Delayed hyperbaric oxygen therapy for air emboli after open heart surgery: case report and review of a success story
Niyibizi et al. Journal of Cardiothoracic Surgery
Delayed hyperbaric oxygen therapy for air emboli after open heart surgery: case report and review of a success story
Eva Niyibizi 0 1 4
Guillaume Elyes Kembi 3
Claude Lae 2
Rodrigue Pignel 6
Tornike Sologashvili 5
0 Division of Emergency Medecine, County Hospital, University of Geneva , Geneva , Switzerland
1 Emergency Medicine Division, Hopitaux Universitaires de Genève , Rue Gabrielle-Perret.Gentil 4, 1205 Geneva , Switzerland
2 Department of Emergency and Primary Care Medecine, County Hospital, Hyperbaric Center, University of Geneva , Geneva , Switzerland
3 Department of Anesthesiology Pharmacology and Intensive Care, County Hospital, University of Geneva , Geneva , Switzerland
4 Emergency Medicine Division, Hopitaux Universitaires de Genève , Rue Gabrielle-Perret.Gentil 4, 1205 Geneva , Switzerland
5 Division of Cardiac Surgery, County Hospital, University of Geneva , Geneva , Switzerland
6 Department of Emergency and Primary Care Medicine, County Hospital, Hyperbaric Center, University of Geneva , Geneva , Switzerland
Background: The current case describes a rare diagnosis of iatrogenic air emboli after elective cardiopulmonary bypass that was successfully treated with delayed hyperbaric oxygen therapy, with good clinical evolution in spite of rare complications. Case presentation: A 35 years old male was admitted to the intensive care unit (ICU) for post-operative management after being placed on cardiopulmonary bypass (CPB) for an elective ventricular septal defect closure and aortic valvuloplasty. The patient initially presented with pathologically late awakening and was extubated 17 h after admission. Neurologic clinical status after extubation showed global aphasia, mental slowness and spatiotemporal disorientation. The injected cerebral CT scan was normal; the EEG was inconclusive (it showed metabolic encephalopathy without epileptic activity); and the cerebral MRI done 48 h after surgery showed multiple small subcortical acute ischemic lesions, mainly on the left fronto- parieto- temporo-occipital lobes. He was taken for hyperbaric oxygen therapy (HOT) over 54 h after cardiac surgery. The first session ended abruptly after 20 min when the patient suffered a generalised tonico-clonic seizure, necessitating a moderately rapid decompression, airway management, and antiepileptic treatment. In total, the patient received 7 HOT sessions over 6 days. He demonstrated full neurological recovery at 4 weeks and GOS (Glasgow Outcome Scale) of 5 out of 5 even after a long delay in initial management. Convulsions are a rare complication of HOT either due to reperfusion syndrome or hyperoxic toxicity and can be managed. Prior imaging by MRI or tympanic paracentesis (myringotomy) should not add further delay of treatment. Conclusion: HOT should be initiated upon late awakening and/or neurologic symptoms after CPB heart surgery, after exclusion of formal counter-indications, even if the delay exceeds 48 h.
Iatrogenic cerebral air emboli; Neurologic deficit; Cardiopulmonary bypass (CPB); Cardiac surgery; Hyperbaric oxygen therapy (HOT)
Iatrogenic air emboli is a 0.1% complication of CPB,
largely under-diagnosed and under-reported with high
morbidity (13–71%) and mortality (5–23%). Cerebral
Arterial Air Embolism is a clinical diagnosis; its risk
factors should be known and a high index of suspicion
should be maintained. HOT should be considered and
initiated in the absence of formal counter-indications,
even if the delay is over 48 h.
A 35 year old male was admitted to the hospital for
elective cardiovascular surgery for a congenital
Ventricular Septal Defect with a moderate left-right shunt and
aortic insufficiency, also known as the Laubry-Pezzi
Syndrome. He was diagnosed at age 25. Relevant
medical history included severe penicillin allergy, type 2
diabetes, hypertension, dyslipidemia, and history of
endocarditis of the pulmonary valve with resultant
moderate pulmonary valve insufficiency.
