Dive Medicine Aide-Memoire Lt(N) K Brett Reviewed by LCol A Grodecki Diving Physics Physics

• Air ~78% N2, ~21% O2, ~0.03% CO2

Atmospheric

Absolute Pressure Hydrostatic/ gauge Pressure Hydrostatic/ Gauge Pressure Conversions • Hydrostatic/ gauge pressure (P) = • 1 bar = 101 KPa = 0.987 atm = ~1 atm for every 10 msw/33fsw ~14.5 psi • Modification needed if diving at • 10 msw = 1 bar = 0.987 atm altitude • 33.07 fsw = 1 atm = 1.013 bar • Atmospheric P (1 atm at 0msw) • Absolute P (ata)= gauge P +1 atm • Absolute P = gauge P + • °F = (9/5 x °C) +32 atmospheric P • °C= 5/9 (°F – 32) • Water virtually incompressible – density remains ~same regardless • °R (rankine) = °F + 460 **absolute depth/pressure • K (Kelvin) = °C + 273 **absolute • Density salt water 1027 kg/m3 • Density fresh water 1000kg/m3 • Calculate depth from gauge pressure you divide press by 0.1027 (salt water) or 0.10000 (fresh water) Laws & Principles • All calculations require absolute units • Henry’s Law: (K, °R, ATA) • The amount of gas that will dissolve in a liquid is almost directly proportional to • Charles’ Law V1/T1 = V2/T2 the partial press of that gas, & inversely proportional to absolute temp • Guy-Lussac’s Law P1/T1 = P2/T2 • (pp) – pressure • Boyle’s Law P1V1= P2V2 contributed by a single gas in a mix • General Gas Law (P1V1)/ T1 = (P2V2)/ T2 • To determine the partial pressure of a gas at any depth, we multiply the press (ata) • Archimedes' Principle x %of that gas Henry’s Law • Any object immersed in liquid is buoyed up by a equal to of the fluid • Gas molecules enter liquid – add to gas displaced by the object tension (=partial press gas in liquid) • Pressure gradient = Δ between gas • Daltons’ Law P(total) = P1+P2+…+Pn tension in the liquid and gas partial • The total pressure exerted by a mixture of gases is the sum of the that press outside liquid would be exerted by each gas if it alone • High gradient (low tension high PP) = high were present and occupied the total rate absorption of gas into liquid volume Physiologic Implications Underwater Apparatus Physiologic Implications Underwater Breathing

• Increased CO2 levels • Immersion Effects • CO2 retention if breathing inadequate • P Δ feet to chest ~120cm H2O, to eliminate CO2 produced. negative static lung load dev when • Common in all diving due to ↑WOB lungs deeper than reg/counterlung • Immersion effects • Fluid shift to central circulation • Gas density • ↑cardiac afterload, ↑blood to lungs = • Equipment effects ↓lung compliance, ↓ VC, ↑ airway resistance, • Exacerbated by exercise/work, , , dynamic airway • Equipment Effects compression • All underwater breathing equipment • Gas Density increases breathing resistance • i.e. Demand valve, in • increased depth = increased density helmet/face masks/hoses (Gas law) = decreased flow • Movement of CO2 from blood to (Poiseuille’s law) = increased WOB lungs based on gradient/press Δ

• – if inhaling Co2 = smaller Δ = less CO2 ventilated Dynamic Airway Compression (DAC)

 • Normal Expiration – gas flows out   along airway because P1 >P2 • P1 -> P2 declines more quickly with  Palv P1 P2 dense gas   • At some point along the tube,  airway P = intrapleural P (Ppl ) = equal pressure point (EPP) Equal • Beyond this point, P along airway is Pressure less than Ppl = airway compression     Point • Catch 22  P  Pl • Harder you try to exhale,   • higher the PPl = shift EPP to the left  • ↑ WOB which ↑ CO Palv P1 P2 2   • Distal movement of EPP  • Increased a/w resistance (, gas     density), reduced lung elastic recoil, negative static lung load Gas Issues in Diving Gas Issues • TOO MUCH

• O2, CO2, inert gas narcosis, High Pressure Neurological Syndrome • TOO LITTLE • , hyperventilation • WRONG GAS • CO poisoning, contaminants Toxicity Ocular OxTox

• Toxic effects due to PPO2 (not %) • Decreased peripheral vision • CNS main concern but pulm may ~2.5-3.0 hrs at 3.0 ATA become an issue with extended • Central vision unaffected, usually dive ops (serial bounce, sat) resolved within 30-45mins after treatment stops • PPO2 limits CF diving • Progressive myopia • 1.6 ATA routine • Generally 2-4 weeks of treatment • 1.8 ATA exceptional (requires CO and usually completely reversed sign-off) after ~3-4 weeks (sometimes up to 1 year) • DM, elderly more susceptible • Unclear whether hood/monoplace increase risk vs. facemask CNS Ox Tox • Vision changes (↓acuity, dazzle, lat • Risk Factors movement, constricted fields) • Exercise • Ears (tinnitus, auditory hallucinations, • Hyper/ music, bells, knocking) • , • Immersion • Nausea/vomiting • Metabolic activity, blood flow to brain • Twitch (lips, cheek, eyelid, tremors…) • Hypoglycemia (DM) • Irritability, behaviour, mood changes • Seizure D?O, +/- meds that lower sx (incl apprehension, apathy, euphoria) threshold • VitE deficiency • Dizzy • Pseudoephedrine, amphetamines, ASA, • Convulsions acetazolamide • Spherocytosis, hypercortisolism • Also pallor, sweaty, palpitations, brady, tachy, panting, grunting, unpleasant gustatory/ olfactory sensations, CNS OxTox • No consistent pre-convulsion • Tx warning sx • Remove O2 Often not preceded by other sx • Protect from injuries if seizing • • Check DDx (don’t forget hypoglycemia) • O2 convulsions not inherently • Keep patient off O2 for 15 mins after all sx harmful are gone • Ignore treatment time lost and resume • No pathologic changes in human table where last interrupted brain, no evidence of clinical sequelae • Don’t forget to compensate for extra • No apparent predisposition to future time for chamber attendants sz disorder • Preventive Measures • Harm based on context (seizure • Air breaks underwater = ) • Clinical HBOT setting (rarely used) • Glutathione • Very high intra & inter-individual • Lithium variation in susceptibility • GABA agonists • ?increased risk with drugs that lower sz threshold (not much evidence) Pulmonary • Cumulative dose = fx of exposure time, ATA, and • Acute Exudative (reversible) FiO2 • Interstitial and alveolar edema, hemorrhage, • Acute Δ with FiO2 > 0.8 ATA destruction of pulm capillary endothelium, • Chronic Δ with FiO2 > 0.5 ATA loss of type I alveolar cells (), inflam. cell infiltrates • Typically insidious mild substernal irritation, chest tightness -> ↑ -> constant burning • Acute Proliferative (non-reversible) exacerbated by inspiration -> dyspnea (exertion or • Type II alveolar cells replace damaged type I rest) (blood-air barrier thickens), fibroblast • ~12-16 hrs @ 1 ATA, ~3-6 hrs @ 2.0 ATA infiltration, increased alveolar-capillary • CXR usually N, +/- patchy infiltrates distance, ↓alveolar air vol, ↑collagen content • Mechanical fx impaired earlier than • Chronic (CO diffusing capabilities) • Progressive , similar to • No change FEV1 ARDS • ↓FVC • Preventions: • 2%, asx, completely reversible over hrs • Air breaks • 10% = mild sx, reversible over several days • Unit Pulmonary Toxicity Dose (UPTD) • 20% = mod sx, probably reversible over • 1 UPT = pulm poisoning produced by 100% O2 weeks, acceptable for a TT x 1 min at 1 ATA • ↓ capacity, FEF 25-75, V/Q defect • HBOT Max 1440 UPTD/24hrs (TT6 = 750 UPTDs) CO2 Toxicity • Inadequate ventilation • S/Sx • Helmet diving, hyperbaric chamber • H/A, flushing, sweating • Alveolar hypoventilation • Dizzy • Dyspnea • Higher inspired CO2 = failure of CO2 scrubbers in systems • Decreased cognition, disorientation • LOC/convulsions • CO2 retention (increased WOB • Makes everything else worse (NN, underwater) OxTox) • Increased CO2 levels unpredictable, even in normal healthy divers • Tx • End dive • Inadequate pulmonary ventilation • Fresh air, +/- O • Increased density of gas 2 • Deliberate hypoventilation or ‘skip- breathing’ – NEVER skip breath, esp. at high PP “Rapture of the deep” • Reversible depression of neuronal • S/Sx excitability due to inert gas • ↓performance mental/manual work • Potency Xe > Kr > Ar > N > H > Ne > (higher fx affected most) He • Dizzy, euphoria, uncontrolled laughter • Interfere with transmission of EP • Overconfidence, overly talkative across synaptic gap • Memory loss/post-dive amnesia • Immediate onset at depth, stable after • Perceptual narrowing (fixation) few mins at depth, rapid resolution • Impaired sensory functioning upon ascent • LOC >100msw • Potentiated by ↑CO2 levels • Prevention • No true acclimatization, divers may • Depth <30msw, plan dive ahead & dev short term tolerance practice tasks • RFs • If affected – decrease depth • Depth, gas mix, , , • cold, fatigue, exercise, EtOH, sedatives, ↑CO2 High Pressure Neurological Syndrome (HPNS) • General excitation of brain • Prevention • Opposite to narcosis • Diver selection • Occurs in very >16 ATA • ↓compression rate, long • Usually Heliox mixtures at this depth stages/holds (allow adaptation)

