NEONATAL RADIOLOGY

Meconium Aspiration
Syndrome
Chritiine Svec Moore, RNC, MSN, NW
COLUMN EDITORS
Carol Trotter, RNC, MPH, NNP
Barbara Carey, RNC, MN, NNP
M
econium staining of amniotic fluid is present in
approximately 8-10 percent of all deliveries. It
usually affects the fetus who is 37 weeks gestation or
greater, postmature and/or growth retarded, and has
experienced some degree of feta1 distress. However, meco-
nium-stained fluid may be present in the premature fetus
with Listeria sepsis2
PATHOPHYSI OLOGY
Fetal respiratory activity is a normal physiologic process
that causes lung fluid to move from within the tracheo-
bronchial tree out into the amniotic fluid. This movement of
tluid during each fetal breath is minimal but consistent
with a steady movement outward from the trachea.s Under
normal conditions, amniotic fluid does not enter the tracheo-
bronchial tree. When fetal distress occurs, apnea resulting in
fetal gasping allows amniotic fluid into the larger airways of
the tracheobronchial tree.
Fetal distress can also trigger the passage of meconium
from the fetal intestine secondary to vagal activity, which
results in hyperperistalsis and sphincter relaxation. In this sit-
uation, the fetus may aspirate amniotic fluid along with
meconium and other debris (such as vernix and squamous
cells). Because of the viscosity of fetal lung fluid, it is uncom-
mon for aspirated meconium and debris to penetrate the
smaller airways before delivery.4
In the neonate, when meconium has penetrated below the
vocal cords and into the trachea and large airways, it causes
partial and/or total occlusion of terminal airways and air sacs.
This results in atelectasis distal to the areas of total occlusion
and gas trapping with alveolar overdistension in the areas of
partial occlusion.
In this situation, the meconium in the airway acts like a
ball-valve mechanism. On inspiration, air moves in around
the meconium debris. On expiration, when airways constrict
around the meconium particles, air is trapped distally. This
results in overdistension of airways and terminal saccules
leading to alveolar rupture and air leaks (Figure 1).
Because the aspirated meconium and amniotic debris are
foreign substances introduced into the lung parenchyma,
clearing of these substances by the ciliary apparatus is often
inadequate. This causes an intlammatory process in the ter-
minal airways and air sacs5 Inflammation results in unstable
alveoli causing alveolar collapse, which in turn results in an
abnormal ventilation-to-perfusion (\i&) ratio.
SIGNS AND SYMPTOMS
Clinically, the infant nith meconium aspiration syndrome
may be quite depressed at birth, demonstrating pallor,
cyanosis, tachypnea, grunting, and retractions. Because of gas
trapping and alveolar overdistension, a barrel chest appear-
ance is observed. Rales and rhonchi may be auscultated on
physical exam.
Depending on the severity of meconium aspiration, both
respiratory and metabolic acidosis can develop due to hypox-
emia and hypercarbia. The hyposemia and hypercarbia are
secondary to the \i/G mismatching described above. Acidosis
of any origin can increase the
PPHN.
risk for and/or potentiate
CHEST X-RAY FINDINGS
Inf2trate.s
Complete occlusion of the airway results in atelectasis.
Atelectatic areas on x-ray film appear more gray/white than
the air-filled normal alveoli. This is because atelectatic areas
have a greater density than air-filled alveoli and therefore
block the beam from reaching the x-ray cassette. This pro-
duces an x-ray film with bilateral, diffuse, patchy, fluffy, or
nodular (more dense, gray/white areas) infiltrates and asym-
metric areas of opacity. These infiltrates may present in a focal
or generalized manner (Figure 2).
Infiltrates may also occur as a result of infl ammation of the
airways and air sacs. With inflammation, the linings of the air
sacs become injured, predisposing them to cellular necrosis.
Cellular necrosis causes tluid accumulation within the alveoli,
resulting in atelectasis. Cellular damage to capillary walls also
results from inflammation, leading to pulmonary edema and
pleural effusions secondary to leaky capillary beds.
Hyperinflation and Air Leaks
Partial occlusion of the airvvay and air sacs by meconium
debris causes air trapping. Partial occlusion can be demon-
strated by hyperinflation of the lungs, which is seen in the
flattening of the diaphragm along with generalized inter-
spersed radiolucency. This may also cause overdistension of
airways and terminal air saccules, which can lead to alveolar
rupture. Free air dissects into the pleural space, causing
pneumothoraces (Figure 3).
