 26 – 45 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

32


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

34


WMH Comparison – U-2 Pilots11/9/2012

Significant difference between control (DOC + FSG)

and all U-2 (scaled and unscaled) irrespective ofclinical NDCS symptoms

• Among only U-2 pilots significant difference betweenclinical NDCS vs. no clinical NDCS (p=0.026)

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 cm3 0.04±0.07 cm3 0.004

Subcortical WMH vol (unscaled) 0 .13±0.27 cm3 0.04±0.07 cm3 0.009

Subcortical WMH count (scaled) 9 .67±18.26 3.29±4.49 <0.001

Subcortical WMH count(unscaled)

7 .57±14.31 3.29±4.49 0.020

McGuire et al. Neurol 2013 (submitted)35 Distribution A: Approved for public release; distribution is unlimited. Case Number: AFMC-2013-0137, 3 Sep 2013

Hypothesis

If pilots exposed tohighaltitudes demonstratechanges onMRI…

what about these folks?

36

C-7




Typical Altitude ChamberExposure

25K ft

18K ft

5K ft-ear/sinuscheck

30 min

denitrogenation


MRI Abnormalities in AltitudeChamber Technicians

38


MRI Abnormalities in AltitudeChamber Technicians


WMH Comparison – Chamber12/31/2012

Significant difference between control(DOC+FSG) and PHY (hypobaric physiologypersonnel)• 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

PHY (n=57) DOC+FSG(n=102)

p-value(2-tailed Mann-Whitney)

Subcortical WMHvol

0.157±0.481 cm3 0.042±0.076 cm3 p=0.029

Subcortical WMHcount

7.4±12.8 3.3±5.6 p=0.022

40


Cortical Thickness(n= 52 PHY; 75 DOC+FSG)

Blue-shaded regionsrepresent areas of relativethinning of cortexcompared to normativecontrols


WMH in Other Populations WMH nonspecific – seen in a variety of

neurological conditions as well as a consequenceof aging

WMH reported in high-altitude mountainclimbers, even in the absence of clinicalsymptoms of mountain sickness – attributed to acombination of hypoxia and hypobaria

WMH change present in 23% (26/113) of Turkishmilitary divers with no history of DCS comparedwith 11% (7/65) of controls

WMH change was found in 43.7% of Frenchmilitary divers with no history of DCS comparedwith 21.8% of controls

Fayed et al. A mJ Med 2006; 119(2):168.e1-6Erdem et al. Aviat Space EnvironMed 2009;80:2-4Gempp et al. AviatSpace EnvironMed 2010; 81:1008-12

42

C-8




Pathophysiology of NDCS(Classic View)

Believed to be secondary to nitrogen gas bubble formation

• Subsequent application of direct pressure on nerves and othertissues, blockage of small arteriolar vessels, and interactionwith proteins in the blood

Venous bubble formation occurs in 47%-66%of subjects exposedto 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 labDCS events 1983-2003

Standard DCS therapy is U.S. Navy Treatment Table 6 (100%FIO2; 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 Space Environ Med 2002;73:1161-6.

Balldin et al. Aviat Space Environ Med 2004;75:969-72

Bennett et al. Cochrane Database of Systematic Reviews 2007 (2) DOI: 10.1002/14651858.CD005277.pub2


Pathophysiology(Alternative Mechanism)

Lesion distribution pattern suggests simple compression ofwhite matter by arteriolar gas bubble not completeexplanation

Microbubble (<30 μm) shower

Accelerated coagulation of human whole blood and cell-freeplasma 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 andactivation orchestrates a “thrombo-inflammatory” cascadenot dependent upon platelet aggregation and thrombusformation

Pontier et al. J Appl Physiol 2011;110:724-729.

Hallenbeck et al. Aerospace Med 1973;44:712-714.

Tanoue et al. J Appl Physiolo 1987;62(5):1772-1779.

Pontier et al. Aviat Space Environ Med 2008;79(12):1096-9.

Nieswandt et al. J Thromb Haemost 2011;9(suppl. 1):92-104.Thom et al. J Appl Physiol 2012;112:1268-1278

44


Implications?