• Affected by rate of compression • Use of N2 (or other narcotic) in • Rapid rate = increased severity at shallower depth • S/Sx • Marked tremor hands/arms/whole body, dizzy, anorexia, nausea, vomiting • Fatigue, • Can progress to myoclonic jerks -> clonic seizures Hypoxia • Same sx as on the surface • Shallow-Water Blackout • Important to know onset for • Breath-hold diving rebreathers • Remember – CO2 produces drive to breathe • Open circuit • Hypoxia at depth – almost never O • Hyperventilation reduces CO2 2 levels below normal levels issue, gen CO2 issue • Hypoxia at surface – almost always • O2 levels may fall to a level causing LOC before CO increases to O2 issue 2 breakpoint trigger for breathing • Closed circuit LOC underwater is never a good • Hypoxia – sensor failure • thing… • Prevention • Maintain gear & checks • Don’t run out of CO Toxicity • Typically contaminated air from • S/Sx improperly directed compression • Headache, N/V, dizzy, weakness, vision engine exhaust changes, disorientation, ↓LOC, auditory dysfunction, cardiac arrhythmias, skeletal • Pathophys muscle necrosis -> ARF, pulm edema • CO relative affinity for Hb 250x greater than • Concomitant smoke inhalation sx O2 • Cherry red skin colour rare, very late • ↓O2 carrying capacity, ↑unbound Hb = left shift = ↓tissue/intracellular O2 • CO best assessed by blood • Disturbs mitochondrial e- transport, ↑NO carboxyhemoglobin (COHb) radicals, peroxidation in brain • Mortality/morbidity not correlated with • Cerebral vessels dilate, ↑coronary blood COHb level flow with ↓central resp -> cerebral hypoxia • Pulse oximetry overestimate arterial O2 & cardiac arrhythmias • Acute mortality often due to ventricular • Tx arrhythmias due to hypoxic stress, • ABCs, preserve airway myocardial impairment • Ventilation, oxygenation • HBOT hastens CO dissociation beyond rate achievable by surface 100% O2 Illness DCI • (DCI) includes DCS and • Diagnosis – generally hx, estimation of AGE likelihood • ~1-10/10,000 dives • Sx depend on location of insult • Higher in cold water, deep; lower in recreational • <24 hrs possible, >24 hrs unlikely, >36 hrs warm water diving (1-4/10k) very unlikely, >48 hrs almost impossible • Traditional/Golding Classification unless altitude change • Type I (MSK, skin, lymph, fatigue) • There is no pathognomonic test for DCI • Type II (neuro, cardio-resp, ENT, shock) • AGE • Tx 100% Surface O2 • Descriptive/Francis Smith Class • • Evolution (spontaneous recovery, static, relapsing) • IVF • Progressive (increasing #, severity of s/sx) • Evacuation considerations • Organ System • Airway, foley, pressurized cabin or as low as • Neuro, cardio-pulm, MSK, skin, lymph, ENT possible • Time of onset (before or after surfacing) • HBOT • Gas burden • Low (conservative within NoD), Med (D Dive), High (violation dive table) • Evidence of DCS Pathophysiology • Henry’s Law – amount of inert gas • Inflammatory & thrombogenic absorbed by blood/tissue increased at processes depth • Association with oxidative stress, microparticles • Boyle’s Law P1V1= P2V2 • Bubbles biologically active – form • Bubble effects plasma-protein coat activating WBC, plts, • Intravascular - embolism, vasospasm, fibrin web ischemia, transbolism, venous stasis, • “Thick skin” stabilizes bubble, decreases hemorrhage, blood-bubble interactions, diffusion of inert gas out of bubble mechanical stripping of endothelial cells • Recurrence of sx likely due to secondary • Extravascular -tissue disruption, tearing, rxn vice initial bubble hemorrhage, localized “compartment syndrome” – ischemia, stasis • Typically peri-alveolar capillary network ‘traps’ venous gas – but can be overcome (# bubbles, repet diving) Cutaneous, PNS • Cutaneous angio-lymphangiologic • PNS DCI • All that tingles is not the bends!!! • Erythema, lymphedema • Don’t forget about non-dysbaric • Cutis Marmorata – neuropraxias: ulnar, median, inferior • Venous congestion, infl, WBC brachial plexus, lateral cutaneous activation, and endothelial damage femoral and sciatic • Associated with pulmonary and neuro • Tight wet suit, weight belts, heavy DCI, thus requires careful monitoring equipment, BCD straps, sitting on side • Cutaneous diffusion of boat etc. • ‘Diver’s Lice’: erythematous rash, typically with dry chamber dives or dry suits • ?inert gas enters skin directly, causing dermal bubbles and histamine release on decompression • Benign, no RCC required • Tx if dx in doubt MSK • Most common presentation of DCS • MSK speculation • “Bends” typically only affects long • Unk if any long-term effects for #2-3 bones of appendicular skeleton if no RCC (if this is DCS) (not axial skeleton) Pain Potential Cause • Adult long bones contain fatty 1. Localized Affected by Tendon/muscle marrow cavity ?reservoir for inert gas sharp movement injury • Pain mechanisms (this is what • Intra-articular moves) • “Niggles”/ marginal DCS if mild sx that 2. Localized Unaffected by Local infl; begin to resolve 10min after onset sharp movement (?DCS) • Peri-articular - (within tendon, muscle); “niggles” if brief “diver rubs at it” • Medullar/sinusoids - gas expansion 3. Poorly Affected by Intra-articular, within medullary cavity, fatty marrow localized, deep movement joint capsule and bone sinusoids boring pain tension; (?DCS) • Referred pain - injury to nerve roots assoc with joint, generalized release 4. Poorly Unaffected by Bone medulla of infl modulators localized, deep movement injury (DCS!) boring pain Spinal Cord DCS Pathophys • Spinal cord white matter in a C-shaped area around the spinal cord grey matter • Autochthonous bubbles – spontaneous bubble formation in spinal cord white matter • Watershed zone between ant and post spinal • Direct axon destruction with 2° effects cord circulation – susceptible to both inert gas (hemm, infl, stretch/compress) accumulation and bubble-related ischemia • Explains rapid onset, lesions in white • Cervical and lumbar enlargements particularly matter vulnerable • But how are these small isolated lesions able to produce such significant sx? • Presentation is likely combo of interacting • Hemorrhage and inflammation compressive/ ischemic mechanisms • Observed in same areas where • Gas embolism autochthonous bubble injuries were seen • But blood flow favours embolization to the brain, and experimental spinal cord • Could explain why some cases of rapid embolism generally produces grey onset spinal cord DCS resistant to matter pathology vs. white matter recompression • Venous infarction – bubble accumulation in epidural venous plexus • Can’t explain ultra-short-latency cases • Usually produces grey matter lesions, not white like DCI IE DCS Pathophys Theories 1. Counter diffusion 3. Explosive/hemorrhagic • Conditions where inert gas in middle ear • Gas accumulation in temporal bone differs from gas in the breathing mixture osteoclast pockets that explosively (gas switch) rupture into inner ear during • -> Diffusion through round/oval window decompression could result in accumulation of inert gas • Plausible for deep mixed diving, blow-up with bubbling from saturation • Blood supply to inner ear isn’t uniform (stria vascularis supplies endolymph 4. Embolism directly, then diffuses to perilymph) • Inner ear blood supply is end-arterial, • Endolymph could rapidly take up new inert thus would be prone to embolic or gas before perilymph had time to eliminate vascular injury former inert gas -> bubbles form in endolymph 2. Gas induced osmosis • Similar to #1, inert gas accumulation in endolymph induces osmotic fluid shift toward endolymph -> hydrops endolymphaticus (similar to Meniere’s) AGE • Subset of DCI • S/Sx • ~1/5000 USN experimental dives • Rapid onset <10 mins, rapid progression • Low among mil working divers on standard tables, • Neuro sx occurring immediately after surfacing (esp. ~1/10k shallow, short dive) should be considered AGE until • 2nd most common cause diving fatalities proven otherwise • Australian dive fatalities 1972-2005, AGE cause in 25% of • +/- POS Sx cases (2nd most common) • Neuro deficits based on bubble location (LOC, • Mechanisms , paresis, sensory loss, , aphasia, • PBT visual loss (field >acuity), , ataxia, seizure, isolated personality or cognitive change etc.) • Intracardiac shunt (“safe dives make bubbles”) • +/- neuropsychiatric, EEG changes • Trans-pulmonary shunt • 5% dead on the spot –cardiac • A-V or bronchopulmonary fistula (rare) • Systemic hypertension and bradycardia • In-situ bubble formation (not likely) • Liebermeister’s sign (sharply demarcated pallor on • 50% diving cases no identified cause, most one half of tongue) neuropath info from iatrogenic CAGE • CK increased with peak 12hrs post onset • DDx: Neuro DCS, CVA, carotid artery • Correlates with severity, outcome (<1000 likely full dissection, cardiac, other neuro process resolution) • MR head: nothing -> focal or multifocal ischemia -> • RFs – same as POS edema AGE • Tx - ABCs • Complications • Supine, recovery position if LOC or