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PULMONARY

DISEASES OF THE
NEWBORN

Respiratory Distress
Syndrome
(Hyaline Membrane Disease)
RDS

is the leading cause of


respiratory failure in preterm
neonates. It is more common in
males than females.

Incidence

occurs

primarily in primarily in
premature infants
it occurs in 60-80% of infants < 28
week of gestational age
15-20% of those between 32 and 36
week
5% beyond 37 week

Predisposing Factors:
Premature

infant.
Asphyxia at birth.
Infant of diabetic mothers.
Cesarean Section delivery.
Previous history of hyaline
membrane disease (HMD) in sibling.
Multiple pregnancies.

Pathophysiology of HMD:
Surfactant

deficiency is the primary


cause of RDS
If surfactant is deficient, the alveoli
cannot be easily distended during
inspiration
which
leads
to
respiratory distress and hypoxemia.

Clinical Manifestations:

Tachypnea (80 to 120 breaths/min).


Dyspnea.
Substernal retraction.
Fine inspiratory crackles.
Audible expiratory grunt.
Flaring of the nares.
Cyanosis or pallor.

Diagnostic Tests:
Chest x-ray shows congested lung
field with a ground- glass
appearance that represents alveolar
atelectasis, and dark streaks.

Respiratory and metabolic acidosis


is determined by blood gas
analysis.

Therapeutic Management

*Maintain

*Oxygen

adequate ventilation and


oxygenation.

should

be

warmed

and

humidified

*Maintain

a neutral thermal environment

Therapeutic Management
Maintain

acid-base
balance by correct
respiratory
acidosis
through
assisted
ventilation and correct
metabolic acidosis by
IV administration of
sodium bicarbonate.

Maintain

adequate hydration and


electrolytes level.
Nutrition is provided by parenteral
therapy during the acute stage.
Surfactant therapy installed in
trachea.

Nipple and gavage feeding are


contraindicated in any situation
that creates a marked increase in
respiratory rate because of the
greater hazards of aspiration.

Prevention of HMD

prevention of premature delivery.

Administration

of corticosteroids to the
mother (24 hours to 7 days before
delivery).

Prophylactic

administration of artificial
surfactant into trachea of premature
neonate.

Prognosis

RDSisaselflimitingdiseaseifmild,
andfollowingaperiodof
deterioration(approximately48hrs)
andintheabsenceofcomplications,
affectedneonatesbegintoimproveby
72hours.

Prognosis

Neonates who survive the first


96 hours have a reasonable
chance of recovery. Surfactant
therapy decreased the use of
long term ventilation and
decreased period of stay in
hospital. It also improves the
outcome.

Prognosis

Neonates who survive the first


96 hours have a reasonable
chance of recovery. Surfactant
therapy decreased the use of
long term ventilation and
decreased period of stay in
hospital. It also improves the
outcome.

Transient Tachypnea of the Newborn

Transient Tachypnea of the


Newborn

usually follows uneventual normal preterm


or term vaginal delivery or CS delivery

Is encountered by all physicians who take


care of newborn infants

Clinical Manifestations

early onset of tachypnea


Retractions respiratory grunting
Occasionally cyanosis that is relieved by
minimal oxygen(<40%)
Patient recovered rapidly within 3 days
No rales or rhonchi
X rays shows prominent vascular markings,
fluid in the intralobar fissures, ovearation, flat
diaphragms

TTN vs RDS

TTN sudden recovery of infants

X ray findings of RDS ( hypoaeration, diffuse


riticulogranules pattern, air bronchogram

Etiology

secondary to slow absorption of flat lung


fluid resulting in decrease pulmonary
compliance and tidal volume, increased dead
space

Treatment and Management

supportive
Observe for the development of respiratory
fatigue and signs of clinical deterioration that
may suggest some other diagnosis

NEONATAL PNEUMONIA

Introduction
Pneumonia
is an important cause of neonatal
infection
Accounts morbidity and mortality
aspecialy in developing country

Pathogenesis
Routes of acquisition: Varies in part
with
the time of onset of pneumonia

