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1) Respiratory Distress Syndrome (RDS) Hyaline Membrane Disease (HMD)

Respiratory distress syndrome (RDS), also known as hyaline membrane disease, affects premature infants due to underdeveloped lungs that cannot produce enough surfactant. This leads to breathing difficulties. The condition results from low surfactant levels causing alveoli collapse and impaired gas exchange. Management includes oxygen supplementation, respiratory support like CPAP if needed, and surfactant replacement therapy. Nurses monitor infants closely, maintain airway and temperature stability, and provide respiratory support.

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ُEssraa Adeel
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144 views9 pages

1) Respiratory Distress Syndrome (RDS) Hyaline Membrane Disease (HMD)

Respiratory distress syndrome (RDS), also known as hyaline membrane disease, affects premature infants due to underdeveloped lungs that cannot produce enough surfactant. This leads to breathing difficulties. The condition results from low surfactant levels causing alveoli collapse and impaired gas exchange. Management includes oxygen supplementation, respiratory support like CPAP if needed, and surfactant replacement therapy. Nurses monitor infants closely, maintain airway and temperature stability, and provide respiratory support.

Uploaded by

ُEssraa Adeel
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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1) Respiratory distress syndrome (RDS) = Hyaline membrane

disease (HMD).

Definition:
 baby's lungs are not fully developed and cannot provide enough
oxygen, causing breathing difficulties. It usually affects premature
babies.
 It's also known as infant respiratory distress syndrome, hyaline
membrane disease or surfactant deficiency lung disease.

Incidence:
 It occurs in about one quarter of infants born at 32 weeks of
gestation and the incidence increases with shorter gestational
periods.
 30% of low birth weight infants (2500 gm).
 50% of very low birth weight infants (1500 gm)
Pathophysiology :-
The disease results from low level or absence of surfactant system.
Surfactant is a phospho-lipid (lipoprotein) substance secreted by
alveolar epithelium, which acting like a detergent, this substance
reduces the surface tension of fluids that line the alveoli and
respiratory passages, resulting in uniform expansion of the lungs and
maintenance of lung expansion.
The immature development of these functions deficient surfactant
cause unequal expansion of alveoli on inspiration and collapse of
alveoli on end of expiration.
Without surfactant infant is unable to keep lung inflated and therefore,
excretes a great deal of effort to expand the alveoli with each breath ,
as a result infant use more O2 to expend more energy than he take in
which rapidly lead to exhaustion . With increase exhaustion number of
alveoli he is able to open is decreased and this will lead to atelectasis.
With progressive atelectasis, pulmonary vascular resistance is
increased .Consequently; there is hyperfusion to lung tissue with a
decrease ineffective pulmonary blood flow. Inadequate pulmonary
perfusion and ventilation produce hypoxemia and hypercapnea.
Prolonged hypoxia lead to metabolic acidosis and retention of CO2
cause respiratory acidosis.
Risk factors (High risk group):

 Prematurity and low birth weight.


 Male sex.
 Infant of diabetic mother (IDM).
 Perinatal infection.

 Secondary to decreased blood perfusion to the lungs impaired


synthesis of surfactant.
 Infants with pathogenic organisms affecting their lungs.
 Around half of all babies born between 28 and 32 weeks of
pregnancy develop RDS.
 Previous birth of baby with newborn respiratory distress syndrome
 Perinatal asphyxia (lack of air immediately before, during or after
birth)
 Cold stress (a condition that suppresses surfactant production)
 Multiple births (multiple birth babies are often premature)
 Infants of diabetic mothers (too much insulin in a baby’s system due
to maternal diabetes can delay surfactant production)
Clinical Presentation:
The symptoms of RDS are often noticeable immediately after birth

 Grade I (Mild distress):

 Rapid respiratory rate (tachypnea >60 breaths per minute)

 Nasal flaring (alae nasai).

 Grade II: (Moderate distress):

 Intercostals and substernal retractions.

 Manifestation of mild distress.

 Grade III: (Severe distress):

 Expiratory grunting.

 Manifestation of mild and moderate distress.

 Grade IV: (Advanced distress)

 All of above.

 Central cyanosis
 Diminish cardiac return frequent apnea episode.

 Disturbed consciousness.

Diagnosis:

 Physical examination:

 Most newborns whom will later develop respiratory distress have


difficulty to initiate respiration at birth, followed by hypothermia and
nasal flaring within a short period of time.

 Expiratory grunting (prolonged expiratory time) due to accumulation


of CO2 or due to air trapping.

 Sea saw respiration: on inspiration the anterior chest wall is retracted


and the abdomen protruded.
 pulse oximetry test to measure how much oxygen is in the baby's
blood using a sensor attached to their fingertip, ear or toe

 Lab, investigation and radiological exam. : - .


 Chest X-ray. Show congested lung field with a ground-glass
appearance that represent alveolar atelectasis and dark streak
 Blood gases reveal hypoxia, hypercapnia and acidosis.
 Serum glucose levels are usually low.
 blood tests to measure the amount of oxygen in the baby's blood
and check for an infection.

Long-term complications may develop due to:

 Too much oxygen.


 High pressure delivered to the lungs.
 More severe disease or immaturity. newborn respiratory distress
syndrome can be associated with inflammation that causes lung or
brain damage.
 Periods when the brain or other organs did not get enough oxygen.

Management:

1) General:
Suction
 Suction is performed only as necessary based on the individual
newborn assessment include: auscultation of the chest, evidence of
decrease O2, excess moisture of ETT or increase newborn irritability.
 Close suction system (the use of specially designed catheter is
usually introduced into airway without disconnecting the neonate
from the ventilator) is more effective than open suction
 suction is harmful procedure as it may cause bronchospasm due to
vagal nerve stimulation , hypoxia and increase intracranial pressure

 Improper suctioning cause infection, airway damage, or even


pneumothorax

Chest physiotherapy
 Percussion and vibration to chest wall but cupped hand is much too
large to be used .commercial devices are available for this purpose.
vibration is difficult to accomplish if respiratory rate is 60 -80 b\m.

 Change position of newborn (Fowler's position is the best )

 Trandelenburg position shouldn't be used as it leads to increase


intracranial pressure

 Basic support including thermal regulation and parentral nutrition


and medications (antibiotics).

N.B: Nipple feeding and gavage feeding are contraindicated; they


increase respiratory rate and effort with greater hazards of aspiration.

 Oxygen administration, preferably heated and humidified, provide


30-40% O2 by head box.

 Respiratory support is needed if the patient continues to deteriorate.


If the PaO2 is less than 50 mm Hg, Continuous Positive Airway
Pressure (CPAP) is highly recommended.
 If under CPAP; (pH < 7.2 Or PaO2 < 40 mmHg Or PaCO2 > 60
mmHg Fi O2 > 60%

2) Specific:

Surfactant replacement therapy through ET tube.

Nursing intervention :
 Assess pre-term infant for respiratory and general status :
 Oxygen saturation
 Cyanosis
 ABG
 Axillary temperature
 Respiratory pattern
 Maintain airway and administer oxygen 4-6 lit/min.
 Provide ventilatory support in case of need.

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