airway not • Relapse seen in ~30% as late as 68hrs controlled • Edema, re-embolization, ischemia reperfusion, • 100% O2, euvolemia with IVF (RL) endothelial damage, • +/- ETT (low press/volume) • Concurrent DCS – can be resistant to Tx • Lidocaine (neuroprotective) 1mg/kg slow IV bolus, then 1-4mg/min (*controversial, may lower sz • Drowning threshold) • IV Benzo for seizures, agitation • Investigations • Chest tube if concurrent pneumo • Carotid Doppler, contrast echo, CXR, CT • HBOT - TT6 or Comex 30 chest, MRI brain (residual damage), PFTs • ?Helium benefit after CVA (Comex 30 on 50/50) • Tx until plateau (h/a not indication for re-tx) • Prognosis/RTD • Medevac ASAP – pressurized aircraft • Most have good outcome w/ resolution if prompt tx to 1 ATA, or fly as low as safely • R/O predisposing factors possible • ? Risk of recurrence if no RF identified • Unknown if 2nd occurrence means worse outcome than 1st • AUMB decision RTD • Any residual sx – unfit dive • Asx after HBOT – case-by case Pulmonary Barotrauma Pulmonary Overpressure Syndrome (POS) • POS • ? Role of obstructive airways. Mixed evidence • , subQ emphysema • FEV 1 has low correlation to PBT risk • (rarely seen in diving) • MEF 25 has moderate correlation to PBT risk • AGE • FEV1/FVC does not correlate • Asthmatics don’t bear a much greater risk for diving-related • Overexpansion of lungs (breathing compressed intrinsic PBT than non-asthmatics gas) & can’t properly ventilate expanding gas • 50% of PBT/AGE survivors, no abnormality of lung fx volume with ↓press detected • Boyle’s law: Largest volume changes near surface, breath- ? Role of compliance hold ascent from 4fsw sufficient • • Pathology more consistent with shear than rupture, implies • Air tracks along bronchi to outside the lung, or into regional differential compliance adjacent blood vessels FVC correlated with PBT risk • Extrinsic: breath-holding on ascent – panic, out of air, • buddy breathe, , sub escape • Chest binding (reducing relative regional difference in compliance) ↓risk for PBT • Intrinsic – obstruction or -> local air trapping, Δlung tissue compliance • Higher incidence PBT while immersed vs RCC (pulm blood pooling with immersion reduces interstitial compliance) • Most pathological studies indicate shear at • Pathology - weak correlation between shear site and terminal bronchioles and marginal alveoli rather location of pre-existing scars/fibrosis than rupture of alveoli • ?Blebs and bullae • COPDers with B&B don’t have ↑incidence of PBT during HBOT (BUT no immersion, slow ascent rates) • B&B found post PBT may be either cause or consequence POS • S/Sx • Screening – controversial • Asx or if sx, usually on ascent or shortly after • CXR low predictive power surface – cough, , CP, SOB, resp distress, • CT – many abnormalities (?clinical significance), pleuritic/substernal CP expensive, ++radiation • +/- sx of AGE • Spiro – poor correlation to PBT risk • Pneumomediastinum – decreased heart sounds, • FEF 25-75% abnormalities – small airway Fx (ensure dysphonia (brassy, monotone), Hamman’s sign, adequate curve before interpreting numbers) recurrent laryngeal paresis, pseudo-tamponade • MTC – not adequate sens/spec • SubQ emphysema – crepitations felt in soft tissues • Asthma Exercise Challenge • CXR • 80% HHR x 8 mins with FEV1 at 15, 30, 60 mins post • FEV1 decrease by 15% or more is positive • Free gas at margin of heart/vessels, pseudo- pneumopericardium, subQ gas • Eucapnic voluntary hypercapnea, hypertonic (4.5% saline) and mannitol • Pneumothorax • • Disposition (case by case) • Intravascular gas with massive AGE • CDSM/AUMB based on cause, investigations • Tx - ABCs • PFT, HRCT (insp, expiration) • ‘Deserved’ with normal f/u invs – potential RTD • O2 • ‘Undeserved’ or persistent sx/pathology – likely • Needle deco/CT for tension pneumo (rare) unfit diving • RCC only if AGE • Supportive SC/mediastinal emphysema • ER/Thoracic referral – urgency based on sx PBT of Descent (Lung Squeeze) • Risk with deep breath hold diving • As descend, compresses lungs (Boyle’s law, gas is compressible) • At surface, hold ~6L • At 6 ATA (50 msw) ~1L • Breath hold divers go much deeper than this! >150msw • Lungs begin to fill with fluid and blood, now more liquid and less compressible Non-pulmonary Barotrauma Non-pulmonary BT • Sinus Squeeze • Treatment is symptomatic • 12% divers experience • Nasal, PO decongestants • Air trapped in sinus (i.e. sinus passageway • Abx if dev infection blocked) decreases in volume as you descend • Refer if # • Can “suck” soft tissues into gas space -> blood vessels engorge and leak blood • RFs • Blood will often drain during ascent • URTI, allergic rhino-, acute or chronic • Air expands, open passageway infectious sinusitis, nasal polyps, mucosal • H/A commonly accompanies retention cysts, deviated , congenital osteo-meatal dystrophy, • Sinus BT Wegener’s, medicamentosa • Air in sinuses that expands on ascent • Prevention • Don’t dive with URTI, , nasal S/Sx deformities (deviation, polyps) • • Caution med use while diving – can wear off • Pain, press, bloody nasal discharge, odontalgia • ENT referral PRN, eg if recurrent Non-pulmonary BT • Mask/Face Squeeze • Dental BT (rare) • Air in mask also follows Boyle’s law • Air trapped within tooth expands on ascent or • Need to add air to space during descent air pocket distorted during descent otherwise gas compressed and “sucks” facial soft • Decay, dental surgery, improper/loose fillings tissues/eyes in • Tx: Dental assessment, analgesia • Tx largely symptomatic • Prevention • Prevention - ensure to equalize your mask • Dental hygiene, dental fillings replaced if loose, during descent ?appropriate time between dental surgery & • Suit Squeeze diving • Air in drysuit compresses against skin on • GI BT (rare) descent, skin forced into folds • Air expands/contracts in GI tract • Seal around can constrict • Perf rare – if occurs likely lesser gastric • Tx – symptomatic (ensure DDx) curvature with panic ascent • Prevention - light garment under suit, ensure • Prevention - avoid swallowing gas (anxious, adequate air layer nausea, head down ascent with Valsalva, excess reg press) • Ear Squeeze/BT • If on ascent, stop and remove gas • See ENT section Non-Dysbaric Dive Injuries Underwater Blast Injuries • EOD, explosives in salvage, UW • Tx cutting/welding, thunderflashes, • ABCs, ABCs, ABCs combat explosives • O2– lung damage may not be • UW blast injuries immediately apparent • HBOT only if signs of AGE, DCS • Primary due to shock wave = damage to gas containing organs (GI, lung, • If require ventilation ENT, CNS) • Risk of AGE, pneumo • Secondary due to displaced debris • Judicious use of fluids • Tertiary due to collision with • Avoid worsening stationary objects • Early use pressors vs IVF • Misc. - burns, radiation, etc. • NPO - May not absorb from GI • Press wave travels 4x faster UW than • Specialist consult as PRN in air • Typically no damage to non-gas containing organ unless impact/penetration wounds Heat-related Illnesses • Heat cramps • Heat Exhaustion (temp <40 °C) • Exertion, significant sweating, excess • Vague malaise, fatigue, headache, hypotonic fluid replacement -> salt thirst, weakness, anxiety depletion • Tachycardia, orthostatic hypotension, • Tx – PO salt (1/4 -1/2 tsp salt +/- in quart of water), rest in cool env • Tx • Cooling – ice packs (axillae, groins, • Heat Edema neck), skin wetting/fans • Minimal edema, esp. feet & ankles • Fluids, oral salt solution, +/- IVF • Diuretic not indicated • Tx – leg elevation +/- support stockings • (temp > 40 °C) • Mild to severe CNS dysfx (delirium, • Heat LOC, seizure), skin hot/dry • Generally elderly due to cutaneous vasodilation, pooling blood in lower • Tx limbs • Cooling – ice-water immersion, cold packs, skin wetting, fan, iced etc. • IVF (hypovolemic, rhambo -> ARF) • Lytes, glucose replacement PRN Cold Water Immersion • Thermal conductivity water >> air • Stage IV – post-immersion/ circumrescue • Body cools ~4-5x faster in water collapse • EtOH impairs thermal perception • ~15-20% immersion during/immediately • Stage I – Initial immersion (0-3 mins) following rescue • Cold shock rxn= initial gasp, hypervent, intense vasoconstriction (due to rapid skin cooling) • Heart muscle cold, less efficient, increase viscosity blood, prone to arrhythmias • Stage II – Short-term response (3-30mins) • Rapid tissue warming may increase off-gassing • Superficial nerves & muscles cool before adequate periph blood flow restored, • Immediate chilling hands/feet = inability to ?bubbles complete survival actions, swimming failure • During rescue – maintain pt horizontal • Stage III – Long-term immersion • Collapse worse if rescued vertically, (>30mins) = hypothermia increased time of immersion • Age, cold habituation delay onset shivering – faster fall body temp • Cephalic redistribution of blood, BP • Mild (35°C), mod (32-35°C), severe (25-32°C), maintained due to hydrostatic pressure profound (<25°C)

