HYALINE MEMBRANE

DISEASE/
RESPIRATORY DISTRESS
SYNDROME

MKS/19
INTRODUCTION
 RDS previously called hyaline membrane
disease is a syndrome in premature infants caused
by developmental insuficiency of surfactant
production and structural immaturity in the lungs
 It also results from genetic problem with
production of surfactant associated proteins
 It affects about 1% of newborn infants and its
leading cause of deaths in pre term infants
DEFINITION
 This is the condition of the newborn infant in which the
lungs are imperfectly expanded (Martin A.E, 1994).
 CAUSE
• Insufficient surfactant in the immature lungs at birth.
CAUSES
 Surfactant is a complex system of lipids, proteins and
glycoprotein which are produced in specialised lungs
cells. It begins to be made in the foetus at about 24 – 28
weeks of pregnancy. Surfactant is found in amniotic
fluid between 28 and 32 weeks.
CAUSES CONT.
By about 35 weeks gestation, most babies
have developed adequate amounts of
surfactant. Surfactant is normally released into
the lung tissue by the 37th week where it helps
lower surface tension in the airways.
By reducing surface tension, surfactant prevents
the air spaces from completely collapsing on
exhalation and allows re-opening of air spaces
with a lower amount of force
 Deficiency of surfactant leads to collapse of the
lungs during exhalation.
 PREDISPOSING FACTORS

 Prematurity

 Perinatal asphyxia and hypoxia

 Hypothermia/cold and stress suppresses the

production of surfactant
 Hypoglycaemia

 Hypovolaemia

 Perinatal infection
PREDISPOSING FACTORS CONT.
 Multiple births (multiple births are often premature)
 Infants of diabetic mothers (too much insulin in a baby’s
system due to maternal diabetes can delay surfactant
production)
 Babies with patent ductus arteriosus.
PATHOPHYSIOLOGY
 Respiratory distress syndrome results from
deficiency in pulmonary surfactant activity
due to lung immaturity.
 If birth occurs before 35 weeks the premature
infant may not be able to cope for a long time
as a result of immature lungs.
 Immature lungs with deficient pulmonary
surfactant develop pulmonary vascular
resistance.
PATHOPHYSIOLOGY
 The infant may breath with minimal difficulties initially
but as the surfactant present progressively reduces, the
respiration become laboured.
 As a result, infant becomes fatigued and more alveoli can
not be opened.
 A surfactant deficient lung is characterised by collapsed
air spaces alternating with vascular congestion and
hyaline membrane
 Pulmonary vascular congestion may lead to pulmonary
hypo perfusion.
PATHOPHYSIOLOGY
 Hyaline membrane lines the air spaces hence blocking
gaseous exchange, as a result blood passing through the
lungs is unable to pick up O2 and unload CO2
 Blood O2 levels falls and CO2 rises resulting in blood
acid level and hypoxia
PATHOPHYSIOLOGY
 Owing to progressive atelectasis and pulmonary
hypoperfusion, hypoxia and hypercapnia may result.
 Hypoxia consequently results into anaerobic glycolysis
causing the production of glucose from glycogen thereby
forming lactic acid which in turn leads to metabolic
acidosis and drop in blood ph.
PATHOPHYSIOLOGY
 Increased acidosis in turn leads to capillary damage and
necrosis of the alveoli, which again suppresses the
production of surfactant with increasing atelectasis –
thus respiratory distress syndrome.
CLINICAL MANIFESTATIONS
Within an hour of birth, the baby presents with the
following
 Tachypnoea

 Cyanosis with increasing hypoxia.

 Flaring of the nostril

 Infant is lethargic and assumes frog position

 Grunting sounds with breathing

 Chest retractions (pulling in of the ribs and sternum

during breathing).
CLINICAL MANIFESTATIONS CONT.
 Apnoea especially In preterm babies.
 Diminished air entry on chest auscultation.

 Characteristic granules or rice grains appearance on chest

x-ray.
 Generalised oedema within 24hours.

