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Respiratory Distress Syndrome

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Respiratory Distress Syndrome (RDS)

Introduction and Etiology


Respiratory Distress Syndrome (RDS) is a life threatening pulmonary
disease primarily of the premature infant caused by surfactant deficiency

Pulmonary surfactant is a complex lipoprotein composed of


phospholipids and apoproteins synthesized by alveolar type 2 epithelial
cells and airway Clara cells. These lipoproteins function to decrease
surface tension at the air-liquid interface of the lung and also play a role
in host defense against infection and inflammation [1-3].

Impairment in the synthesis and/or secretion of surfactant leads to an


increase in dead space due to atelectasis and a decrease in lung
compliance. Consequences include ventilation-perfusion mismatch,
hypoxemia and hypercarbia that in turn lead to respiratory acidosis.

Acidosis causes vasoconstriction that impairs the endothelial and


epithelial integrity in the lungs, thus leaking an exudate that forms the
hyaline membrane from which the name of the disease is derived.

Epidemiology
About 1 in 20,000-30,000 newborn US infants will have RDS.
Approximately half of neonates born at gestation age of 26-28 weeks
will develop RDS, while about 30% of 30-31 gestation week neonates
will develop it [4]. Although prematurity is the primary risk factor, there
are several other risk factors including maternal diabetes, cesarean
section, asphyxia, rapid labor, and complications that reduce blood flow
to the fetus [5, 6].

Internationally, RDS occurs less frequently than in the US but overall, it


is more common in white premature infants.

Clinical presentation
Symptoms observed in infants with RDS are indicative of difficulty with
breathing. They typically present shortly after birth, at times hours
afterwards, and include:
 Cyanosis
 Tachypnea
 Nasal flaring
 Subcostal and intercostal retractions
 Expiratory grunting
 Apnea
 
Potential complications
Several of the complications of RDS are reduced with adequate
treatment. In certain cases, a combination of the disease and its treatment
result in the complications of:
 Patent ductus arteriosus (PDA)
 Pulmonary hemorrhage
 Pneumothorax
 Bronchopulmonary dysplasia (BPD)
 Septicemia
 Hypertension
 Failure to thrive
 Apnea
 Intraventricular hemorrhage (IVH)
 
Differential diagnosis
With hyaline membrane disease causing respiratory distress syndrome,
there are quite a few other diseases or conditions that can present
similarly. Some of which are:
 Transient tachypnea of the newborn
 Pneumonia
 Sepsis
 Pneumothorax
 Persistent pulmonary hypertension
 Congenital lung malformations
 Aspiration syndromes
 
Treatment
Urgent delivery of care to infants with hyaline membrane disease is very
important. With prematurity being the most common risk factor
responsible for RDS, neonatologists are on hand for the delivery and can
administer immediate treatment required.
Resuscitation is the primary treatment required so as to minimize
sequelae of the disease. It entails administration of warm, moist oxygen
and assisted ventilation. The oxygen is critically important but can also
cause damage to the lungs via generation of radical ions [7]. As such,
great care is taken to ensure that the patients are receiving the smallest
possible amount of oxygen required.
Continuous positive airway pressure (CPAP) is often used to promote
ventilation, by keeping the alveoli open at the end of expiration thereby
reducing the chances of atelectasis [8]. Using CPAP reduces the
associated side effect of lung damage due to mechanical ventilation.
Surfactant replacement therapy is also being used to treat HMD and
has reduced the mortality rate from respiratory distress syndrome by
about half. The surfactant protects the immature lung from inflammation
and also partially restores the surface tension that helps keep alveoli
from collapsing. It is typically administered shortly after birth [9].
Interestingly, the ideal type of surfactant that will be most beneficial to
these patients is yet to be ascertained [10].
Corticosteroids are another group of medications used in the
management of infants at risk for HMD. In this case, mothers at an
increased risk of having children with hyaline membrane disease are
given a single dose of corticosteroid. Several doses have been shown to
have no additional benefit but a repeat dose can be considered in the
event that the woman does not deliver within a week of prior
corticosteroid administration [11, 12].
Other forms of management include supportive therapy to promote
circulation and aid in respiration such as fluid and metabolic support. In
addition, antibiotics may be administered if there also risk factors for
infection.
 
Prognosis
Typically, the symptoms worsen a few days after birth but slowly
improve afterwards. The goal is to support the infant while the lungs
begin producing surfactant.  Providing adequate nutritional
requirements is also important for recovery and growth.
Many infants with RDS suffer the complications of oxygen and
ventilation therapy but recover within the first couple of years of life as
the lung tissue is replaced with new and functional tissue.
Damage to other organs such as the brain may also occur which is due to
a combination of factors including hypoxia and intraventricular
hemorrhage, so it is imperative to begin therapy early and monitor organ
damage.
 
References:
1. Goerke, J., Pulmonary surfactant: functions and molecular
composition. Biochim Biophys Acta, 1998. 1408(2-3): p. 79-89.
2. Whitsett, J.A., et al., Human surfactant protein B: structure,
function, regulation, and genetic disease. Physiological reviews,
1995. 75(4): p. 749-57.
3. Wright, J.R., Immunomodulatory functions of
surfactant. Physiological reviews, 1997. 77(4): p. 931-62.
4. Hintz, S.R., et al., Neurodevelopmental outcomes of premature
infants with severe respiratory failure enrolled in a randomized
controlled trial of inhaled nitric oxide. The Journal of pediatrics,
2007. 151(1): p. 16-22, 22 e1-3.
5. Gerten, K.A., et al., Cesarean delivery and respiratory distress
syndrome: does labor make a difference? American journal of
obstetrics and gynecology, 2005. 193(3 Pt 2): p. 1061-4.
6. Qiu, X., et al., Comparison of singleton and multiple-birth
outcomes of infants born at or before 32 weeks of
gestation. Obstetrics and gynecology, 2008. 111(2 Pt 1): p. 365-71.
7. Wells, D.A., D. Gillies, and D.A. Fitzgerald, Positioning for acute
respiratory distress in hospitalised infants and children. Cochrane
database of systematic reviews, 2005(2): p. CD003645.
8. Murray, P.G. and M.J. Stewart, Use of nasal continuous positive
airway pressure during retrieval of neonates with acute
respiratory distress. Pediatrics, 2008. 121(4): p. e754-8.
9. Engle, W.A., Surfactant-replacement therapy for respiratory
distress in the preterm and term neonate. Pediatrics, 2008. 121(2):
p. 419-32.
10. Pfister, R.H., R.F. Soll, and T. Wiswell, Protein containing
synthetic surfactant versus animal derived surfactant extract for
the prevention and treatment of respiratory distress
syndrome. Cochrane database of systematic reviews, 2007(4): p.
CD006069.
11. Doyle, L.W., et al., Outcome at 2 years of age of infants from
the DART study: a multicenter, international, randomized,
controlled trial of low-dose dexamethasone. Pediatrics,
2007. 119(4): p. 716-21.
12. Wapner, R.J., et al., Long-term outcomes after repeat doses
of antenatal corticosteroids. The New England journal of
medicine, 2007. 357(12): p. 1190-8.

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