Air Embolism in the Newborn: Rare

Complication of Intensive Care Therapy

in Children
Giampiero Beluffi, M.D.,1 and GianFranco Perotti, M.D.2

ABSTRACT

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Systemic air embolism in neonates, either premature or full term, necessitating
mechanical ventilation is a devastating and usually fatal condition. We describe three cases
of this complication, two in mechanically assisted preterm babies, and one in a full-term
dysmorphic patient. Causes and possible management are described.

KEYWORDS: Systemic air embolism, premature, mechanical ventilation,

complications of mechanical ventilation

S ystemic air embolism (SAE) has been described
and documented as the most catastrophic complication
of hyaline membrane disease in very small premature
infants undergoing mechanical ventilation.1–13 SAE can
also be found in necrotizing enterocolitis14,15 and fol-
lowing surgical procedures, trauma,16 and asthmatic
spells. This dramatic complication is related to pressure
and dissection of air into the pulmonary veins and the
systemic circulation, although the mechanism of intra-
vascular air embolism is still not very clear. We report on
three patients, two premature infants and one full-term
infant, in whom we had the opportunity to document
this fatal complication.
CASE REPORTS
Case 1
T.D. was a 720-g premature female baby born by the
vaginal route at 25 weeks of gestational age (wga), due to
prolonged and premature rupture of the membranes.
Prophylaxis with antenatal steroids was performed with
one dose only of betamethasone. Apgar score was 4 at 1
minute and 6 at 5 minutes after oral-tracheal intubation
and ventilation. At admission to the neonatal and
intensive care unit, the clinical condition of the neonate
appeared immediately compromised (clinical risk index
of babies was 17),17 and she was ventilated with aggres-
sive settings as follows: synchronized intermittent man-
datory ventilation (SIMV) 50 breaths/min, positive
inspiratory pressure (PIP) 23 cm H2O, positive end-
expiratory pressure (PEEP) 3.9 cm H2O, mean airway
pressure (MAP) 9 cm H2O, inspired oxygen partial
pressure (FiO2) 1, and two consecutive doses of surfac-
tant (Curosurf1, Chiesi Farmaceutici SpA, Parma, Italy,
200 mg/kg each) were administered through the endo-
tracheal tube (ET). Arterial blood gas analysis gave the
following results: pH 7.15, PaO2 35 mm Hg, PCO2
67 mm Hg, base excess (BE) 14.5 mmol/L, HCO3
18 mmol/L. Chest X-ray showed diffuse bilateral lung

1
Sezione di Radiologia Pediatrica; 2Divisione di Patologia Neonatale e
Terapia Intensive Neonatale, Fondazione IRCCS Policlino S. Matteo,
Pavia, Italy.
Address for correspondence and reprint requests: Prof. Giampiero
Beluffi, M.D., Giampiero Viale Golgi, 19 Pavia I-27100 Pavia, Italy
(e-mail: g.beluffi@smatteo.pv.it).
Am J Perinatol 2009;26:393–397. Copyright # 2009 by Thieme
Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001,
USA. Tel: +1(212) 584-4662.
Received: June 30, 2008. Accepted after revision: November 19,
2008. Published online: March 6, 2009.
DOI 10.1055/s-0029-1214236. ISSN 0735-1631.
393
394 AMERICAN JOURNAL OF PERINATOLOGY/VOLUME 26, NUMBER 5 2009

opacities with a central air bronchogram. Saturation
remained less than 40% and adrenaline was instilled by
ET due to bradycardia without significant improvement.
Seven hours later, despite a third dose of surfactant
(Curosurf1 100 mg/kg) and more aggressive high-
frequency oscillation ventilation (HFO, Sensor Medics,
Viasys Healthcare Europe, Hoechberg, Germany) with
the following parameters: oscillation frequency Hz 15,
Delta P 37, MAP 16, FiO2 1 (arterial blood gas analysis
not available), the child’s clinical condition abruptly
deteriorated. A second chest-abdomen X-ray (Fig. 1)
showed bilateral interstitial emphysema and air within
the right heart chambers, superior and inferior vena cava,
the hepatic and splenic veins, iliac and femoral veins, both
axillary and upper-limb veins, as well as in the supraclavear
soft-tissue small vessels. In addition, free air was present
in large amounts within the abdominal cavity. Demise
followed. Postmortem examination was not performed.
and mechanical ventilation with aggressive settings
(SIMV 45 breaths/minute; PEEP 4 cm H2O, PIP
18 cm H2O, MAP 7.7 cm H2O; FiO2 1,). Surfactant
(Curosurf1) was administered by ET 45 minutes after
delivery with improvement of gas exchange. An emer-
gency X-ray showed diffuse bilateral lung opacities with
exclusion of the lower-right lung, which was partially
hyperlucent. The tip of the umbilical vein catheter was
slightly bent to the right above the diaphragm, and signs
of free air within the liver were detectable. The nasogas-
tric catheter was bent within the stomach and its tip
pointed below the distal third of the 10th rib. Seven
hours later, the clinical conditions of the baby abruptly
worsened with desaturation, pallor, and an increase in
oxygen demand. Ventilation was changed from conven-
tional to HFO (Sensor Medics; Hz 15, Delta P 33, MAP
18, FiO2 1) due to hypoxemia and hypercapnia (arterial
blood gas analysis was: pH 7.11, PaO2 29 mm Hg, PCO2

