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144 VOLUME 34 | NUMBER 3 May/June 2009
Annie J. Rohan, MSN, RNC, NNP/PNP, andSergio G. Golombek, MD,
MPH, FAAP
HYPOXIAIN
THE Term Newborn:PART TWO—PRIMARY PULMONARY DISEASE,
OBSTRUCTION,AND EXTRINSIC COMPRESSION
AbstractPediatric care providers are repeatedly called upon to
evaluatea cyanotic newborn in the labor and delivery suite, or in
thewell-baby nursery. A myriad of disorders spanning
all-organsystems exist as possibilities for each of these problems,
al-though several causes for newborn cyanosis are
particularlycommon. In this second of a three-part series, primary
pul-monary disease, airway obstruction, and extrinsic compressionof
the lungs as causes for newborn hypoxia are explored. It is inthis
group of disorders that we find the answers for the greatestnumber
of these cyanotic dilemmas. Knowledge of the breadthof diagnoses,
and respect for the variety of clinical possibilities,is the first
step in providing a patient with accurate diagnosis,treatment, and
referral.Key Words: Evaluation; Hypoxia; Newborn;
Pulmonary;Respiratory.
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decreased lung compliance, ventilation-perfusion
inequality,intrapulmonary right-to-left shunts, and a resultant
varyingdegree of hypoxia in the newborn. Logically, as such,
theentire spectrum of neonatal respiratory disorders may pres-ent
with cyanosis. In general, hypoxia associated with pul-monary
disease presents as tachypnea, grunting, flaring,chest retractions,
arterial blood gas usually showing carbondioxide retention, rise in
PaO2 when supplemental oxygenis used, and evidence of lung disease
on chest radiograph.There are numerous diagnoses included in the
category of“primary pulmonary disease,” including:• Transient
Tachypnea of the Newborn• Tracheoesophageal Fistula and Esophageal
Atresia• Aspiration Syndromes• Respiratory Distress Syndrome•
Pneumonia• Pulmonary Hemorrhage• Pulmonary Hypoplasia• Pulmonary
Lymphangiectasia• Congenital Pulmonary Cysts• Pulmonary Lobar
Emphysema
Transient Tachypnea of the Newborn (TTN). TTN is per-haps the
most common respiratory disorder of the termnewborn (Levine, Ghai,
Barton, 2001). Like most primaryrespiratory diseases, TTN is a
spectrum disorder—it rangesfrom a mild intermittent tachypnea,
perhaps more
May/June 2009 MCN 145
What do newborn care providers need to know tomeet the challenge
of evaluating hypoxia in theterm newborn infant? The first article
in thisthree-part series (see Rohan & Golombek, 2009),
discussedcardiopulmonary adaptation of the term newborn,
defini-tions and features of neonatal hypoxia, cardiac causes
ofhypoxia in the newborn, and neonatal pulmonary hyper-tension. In
this Part Two article, we describe causes of new-born hypoxia that
have close origins to the respiratorysystem. These causes can be
broken down into three dis-tinct categories: (1) primary pulmonary
disease (wherepathology originates in the lung parenchyma), (2)
airwayobstruction (where pathology originates in the upper
air-ways), and (3) extrinsic compression of the lung and
airway(where pathology originates outside of the lung but im-pinges
upon respiratory structures). In each of these sepa-rate categories
is found an array of disorders that can causerespiratory
dysfunction and resultant hypoxia (Table 1).
Primary pulmonary disease is the most common etiologyfor
cyanosis and hypoxia in this population (AmericanAcademy of
Pediatrics, 2002). The prudent clinician, how-ever, will routinely
consider alternatives, so as not to causedelayed diagnosis and its
associated negative consequencesfor the infant with a less common
disorder.
