L25 Diving and Marine Medicine

• Sea level: 1 atm, 14.7psi, 760mmHg
• 33 feet sea water (fsw): 2atm
• 66fsw: 3atm

• 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

• 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

• *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

• 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
• 

• 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%)

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

• 1. Physical obstruction:
• -lymphatics
• -vasculature
• -endothelial cell injury

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

• 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

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

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

• Primary effects:
• -Direct pressure
• -Hyper-oxygenation

• Secondary effects:
• -Antimicrobial effect
• -Blunt Ischemia-Reperfusion Injury
• -Vasoconstriction
• -Angiogenesis - stimulates vasculogenic stem cell mobilization
• -Wound healing

• 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)

• ...tissue ischemia, fibrosis, eventual necrosis
• -subsequent hypovascular lesions are frequently nonhealing
• -Grafts or flaps into an irradiated field are often unsuccessful

HBO stimulates angiogenesis

• -HBO stimulates macrophages to produce growth factors
• -Fibroblasts produce more surface GFR
• -Fibroblast proliferation rate increases after HBO exposure
• -Stimulates angiogenesis

• 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

• 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