DISEASES OF THE NEWBORN I

MED 7710
CHILDREN’S HEALTH
 COURSE OBJECTIVES
At the end of the session the student:
1. Should be able to recognise the life-threatening condition in
the newborn

2. Should have understood the pathoshysiology of these

different life-threatening conditions

3. Should be able to apply appropriate management to the

conditions that they have recognized
 CONTENTS

RESPIRATORY DISTRESS IN THE NEWBORN

HYPERBILIRUBINEMIA IN THE NEWBORN

HEMOLYTIC ANEMIA IN THE NEWBORN

GASTROINTESTINAL CONDITIONS IN THE NEWBORN

I. RESPIRATORY DISTRESS IN THE NEWBORN INFANT:1

Transition from intrauterine life to extrauterine life is a difficult adjustment for

newborn infants.
It requires:
1. effective pulmonary gas exchange
2. rapid removal of fluid in the potential pulmonary air space

Fetal circulation in utero is not the same as that in the adults.

It consists of a parallel circuit where different openings allow blood to enter the
left atrium, the descending thoracic aorta and to the lower half of the body .

https://www.youtube.com/watch?v=75fj1eoUZcoA
 The three major openings that allows blood to go to different parts of the body
are the following:
Blood going to the left atrium passes through the FORAMEN OVALE
Blood going to to the descending thoracic artery passes through DUCTUS
ARTERIOSUS
Blood going to the lower half of the body passes through the DUCTUS
VENOUSUS

During intrauterine life, the following conditions exists in the fetal circulation:
Pulmonary vascular resistance is high
Pulmonary blood flow is low
Most of the blood from the right side of the heart goes to the aorta through
the foramen ovale
Once the umbilical cord is clamped, the following conditions happen:
The resistance in the placental circuit becomes low
There is increase in the systemic blood flow
Pulmonary blood flow increases more than 10 times its original situation
The most important stimuli for increasing pulmonary blood flow is pulmonary
ventilation of the lung and increased oxygen tension
Crying is a significant part of the transition because it helps in lung expansion
and protect lung volume.
In order for breathing to be successful, the following factors should be
achieved:
• sufficient gas exchange surface area
• Adequate pulmonary vasculature
• Compliant lung
• Structures that control respiration must be mature
Three groups of skeletal muscles are involved in respiration:
Diaphragm - this is the primary muscle involved in respiration
Intercostal and accessory muscles
Abdominal muscles

DEFINITION OF RESPIRATORY DISTRESS

It is defined as:
• Tachypnea with respiratory rate of 60/min
• Chest retractions
• Intercostal. subcostal and substernal retractions
• Expiratory grunting
• With or without cyanosis

Causes of Respiratory Distress:

1. Pulmonary
2. Non-pulmonary
• Non-pulmonary causes of respiratory distress:
• Cardiac
• Sepsis
• CNS
• Metabolic
• Hematologic

Pulmonary Causes are myriads, but the following are most common:
Congenital anomalies
Transient tachypnea of the newborn
Respiratory distress syndrome
Meconium Aspiration syndrome
Pneumonia
Pneumatocoele
 TRANSIENT TACHYPNEA OF THE NEWBORN

CHEST X-RAY FINDINGS IN TRANSIENT TACHYPNEA

OF THE NEWBORN:
Hyperinflation
Prominent perihilar vascular markings
Fluid maybe present in the fissures
Small pleura

Benign, self-limited condition noted after birth

It is common in newborns delivered by caesarean section without going through
labor
Predominance of male sex
Occur in preterm infants, but commonly between the 37 - 40th week of
gestation
 Risk factors consist of the following:
1. perinatal asphyxia
2. prolapse of the umbilical cord
3. maternal complications i.e. asthma or diabetes
4. use of anesthesia or analgesia during delivery
PATHOPHYSIOLOGIC MECHANISM:
Delayed clearance of lung fluid by the lymphatics and pulmonary circulation
which results in pulmonary oedema that is transient.