Primary Pulmonary DiseasePrimary lung disease causes alveolar
hypoventilation,
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appropriately defined as “delayed transition to
extrauterinelife,” up to and including a disease with tachypnea,
oxygenrequirement and physical signs closer to respiratory
distresssyndrome. Typically, these infants have benign
intrapartumcourses and are not at risk for other illnesses. Many
ofthem are delivered by cesarean section; some without labor.The
most significant discriminatory findings are the onsetof the
illness and the degree of distress exhibited by theinfant. Cyanosis
and carbon dioxide retention are not hall-marks of the disease,
however, are observed on occasion.Typically, the infant becomes
tachypneic immediately afterbirth and has very mild respiratory
distress. Infants are neu-rologically normal. The chest radiographs
generally revealhyperinflation with clear lung parenchyma except
for peri-hilar linear densities and fluid in the fissures. There
shouldbe no areas of consolidation.
The pathophysiological mechanism is the delayed resorp-tion of
fetal lung fluid which eventually clears over the nextseveral hours
to days (Kopelman & Mathew, 1995). If fol-lowed closely,
infants remain stable for several hours and/or
begin to improve. A worsening clinical picture shouldsuggest
another diagnosis.
Tracheoesophageal Fistula and Esophageal Atresia.Esophageal
atresia and tracheoesophageal fistula occurswhen the esophagus
fails to differentiate and separate fromthe trachea. The most
common anatomic type of this disor-der is when the upper esophagus
ends in a blind pouch,and there is a fistula connecting the lower
esophagus to thetrachea (Martin & Alexander, 1985). The infant
typicallypresents with cyanosis and “choking” as a result of
in-creased oral secretions. During physical examination,
anorogastric catheter is typically unable to be advanced to
thestomach, and if left indwelling during chest radiograph,
thecatheter is usually seen coiled in the area of the mid
thorax.Pediatric surgical consultation is uniformly indicated.
Aspiration Syndromes. The pathophysiologic mechanismfor illness
in aspiration syndromes is the obstruction oflarge and small
airways with the aspirated material (meconi-
146 VOLUME 34 | NUMBER 3 May/June 2009
PRIMARY PULMONARY DISEASE AIRWAY OBSTRUCTIONEXTRINSIC
COMPRESSION OF THE
LUNGS AND AIRWAY
Transient tachypnea of the newborn Choanal atresia, choanal
stenosis Pneumothorax
Tracheoesphageal fistula, esophagealatresia
Pierre-Robin sequence Pneumomediastinum
Aspiration syndromes Macroglossia Pleural Effusion
Respiratory distress syndrome Right aortic arch Chylothorax
Pneumonia Thyroid goiter Congenital diaphragmatic hernia
Pulmonary hemorrhage Cystic hygroma Mediastinal masses
Pulmonary hypoplasia Laryngomalacia, tracheomalacia,tracheal
stenosis, subglottic stenosis
Thoracic dystophies, thoracicdysplasias
Pulmonary lymphangiectasia Subglottic hemangioma/hematoma
Extralobar sequestration
Congenital pulmonary cysts Bronchomalacia, bronchial stenosis
Right/double aortic arch
Pulmonary lobar emphysema Laryngeal web Tracheal vascular
ring
Vocal cord paralysis Pulmonary artery sling
Foreign body aspiration Cricoid cartilage malformation
Mucous plugging
Table 1. Classification of Disorders: Primary Pulmonary Disease,
Airway Obstruction, and ExtrinsicCompression of the Lungs and
Airway
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um, blood, amniotic fluid, formula or breast milk). As
thedisease process progresses, the symptoms and severity
ofhypoxemia increase over the subsequent hours.
Pulmonaryhypertension may develop when aspiration occurs in
con-junction with varying degrees of in utero asphyxia.
Meconium in the amniotic fluid occurs in approximately20% of
pregnancies; as a consequence, meconium aspira-tion syndrome (MAS)
is considered to be a relatively com-mon event (Wiswell, 2001).
Infants with this disorder, andother forms of aspiration, typically
have symptoms similarto infants with TTN, but an exaggerated
presentation sug-gesting a more severe condition. In addition,
while manyinfants have the onset of symptoms at birth, some
infantshave an asymptomatic period of several hours before
respi-ratory distress becomes apparent. Infants with
aspirationsyndromes may require more oxygen, and have
greaterdegrees of tachypnea, retractions, and lethargy. The
arterialblood gases may reveal more acidosis, hypercapnia,
andhypoxemia than in infants with TTN. The chest radi-ographs
differ from that of TTN with significant heteroge-neous lung
disease, hyperinflated and hypoinflated areas,patchy and linear
infiltrates and atelectasis.
