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Steve Berrill

Provisional Fellow
Arterial Gas Embolism 2006
Photos Dr Robert Wong.
What Causes it?
• Diving accidents. 10% of Fremantle’s 40 per year
– Presentation.
– Pathophysiology.
– Treatment.
– Case report
• Iatrogenic.
– Review of Diagnosis and management.
Venous Versus Arterial Air.

• Venous air isn’t too bad.


– Studies show that systemic venous bubbles are trapped
in the pulmonary arterial tree and are usually completely
eliminated from that site. The lung traps the air and
excretes it into alveoli from the arterioles. (RG Presson,
J Appl Physiol; 1989;67(5),1898-1902)
• Dyspnoea, Pulmonary hypertension, ARDS, Overload
pulmonary filter.
– How much is too much?
– Dogs can survive 1 litre over 1-2 hours!
• Die with 100mls suddenly.
• Humans, unsure, probably similar. 1ml/kg?-2ml/kg
Reach Arterial System, Dense CVA,
Cardiovascular and Respiratory instability.

1. Venous gas embolism with breach of the pulmonary


vascular filter (paradoxical gas embolism).
2. Shunt
patent foramen ovale (paradoxic gas
embolism)
3. Tear of the pulmonary parenchyma with entry of
gas into pulmonary venous outflow.
Diving Related Cerebral.A.G.E
• Pulmonary barotrauma upon ascent.
– Lung volume doubles from 10m to surface.
– Holding breath
– Asthma/Gas trapping
• 1/50,000 dives
– Only need 1.2m (4ft) change in pressure!
• Terminal bronchiole/alveolar rupture, into vessel.

• Arterial embolisation of air.


• Cerebral air.
Onset

• In a series of 24 USNavy cases in which the time was


known,

– 9 occurred during ascent in the water,


– 11 within one minute at the surface and
– 4 occurred within 3-10 minutes at the surface.

– DDx: Medical Cause, ‘The Bends’, Impure Air


supply, Marine sting, panic and drowning.
Classic Symptoms and
Signs
– Group A: Die. Unconscious, cardiac arrest. 5-10%
– Group B:
– Loss of consciousness upon ascent.
– Disorientation
– Chest pain
– Paralysis or weakness
– Dizziness
– Blurred vision
– Focal or generalised convulsions
• Symptoms Bloody froth from mouth or nose
• Marbling of the skin.
• 30 % Remain unwell.
• As bubbles move on... 60% improve.
• 1/2 of these relapse minutes to hours later
due to secondary inflammation.
Management.
– Safety, Response?ABC.
– Give O2,
– Place in horizontal, neutral position
– Removal to the nearest recompression chamber.
– Air evacuation should be at sea level, (1 ATM Pressure.)
• Any bubbles will expand if ambient pressure drops.
• Including pneumothoraces.
Pulmonary barotrauma
• Less than 50% have demonstrable PBT.
• CXR/clinical examination.
• Concern about
• chamber ascent expanding PTX.
• Pneumothorax
• Tension
• Mediastinal emphysema
Tension Pneumothorax
Pneumomediastinum
CAGE
Impaired Cerebral autoregulation:
flow is maintained over a range of perfusion pressure

Promotes redistribution of bubbles:


arterial BP
surface tension of the trailing end

Promotes trapping:
surface tension at the leading end
CAGE
Bubble size is important:
small bubbles redistribute
large bubbles occupying several branching arteries
may trap, 50-60micron bubbles.
Blood Pressure:
hypotension promotes trapping
hypertension and vasodilatation promote
redistribution
• Bubbles that trap cause ischaemia in the
downstream territory
• Ischaemic neurones - loss ion homeostasis
• cascade of events leading to necrosis
• duration of trapping is critical (bubble size)
CAGE
• Bubbles that redistribute damage endothelium
• stripping surfactant => leakiness of capillaries
• impaired autoregulation
• expression of adhesion molecules - leukocytes
accumulation, secondary ischaemia.

• Secondary injury. Explains ongoing symptoms and


HBOTs effects in delayed treatment.
• DCS
• CAGE
• CO
How Does HBO2 Work?
1.

1. Bubbles move on.


2. Favours bubble shrinkage by denitrogenating
surrounding cerebral tissue.
HBOs Effects Continued.
• Decreases cerebral oedema.
• Enhances oxygenation in watershed areas.
• PaO2 2000mmHg, Oxygen content 6mls/100mls
• Anti-inflammatory effects
– Decreases Neutrophil adhesion through down-
regulating ICAM-1.
– Decreases Platelet aggregation.
– Decreases Capillary leakiness.
• Basis of daily treatment, relapses, CO and Divers.
ICAM-1
• Intercellular adhesion molecule-1 (ICAM-1)
• Ischaemia-reperfusion injury increases the
expression of CD18 and ICAM-1 and
causes increased adhesion of leucocytes on
the endothelium; hyperbaric oxygen
decreases the expression of ICAM-11:
• Ann Plast Surg. 2003 Nov;51(5):478-87
FREMANTLE TREATMENT TABLE
Multiplace - Table - USN 6 / RN 62
100% Oxygen
Air
0-5 20 5 20 5 20 5 30 15 60 15 60 30

Ascent Rate
3 metres in
10 minutes

9 Metres
Attendant commences
Ascent Rate 100% Oxygen for 30 mins
3 metres in É 9 metres to surface
10 minutes

Any extension at an y depth


É Atte ndant re quir es 90 minutes on 100% Oxyge n
18 Metres É last 60 mins @ 9 metres and 30 minutes on ascent

Treatment Time 4Hr 35min (275 mins) Revised May 2002


50/50 Heliox
FREMANTLE TREATMENT TABLE 20/80 Heliox
Multiplace - Table Comex 30 100% Oxygen
Air

