NEONATAL RESPIRATORY

DISORDERS

By Dr abdulkadir S.(Ass professor)

Outlines
 Overview of respiratory distress in newborn

 Respiratory distress syndrome

 Transient tachypnea of the newborn

 Meconium aspiration syndrome

 Neonatal pneumonia
Introduction
 Respiratory distress is one of the most common
reasons a neonate is admitted to intensive care unit.

 Birth initiates a dramatic change from the

intrauterine state in which the placenta is the
primary organ of respiration, to life outside the
uterus in which the lung is the organ of gas
exchange.
 Respiration involves a system that includes the lung
and muscular structures of the diaphragm and chest,
as well as complex neural, chemical, and sensory
centers in the brain.
 Neonatal respiratory diseases result from problems
with any or all of these structures or neural
pathways .
RESPIRATORY DISTRESS IN THE NEW
BORN
Definition
 RR>/=60/min
 Retractions /chest in drawing
 Flaring of alanasi
 Grunting
 Cyanosis
Causes
1. Pulmonary causes
Intrathoracic
• HMD

• Congenital pneumonia

• MAS

• TTN

• Air leak syndromes

• Pulmonary Hemorrhage

• Bronchopulmonary dysplasia
 Intrathoracic Malformations
• Diaphragmatic hernia
• Pulmonary hypoplasia
• Congenital lobar emphysema

Extrathoracic
 Congenital air way obstruction

congenital obstructive air way anomalies

2. Extrapulmonary causes
A. Cardiac Causes
• CHD
• CHF
• Hypovolemia
• Cardiac arrhythmia
B. Metabolic Causes
• Hypoglycemia
• Hypothermia
• Hypocalcemia
• Metabolic acidosis
C. Neurological Causes
 Neonatal Meningitis
 Neonatal seizure
 Hypoxic Ischemic Encephalopathy
D. Hematological Causes
 Anemia
 Polycythemia
Evaluation of Infant with Respiratory
Distress
 History
 Pregnancy- Hydramnios, Diabetes
 Labor

 Delivery: C/S or vaginal

 Evidence of Infection

 Meconium

 Apgar Scores

 Resuscitation
Physical examination
 Degree of respiratory distress
 Cyanosis
 Air entry
 Heart murmur
 Temperature
 Scaphoid abdomen
 Position of PMI
Common Neonatal Respiratory
Disorders
 Respiratory distress syndrome (RDS ).
 Transient tachypnea of the newborn (TTN).
 Meconium aspiration syndrome (MAS).
 Apnea.
 Air leak syndrome.
 Pneumonia.
Respiratory Distress Syndrome (RDS)

 Respiratory distress syndrome (RDS), also called

Hyaline membrane disease (HMD), is a respiratory
disease that primarily affects preterm infants.

 The primary dysfunction is reduced surfactant

synthesis

 The diagnosis can be established pathologically or

by biochemical documentation of surfactant
deficiency.
Epidemiology
 Mostly occur in babies born before 37 weeks of
gestation.
 Incidence is inversely related to gestational age
and birth weight.
 The incidence based on gestational age is as
follows:
 Lessthan 28 weeks 60 – 80%,
 32-36 weeks 15-35% in

 >37 weeks 5%.

Risk factors
Increase Risk Decrease Risk

 Prematurity.  Chronic intrauterine

 Male sex. stress.
 Familial  Prolonged rupture of
predisposition. membranes.
 Cesarean section  Maternal hypertension.
without labor.
 Perinatal asphyxia.  Narcotic use.
 Chorionamnionitis.  IUGR or SGA.
 Infant of a diabetic  Corticosteroids
mother (IDM). (prenatal).
 Hydrops.  Tocolytic agents.
Surfactant metabolism
 Surfactant recovered from lungs of all mammalian
species by alveolar wash procedures contains 70%
to 80% phospholipids, about 8% to 10% protein,
and about 10% neutral lipids, primarily cholesterol

 The phosphatidylcholine species of the

phospholipids represents about 60% by weight of
the surfactant and about 80% of the phospholipids
• The type II cell is responsible for the major
pathways involved in surfactant metabolism

 Synthesis and secretion of surfactant is a complex

sequence

 Specific enzymes within the endoplasmic reticulum

use glucose, phosphate, and fatty acids
Surface tension
According to LaPlace's law, the pressure (P) necessary
to keep the sphere open is proportional to the surface
tension (T) and inversely proportional to the radius (R)
of the sphere, shown by the formula
P = 2T/R

