RESPIRATORY DISEASES

OF THE NEWBORN

By: dr Ismah, Paeds department

1

2

Respiratory diseases

of the newborn

Respiratory distress syndrome - RDS

(hyaline membrane disease)

Transient tachypnea of the newborn (TTN)

Meconium aspiration syndrome (MAS)

Primary pulmonary hypertension of the newborn

(PPHN)

Apnea of prematurity

Congenital pneumonia

3

Preterm infant Term infant Both

• RDS

• Erythroblastosis

fetalis

• Nonimmune

hydrops

• Pulmonary

hemorrhage

• PPHN

• MAS

• Polycythemia

• Amniotic fluid

aspiration

• Bacterial sepsis e.g. GBS

• TTN

• Spontaneous pneumothorax

• Congenital anomalies e.g.

congenital lobar

emphysema, diaphragmatic

hernia

• Congenital heart disease

• Pulmonary hypoplasia

• Viral infection e.g. CMV,

herpes

• Inborn metabolic errors

4

1. Respiratory distress

syndrome

- RDS

(hyaline membrane

disease)

Occurred after the onset of breathing

and is associated with an insufficiency

of pulmonary surfactant

Incidence of RDS increase with decrease gestational

age

RDS develops in 30-60% in infant 28-32 W

Others risk factors: delivery of previous preterm infant

with RDS, maternal DM, male sex, 2nd born of twins, c

sec not in labor

May develop immediately in extremely immature infant

or 3-4 hrs after birth in 34W infant 5

LUNG DEVELOPMENT

Lining of alveolus consists 90% type 1 and 10% types

II cells

The surfactant production depends on the fetal

cortisol, begins between 32-34 W of gestation

Surfactant produced by type II cells sufficiently by 34-

36 W

6

Contents of surfactant are 90% lipids (lecithin,

phosphatidylglycerol) and proteins SP-A, SP-B, SP-C

and SP-D

Surfactant prevents atelectasis and contributes to the

lung recoil by manipulates the surface tension of the

lungs

Lecithin/Sphingomyelin ratio 2:1 in amniotic fluid

usually indicate fetal lung maturity or the presence of

minor phospholipids e.g. phosphatidylglycerol

7

CLINICAL MANIFESTATION

Tachypnea

Nasal flaring

Intercostal, sternal recession

Grunting; closure of glottis during expiration

Cyanosis

8

CXR

Shows air bronchogramsand reticulonodularshadowing throughout the lung fields (often termed ‘ground glass’ appearance)

9

10

PREVENTION AND TREATMENT

Prevent preterm birth; treatment of infections, cervical

cerclage

Prevention of neonatal cold stress, birth asphyxia,

hypovolemia reduces risk of RDS

Administration of corticosteroid before delivery for lung

maturity

Surfactant usage

Aim SPO2 ≥ 90%, PaO2 60-70 mmHg, pH> 7.25

Start antibiotic for 48-72 hrs (difficult to differentiate

sepsis, pneumonia from RDS)

11

SURFACTANT

Surfactant therapy reduces mortality rates most

effectively in infants <30 weeks and those of birth weight

<1250 gm

12

WHO TO GIVE?

Depressed preterm infants who have no spontaneous respiration

after 30 seconds of ventilation that require positive pressure

ventilation (PPV)

Preterm infants below 28 weeks gestation who are given only

CPAP from birth in delivery room, i.e. the infant has spontaneous

respiration and good tone at birth. Surfactant to be given within

30 minutes after birth

Preterm infants between 28-32 weeks – to have CPAP from birth

in delivery room. To assess requirement for surfactant in NICU

based on oxygen requirement of FiO2 > 30% and respiratory

distress

More mature or larger infants should also be given surfactant if

the RDS is severe13

TIMING OF SURFACTANT

THERAPY

The first dose has to be given as early as possible to the

preterm infants requiring mechanical ventilation for RDS but

not in 1st minute OL

The repeat dose is given 4-6 hours later if FiO2 is still >

0.30 with optimal tidal volume settings for those below 32

weeks;

And if FiO2 > 0.40 and CXR still shows moderate to severe

RDS (“white” CXR) for those infants > 32 weeks gestational

age.

14

TYPES OF SURFACTANT

Survanta , a natural surfactant, bovine derived

Dose : 4 ml/kg per dose.

Curosurf , a natural surfactant, porcine derived

Dose: 1.25 mls/kg per dose.