The deleterious effects of gastroesophageal reflux (GER)
ininfants have been recognized with increasing frequency, andput
the neonate at risk for aspiration of stomach contents.The spectrum
of symptoms caused by GER in the infant isdistinctly different than
in the adult, but is frequently recog-nized in the neonatal period
with intermittent episodes of hy-poxia, during, after or between
feedings, with or withoutvomiting. When presenting with cyanosis,
diagnosis is gener-ally made in the term infant by pH probe or
esophagramstudy, only after other causes of hypoxia have been ruled
out.
Respiratory Distress Syndrome. Respiratory distress syn-drome
(RDS), once known as hyaline membrane disease, isone of the most
predominant lung problems experienced byneonates. It mainly strikes
infants under 35 weeks gestation,however, it has been well
documented in the term and latepreterm infant (Golombek &
Truog, 2000), classically in the in-fant of a diabetic mother, or
in cases of perinatal hemorrhage.
The etiology of RDS is understood to be a deficiency inpulmonary
surfactant either by lack of production, or, morecommonly in the
late preterm infant, by inactivation of thissurfactant. Surfactant
is thought to be produced near the22nd week of gestation; however,
production can easily bedisrupted by hypoxemia, hypothermia, or
acidosis.
Infants with RDS have progressively more severe respira-tory
distress after birth. The classic findings of cyanosis,
nasalflaring, intercostal and subcostal retractions, and
tachypneaare present. Grunting classically occurs as the infant
attemptsto maintain the gas volume within the lung by causing
expi-ratory braking using the vocal cords and glottis. Apnea
mayoccur as work of breathing increases. There is decreased
lung
compliance, decreased lung volumes, atelectasis,
decreasedalveolar ventilation, hypoperfusion, and subsequent
hypoxia.The symptoms of RDS usually worsen gradually for the
first48 to 72 hours, followed by stabilization, and a slow
recov-ery period. Stabilization of the disease is often
associatedwith diuresis. Like aspiration syndromes and
pneumonia,pulmonary hypertension may develop when RDS occurs inthe
context of an opportune setting.
Chest radiograph in RDS has features suggesting general-ized
atelectasis. In the preterm infant, this presents with ageneralized
reticulogranular “ground glass” appearance ofthe lung fields with
air bronchograms. In the term infant,however, there is not as
typical a picture, and features ofatelectasis vary from generalized
to patchy. One must use his-tory and clinical evaluation to
differentiate between RDS andother generalized pulmonary diseases,
although distinctionfrom pneumonia, in particular, is very
difficult at the onset.
Pneumonia. Enteric organisms such as Escherichia coli andGroup B
Streptococcus are the frequent causative bacterialagents of
congenital pneumonia, and viruses are increasinglyrecognized as
culprits for this infection. Rarely, a postnatallyacquired
pneumonia is observed in the early newborn. A tableof organisms
that can cause pneumonia in the neonate is inTable 2.
The diagnosis of neonatal pneumonia is typically animprecise
science. It is generally based on the history, physi-cal
examination, chest X-ray results, and lab data. Whilepneumonia in
newborns is relatively rare, premature infantshave at least a
10-fold increased incidence of infectionswhen compared to term
infants. Mothers with intrapartumfever and prolonged rupture of
membranes have a greaterrisk of transmitting infections to their
infants. Symptoms ofpneumonia in a neonate, which often present
within 48hours of delivery, include vital signs instability and
respira-tory distress. Laboratory data often suggests
infection.Chest radiograph typically depicts unilateral or
bilateralstreaky densities of the perihilar region in bilateral
lungfields. Like RDS, symptoms are highly variable and dictatethe
degree of supportive care.
Pulmonary Hemorrhage. Rarely occurring in isolation,pulmonary
hemorrhage is typically found in an infant sickwith RDS, pneumonia,
heart disease, or asphyxia. It hasbeen noted with higher incidence
in infants receiving pul-monary surfactant. Significant bleeding
may also occur as acomplication of trauma to the respiratory
epithelium duringairway suctioning.