• Inability to breath hold, control breathing cycle • Sudden strain on heart, Predispose cardiac arrhythmias Near-Drowning/Drowning • Drowning ~100-150 scuba deaths • Tx per year • Ventilation must be reestablished • Entanglement, running out of air, prior to developing end-organ injury cardiac events from • Secondary to other injury, ?AGE/POS • ABCs, 100% O2 • +/- ETT, NG tube • Major pathophys is hypoxemia • Monitor serial Arterial Blood Gas • 10-15% do not aspirate water – laryngospasm • Antibiotics • Ocean water/pool generally not • V/Q mismatch required unless dev fever, purulent • Fluid-filled alveoli – perfused, not excretions, new infiltrates on CXR ventilated • If aspirate known contaminated water, • Decreased ventilation -> increase consider Abx PaCo2, cardiovascular collapse • Ventilation – based on clinical • Dilute surfactant presentation • Elevation diaphragm from gastric • BiPAP, PEEP etc. distention -> vomit & aspirate gastric contents Immersion Effects Effects of Immersion • CV Effects of Immersion • Pulmonary Effects of Immersion • Increased central volume (700 ml) – • Reduced vital capacity (5%) hydrostatic P effect • Reduced compliance • Increased stroke volume • Increased closing volumes – • Dive reflex – bradycardia, peripheral functional gas trapping, increased FRC vasoconstriction • Increased diffusion capacity • Increased pulmonary artery pressure • Relative V/Q mismatch apical vs basal • Increased pulmonary capillary • Active Na channel transport in pressure alveolar epithelial cells impaired in cold -> reduced clearance alveolar fluid • Negative intra-alveolar pressures – dense gas, turbulent flow, regulator Immersion Pulmonary Edema • Acute resp distress with pulm • Tx congestion, +/- hypoxia • Generally resolves within few hours ( 5 mins • No resolution on ascent (i.e. bad gas) - 25hrs) • S/Sx • O2 • Dyspnea, cough, +/- frothy or blood tinged • Resistant cases • +/- β-agonist inhalation, • , hypoxia • Rapid diuretic (IV lasix 20-40mg) • Rales ~25%, ~10% • +/- BiPAP • Frequently become symptomatic during • Usual CAF workup ascent or surface swim • BP, ECG, cardiac enzymes • Diagnosis • Echo • CXR – no findings, interstitial edema, • EST diffuse alveolar densities • PFTs • ?CT more sensitive but ?significant • ABG: avg Sat 88%, PPO2 66mmHG, eucapnia Immersion Pulmonary Edema • Prognosis • Combination of immersion and: • Recurrence 15-30%, unpredictable • Inspiratory restrictive load (high breathing • CAF case by case RTD if all w/u negative resistance – faulty regulator) • Risk Factors • Negative pulm pressure • Fluid overload • Incidence, mortality likely under-reported • High intensity exercise • Depth independent (2.9 msw), even surface only • LV diastolic dysfunction • Exertion during dive freq absent • Prevention • Cold increases incidence but not necessary • Equipment checks • Over hydration pre-dive may contribute • Consider pre-dive hydration carefully (association) • Sildenafil decr MPAP/CVP, incr venous • ?tight create neg intrathoracic press, capacitance/pulm vasodilation BUT possible ?NSAIDs – contrary or weak evidence risk DCS • Pre-immersion hyperbaric may protect in thermo-neutral water, not for cold water Pulmonary Edema: Other Considerations • Salt Water Aspiration Syndrome • Exercise on dry land • Aspiration fine mist of seawater from • Neurogenic Pulmonary Edema leaking/flooded demand valve (elevated catecholamines -> • May coexist with IPE peripheral vasoconstriction, increased • Tends to onset post-dive rather than on pulm art P, pulm capillary leak) ascent • Often provoked by exercise, movement or cold • Hyperbaric hyperoxia in absence of exposure immersion/exercise • Cough, fever, rigors, nausea, myalgia, SOB, • ~14% N. Americans have genetic β-2 mild leukocytosis adrenergic receptor polymorphisms • CXR – patchy consolidation v. interstitial predisposes to pulmonary edema with edema IVF • Tx – self-limiting, resolves without treatment within 2-24hrs • Rest, 100% O2 Systems Focus: ENT Physiology Otitis Externa Fungal Otitis Externa • Prevention • Aspergillus/Candida • No Q-Tips • Can cause malignant OE • Olive oil/2% acetic acid/domeboro/ tea tree oil • Tx • Tx • H2O2 irrigation, wick • Clotrimazole 1%/Locacorten-Vioform • +/- gentle irrigation ottic gtts • VoSol HC • Lamisil/Sporanox PO • Cortisporin/Cipro HC/CiproDex/Garasone • Wick (betnovate 0.05%, gentamicin sulfate 0.1%, tolnaftate 1%) Malignant (necrotizing) • Pseudomonas • Osteomyelitis/erosion skull base, CN paresis • Cipro IV 400mg q8h or 750mg PO BID • Levoflox if increase resistance to Cipro Barotitis Externa Exostoses & Osteoma • Canal occluded • Periosteal rxn to cold water • Hood, cerumen, oxostoses • “Surfer’s ear” • Doc’s ProPlugs • Benign bony neoplasms • Blocks water from entering ears in • Typically single osteoma, multiple <20 fsw exostoses • Vented plug reduces abrupt press • Occlusion -> hearing loss, changes, ?easier equalization infection, difficulties equalizing • Surgical excision has high rate of associated HL & recurrence Equalization • Equalization • First equalization press felt at ~30cm • ET collapses if not equalized by 1.5msw • TM rupture if not equalized by ~10msw • General Principles • Start early, blow gently • Don’t smoke, avoid agents causing vasomotor rhinitis (PDE -5) • Consider polyposis/deviated septum if persistent probs • Don’t dive when congested • Decongestants may allow descent and become ineffective for ascent • Don’t use if: • Unable to equalize without them • New diver • >4-5d continuously • CI present (anxiety, HTN…) • ↑ pO2 / ↑ pN2 (deep / mixed gas) Equalization Techniques • Beance Tubaire Voluntaire (BTV) • Frenzel • Voluntarily open ET by “twitching” • Closed glottis, move the tongue throat backwards quickly and forcefully • Tensore veli palatini muscle against soft palate • 30% pop can perform consistently • Pinch nose for better effect • Swallow/yawn • Gentle, safe for ascent • Edmonds • Valsalva • Jut jaw forward • Mod forceful attempted exhalation against closed airway • Combine with other techniques • Never on ascent, never >5s • Lowry • Toynbee • Pinch nose, gentle blow against blocked nose & swallow • Pinch nose & swallow • Difficult to perform • Small pressure diff, safe on ascent • Head tilt (bad ear up) • Combine with other techniques MEBT • TEED 0 • Teed 1 • Sx of fullness/pressure with no • Pressure, typically no pain otoscopic findings • Erythema, retraction of TM • Resolves in 2-24hrs • Resolves 24-48hrs • No Tx required • +/- decongestants • +/- decongestants MEBT • Teed 2 • Teed 3 • Pressure > pain • Pain & pressure • Mild hemorrhage within TM • More extensive hemorrhage • Erythema extending to umbo within TM • Resolves 48-72hrs • Resolves 4-5 days • Decongestants recommended • Decongestants recommended MEBT • Teed 4 • Teed 5 • Prominent pain • TM rupture • Blood behind TM, TM bulge • Often initial relief of pain, resumes • Resolves 5-14d several hrs later • Decongestants recommended • +/- acute dizzy/vertigo • +/- Abx if secondary infection • Usually diminished hearing • Consider myringotomy if not • Avoid diving until TM healed (2-6 resolved at 7d weeks) • Abx drops (Cipro, Floxin) vs PO vs observation • ?serial audiograms • ENT referral if fails to heal • 90% heal within 90d TM Perforation • Central perf =‘good’ perf

