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Decompression sickness
Mattijn Buwalda
Anesthetist-intensivist
& dive medical physician
Runtime: 60 min
Slides: 42
Movie clips: 2
• Male 52 Jr, PMH: nil of note, > 800 dives • 2 decompression dives Zenobia wreck (Cyprus) • 1e: 50 min @ 38 msw • 2e: 49 min @ 35 msw, unexpected current, high
waves, very difficult to climb back into boat, • Strained muscles left arm! • > 15 min numb pain left schoulder radiating to hand,
dig 5......???
DCS case
Zenobia sunk 1980
42 msw
• After 30 min @ shore, increasing numbing pain unrelated to movement, + tingeling left am.
• DD: muscular strain, myocardial infarction & DCS • after 10 min 100% O2: pain dissapeared, ECG: GB • DCS muscular/ joint due to unexpected increased
N2 absorption • Excessive use of left arm muscles caused extra
bubble formation (tribunucleation)
Case
• definition & stats
• signs & symptoms
• first aid
• recompression
• provocation
• prevention
DCS content
• Decompression sickness: clinical signs & symptoms due to bubbles in tissues and venous blood as result of insufficient inert gas washout
• Arterial Gas Emboli: occlusion of arteries
• Decompression Illness is the umbrella term
AGE + DCS = DCI
The distinction between DCS
and AGE is fading!
Classification of DCS
1991 classification • Evolution
– progressive – static – improving – relapsing
• Organ system – musculoskeletal – cutaneous – neurological – vestibulocochlear – lymphatic – cardiopulmonary
• Additional information
Golding 1960 • Type 1
– joint pain – itching – cutis marmorata – localized pitting edema
• Type 2 – cardiovascular – pulmonary – neurological
• Type 3 – inner ear – vestibular
• Type 4 – dysbaric osteonecrosis
Francis T. Describing decompression illness: the forty second undersea and hyperbaric medical society workshop. Bethesda, Maryland: Undersea an Hyperbaric Medical Society. 1991
• Diver with worsening pain in shoulder and elbow: “progressive musculoskeletal DCI”
• A diver with sudden loss of consciousness immediately after a rapid ascent and who is subsequently recovering: “remitting neurological DCI”
Examples
Stats
• DCI is rare, huge variation in incidence
• due to incomplete reporting
• due to differing circumstances
– 2-4 per 10.000 dives (recreational, DAN)
– 30 per 10.000 dives (Scapa Flow)
– 0.32 per 10.000 dives (scientific diving)
– 1-10 per 10.000 dives (commercial diving
– AGE 3.9 – 8 % of DCI
• DCI correlates with:
– depth
– age
– less experience
?
? Number of
dives
incidents
Fatality rate:
1 -2.5 per 100.000 dives
pathofysiology
tissue bubbles
tissue distortion/ compression:
• joints
• peripheral nerves
• spinal cord
• inner ear
arterialized bubbles
Ischemia/ obstruction:
• skin: cutis marmorata
• cerebral
• inner ear
• spinal cord
generalized effects:
• activation of inflammatory pathways (SIRS)
• activation of coagulation
• endothelial damage > extravasation of fluid
• microparticles
Musculoskeletal
• proximal joints
• usually unilateral
• shoulder/arm (most common)
• knee/ leg
• usually no signs on examination
• deep nagging pain
• numbing pain
• no relation to joint movement
• exact cause unknown:
– bubbles in ligament/ tendon?
– bubbles in marrow give high intramedullary pressure
• bilateral back, abdominal, girdle type of pain is not musculoskeletal! but probably neurological in origin!
Cutaneous
• superficial erythematous rash + itch
– if only symptom then DCS is mild
– good response to oxygen
• cutis marmorata
– marbled blotchy
– can be itchy or painful
– associated with neurological DCS
– is not mild!
• subcutaneous swelling
• blocked lymfe vessels
• not painfull
• if no other symptoms: mild DCS
lymfatic
Neurological signs
• severe cases: difficult to differentiate between massive DCS and AGE due to lungrupture
• coordination and balance are affected disproportionately!
• dysexecutive syndroms:
– concentration
– memory, mood
• sensory abnormalities:
– patchy
– may not follow cortical or dermatome distribution
– multifocal, combinations of cortical, brainstem, spinal cord or peripheral nerve damage
Pathophysiology of cerebral DCS
• no autochtonous bubble formation
– high tissue blood flow > fast washout
– reuptake of N2 in brain tissue > bubbles shrink
• only bubble emboli
– AGE after lung rupture
– arterialized VGE (massive DCS or pulmonary shunting)
• short latency
– 75% < 10 min
Spinal cord
• arterial blood supply – deep dives, close to NDL
– fast tissues
– < 30 min of surfacing
• venous infarction – overload of venous capillary
network > thrombosis + infarction
– < 2 h of surfacing
– usually cause of paralysis
– venous plexus has no valves
• autochthonous bubbles
Neurological exam
• most important for prognosis, severity and HBO treatment
• for (hyperbaric) physicians: – standard neurological exam
– special emphasis on: coordination and balance
• for divers and dive masters: – DAN course: neurological assessment
– 3-4 hours training
https://www.daneurope.org/web/guest/training/programs
5 min neuro short video
Professional neuro exam
• standard neuro exam
• Romberg: proprioception > dorsal colum function
• sharpened Romberg is more sensitive!
