Objectives Review physics of compressed air diving Complications

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

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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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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

Dive Medicine and Hyperbaric Therapy 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 �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% O 2 at 3 ATM) CNS toxicity Occurs when breathing 100% O 2 at high ambient pressures Causes oxygen-induced seizures in hyperbaric chambers Treatment: removal of supplemental O 2

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 mm. Hg (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% O 2; 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 6 A) 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% O 2 to facilitate washout of N 2 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 Air breathing O 2

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

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