• Attic Perf = ‘bad’ perf IEBT • May present • At time of forced equalization • At depth or immediately post dive with exertion (lift gear) • During otherwise normal ascent • Days later (usually hx of strain) • Pathophys theories (likely combo) • Perilymphatic fistula (explosive or implosive force on windows 2° to press wave generated by TM or CSF) • Intralabyrinthine membrane tear • IE hemorrhage & gas • RFs • URI or active , hx of difficulty equalizing or poor equalizing technique (too late, too hard) • Forced Valsalva on ascent = sudden equal & implosion of stapes -> round window explosion • Wave trauma • Removing wetsuit hood • Heavy lifting (during, post dive) • Enlarged aqueducts (bigger wave) • Weakness of annular ligament of stapes IEBT • S/Sx • Tx – involve ENT! • Constant disequilibrium, loss of balance, ataxia, • Bed rest with head elevated 30° until 7days post positional vertigo, nystagmus, N/V plateau of sx (~1-2 weeks) • Subjective ear fullness, high pitched tinnitus • Avoid cough, sneeze, Valsalva, strain at stool, sex, • Hearing loss of various degrees (progressive, air travel, loud noises fluctuating or positional) • Anti-nauseants, decongestants, sedative, • Divers tend to have vertigo > SNHL compared to laxatives – OK other causes IEBT • Steroids – no evidence for IEBT, but make sure to • Acoustiphobia consider SSNHL when HL is the only s/sx • NSAIDS CONTRAINDICATED • Initial Exam • Otoscopy: N, +/- MEBT • Surgery – tympanostomy and window graft • Neuro exam • Severe sx (repair within 48hrs), no improvement @ 7-10d, serial audiometry shows deterioration, • Hennebert (cough, sneeze, Valsalva) & Tullio co-existing TM rupture (noise) • ~90% successful vestibular sx, improve vertigo & • Serial audiometry tinnitus >HL (10% recurrence post surgery) • Gen global (conductive) or HF SN loss • Positional – hearing gain of >10dB when supine with • RTD may be ok - CAF case-by-case affected ear turned up • No non-compensated vestibular sx • Special Investigations • HL stable, narrow, doesn’t affect speech band • VNG/VEMP – may show vestibular dysfx • No anatomical risk factors, no issues equalizing • ABR – differentiates central from peripheral injury • HRCT of temporal bones – consider for divers • 6-12 weeks post (min no diving x 6 weeks without other defined RFs post sx resolution or sx plateau) IE DCS • Typically deep and deco dives, deco • S/Sx violation, mixed gas • Usual onset near surface, on deco stop, or • Pathophys theories: v. shortly after surfacing • Bubbles in osteoclasts – rupture bone lining • Vertigo & SNHL > tinnitus otic spaces • N/V, staggers, nystagmus • Inert gas into perilymph from both blood • +/- presence of other DCS sx (<50%) and diffusion from ME via windows = • Usually MEBT absent supersaturation • Neg Dix-Hall-Pike, Henneberts, Tullio • Vascular emboli • Autochtonous bubbles arise in organs of • Tx inner ear • Rxn reasonably well to early RCC (TT6) • **Counterdiffusion -> total inert gas • High rate of residual sx if Tx delayed supersaturation • If unsure IE DCS vs. IEBT vs both: • Gas switch from He to air – N2 diffuses in • Myringotomy then RCC, slow ascent vascular space from blood, He from ME • Some evidence ok to compress without myringotomy if no prob equalizing IEBT vs. IEDCS