Pt remains on BIBS from descent until 18m air breaks


5 60 25 5 25 5 25 5 25 5 25 5 25 5 25 5 25 5 25 5 25 5 25 5 25 5 30

Ascent Rate
3 metres in
12m 5 minutes

Ascent Rate
3 metres in
5 minutes
18m At 12 metres
First Atte ndant
Ascent Rate bec omes ‘patient' on
24m 3 metres in
5 minutes
100% Oxygen
Sec ond Attendant
Ascent Rate
3 metres in lock s in for remaind er
30m 5 minutes of tre atment

Total Duration 7 hrs 30 mins (450 mins) Revised May 2002


Mr JC. 44 year old.
• Beer gut.
• Illiterate
• Diabetic
• Previous panic under water.
– Passed his diving test?!
Boat Dive to 25m
• Over weighted
• Steel tank, borrowed gear
• Witnessed by buddy to plummet to 25m
• Clear water, buddy at 10m
• Flailed and inflated BCD.
• Rocketed to surface
• Buddy slowly ascended to help.
• Lost consciousness, started to sink!
• Help summoned to remove JC from water.
• 20min trip to boat ramp.
• GCS 7/15 by ambulance crew.
• Bends vs CAGE??
Peripheral ED.

• Erect CXR
– Bubble load to CNS.

• GCS 14/15 in Fremantle HBMU.


• No clear neurological deficit. Looked
unwell, very slow mentation
Treatment.
• Recompressed to 18 metres (2.8 ATA) 2.5
hours after accident.
• Bilateral Myringotomies in the chamber.
• IVFluids
• Concern about expanding pneumothorax
upon ascent from treatment.
Progress
• 45 minutes into 18m treatment felt much
better, looked brighter, felt normal.
• Standard RN62.
• Minor relapse each night and improved with
repeat daily treatments.
• Plateau in improvement at 4 days.
• Discharged, no residual deficit.
• Not fit to dive again.
Iatrogenic Air Embolism
• Peripheral iv line infusion of air.
• Central venous catheterisation (60%)
• often tunnelled CVCatheters by surgeons.
• Removal CVC.
• Cracked or disconnected CVC.
• Cardiopulmonary Bypass Circuit
• Range of Surgical Procedures.
Surgical
– Subatmospheric pressure in the vein/Non collapsing
Vein.
– Neck, Neurosurgery and Major ENT
– Dural Veins
– Myometrial Veins, C-Section/ Gynae
Laparoscopy
– Coagulated
– Haemodialysis.
– Laparoscopic
– THJR and Arthroscopy.
– TURP
– CEA.
– Gastroenterologists. Upper and lower GI scopes.
THJReplacement gasnet
• 57% THJR
• thought to be alternate explanation to cement
reaction.
• 10% could aspirate air.

• 80% sitting neurosurgery


• 10% cervical laminectomy
• 0.1% CVC
C-Sections Obstet Gynae Surv 1994 Jan;49(1);72-6
• 50% detectable VAEmbolism
• 25% had Chest pain or Dyspnoea.
• Usually uterine incision.
– Placenta previa
– Externalisation of uterus
– Is this clinically significant??
• Detect 1ml of air.
– Rare case reports of death/neurology.
Think of it when:
• Sucking sound when you site a CVP.
• Drop in cardiac output/capnograph, PAP
rises,
– arrhythmias,
– V/Q mismatch and hypoxia
– Cardiac arrest.
• When your patient doesn’t wake up
normally.
Rare, ?1 per year
Diagnosis
• Clinical
• Doppler in Neurosurgery
• TOEcho
• “Millwheel murmur is often present” NEMJ 2000 342
(7) 476-483

• CT need 1.3mm or larger bubbles.


• 30-60 microns.
Treatment
• Pressure on vein.
• Flood field,
• Stop surgeon
• ABC 100% Oxygen. Cease Nitrous.
• Multiorifice atrial CVC may remove some
air. 2cm past SVC into RAtrium
• Head down? 10 min right side up?, no evidence
• ?HBO.
Whats the natural history of
Gas embolism untreated?
• Summary of 27 case series, 976 cases.
Bennett and Elliot Dive Medicine 2003

• Mainly divers, some iatrogenic.

HBOT No HBOT
Full Recovery Dead Full Recovery Dead

346/436 45 74/388 151


Iatrogenic Cerebral air embolism 86
patients Marseille 1980-1999
Intensive Care Medicine 2002 28:559-563

• 1980-1999
• Retrospective study of all patients who
received HBOT for CAGEmbolism.
• Better outcome if treated within 6 hours.p<0.05
• Venous 3hour delay versus 8 hours Arterial
– Most arterial source was CBP, anesthetised
patients.
• Impaired consciousness 70%
• Focal motor deficit 60%
• Seizures 11%
• Visual 10%
• Dysarthria/Aphasia 5%
• Cardiovascular instability in 26%
• Respiratory disturbances in 23%.

• Neurological improvement in 55% after first HBO


Session.
– 40% full recovery
• 40% following second session.
– 50% full recovery.
12 year 17 patients Minneapolis
UHMS 2003 30(2) 117-122

• 5/17 immediate complete resolution of


symptoms
• 11/17 some improvement
• 1/17 no change.
• GCS 3 pre-HBOT all died.(5/17)
• One patient CVC leak over 6 days!
– Dyspnoea TNT rise Neurology. TTE day6.
HBO NEJM Feb17 2000 342(7) 476-3
• Neurology.

• Not if too critically unwell to transfer


• IABP failed at 18 metres!!
• Inotropes.
• Ventilator.
Case reports of improvement with HBOT up to 52 hours later!