NEONATAL NETWORK / OCTOBER 1994 Vol. 13 No. 7 57
FIGURE 1 n Effects of meconium on pulmonary function: (A) normal alveolar function and gas exchange, (B) complete obstruction with atelectasis
and intrapulmonary shunting, (C and D) ball valve effect, (C) partial obstruction on inspiration and air entry, (D) airway collapse on expira-
tion and air trapping plus distention and impingement on vasculature, (E) overdistention and rupture with air leak, (F) surfactant displace-
ment and atelectasis.
From: Turnage CS. 1989. Meconlum aspiration syndrome. /ournal of Pemnatai and Neonatal Nursing 3(2): 72. Reprinted by permission
Pleural Efhsions
Pleural effusions, lvhich represent tluid in the pleural space
(usu,dl!~ o\rer the l ung bases), may be present in the neonate
with meconium aspiration syndrome (Figure 2 1. Pleural effu-
sions result from the inflammatorv process set up b!. meconi-
urn in the lungs. Inflammation causes cellular necrosis and
atelcctasis, which prevents the airvvavs and air sacs from clear-
ing lung fluid effectivehr.
TABLE 1 n Chest X-ray Findings in Infants with Meconium
Aspiration Syndrome
1. Diffuse, patchy/nodular Infiltrates:
focal or general, asymmetric or symmetric
2. Hyperinflalion of lung fields
3. Air leaks
4. Pleural effusion
5. Cardiomegaly
Cardiomegaly
Cardiomegaly may be noted on the chest x-ray of a
neonate \\ith meconium aspiration syndrome. Cardiomegal)
is a resuh of intrauterine asphyxia associated with meconium
aspiration and/or the frequent hyposemia associated with
the disease process postnatally. These events cause a car-
diomyopathy and decreased cardiac contractility that results
in an enlarged heart. The chest x-ray findings are summa-
rized in Table 1.
CASE STUDY
A 40-UIZ& gestation, 3.9 kg, AGA male n-as delivered b!~
cesarean section due to breech position to a SO-year-old,
gra\.ida 2. para 0 mother. The pregnancz \\.as complicated b>
upper respiratory infections during.the first and third
trimesters; the mother \vas treated \\ith ampicillin and anti-
histamines early in the third trimester.
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.
,
FIGURE 2 n Term neonate with meconium aspiration syndrome.
Note the diffuse, bilateral, dense infiltrates as well as the
right pleural effusion. The heart size is within normal limits.
The tip of the endotracheal tube is properly located
between the clavicles and the carina.
FIGURE 3 m A 41-week gestation male with history of meconium
aspiration syndrome. This admnslon chest x-ray film
demonstrates a right tension pneumothorax. The heart and
mediastinal structures are shlfted to the ieft. Heavy infiltrates
are noted in the upper and lower lunq fields.
Labor began spontaneously with rupture of amniotic
membranes four hours prior to delivery. Light meconium-
stained fluid was noted at that time. Apgar scores were 6 and
9 at one and five minutes.
The baby was intubated and suctioned at delivery with
only a scant amount of meconium fluid aspirated.
Stimulation and continuous positive airway pressure by face
mask were provided to elicit respirations. Physical exam was
normal except for dark staining of the umbilicus and the
development of respiratory distress shortly after birth. The
neonate demonstrated mild retractions, grunting, and
tachypnea and required free-flow oxygen to remain pink.
Upon admission to the NICU, the baby was placed in 100
percent oxygen per osyhood. A radial arterial gas revealed a
mild respiratory acidosis: pH of 7.33, PCO, of 50, and PaOz
of 111. A sepsis evaluation was performed and antibiotics
were initiated.
An admission s-ray examination (Figure 4) was indicated
because of respiratory distress consisting of grunting, retract-
ing, tachypnea, and an osygen requirement. Findings were as
follows:
, yaw
I
\
e
- CI
i
shifted to left
Penetration appears to be normally exposed.
L
No significant rotation is noted.
The soft tissues of the neck, chest, and extremities are of
normal thickness and without emphysema.
The bony framework is intact, with 12 ribs bilaterally and
normal vertebrae. Clavicles are intact.
