Dive Medicine and Hyperbaric Therapy by ozC7Hx

VIEWS: 10 PAGES: 35

									                       Dr. Michael Feldman
Sunnybrook-Osler Centre for Prehospital Care
Objectives
 Review physics of compressed air diving
 Complications during descent
 Medical problems at depth
 Complications during ascent
 Prevention of complications
 Prehospital care of dive injuries
 Hyperbaric therapy for dive injuries
Case Report
 Veteran police diver is pulled from the water with no
  vital signs during a training exercise
 The 50-year-old diver signalled her partner that she
  had encountered some sort of difficulty
 The partner pulled the officer back into the boat and
  began administering CPR enroute back to land
 On arrival, paramedics encounter a female police
  officer with no vital signs
 The partner, a 48 year old male officer is short of
  breath and complaining of back pain
Your next steps?
 What do you want to know?
 What do you want to do?
 What triage decisions do you make?
 What resources do you need?
A brief history of diving
 Breath-hold diving for food and resources for
  thousands of years
 Evidence of Neanderthal divers 40,000 years ago
 Fires built by Fuegian Indian divers in Straits of
  Magellan to warm themselves (hence “Tierra del
  Fuego”)
 Ancient Greece and Persia recorded military use of
  diving bells (e.g. to cut anchor cables, bore holes in
  ships)
Compressed air diving
 Mid-1800’s – first practical surface-supplied diving suit
 French engineers pioneer compressed air to keep
  underwater chambers dry for work on bridge footings
 1943 – Cousteau and Gagnon invent SCUBA
 Presently has recreational, scientific commercial, and
  military applications
 Enhancements: rebreather systems, mixed gas diving
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             Physics
        Resistance is Futile.
Sea level
 1 ATM

            Effects of ambient
            pressure
 10 m
2 ATM




            Boyles Law:
            As ambient pressure increases,
 20 m
3 ATM
            volume decreases

            SCUBA delivers increasing
            amounts of gas to maintain
            normal volume against
            ambient pressure
 30 m
4 ATM
Henry’s Law
Descent                             Ascent