WMH associated with impairment of executive

processing in other neurological diseases

• Statistical but not clinical deficits noted in U-2pilots

• 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?

46

B-8



JOIN NDMS/DMAT

• [email protected]

• https://www.showmeresponse.org/

• http://www.mo1dmat.org/

• https://phix.kdhe.state.ks.us/VolunteerRegistry/

• Your own state!

How goodlyare your tents,O Jacob, and

your dwellingplaces O Israel!

-Num 24:5

BON KOURAJ

MO1-DMAT, IMSURT-W, 82nd ABN AT GHESIKO FIELD HOSPITAL, HAITI:

JANUARY-FEBRUARY 2010

References

• Department of Health and Human Services,Centers for Disease Control, EmergencyPreparedness and Response:http://emergency.cdc.gov/

• U.S. Government Response to the HaitiEarthquake:http://www.state.gov/r/pa/prs/ps/2010/01/135308.htm

• http://www.whitehouse.gov/issues/foreign-policy/haiti-earthquake

D-1


Tuesday, October 1, 2013, Medicine Aerospace Day

Hyperbaric Oxygen forIdiopathic Sudden

Sensorineural HearingLoss

Leonardo Profenna, MD, MPH

Medical Director of Wound Care and Hyperbaric Medicine

Connally Memorial Medical Center

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

15th leading cause of burden of disease

Introduction - ISSHL

Definition

Per ceptivehearing loss

Hear ing loss occurred w ithin 72 hours

Sever ity of the hear ing loss averages at least 30 dB HL for three subsequent oneoctave steps in fr equency as shown in the standard pure-tone audiogram

Hear ing loss is nonfluctuating

Etiology r emains unknown after clinical, labor atory and imaging studies

Blank otological histor y in an otherwise healthy individual

Unilater al in >97% of cases

Common presentation – Sudden unilater al hearing loss

Tinnitus (70%-90%)

Sensation of aur al fullness (blocked or full ear )

Dizziness

Ver tigo (20-60%)

Diagnosis

Symptom complex

On phone – ask pt to hum – if sound lateralizes to side of hearing loss – suspectconductive (non-urgent)

If doesn’t later alize or lateralizes to opposite ear, ur gent eval

History: trauma, pain, drainage, fever, FNS, HA, diplopia,eye pain, pr ior historyof hearing loss

Otoscopic exam (OM, foreign body, perforation, OE, cholesteatoma

Neuro exam exclude stroke

Rinne/Weber

Audiometr ic exam

MRI with contrast (2.7-10.2%) – normalin ISSHL – r/o acoustic neuroma, perilymphfistula, Meniere’s, vascular, MS

Differential Diagnosis

Acute stroke

Anterior inferior cerebellar artery

Ipsilateral Horner syndrome, diplopia, nystagmus, facialweakness, limb sx, ataxia, contralateral pain or temp sensationloss

MS, meningitis, schwannoma, migrainous infarction

D-2



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. – 25 - 68% spontaneous full remissions and47 – 89% partial remissions

Difficult to judge efficacy of therapy given highremission rate and low incidence

Costs

Hearing aids $1,500 – 3,000 per pair

Replace 3-5 years

Cost of ten HBO2 treatments $2,000 – 5,000

D-3



Corticosteroids and ISSHL

Rationale

Decrease inflammation and edema

Scant data – Cochrane review – two randomized, controlled trials

Results conflicting – one no difference, one statisticallybetter outcome with steroids

1980 – 67 pts with SSHL within 10 days (poor study)

Glucocorticoid (varying dose) vs. Placebo – overall 61% vs.32% recovery, RR 1.3, 95% CI 0.91-1.86

Pts with mild loss recovered regardless

Profound hearing loss no benefit

Moderate loss – GC 78% vs. placebo 38%, RR 1.74, CI 1.19-2.55

Corticosteroids, cont.

