RESPIRATORY DISTRESS SYNDROME RDS
Category: Child Health
Abstract : Respiratory distress syndrome (RDS), also known as hyaline membrane disease
(HMD), occurs almost exclusively in premature infants. The incidence and
severity of RDS are related inversely to the gestational age of the infant. The
outcome of RDS has improved in recent years with the increased use of antenatal
steroids to improve pulmonary maturity, early postnatal surfactant therapy to
rep
Respiratory distress syndrome (RDS), also known as hyaline membrane disease
(HMD), occurs almost exclusively in premature infants. The incidence and
severity of RDS are related inversely to the gestational age of the infant.
The
outcome of RDS has improved in recent years with the increased use of antenatal
steroids to improve pulmonary maturity, early postnatal surfactant therapy to
replace surfactant deficiency, and gentler techniques of ventilation to minimize
damage to the immature lungs. These therapies have also resulted in the survival
of premature infants who are smaller and more ill. Although reduced, the
incidence and severity of complications of RDS continue to present significant
morbidities.
The sequelae of RDS include intracranial hemorrhage and/or
periventricular leukomalacia with associated neurodevelopmental delay,
septicemia, bronchopulmonary dysplasia (BPD), patent ductus arteriosus (PDA),
and pulmonary hemorrhage. Direct attention to anticipating and minimizing these
complications and also toward preventing premature delivery whenever possible
are strategic goals.
Pathophysiology:
A relative deficiency of
surfactant, which leads to decrease in lung compliance and functional
residual capacity with increased dead space, causes RDS. The resulting large
ventilation-perfusion mismatch and right-to-left shunt may involve as much as
80% of cardiac output. Macroscopically, the lungs appear airless and ruddy (ie,
liverlike). Thus, the lungs of these infants require a higher critical opening
pressure to inflate. Diffuse atelectasis of distal airspaces along with
distension of some distal airways and perilymphatic areas are observed
microscopically. With progressive atelectasis along with barotrauma or
volutrauma and oxygen toxicity, endothelial and epithelial cells lining these
distal airways are damaged, resulting in exudation of fibrinous matrix derived
from blood.
Hyaline membranes that line the alveoli are formed within a
half hour after birth. At 36-72 hours after birth, the epithelium begins to
heal, and surfactant synthesis begins. The healing process is complex; in
infants who are extremely immature and critically ill and in infants born to
mothers with chorioamnionitis, a chronic process often ensues, resulting in
BPD.
Surfactant is a complex lipoprotein comprised of 6 phospholipids and
4 apoproteins. Functionally, dipalmitoyl phosphatidylcholine (DPPC), or
lecithin, is the principle phospholipid. DPPC along with apoproteins SP-B and
SP-C or with the addition of other substances (eg, nonionic detergent tyloxapol,
C16:0 alcohol hexadecanol [Exosurf]) facilitates adsorption and spreading of
DPPC as a monolayer, which lowers the surface tension at the alveolar air-fluid
interface in vivo.
The components of pulmonary surfactant are synthesized
in the Golgi apparatus of the endoplasmic reticulum of the type II alveolar
cell. The components are packaged in multilamellar vesicles in the cytoplasm of
the type II alveolar cell and are secreted by a process of exocytosis, the daily
rate of which may exceed the weight of the cell. Once secreted, the vesicles
unwind to form bipolar monolayers of phospholipid molecules that are dependent
on the apoproteins SP-B and SP-C to configure properly in the alveolus. The
lipid molecules are enriched in dipalmitoyl acyl groups attached to a glycerol
backbone that pack tightly and generate low surface pressures.
Tubular
myelin stores surfactant and may depend on SP-B. Corners of the myelin lattice
appear to be glued together with the larger apoprotein SP-A, which may also have
an important role in phagocytosis. Hypoxia, acidosis, hypothermia, and
hypotension may impair surfactant production and/or secretion of
surfactant.
Frequency:
• In the US: While the greatest risk factor for
developing RDS is prematurity, maternal diabetes and asphyxia are also risk
factors. Not all premature infants develop RDS. Approximately half of infants
born at 28-32 weeks' gestation develop RDS. In the United States, RDS occurs in
approximately 40,000 infants each year and in 14% of low birth weight infants.
Incidence of RDS increases with decreasing gestational age and may occur in as
many as 45-80% of infants born when younger than 28 weeks' gestation.
•
Internationally: RDS has been reported in all races worldwide, occurring more
often in premature infants of Caucasian ancestry.
History:
• RDS
frequently occurs in the following individuals:
o Male infants
o Infants
born to mothers with diabetes
o Infants delivered via cesarean without
maternal labor
o Second-born twins
o Infants with a family history of
RDS
• In contrast, the incidence of RDS decreases with the
following:
o Use of antenatal steroids
o Pregnancy-induced or chronic
maternal hypertension
o Prolonged rupture of membranes
o Maternal narcotic
addiction
• Secondary surfactant deficiency may occur in infants with the
following:
o Intrapartum asphyxia
o Pulmonary infections
o Pulmonary
hemorrhage
o Meconium aspiration pneumonia
o Oxygen toxicity along with
barotrauma or volutrauma to the lungs
Physical:
• Physical findings are consistent with the infant's maturity
assessed by Dubowitz examination or its modification by Ballard.
•
Progressive signs of respiratory distress are noted soon after birth and include
the following:
o Tachypnea
o Expiratory grunting (from partial closure of
glottis)
o Subcostal and intercostal retractions
o Cyanosis
o Nasal
flaring
• Extremely immature infants may develop apnea and/or
hypothermia.
Causes: Surfactant deficiency and risk factors are outlined
in History.
DIFFERENTIALS
-Anemia,
- Acute Aspiration
Syndromes
- Gastroesophageal Reflux
- Hypoglycemia
- Hypothermia
-
Circulatory Arrest and Cardiopulmonary Bypass
- Pneumomediastinum
-
Pneumonia
- Pneumothorax
- Polycythemia
- Sudden Infant Death
Syndrome
- Transient Tachypnea of the Newborn
Other Problems to be
Considered:
Several diagnoses may coexist and further complicate the course
of RDS, including the following:
Pneumonia is often secondary to group B beta
hemolytic streptococci (GBBS) and often coexists with RDS.
Metabolic problems
(eg, hypothermia, hypoglycemia) may occur. Hematologic problems (eg, anemia,
polycythemia) may occur.
Transient tachypnea of the newborn usually occurs in
term or near-term infants, usually after cesarean delivery. The chest radiograph
of an infant with transient tachypnea exhibits good lung expansion and, often,
fluid in the horizontal fissure. Aspiration syndromes may result from aspiration
of amniotic fluid, blood, or meconium.
Aspiration syndrome is also
observed in more mature infants and is differentiated by obtaining a history and
by viewing the chest radiograph findings.
Pulmonary air leaks (eg,
pneumothorax, interstitial emphysema, pneumomediastinum, pneumopericardium) may
occur. In premature infants, these complications may occur from excessive
positive pressure ventilation, or they may be spontaneous.
Congenital
anomalies of the lungs (eg, diaphragmatic hernia, chylothorax, congenital cystic
adenomatoid malformation of the lung, lobar emphysema, bronchogenic cyst,
pulmonary sequestration) and heart (eg, cardiac anomalies) are rare in premature
infants. These entities can be diagnosed based on chest radiograph or ultrasound
examination findings and, on rare occasion, may coexist with RDS.
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