Increased pressure    Dissolved gas comes
increases dissolved    out of solution and
gas                              is exhaled
Descent
 Ambient pressure increases tremendously
 Body tissues act as a non-compressible fluid and the
  force is not perceptible
 Gas-filled spaces (sinuses, middle ear, lung,
  gastrointestinal tract) are compressible
 Lung is filled with SCUBA-supplied gas at increased
  pressures, which resists the compressive force of water
 Increased partial pressures in lungs responsible for
  increased dissolved gases in the bloodstream
Barotrauma of Descent
 Mask barotrauma
 Sinus barotrauma
 External ear barotrauma (if air is trapped by hood)
 Barotitis media
 Inner ear barotrauma (round or oval window can be
  ruptured by either increased pressure in middle ear or
  forceful Valsalva maneuver)
 Suit squeeze
 Dental barotrauma
 Lung squeeze (breath-hold divers, >30 m depth)
Mask Barotrauma
 As diver descends, air must be added to
  airspace between mask and face
 If the diver forgets, periorbital edema,
  ecchymosis, and subconjunctival
  hemorrhage may result
 This is usually benign despite the dramatic appearance
Sinus barotrauma
 If any of the sinuses are blocked, a relative vaccuum
  develops
 Patient presents with severe pain in the affected sinus
  (usually frontal sinus)
 On ascent, the expanding gas may result in expulsion
  of blood and mucous into the nose and mask
Barotitis Media
 During descent, pressure in
  the middle ear must be
  equalized at regular intervals
 Diver may experience ear pain
  as water pressure distorts the
  tympanic membrane
 Rupture of tympanic
  membrane will relieve the
  pain, but may be
  accompanied by severe
  vertigo as cold water enters
  the middle ear
Lung Squeeze
 Rare complication in breath hold
  diving
 “No limits” diving – men’s world record
  172 m; women’s record 160 m
 Well-documented dive in which a
  Belgian diver flooded his sinuses and
  eustachian tubes during descent;
  reached 210 m
 Lungs get compressed to very small
  volumes, causing pulmonary edema
Complications at Depth
 Nitrogen narcosis – increased dissolved nitrogen acts
 as an intoxicant, possibly by altering electical
 properties of excitable membranes
   Begins at 20-30 m: euphoria, deterioration in judgment
   70-90 m: auditory and visual hallucinations
   120 m: loss of consciousness
 Treated by ascent
 Prevented by heliox commercial diving gas mixtures
Oxygen Toxicity
 Pulmonary toxicity
    Can cause alveolar damage and pulmonary edema
    Not a problem in diving (but a consideration in
     hyperbaric chambers – breathing 100% O2 at 3 ATM)
 CNS toxicity
    Occurs when breathing 100% O2 at high ambient
     pressures
    Causes oxygen-induced seizures in hyperbaric chambers
    Treatment: removal of supplemental O2
Ascent
 Decreased ambient pressure allows gas-filled spaces to
  expand
 Decreased partial pressure of gases in lungs allows
  dissolved gases to come out solution
   Bubbles form in tissues
   Pressure in lungs forces air across alveolar membrane
   Alveolar rupture
Pulmonary Barotrauma
 Expansion of trapped alveolar gas (e.g. against a closed
  glottis)
 Divers usually have a history of rapid or uncontrolled
  ascent (out of air, uncontrolled positive buoyancy)
 A pressure difference of 80 mmHg (1 m ascent) is
  sufficient to force air across pulmonary alveolar
  membrane into interstitial space or vascular system
 May result in pneumothorax, pneumomediastinum,
  pneumoperitoneum, or arterial gas embolism
Pulmonary Overpressurization
 26 year old naval
  seaman
 One hour dive
  between 3 and 10 m
  depths
 Chest pain, neck
  swelling, hoarse
  voice immediately
  on surfacing
 Treated with 100%
  O2; resolved within
  2 days without
  sequelae
Arterial Gas Embolism
 The most dramatic injury associated with compressed air
    diving
   Air bubbles forced into pulmonary microcirculation and
    through to left atrium, where they are dispersed to arterial
    circulation
   Result in mechanical occlusion of small arteries and
    disruption of BBB resulting in cerebral edema
   Clinical presentation is usually sudden and dramatic
   Anyone who has neurologic symptoms or loss of
    consciousness within 5 minutes of surfacing should be
    presumed to have AGE
Cerebral Arterial Gas Embolism
 42 year old recreational diver with 2 years experience
 Seen to have suddenly surfaced
 When reached by the boat, he had no vital signs. His air
    tank was empty and his buoyancy compensator fully
    inflated
   CPR started immediately, with return of circulation 12
    minutes later
   Seizures and decorticate posturing in ED
   Hyperbaric treatment (USN table 6A) for 7 hours
   Now confined to wheelchair; able to carry out most ADLs
Cerebral Arterial Gas Embolism
Decompression Sickness I
 Pain in joints with the
  consequent loss of function
 The pain often described as
  a dull ache, most common
  in shoulders or knees
 The pain is initially mild
  and divers may attribute
  early DCS symptoms to
  overexertion
 Skin bends: rashes,
  mottling, itching and
  lymphatic swelling
Decompression Sickness II
 CNS, pulmonary, or circulatory involvement
 Spinal cord is the most common site for Type II DCS
 Low back pain may start within minutes and may progress to
    paresis, paralysis, paresthesias, and loss of sphincter control
   Other symptoms may include headaches, visual disturbances,
    dizziness, and changes in mental status or cognition
   Labyrinthine DCS (the staggers) causes nausea, vomiting,
    vertigo, nystagmus, tinnitus and hearing loss. Labyrinthine
    disturbances not associated with other symptoms of DCS likely
    due to barotrauma
   Pulmonary DCS (the chokes) causes (1) substernal discomfort,
    (2) non-productive cough, and (3) respiratory distress
   Hypovolaemic shock – fluid shifts from intravascular to
    extravascular space
Prevention of Decompression
Sickness
 Limit time spent at depth
 Slow and staged ascents (decompression stops) so that
  body’s burden of nitrogen is eliminated without
  forming bubbles
 USN and commercial dive tables
 Dive computers to track dive profile and calculate
  decompression requirements
 Avoidance of flight for 24 hours after last dive
 Protective effect of vigourous exercise
USN Navy Dive Table
Prehospital Care of Diving Injuries
 100% O2 to facilitate washout of N2
 Crystalloid infusion – maintains capillary perfusion for
  elimination of bubbles
 Diazepam may relieve labyrinthine vertigo (if not
  responsive to dimenhydrinate)
 ASA (bubbles may cause platelet aggregation)
 ALS procedures as appropriate (e.g. needle
  decompression)
 Transport to hyperbaric facility
Hyperbaric Oxygen Therapy
 Toronto hyperbaric
  chamber at UHN
  General site
 Multiplace chamber
  can dive to 2 to 5 ATM
 Other Ontario
  chambers in
  Hamilton, Ottawa,
  Tobermory
 Access via DAN or
  Criticall
HBOT - Indications
   Air or gas embolism
   Carbon monoxide poisoning ± cyanide
   Clostridal myositis (gas gangrene) and necrotizing soft tissue infection
   Crush injury, compartment syndrome (acute traumatic ischemia)
   Decompression sickness
   Problem wound healing
   Exceptional blood loss (anemia)
   Intracranial abscess
   Osteomyelitis (refractory)
   Delayed radiation injury (soft tissue and bony necrosis)
   Compromised skin grafts and flaps
   Thermal burns and frostbite
Recompression Treatment
                             O2
             Air breathing
Objectives
 Review physics of compressed air diving
 Complications during descent
 Medical problems at depth
 Complications during ascent
 Prevention of complications
 Prehospital care of dive injuries
 Hyperbaric therapy for dive injuries
Questions?

								
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