Respiratory Distress in Newborn

Presenter
Noorul Nadia Salwani Binti Mohd Tajuddin
Nurul Nabilah Farhana Binti Noordin

Supervisor
Dr Muhaireen binti Arshad
 Definition of Respiratory Distress

Clinical condition characterized by the presence of one or more

signs of increased work of breathing in newborn.
• Respiratory distress is frequently encountered in newborns and
may be a potentially life threatening condition.

• The key to successful management of the infant who has

respiratory distress is based on the ability to
Obtain a complete maternal and newborn history
Perform a thorough physical examination
Recognize the common respiratory disorders
Differentiate among various diagnostic entities
Identify severity of respiratory distress
 Relevant maternal history
• Hypertensive disorders – pulmonary edema, prem delivery
• Gestational diabetes - RDS
• Maternal pyrexia / infection – congenital pneumonia
• History of complicated past pregnancies / deliveries
• Gestational age at delivery – RDS in prem, MAS in post
date
• Mode of delivery – TTN in LSCS, short 2nd stage of labour
• Obstetric complications during labour – birth trauma, injury or
hypoxic insult to the brain cause central respiratory distress
 Relevant birthhistory
 Meconium stained liquor
 Short 2nd stage of labor
 Perinatal events
 Leaking >18H
 Signs and Symptoms of RespiratoryDistress
• Weak cry - sign of fatigue
• Stridor – partial obstruction of upper airway
• Wheeze – narrowing or obstruction of small airways by secretions/inflammation
• Sweating – to regulate temperature due to high energy spend for brething
• Nasal flaring – infant attempting to decrease airway resistance
• Tachypnea - infant breathes at a faster rate to maintain ventilation in the face of decreased tidal
volume.
• Grunting - An infant in respiratory distress may try to maintain lung volume with adequate gas
exchange by partially closing the glottis during expiration.
• Cricoid tug/tracheal tug - Increase pull of diaphragm is transmitted as a downwards tug on the
trachea during inspiration.
• Cyanosis – poor saturation level
• Gasping
• Retractions
• Head bobbing – due to high use of sternocleidomastoid (SCM) and scalene muscles
 PhysicalExamination
Vital signs
◦ Tachypnea, tachycardia, decreased oxygen saturation, temperature instability
Inspection
◦ Increased workof breathing (retractions), cyanosis, pallor, scaphoid abdomen, meconium
staining, asymmetric chest wall movement
Palpation
◦ Tracheal deviation, displaced apical beat, thrill may be palpable inthe precordium
Auscultation
◦ crackles, wheeze
◦ heart sounds for the presence of any pathological murmurs.
◦ Absent/reduced breath sound

Special test: Transillumination test of chest wall

Retractions
Respiratory distress = Pulmonary
problem?

NOT 100%
 Respiratory system Cardiovascular system
1. Transient Tachypnea of Newborn 1. Congenital heart disease
(TTN) 2. Persistent pulmonary
hypertension of newborn Anatomic
2. Meconium Aspiration Syndrome 1. Tracheoesophageal fistula
(MAS) 2. Congenital diaphragmatic
3. Congenital pneumonia hernia
4. Respiratory Distress Syndrome
(RDS) Differential Diagnosis
5. Pneumothorax
6. Pleural effusion of
Respiratory Distress
CNS Hematological
1. Trauma or intracranial 1. Polycythemia
bleed Metabolic 2. Blood loss
2. Drug withdrawal 1. Hypoglycemia
syndromes 2. Inborn errors of
metabolism (IEM)
3. Acidosis
 1. Pneumothorax
• May occur as the lungs is filled with air after birth
• Increased risk in
Infants requiring PPV after birth
Preterm babies
Meconium aspiration
• Causing collapse of lungs
• May interfere with blood flow causing severe respiratory distress,
oxygen desaturation and bradycardia (Tension pneumothorax)
• Suspected when there is reduced breath sound and positive
transillumination test
 Management
Tension pneumothorax: needle thoracocentesis
• An emergency measure to decompress the chest until a chest
tube is inserted.
• Attach a 10ml syringe already filled with 2ml sterile normal saline
to a 16 to 20 gauge angiocatheter. Gently insert catheter
perpendicularly through the second intercostal space, over the
top of the third rib, at the midclavicular line
• Air will be aspirated on successful needle thoracocentesis
• Then, insert a chest tube as soon as feasible.
-“Safety triangle” – anterior to mid-axillary line, posterior to
pectoral groove and above 5th ICS
 2. Pleural effusion