2001 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 10-14 days

Can give intratympanic glucocorticoids – recommended if noimprovement with oral or oral contraindicated

Antivirals and ISSHL

Not recommended by AAO-HNS due to lack of evidenceof efficacy and risk of side effects

Rationale for HBO2 use

High metabolism and scant vascularity to cochlea

Cochlea and inner structures require a high O2 supply

Oxygen to supply to inner cochlea is via oxygen diffusionthrough perilymph

Studies of perilymph pO2 showed trend toward low O2 inISSHL

Normobaric O2 (3.4 X) and HBO2 (9.4 X) raise perilymphO2 compared to room air

HBO2 also is anti-inflammatory, reduces edema andblunts ischemia-reperfusion injury

Cochrane reviews

2005, 2007, 2009, 2010, 2012 reviewed corticosteroids,vasodilators and HBO2

Only HBO2 received conservatively favorable review

2007 and 2010 – “For people with acute ISSHL, theapplication of HBO2 significantly improved hearing, butthe clinical significance remains unclear.”

Average hearing gains of 19.3 dB for moderate loss and37.7 dB for severe

Cochrane Review 2012

7 studies, 392 participants form 1985 to 2004

207 received HBOT and 185 control

Dosages from 1.5 ATA for 45 minutes daily X 15 days to 2.5 ATAfor 90 minutes daily X 25 days

Exclusions and comparator regimens were different – some to notreatment, some to pharmacologic treatment, some to sham.

F/U periods varied 10 days to 3 months

Entry criteria also different (time, dB loss, pharmacologicfailure, etc)

Overall blinding and randomization procedures were poor

D-4



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 to2.78.

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 to1.84, NNT 5 for improvement in 1

Mean improvement in pure tone average as percentage ofbaseline

1 trial, 50 participants, with HBOT 61%, without 24%, so 37%better with HBOT, statistically significant

Cochrane Review 2012 Results

Mean improvement in hearing over all frequencies

4 trials (169 participants), 2 dropped due to lack ofstandard deviations (both were positive), so 91 participants

HBOT 15.6 dB improvement over controls, p=0.03, CI 1.5 to29.8

Severe and moderate did better than mild

Cochrane 2012 Review Conclusions

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

Impairment ranges

Slight

26 – 40 dB – hear and repeat spoken words at 1 meter

Moderate

41 – 60 dB – hearing aids

Severe

>61 dB – hearing aids, lip-reading, sign language training

Additional data

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

UHMS conclusion

Given the large amount of positive data - recommendtreatment 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% O2 at 2 to 2.5 ATA for 90 minutes daily X 10-20treatments

D-5



AAO-HNS Clinical Practice Guideline

Although hyperbaric oxygen therapy (HBOT) is notwidely available in the United States and is notrecognized by many US clinicians as an intervention forISSNHL, the panel felt that the level of evidence forhearing improvement, albeit modest and imprecise, wassufficient to promote greater awareness of HBOT as anintervention for ISSNHL.

Questions?

E-1



Hypoxia

• COL Brian W. Smalley DO, MSPH, CPE

Office

Or this… Or even this…

Hypoxia

• State of oxygendeficiency in theblood cells andtissues sufficient tocause impairmentof function

• 4 Types– Hypoxic

– Hypemic

– Stagnant

– Histotoxic

E-2



TYPES OF HYPOXIA

HISTOTOXIC(POISONING)

STAGNANT(POOLING)

HYPEMIC(BLOOD)O2

O2

O2O2

HYPOXIC(ALTITUDE)

Reduced pO2

in the lungs(high altitude)

Body tissue

Redblood cells

Hypoxic Hypoxia

ALVEOLAR PO2AIR

Po2 = 152 mm HgPco2 = 0.3 mm Hg

ALVEOLIPo2 =

103 mmHg

Pco2 =

40 mm Hg

Po2 = 40 mm Hg Po2 = 100 mm Hg

Pco2 = 46 mm Hg Pco2 = 40 mm Hg

LUNGCAPILLARIES

RIGHTHEART

LEFTHEART

VEINSARTERIES

PH2O = 47 mmHg

increased temp,Pco2,ordecreasedpHshift curveto the right

OxyhemoglobinDissociation Curve

ALVEOLAR AIR AT SEA LEVEL

GAS mmHg

N2 563

O2 103

CO2 40

H2O 47

TOTAL 760

O2Hb SAT = 98%

ALVEOLAR AIR AT 10,000 FT

GAS mmHg

N2 376

O2 61

CO2 35

H2O 47

TOTAL 522

O2Hb SAT = 87%

E-3




GAS mmHg

N2 179

O2 30

CO2 27

H2O 47

TOTAL 283

O2Hb SAT = 55%


GAS mmHg

N2 90

O2 26

CO2 24

H2O 47

TOTAL 187

O2Hb SAT = 42%

ALVEOLAR AIR AT 34,000 FTON 100% OXYGEN

GAS mmHg

N2 0

O2 100

CO2 40

H2O 47

TOTAL 187

O2Hb SAT = 98%

OTHER CAUSES:

• Hypoventilation

• Airway obstruction

• Reduction in gas exchange area

• Impairment of gas exchange

Hypemic Hypoxia

+

+

+

+

++

+

++

+

+

+

+ ++

Inability of theblood to accept

oxygen inadequate amounts

+

CAUSES

• Reduced RBC count

– blood donation

– hemorrhage

• Carbon Monoxide (CO)

– incomplete combustion

– forms carboxyhemoglobin

• Sulfa drugs/Ferricyanide– forms methemoglobin

E-4



Reducedbloodflow

Bloodmovingslowly

Adequateoxygen

Red blood cellsnot replenishing

tissue needsfast enough

Stagnant Hypoxia CAUSES

• SYSTEMIC– Sustained high G– Sustained PPB– Shock– Reduced cardiac output

• LOCAL– Body posture– Hyperventilation– Emboli– Extreme temperatures

Red blood cellsretain oxygen

Inability of thecell to acceptor use oxygen

Poisonedtissue

AdequateOxygen

Histotoxic Hypoxia

HISTOTOXIC HYPOXIA

• Inability of tissues to accept and/or utilizeoxygen

• Causes:

– Carbon monoxide

– Alcohol

– Cyanide

– Hydrogen sulfide

REMEMBER:

• Can occur at any altitude

• Different types are additive

• Individual and daily variability

E-5



Reduced pO2

in the lungs(high altitude)

Body tissue

Redblood cells

Hypoxic HypoxiaPHYSIOLOGICAL RESPONSES TO HYPOXIC

HYPOXIA

• RESPIRATORY

• CARDIOVASCULAR

RESPIRATORY RESPONSE TO HYPOXIARESPIRATORY RESPONSE TO HYPOXIA

Decreased arterial PO2

Stimulate ventilation (8-10K feet)

Decrease PACO2

Less Reduction in PAO2

Decreased arterial PO2

Stimulate ventilation (8-10K feet)

Decrease PACO2

Less Reduction in PAO2

CARDIOVASCULARRESPONSE TO HYPOXIA

CARDIOVASCULARRESPONSE 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

• 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

CEREBRAL CIRCULATIONCEREBRAL CIRCULATION

• Below 15,000 ft– Decrease PCO2 predominates

– Reduced blood flow

• Above 16,000 ft– Decreased PO2 predominates

– Increased blood flow

• 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 muscleresistance

E-6



SYMPTOMS(subjective )

apprehension headache

euphoria hot/cold flashes

tingling nausea

dizziness numbness

blurred vision belligerence

tunnel vision fatigue

SYMPTOMS(objective)

hyperventilation

cyanosis

poor judgment

mental confusion

loss of muscle coordination

unconsciousness

STAGES OF HYPOXIA

• INDIFFERENT

• COMPENSATORY

• DISTURBANCE

• CRITICAL

STAGES OF HYPOXIA

Indifferent Stage

• Altitudes: Sea Level - 10,000 feet

• Symptoms: decrease in night vision @ 4000feet– acuity

– color perception

Compensatory Stage

• Altitudes: 10,000 - 15,000 feet

• Symptoms: impaired efficiency, drowsiness,poor judgment and decreased coordination

E-7



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, slurredspeech, illegible handwriting

Critical Stage

• Altitudes: 20,000 feet

and above

• Signs: loss of

consciousness,convulsions anddeath

When hemoglobin saturation fallsbelow 65% seriouscellular dysfunction occurs; and if prolonged, can causedeath!

WARNING!