The manifestation of pulmonary hemorrhage is the presenceof
blood or bloody fluid from the airway, and runs the spec-trum from
scant bloody aspirate to massive bleeding. It followsthat clinical
examination may be minimally altered frombaseline, or range up to
sudden deterioration with shock,
May/June 2009 MCN 147
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bradycardia and death. Clotting factors can be consumed
rap-idly, and supportive care may include management of
coagu-lopathy blood product loss/consumption with transfusion.
Pulmonary Hypoplasia. Pulmonary hypoplasia is part ofthe
spectrum of malformations characterized by incompletedevelopment of
lung tissue. Circulating amniotic fluid,composed primarily of fetal
urine, is an important factor inthe development of the fetal lung.
When a fetus has absentor minimal urine production because of renal
agenesis orother severe renal malformation, the result is
oligohydram-nios and concomitant pulmonary hypoplasia or
pulmonaryaplasia.
Originally described by Potter (1946), the “oligohydram-nios
sequence” (formerly called “Potters syndrome”) pro-duces severe
pulmonary hypoplasia with typically flattenedfacial features and
limb deformation on the physical examina-tion. There may be renal
findings on abdominal exam, andthe obvious oliguria. Lung
hypoplasia can be seen on chestradiograph, but is overwhelmingly
evident on clinical examwhere the conscious infant has marked
respiratory distress.
Pulmonary hypertension leads to cyanosis and hypoxia, andfailure
of mechanical ventilation is often associated with pneu-mothorax.
The spiral to death is inevitable in severe cases, dueto failure of
ventilation and advanced renal dysfunction. This“oligohydramnios
sequence” can also occur, although oftenless dramatically, in the
presence of a more benign renalabnormality, or when there is
prolonged rupture of the mem-branes and chronic loss of amniotic
fluid before 26 weeksgestation. In these cases, and depending on
severity along thespectrum, less severe pulmonary hypoplasia can be
supportedwith mechanical ventilation in the NICU.
Pulmonary Lymphangiectasia. This rare entity is also a re-sult
of developmental abnormality where there is congenitaldilation of
the pulmonary lymphatic channels. Prenatalsonography can typically
detect the lobulation caused bydiffuse dilation of the pleural
lymphatics. At birth, in addi-tion to severe respiratory distress,
these infants may alsohave coexistent lymphedema. Congenital
cardiac malfor-mation is also common. Chest radiograph reveals
variablepatterns of marked hyperinflation and atelectasis. When
148 VOLUME 34 | NUMBER 3 May/June 2009
BACTERIAL VIRAL OTHER
Group B streptococcus Cytomegalovirus Candida albicans (and
other fungi)
Escherichia coli Adenovirus Ureaplasma
Klebsiella Rhinovirus Chlamydia
Staphylococcus aureus Respiratory syncytial virus Syphilis
Listeria monocytogenes Parainfluenza Pneumocystsis jiroveci
(carinii)
Enterobacter Enterovirus Tuberculosis
Haemophilus influenza Rubella
Pneumococcus
Pseudomonas
Bacteroides
Citrobacter
Streptococci viridans
Acinetobacter
Stenotrophomonas maltophilia
Table 2. Organisms That May Cause Pneumonia in the Neonate
Note: Adapted from Fisher & Boyce (2005).
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unanticipated, diagnosis of this rare disorder is
difficult,since the clinical presentation often mimics more
commonforms of severe respiratory distress.
Congenital Pulmonary Cysts. Like pulmonary lymphang-iectasia,
congenital pulmonary cysts are uncommon, butcan often be detected
on prenatal sonography. Cysts cancause disease either as a result
of pulmonary hypoplasiawhen there is generalized intrapulmonary
cyst formation,or as a result of airway compression in the face of
a largeextrapulmonary cyst. The most common congenitalpulmonary
cyst is the congenital cystic adenomatoid mal-formation (CCAM)
(Al-Bassam et al., 1999). This intrapul-monary disease has a wide
range of presentations, fromsingle to multiple cysts, affecting
some or all the lung. Cys-tic adenomatoid malformations most
commonly presentwith acute respiratory distress in the first few
hours of life.Alternatively, it can present at several months of
age asrecurrent pneumonias.
