L25 Diving and Marine Medicine

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Author:
jknell
ID:
201822
Filename:
L25 Diving and Marine Medicine
Updated:
2013-02-19 17:11:18
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Pulmonary II
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Hyperbaric medicine
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  1. Atmospheric pressure and diving
    • Sea level: 1 atm, 14.7psi, 760mmHg
    • 33 feet sea water (fsw): 2atm
    • 66fsw: 3atm
  2. Principles in diving medicine
    • Boyle's law: pressure and volume are inversely related
    • -P1V1 = P2V2

    Henry's law: amount of gas which dissolves in a liquid is proportional to the pressure of the gas in contact with the liquid

    Dalton's Law: total pressure of a mixture of nonreactive inert gasses is the sum of the partial pressures of the individual gas
  3. Diving medicine
    types of injury
    • 1. Barotrauma (pulmonary)
    • -feared injury is the Arterial Gas Embolism (AGE)
    • -nonpulmonary barotrauma: mask, sinus, ear, GI, dental...

    • -2. Decompression sickness
    • -DCS type I
    • -DCS type II
  4. Barotrauma
    pulmonary (PBT)
    • *Problem of ascent, often when the diver voluntarily (or involuntarily) holds their breath
    • Causes:
    • -Excessive intrapulmonary pressure during positive pressure breathing
    • -Failure of expanding gas to escape during ascent (breath-holding or local pulmonary obstruction)

    • Pathophysiology:
    • -Overdistension and overpressurization (transpulmonic pressure ~100cmH2O

    • Presentation:
    • 1. Local lung injury: chest pain, cough, hemoptysis (no need for recompression)

    • Pneumediastinal: most common form of PBT
    • -Substernal chest pain, dyspnea.
    • -Can lead to subcutaneous emphysema: crepitance, hoarseness, dysphagia
    • -Hamman's sign: crunching sound with cardiac activity
    • *thin line along the L heart border
    • Tx: conservative, detailed neuro exam

    Subcutaneous

    • Pneumothorax
    • -Infrequent (<10% of cases)
    • -Air vents through visceral pleura (which has greater resistance)
    • -Must exclude prior to recompression
    • (hemo-pneumo-thorax)

    Arterial gas embolism
  5. Arterial gas embolism
    • Ruptured alveoli causes air to enter pulmonary capillaries and venous circulation (systemic circulation)

    • Pathophysiology:
    • -Air blocks arteries 30-60 microns
    • -reactive hyperemia causes increased ICP, leading to systemic hypertension and loss of autoregulation
    • -opening of BBB, vasogenic edema
    • -Neuronal ATP decreases and lactic acid increases

    • AGE sudden death:
    • -large amounts of air in central vascular bed
    • -CxR shows complete gas filling of central vascular bed
  6. Arterial gas embolism
    clinical presentation
    • Presentation:
    • -Immediate death (<5% all cases)
    • -Immediate onset of sx within 10 minutes of surfacing:
    • -Chest pain, SOB, dysphagia, hoarseness
    • -Sudden neurologic symptomes (i.e. confusion, LOC, seizures, blindness, paralysis, paresthesias, focal neuro symptoms, memory, fine motor abnormalities)

    • PE:
    • -barotrauma, crepitus

    • Labs:
    • -Hemoconcentration (elevated Hct)
    • -Elevated creatinine kinase (CPK), SGOT, SGPT, LDH, Troponin

    Radiograph: only minority of patients show evidence of barotrauma with CxR

    • Dx: high clinical suspicion
    • -Any LOC or serious neurologic injury within minutes of surfacing
    • -Increased CK (may not elevate for hours)
    • -Mediastinal air (<50%)
  7. Decompression sickness (DCS)
    aka Caisson disease, Diver's palsy, the bends

    History, pathophysiology, etiologies
    History: Caissons - bridge building had workers breathing in pressurized air for long periods of time. Illness with too rapid an ascent

    • Partial pressure of nitrogen increases with depth:



    • Pathophysiology:
    • -Rapid reduction in pressure without adequate time for the elimination of N2 from the tissue (breathing it off)
    • -N2 comes out of solution and forms bubbles

    • Etiologies:
    • -divers on ascent
    • -pilots on rapid altitude changes
    • -astronauts
  8. Consequences of vascular bubbles
    • 1. Physical obstruction:
    • -lymphatics
    • -vasculature
    • -endothelial cell injury