IEBT IE DCS More common More rare Typically during descent (+/- delay) Typically ascent (+/- delay) Hx of trouble equalizing, shallow dive, pain Hx – painless, no issues equalizing, typically +/- HL, tinnitus, N/V deep/mixed gas (Heliox) dive +/- HL, tinnitus, N/V Signs of MEBT, abnormal TM/perf No external signs Hennebert/Tullio Tx Tx -No RCC -Urgent RCC -Head elevated, avoid CSF, steroids -?steroids

• Delay situation = Valsalva after surfacing (ie. carrying tanks, lifting ) • When in doubt - myringotomy & recompress Myringotomy • Myringotomy • Don’t do it for the first time on your own, with a diver requiring immediate RCC • Procedural otoscope, 22G spinal needle • • 10 drops of 8% tetracaine base in 70% isopropyl alcohol applied to TM for 15 mins or 1cc of 5% EMLA applied to TM for 60 mins • Then dab incision site with 20-25% phenol Transient Caloric Stim • Up to 25% divers, females 4x> males • Unequal vestibular caloric stimulation • Due to press diff between two ME • Cold water enters one ear • Esp. if horizontal canal is in vertical spaces position – supine with head elevated • Δ0.6msw sufficient 30°/prone head depressed 30° • Rotational vertigo, nausea, nystagmus • Can also occur if TM perf with MEBT • Spinning toward side with related ETD • Common RFs dysfx • Obstruction one canal (cerumen, FB, • Resolves in mins(usually) to hours (v. exostoses, OE, ear plus, diving hoods) unusual) • TM perf • No HL or tinnitus • Prevention: • Don’t dive with sticky ears • Descend little bit until sx resolve then ascend slowly • Toynbee or Frenzel, NOT Valsalva • Recurrence may be indication to discontinue diving – case-based ”Dizzy” Diver DDx • Disorientation • Impaired vision/proprioception, N2 narcosis, hyper/, hyper/hypoxia, gas contaminants (CO), HPNS • Diving Causes Vertigo • Caloric (poor fitting hood, unilat canal obstruction, TM perf) • Positional (prone with head down) • Pressure Δ (ABV) • MEBT, IEBT, IEDCS • HPNS • Non-Diving Causes • BPV, Meniere's, vestibular neuronitis, labrynthitis • Acoustic neuroma, MS, migraine • AOM • • Meds • Factitious Facial Baroparesis • Facial n. runs through facial canal • Tx along walls of middle ear cavities • 100% O2 • Bony canal separates n. from middle ear • Toynbee or Frenzel, no Valsalva space • Decongestants • ~50% of people have “dehiscences” • Dive (or RCC) to 1-2msw on O2, slow where nerve is covered by soft ascent • Some authorities opine that HBOT at tissue/mucosa rather than bone >10msw may be detrimental • PΔ of only 0.8msw can cause relative ischemia of n. • Myringotomy – rarely if ever required • Compression lasting >3.5 hrs can lead to • No evidence to support corticosteroid permanent damage • Usually resolves within 1-2 hrs after equalization (unless compression • S/Sx >3,5hrs) • Setting of difficult equalization • DDx • LMB facial palsy, always unilateral • DCS – provocative profile, no signs of • Onset shortly after surfacing MEBT, +/- other signs of DCS • s/sx of MEBT usually evident • Never reported as isolated DCS finding • +/- coexist with IEBT • CAGE/Stroke – UMN vs LMB • Able to frown and close eye normally = UMN Systems Focus: Cardiology CVS & Diving • ↑cardiac demand • CAF RF Screening • Heat generation, exercise, vascular • Hx – CVD, smoker, DM, , FHx, redistribution due to immersion HTN, exercise tolerance • Cold/stress can induce coronary • Anthropomorphics • Labs – lipids, fasting gluc, A1C > FRS • ECG q4yrs to 40, then q2yrs >40 y.o. • CVS D/O in diving: • +/- EST, stress echo, nuclear • Sudden – underwater usually , CT Coronary Ca if indicated due to CVD, arrhythmia • Acute MI • Why screen Asx? • Stroke • Most ACS due to plaque rupture, often without flow limitation pre-ACS • Syncope event • Arrhythmias • Up to 50% initial presentation CVD is • Pulmonary edema sudden cardiac death • Paroxysmal dyspnea • Vascular rupture/occlusion • Gas embolism CHD • Septal defects • PFO & Diving • VSD most common upper septum • Controversial- significant opinion (based • Small deficits gen no significant R to L on epi, animal models, path exam, shunt (unlikely to ↑risk AGE) pathophys reasoning) that shunt likely does not contribute to isolated spinal • Aortic stenosis DCS • Exercise syncope, sudden death • Relative risk DCS in significant shunt vs. no shunt ~5-25 • Patent ductus arteriosus • Includes incidence of isolated spinal DCS, • HF if severe thus likely overestimate shunt-attributable risk • Cardiomyopathy • Consider underlying condition • Hypertrophic often asx, may hear • CAF Screening – CDs, unexplained murmur on exam if valve abN DCS/AGE hit • Dilated – ↓LV fx may = exercise • Echo with bubble contrast & Valsalva intolerance • * Any FHx of sudden death needs investigation to r/o cardiomyopathy! • CI’s to diving • AbN LV Fx – EF <50% (risk arrhythmia) • Hx ICD, arrhythmias, syncope • Hx of HF (lose cardiac reserve to prevent syncope) Valvular Disease • Stenotic valves • Aortic insufficiency – HF if severe • ↓exercise tolerance (worse with immersion) • Mitral stenosis – exercise induced • Lead to circulatory obstruction pulmonary edema • Regurgitant valves • Mitral insufficiency – HF if severe • Tolerated if mild • HF, pulm congestion if severe -> ↑dyspnea • Mitral prolapse - +/- arrhythmia (exercise, immersion) • Assoc with palpitations, tachy, extra beats, CP, regurg • Volume overload -> hypertrophy • ↑muscle mass demands requires ↑blood • Pulmonic stenosis – reduced exercise flow (risk underperfusion of endocardium) tolerance if severe • Bicuspid aorta (*requires cardiology W/U) • Tricuspid stenosis – reduced exercise • Assoc with abnormal coronary arteries, aortic tolerance if severe root dilation, PDA, Turner syndrome, aortic stenosis, aortic insufficiency • Prosthetic valves • What is fx status • Aortic stenosis – exercise syncope, • ?anticoagulation required (increase hemorr sudden death risk in BT) • Low risk if no LVH on ECG, HF, arrhythmias, • Likely low stress warm water diving only syncope or angina Arrhythmias • Supraventricular • Long-QT syndrome • Episodic SVT, Afib can be N variant in • QT > 440 msec young population • Assoc with sudden death/VF, syncope • R/O Mitral sten, TSH, HTN, nicotine, • Ppt by stress, exercise, lyte abN, drugs, stress, EtOH, caffeine, supplements meds etc. etc. • Increase risk combo of exercise & • Gen ok to dive if no organic heart immersion disease, resolves with stim remove • Unfit dive • CDSM review if requires BB/CCB • Increased vagal tone • Ventricular • Bradycardia may be N variant in well • PVC may be N variant – assess with conditioned applicants exercise • Fit dive if asx • No go diving if multifocal, R-on-T, freq • If palpitations (Afib), severe brady coupling, ICD, LV dysfx (increase