Differential Diagnoses:
1. Respiratory Distress Syndrome
2. Neonatal Pneumonia
3. Neonatal infection
LABORATORY OR DIAGNOSTIC PROCEDURES:
• CBC with blood typing
• Chest x-ray
• ABGs

TREATMENT:
Most do not require treatment
Supplemental oxygen through nasal cannula
Mechanical ventilator if required, although very rarely
Antibiotics if sepsis has not yet been excluded
Hydration and nutrition
Avoid overload
Diuretics has not been proven to be effective
Aerosol β agonist may play a role in the management of TTN
 RESPIRATORY DISTRESS SYNDROME2
It is common in preterm infants < 28 weeks AOG in 60 - 80%
The incidence increase in maternal diabetes , multiple births, precipitous labor,
and in casearean sections, among others
The risk is reduced in:
1. Chronic or pregnancy- associated hypertension
2. Maternal heroin use
3. Premature rupture of the bag of water
4. Antenatal corticosteroid used

ETIOLOGY AND PATHOLOGY:

• Absence or decrease in the amount of surfactant in the lungs
SURFACTANT: fluid secreted by the cells of the alveoli that serves to
reduce the surface tension of pulmonary fluids
surfactant contributes to the elastic properties of pulmonary tissue,
preventing the alveoli from collapsing.
 The absence of surfactant increases alveolar tension, leading to atelectasis,
FRC is not attained, producing further damage to the endothelial and
epithelial cells from atelectasis
Absence or deficiency of surfactant further results to ischemic injury and
toxicity, forming and collecting proteinacious and cellular debris in the alveoli
(hyaline membrane) further preventing oxygenation.
3 situations that prevent the alveoli from expanding:
1. Alveolar atelectasis
2. Hyaline membrane
3. Interstitial edema

• Surfactant appear in the lungs at the age of 28 - 32 weeks AOG

• Mature levels are found after the 35th week of gestation

• The initial component of surfactant contains lecithin, phosphatidylglycerol,

apoproteins and cholesterol.
• As the gestational age increases, phospholipids are synthesized and
deposited in alveolar cells type II
• These surface-agents are released into the alveoli so they can reduce surface
tension and maintain alveolar stability at end expiration.
CLINICAL MANIFESTATION:
Usually appears within minutes after birth
Tachypnea, grunting, subcostal and intercostal retractions, nasal flaring
and cyanosis
Breath sounds maybe normal, diminished or tubular in character and
auscultation findings will produce fine crackles during deep inspiration

The natural course of untreated RDS will constitute of:

• Progressive worsening of the cyanosis and dyspnea
• There will be hypotension
• Grunting will disappear and anemia will worsen
• Warning signs i.e. apnea and irregular respiration are indication for a
more aggressive management.
OTHER LABORATORY FINDINGS CONSIST OF:
Mixed metabolic and respiratory acidosis
Oliguria
Edema
Ileus

Condition may peak on the 3rd day, with gradual improve and may manifest as:
Spontaneous diuresis
Gradual improvement of the values of blood gases with lower p02 and
ventilatory support
Deaths maybe due to:
1. Severe impairment of gas exchange
2. Pneumothorax, pulmonary interstitial emphysema,
3. Intraventricular haemorrhage
4. Pulmonary haemorrhage
DIAGNOSIS:
Clinical course of the disease
Chest x-ray finding
Blood gas values Air bronchogram

air-filled oesophagus
Fine reticular granules

Chest X-Ray Findings - characteristic but

not pathognomonic of RDS:
Low lung volumes
Diffuse, fine, reticular granularity of the
parenchyma (ground glass appearance)
Air bronchogram
BLOOD GASES
BLOOD GASES IN PATIENTS WITH RESPIRATORY DISTRESS SYNDROME
WILL BE AS FOLLOWS:
• There will be initial hypoxemia which progresses to severe hypoxemia
• Metabolic acidosis
• Hypercapnia

WHAT IS METBOLIC ACIDOSIS?B

The presence of a low serum bicarbonate concentration (normal range is 22
- 28 mEq/L)
It is also generally associated with low urine pH
In short it is a condition where there is excess acid in the plasma
SOME DIFFERENTIAL DIAGNOSIS:
1. Transient tachypnea of the newborn
2. Neonatal pneumonia
3. Cyanotic heart disease
4. Sepsis
5. Meconium aspiration syndrome
6. Persistent pulmonary hypertension

PREVENTION:
Avoid untimely scheduling of caesarean section or induction of labor if AOG
is not definite
Administration of antenatal corticosteroids beefier the 37th week of
gestation The administration of antenatal aorticosteroids can:
1. Reduce overall mortality
2. Reduce the incidence of admission to the NICU and prolonged use of
ventilator support
3. Reduce the incidence of intraventricular haemorrhage (IVH), necroticing
enterocolitis and neurodevelopmental impairment
 TWO CORTiCOSTEROIDS FOR USE:
Betamethasone - reduces neonatal death more than Dexamethasone
Dexamethasone

ADMINISTRATION OF BETAMETHASONE HAS BEEN RECOMMENDED BY

THE AMERICAN COLLEGE OF OBSTETRICS AND GYNECOLOGY IN THE
FOLLOWING CONDITIONS:

All women, between 24th - 36th week of gestation, who are on preterm labor
and may likely deliver within a week’s time, administration of antenatal
cortcosteroids should be considered.
 TREATMENT

The basic problem in RDS is primary O2 - CO2 exchange

1. Basic supportive measures consist of:
Monitoring of temperature
Monitoring of fluid and electrolytes and adequate circulation
Respiration
Other parameters to monitor would be
glucose level
PaO2, SaOs, pH, electrolytes
Hematocrit
Blood pressure
Temperature
 2. NCPAP ( Nasal Continuous Positive Airway Pressure)
Utilized if there is significant respiratory distress or SaO2 can not be
maintained at >90% @FiO2 of > 40-70%
It produces rapid improvement in oxygenation
It reduces collapse of the surfactant dependent valveoli
It reduces the risk for the use of mechanical ventilation

3. SURFACTANT:
They are recognised to aid in the management of RDS
They are called prophylactic or early rescue surfactant replacement therapy
Administered as follows
1. Intubate surfactant extubatne (INSURE)
2. Minimally invasive surfacent therapy (MIST)
3. Less invasive surfactant administration
Neonates who needs mechanical ventilation should be given surfactant
immediately, every 6-12 hours for a total of 2-4 doses.
The total dose of surfacent is 100 mg of phospholipids (4 ml/kg) in 4 divided
doses
 MECONIUM ASPIRATION SYNDROME1
It is a respiratory syndrome produced when an infant is born through
meconium stained amniotic fluid
It is a diagosis that can be used if all other causes for distress in the newborn
has been ruled out
Miconium consists of water and pieces of materials from the GIT, bile
pigments including lipids from vernix
Aspiration may occur during fetal gasping or during the first breath
Although sterile, when it enters the lungs, it stimulates inflammatory reactions
through cytokines and vasoactive production.

CLINICAL MANIFESTATION OF MAS:

Respiratory failure, hypoxia due to poor lung compliance
Increased airway resistance and smaller tidal volume
Airways are plugged with meconium resulting to ventilation-perfusion
abnormalities, which lead to right to left shiunting through the FORAMEN
OVALE or DUCTUS ARTERIOSUS
1
RADIOLOGIC FINDINGS:
Streaky, linear or patchy inflitrates
Hyperaeration
Radiologic changes may resolve in
7-10 days
In some infants however, changes may
take weeks

Other laboratory procedures:

1. CBC with blood typing
2. Blood culture and sensitivity
3. Blood gases

Differential Diagnoses:
1. Respiratory distress syndrome
2. Transient tachypnea of the newborn
3. Neonatal infections particularly
neonatal pneumonia
 TREATMENT:
RESPIRATORY SUPPORT:
1. Oxygen hood to maintain oxygen saturation at >95% (pAO2 at 55 - 90
mmHg)
2. CPAP
3. Assisted ventilation
4. Exogenous and surfactant lavage
5. ECMO
6. Sedation

SUPPORTIVE TREATMENT:
Antibiotic treatment
Maintenance of fluid and electrolytes
Monitoring vital signs and chest x-ray
ROLE OF SUCTIONING IN INFANTS WITH MAS:
Intrapartum suctioning of the infant while the shoulder is being delivered is
not recommended
Tracheal suctioning may remove some of the meconium that is lodged in the
trachea even after suctioning intrapartum
It is recommended that tracheal suctioning be done before positive
pressure ventilation is done
Suctioning is not recommended for vigorous infants even when born with
MSAF
 iNFECTIONS IN THE NEWBORN INFANTS 2,C

CLASSIFIED ACCORDING TO THE TIME IT WAS ACQUIRED IN RELATION TO

THEIR BIRTH:
Congenital infections - infections acquired in utero
Perinatal infections - acquired within the time of delivery
Early onset - occurring within 7 days after birth (1st 72 hours)
Late onset - occurs between 7 - 30 days of life
Hospital acquired - usually acquired after the 30 days of life
COMMON MICROORGANISMS THAT CAUSE THE INFECTIONS:
1. Group B haemolytic streptococcus
2. E. Coli
3. H. Influenza
4. Viral organisms:
Herpes simplex Listeria Monocytogenes
Hepatitis B HIV
EARLY ONSET - Usually occurs within 7 days of life
They usually occur during or before delivery (vertical transmission)
The organisms that usually cause the infection are Group B Hemolytic
Strep and E. Coli
Other viral infections can cause early onset sepsis, i.e. herpes
In majority of cases, the neonate is not exposed to pathogenic bacteria until
the membrane ruptures and the infant passes through the vaginal canal or is
exposed to the external environment.