TUC

(time of useful consciousness)

• The time from an interruption of anadequate oxygen supply to the time usefulfunction is lost.

TUC

Altitude TUC

FL 430 & up 9-12 sec

FL 400 15-20 sec

FL 350 30-60 sec

FL 300 1-2 min

FL 280 2-3 min

FL 250 3-5 min

FL 180 20-30 min

Signs of Hypoxia (what you might see)

• Hyperventilation

• Cyanosis

• Mental confusion

• Poor judgment

• Lack of muscle coordination

Mental Disturbance

E-8



Performance Disturbance

CAUTION! Failure to recognize your signs and symptoms by thedisturbance stage may result in an aircraft mishap

Back on oxygen

Time off Oxygen

1 minute

2 minutes

3 minutes

4 minutes

5 minutes

6 minutes

Handwriting at 25K

Factors InfluencingHypoxia and TUC

• Altitude (cabin)

• Rate of Ascent

• Duration of Exposure

• Fitness Level

• Activity at Altitude

• Temperature

• Self-imposed stress

Hypoxia

• Prevention– Limit time at

altitude

– Know yoursymptoms

– Pressurized

cabin

– Minimize selfimposed

stressors

– 100% O2

• Treatment

– Descend to a safe altitude

– 100% O2

RECOVERY FROM HYPOXIARECOVERY FROM HYPOXIA

• RAPID AND COMPLETE

• O2 PARADOX– DECREASE IN PCO2

– INTRODUCTION OF HIGH FIO2

• RAPID AND COMPLETE

• O2 PARADOX– DECREASE IN PCO2

– INTRODUCTION OF HIGH FIO2

QUESTIONS?

F-1



Lectures References Link

www.baromedical.com/clarkefiles.asp

Hyperbaric Medicine 2013

Best Evidence and Practice Standards

American Osteopathic College ofOccupational 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-2



National Board of Diving & Hyperbaric Medical Technology

Position Statement (2009-04)

Intermittent Air BreathingIt is the position of the National Board of Diving & Hyperbaric Medical Technologythat every recompression treatment facility and every clinical hyperbaric oxygenchamber, regardless of type or class, be equipped to provide intermittent airbreathing. Intermittent airbreathing, commonly referred to as an ‘air break’,serves to prophylax against and lower the incidence of central nervous systemoxygen toxicity. Intermittent air breathing also serves to treat premonitory signsand symptoms of oxygen toxicity, thereby reducing the potential for symptomprogression to overt seizure.

The application and sequencing of intermittent air breathing will be at thediscretion of the hyperbaric physician. However, intermittent air breathing shouldbe immediately instituted (by either multiplace chamber tender or monoplacechamber operator) whenever an acute change in patient status occurs and isconsistent with, or suggestive of, CNS oxygen toxicity.

www.nbdhmt.org

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

Delay(h) N CR IR Effectiveness

1 – 6 2,559 2,401 (94%) 135 (5%) 2,536 (99%)

6 – 12 1,802 1,579 (88%) 216 (12%) 1,795 (97%)

12 – 24 555 473 (85%) 80 (14%) 553 (100%)

24 – 36 234 189 (81%) 43 (18%) 232 (99%)

> 36 119 90 (76%) 29 (24%) 119 (99%)

~ 5,278 consecutive cases

Xu W, et al. PLoS One 2012;7(11):e 50079

Decompression Sickness

Cochrane: recompression universally accepted standard

US Navy Diving Manual Rev. 6; 2005 TT6 (Comex Cx 30)

Serial dosing protocol


Effects of treatment delay; current controversy

Monoplace aspects

F-3



Carbon Monoxide Poisoning

Oxygen is the antidote…

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, et al. 1989 Ducasse, et al. 1995 Thom, et al. 1995

Scheinkestel, et al. 1999 Weaver, et al. 2002

Annane, et al. 2011 Garrabou, et al. 2011

Carbon Monoxide Poisoning

1. Lab studies uniformly (less 1) support HBOdemonstrate HBO mechanisms; superiority of HBO

at 3 ATA oxygen

2. Pregnant pts. not studiedlab, retrospective and prospective (Elkharrat, et al. 1991)

data produce an essential ‘hyperbaric’ consensus; nocontrarian views

trans-placental physiology ‘fetus as a sponge’

Annane group treat pregnant pts.

