Idiopathic respiratory distress syndrome

Idiopathic respiratory distress syndrome
Neonatal respiratory distress syndrome (RDS) is a disease of premature babies which results primarily from a deficiency of surfactant.


Is common in several neonatal disorders e.g.:

Hypovolemia
Hypoglycemia
Congenital heart disease
Cerebral hemorrhages


Respiratory distress syndrome (RDS), and Hyaline membrane disease (HMD) are applied to the severe lung disorder responsible for more deaths in pediatric population and carries the highest risk in long term-neurological complications, and is most common in preterm infants.
It is rare in infants born to narcotic addicted mothers or infants subject to intra-uterine stress e.g. maternal preeclampsia or hypertension


Neonatal respiratory distress syndrome is a form of respiratory distress usually occurring within 4 hours of birth and persistently worsening for 48 to 72 hours.
If not fatal, it resolves by 72 hours.
Surfactant replacement therapy has shortened the duration of the disease and reduced mortality by 40%.
Surfactant deficiency results in high alveolar surface tension; with each breath the baby must re-inflate the collapsed alveoli. Thus every breath is like the first - a large effort for relatively poor expansion.

This condition is now being treated with administration of synthetic or animal surfactant.

Pathophysiology
The preterm is born before the lungs are ready for functioning & IRDS can develop acutely within 30 minutes or few hours after an achievement of normal breathing after birth.
Surfactant is the responsible factor, it is a surface-active phospholipids secreted by the alveolar epithelium. It decreases the tension of the fluid that line the alveoli & respiratory passages causing a uniform expansion of the lungs & maintain their expansion at the end of expiration.


If no surfactant great deal of effort is needed to expand the alveoli with each breath leading to:
Atelectasis
Hypoxia
Hypercapnia (?CO2 in the blood)

To over come this situation, high lactic acid is formed & produce metabolic acidosis

& with the inability of the collapsed lungs to blow excess CO2 respiratory acidosis occur
leading to vasoconstriction in the lungs this diminish pulmonary circulation that limit the amount of materials needed for the production of surfactant

this lead to the formation of hyaline membrane which decreases the elasticity of the lungs so they become stiff needing high pressure to expand.

predisposing factors
Prematurity
Small for dates
Male sex
Maternal diabetes mellitus
Hypothermia
Perinatal asphyxia

Clinical manifestations of respiratory distress
Respiratory rate of greater than 60/min for more than an hour, it may reach (80/min)
Grunting expiration
Subcostal or sternal recession on inspiration
flaring of the nasal alae
Fine inspiratory rales heard over both lungs
Cyanosis
As the disease progresses:
Flaccidity
Inertness
Unresponsiveness
Frequent apneic episodes
Decrease breath sounds
Severe disease is associated with:
Shock like state
Decreased cardiac return
Decrease blood pressure

Treatment
Treatment can be considered in terms of prevention and subsequent management:
Prevention:

Avoiding preterm delivery where possible

Careful control of diabetes in pregnancy

Administration of Dexamethasone to mothers before preterm deliveries

Avoidance of hypothermia after delivery

Management:
Mechanical Ventilation and oxygen administration
Surfactant is given endotracheally .

Supportive measures:
** Maintain neutral thermal environment to decrease O2 utilization
** Provide additional fraction of inspired O2(FIO2) by assisted ventilation


Cont. Supportive measures:
** Prevent hypotension and Hypovolemia
** Correct respiratory acidosis by assisted ventilation

**Correct metabolic acidosis by I.V NaHCO3 which also dilates the pulmonary vessels and decrease constriction response
** Oral feeding and are contraindicated with increased respiratory rate because of the risk of aspiration
** Nutrition is by I.V parentral therapy during acute stage

complications

Early complications include:

Patent ductus arteriosus with congestive heart failure
Pneumothorax
Pulmonary interstitial emphysema
Lobar collapse
Cerebroventricular haemorrhage

Late complications are principally the result of therapy:
Oxygen toxicity e.g.

Retinopathy of prematurity

Bronchopulmonary dysplasia.

Necrotizing Enterocolitis

Neurological sequels

Nursing considerations:
Assessment:
Close observation to assess infant’s response to therapy
Continuous monitoring and close observation of vital signs, color, general condition, and Lab results
Nursing diagnosis:
Ineffective airway clearance R/T flexible rib cage, fatigue, weak or absent cough reflex
Ineffective breathing pattern R/T increased surface tension of alveoli, flexible rib cage
Impaired gas exchange R/T inability to maintain lung expansion, presence of hyaline membrane
High risk for trauma (brain tissue) R/T hypoxia and Hypercapnia
High risk for infection (pneumonia) R/T accumulation of pulmonary secretions


Planning:
Facilitate respiratory effort
Prevent complications

Implementation:
Remove secretions
Positioning, skin care, and mouth care
Postural drainage
Vibration of chest wall
Suctioning
Care of the infant on ventilator
Monitor blood gases and vital signs
Give medications as prescribed and observe
their effect


Evaluation
Continuous assessment for:
Respiration
Behavior of infant: body
weight, V.S and signs of
sepsis or other complications

Expected out come:
Adequate breathing
Normal PO2 levels
No complications