• Collection of fluids in pleural space

• Large pleural effusion can interferes with lungs expansion
• Caused by edema,infection or leakage from the baby’s
lymphatic system
• Large pleural effusion can be diagnosed before birth by
ultrasound
• Excess fluid may also be seen in subcutaneous
tissues/scalp,abdomen(ascites),and
heart(pneumopericardium)hydrops fetalis
• Managementthoracocentesis
 3. Infants with airway obstruction
• Thick secretions
Meconium,blood,mucous or vernix
Should be suspected when baby not improving and no chest
movements with endotracheal intubation
These secretion may be thick enough to completely obstruct the
airway where suction catheter unable to completely removed
In this case,directly suction the trachea with a meconium aspirator
attached to an endotracheal tube
 4. Robin sequence
• Combination of facial anomalies,either isolated or part of genetic
syndrome
• Usually associated with cleft palate
• Lower jaw is small in relation to upper jaw
• Tongue is positioned further back in the pharynx and obstruct
airway
• Management:
Turn into prone position
Endotracheal tube insertion through the nose into posterior pharynx
In severe respiratory difficulty which requires resuscitation,consider
laryngeal mask
 Newborn with normal
anatomy(left) and newborn with
Robin sequence(right)

Endotracheal tube placed deep in

posterior pharynx,above the vocal cord
 5. Transient Tachypnea of Newborn (TTN)

oSelf-limiting disease commonly seenin neonates,usually resolved

spontaneously
oPresent within the first few hours of life with tachypnea and other signs
of respiratory distress,needs for oxygen requirement, and ABGs that do
not reflect carbon dioxideretention
oCharacterized by an airspace-fluid burden secondary to the inability to
absorb fetal lung fluid
TTN –Pathophysiology
Normal deliveryprocess

Catecholamine surge during labour aid lymphatic vessels dilatation

Lung epithelium switches from fluid secretion to fluid absorption

Lungs fluid absorbed, as infant cries alveoli now filled with air, remaining
fluid continues to be absorbed until full clearance
 Chest X-ray
interstitial oedema -prominently
perihilar
◦ often seen as perihilarstreakiness
Small pleural effusions

Fluid in fissures
 TTN -Management
Supportive management – treatment of choice
• Oxygen supplement
• Withold oral feeding in extremetachypnea

As the retained lung fluid is absorbed by the infant's lymphatic system,

the pulmonary statusimproves.
 Meconium Aspiration Syndrome
(MAS)

Aspiration of stained amniotic fluid, which can occur before, during, or

immediately after birth.
Meconium:
First intestinal discharge fromnewborns
Viscous, dark-green substance composed of intestinal epithelial cells,
lanugo, mucus, and intestinal secretions, mucosal cells, and solid
elements of swallowed amniotic fluid, such as proteins and lipids.
Sterile and does not contain bacteria, which is the primary factor that
differentiates it from stool.
 MAS – riskfactors
Intrauterine distress can cause passage of meconium into the amniotic
fluid.
Factors that promote the passage inutero:
a) placental insufficiency
b) maternal hypertension
c) preeclampsia
d) oligohydramnios
e) Infection
f) Acidosis
g) maternal drug abuse, especially use of tobacco and cocaine.
MAS -Pathophysiology
Fetal distress

Neural stimulation of maturing GItract

Peristalsis and relaxation of rectalsphicter

Passage of meconium inutero

 MAS – 4 majorpulmonary
Airway obstruction
effects
• Complete obstruction of the airways by meconium results in atelectasis
• Partial obstruction causes air trapping and hyperdistention of the alveoli, (ball-valve effect).
• Trapped gas (hyperinflating the lung) may rupture into the pleura (pneumothorax),mediastinum
(pneumomediastinum), or pericardium(pneumopericardium).
Surfactant dysfunction
• Meconium deactivates surfactant and may alsoinhibit surfactant synthesis
• Several constituents of meconium, especially the free fatty acids have a higher minimal surface tension than
surfactant and strip it from the alveolar surface, resulting in diffuse atelectasis.
Chemical pneumonitis
Enzymes, bile salts, and free fatty acids in meconium irritate the airways and parenchyma, causing a release of
cytokines which initiate a diffuse pneumonitis that may begin within a few hours of aspiration.
Persistent pulmonary hypertension of the newborn
• Many infants with meconium MAS have primary or secondary PPHN as a result of chronic in utero stress and
thickening of the pulmonary vessels.
• PPHN further contributes to the hypoxemia caused by meconium aspiration syndrome. [5]
MAS -Diagnosis
Diagnosis of MAS requires
•Presence of meconium-stained amnioticfluid
•Neonatal respiratory distress
•Characteristic radiographic abnormalities.
Chest x ray (high lungs volume)
◦ Hyperinflation (air trapping)
◦ Diaphragmatic flattening
◦ Patchy of atelectasis/consolidation
◦ Pneumothorax
MAS -Management
NRP – Born not vigorous  under vocal cord suction
CPAP or intubation in severeMAS
Oxygen therapy (supportive care)
ABG