15

COMPLICATIONS

PDAPulmonary air

leaks

Bronchopulmonarydysplasia

(chronic lung disease)

ROP

16

RDS

increased

pulmonary

pressure

prevent

closure of

ductus

arteriosus

Associated

with

ventilation

that may

lead to

ruptured

alveolar

O2 dependent ≥

CGA 36W

Excessive

O2

developing

blood

vessels of

premature

infant retina

blindness

Tachypnea, mild retraction, hypoxia, occasional

grunting, rarely cyanosis which may persist for up to

48 hrs

Caused by retained lung fluid or slow resorption of

lung fluid

Associated in larger premature infant or term infant in

precipitate delivery (not in labor), infant DM mother or

use of analgesia intrapartum

17

2. TTN

PATHOPHYSIOLOGY

The lungs in utero are constantly secreting fluid to aid lung

growth and development

However the rate of lung fluid production and volume of foetal

lung lumen decreases before birth, most during labour

The mechanism for fluid absorption is triggered by

neuroendocrine hormones, which cause lymphatic vessel

dilatation

As the lung pulmonary circulation increases following the first

breath, the fluid in the lungs is cleared thus interruption of this

process of clearing fluid from the lungs may result in

respiratory distress. 18

19

MANAGEMENT

It is often managed conservatively by a period of close

observation on the postnatal ward or in the neonatal unit

but must be weighed against other differential diagnoses

including RDS and pneumonia which may progress rapidly

in newborn infants

Oxygen therapy

Antibiotics may be used if persistent (consider other

associated condition e.g. sepsis)

20

3. MAS

Term and post term delivery

Tachypnea, hypoxia, hypercapnia, small airway obstruction,

air trapping, overdistention and extra alveolar air leaks

Meconium stained liquor suggest utero distress with

asphyxia, hypoxia and acidosis

21

The inhaled meconium can cause:

• Mechanical obstruction of the airways leading to

mismatched ventilation/ perfusion

• Chemical pneumonitis (in 24-48 hrs)

• Infection which inhibit surfactant function and leads to

inflammation and swelling, which also can obstruct small

airways

• The combination of ventilation/perfusion mismatch and

pulmonary inflammatory can trigger vasoconstriction of

the pulmonary vasculature leading to PPHN

22

MANAGEMENT

Mostly supportive therapy

Most cases of MAS will recover within 2–3 days

However, some infants will progress to develop severe

MAS requiring intubation and ventilation

Start on antibiotic in view of distinguishing MAS from

pneumonia can be difficult

• The initial chest radiograph is often similar to findings

associated with pneumonia with bilateral patchy infiltrates and

possible pleural effusion

23

CXR

24

Bilateral diffuse

grossly patchy

opacities

4. PPHN

Term, post term

Defined as a failure of normal pulmonary vasculature

relaxation at or shortly after birth, resulting in

impedance to pulmonary blood flow which exceeds

systemic vascular resistance, such that unoxygenated

blood is shunted to the systemic circulation

25

PPHN can be:

• Idiopathic - 20%

• Associated with a variety of lung diseases:

Meconium aspiration syndrome (50%)

Pneumonia/sepsis (20%)

RDS (5%)

Congenital diaphragmatic hernia (CDH)

Others: Asphyxia, Maternal diabetes, Polycythemia

26

DIAGNOSIS

History

- Precipitating factors during antenatal, intrapartum, postnatal

periods

Respiratory signs

- Signs of respiratory distress

- Onset at birth or within the first 4 to 8 hours of life

- Marked lability in pulse oximetry

Cardiac signs

- Central cyanosis

- Prominent precordial impulse

- Murmur27

Radiography

- Lung fields: normal, parenchymal lesions if lung disease is

present, or oligaemia

- Cardiac shadow: normal sized-heart, or cardiomegaly (usually

right atrial or ventricular enlargement)

Echocardiography

- Exclude congenital heart disease

- To look for pulmonary artery pressure

- Define the presence, degree, direction of shunt through the

duct / foramen ovale

- Define the ventricular output.

28

Differentiate PPHN from Congenital

Cyanotic Cardiac diseases.

