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Decompression Illness Decompression Illness DCI • Decompression illness (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 barotrauma 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 confusion, paresis, sensory loss, apnea, aphasia, • PBT visual loss (field >acuity), vertigo, 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 airlock • 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/TT6A 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 .
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