Other rare forms of congenital pulmonary cyst
includebronchogenic cyst and pulmonary sequestration. Similar tothe
case of pulmonary lymphangiectasia, without a sugges-tive prenatal
sonogram, congenital pulmonary cysts as anetiology for newborn
hypoxia can be an elusive diagnosis.
Pulmonary Lobar Emphysema. This congenital disorder
ischaracterized by overdistention of one or more lobes of
aninfant’s lungs. This overdistension can be due to an
intrinsicairway obstruction or alveolar overgrowth. Severity of
symp-toms depends upon the degree of overinflation, and
theresultant compression of surrounding lung tissue. Symptomsoften
begin at 1 to 2 months of age, but also can present ear-lier in the
neonatal period. Similar to pneumothorax, physi-cal examination may
reveal decreased breath sounds over theaffected lobe and apical
heartbeat displaced to the contralat-eral side. Chest radiograph
will demonstrate the hyperinflat-ed lobe, but may be difficult to
differentiate from atypicalpneumothorax, congenital pulmonary
cysts, or diaphragmat-ic hernia. Diagnosis is
radiographic—generally by CT scanafter conventional radiograph is
markedly abnormal. Becausenearly 10% of infants displaying this
condition have associat-ed anomalies, especially congenital heart
defects, genetic eval-uation is suggested (Lacy, Shaw, Pilling,
& Walkinshaw,1999).
Airway ObstructionThe newborn is particularly disadvantaged to
deal with air-way obstructions because of very small tracheal
andbronchial diameters. The risk of obstruction, even frommucus
plugging is much increased in neonates than inadults. In addition,
chest musculature is weak and the chestwall is relatively
compliant, so coughing and deep breathingis comparatively
ineffective.
Airway obstruction causes mechanical interference
withventilation and results in alveolar hypoventilation. Theneonate
with an airway obstruction is usually in obviousdistress.
Fortunately, physical examination or chest radi-ograph can usually
reveal the source of the obstruction.Both physical examination and
chest radiograph are highlyvariable, depending on the etiology of
the obstruction, butin many cases, are diagnostic.
Some of the more common airway obstructions are:
Choanal Atresia and Stenosis. This is a complete or par-tial
blockage at the posterior nasal chamber, which can beunilateral
(80%-90%) or bilateral (Keller & Kacker, 2000).Infants usually
present with respiratory distress immediatelyafter birth, because
the infant is an obligate nasal breather.Unusually, they become
more pink with crying. Duringphysical examination, a 6-Fr catheter
cannot be passed intothe nasopharynx. An artificial airway should
be providedas soon as possible, until pediatric otolaryngologic
evalua-tion is available.
Pierre-Robin Sequence. In this disorder, there is a hy-poplastic
mandible, usually associated with a cleft palate,and readily noted
on physical examination. Hypoxia occurssecondary to airway
obstruction when the tongue falls tothe back of the oral cavity,
obstructing the oropharynx.Pulling the tongue forward, caring for
this neonate in theprone position, and possibly providing a
nasopharyngeal orendotracheal airway may be necessary until
otolarygologicevaluation can be obtained.
Macroglossia. In a similar scenario to the Pierre-Robin
se-quence, macroglossia results in airway obstruction and hypox-ia
when the oversized tongue obstructs the oropharynx. Onphysical
examination, the large—or relatively large—tonguecan be realized,
and often is noted as one of several features ofa genetic syndrome,
such as Beckwith-Wiedemann syndromeor Trisomy 21.
Thyroid Goiter. Neonatal hyperthyroidism is rare inneonates, but
is serious and potentially life threatening. Inutero exposure to
PTU or excessive iodine may result ingoiter formation, or can
result from the transplacental pas-sage of immunoglobulins in
mothers with Graves disease.Occasionally, a goiter is sufficiently
large to compromisethe neonatal airway, resulting in respiratory
difficulty andhypoxia. These large goiters are typically diagnoses
in uteroby ultrasonography, but are readily evident on physical
ex-amination at birth.