risk while diving – can increase risk sudden death) syncope Conduction Abnormalities • Often underlying cardiac disease • RBBB • 1° AV • Incomplete • May be due to excess vagal tone • If stable, usually N variant, benign • Asx generally ok • Complete • May be N variant or congenital HD • Fixed 2° AV block • Requires workup to r/o anatomic • Often lead to complete block = CI cardiac abnormality • LBBB • Pacemaker • Often due to cardiomyopathy or • If no other heart disease, coronary dz pacemaker tested to pressure and • Requires workup good exercise tolerance • May be ok for • Unfit CF diving • ICD – unfit diving Conduction Abnormalities • Brugada Syndrome • Pre-excitation syndromes • Mutation Na channel • Short PR not in itself CI • Type 1 – ST elevation >2mm in >1 of • Asx, low risk arrhythmia may be ok V1-V3 followed by a negative T Wave sport diving • Type 2 - >2mm saddleback shaped ST • Recurrent paroxysmal or exercise- elevation induced tachy requires w/u • Type 3 – morphology of Type1/2 but • WPW <2mm • Risk exercise induced tachy, • Accompanied by documented VF/VT, palpitations, SOB, syncope, sudden cardiac death FHx of sudden cardiac death <45, similar ECG in family mbrs, syncope, • If successful ablation – ok to dive nocturnal agonal , • If sx – Unfit Diving inducibility of VT with electrical stimulation • Tx = ICD, CI to diving Long-term Effects of Diving Noise-Induced Hearing Loss • Risk Factors (RF) • CAF screening • Noise in environment – topside • Audiogram qYear & on clinical • Ship/boat noise, equipment/tools indication • Gas into chamber • Occupational med (effect of diving • Noise in environment – underwater on person) – audiogram • No hearing protection • considerations • Helmet, reg, ship/boat noise, tools, underwater explosions (whisper test, word discrimination, • Barotrauma audiology) • Inner ear DCS • New studies show no difference • ↓Sound localization under water between divers and those • ↑sound velocity in water vs air = exposed to similar levels of reaches both ears at same time surface noise DON • Type of due to • Dx based on imaging studies hyperbaric exposures; in long bones with • Long-Bone Survey (LBS) fatty marrow • B/L upper humeri (including rotational view of • Relatively ↓blood flow = prolonged wash- shoulder), AP & lat knees (upper tibia & lower out femur) & b/l hip • Xray changes may not be observed for • N2 is 5x more soluble in marrow fat than in months/years after lesions devo blood • MRI preferred – more sensitive & specific • Location: prox humerus, prox/distal • Able to detect DON as early as 2 weeks post onset, and by 2 months virtually all lesions are femur, prox tibia demonstrable • “wet” (divers) – femur, shoulders, rarely hip • Bone scan • “dry” (caisson) – hip most common • High sens but low specificity, not diagnostic • Juxta-articular (A) or shaft (B) lesions • Prevention • A lesions often become sx – pain, ↓ROM • Timely Tx of DCS with HBOT likely to reduce • B lesions often remain asx incidence of DON • RF • Avoid RFs • Depth exposures >30msw, or >4hrs at <30msw, hx of DCS (any depth), significant omitted deco • Submariner escape – DON risk after single provocative deco exposure even if no DCS • >40, obesity, EtOH, fatty liver, dyslipidemia • Hx of DON DON Classification UK MRC • Ficat 0 • Juxta-articular A Lesions: • Ischemia, intravascular coag • A1 – Dense areas with intact articular cortex • Asx, no radiographic changes • A2 – Spherical opacities • Ficat 1 • A3 – Linear opacities • Dead bone without repair, asx • A4 – Structural failures: translucent cortical • Xray N, MR shows marrow edema by ~ 4weeks bands, collapse of articular cortex, sequestration of cortex • Ficat 2 • A5 – Secondary degenerative arthritis • Dead bone with repair, no collapse, asx until late • XR: sclerosis with irreg margins, spherical opaque • Shaft B Lesions: areas (“snowcap”) and linear opacities • B1 – Dense areas • MRI: rings of low intensity surrounding necrotic • B2 – Irregular calcified areas center • B3 – Translucent and cystic areas • Ficat 3 • Dead bone with repair & collapse • Sx – pain with joint motion or weight-bearing • Xray: subchondral # - radiolucent “crescent” line • MRI: necrotic centre, collapse of articular surface • Ficat 4 • Secondary degenerative arthropathy • May progress to complete destruction of joint DON • Screening • Management • ALL divers complete DON questionnaire • All DCS, significant omitted-D, sub @ PHA escape, or DON lesions require CDSM • LBS only if at risk review • Student divers • If ID DON – R/O lesions at other sites • DWD candidates LBS at end of course • Juxta-articular A lesion • SWD only if Q shows ↑risk = LBS within 1 • Shall be further characterized by MRI, month completing course staged • Divers with ongoing exposure to DON RFs • MRI of b/l shoulders, hip and knees (all DWD, SWD with increased risk) = LBS • Followed by XRq6 months x 2 years, then q5yrs annually until no further interval change • Any diver with DCS, significant violation • Referred to ortho deco or sub escape = LBS within one • Declared “unfit CF diving or hyperbaric env” week of event, followed by MR (hips, • Strongly advised to d/c civi diving >30msw, knees, shoulders) @ 2 months post-event avoid load-bearing activities on involved • All DWD, and any SWD who have joint required LBS = LBS at termination of • Shaft lesion diving career • MR of b/l shoulders, hip and knees • LBS q5years until end of diving career, exit LBS • F/U required if dev sx • May be able to continue diving as per their quals vs. <30msw – requires CDSM review Aquatic Hazards Categories • Bites • Biological contaminants • Barbs and Venoms • Chemical contaminants • Toxins • Radiological contaminants • Infectious agents • Contamination Coelenterates (Jellyfish, sea anemones, fire coral…) • Nematocysts • Irukandji syndrome • Vinegar ↓nematocyst discharge • Can follow negligible sting from • Box jellyfish/sea wasps variety of jellyfish • Multiple interlacing whiplash lines in • Stinging -> papules, dyshidrotic, beaded/ladder pattern -> wheal -> severe abdo pain, muscle cramps, necrosis/ulceration ~7-10d hypertonicity, ↑HR, ↑BP, resp distress • Excruciating pain • Death can be within 10mins, likely • Sea Bather’s eruptions survival after 1st hr • Thimble jellyfish larvae “sea lice” • HTN, then hypo/hypertensive when nematocysts trapped under oscillations, VF, resp distress, apnea, bathing suit/wetsuit discharge edema, , paralysis • Painful, erythematous, pruritic rash • Tx under dive suit • Vinegar, remove tentacles asap • If freq exposure, can dev allergies to • IV morphine, IV steroids, anxiolytics, toxin antivenom • Tx = topical steroids, avoid trigger Stings/Spines/Bites