The vaginal canal is colonized by aerobic and anaerobic organisms that can
infect the infants through the ascending route.
PATHOGENESIS:2
• Prolonged rupture of the membrane is one of the reasons why infants get
infected while in utero.

• Chorioamnionitis is caused by invasion of the amniotic fluid by organisms

brought about by premature rupture of the membranes

• Chorioamnionitis is a clinical syndrome consisting of maternal fever,

with or without tenderness, foul vaginal discharge, maternal leukocytosis
and maternal/fetal tachycardia
CHORIOAMNIONITIS is now known as Intrauterine Inflamation or Infection at birth
(Triple I)
It consists of the following:
Fetal tachycardia
Maternal leukocytosis (>15,000 in the absence of steroids)
Purulent secretions from the vaginal opening
Microscopic changes consistent with infection
Fever

• Rupture of the membranes for more than 24 hours was thought before as a factor
causing intrauterine infections.
• However, it has been found out that PROM of 18 duration has been attributed to
early onset of infection with group B streptococcal infections in the newborn.
• Today, PROM of 18 hours duration is considered as the appropriate cut-off time
for increased risk of neonatal infection
 LATE-ONSET INFECTION

FACTORS CAUSING LATE-ONSET INFECTION:

Prematurity
Prolonged used of IV catheters
Associated illness
Use of antibiotics to which the organism is resistant to
Hospitalization
Infected IV catheters or contaminated enteral solutions

ORGANISMS MOSTLY INVOLVED:

Gram-positive organisms (staph aureus
Gram-negative enteric bacteria
Candida spp
 CLINICAL MANIFESTATIONS:
Most of the clinical signs and symptoms of infections in the newborn are varied
and subtle. They may present as:
Lethargy
Poor feeding
Hypothermia
Tachypnea
Irritability
Poor cry

Signs and symptoms may occur in any organ system and may manifest as
any of the above mentioned clinical manifestations.

The IMCI and the WHO has come up with clinical criteria for severe infection in
children
2
 DIAGNOSTIC EXAMINATIONS
1. Complete blood count with blood typing
2. Blood culture and sensitivity
3. PRC
4. Lumber tap

GENERAL APPROACH TO MANAGEMENT:

Without specific signs of focal lesion, treatment for neonatal infection is
usually empirical.
Antibiotics are chosen specially to cover the organisms that are known to
cause the infection
Coverage for GBS, gram-negative organisms, Listeria and Enterococcus
ANTIBIOTICS FOR EMPIRIC TREATMENT OF NEONATAL INFECTION
2
 EMPIRIC ANTIBIOTIC TREATMENT FOR NEONATAL INFECTIONS

An empiric treatment for suspected early onset sepsis in term or late preterm
infants is Ampicillin at 150 mg/kg/dose IV every 12 hours and Gentamicin at 4
mg/kg/dose IV every 24 hours.
These antibiotics have been the standard regimen because it covers almost all of
the organisms that causes neonatal infections
After discharge from the nursery, Ampicillin plus Cefotaxime or Cefepime may be
used, especially if the infection is due to E. Coli that is resistant to Ampicillin
Ceftrixone maybe used in preterm infants >41 weeks after birth
Initial antibiotics can be discontinued once results of culture and sensitivity is
available and the antibiotics are not the drug of choice for the organism.
Before shifting to another antibiotic, consider the clinical status of the infant.
 SYNTHESIS

Discussed in Diseases of the Newborn I are the following:

1. Transient Tachypnea of the Newborn
2. Respiratory Distress Syndrome
3. Meconium Aspiration Syndrome
4. Neonatal Infections

The topics were discussed based on the following:

1. Etiology
2. Pathophysiology
3. Symptomatology
4. Laboratory or diagnostic procedures to arrive at a diagnosis
5. Differential diagnoses
6. Management/Prevention
 ASSESSMENT:
An 8 hour old full term male infant, delivered through spontaneous vaginal
delivery was brought to you by the midwife because of flaring of the ala nase,
intercostal, subcostal retractions, associated with grunting and an RR of 70/min.
Physical findings on auscultation revealed crackles occasionally on the right
lung fields.
Questions:
1. What laboratory exams would you request?
2. What is your diagnosis?
3. How are you going to manage this patient?
 REFERENCES:

1. Thomas K. McInerny, M.D., American Academy of Pediatrics, Textbook of

Pediatric Care, 2nd ed 2017
2. Nelson’s Textbook of Pediatrics, 21st ed

OTHER REFERENCES:

A. https://www.youtube.com/watch?v=75fj1eoUZco
B. https://www.renalandurologynews.com/.../acid-base-disorders-metabolic-
acidosis/

C. https://emedicine.medscape.com/article/978352-overview