 Hypothermia

 Hypotension, Asphyxia

 Reduced urine output.

MANAGEMENT
 The baby is nursed in an incubator or covered
with blanket to maintain body temperature.
 If necessary, the baby may also be dressed in order to
conserve some heat.
OBSERVATION
 Frequent observation of temperature, heart rate,
respirations and colour of the skin.
 Temperature of the baby is taken rectally at regular
intervals of not less than four hours to detect
hypothermia.
 Normal temperature should be maintained in the range
between 36.5 – 37.5oc.
 The temperature of the incubator should be between 34
&37oc, depending on baby’s condition.
OBSERVATION CONT.
 Cardiac monitor to record heart rate and
viability.
 Urine samples are taken to the lab for glucose
osmolarity to exclude renal failure.
 Baby is observed for oedema, oxygen flow,
intravenous infusions and passage of stool.
OBSERVATION CONT.
 The general behaviour, muscle tone, colour of skin and
response to stimuli should be observed.
 Observations for secretion if present, suctioning done to
clear air way. Aseptic technique maintained when
suctioning.
 Observe the infusion line since the baby may be on 10%
dextrose 60ml/kg bwt to correct acidosis.
OXYGEN THERAPY
 The aim is to maintain arterial tension in the normal
range i.e. 7-10kpa in mature babies and 6-9kpa in preterm
babies.
 Administration of oxygen helps prevent brain damage by
relieving hypoxia.
 Acute measurement of oxygen partial pressure is
important as this may prevent hypoxaemia, which may
result in lung and brain damage.
OXYGEN THERAPY
 Intermittent positive pressure may be used in severe
cases, continuous arising pressure (cap) can be used.
 CAP prevents collapse of the alveoli on expiration by
maintaining positive pressure
 This can be maintained by use of an endotracheal tube.
OXYGEN THERAPY CONT.
 Humidified oxygen is given at 60% while gas is
monitored as baby’s condition improves.
 O2 concentration is reduced followed by gradual
reduction in positive airway pressure.
• Look out for signs of CAP like pneumonia,
intraventricular haemorrhage and hydrocephalus.
FEEDING
 During the early stages, baby may not be fed via GIT to
prevent milk aspiration. Paralytic ileus may also be
present in RDS especially during the first day.
 This may cause accumulation of milk in the intestines
once the baby is fed.
 This can cause bacterial proliferation in the intestines
leading to septicaemia. Parenteral feeding is required in
the first few days.
 Later feeding into the stomach or intestines are started.

 A NGT can be used to feed baby on expressed milk.

HYGIENE
 Eye
 If nursed in radiant heater with phototherapy baby’s eyes
should be padded to prevent corneal damage.
 May require installation of artificial tears to prevent
drying of cornea.
 Mouth

 Mouth care is done regularly and ant thrush medication

may be given to prevent risk of infection.
HYGIENE CONT.
 Skin
 Skin cleaning should be done gently. Soiled nappies are
changed to prevent excoriation. A barrier cream is then
applied to protect the skin.
 Position of baby is changed after cleaning.
PREVENTION OF INFECTIONS.

 Frequent and effective hand washing.

 Maintenance of high standards of care at all times.
 Restriction of visitors and personal handling the infant.
 Reverse barrier nursing.
COMPLICATIONS
 Intraventricular haemorrhage.
 Pneumothorax.

 Patent ductus arteriosus.

 Bronchopulmonary intravascular coagulation

 Sepsis

 Pneumopericardium

 Pulmonary interstitial emphysema.

PREVENTION OF RDS
 Prevention of preterm labours and births.
 If preterm labour is inevitable, mother may be given
betamethasone for atleast 24 hours before delivery to
increase production of surfactant in the foetal lungs.
 Amniocentesis may be done to determine leci-thin
sphyngomyelin.
 If no sufficient surfactant in liquor, delay caesarean
section or induction of labour.
THE END

28