5 min neuro exam
5 minute neuro exam
• http://www.bramkov.cz/?v=0Y54aQ8bdOQ
• https://www.diversalertnetwork.org/medical/neuroexam.asp
Skills session: 5 min neuro exam
• groups of 3-4 students
• one patiënt (prepared cases)
• one examiner
• one fills in the DAN neuro assessment sheet
• Rotate 4 times!
See skill station 5 min neuro exam
Outcome neuro DCS
• Spinal cord DCS n=63:
– 67% complete resolution @ 1 month
• DCS n=268: 86% complete resolution
• DCS n=1763: 80% complete resolution
• DCS, chamber on site:
– immediate recompression n=166
– 97% complete resolution after 1 session
– eventually 100% complete resolution
Gempp E, Blatteau JE. Risk factors and treatment outcome in scuba divers with spinal cord decompression sickness. J Crit Care 2010;25:236-42
Thalman ED. Principles of US Navy recompression treatments for decompression sickness. In: Moon RE, Sheffield PJ, eds. Treatment of decompression illness. Kensington, MD: Undersea and
Hyperbaric Medical society. 1996:75-95
Vestibulocochlear
• inner ear decompression sickness
• symptoms: vertigo, nystagmus, nausea, vomiting, hearing loss
• large differential diagnosis
• AGE: blood supply is end-arterial
• isobaric counterdiffusion temporary super saturation on switching from He to N2 during ascend after deep dives
Wait for lecture:
ENT & diving
• very rare
• large volume of gas in right atrium, ventricle, pulmonary artery
• etiology: VGE, massive DCS
• pathophysiology:
• pulmonary hypertension
• right ventricular strain
• endothelial activation
• signs & symptoms:
• cough, dyspnoea
• pulmonary edema
• arrhythmias
The lung: chokes
Ence TJ, Gong H.Jr. Adult respiratory distress syndrome after venous air embolism. Am Rev Respir Dis 1979;119:1033-7
Frim DM, Woilman L, Evans AB, Ojemann RG. Acute pulmonary edema after low-level air embolism during craniotomy. Case report. J neurosurg 1996;85:937-40
23
Constitutional signs
• endothelial activation/ damage
• increased permeability > fluid shift to interstitium
• leucocyte & platelet activation, adherence to endothelium
• microthrombi
• SIRS/sepsis like reaction!
• hypovolemia
• tired after dive
• constitutional signs
– SIRS or neurological???
– light headed, dizzy
– headache
– bit unsteady on feet
Being tired without any other signs is not DCS!
Symptoms of DCS in rec. divers
DAN network report on DCI, Durham, NC, Divers Alert Network, 2005
Symptoms Frequency
local joint pain 89%
arm symptoms 70%
leg symptoms 30%
dizziness 5.3%
paralysis 2.3%
shortness of breath
1.6%
extreme fatigue
1.3%
collapse 0.5%
Time to onset Percentage of
cases
within 1 hour 42%
within 3 hours 60%
within 8 hours 83%
within 24 hours
98%
within 48 hours
100%
Frequency timing & symptoms
Symptoms starting > 24 h are most unlikely due to DCS
Navy department. US Navy Diving Manual. Revision 6. vol5:Diving medicine and recompression chamber operations. NAVSEA 0910-LP-106-0957.
washingto, DC: naval Sea Systems Command, 2008
• joint pain only
– but not bilateral back, abdominal pain!
• superficial rash only
– but not cutis marmorata
• subjective sensory change only
– patchy tingling, may migrate
– non dermatomal
– not objective!
• constitutional signs only
Mild DCS I
• worsening symptoms are never mild!
