Neonatal respiratory distress syndrome is a breathing disorder that mainly affects premature newborns. It occurs due to immature lungs that cannot produce enough surfactant, a substance that keeps the lungs from collapsing. Without sufficient surfactant, the lungs collapse and the infant must work hard to breathe, risking organ damage from lack of oxygen if untreated. The case study describes a premature newborn, Kristin, exhibiting several clinical signs of respiratory distress syndrome, including a fast respiratory rate, expiratory grunting, and cyanosis around the mouth. Her blood tests also indicate low oxygen levels incompatible with life.

1. Neonatal Respiratory distress syndrome;
is a breathing disorder that mainly occurs in premature newborns.
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This is due to the fact that premature infants
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have immature lungs that aren't able to produce
enough surfactant, which coats the insides of
the lungs to keep them from collapsing.
Without enough surfactant, the lungs collapse
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and the infant has to work hard to breathe.
The lack of oxygen can damage the baby's brain
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and other organs if proper treatment isn't given.
Other names for RDS include Hyaline
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membrane disease, Neonatal respiratory
distress syndrome, Infant respiratory distress
syndrome, and Surfactant deficiency.
Pathogenesis;
The fundamental defect in RDS is a deficiency of pulmonary surfactant.
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The incidence of RDS is inversely proportional to gestational age.
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It occurs in about 60% of infants born at less than 28 weeks of gestation, 30% of those born between 28 to 34
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weeks’ gestation, and less than 5% of those born after 34 weeks’ gestation.
surfactant consists; predominantly of dipalmitoyl phosphatidylcholine (lecithin), smaller amounts of
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phosphatidylglycerol, and two groups of surfactant-associated proteins.
The first group is composed of hydrophilic glycoproteins SP-A and SP-D, which play a role in pulmonary host
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defense (innate immunity).
The second group consists of hydrophobic surfactant proteins SP-B and SP-C, which, in concert with the
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surfactant lipids, are involved in the reduction of surface tension at the air-liquid barrier in the alveoli of the
lung.
surfactant caused by mutations in the SFTPB or SFTBC genes.
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Surfactant synthesis is modulated by a variety of hormones and growth factors, including cortisol, insulin,
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prolactin, thyroxine, and TGF-β. The role of glucocorticoids is particularly important.
MORPHOLOGY
The lungs are distinctive on gross examination.
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Though of normal size, they are solid, airless, and reddish purple, similar to the color of the liver, and
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they usually sink in water.
Microscopically, alveoli are poorly developed, and those that are present are collapsed.
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When the infant dies early in the course of the disease, necrotic cellular debris can be seen in the terminal
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bronchioles and alveolar ducts.
The necrotic material becomes incorporated within eosinophilic hyaline membranes lining the respiratory
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bronchioles, alveolar ducts, and alveoli.
The membranes are largely made up of fibrin admixed with cell debris derived chiefly from necrotic
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type II pneumocytes.
The sequence of events that leads to the formation of hyaline membranes is depicted in.
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There is a remarkable paucity of neutrophilic inflammatory reaction associated with these membranes.
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The lesions of hyaline membrane disease are never seen in stillborn infants.
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In infants who survive more than 48 hours, reparative changes occur in the lungs.
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The alveolar epithelium proliferates under the surface of the membrane, and may detach into the airspace
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where it undergoes partial digestion or phagocytosis by macrophages.
Kristin's clinical Features;
Kristin's RR was 70 breaths/min after birth, this is considered fast for premature newborns, the normal range for
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term newborns is 30-60 respirations per minute and for preterm 40-70 breaths/min.
This could be one sign of RDS showing that her lungs are trying to work harder to breathe.
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2. Expiratory grunting, nasal flaring, substernal
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retractions, cyanosis in hands feet and around her
mouth.
These signs and symptoms are indicative of RDS.
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Kristin's pH would be considered low but still in
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the rage with a pH of 7.28, her PCO2 of 50 is still
within rage but on the lower side, and her PO2 of
40 shows that her CO2 is exceeding her O2 levels
therefore she is not receiving the necessary
amount of oxygen that is compatible with life.