 If the surface tension is high and the alveolar

volume is small (ie, the radius is low), as occurs at
end expiration, the pressure necessary to maintain
the alveolus open is high.
 If this increased pressure cannot be generated, the
alveolus collapses.
 If this occurs throughout the lung, alveolar collapse
results in diffuse atelectasis, which in turn leads to
hypoxemia.
 Pulmonary surfactant reduces the surface tension,
even at low volumes, leading to a decrease in the
required pressure and maintaining alveolar stability
Clinical presentations
 RDS usually presents at birth but may appear up to
12 hours after birth.
 It presents with worsening respiratory distress:
 Cyanosis in room air that persists or progresses over
the first 48 hours of life.
 Increasing tachypnea (> 60 breaths/minute),
grunting on expiration, and retractions of the chest
wall.
 The uncomplicated clinical course is characterized
by a progressive worsening of symptoms with a
peak severity by days 2 to 3 and onset of
recovery by 72 hours.
 Retractions are prominent and are the result of the
compliant rib cage collapse on inspiration
 Surfactant therapy often greatly shortens this
course.
 Additional clinical features include pallor resulting
from anemia or peripheral vasoconstriction.
 Auscultatory findings – markedly decreased air
entry bilaterally.
 Peripheral edema, often present in RDS, is of no
particular prognostic significance unless it is
associated with hydrops fetalis .
 The recovery phase is characterized by
regeneration of alveolar cells, including the type II
cells, with a resultant increase in surfactant activity.
Investigations
 Laboratory Studies
 Blood gases reveal hypoxia, hypercapnia, and
acidosis.
 Complete blood picture to rule out infection.

 Chest X-ray
 Reveals
bilateral reticulogranular density (ground glass
appearance) and opaque lungs (air- bronchogram).
Shake test
 Gastric aspirate- 2 ml
 Alcohol – 0.5 ml
 Shake for 15 seconds
 When no bubbles are seen- 60% chance of HMD
 When bubbles cover 1/3 of the liquid surface or
less- 20% chance of HMD
Lecithin sphingomyeline ratio
 Risk of HMD less if L/S > 2
Exceptions -Infant of diabetic mother
- Perinatal asphyxia
- Erythroblastosis fetalis
Lamellar body count
 Lamellar bodies are packages of phospholipids
produced by type II pneumocytes

 Present in amniotic fluid

 Numbers increase with gestational age

 >50,000 bodies/ul predicts lung maturity

Management
General
 Basic support including thermal regulation,
parenteral fluid, and medications (antibiotics).
 Oxygen administration: Preferably heated and
humidified 30-40% O2 by head box.
 Respiratory support is needed if the patient
continues to deteriorate under FiO2 of more than
60% and/or if the PaO2 is less than 55-60 mmHg.
Continuous positive airway pressure (CPAP) is
then tried.
 IF under CPAP, two successive blood gas analyses
20 minutes apart reveal the following values:
 PH < 7.2
 Or PaO2 < 55 mmHg

 Or PaCO2 > 60 mmHg

 Proceed to endotracheal intubation and mechanical

ventilation.
Surfactant therapy
Indications
 Prophylactic treatment:

 For all infants > 32 weeks who require a ventilator.

 For all infants < 29 weeks.
 For infants between 32 and 29 weeks, the physician
should use his/her clinical judgment on a case by case
basis.
 Rescue treatment:
 For infants with moderate to severe RDS
who require mechanical ventilation.
 If the infant remains ventilated at 12 hours
after his/her first dose of surfactant, a
second dose of surfactant should be
considered.
Dosage and administration

 Dose: Should be guided according to the type of

surfactant used.

 Timing: Usually within 1-2 hours of age, but

without delaying resuscitation measures.
Complications
 Pulmonary air leaks

 Intubation related

 Bronchopulmonary dysplasia
Prevention
 Prevention of premature labor and delivery

 Antenatal corticosteroid therapy

 Surfactant administration
Transient Tachypnea of the newborn

 TTN is a benign disease of near-term or term

infants who display respiratory distress shortly after
delivery.
 Pathologic conditions must be excluded.

 It is caused by failure of adequate lung fluid

clearance at birth, resulting in excess lung liquid.
 Risk factors
 Cesarean section
 Precipitous labour
 Macrosomia.
 Maternal diabetes
 Male sex.
 Excessive maternal sedation.
Clinical presentations
 The infant is usually near-term or term, and shortly
after delivery exhibits tachypnea (> 80
breaths/min).

 The infant may also display grunting, nasal flaring,

rib retraction, and cyanosis.

 An important marker of TTN is the spontaneous

improvement of the neonate.
Investigations
 Laboratory investigations
 Blood gases.
 Complete blood count (CBC) to rule out
infection.
 Radiological studies
 Chest X-ray findings consistent with TTN include
perihilar streaking, mild cardiomegaly, increased lung
volume, fluid in the minor fissure, and perhaps fluid in
the pleural space.
Management
General
 Oxygenation.

 Fluid restriction.

 Feeding as tachypnea improves.

 Confirm the diagnosis by excluding other causes of

tachypnea, e.g., pneumonia, congenital heart
disease, Respiratory distress syndrome (RDS), and
cerebral hyperventilation.
Outcome and prognosis
 The disease is self-limiting and there is no risk of
further pulmonary dysfunction.

 Respiratory symptoms improve as intrapulmonary

fluid is mobilized, usually occurring with diuresis.
Meconium aspiration syndrome
Definition
 This respiratory disorder is caused by meconium
aspiration by the fetus in-utero or by the newborn
during labor and delivery.
 The aspirated meconium can cause airway
obstruction and an intense inflammatory reaction.