The trachea shows a straight air column.
The hilar area on the left is difficult to distinguish because
of patchy infiltrates.
The heart is of normal configuration, location, and size.
FIGURE 4 n A 40-week gestation male with history of meconium
aspiration syndrome. This admission chest film has a very
characteristic pattern of diffuse, patchy infiltrates. The
lucency on the right mediastinal and right subpulmonic
areas most likelv reoresent free air.
NEONATAL NETWORK / OCTOBER 1994 Vol. 13 No. 7 59
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e
The tl-ymus is present.
.
.
.
The diaphragm is between the ninth and tenth rib
bilaterally.
Gastric air is present on the left.
The intercostal spaces are normal in size.
The lung fields demonstrate bilateral, diffuse, patchy infil-
trates. The areas of lucency on the right represent a
pneumothorax in the right subpulmonic area and the right
lower lobe. There may also be free air located at the right
mediastinal area, although a lateral film may be required
to distin_tish it.
Impression: The history, clinical, laboratory, and x-ray
data support the diagnosis of meconium aspiration with a
small right pneumothorax.
REFERENCES
1. Gregory GA, et al. 1974. Meconium aspiration in infants-a
prospective study. Journal of Pediatrics85(6): 848-852.
2. Brady J, and Goldman S. 1986. Management of meconium aspi-
ration syndrome. In Neonatal Pulmonary Care, 2nd ed.,
Thibeault DW, and Gregory GA, eds. Norwalk, Connecticut:
Appleton-Century-Crofts, 483498.
3. Hodson WA. 1992. Normal and abnormal structure development
of the lung. In Fetal and Neonatal P@siolo~, Polin RA, and Fox
WW, eds. Philadelphia: WB Saunders, 771-782.
4. Fanaroff A, and Martin R 1992. Neonatal-Perinatal Medicine,
Diseases of t he Fettu and Infant, 5th ed. St. Louis: Mosby-Year
Book 835.
,
5. Dennehy I? 1987. Respiratory infections in the newborn. Clinics
in Perinatolom 14( 3): 667-682.
About the Author
Christine Svec Moore, RNC, MSN, NNP, is current& working in
the NICU at St. J ohns Mercy Medical Cent er as a PaeonataI nurse
practitioner. She has worked a5 a neonatal manspor t nurse, ,NICU staff
nurse, and neonatal clinical specialirt. She is a member of NANN and
was t hej i r st pr esi dent of t beSt . Loui s, Mircourz,chapter of NANN.
~E~~~~~ELONGAT
Bhiii%mR
B
aylor University Medical Center in Dallas, Texas is seeking
quality candidate to fill a key position in our progressive
organization. In addition to professional growth opportunities, we
are pleased to offer a most competitive compensation program,
subsidized on-site child care and on-site kindergarten for
employees children and the opportunity to work in a nationally
recognized organization. And, living in Dallas offers a
comfortable lifestyle with a moderate cost of living. .
Excellent opportunities for experienced professionals seeking a
new challenge. As a teaching and research hospital, we are expcsed
to a wide variety of clinical cases. We offer flexible scheduling and
educational opportunities through weekly in-services.
NEONATALNURSE
PRACTITIONERMANAGER
Opportunity available for a Neonatal Nurse Practitioner with well
developed clinical, teaching and managerial skills. Responsible for
overseeing a practice group of 10 NNPs in a 5500 birth multi-
hospital setting with regional High Risk OB and Neonatal
refer& with covemge provided in our university medical center
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facilities. Practice settings include delivery room and ground/air
transpoa Perinaml outreach and nursing staff development are
integral components of the role. Clinical responsibilities are an
important priority as well as assisting other NNPs with their
professional development.
Development of a NNP certificate program is in process. NNP
Manager will have adjunct clinical faculty appointment.
Requires NNP with Masters degree in Nursing and 2 years
experience in NNP role.
To inquire about this opportunity, please call or send your resume
to: BAYLOR UNIVRRSITY MEDICAL CENTER, Dept.
NNlop4, P.O. Box 150647, Dallas, TX 75315. An equal .
zqpommity employer and a smoke- free facility. Baylor conducts a
drug screen as part of its preemployment health screening.
60 Vol. 13 No. 7 OCTOBER 1594 / NEONATAL NETWORK
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