1Topic 2.6 DCI AVMO 0019

  1. Learning Outcomes?
    • • Describe the physics of evolved gases in decompression, and the pathophysiology of DCI
    • • Describe the clinical manifestations of DCI and their diagnostic features
    • • State the pre-disposing and precipitating factors for DCI
    • • Describe methods of preventing DCI from hypobaric exposures
    • • Describe treatment of suspected DCI in-flight and post- flight
    • • Locate the reference documents regarding hypobaric exposures in the ADF
    • • Recognise, manage and recommend prevention strategies for decompression illness from hypobaric exposures
  2. Definitions Dysbarism?
    • • any disease induced by change in pressure, includes both trapped AND evolved gases
    • • decompression sickness, arterial gas embolus and barotrauma
    • • Decompression Sickness (DCS)
    • • evolved gas disease
    • • Arterial Gas Embolus
    • • pulmonary barotrauma with embolisation (usually cerebral)
    • • Decompression Illness (DCI)
  3. Decompression Illness?
    • • Decompression illness is a risk with any exposure to reduced ambient pressure and can occur in:
    • • compressed gas divers
    • • estimated to occur <0.05%
    • • aviators
    • • astronauts
    • • pressurised chamber workers
  4. Incidence of Sub-atmospheric DCI?
    • • Diving (sub-aquatic) vs. aviation (sub-atmospheric)
    • • Large diving study (DAN) with incidence of ~0.05%
    • • DCI in aerospace operations:
    • • most cases arise from hypobaric chamber training
    • • cases do happen operationally:
    • • rapid decompressions (rare)
    • • HAPO
    • • pressurisation ground checks
    • • specific risk factors in crew
    • • space
  5. PATHOPHYSIOLOGY
    Decompression Illness
  6. Inert Gas (N2) Uptake
    • • Determined by:
    • • Tissue perfusion
    • • Tissue solubility
    • • Blood solubility
    • • Rate of diffusion
    • • Temperature
    • • Tissue pH & PCO2
    • • At depth, inert gas diffuses into tissues down concentration gradient
    • • On ascent, the elimination of inert gas mirrors the process of uptake
    • Dalton’s Law
  7. The Physics of DCI - Henry’s Law?
    • At a constant temperature, the amount of a given gas dissolved in a given type & volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid
    • “Fizzyology” - “Coke Bottle Law”
  8. With a reduction in ambient pressure, a pressure differential exists between the partial pressures of N2 in the tissues &
    • environment (until equalisation)?
    • jQuery1101021855516431892696_1488026318906
  9. If a state of “supersaturation”?
    develops, bubbles can form out of solution
  10. Haldane’s hypothesis?
  11. The Physics of Bubbles?
    • • Formation of bubbles depends on:
    • • Henry’s law
    • • Haldane’s critical supersaturation theory
    • • Pre-existing conditions:
    • • Bubble micronuclei
    • • Hydrophobic interfaces
    • • Vascular turbulence
    • • Tribonucleation/ cavitation
  12. Pathophysiology of DCI?
    • Bubbles – evolved or embolic
    • Primary effects of bubble formation:
    • • fragment
    • • compress
    • • obstruct

    • Secondary effects of bubble formation?
    • • Stimulation of inflammatory processes
    • • Complement cascades
    • • Kinin
    • • Coagulation (and platelets)
    • • Damage endothelial cells
    • • Immune system eg. leucocytes
    • • Often delayed
  13. Venous Gas Emboli?
    • • Arise de novo
    • • low pressure
    • • flow in venous plexi may favour formation
    • • promoted by presence of micronuclei
    • • Effects:
    • • haematological consequences
    • • venous infarction
    • • embolic via right heart to the lungs
    • • Increase in MPAP
    • Incidence of VGE
    • • Poor correlation to clinical DCI
    • • Measured by precordial Doppler US
  14. Arterial bubbles?
    • • Unlikely to form de novo
    • • High pressure
    • • Rarely supersaturate
    • • Arise via:
    • • VGE (paradoxical gas embolism)
    • • R to L shunts (eg. PFO)
    • • Passage through bubble filter
    • • Pulmonary barotrauma
    • • Effects:
    • • Damage endothelium
    • • Strip surfactant
    • • Increased permeability
    • • Haemoconcentration
    • • Activate inflammatory cascades
    • Role of PFO
  15. • Incidence - ~30% of general population?