 Rare occurrence before 37 weeks of

gestation.
 Meconium aspiration syndrome (MAS) is often a sign
that the neonate has suffered asphyxia before or
during birth.
 The mortality rate can be as high as 50% and
survivors may suffer long-term sequelae including
bronchopulmonary dysplasia and neurological
damage.
 Risk factors
 Post-term pregnancy.
 Maternal hypertension.
 Abnormal fetal heart rate.
 Pre-eclampsia.
 Maternal diabetes mellitus.
 Small for Gestational Age (SGA).
 Maternal respiratory or CVS disease.
 Meconium
 Meconium is a thick, black-green, odorless material.
 Meconium results from the accumulation of debris,
including desquamated cells from the intestine and
skin, GI mucin, lanugo hair, fatty material from the
vernix caseosa, amniotic fluid, and intestinal
secretions.
 The black-green color results from bile pigments.
 Meconium is sterile.
 Passage of meconium occurs early in the first
trimester of pregnancy.
 Fetal defecation slows after 16 weeks gestation
and becomes infrequent by 20 weeks due to
innervation of the anal sphincter.
 fetal passage of meconium remains infrequent from
approximately 20 to 34 weeks.
 Almost all fetuses and newborn infants who pass
meconium are at term or postterm gestation.
 Aspirated meconium can interfere with normal
breathing by several mechanisms.
 Airway obstruction
 Chemical irritation and inflammation
 Infection
 Surfactant inactivation.

 However, it is likely that most cases of severe MAS

are primarily caused by intrauterine pathologic
processes, primarily asphyxia and infection, rather
than the aspiration of meconium by itself
Clinical presentations
 Meconium staining of amniotic fluid before birth.
 Meconium staining of neonate after birth.
 Airway obstruction.
 Respiratory distress leading to an increased
anteroposterior diameter of the chest.
Investigations
 Laboratory investigations
 Blood gas analysis.
 Radiological studies
 Chest X-ray will show patchy infiltrates, coarse
streaking of both lung fields, an increased
anteroposterior diameter, and flattening of the
diaphragm.
Management
 Prenatal management
 Identification of high-risk pregnancy.
 Monitoring of fetal heart rate during labor.
 General management
 Emptying of the stomach contents to avoid further
aspiration.
 Correction of metabolic abnormalities, e.g., hypoxia,
acidosis, hypoglycemia, hypocalcaemia, and
hypothermia.
 Surveillance for end organ hypoxic/ischemic damage
(brain, kidney, heart, and liver).
 Respiratory management
 Frequent suctioning and chest physiotherapy.
 Pulmonary toilet to remove residual meconium if
intubated.
 Antibiotic coverage (ampicillin and gentamicin).

 Oxygenation (maintain a high saturation > 95%).

 Mechanical ventilation (to avoid hypercarbia and

respiratory acidosis).
 Surfactant may be required if clinical condition
continues to deteriorate.
 Cardiovascular management
 Correct systemic hypotension (hypovolemia and
myocardial dysfunction).
 Treat persistent pulmonary hypertension.
 Maintain a PaCO2 level < 40mmHg, and ensure an O2
saturation of > 95%.
Neonatal pneumonia
Definition

 Pneumonia is an important cause of neonatal infection

and accounts for significant morbidity and mortality.

 In developed countries, the incidence of pneumonia in

full-term infants is less than 1 percent & 10 percent in
preterm infants.

 Neonatal pneumonia can have early or late onset.

 Bacteria are the principal pathogens for both types.
 Risk factors

 Prolonged rupture of membrane

 Premature delivery
 Chorioaminioitis
 Maternal intrapartum fever
 Fetal tachycardia
 Routes of acquisition : The route of acquisition varies
in part with the time of onset of the pneumonia.

 Early-onset pneumonia generally within three days

of birth, is acquired from the mother by one of
three routes:
 Intrauterine aspiration of infected amniotic fluid
 Transplacental transmission of organisms
 Aspiration during or after birth of infected amniotic
fluid.
 Late-onset pneumonia occurs during hospitalization
or after discharge

 Generally arises from organisms colonizing the

hospitalized newborn or is nosocomially acquired
from infected individuals or contaminated
equipment.
Clinical presentations
 Onset occurs 1-2 days after delivery.

 Moderate to severe respiratory distress in the

presence of one or more risk factors for infection.
Investigatons
 Chest X-Ray
 Finding may be identical to other causes of respiratory
distress.

 Bacterial cultures
 Some cases of pneumonia may be culture negative.
Management of pneumonia
 Respiratory support.
 If the culture is negative for pneumonia, treatment
consists of parenteral ampicillin and gentamicin for
10 days.
 If the culture is positive for pneumonia, treatment
consists of the appropriate antibiotic according to
culture result.
Complications
A. Air leak –pneumothorax,Pneumomediastinum

B. Persistent pulmonary hypertension

 Ten q