Differentiating points between the two are:

• Infants with PPHN usually had some perinatal hypoxia

• Bradycardia is almost always due to hypoxia, not a

primary cardiac problem

• Babies with congenital cyanotic heart diseases are

seldom critically ill at delivery

• Infants with cyanotic lesions usually do not have

respiratory distress

• The cyanosed cardiac baby is usually pretty happy, but

blue

29

MANAGEMENT

30

• Preventing and treating; hypothermia, hypoglycaemia, hypocalcaemia, hypovolemia, anaemia

General measures

• Morphine, midazolamSedation

Ventilation

31

• Aim MAP>50 mmHg

• Inotropes to increase COCirculatory

• Inhaled NOVasodilators

• Extracorporeal membrane oxygenation

ECMO

5. APNEA OF PREMATURITY

Defined as sudden cessation of breathing that lasts for

at least 20 seconds or is accompanied by bradycardia

or oxygen desaturation (cyanosis) in an infant less

than 37 weeks’ gestational age

Incidence increase with decrease gestational age

32

CLASSIFICATION

Central

Complete cessation of airflow and respiratory efforts with

no chest wall movement with no evidence of obstruction

Obstructive

Absence of noticeable airflow but with continuation of

chest wall movement

Mixed apnea – most common

33

ETIOLOGY

Symptomatic of underlying problems, commoner ones

of which are:

• Respiratory conditions (RDS, pulmonary haemorrhage,

pneumothorax,

upper airway obstruction, respiratory depression due to drugs).

• Sepsis

• Hypoxemia

• Hypothermia

• CNS abnormality (e.g. IVH, asphyxia, increased ICP, seizures)

• Metabolic disturbances (hypoglycaemia, hyponatraemia,

hypocalcaemia)

• Cardiac failure, congenital heart disease, anaemia

• Aspiration/ Gastro-oesophageal reflux

• Vagal reflex: Nasogastric tube insertion, suctioning, feeding

34

Differentiate from Periodic

breathing

Regular sequence of respiratory pauses of 10-20 sec

interspersed with periods of hyperventilation (4-15 sec) and

occurring at least 3x/ minute, not associated with cyanosis

or bradycardia

Benign respiratory pattern for which no treatment is

required

Respiratory pauses appear self-limited, and ventilation

continues cyclically

Periodic breathing typically does not occur in neonates in

the first 2 days of life35

MANAGEMENT Immediate resuscitation.

36Pediatrics Protocol 3rd ed

Review possible underlying causes and institute specific

therapy, e.g. septic workup if sepsis suspected and

commence antibiotics

Remember to check blood glucose via glucometer

Management to prevent recurrence

- Nurse baby in thermoneutral environment

- Nursing prone can improve thoraco-abdominal wall synchrony and

reduce apnoea

Monitoring:

- Pulse Oximeter, cardio-respiratory monitor

37

Drug therapy

- Methylxanthine compounds:

Caffeine citrate (preferred if available)

IV Aminophylline or Theophylline

• Start methylxanthines prophylactically for babies < 32

weeks gestation

• For those > 32 weeks of gestation, give methylxanthines if

babies have apnoea

• To stop methylxanthines if

- Gestation > 34 weeks

- Apnoea free for 1 week when the patient is no longer on CPAP

- Monitor for at least 1 week once the methylxanthines are stopped

38

After discharge, parents should be given advice

- Supine sleep position

- Elimination of exposure to tobacco smoke

39

6. CONGENITAL PNEUMONIA

Acquired through the birth passages especially after

prolonged rupture of membranes

Pneumonia in newborn infants is often difficult to

diagnose and often difficult to distinguish from other

causes of respiratory distress including RDS and TTN

Investigations including blood white cell counts, blood

cultures, C-reactive protein, CXR

40

PATHOPHYSIOLOGY

Pneumonia may be acquired due to ascending

infection especially when chorioamnionitis is

present

Common pathogens include • Bacteria, such as group B Streptococci (GBS), Streptococcus

pneumonia, Staphylococcus aureus, Listeria and gram-

negative enteric rods (e.g. E.Coli)

• Viruses, such as Herpes simplex virus, Respiratory syncytial

virus and Influenza A & B viruses

• Atypical organisms such as chlamydia

• Fungi such as Candida albicans.

41

RISK FACTORS

Prolonged rupture of membranes (PROM)

Prematurity

Maternal infection (maternal fever or raised

white cell count) e.g. GBS

42

MANAGEMENT

Blood gases and pulse oximetry monitoring will guide

the respiratory support required by the infant

Antibiotic; Penicillin and gentamicin

Supportive care such as oxygen, thermoregulation,

prevention of hypoglycaemia and parenteral nutrition

or nasogastric tube feeding

43

CXR

A chest radiograph may show bilateral patchy

shadowing with or without pleural effusion.

44

TAKE HOME MESSAGE

Gestation age

Risk factors

Recognize signs of respiratory distress

Early intervention, consultation and close monitoring

45

THANK YOU

Ref:

1. Nelson Essential of Pediatrics 6th ed

2. Pediatrics Protocol 3rd ed

3. http://www.learningradiology.com

46