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Case 2
O.F. was an 830-g premature male baby, delivered by
urgent caesarean section at 25 wga due to vaginal bleed-
ing in abruptio placentae. No antenatal prophylaxis with
steroids was performed. The Apgar score was 3 at 1
minute; he was immediately resuscitated by endotracheal
intubation, cardiac massage, adrenaline administration,
83 mm Hg, BE 12 mm Hg, HCO3 20 mm Hg).
Chest/abdomen X-ray (Fig. 2) showed a left pneumo-
thorax and signs of diffuse interstitial emphysema in
association with free air within the hepatic, iliac, femoral,
and popliteal veins as well as in the upper-limb veins and
within the jugular veins. The stomach was distended by
air. The tip of the umbilical vein catheter had bent to the
left below the diaphragm. Demise followed and post-
mortem examination was not performed.

Figure 1 At admission (A), supine chest-abdomen X-ray shows complete ‘‘whiteout’’ of both lungs and central air
bronchogram. Seven hours later (B), supine chest-abdomen X-ray shows bilateral interstitial emphysema and massive air
within the right heart chambers, superior and inferior vena cava, hepatic and splenic veins, iliac and femoral veins, axillary and
upper-limb veins as well as in supraclavicular soft-tissue tiny vessels and a large pneumoperitoneum. An umbilical vein catheter
bent to the left is detectable.
 AIR EMBOLISM IN THE NEWBORN/BELUFFI, PEROTTI 395

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Figure 2 The first chest-abdomen X-ray taken (A) shows bilateral lung opacities, partially hyperlucent right-lower lobe, tip of
the umbilical venous catheter slightly bent to the right above the diaphragm, and signs of free air within the liver. The second
chest-abdomen X-ray (B) shows left pneumothorax, diffuse interstitial emphysema, and free air in hepatic, iliac, femoral, and
popliteal veins as well as in the upper-arm veins and, bilaterally, the jugular veins. The stomach is distended by air. The tip of the
umbilical vein catheter is below the diaphragm and bent to the left.