  16. Theoretical risks:?
    • •R to L shunting
    • •Increased R atrial pressure (eg. lung bubble load)
    • •CAGE
    • •Anti-G straining
    • •PPB
  17. Manifestations of DCI?
    • • Musculoskeletal
    • • Cutaneous
    • • Gastrointestinal
    • • Cardiopulmonary
    • • Neurological
    • • Peripheral nerves
    • • CNS
    • • Cerebrum
    • • Cerebellum
    • • Spinal cord
    • • Audio-vestibular
  18. DCI in Aerospace Operations?
    • • First symptom is almost always joint awareness or discomfort
    • • May be masked by operational distractions
    • • Staying at altitude leads to evolution/ more severe symptoms
    • • Many resolve on recompression to sea level
    • • differs from sub-aquatic DCI
    • • “Landing is treatment”
    • • ALL require presentation to Health Services
    • • Joint pain - 60 %
    • • usually knee, shoulders, elbows
    • • Neurological - 34%
    • • motor, sensory, visual, cerebellar
    • • Both - 23%
    • • Respiratory - 8%
    • • Collapse is rare in aviation
    • • 1 in 140 cases, 136,000 exposures
    • • 40-54% have symptoms persisting on return to sea level
  19. Musculoskeletal DCI?
    • • “The Bends”
    • • Peri-articular joint pain is the most common symptom
    • • minor niggle to severe pain
    • • Onset usually early, but can be delayed (24-48 hrs)
    • • Better with pressure, worse with use
    • • Migratory polyarthralgia/myalgia
    • • Examination is usually unremarkable
    • • Exact cause of bubble-induced pain is uncertain:
    • • ?peri-osteum, medullary cavity, ligaments or tendons
    • • ?due to mass effects &/or inflammatory mediators
  20. Cutaneous DCI?
    • • “The Creeps”
    • • Subcutaneous bubble formation
    • • Initiates inflammatory reaction, generally causing symptoms such as pruritis or hyperaesthesia
    • • May also have erythematous macular rash/marbling
    • • Severe form is “cutis marmorata”
  21. Respiratory DCI?
    • • “The Chokes”
    • • Lungs act as “bubble filters”, but can be overwhelmed
    • • This can lead to arterial bubbles
    • • Increase in pulmonary venous pressure
    • • Can lead to shunting across PFO
    • • Pain, chest tightness, cough
    • • Rare - ?other causes with similar presentation
    • • Beware associated pulmonary barotrauma
  22. Neurological DCI?
    • • Neurological DCI includes:
    • • Brain
    • • Cerebrum
    • • Cerebellum - “The Staggers”
    • • Spinal cord
    • • Peripheral nerves
    • • Inner ear
    • • Embolic vs autocthonus
    • • de novo bubble formation in the brain is unlikely due to the large perfusion such that supersaturation is unlikely to develop
    • • most cases of CNS DCI are consistent with a vascular event (CAGE)
    • • bubbles can cause secondary CNS effects due to BBB permeability changes and initiation of inflammatory reactions
    • • Symptoms are varied in both presentation and severity
    • • eg. mild short-lived paraesthesia to permanent paralysis
  23. Spinal cord DCI?
    • • Multiple possible aetiologies:
    • • vascular
    • • arterial emboli
    • • venous infarction
    • • compression - tissue bubbles
    • • Poor prognosis generally
  24. Other Symptoms of DCI?
    • • Constitutional DCI
    • • Non-specific symptoms such as malaise, lethargy, headache, myalgias
    • • likely secondary to inflammatory activation
    • • Lymphatic DCI
    • • Lymphoedema, unusual swelling
    • • Inner ear DCI
    • • Need to distinguish from inner ear barotrauma
    • • Unique inert gas kinetics of labyrinth – very rare in aviation
    • • Other effects:
    • • Haemoconcentration, pro-coagulant
  25. Cerebral Arterial Gas Embolism (CAGE)?
    • • Rare in aviators, incidence unknown
    • • Typically due to breath holding with diving
    • • increased risk with pulmonary disease that can predispose to gas trapping or shearing forces
    • • can occur at trans-pulmonary pressures of >60-80mmHg (eg. ascent to surface from ~1m depth!)
    • • Usual presentation is sudden collapse immediately or very soon after decompression
    • • Gas embolism can also affect other vascular beds
    • • eg. coronary, splenic, hepatic, renal
    • • Don’t forget PBT (risk of pneumothorax)
  26. RISK FACTORS Decompression Illness Predisposing Factors?
    • • Most important risk factors are:
    • • “Dose”
    • • altitude/pressure
    • • duration of exposure
    • • Rate of decompression
    • • ?pre-oxygenation
    • • Risk factors for DCI classified as:
    • • Individual
    • • Sortie
    • • Post-sortie period
  27. Predisposing Factors DCI?
    • • Individual risk factors:
    • • Anatomy, eg. PFO, other shunts
    • • Physiology:
    • • Likely - age and fitness
    • • Unproven - BMI (body fat %), gender), diet (fat), hydration
    • • Individual susceptibility - increased risk if previous DCI
    • • Sortie risk factors:
    • • Recent exposure to hyperbaric environment
    • • eg. SCUBA, aircraft pressurisation testing, HEED training
    • • Sortie profile – repetitive, high altitude
    • • Exercise
    • • Cold
    • • Post-sortie risk factors:
    • • Level of exercise post-sortie
    • • Rewarming
  28. Flying after diving ?
    • • DI(AF) OPS 6-13 (DI(G) OPS 22-1)
    • • No decompression diving
    • • CA<8,000ft – TMUFF 12hrs for aircrew; 9 hours others
    • • CA>8,000ft – TMUFF 48hrs for all
    • • Decompression diving
    • • CA < 8,000ft – TMUFF 24 hrs
    • • CA > 8,000ft – TMUFF 48hrs
  29. • Flying after HEEDs/HABD ?
    • 9hrs for Navy, ?for Army
  30. • Flying after chamber runs ?
    • • Traditional
    • • CADO (nil restriction)
  31. Individual susceptibility?
    • Reports of unprovoked DCS at:
  32. Decompression Illness Prevention?
    • • Operational sortie (“dose”) limits:
    • • Altitude limits
    • • Minimise time of exposure
    • • Denitrogenation (pre-oxygenation)
    • • Keep warm
    • • Pressure suits
    • • Mission planning
    • • DI(G) OPS 22-2
    • • Only fly when healthy
    • • Do not fly after compressed air diving
    • • Restrictions depend on gas mix and dive profile
    • • DI(G) OPS 22-1
    • • Pre-oxygenation regulations
    • • DI(AF) OPS 3-5
    • • AVMED SI(OPS) 1-1
  33. Pre-oxygenation?
    • • 100% oxygen (good seal required)
    • • Longer = better (diminishing returns)