Cystic Hygroma. Cystic hygroma arises as a result of ab-normal
development of the lymphatic channels, usually inthe lateral neck.
A large ill-defined mass presents in this
May/June 2009 MCN 149
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area, and can extend to the scapular, axilla or thorax. Cys-tic
hygroma of the mediastinum has also been reported, al-though this
more likely presents as a supraclavicular mass.When evident, cystic
hygroma distorts the subglottic areaand usually compromises the
airway, often requiring endo-tracheal intubation to secure
oxygenation and ventilation.
Laryngomalacia, Tracheomalacia, Subglottic Stenosis,and Tracheal
Stenosis. In some infants, a combination of anarrow tracheal
diameter and insufficient cartilaginous sup-
port in the neck results in luminal compromise with
eachinspiration. A characteristic stridor is evident on
physicalexamination, and is accentuated with crying. Usually this
isa self-limiting condition that resolves by 6 to 12 months ofage.
In the rare case where excessive work of breathing andhypoxia is a
feature, the high degree of airway obstructionmay require
tracheostomy (Gatz, 2001).
Other less common causes of airway obstruction in thenewborn
include, but are not limited to the following:• Subglottic Hematoma
or Hemangioma• Bronchomalacia or Bronchial Stenosis• Laryngeal Web•
Vocal Cord Paralysis• Foreign Body Aspiration• Mucous Plugging
Extrinsic Compression of the Lungsand AirwayExtrinsic lung
compression occurs when a space-occupyinglesion consumes volume
within the thoracic compartment.Similar to the case of primary
pulmonary disease, oxygenwill usually improve a patient’s PaO2 if
ventilation is ade-quate. In many cases, however, oxygenation and
ventilationis still inadequate despite supplemental oxygen, and
me-chanical ventilation needs to be provided to treat hypoxiaand
hypercarbia.
Pneumothorax and Pneumomediastinum. The dissectionof air from
the alveoli into the mediastinum, and further in-
to the pleural cavity, creates a pneumomediastinum
and/orpneumothorax. This air leak occurs more frequently in
theneonatal period than any other time in life (Fanaroff,
Miller,& Martin, 2002). Spontaneous air leak typically presents
asa complication of meconium aspiration, pneumonia, RDS,pulmonary
hypoplasia, or any other disease associated withpoor lung
compliance, but can also occur in infants withoutunderlying
pathology. It is also commonly associated withpositive pressure
ventilation or vigorous resuscitation. Pneu-mothorax is reported to
occur in approximately 1% of all
live births, but this is probably underreport-ed since
asymptomatic air leaks often go un-detected (Al-Bassam et al.,
1999).
Clinical signs of pneumothorax includerespiratory distress,
tachypnea, nasal flaringand grunting, cyanosis, and even movementof
the apical pulse away from the side of thepneumothorax. The most
accurate diagnosiscan be made from radiographs,
althoughtransillumination of the chest by a skilledclinician can be
suggestive with large pneu-mothorax. Severe distress and
displacementof the mediastinum (“tension pneumotho-rax”) may
require evacuation of air with a
needle or small catheter, or insertion of a closed system
chesttube with continuous suction.
Pleural Effusion or Chylothorax. Fluid accumulation in
thepleural space most typically represents a chylothorax in
theneonate; however, a pleural effusion, empyema, or
pleuralhemorrhage can produce similar radiographic changes
andclinical findings. Chylothorax is the accumulation of lymphat-ic
fluid in the pleural space, and when found in the otherwisehealthy
term newborn, may represent. Thoracic duct ruptureat delivery. This
is the most frequent cause of a large pleuraleffusion in newborn.
In chylothorax, pleural fluid is initiallyserous, but usually turns
chylous after milk feedings. Chy-lothorax, and other types of
pleural accumulations, are typi-cally diagnosed and managed
successfully with thoracenteses.
Congenital Diaphragmatic Hernia. Diaphragmatic hernia,which
occurs in about 1 in 2,200 births, is an emergency atbirth, and
must be treated upon diagnosis (Golombek,2002). Usually detectable
on prenatal sonography, thisanomaly presents with herniation of
abdominal contentsinto the thorax because of incomplete formation
of thediaphragm. Left sided hernias occur five times more oftenthan
those on the right (Braby, 2001; Golombek, 2002).