3. Pediatric pts. not studiedsofter 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

5. Less severe* cases, no compelling data HBO vs. NBO

* arguably: headache; nausea; vomiting; dizziness; fatigue;

malaise; syncope; confusion; subtle cognitive, visual orauditory changes; tachycardia; tachypnea

6. Data argues for high (3 ATA) initial tx. pressureprecise dosing course not reconciled

7. HBO ‘harms’; good patient safety profile

8. HBO economics arguably favorable

Problem Wound Healing: Diabetic Foot Ulcers


Controlled trials

Cochrane

Meta-analysis update

Efficacy vs. effectiveness

Tissue oximetry case management

Modern dosing

F-4



HBO Cell Signaling Mechanisms in Wound Repair

Enhanced VEGF expression, Feng J, et al. 1998

HBO induced VEGF per c-Jun/AP-1 activation, Lee C-C, et al. 2006

Simultaneous activation of ERK and JNK pathways, Lee C-C, et al. 2006

Enhanced SPC mobilization via NO elevation, Thom SR, et al. 2006

NO mediated inhibition of neutrophil adhesion, Thom SR, 2004

NO mediated reversal of impaired EPC mobilization, Gallagher KA, 2007

NO mediated enhancement of Ang2 gene expression, Lin S, et al. 2002

0

-5

∆ N

O (

nM

)

0 5 10 15 20

200

400

600

800

1000

HBO

SNP

4mg/kg

Time (min)

A

Thom SR, et al. 2006Am J Physiol. Heart Circ;290C

Problem Wounds Healing: Diabetic Foot Ulcers


Controlled trials

Cochrane




Modern dosing

HBO seems to improve chances of healing in pts. withDFU’s and may reduce the number of major amputations

Cochrane (2012)

F-5





Controlled trials

Cochrane




Modern dosing



Controlled trials

Cochrane

Meta-analysis updates



Modern dosing

F-6



Crush Injury, Compartment Syndrome, Acute TraumaticPeripheral 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-7



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-saving because 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-8








10-20 mmHg

5 5 10 15 20 35 40 55

5 15 25 40 55






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-9



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

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 confusionpre and post-op timing issues

Radiation Tissue Injury Prophylaxis Skin Flaps-Skin Grafts

Compromised Skin Flaps

Surgical exploration vs. immediate hyperbaric referral

Tissue oxygen tension screening

Dosing protocol

Evidence-based appraisal

F-10



Skin Flaps-Skin Grafts

Compromised Skin Grafts

Preparation vs. preservation

Tissue oxygen tension screening

Autologous vs. bioengineered

‘Preparation/preservation of Compromised SkinGrafts …’excludes artificial skin’

Medicare Hyperbaric LCD’s:Clearly meeting the intent of this policy limitation…

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-11



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

Gibson 1986 41 46 9/29 (31) 7/12 (58) <0.05

Riseman 1990 29 41 4/17 (23) 8/12 (67) <0.02

Brown (1994) 54 35 9/30 (30) 10/24 (42) 0.40

Shupak (1995) 37 32 9/25 (36) 3/12 (25) 0.71

Holllabaugh (1998) 26 23 1/14 (7) 5/12 (42) 0.5

Wilkinson (2004) 44 14 2/33 (6) 4/11 (36) 0.03

Mindrup (2005) 42 21 2/16 (13) 7/26 (27) 0.44

George (2009) 78 10 4/48 (8) 4/30 (13) 0.48

Hassan (2010) 67 22 5/29 (17) 10/38 (26) 0.37

TOTALS 418 27 45/241 (19) 58/177 (33) 0.001

Study N Overall Rate HBORate Non-HBOMortality (%) Mortality (%) Mortality (%) P Value

Necrotizing Soft Tissue Infections

Softer evidence support than gas gangrene

Confusion re mixing this condition with gas gangrene

Dosing issues

F-12



Refractory Osteomyelitis

Scientific and laboratory basis

Limited and poorly clinical data

Abuse issues


Bone pO2 (mmHg)

