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 adequate ventilation and oxygenation.

*Oxygen 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

• RDS is a self- limiting disease if mild, and following a period of

deterioration (approximately 48 hrs) and in the absence of complications,

affected neonates begin to improve by 72 hours.

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 beta- hemolysis- 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 pneumonia1. Bacterial infections

1. Escherichia coli2. Group B streptococcus3. Kleibsiella spp4. Staphylococcus aureus5. Streptococcus pneumonia6. Mycobacterium tuberculosis

transplacentally7. Listeria monocytogenes

2. Viral infections1. Herpes simplex virus ( HSV) 2. Adenovirus3. Enteroviruses4. Mumps 5. Rubella6. Cytomegalovirus

3. Fungal infections1. Candida sp

4. Other patogens 1. Toxoplasma2. Syphilis

Late – onset pneumonia

1. Bacterial infections1. Staphylococcus2. Kleibsiella3. Escheichia coli4. Enterobacter cloacae5. Streptococcus pneumoniae6. Pseuodomonas aeroginosa7. Serratia marcescens

2. Viral infections1. Adenovirus 2. Parainfluenza virus3. Rhinovirus 4. Enteroviruses5. Influenza 6. RSV

3. Fungal infections1. 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 radiographyBilaterall alveolar densities + air bronchogramsIrregular patchy infiltratesNormal pattern

Treatment Early- onset pneumonia

Ampicillin + gentamycinCephalosphorin

Late - onset pneumonia Vancomycin + aminoglycoside

viral infection Acylovir