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The elective surgery consisted of a closure of the
ventriculo-septal defect (VSD) and aortic valvuloplasty,
under cardiopulmonary bypass (CPB). The whole
operative procedure lasted five hours and thirty-five minutes,
with aortic clamping duration of one hour and nine
minutes, and extracorporeal circulation time of one hour
and twenty-nine minutes. The patient underwent
combined general and epidural anesthesia. Perioperatively he
was hemodynamically stable, and weaning from CPB
was uneventful. The transoesophageal echocardiography
(TOE) performed by the anesthesiologist after the
declamping of the aorta, however, showed a significant
amount of residual air bubbles, which were then
immediately extracted through the aortic canula until
The patient was transferred to our multidisciplinary
intensive care unit around 5 pm right after the surgery.
Upon his arrival, he was still intubated but not sedated.
The primary clinical examination showed GCS of 11,
bradypnea, poor vigilant state, both pupils constricted in
myosis but no neurologic focal deficit. His first arterial
blood gas showed a respiratory acidosis. All of these
findings were consistent with opioid impregnation or a
slow metabolic clearance of anesthetic agents. His
conscious state and frequents apneas required him to stay
on mechanical ventilation with assisted and controlled
mode until the end of the night.
On day 1 he was extubated and his neurological
examination showed slowness, spatio-temporal disorientation,
severe motor and sensory aphasia, no response to simple
orders, and no limb deficit. The brief neuropsychological
examination in his native tongue at his bedside with a
certified interpreter confirmed similar findings. At that
stage, the differential diagnosis was a cerebral vascular
event - ischemic or haemorrhagic, epilepsy, or an air
emboli. The hypothesis of an air emboli was discussed with
the operating surgeon and the anesthesiologist, who
both confirmed that during the procedure there had
been a considerable amount of air bubbles after
decanulation of the aorta, an occasional event occurring with
CPB; however, no additional transoesophageal
echocardiograpy was performed in the ICU at that time.
An injected cerebral CT scan was performed and
excluded a recent ischemic attack or secondary bleeding;
all arteries were patent. After neurologist consultation,
the patient was treated for a small vascular ischemic
attack, based on the sole clinical diagnosis, and without
specific radiographic findings. He received intravenous
aspirin (250 mg) and appropriate hemodynamic monitoring.
On day 2, an MRI showed restricted diffusion and
cortical lesions (Fig. 1) in the left temporal-parietal and
occipital areas, and additional multiple small punctiform
lesions in the subcortical areas (in frontiers territories)
(Fig. 2) left frontal superior, left precentral, and two
Fig. 1 MRI diffusion sequences showing restricted diffusion in the
left temporal parietal and occipital areas
other bilateral milimetric lesions on the posterior part of
the body of the corpus callosum. All of these small
lesions were compatible with acute ischemic lesions.
However the small size of the lesions was not consistent
with the loud clinical status and a potential subclinical
status epilepticus was evoked. The EEG done on day 2
excluded the presence of epileptiform activity and
showed a slow tracing compatible with metabolic versus
toxic encephalopathy, a nonspecific finding in ICU
patients; but a definitive diagnosis could not be confirmed.
Because of the pathologic awakening, persistent
neurologic deficit of global aphasia, recent open heart surgery,
and the results of outside clinical investigations, we
decided collegially to reconsider the possible diagnosis of
an air emboli, and assess for hyperbaric oxygen therapy.
Luckily, our university medical center in Geneva
possesses a renovated hyperbaric chamber with a medical
team available 24/7. We contacted them to get their
expert opinion, and considering the delay of over 45 h
but of less than 72 h, they agreed to take the patient for
a few sessions over 3–4 days in the hyperbaric chamber
since there was no known contraindications (i.e: undrained
pneumothorax, cardiac failure, uncontrolled hypertension,
untreated epilepsy and acute severe asthma). The patient
entered the hyperbaric chamber accompanied by an
intensive care resident doctor, an anesthesiologist and a nurse at
11:30 pm (day2); i.e. 54 h after surgery.
The initial plan (Fig. 3) was to do a first profound
compression session CX30 of 7 h and 30 min, starting
the first 10 min with pure oxygen up to 2.8 ATA in
order to crush the gaz bubble; followed by with a 50%
helium-oxygen mix at 4 ATA for the rest of the session.
The compression went smoothly. However 20 min after
the beginning of the session, at a level of 4 ATA the
patient suffered a generalized tonico-clonic seizure,
followed by new onset rapid atrial fibrillation and
massive bronchoaspiration requiring a moderately rapid
decompression, interruption of the session and evacuation
of the patient from the chamber. The patient was
transferred back to the ICU for stabilisation, airway
management with re-intubation and sedation, hemodynamic
stabilisation and antiepileptic treatment with adequate
therapy (propofol, midazolam, clonazepam, levetiracetam).
