Case report

Cerebral air embolism from a Central Venous
Catheter: A timely reminder of the importance of
rapid diagnosis
Muhammad Farhan Khaliq,1 Maria Shoaib,2 Syed Maaz Tariq,3
Muhammad Taimoor Khan4
1

Department of Internal
Medicine, CAMC Health System,
Charleston, West Virginia, USA
2
Department of Neurology,
University of Oklahoma Health
Sciences Center, Oklahoma City,
Oklahoma, USA
3
Jinnah Sindh Medical
University, Karachi, Sindh,
Pakistan
4
Department of Neurology,
CAMC Health System,
Charleston, West Virginia, USA
Correspondence to
Dr. Muhammad Farhan Khaliq,
​muhammadfarhankhaliq@​
gmail.​com
Accepted 23 July 2018

Summary
Cerebral air embolism (CAE) is a rare, avoidable and
potentially fatal iatrogenic complication. Here, we
report a case of CAE associated with a central venous
catheter in the internal jugular vein that resulted
in neurological deficits and generalised epileptic
seizures. A 64-year-old man admitted for fasciotomy
for compartment syndrome developed CAE with leftsided neurological deficits. The suspected origin was
retrograde air flow from the right internal jugular
venous catheter. The air spontaneously resorbed
without the need for specific therapy, and he made
a good recovery. CAE is an infrequent iatrogenic
complication that requires prompt diagnosis to avoid
significant morbidity and mortality. This case serves
as a timely reminder that adverse outcome such as
stroke, seizures or death can be avoided by a high
index of suspicion and prompt diagnosis. Hyperbaric
oxygen is the prime therapeutic measure, but highquality evidence on its clinical value is lacking.

Background
Cerebral air embolism (CAE) is a preventable
iatrogenic complication. Aetiologies include
diagnostic and therapeutic interventions such as
manipulation of central venous catheters (CVC),
bronchoscopy, endoscopy, open heart surgery,
thoracotomy and neurosurgical procedures.
Non-iatrogenic causes have also been reported
including deep sea diving, high altitude accidents, trauma, childbirth and oral-genital sex.1–3
Here we present a case of a 64-year-old man who
developed left-sided sensorimotor defects and
status epilepticus due to an air embolism originating from right-sided internal jugular venous
catheterisation. This case highlights the importance of prompt diagnosis to avoid adverse and
potentially fatal sequelae.
© BMJ Publishing Group
Limited 2018. No commercial
re-use. See rights and
permissions. Published by BMJ.
To cite: Khaliq MF, Shoaib M,
Tariq SM, et al. BMJ Case
Rep Published Online First:
[please include Day Month
Year]. doi:10.1136/bcr-2018225120

Case presentation
A 64-year-old man with a medical history of
chronic obstructive pulmonary disease underwent fasciotomy for compartment syndrome
arising from acute limb ischaemia. He had an
uneventful recovery and was transferred to
the general telemetry floor in stable condition.
A CVC was placed in the right internal jugular

vein in the intensive care unit for medicine and
fluid administration.
Next day, the patient developed severe, leftsided leg pain that required repeat exploratory
fasciotomy resulting in evacuation of a large
haematoma. The patient required fluid resuscitation with several bags of normal saline. During
fluid resuscitation, he was sitting in a semirecumbent position. Several minutes later, a nurse
walked in the room and noticed that he was unresponsive with his hands and feet curled up. His
body was noted to have increased tone and bent
towards the left side with left-sided tonic-clonic
convulsive activity witnessed by the staff. His
vital signs obtained at that time were heart rate
120 bpm, blood pressure 85/40 mm Hg, respiratory rate 30 per min and oxygen saturation 60%
on ambient air. On chest auscultation, patient had
no cardiac murmur and bilaterally equal breath
sounds. Neurological examination revealed a
lethargic patient who was disoriented and could
only follow one-word commands with difficulty.
Further examination revealed left-sided hemiplegia with left facial droop. Due to this sudden
change in his haemodynamic and neurological
status, a medical emergency teamwas calledto
stabilise the patient. The patient was treated
with 100% oxygen via a non-rebreather mask
with little improvement, so bedside intubation
was performed.