• complete neurological exam
• patients needs review after 12,24,36 h
• surface oxygen will accelerate recovery
• not treating mild DCS will probably not have residual effects
• which is a consideration in remote areas
• Mild DCS is not a reason not to contact DAN or not refer for recompression treatment
Mild DCS II
2004 workshop: mild DCS, DAN & UHMS
DCS – the big picture
tissue super saturation
lungs:
exhalation
veins: gas in
solution/
bubbles
tissue gas bubbles venous gas bubbles
growth by diffusion
tissue: ischemia and
distortion
• vestibulocochlear
• spinal
• joints bends
• osteonecrosis
growth by coalescence
endothelial effects
respiratory: chokes
arterialization
• neuro DCS
• cutis marmorata
• vestibulocochlear
• spinal
Differential diagnosis
• difficult diagnosis, no lab test
• inner ear barotrauma
• alternobaric vertigo
• fascial nerve compression
• contaminated breathing gas (CO)
• musculo skeletal strain
• immersion pulmonary edema
• water aspiration
• allergic/toxic skin rash
• coincidence of neurological & cardiac symptoms in the unfit older diver
lecture:
ENT & diving
First-aid treatment
• ABC approach
• Recue diver training
• supine (or lateral decubitus if unconscious)
– buoyancy has no effect on distribution of arterial or venous air
– mild DCS (pain only) can sit.
Butler BD, Laine GA, Leiman BC, et al. Effects of trendelenburg position on the distribution of arterial air emboli in dogs. Ann Thorac Surg 1988;45:198-202
First aid treatment
• 100% oxygen
– FiO2 as high as possible, enriched air, CCR
– continue after symptoms reversal until recompression
• fluid administration oral or IV
– no hypotonic fluids
– no firm guidelines
– 1 liter 0.9% saline/ hartman every 4 h
– aim at diuresis 1-2 ml/kg/h
– severe DCS requires aggresive fluid suppletion
• contact DAN
Longphre JM, et al. First aid normobaric oxygen for the treatment of recreational diving injuries. Undersea Hyperb Med 2007;34:43-49
Additional therapy
• seizures
– diazepam rectal
– phenytoin (Dilantin): 500 mg in 10’ , 100 mg in 30’ i.v.
• bladder catheter if spinal DCS
• air evacuation
– < 1000ft
– no entonox
Bennett M, et al. Adjunctive treatment of decompression illness with a non-steroidal anti-inflammatory drug (tenoxicam) reduces compression requirement. Undersea
Hyperb Med 2003;30:195-205
Evacuation
• preferably pressurized airplane or < 1000 ft
• remote location, no air evac to be expexted soon:
– pain only: short commercial flight + O2 suppl.
– mild neuro signs: wait 24 h then commercial flight + O2 suppl.
Mitchell SJ, et al. Management of mild or marginal decompression illness in remote locations. Durham, NC: Divers Alert Network;2005
Recompression therapy
Why recompression?
• bubble compression
• increased inert gas washout
• tissue oxygenation
• decreased PMN/platelet adhesion
table 6
• extension possible
• deeper ? if symptoms progress or don’t change within first 20 min
U.S. Navy table 6
Post recompression
• flying after treatment
– symptom free
– 72 hours
• diving after DCS (civilian)
– symptom free +
– 30 days following treatment
• evaluation: why did this diver have DCS?
• MRI brain/ spinal cord @ 1 wk, 4 wks
– if persistent signs/symptoms
UHMS best practise guidelines, prevention and treatment of decompression sickness and arterial gas embolism, 28 April 2011
Provocative mechanisms
• Pre dive
– dehydration
• Bottom phase
– vasodilation (warm water, exertion)
– more N2 uptake
• Decompression phase
– lack of movement
– less N2 mobilization
• Post dive
– vasodilation (hot shower?, exertion)
– straining (bubble release, valsalva)
Protective/preventive actions
• Pre dive
– physical condition
– no dehydration
– exercise (micro nuclei)
– vibration (micro nuclei)
– sauna (micro nuclei, HSP?)
– oxygen (denitrogenation)
• Bottom phase
– cold water
– no exertion
– decrease depth & time
• Deco phase
– no hypothermia
– mild exercise
– oxygen
• Post dive
– avoid exertion
– avoid hyperthermia
– hydration
– oxygen
Gempp E, Blatteau JE. Preconditioning methods and mechanisms for preventing the risk of decompression sickness in scuba divers: a review. Research in sports medicine 2010:18:205-218
Hydration
Golden rules DCS
• symptoms occurring at depth or during compression can’t be DCS
• symptoms starting > 24 h are most unlikely due to DCS
• symptoms onset < 10 min pulm barotrauma with CAGE more probable
• no DCS after dive to less then 6 m depth (rare up to 10 m dive)
• DCS is a clinical diagnosis, don’t let lab/radiology delay treatment
• DCS is 100% curable if immediate recompression
• good review: Lancet 2011;377:153-164
• There is no lab test for DCS, it is a difficult clinical diagnosis. Always confer with a dive medical physician (DAN)
Van Liew HD, Flynn ET. Direct ascent from air and n2-O2 saturation dives in humans: DCS risk and evidence of a threshold. Undersea Hyperb Med 2005;32:409-19
• good review: Lancet 2011;377:153-164
• Pollock NW and Buteau D. Updates in decompression illness. Emerg Med Clin N Am 2017;35: 301–319