Another cerebral CT scan did not show any new lesion.
After stabilisation, he was taken back to the hyperbaric
chamber and the rest of the session (170 min with 50%
helium-oxygen mix at 4 ATA) went without any new
complications. He suffered a new episode of focal convulsion
of the left superior arm one hour after his return from the
session that necessitated the adjunction of thiopenthal
He received a third session of HOT later (day 3) under
mechanical ventilation during 150 min at 2.5 ATA with
pure oxygen. On day 4, he also received a 150 min
session of HOT while still intubated. He was extubated on
day 5, and for the next 2 days the patient underwent
each day (day 5-6-7) 1 short session of 95 min under
simple mask at 2.5 ATA. In total, the full treatment of
HOT consisted of 7 sessions over 5 days.
Except for the adverse events of the first session, all of
the remaining sessions went smoothly without
complication. The patient recovered rapidly, and was transferred
out of the intensive care unit into the cardiovascular
surgery ward 6 days after admission. The EEG done at
day 5 showed no epileptic activity and the antiepileptic
agents were stopped after the HOT sessions were
resumed. After the 7th session of HOT at day 7, the
patient’s neurological status showed a slight residual
spatio-temporal orientation, slowness of speech and a
Fig. 3 Timeline of Hyperbaric Sessions
moderate loss of words but his language was informative
and he showed no more comprehensive deficit.
Considering the good neurological response and improvement on
orientation, speech, and psychomotor slowness, HOT
sessions were resumed.
On day 14, a control cerebral MRI was done and showed
subacute ischemic small punctiform lesions in the right
fronto-orbitary region, left pre-central and left
temporooccipital region. The previous extended left cortical
occipitoparieto-temporal lesion had disappeared, and was probably
due to vasogenic edema. The neurovascular specialists and
neuroradiologists concluded that the subcortical and
bilateral corpus callosum punctiform lesions were highly
compatible with air emboli lesions and therefore there was no
indication to pursue aspirin medication upon discharge.
On day 19, a neuropsychological evaluation in English
was done, although not in his native tongue, and showed
good neurological recovery without pathological
sequellae compared to the adult reference population. Detailed
examination revealed no orientation disorders. The
behavioural analysis showed a slight psychomotor slowness
with a lack of task initiation, a discrete lack of verbal
spontaneity in the executive area, and borderline
memory tests results showing a slight weakness in the
episodic, verbal and visuo-spatial memory. There were
no language, calcul, or graphic deficits, no speech
impairment, and no sign of corpus callousum defect. All of
these findings showed mild weaknesses in the mnesic,
executives and attentional areas which were compatible
with the MRI lesions.
Figure (Fig. 4) summarizes the Timeline of events as
they occured sequentially. The patient was discharged
from the hospital on post-operative day 23 in good
clinical condition, with a neurologic follow up scheduled
8 weeks later. Upon discharge, the Glasgow Outcome
Score was of 5 out of 5. (GOS 1: death. GOS 2: vegetative
state with no obvious cortical function. GOS 3: severe
disability –conscious but disabled with dependency.
GOS 4: moderate disability but independent. GOS 5:
complete recovery with resumption of activity, although
the patient might show some minor neurological
Over 5 months after his surgery, a follow-up phone
call was made. The patient reported a good recovery. He
had mild overall fatigue and had not yet gone back to
work, but was without neurological deficit.
Discussion and literature review
Open heart cardiac surgery with extracorporeal circulation
is one of the known causes of air embolism  most of the
time by entry of air into the extracorporeal bypass pump
circuit directly into the systemic circulation, or into the
pulmonary veins in case of paradoxical embolism, or in
case of incomplete removal of the air from the heart after
cardiac arrest [2, 3].
The precise incidence of iatrogenic cerebral arterial air
embolism is unknown mostly due to underdiagnosis,
underestimation, underreported cases, and seldom
nonspecific or transient symptomatology [4, 5]. Some
previous authors estimated the incidence of 0.1% of all
extracorporeal circulation . In 2010, the risk was estimated
at 2.6/100 000 procedures. However, although rare, it
compasses a prolonged hospital stay with a high
morbidity (13–71%), and a high mortality (5–23%) .
There are a few common risk factors for post cardiac
surgical stroke, such as age, hypertension, diabetes, and
previous history of vascular ischemic attack [8–13].