Investigations

An emergent CT scan within 30 minute of
symptom onset revealed serpiginous gas attenuation over the right posterior parietal lobe indicating gas in the cerebral vessels (figures 1). CT
angiography (CTA) (performed only in the arterial phase) within an hour of the first CT scan
and 2 hours after symptom onset demonstrated
good blood flow without any filling defects.
Magnetic Resonance imaging (MRI) with diffusion-weighted imaging performed within 3 hours
of symptom onset did not reveal any significant
pathology. The possibility of vascular air embolism originating from a mishandled central venous
line was considered. The line was checked. All
unused hubs on the line were closed, the CVC
and delivery devices showed no evidence of
leakage. At the time of the event, the patient was

Khaliq MF, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2018-225120

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Reminder of important clinical lesson

He underwent successful extubation. The rest of the clinical course was uneventful and, by discharge, he had made a
complete recovery.

Discussion

Figure 1 Axial view of head CT demonstrating air in the cerebral
vessels.
resuscitated with fluids in a semirecumbent position. Authors
suspect that it could be due to lack of priming or hubs being
open or connections not tight for a shorter amount of time
that could have resulted in 15–20 mL of air entry.
CTA of the chest remained negative for pulmonary embolism and showed no air on the right side of heart. Transoesophageal echocardiography (TOE) with agitated normal
saline did not reveal right-sided opacification or microbubbles in several cardiac cycles, ruling out intracardiac (right
to left atrial shunts) and intrapulmonary shunts, respectively.

Treatment

Over the next few hours, the patient continued to have
tonic-clonic jerks on the left side. Electroencephalogram
was performed that confirmed the presence of epileptiform
discharges. The patient required intravenous levetiracetam.
The CVC was removed and alternative access was established. Due to resolution of air on CTA and unavailability
of hyperbaric oxygen therapy, he was treated conservatively
with 100% oxygen.

Outcome and follow-up

The next day, he was given an awakening trial and did not
have neurological deficits on neurological examination.
2

CAE is a rare, preventable, but serious iatrogenic complication resulting in significant morbidity and mortality.4 CAE
is widely under-reported. CAE should be considered in
patients with sudden neurological deterioration, particularly
after central venous or arterial manipulations, neurological
procedures, or interventional procedures such as bronchoscopy, endoscopy and haemodialysis when the patient is in
the sitting, semi-sitting, or standing posture.1–3 The most
common neurological symptoms reported are focal neurological deficits, coma, seizures, encephalopathy and headache. Neurological manifestations mainly arise from damage
occurring in the right brain hemisphere owing to the more
central position of the right carotid artery and right internal
jugular vein, as was the case with our patient, who developed
left-sided sensorimotor deficits.
CAE can be arterial, venous or both. It is difficult to
differentiate arterial from venous embolism as air entry can
occur concomitantly. Air embolism can take different pathways depending on patient position during CVC insertion or
manipulation. Cerebral air entry can take place in a retrograde fashion in the venous circulation when the patient is
in an upright position, which we suspect in our case.5 More
commonly, air can travel to the heart while the patient is
in the supine position and pass into the ventricle and lungs,
causing dyspnoea, cough, chest tightness and arrhythmias. It
can also migrate to the arterial side from the venous side via
intracardiac shunts (eg, patent foramen ovale) or intrapulmonary shunts (eg, arteriovenous malformations, intrapulmonary physiological shunts).6 Physiologically, pulmonary
capillaries can filter out air bubbles, thereby protecting the
venous and arterial circulations. However, if the air bubble
exceeds the filtration capacity threshold of the pulmonary
capillaries, pulmonary oedema or arterial air emboli can
occur as mentioned above.7 8 History, physical examination,
imaging including CT/CTA/MR angiography/MR venography, CTA chest, transthoracic echocardiography, TOE and
transcranial Doppler can provide helpful cues to the aetiology and for differentiating arterial from venous embolism.
Early diagnosis and urgent intervention are crucial and
may reduce morbidity and mortality from CAE.4 Current
treatment includes immediate stopping of the embolic procedure, placing the patient in the supine position in cases of
retrograde ascension of air (rather than in a Trendelenburg position to avoid any potential worsening of cerebral
oedema), aspirating air through a CVC, external cardiac
massage and administering 100% supplementary oxygen to
decrease nitrogen in the alveoli.6 9
Hyperbaric oxygenation (HBO) should be considered in
the presence of neurological deficits and is probably the
only management approach that is proven effective for both
venous and arterial air embolism.10 HBO works by increasing
the partial pressures of dissolved oxygen in the plasma,
leading to increase oxygenation in the ischaemic tissue and
favouring denitrogenation.10 The optimal time frame for
initiating HBO is uncertain. The evidence suggests early
initiation is preferred and improves outcomes.10 However,
a delayed diagnosis should not discourage treatment with
hyperbaric oxygen, and there is some evidence of recovery of
Khaliq MF, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2018-225120