Early onset pneumonia


Late - onset pneumonia

Early onset pneumonia

Generally within three days of birth


Aquired from the mother by one of three routes

Intra uteri aspiration of infected amniotic fluid


Transplacental tranmision of organisms from the
mother to the fetus
Aspiration during or after birth of infected amniotic
fluid or vaginal organisms

Late - onset pneumonia

Occures during hospitalization or after


discharge
Nosocomial acquired from

Infected individuals
Contaminated equipment

Microorganisms can invide through

injury tracheal
bronchoia mucosa
bloodstream

Mechanisms of injury in GBS


pneumonia

In GBS pneumonia,

the level of beta hemolysin expression


correlate directly with the abilility of the
organism to injure of epithelial cell
Hemolysin act as pore forming cytolysis
alveolar edema and hemorrhage
Surfactant phospholipid inhibits betahemolysis- associated lung epithelial cell injury
premature infants more severelly affected

Pathology
(The patologic changes very with type of
organisms)

Bacteria :
Inflammation of pleura
infiltration / distruction of
brochopulmonary tissue
leukocyte and fibrious exudate within
alveoli and bronchi/ bronchioles
Bacteria are seen within interstitial
spaces, alveoli,bronci/bronchioles

Virus

Cause an interstitial pneumonia


Infiltration of mononuclear cell and
lympocytes hyalin membrane formation -
interstitial fibrosis and scarring

Microbiology
Cause :

Bacterial
Viral
Spirochetal
Protozoan
Fungal pathogens

Early- onset pneumonia


1.

Bacterial infections
1.
2.
3.
4.
5.
6.

Escherichia coli
Group B streptococcus
Kleibsiella spp
Staphylococcus aureus
Streptococcus pneumonia
Mycobacterium tuberculosis
transplacentally

7.

Listeria monocytogenes

2.

Viral infections
1.
2.
3.
4.
5.
6.

3.

Fungal infections
1.

4.

Herpes simplex virus ( HSV)


Adenovirus
Enteroviruses
Mumps
Rubella
Cytomegalovirus
Candida sp

Other patogens
1.
2.

Toxoplasma
Syphilis

Late onset pneumonia


1.

Bacterial infections
1.
2.
3.
4.
5.
6.
7.

Staphylococcus
Kleibsiella
Escheichia coli
Enterobacter cloacae
Streptococcus pneumoniae
Pseuodomonas aeroginosa
Serratia marcescens

2.

Viral infections
1.
2.
3.
4.
5.
6.

3.

Adenovirus
Parainfluenza virus
Rhinovirus
Enteroviruses
Influenza
RSV

Fungal infections
1.

Candida sp

Risk factors

Early onset pneumonia

PRM > 18 hours


Maternal amnionitis
Premature delevery
Fetal tachycardia
Maternal intrapartum fever

Late onset pneumonia

Assisted ventilation

Other factors

Anomaly of the airway (choanal atresia,


tracheoesophageal fistule)
Severe underlying disease
Prolonge hospitalization
Neurologic empairment aspiration
gastroentestinal contents
Poor hand washing
Overcrowding

Clinical manifestation
Early- onset pneumonia

Respiratory distress beginning at / soon after birth


May have associated

Lethagy
Apnea
Tachycardia
Poor perfusion
Septic
Shock

Other sign

Temperature instability
Metabolic acidosis
Abdominal distentions

Late onset pneumonia

Respiratory distress
Apnea
Tachypnea
Tachycardia
Poor feeding
Abdominal distention
Jaundice
Emesis
Circulatory collapse

Diagnosis

Sudden onset of respiratory distress or other


sign of illness should be evaluated for
pneumonia / sepsis
culture: Blood,cerebrospinal fluid, pleural fluid
Chest radiography
Bilaterall alveolar densities + air bronchograms
Irregular patchy infiltrates
Normal pattern

Treatment

Early- onset pneumonia


Ampicillin

+ gentamycin
Cephalosphorin

Late - onset pneumonia

Vancomycin + aminoglycoside

viral infection

Acylovir