Chest X-ray
Echo - to evaluate forPPHN
Complications ofMAS
Pneumothorax
PPHN
Chronic lung disease (associated with severe MAS)
Hypoxic insult
 CongenitalPneumonia
Pneumonia that presents within the first 24 hours after birth.
Pathophysiologically
◦ True congenital pneumonia
◦ Aready established at birth.
◦ Transmission of congenital pneumonia usually occurs via 1 of 3 routes:
◦ Hematogenous
◦ Ascending
◦ Aspiration

◦ Intrapartum pneumonia
◦ acquired during passage through the birthcanal
◦ may be acquired via hematogenous or ascending transmission, from aspiration of infected or
contaminated maternal fluids, or from mechanical or ischemic disruption of a mucosal surface that has
been freshly colonized with a maternal organism of appropriate invasive potential and virulence.

◦ Postnatal pneumonia
◦ originates after the infant has left the birthcanal.
◦ infection occurs after the birthprocess.
 Etiologyof CongenitalPneumonia
Group B streptococcus(70%)
E. Coli
H. influenzae
S. pneumoniae
K.pneumoniae
L.monocytogenes
Viruses (CMV, HSV)
Fungi (candida albicans)
 RiskFactors CongenitalPneumonia

PROM > 18 hours

GBS positive mother
Maternal pyrexia
Chorioamnionitis
Maternal UTI
Presentation CongenitalPneumonia
Respiratory distress (tachypneic, nasal flaring, grunting,recession)
Sign of sepsis
◦ Lethargy/poor feeding/weak cry
◦ Vomiting/abdominal distension
◦ Abnormal temperature
◦ Seizure
◦ Hypoglycemia/hyperglycemia
◦ Severe jaundice
 Diagnosis
Risk factor
Chest Xray

Blood investigation
◦ FBC (leucopenia/leucocytosis/thrombocytosis/thrombocytopenia)
◦ Blood culture
◦ CRP after 24H oflife
Management CongenitalPneumonia

Antibiotics
Respiratory support

Treatment of complications – empyema, effusions

 Respiratory DistressSyndrome
(Hyaline Membrane Disease)
Most common respiratory distress in premature infant
Characterized by surfactant deficiency
Pathophysiology
◦ Production of surfactant by Type II Pneumocyte started around 24-25w of
gestation, at 37w adequate forbreathing
◦ Prematurity  Lack of surfactant  increase surface tension in alveoli 
alveoli collapse  reduce lungs volume  respiratory distress
Surfactant
Composed of lipid and protein
Produced by type IIpneumocyte
Surfactant therapy - Standard care for preterminfants
Preparation that available
◦ Survanta, a natural surfactant, bovinederived
◦ 4mls/kg per dose
◦ Curosurf, a natural surfactant, porcine derived
◦ 1.25mls/kg per dosed
 RiskFactors RDS
Prematurity (the lower gestation weeks the higherrisk)
Male gender
Maternal diabetes
Maternal hypertension
IUGR in babies <28weeks
Perinatal hypoxia/acidosis
Sepsis
Hypothermia
Second twin
Family history with RDS
MAS
Congenital pneumonia
 Diagnosis RDS
CXR
◦ Ground glass opacification
◦ Air bronchogram
◦ Low lungs volume
 Management RDS
Oxygen support
Surfactant therapy
◦ Survanta, a natural surfactant, bovinederived
◦ 4mls/kg per dose
◦ Curosurf, a natural surfactant, porcine derived
◦ 1.25mls/kg per dosed
Normal newbornCXR
TTN
MAS
RDS CONGENITAL
PNEUMONIA
 References
• Nelson Textbook of Pediatrics 19th Edition
• NRP 7th Edition
• Sunflower textbook paediatrics
• Medscape