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Reminder of important clinical lesson

neurological function in patients treated late with HBO.11 12
In our case, the patient developed sudden neurological deficits and was found to have air on CT scan that resolved
within an hour on repeat CT with 100% oxygen. Lack of
availability of HBO in our tertiary care centre, full resorption
of air on repeat CT scan and the critical condition of our
patient prevented transfer to an HBO facility.
In our case, no mishandling was reported by the staff
during CVC use, but we suspect this was due to under-reporting, lack of knowledge or awareness. The patient had
fluid administration prior to the event, and CAE could be
attributed to the lack of priming or capping of the unused
hubs. Further, his semirecumbent position made him vulnerable to air aspiration during inspiration, hence retrograde
ascension of air directly to the brain. Some studies have
reported rapid symptom onset; however, we noticed a delay
in our case as reported by Yesilaras and colleagues.13 This
could be due to only a small volume of air entering at a slow
rate.14
Since CAE associated with CVC is largely preventable, we
emphasise the importance of careful handling of CVCs and
reiterate some precautions. After catheter is inserted, adhesive tape and sutures should be applied to prevent dislodging.
It is imperative to ensure all connections are tight and unused
hubs are locked when the catheter is not in use. As learnt
from our case, it is crucial to prime the tubing and expel
air from all syringes to be connected to the catheter. During
CVC removal, the same position, that is, head down or Trendelenburg, should be used. This prevents the central venous
pressure (CVP) from dropping below atmospheric pressure, and the patient should be instructed to avoid talking,
coughing and breathing in. If possible, the highest CVP can
be achieved with the Valsalva manoeuvre, resulting in the
greatest protection against air embolism. Adequate pressure should be applied to achieve haemostasis after catheter
removal followed by application of an air-occlusive dressing
for 24 hours. It is recommended that the patient remains
supine for 30 min after central venous access removal. Institution protocols should be followed for insertion and removal,
along with regular training of staff to reduce or prevent any
complications.6
This iatrogenic case is an important reminder of the danger
of CAE and that clinical vigilance by all staff is required
to prevent this avoidable complication and unnecessary
morbidity and mortality.

Learning points
►► Cerebral air embolism is an avoidable complication that can

result from central venous catheterisation.

►► Early diagnosis by relevant imaging is important to reduce

morbidity and mortality.

►► Treatment with hyperbaric oxygen should be considered, if

available.

►► Precautionary measures can significantly reduce the chances

of developing air embolism.

Contributors MFK was involved in the care of the patient. MFK and MS came up
with the initial plan. SMT prepared the initial draft of the manuscript. MTK searched
for the literature and critically reviewed it. MS, MFK and SMT prepared the final
manuscript. In the end, all authors read and approved the final manuscript.
Funding The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.

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Reminder of important clinical lesson