    • 2. Activation of:
    • -platelets
    • -neutrophils (inflammatory cascade)
    • -coagulation cascade
    • -capillary permeability (increased)

  9. Decompression sickness
    clinical
    • DCS Type I: 50%
    • -Joint pain
    • -Extreme fatique
    • -Skin and lymphatic bends

    • DCS Type II: 50%
    • -Neurologic or spinal cord
    •          -paresthesias, numbness, weakness, paralysis, urinary retention
    • -Pulmonary DCS "chokes"
    • -Vestibulr DCS

    • Onset:
    • -50% present within 30 min of surfacing
    • -85% present <1hr
    • -95% present <3hrs
    • -rare (<1%) present delayed, >6hrs
  10. Treatment of DCS and AGE
    Prehospital: ABCs, position, oxygen, fluid, transport

    • Hyperbaric medicine (recompression)- rationale:
    • -decrease bubble size
    • -restore blood flow
    • -Increase diffusion gradient for N2
    • -Oxygenate hypoxemic tissues
    • -Reduce ischemia-reperfusion injury (decrase activation of leukocytes and platelets)
    • -Decrease cerebral edema
  11. Standard treatment for severe DCS
  12. Standard treatment for AGE
  13. Hyperbaric oxygen therapy
    aka HBOT, HBO, HBO2
    Breathing 100% oxygen while under increased atmospheric pressure

    • Hx: "life without blood"; surgeon kept pigs alive at 3atm after removing their RBCs
    • -able to increase partial pressure of oxygen in plasma high enough to sustain life

    • -Sea level air (PaO2 100mmHg) = 0.3 vol%
    • -3atm 100% O2 (PaO2 2100mmHg) = 6.6 vol%

    • Indications:
    • -AGE
    • -CO poisoning
    • -Gas gangrene
    • -DCS
    • -Crush injury, compartment syndrome
    • -compromised graft/flap
    • -necrotizing soft tissue infections
  14. HBO
    mechanism of action
    • Primary effects:
    • -Direct pressure
    • -Hyper-oxygenation

    • Secondary effects:
    • -Antimicrobial effect
    • -Blunt Ischemia-Reperfusion Injury
    • -Vasoconstriction
    • -Angiogenesis - stimulates vasculogenic stem cell mobilization
    • -Wound healing
  15. Gas gangrene
    • Clostridial myonecrosis caused by C. Perfringens (80-90%)
    • -Aneaerobic, spore-forming, GP encapsulated bacillus
    • -Alpha toxin is the most prevalent and lethal toxin

    • Hyper-oxygenation is antimicrobic:
    • -Multiplies freely at 30mmHg, restricted growth at 70mmHg
    • -inactivated at high pressure (>250mmHg)
  16. Radiation injury
    • ...tissue ischemia, fibrosis, eventual necrosis
    • -subsequent hypovascular lesions are frequently nonhealing
    • -Grafts or flaps into an irradiated field are often unsuccessful


    HBO stimulates angiogenesis
  17. Chronic wound healing and HBO
    • -HBO stimulates macrophages to produce growth factors
    • -Fibroblasts produce more surface GFR
    • -Fibroblast proliferation rate increases after HBO exposure
    • -Stimulates angiogenesis
  18. Central retinal artery occlusion
    HBOT
    • Sudden painless vision loss due to:
    • -atherosclerosis-related thrombus
    • -vasospasms
    • -giant cell arteritis

    -Inner retinal layer becomes ischemic

    • HBOT is successful within first 24 hours
    • -choroidal circulation may supply enough O2 to inner retinal layers by diffusion
  19. CO poisoning
    • HBOT:
    • -accelerates of carboxyhemoglobin dissociation (nl half-life is 320 min at RA; 23 min at 3atm)
    • -prevents CO-mediated brain lipid peroxidation and leukocyte mediated inflammatory changes in the brain
    • -Tissue oxygenation
    • -reduced edema

    • Indications:
    • -transient or prolonged unconsciousness
    • -CV dysfunction
    • -severe acidosis
    • -neurological impairment
    • -COHgb >25-30%
    • -Pregnancy with COHgB>15%
    • -Abnormal neuropsychiatric testing

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