Healthy bone…~ 45 mmHg

Infected bone… ~ 20-22 mmHg

Infected bone & HBO… ~ 109mmHg

Stimulates osteoclasts, fibroblasts and angiogeneis

Bacteriostatic (anaerobes); Enhances PMNL function

Enhances aminoglycoside transport across cell wall

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


Reduced edema

Enhanced collagen synthesis

Improved dermal element preservation

Better preservation of ATP levels

Improved infection control

Improved microcirculation

Cochrane 2005)

Insufficient evidence to support-refute HBO effectiveness

Evidence from two RCT’s don’t produce clear guidelines

F-13



Clinical Practice and Hyperbaric Dosing

G-1



The Disappearing 24/7 Hyperbaric Medicine Service

A National Crisis

American Osteopathic College of Occupationaland Preventative Medicine

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

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

Dominating today‘s practice is a model designed toeliminate from contention those in immediate need

This model and the loss of 24/7 care at established facilities serves

to critically compromise patient access

Early hyperbaric chambers not hospital-based

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-2



1970’s: Increasing availability of hyperbaric medicine

All such facilities operated with a 24/7 call response;early outpatient element to the service evolves

Refractory bone infections

Lower extremity chronic wounds

Late radiation tissue injury

1980’s: Outpatient application dominates

Monoplace chambers widely adopted; increased geographic access

~ ancillary equipment advances for ‘critical’ patients

~ continues to ensure that all facilities are 24/7

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 fit this model

By design, access fails those who might benefit most

Competitive & financial pressure on 24/7 services

…began to lose market share

…usually the less clinically demanding cases/skills

…invariably those with better reimbursement

…burdened with costs of higher clinical skills & 24/7 staffing

~ increasing geographic availability comes at a price

The net effect of all of this…

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

By-product of this dilemma: loss of key ancillary equipment

G-3



Those for which inclusion of HBO therapy can make a difference

between a good outcome and a bad one have much to worry about

Several dimensions to this dilemma

Erosion of best medical practice

Failure of patient/beneficiary access

Quality of life impact

Ethical and moral questions

Medical-legal threat

Evacuated to nearby hospital with HBO

ED unable to contact HBO team (weekend)

Eventually advised HBO service not 24/7

DAN referral to Hospital, South Miami

Eventual medical transfer

Succumbed during initial HBO treatment

Retired nurse suffered decompression-induced CAGE

Patient suffers iatrogenic CAGE during heart surgery

Immediate and significant compromise

None of 12 local hyperbaric programs would treat

Hospital in adjacent state agrees to accept

Risk benefit analysis of ‘fresh heart’ transfer

No significant benefit to delayed yet aggressive care

Long term supportive care

Recreational decompression sickness

Central Florida fresh water lake dive

Nearby trauma center; long-standing DCI tx.

facility not available 24/7 on Tuesdays!

Arrangements made via DAN to transfer

elsewhere in the state

Treatment delay but good clinical outcome

Severe carbon monoxide poisoning

Coal miner trapped for several days

University medical center receives patient; seeks HBO

Nearby hyperbaric facility will not accept

Patient transferred out of state several days later

Protracted hospitalization, incomplete recovery

What possible solutions might exist?

G-4



Reimbursement rates increased for HBO therapyinitiated outside of normal working hours

Reimbursement rates increased for all treatments for those who

maintain a 24/7 call response

Decreasing reimbursement rates to those facilities that do not

offer a 24/7 call response

This could be worked into a revenue neutral situation by

respective purchasers of health care by…

Development of a regional network of 24/7 hyperbaric

treatment facilities

Require those who don‘t offer 24/7 to contribute to the

costs of those who do

May prompt some to adopt 24/7 coverage

Health insurance companies mandate those who file claims for

HBO therapy be available to provide such therapy for all of their‘medically necessary’ conditions

Institution of any such corrective steps will require collective

involvement of the many stakeholders

Those related medical science associations

Those related safety and technology bodies

Those who underwrite health care costs

Those who regulate this technology

Those who organize and effect patient transfers

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National DisasterMedical American OsteopathicCollegeof … · 2013-09-27 · B-1 American...

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