• General Tx: immerse in hot water • Stonefish • Up to 45°C, including N skin (as control) • Myotoxin – blocks conduction skeletal/ cardiac/involuntary muscles, releases Ach • Stingray • Immediate excruciating pain, edema, swelling, hot with numb centre & extremely • Spine physical damage, envenomation tender surrounding • Tx • Cardiorespiratory collapse • Supine, elevate limb, wash away venom • Tx • Gently remove spine • Elevation, local anaesthetic, hot water bath • Hot water bath • Antivenom if persistent pain • Inject local anesthetic into wound • Debride necrotic tissue • Monitor for 2° complications Sea Urchins • Sea Snake • • 4 bite marks, venom blocks Ach • Spine causes physical damage, Ach-like • Euphoria, restless, thirst, dry throat, N/V, venom myalgias -> weakness -> paralysis (similar to • Tx Guillain-Barre), myoglobinuria • Remove spines vertically • Tx • Hot water bath • Pressure immobilization, antivenom • Local anaesthetic (prophylactic epi/antihistamine), +/- ARF Medical Exam for Divers Diver PHA • Purpose • Physical Exam Highlights • Fit to dive, fit to work, med surveillance, assess • HEENT – TM mobile with Valsalva, TM changes, impairment TMJ ROM/crepitus • CVS • CAF SWD PHA (CFHS Instruction 4000-04) • RESP • Initial • GI – scars, hernias, masses • Type I – P1, P2, 2452, 2552, DON screen, labs • MSK – document well any signs/symptoms, especially in the shoulders, elbows, hips and • Type II – P1, questionnaire review knees • P1 – anthropomorphics, vision, audio, 2452 • Neuro – gait, cognition, CN, pronator drift, Romberg, sharpened Romberg, • P2 – full history and physical bulk/tone/power/sensory/DTR, peripheral vs.. • Initial Investigations dermatome nerve deficits, +/- SCAT • Blood – CBC, ‘lytes, cr, liver enzymes (AST, ALT, GGT, Alk Phos), lipids, FBS q2 years • Urine – dip and micro • CXR – PA insp/expiration, lat (3 views) q5 years • EKG – q4 yrs to 40yo, then q2 yrs • Spirometry screen • DON screening – annual Q’s; LBS if at-risk • CV q4 to 40 then q2 Diver ROS 1. Asthma 5. Significant Head trauma • Asthma after age 12, wheeze, SOB, ILD or COPD • TBI/concussion/LOC >2 mins, skull #, any ICH, • Childhood Hx, ER presentations, hospitalizations post-traumatic amnesia >30 mins, focal neuro sx, post concussive epilepsy or post concussive sx • EIA, respiratory cold tolerance, , lasting >24 hrs , cough (nocturnal, post URTI) • For concussion/head injury • Puffer use • Total # of concussion or head injuries • No go asthma = requires ongoing use of rescue • Date last HI, interval between concussions/HIs inhalers, induced by cold/exercise/anxiety or • Change in threshold of trauma required to induce exposure to airborne concussion/HI sx particulate/chemical/petroleum distillates found in the dive/sub atmosphere • Previous assessment by neurologist/specialist • Previous imaging results 2. Pneumothorax • Hx of spontaneous or traumatic, chest tube 6. ENT • Sinus problems, nasal polyps, deviated nasal 3. Neuro septum, sinusitis • Seizure/epilepsy • ETD problems clearing ears under pressure, • Blackout/LOC flying • Migraines with deficits/impact on fx • Chronic OM/OE, TM perforation 4. MH conditions • Vertigo, Meniere's • Claustrophobia, anxiety, PTSD, phobias, 7. Hx of DI (DCS or AGE), DON, barotraumas substances (CAGE positive – context and consequences) Drugs & Diving Considerations • Considerations: • “Bad” Drugs • Underlying disorder • Affect alert/LOC/cognitive fx, exercise tolerance, change sz threshold • Is drug inherently safe for diving? • I.e. psychotropics, sedatives, BB etc. • What type of diving planned? • “Bad” Diseases • Will performance be impaired – • Affect alert/LOC unsuccessful mission • ↓exercise tolerance/general fx, • Proximity to medical care ↓press equalization, ↑risk DCS • Incapacitation – diver now a threat • I.e. psychiatric, neuro, cardiac, resp, to themselves or safety to others MSK, metabolic, ENT considerations • Change in drug’s efficacy/safety • “Bad” Dives profile due to hyperbaric env • ↑exertion, exposure (hot/cold), elaborate equipment (rebreathers), dangerous env (overhead, combat, EOD, extreme depth/duration/deco), distance from med resources Initial Approach to Dive Injury 1st Principles • DCI • Dead/VSA • Trapped gas -> POS, AGE • At surface vs. depth • Evolved gas -> DCS • Witnessed/unwitnessed • AGE, MI, drowning due to • Not all diving casualties are dysbaric blackout/medical condition • Thermal (hyper/hypothermia) • Near drowning, IPE • Blackout • Environment (blast injuries, tools, • Gas issue (too much, not enough, wrong mechanical dangers, marine life) gas), seizure • Previous med conditions (MI, Sz) • Vertigo and other ENT symptoms • Not all dysbaric casualties have DCS • Vestibular DCS, inner ear BT (pure or combined with vestib DCS), alternobaric • POS, AGE vertigo, Meniere's/BPPV • Other barotraumas • /SOB • Chokes, pneumothorax, immersion pulm edema, ACS/CHF • Headache • CO2 toxicity, DCS (?type?), migraine, plain H/A Initial Approach • Approach • Diver Hx • Onset • • Evolution • Depth, time - estimate of N2 stress • Presentation • ?repet dives – how many, when was last dive • Gas burden – dive profile • Evidence of barotrauma • Dive equipment & gas used • Mod – High risk = Manage as DCI • Mechanism of injury • When did problems start • Low Risk – consider other causes • Descent, at depth, ascent, at surface 1) Non-DCI dysbaric (i.e. BT) • What happened during dive 2) Non-dysbaric diving-related (i.e. marine life) • Uneventful; strong ; aborted; 3) Non-diving-related CLASSICAL (ie. MI) Initial Actions Dysbaric Casualty • ABCDE • Emergency (Red) – immediate, • Vitals life-saving • Severe sx, rapid onset <1hr, • 100% Oxygen progressive, neuro deficits, clearly • Accelerate inert gas elimination & ill improve O2 delivery to hypoxic tissue • BMV, demand valve, rebreather • Urgent (Yellow) – disability • IV Fluids – IL bolus, then titrate preventing (~100-175ml/hr) • Pain only, stable or progressing, overall stable, without sx of severe • Avoid dextrose (can increase ICP) DCS • PO fluids unlikely to benefit • Increase tissue perfusion = increase • Timely (Green) – elective inert gas washout • Unclear/ambiguous sx, long delay st • DDx from when sx 1 appeared (not when 1st reported) Time to Tx – DAN workshop 2004 • Consensus Statements 4. Some patients with mild s/sx after 1. Mild s/sx = limb pain, diving can be treated adequately constitutional sx, some cutaneous without recompression. For those with sensory changes, rash; where these DCI recovery may be slower in the manifestations are static or remitting, absence of recompression. and associated objective neuro dysfx 5. Some divers with mild s/sx after has been excluded by medical exam diving may be evacuated by commercial 2. Untreated mild s/sx due to DCI are airliner to obtain treatment after a unlikely to progress after 24hrs from surface interval of at least 24hrs, and end of diving (unless further deco or this is unlikely to be associated with ascent to altitude) worsening outcomes 3. Level B epi evidence indicates that a delay prior to recompression for a • NB Mild s/sx – need monitoring patient with mild DCI is unlikely to be associated with any worsening of long- term outcome General Approach RTD • Impairment • Key Considerations: • Loss of use or derangement of body • Dive safety (individual & team) part/organ system or fx • Job/mission completion • Disability • Conserve trained resources • Inability to meet demand/need based on • CAF RTD after DCI an impairment • Type I DCS completely resolved • 5 key questions: • No fly 3d, no diving 7d • Diver or patient? • Type II DCS completely resolved after 1 TT • Disqualifying meds • No flying 7d, no diving 30d • Consider both med & indication • Type II DCS residual sx or repeated tx • Ability to do job • No fly 10d, no diving until reviewed by CDSM • Exercise tolerance, cognitive fx, roles • AGE completely resolved after 1 TT (buddy, , dive sup, boat driver, • No fly x 7d, no diving until reviewed by EOD disposal), stressors (pressure, gas CDSM toxicities, thermal, disorientation etc.) • Quantification of impairment • AGE residual sx or repeated tx • No fly x 10d, no diving until reviewed by • Immune function CDSM • Assessment of job - ?tailored diving HBOT HBOT • UHMS Indications • CAF Treatment Tables 1. Air or Gas Embolism 2. CO poisoning • Limits due to OxTox (decreased 3. Clostridial myositis and myonecrosis with air breaks) (Gas Gangrene) • If TT stopped due to CNS OxTox, 4. Crush injury, compartment syndrome, allow 15 mins after sx resolved, other acute traumatic ischemias then resume schedule at point of 5. DCS 6. Arterial insufficiencies interruption 7. Severe anemia • Tx repeated until resolution or 8. Intracranial abscess plateau 9. Necrotizing soft tissue infections • Contraindications – almost all 10. Osteomyelitis (refractory) relative (depends on indication) 11. Delayed radiation injury (soft tissue, bony necrosis) • Largely same as diving 12. Compromised grafts and flaps • Other common treatment tables: 13. Acute thermal burn injury • USN, Comex, Catalina, CO poisoning 14. Idiopathic sudden sensorineural • Proprietary commercial tables hearing loss (new Oct 2011) HBOT Mechanisms • Bubble Compression (Boyle’s Law) • Blunt ischemia-reperfusion injury • Hyperoxygenation (Henry’s Law) • Attenuates PMB-endothelial interaction • 10-15x increase in plasma O2 • Prevent lipid peroxidation • 2-4 x increase in O2 diffusion capacity from capillaries • Decrease edema • Gas Gradient – support gas • Vasoconstriction (while tissues washout, prevent additional uptake remain hyper-oxygenated) of inert gas during HBOT • Angiogenesis/Wound healing • Stimulate vasculogenic stem cell • Antimicrobial effect mobilization Inhibit clostridial alpha toxin • • Increase growth factor synthesis Anaerobic bacteriostasis • • Stim fibroblast proliferation enhance antibiotic activity, • • Angiogenesis, reversal of tissue • improve PMN fx hypoxia Adjuncts • NSAIDs • Other considerations • No diff in final outcome, but with • Hydration, food tenoxicam divers needed fewer TT • Urinary catheter • NNT ~4-5 • DVT prophylaxis • Heliox • Hospital admission • May decrease # of TT required • Specialists consults (i.e. neuro) • Lidocaine may have neuroprotective effect • Insufficient evidence to support routine use

• Perfluorocarbons increased O2 delivery, N2 removal • Animal models only so far • Not recommended: steroid, ASA, Heparin (unless DVT prophylaxis @24hrs)

Treatment Table Summary

Table Indications 5 Type 1 DCS only if sx completely resolved during transport to RCC

Recurrence Type 1 Sx (complete resolved after 1x O2 period at 18msw) Omitted-D, uncontrolled ascent/blow-up – for Asx if omitted D ≤30 mins) 6 DCS, AGE responding to initial 18msw RCC Omitted D, uncontrolled ascent/blow-up: Asx individual with ≥ 30 mins

nd 6 Mod Extension of TT6, if patient remains sx by end of 2 O2 period at 18msw 6A Severe AGE/DCS deteriorating or not responding at 18msw, resolving @50msw nd 6A Mod Extension of TT6A, if patient remains sx by end of 2 O2 period @18msw 7 Heroic measure, used in extreme cases 8 Deteriorating severe AGE/DCS sx @50msw, recurrence of severe AGE/DCS during deco from 50msw-18msw etc.