When the herniation occurs on the left side, the stomachand
intestines may enter the thorax and compress the lung,pushing the
mediastinum to the right. The degree of distressnoted in the
neonate depends on the severity of the herniation.As the neonate
begins breathing, the presence of the abdomi-
150 VOLUME 34 | NUMBER 3 May/June 2009
Primary pulmonary diseaseis the most common
etiology for cyanosis andhypoxia in the newborn
population.
-
nal contents compresses the lungs, making it very difficult
tocomplete inspiration. As swallowed air further distends the
in-testines and stomach, compressing the lungs even more,
theneonate’s respiratory distress worsens.
Symptoms of diaphragmatic hernia include cyanosis, res-piratory
distress, a scaphoid abdomen, and sometimes bowelsounds in the
chest on auscultation. Chest radiograph show-ing the loops of bowel
in the thorax confirms the diagnosis.
Immediate insertion of a nasal gastric tube attached tosuction
to evacuate abdominal gas is indicated. Ventilation isusually
needed and should be done through an endotrachealtube, as bag and
mask ventilation introduces air into the gas-trointestinal tract,
further compromising space in the chestcavity. Respiratory
therapies should address the frequently as-sociated hypoxia of
persistent pulmonary hypertension. Ur-gent evaluation by a
pediatric surgical team is requisite.
Mediastinal Masses. Mediastinal masses in neonates
occurinfrequently. Teratomas and dermoids are the most commonof
these lesions. They are neurogenic in origin, and typicallylocated
in the anterior mediastinum. On chest radiograph,soft tissue
density characteristic, and there may be calcificationor fat
density areas within the region of the mass as well. An-terior
mediastinal masses can displace the trachea, producinga clinical
picture similar to airway obstruction. Middle andposterior
mediastinal masses are less likely to produce respira-tory distress
and hypoxia, as displacement of the esophagus ismore likely.
Ultrasonography, CT, MRI and contrast radi-ographs are all useful
in the evaluation of these lesions.
Thoracic Dystrophies or Dysplasias. Now exceedingly un-common,
these problems result from shortened ribs, anelongated thoracic
cage and a resultant respiratory compro-mise. Many are associated
with other congenital defects ordwarfism. Jeune syndrome (or
“asphyxiating thoracic dys-trophy”) is one such complex disorder,
which often resultsin death during infancy or early childhood.
Extralobar Sequestration. Extralobar sequestration occurswhen
lung tissue develops with no identifiable bronchialcommunication,
and that receives its blood supply fromone or more anomalous
arteries. Infants can be asympto-matic, present with respiratory
distress at birth, or presentlater in infancy with a chronic cough.
In addition to vascu-lar anomalies, the malformation has been
reported in asso-ciation with CHD (Harris, 2004). Diagnosis is
generallymade by CT scan after abnormal radiographic or
sono-graphic evaluation. Surgical intervention or vascular
em-bolization is often indicated.
Other less common causes of extrinsic compression ofthe airway
and lungs in the newborn include:• Right/Double Aortic Arch•
Tracheal Vascular Ring• Pulmonary Artery Sling• Cricoid Cartilage
Malformation
In the final of this three-part series to be found in
theJuly/August 2009 issue of MCN (volume 34, no. 4),neurologic,
metabolic, and hematologic disorders will bereviewed as a basis for
newborn hypoxia. �
Annie J. Rohan is a Senior Nurse Practitioner, Stony
BrookHospital-Stony Brook, and Jonas Nursing Scholar, Colum-bia
University School of Nursing, PhD Program, New York,NY. She can be
reached via e-mail at [email protected]
Sergio G. Golombek is an Associate Professor of Pediatricsand
Clinical Public Health, New York Medical College, NewYork, NY, and
Attending Neonatologist, Maria Fareri Chil-dren’s Hospital of
Westchester Medical Center, Valhalla, NY.
The authors have disclosed that they have no
financialrelationships related to this article.
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