Indian Pediatr 2018;55:
Neonatal Cerebral Air Embolism
and NS Kabra1
From Departments of 1Neonatalogy and 2Radiology,
Surya Children Medicare, Mumbai, India.
Correspondence to: Dr Javed Ahmed, Department of Pediatrics, Surya
Children Medicare Pvt Ltd, Mumbai, India. Email:
Received: December 23, 2017;
Initial review: March 13, 2018;
Accepted: July 21, 2018.
Background: Vascular air embolism (VAE) is
rare but potentially lethal condition, and survival is rarely reported
in newborn. Case Characteristics: A preterm (27+1 weeks)
neonate on Continuous positive airway pressure developed sudden cardiac
asystole on day 3 of life and required 30 minutes of cardiopulmonary
resuscitation. Observation: Infant had air embolism in
liver and brain. He survived but developed cystic encephalomalcia
requiring extensive neuro-rehabilitation. Message: Air
embolism should be considered as differential diagnosis of sudden
unexplained cardiac deterioration in well neonate.
Keywords: Encephalomalacia, Neonatal stroke, Neonatal
ascular air embolism (VAE) is rare but
potentially lethal accident, and survival is rarely reported in newborn
[1,2]. Precise incidence of VAE is not known due to under- recognized
and under-reported nature of this almost fatal catastrophe. We report a
newborn with cerebral air embolism, its acute management, and
neurodevelopment outcome at 4 months.
An extreme preterm (27+1
weeks), 895 gm, male infant was admitted with respiratory
distress syndrome male (RDS) and was commenced on CPAP support (7 cm of
water and 40% oxygen). He also required surfactant replacement therapy
(two doses within 12 hours of birth). Parenteral nutrition was started
through umbilical venous line since admission. Infant’s respiratory
distress improved gradually and he was started on trophic feeds on day-2
of life; intravenous infusion consisted only of parenteral nutrition and
IV Caffeine. There was a sudden episode of cardiac asystole on day-3 of
life with mottled and marbled skin. He required extensive
cardio-pulmonary resuscitation (CPR) (30 minutes) and 4 doses of IV
adrenaline. Blood gas analysis showed severe metabolic acidosis (pH
7.02, HCO3 7.0 meq/L, PCO2
30 mmHg) with normal potassium and calcium. Circulation could be
restored only after 30 minutes of CPR with return of pulses and
auscultable heart sounds. Infant required adrenalin infusion and
mechanical ventilation as post resuscitative care. A bedside
trans-illumination test ruled out pneumothorax, which was later
confirmed with X-ray chest. A neuro-sonogram performed within one
hour of the event showed presence of multiple echogenic specks with
posterior acoustic shadowing in branching distribution suggestive of air
bubbles in bilateral parietal and occipital regions within the cerebral
parenchyma (Web Fig.1). Abdomen sonogram showed presence
of umbilical line in sub-diaphragmatic position, in portal vein with
similar echogenic specks suggestive of air bubbles in the portal vein
tributaries along the umbilical line. A 2D Echo performed 24 hours later
showed normal cardiac function and presence of a PFO. A follow-up
neuro-sonography after 2 days showed disappearance of these lesions
confirming re-absorption of air specks. A continuous ECG tracing did not
show any arrhythmia and QTc interval was normal.
Post-resuscitation, infant developed multiple
multi-focal myoclonic seizure that required treatment with Phenobarbital
and Levetiracetam. Sensorium improved gradually and infant could again
be weaned to CPAP support in another seven days. A term corrected USG
brain showed development of multiple parenchymal cystic spaces
suggestive of cystic periventricular leucomalacia in parietal and
occipital regions bilaterally. An electroencephalogram (EEG) done at 35
weeks was reported to be normal. Infant initially had severe truncal and
axial hypotonia, which improved gradually during NICU stay with
developmentally supportive care. Infant was discharged at 35 weeks Post
Menstrual Age (PMA) on oral feeding at weight of 1920 gm (3rd
percentile) and head circumference of 29 cm (9th
percentile). Infant was started on early stimulation and intensive
physiotherapy after discharge. BERA at 3 months was normal. Cortical
visual impairment was diagnosed and visual rehabilitation was started.
At corrected 4 months of age, head circumference was less than 3rd
centile, and spasticity of limbs was present with grade 3 neck control.
Cerebral air embolism in preterm neonate is mostly
fatal with very few survivors reported till date [1,2]. The largest
reported newborn case series (25 cases) of air embolism is of
pre-surfactant era where very high pressure ventilation was used with
almost universal fatal outcome . The barotrauma causes seepage of air
from ruptured alveoli into systemic circulation . Other potential
sources of VAE in newborn include advance necrotizing enterocolitis,
central or peripheral vascular access, neurosurgery, cardiac surgeries
and ECMO [4,5]. While smaller amount of air may be broken down in the
system and may not cause ill-effects, large amount of air can be fatal.
In the right side of circulation, it can cause air lock of the right
heart resulting in absent right ventricular output and sudden death. The
amounts of air require to cause fatal embolism could be as little as 3-5
mL/kg . Air in cerebral circulation causes not only occlusive
infarcts but also cascade of endothelial injury, disruption of blood
brain barrier and cerebral edema which further expands the occlusive
ischemic infarcts .
Cerebral air embolism can also be seen in preterm
infant after prolonged cardiopulmonary resuscitation. This is likely to
be due to frail pulmonary alveoli which rupture into blood vessels
during neonatal CPR [7-9]. The source of air embolism in our case was
unclear. USG abdomen showed presence of air in portal vein tributaries.
UVC air could also be due to CPR or line handling for emergency
medicines. The PFO in our case could be portal for the systemic air
embolism (paradoxical air embolism). It is possible that cerebral air
embolism in our case could be due to extensive CPR; however, we also
believe that introduction of new air embolism in critical unstable
newborn would have led to unsuccessful CPR . Nevertheless the
neurological devastation caused by air embolism is grave, irrespective
of the source of origin.
Trans-oesophageal echocardiography is the most
sensitive modality, and can detect 5-10 microns of air bubble.
Precordial doppler USG / ECHO is most common used and readily available
and can detect 15 microns of air bubble. . Air embolism is reported
in 89% of preterm neonates in largest reported series of unsuccessful
CPR in post-mortem series . True incidence of air embolism in
survivors of CPR is not known.
Management of VAE includes prevention of further
release of air (e.g., covering the surgical site with wet mop in
neurosurgery), reduction in the size of embolic air, and support of
circulation with effective CPR and vasopressor. Administering 100%
oxygen not only improves tissue oxygenation but also reduces air bubble
volume by eliminating nitrogen. Air lock in the right side of heart may
be relieved by partial left decubitus position. Chest compression in CPR
will support the hemodynamics and will also break the air bubbles into
smaller fragments . Therapeutic hypothermia was found to be
beneficial in an adult in improving neurological outcome .
Air embolism is a potentially preventable
complication and should be kept as differential diagnosis in case of
sudden unexplained deterioration in an otherwise stable neonate.
Contributors: JA,HB,NSK: diagnosis and management
of the patient; JA: neurodevelopment assessment; VA: diagnosis of air
embolism and providing the photographs; NSK: overall guarantor of the
authenticity of the case. The final manuscript was approved by all the
Funding: None; Competing Interest: None
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