Case 3 patients who have survived these usually fatal complica-

B.R. was a 3660-g male infant born by the vaginal route
at 39 wga. The Apgar scores were 2, 6, 7 at 1, 5,
10 minutes, respectively. Hydronephrosis, patent ductus
arteriosus, and some dysmorphic features (low-set ears,
small mandible, and swelling of the soft tissues of the
neck) were present. Twenty days after birth, the neonate
abruptly developed clinical signs of sepsis; blood culture
gave negative results (C-reactive protein was 13 mg/dL,
leukocytes 2800/mm3, neutrophils 500) and secondary
severe multiorgan dysfunction followed. The baby died
20 hours later despite intensive care with no signs of
pneumothorax or air leaks. Postmortem examination was
not performed: nevertheless, total-body X-ray taken
2 hours after demise to further evaluate the presence of
spine or upper- and lower-limb abnormalities showed
(Fig. 3A to C) massive air embolism with air occupying
heart chambers, lung parenchyma (pulmonary interstitial
emphysema, [PIE]), superior and inferior vena cava,
right and left branches of the hepatic veins, bilateral
jugular veins, and upper- and lower-limb veins, without
evidence of pneumothorax.
DISCUSSION
Both SAE and pulmonary vein air embolism are
rare,1–5,7–13,18–23 and there are only a few reported
tions.4,5,18 In the surviving case reported by Kogutt, the
patient had no clinical symptoms and the diagnosis was
based on radiographic findings only,4 and an infant with
such a condition treated by Weiner et al survived
13 days.6 Air has been reported within cerebral
vessels13,18,24 and in two instances within the intracranial
venous sinuses with survival of the infants.25 Rupture of
alveoli into pulmonary capillaries due to barotrauma
through alveolar-capillary or bronchovenous fistulae is
thought to be the main cause of massive air embolism in
infants with an air leak.2,4,5,7,10,26 Systemic venous air was
found always to be predominant over systemic arterial air
in the study of Booth et al,27 in which it was shown that
PIE was statistically more prevalent than pneumome-
diastinum and/or pneumopericardium and was similar in
prevalence to pneumothorax. It was hypothesized that air
within the pulmonary system gained access to the sys-
temic venous system via lymphatic ducts, which resulted
in the clinical entity of neonatal SAE. This readily
explains the venous predominance in neonatal
SAE.27,28 In premature infants, SAE is always due to
respiratory-assisted ventilation, such as insertion of cen-
tral venous lines,12,28 intravenous injections during re-
suscitation,22 and, most of all, long-standing mechanical
high-pressure ventilation.1–11,19,21,22,29 Moreover, it has
also been reported in one full-term infant suffering from
396 AMERICAN JOURNAL OF PERINATOLOGY/VOLUME 26, NUMBER 5
Figure 3 Total-body X-ray taken 2 hours after demise (A), showing massive and diffuse air embolism: air is seen in the heart
chambers, lung parenchyma, superior and inferior vena cava, right and left branches of the hepatic vein, bilateral jugular veins,
and upper- and lower-limb veins as shown in detailed images (B, C).
congenital viral pneumonia and occurred spontaneously
in another full-term newborn with massive aspiration
in the absence of ventilation treatment.2,5 Physiological
intravascular air can appear as early as 25 minutes after
death, so postmortem X-ray films have to be evaluated
with caution when an embolic event is suspected19,30
However, because it is well known that absorption of
intravascular gas, especially oxygen, occurs rapidly after
death, the diagnosis of SAE can be overlooked and
undetected at postmortem examination.3,5,8,9 In the
preultrasound era, air in the fetal circulation was de-
scribed as a sign of intrauterine fetal demise, appearing
within 3 days of the estimated time of death.31 Clinical
signs of SAE are sudden and dramatic19,20,23: cardio-
vascular collapse, sudden deterioration in respiratory
status, pallor, cyanosis, irregularities in cardiac rhythm,
as well as seizures and/or the development of neuro-
logical defects in non-fatal central nervous system
emboli.18 One hundred percent oxygen has been shown
to increase the reabsorption of extra-alveolar air and to
increase the oxygen concentration in the areas distal to
the emboli, thus reducing the chance of hypoxic dam-
age.18 The same applies to hyperbaric oxygen therapy,
as shown in selected adult cases.32 Our first two cases fit
in the SAE category in very low-weight, premature
infants presenting severe respiratory problems at birth
and requiring high-pressure ventilation in the delivery
2009
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room, and in the third patient, SAE may have been
related to the septic state that developed during his last
days of life.
REFERENCES
1. Gwinn JL, Lee FA, Weinberger HD. Radiological case of
the month: massive air embolism. Am J Dis Child 1973;
126:63–64
2. Ponté C, Remy J, Lequien P. Spontaneous air embolism in
the newborn: a complication of pulmonary interstitial
emphysema. Pediatr Radiol 1974;2:231–234
3. Shook DR, Cram KB, Williams HJ. Pulmonary venous air
embolism in hyaline membrane disease. Am J Roentgenol
Radium Ther Nucl Med 1975;125:538–542
4. Kogutt MS. Systemic air embolism secondary to respiratory
therapy in the neonate: six cases including one survivor. Am J
Roentgenol 1978;131:425–429
5. Oppermann HC, Wille L, Obladen M, Richter E. Systemic
air embolism in the respiratory distress syndrome of the
newborn. Pediatr Radiol 1979;8:139–145
6. Weiner JH, Kliegman RM, Fanaroff AA, Carlo WA.
Pulmonary venous air embolism in the neonate. Crit Care
Med 1986;14:67–69
7. Bollinger B, Vinther S. Systemic air embolism in the
neonate. Pediatr Radiol 1988;19:52
8. Richter A, Tegtmeyer FK, Möller J. Air embolism and
pulmonary interstitial emphysema in a preterm infant with
hyaline membrane disease. Pediatr Radiol 1991;21:521–522

