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Background: CCAM is a developmental hamartomatous
abnormality of the lung with adenomatoid proliferation of cysts
resembling bronchioles. CCAM represents approximately 25%
of all congenital lung lesions.
CAM is believed to result from focal arrest in fetal lung
development before the seventh week of gestation secondary to
a variety of pulmonary insults. Depending on the time and type
of insult, 4-26% of cases can be associated with other
congenital abnormalities. However, arrest of pulmonary
development with distortion of architectural differentiation
may take place at any stage of embryonic development.
CAM differs from normal lung tissue because of a combination
of increased cell proliferation and decreased apoptosis. A well-
defined intrapulmonary bronchial system is lacking, and
normally formed bronchi supplying the mass are absent.
Usually, the radiographic pattern appears as an
expansile soft-tissue mass containing multiple air-filled
cystic masses of varying size and shifting of the
Initially and early in life, a homogeneous fluid-opacity
pulmonary mass may present and evolve to demonstrate
an air-filled cystic radiographic appearance over time.
The initial dense appearance is a result of delayed
emptying of alveolar fluid either via the bronchi or
lymphatic and circulatory systems.
In patients with CAM, the pattern in the lung
demonstrates multiple radiolucent areas that vary
greatly in size and shape.
The involved lung may appear honeycombed or spongy,
but occasionally, 1 large cyst may overshadow the
Airtrapping within cystic spaces can cause rapid
enlargement of the CAM and subsequent respiratory
Findings are usually apparent in a symptomatic
individual, but they may not be as apparent in an
(CDH) constitutes a major surgical emergency in the newborn,
and the key to survival lies in prompt diagnosis and treatment.
Symptoms depend on the degree of herniation; small hernias
may initially pass unnoticed, whereas larger ones produce
immediate and severe respiratory distress.
The left-sided Bochdalek hernia is seen in approximately 90%
of cases. The major problem in a Bochdalek hernia is the
posterolateral defect of the diaphragm, which results in either
the failure of the pleuroperitoneal folds to develop or the
improper or absent migration of the diaphragmatic
musculature. Bilateral Bochdalek hernias are rare.
The Morgagni hernia is a less-common CDH, occurring in only
5-10% of cases of CDH. This hernia occurs in the anterior
midline through the sternocostal hiatus of the diaphragm, with
90% of cases occurring on the right side.
The classic radiographic appearance is one which the
left hemithorax is filled with cystlike structures (loops of
bowel), the mediastinum is shifted to the right, and the
abdomen is relatively devoid of gas (Swischuk, 1997). In some
cases, a few loops of intestine can be seen in the abdomen, but
more often, only the stomach remains visible within the
known as hyaline membrane disease (HMD), is an acute lung
disease of the newborn caused by surfactant deficiency. It is
seen primarily in neonates younger than 36-38 weeks'
gestational age and weighing less than 2500 g. In comparison,
HMD tends to occur in neonates younger than 32 weeks'
gestational age and weighing less than 1200 g.
The incidence and severity of RDS is inversely related to
gestational age. RDS is the most common cause of respiratory
failure during the first days after birth. In addition to
prematurity, other factors contributing to the development of
RDS are maternal diabetes, cesarean delivery without
preceding labor, fetal asphyxia, and being the second born of
Pathophysiology: RDS is the result of anatomic pulmonary
immaturity and a deficiency of surfactant. Pulmonary
surfactant synthesis, in type II pneumocytes, begins at 24-28
weeks of gestation, and gradually increases until full gestation.
Pulmonary surfactant decreases surface tension in the alveolus
during expiration, allowing the alveolus to remain partly
expanded, thereby maintaining a functional residual capacity.
In premature infants, an absence of surfactant results in poor
pulmonary compliance, atelectasis, decreased gas exchange,
and severe hypoxia and acidosis. Premature infants must
expend a great deal of effort to expand their lungs with each
breath, and respiratory failure ensues.
In RDS, the classic chest radiographic findings consist of
pronounced hypoaeration, bilateral diffuse reticulogranular
opacities in the pulmonary parenchyma, and peripherally
extending air bronchograms. The reticulogranularity is due to
superimposition of multiple acinar nodules caused by
atelectatic alveoli. The development of air bronchograms
depends on the coalescence of areas of acinar atelectasis
around aerated bronchi and bronchioles. In nonintubated
infants, cephalic doming of the diaphragms and hypoexpansion
Background: Bronchopulmonary dysplasia (BPD) is a chronic
pulmonary disorder that results from the use of high positive-
pressure mechanical ventilation and high concentration oxygen
in neonates with respiratory distress syndrome (RDS). It is
defined as oxygen dependence at 28 days. BPD is
pathologically characterized by inflammation, mucosal
necrosis, fibrosis, and smooth muscle hypertrophy of the
airways. With advances in medical management, BPD has
Preterm delivery (immature lungs): The disease is
common in children delivered before 32 weeks'
gestation and in those weighing less than 1000 g.
oxygen concentration is an etiologic factor in patients
with immature lungs, and any concentration greater
than 60% is associated with a high incidence of the
RDS that requires mechanical ventilation: Sustained
positive-pressure ventilation in preterm infants with
RDS results in dilatation of the terminal bronchioles,
which causes ischemic necrosis of the distal airways.
Resultant pulmonary interstitial emphysema (PIE) and
pneumothorax produce chronic lung damage. Although
mechanical ventilation in RDS may be the original
cause, it also occurs in patients with diaphragmatic
hernia, persistent pulmonary hypertension of the
newborn, meconium aspiration, and other diseases that
require prolonged mechanical ventilation. RDS is not
an absolute requirement for the development of BPD
because the disease can occur in those receiving
mechanical ventilation to manage other diseases.
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