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
10 m
2 ATM
20 m
3 ATM
30 m
4 ATM
Effects of ambient
pressure
Boyles Law:
As ambient pressure increases,
volume decreases
SCUBA delivers increasing
amounts of gas to maintain
normal volume against
ambient pressure
Dr. Michael Feldman
Sunnybrook-Osler Centre for Prehospital Care
Henry’s Law
Descent
Increased pressure
increases dissolved
gas
Ascent
Dissolved gas comes
out of solution and
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
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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
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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
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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
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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
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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
Air breathing
O2
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?