    • • Enhanced by exercise
    • • 30 mins eliminates ~30%
  34. Decompression Illness Treatment Aircrew Immediate Actions?
    • • Descend ASAP
    • • Use 100% oxygen
    • • Keep warm
    • • Minimise activity
    • • Declare emergency
    • • Seek AVMO review
  35. Decompression Illness Treatment Medical Management?
    • • Patient positioning
    • • 100% Oxygen
    • • IV Fluids
    • • Pharmacological adjuncts
    • • Recompression
    • • Transport
  36. DCI & Collapse?
    • • Manage as with all unconscious patients
    • • DRABCDE:
    • • AIRWAY (& c-spine)
    • • BREATHING (100%O2)
    • • CIRCULATION
    • • DISABILITY
    • • ENVIRONMENT
  37. Medical Report on an Aircraft Incident or Accident?
    • • Notifications:
    • • AVMED on call SAVMO (24/7) - 24/7 - MUST be notified ASAP for hypobaric DCI in aircrew
    • • SUMU (HMAS PENGUIN 24/7) - should be contacted as soon as practicable to seek advice and to notify if an ADF member needs recompression
  38. DCI History & Examination?
    • • Signs and symptoms
    • • Medical history
    • • symptoms
    • • evolution
    • • Response to landing/Rx
    • • Risk factors
    • • Sortie history
    • • Sortie profile (inert gas load)
    • • breathing gas
    • • ?pre-oxygenation
  39. DCI History & Examination>?
    • • Systems review
    • • Other injuries
    • • Neurological examination
    • • including MMSE
    • • if stable
    • • thorough
    • • including mini mental state
    • • sharpened Rhomberg’s
    • • Do not stand up if CAGE
  40. DCI Investigations?
    • • DCI is a clinical diagnosis
    • • Ix indicated to exclude other:
    • • Bloods
    • • FBC (increased Hb & Hct)
    • • Biochem
    • • BSL
    • • CPK (elevated in CAGE)
    • • Radiology
    • • CXR
    • • CT
  41. DCI Positioning?
    • • Supine
    • • Do not sit/stand up to examine or transfer if risk of CAGE
    • • Head down not recommended
    • • May contribute to cerebral oedema
    • • Airway challenges
    • • Increases venous return – more bubbles centrally
  42. DCI Oxygen Therapy?
    • • 100% oxygen is mandatory
    • • Don’t forget risk of oxygen toxicity
    • • Must be a good seal
    • • Aviators mask ideal, often impractical
    • • Enhances denitrogenation
    • • HD130 - For “pain only” DCI which resolves
    • • 2 hrs normobaric 100% oxygen and observe
  43. DCI Pharmacological Adjuncts?
    • • Analgesics
    • • Paracetamol +/- opioids PRN
    • • Avoid aspirin
    • • NSAIDs ?
    • • Lignocaine infusion
    • • promising initial studies of benefit in cerebral protection in neurological DCI/CAGE
    • • more recent evidence ?
    • • monitoring requirements are challenging
  44. DCI Recompression?
    • • HD130 - symptoms that clear on descent with normal neurological exam
    • • 100% oxygen for 2hrs
    • • aggressive hydration
    • • observe 24hrs and re-evaluate
    • • recompression may not be required
    • • Always discuss with AVMED +/- SUMU
    • • unfit to fly 72 hours
  45. DCI Recompression?
    • • Symptoms that persist at ground level or recur  recompression
    • • 100% oxygen
    • • IV fluids
    • • hyperbaric therapy
  46. In all cases the nearest hyperbaric facility must be consulted?
  47. Recompression Aims:?
    • • Reduce the size of bubbles (pressure effect)
    • • Denitrogenate bubbles (oxygen effect)
    • • increase diffusion gradient out of bubbles
    • • Relieve ischaemia and hypoxia
    • • help restore normal tissue function in affected areas
    • • Some anti-inflammatory effects
  48. Quiz question 12
    • Patent foramen ovale is thought to increase risk of clinical DCI in aviation activities which:
    • a. Decrease right atrial pressure
    • b. Increase left atrial pressure
    • c. Increase pulmonary artery pressures
    • d. Increase right atrial pressure
  49. Quiz question 13
    • An example of a “fast tissue” in which nitrogen uptake and washout are rapid is:
    • a. Bone
    • b. Muscle
    • c. Fat
    • d. Tendon
Author
david_hughm
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1Topic 2.6 DCI AVMO 0019
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1Topic 2.6 DCI AVMO 0019.txt
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