However, there is some evidence that procedures with
cardiopulmonary bypass are more at risk of stroke as opposed
to “beating heart” cardiac surgery [14–17]. Valvular
replacement surgery is also a greater risk since the ventricle
is opened as opposed to coronary artery bypass grafting
[8, 11, 12, 18]. Along that line, another risk factor
described is any surgery in which the left ventricle and/or
the aorta is opened .
In a brief reminder of the pathophysiology of
cerebral arterial air embolism, we learn that any arterial
gas bubble with a size over 30–60um can obstruct
the circulation and cause damage through various
mechanisms: irritation of the endothelium, cell injury
and intra neuronal oedema, inflammation causing
vasogenic oedema, and tissue hypoxia. All of these
processes will lead to a deficit of perfusion and distal
Over the last 30 years, many efforts have been made
to increase the number of prospective and clinical
studies. Unfortunately, due to technical and ethical
restrictions and the hyperbaric centers accessibility there isn’t
a clear level of scientific evidence .
In 2012, Expert Consensus Societies in Europe (ECHM:
European Committee for Hyperbaric Medicine) and in
America (UHMS: Undersea and Hyperbaric Medical
Society) published recommendations recognizing Iatrogenic
Symptomatic Air Emboli as one of the four indications for
urgent treatment by HOT .
In case of iatrogenic symptomatic air emboli, HOT is
an adjunct treatment, recommended after conventional
treatment of patient positioning, evacuation of air, 100%
oxygenation, retrograde perfusion, optimisation of
cerebral blood flow, and supportive ventilation measures
and/or vasopressors if needed.
Experimental studies showed that delay in initiating
HOT was inversely related to its efficacy . Benefits
were shown, however, even if the treatment started 12 h
after the ischemia when it was a single session treatment
, and 24 h for a daily session during a week of
treatment . One can then think that the delay in initiating
Fig. 4 Timeline of Events
the HOT could be partially reversed by increasing the
number of sessions administered.
Although there is no level of evidence 1A for HOT use
in iatrogenic symptomatic arterial air embolism due to
ethical reasons , there are some indirect proofs of
efficacy since two studies of respectively 86 and 119 patients
showed a better recuperation prognosis when HOT is
done within the first 6–7 h after the incident [7, 23].
In a 22-year retrospective review of 36 patients who
sustained cerebral arterial gas embolism with acute
neurologic deficit and were treated with HOT, over 72%
patients improved after 24 h. A short (less than 6 h)
time to treatment and a young age (less than 45 years)
were the two most favourable prognostic factors. The
two least favourable prognostic factors were oedema or
infarct on the cerebral CT at 24 h after HOT, and the
association of cardiopulmonary symptoms .
The diagnosis of postoperative iatrogenic cerebral
arterial gas emboli is difficult, mostly due to several
confounding factors: general anesthesia limiting or delaying
a precise neurological examination, cerebral imaging
showing different or little results, and low index of
suspicion from the medical team.
Based on the literature review, we can conclude that the
patient discussed here, although younger than 45 years
old, had many risk factors for post-operative stroke (and
iatrogenic cerebral arterial embolism): hypertension,
diabetes, cardiopulmonary bypass and valvuloplasty.
Research shows that the results of cerebral imaging by
CT or MRI in a patient presenting with a neurological
deficit after cardiac surgery are often nonspecific and do
not allow the definitive diagnosis or exclusion of cerebral
arterial gas emboli, and thus should not extend the delay
for initiating HOT [2, 4, 25, 26].
In the initial management of this patient, some of the
type A medical thinking errors were made on clinical
assumptions or tunnel vision, provoking a significant delay
in the management of air emboli. The two main reasons
we self-critically observed are: first, we had a low index
of suspicion, probably due to its very low prevalence;
therefore, we wasted time excluding and confirming
other diagnoses. Secondly, we thought that even if it was
indeed an air emboli, the delay was already too long and
therefore no treatment such as HOT could be effective.
In the risk/benefit analysis of HOT, a few practicalities
must be considered: the patient’s stability, the availability
and accessibility of the nearest HOT center, and the
absence of contraindications. However, many hyperbaric
medicine centers such as ours can now manage
intubated and sedated patient equipped with up to two
continuous IV pumps, along with a one-on-one intensive
and/or anesthesiology specialised caregiver.