9. Sizun J, Giroux JD, Rubio S, Thoma M, Colin A, Alix D.
Embolie gazeuse létale d’origine pulmonaire chez un
nouveau-né atteinte de maladie des membranes hyalines
(cas radiologique du mois). Arch Fr Pediatr 1992;49:819–820
10. Birenbaum HJ, Armiger J. Neonatal radiology casebook.
Massive systemic air embolism in a low birth weight infant.
J Perinatol 1996;16:142–143
11. Shah V, Martin N. Systemic air embolism in respiratory
distress syndrome. Indian J Pediatr 1996;63:809–812
12. Smith J, Els I. Intracardiac air: the ‘‘hospital killer’’ identified?
Case reports and review of the literature S Afr Med J
2003;93:922–927
13. Yikilmaz A, Lee EY. Massive air embolism in a newborn.
Pediatr Radiol 2007;37:607
14. Miller T. Systemic air embolism in necrotizing enterocolitis.
AJR Am J Roentgenol 1979;132:322
15. Daneman A, Woodward S, de Silva M. The radiology of
neonatal necrotizing enterocolitis (NEC) A review of 47
cases and the literature. Pediatr Radiol 1978;7:70–77
16. Mante M, Rossi J, Champey JC, Favier O. Aéroportie post-
traumatique de l’enfant. Ann Radiol (Paris) 1992;35:222–
224
17. The International Neonatal Network. The CRIB (Clinical
Risk Index for Babies) score: a tool for assessing initial
neonatal risk and comparing performance of neonatal
intensive care units. Lancet 1993;342:193–198
18. Savani RC, Merten DF, Brazy JE. Air embolism with
survival in a neonate. Pediatr Radiol 1990;20:480–482
19. Kumar P, Ostrea EM Jr. Ventilatory management casebook.
Systemic air embolism: a potential fatal complication of
ventilator therapy. J Perinatol 1995;15:341–343
20. Laskey AL, Dyer C, Tobias JD. Venous air embolism during
home infusion therapy. Pediatrics 2002;109:E15
21. Tan GH, Sussmane JB. Massive air embolism in a neonate
with pulmonary hypoplasia. N Engl J Med 2002;346:751
AIR EMBOLISM IN THE NEWBORN/BELUFFI, PEROTTI 397
22. Wald M, Kirchner L, Lawrenz K, Amann G. Fatal air
embolism in an extremely low birth weight infant: can it be
caused by intravenous injection during resuscitation? Inten-
sive Care Med 2003;29:630–633
23. Sowell MW, Lovelady CL, Brogdon BG, Wecht CH. Infant
death due to air embolism from peripheral venous infusion.
J Forensic Sci 2007;52:183–186
24. Daneman A, Abou-Reslan W, Jarrin J, Traubici J, Hellmann J.
Sonographic appearance of cerebral vascular air embolism in
neonates: report of two cases. Can Assoc Radiol J 2003; 54:
114–117
25. Al-Hathlol K, Al-Mane K, Al-Hathal M, Al-Tawil K,
Abulaimoun B. Air emboli in the intracranial venous sinuses
of neonates. Am J Perinatol 2002;19:55–58
26. Macklin MT, Macklin CC. Malignant interstitial emphy-
sema of the lung and mediastinum as an important
complication in many respiratory diseases and other con-
ditions. Medicine 1944;23:281–358
27. Booth TN, Royal SA, Allen BA. Lymphatic air embolism: a
new hypothesis regarding the pathogenesis of neonatal
Downloaded by: WEST VIRGINIA UNIVERSITY. Copyrighted material.
systemic air embolism. Pediatr Radiol 1995;25:S220–S227
28. Royal SA. Massive air embolism in a newborn. Pediatr Radiol
2007;37:1060
29. Leicht CH, Waldman J. Pulmonary air embolism in the
pediatric patient undergoing central catheter placement. A
report of two cases. Anesthesiology 1986;64:519–521
30. Quisling RG, Poznanski AK, Roloff DW, Borer RC.
Postmortem gas accumulation in premature infants. Radiol-
ogy 1974;113:155–159
31. Bennet R. Unequivocal radiological evidence of intra-uterine
foetal death, including demonstration of gas formation within
the foetal circulation: report of a case, and review of thirty-
seven cases of foetal death. Clin Radiol 1960;11:200–204
32. Orebaugh SL. Venous air embolism: clinical and exper-
imental considerations. Crit Care Med 1992;20:1169–1177