The main risks of the hyperbaric oxygen therapy are rare,
and are due to oxygen toxicity on the cardiovascular and
neurologic systems. Hyperoxic convulsions are
exceptionally rare and due to the reperfusion phenomenon. They
usually resolve after stopping the oxygen administration.
In order to avoid unexpected tympanic membrane
perforation, our patient had a preventive myringotomy due
to his inability to follow simple commands; however this
procedure is not mandatory and should not extend the
delay to start HOT sessions.
Based on our multidisciplinary experience as intensivist,
anesthesiologist, cardiac surgeon, hyperbaric specialist,
and acute care, these are the main criteria that we
recommend for advising hyperbaric oxygen therapy:
1. Any medical or surgical procedure considered
at risk (extracorporeal circulation, central lines
manipulation, coelioscopy with high abdominal
pressure, open heart-surgery, seated position
2. Perioperative or postoperative neurologic symptom or deficit of any nature, including a late awakening after general anesthesia
3. Accessibility to the hyperbaric chamber
4. Patient stability
5. A well trained team of intensivists or anesthesiologists, provided with the right equipment to care for the intubated and sedated patient while in the hyperbaric chamber
6. Absence of contraindications (i.e: undrained pneumothorax, cardiac failure, uncontrolled hypertension, untreated epilepsy and acute severe asthma)
As stated above, radiographic proof or documentation
is not mandatory before initiating HOT, since air emboli
is first and foremost a clinical diagnosis, and the
neuroradiologic findings are nonspecific in the early hours after
Finally, little is described in the literature regarding the
natural history of iatrogenic cerebral arterial air embolism.
One may argue that with such a delay of over 54 h prior
to HOT, the successful evolution of the patient with
complete recovery at 30 days (Glasgow Outcome Scale of
5 out of 5) could be attributed to the natural evolution of
the disease, and not so much to the HOT. However, the
frequent natural outcome of iatrogenic gas bubble is
to be rapidly removed by the pulmonary filters. In
our experience, when that is the case, the arterial
emboli is eliminated within a few hours with a
spontaneous favourable outcome. Unfortunately, if the bubble
stays trapped for a period longer than 24 or 36 h, the
apoptosis mechanisms are already taking place and
necrosis of the cerebral tissue occurs, with risks of
sequelae comparable to any other blood clot causing
an ischemic cerebro-vascular event.
The fact that our patient’s neurologic deficit did not
improve nor deteriorate during the 54 h preceding the
HOT, but improved drastically after the treatment, is a
strong argument in favour of the beneficial effects of
hyperbaric oxygen therapy.
Post-operative cerebral arterial air emboli is a tricky,
mimicking, underdiagnosed, underreported and rare entity
with a high morbidity and mortality index. Therefore, the
diagnosis should be made as early as possible with a high
index of suspicion and solely on the clinical context
(personal risk factor, surgery at risk, delayed awakening and/or
neurological deficit). The neuro-imaging can exclude
other diagnosis and orient but should not delay the
initiation of hyperbaric oxygen therapy (HOT). In the absence
of contraindications, assessing for patient stability and
center accessibility are important factors that need to be
part of the multidisciplinary discussion early on, in order
to limit delay in management.
To this day, there is no randomised controlled trial or
any other prospective study clearly setting a maximum
delay for initiating HOT when having a suspicion of air
emboli. However, for ethical reasons, and after a review
of the literature, we advocate initiation of HOT, even
with a delay over 48 h, whenever possible.
1 ATA: One atmosphere absolute (=760 mmHg baric pressure at sea level);
CPB: Cardiopulmonary Bypass; CT: Computed tomography;
ECC: Extracorporeal circulation; EEG: Electroencephalogram; GCS: Glascow
coma scale; GOS: Glasgow outcome scale; HOT: Hyperbaric oxygen therapy;
ICU: Intensive care unit; MRI: Magnetic resonance imaging; VSD:
I, the corresponding author, would like to thank all of the contributing authors
for their relecture and correction of the manuscript and for their expert advices.
EN wrote the manuscript, conducted the literature review and obtained the
patient’s consent. GK conducted a relecture of the manuscript and made a
significant contribution to the anesthesiology and intensive care aspects of
the case. CL conducted a relecture of the manuscript and contributed as a
hyperbaric expert on the case. RP conducted a relecture of the manuscript
and contributed as a hyperbaric expert on the case. TS conducted a
relecture of the manuscript and contributed as the treating cardiac surgeon
on the case. All authors read and approved of the final manuscript.
Consent for publication
Obtained with signature.
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