Respiratory Distress of

Newborn
ANTHONY CHIEW HAN YANG
NUR HANISAH ABDUL HALIM
DESMOND LING CHUNG WEI
Overview

 Introduction
 Definition
 Approach to respiratory distress of the newborn
 Meconium
Aspiration
Syndrome
Congenital
Diaphragmatic Congenital
Hernia Pneumonia

RESPIRATORY
DISTRESS OF
NEWBORN
Persistent
Pulmonary
Hypertension Transient
Of Newborn Tachypnea of
Newborn
Respiratory
Distress
Syndrome
Definition

 One or more signs of increased work of breathing e.g. tachypnea,

nasal flaring, chest recessions or grunting
Assessment and approach

 Maternal history ( risk factors)

 Gestational age of infant
 Liquor (colour/ odor/ volume)
 Antenatal and intrapartum history (steroids/ PROM/ fever)
 Clinical presentation
 Xrays
 Lab evaluations
Clinical presentation

 Respiratory rate (>60 breath/min)

 Quality (shallow/ deep breathing)
 Nasal flaring
 Grunting
 Chest recessions
 Breath sound (air entry, adventitious sound)
 Colour (pink, dusky, pale, mottled, cyanosis)
 Heart rate, pulses, perfusion
 Blood pressure
Management

 Depends on the cause

 Supportive
 IV fluid
 Maintain vital signs
 Oxygen therapy
 Respiratory support
1) Meconium aspiration syndrome

 Meconium stained amniotic fluid is seen in 15% of predominantly term

and post-term deliveries
 The presence of meconium in the amniotic fluid suggests in utero distress
with asphyxia, hypoxia and acidosis.
 Risk factors
 Post- term pregnancy
 Pre- eclampsia, eclampsia
 Gestational diabetes mellitus
 IUGR
 Clinical manifestations

 Meconium stained amniotic fluid (meconium stained umbilicus cord, nails,

skin)
 Tachypnea, hypoxia, hypercapnia, small airway obstruction
 Some infants may have mild initial respiratory distress, which becomes more
severe hours after delivery
 Pneumothorax and/or pneumomediastinum
 PPHN in severe cases
 Chest xray features
 Patchy infiltrates
 Hyperinflation
 Flattening of diaphragm
 Increase in AP diameter
Pathophysiology
Chest xray: areas of hyper expansion mixed with patchy
densities and atelectasis
Management

 Tracheal suction if baby not vigorous

 Consider CPAP, if FiO2 requirements >0.4; however CPAP may
aggravate air trapping and must be used cautiously
 Mechanical ventilation: in severe cases( PaCO2> 60mmHg or
persistent hypoxemia PaO2 <50mmHg)
 Correct systemic hypotension (hypovolemia, myocardial
dysfunction)
 Manage PPHN if present
 Surfactant therapy
2) Pneumonia or sepsis

 Risk factor
 Unexplained preterm labour
 PROM>18 hours
 Maternal fever( >38 degree Celsius)
 Signs of chorioamnionitis
 Fetal tachycardia
 Recurrent maternal UTI
 Previous infant with neonatal infection
 Early onset pneumonia( within first 3 or 7 days of life, usually within 48 hours)
 Late onset pneumonia( within 4 and 28 days of life)
 May acquired by intrauterine, intrapartum or postnatal routes.
Clinical manifestations

 Tachypnea
 Nasal flaring, grunting, chest recessions
 Poor feeding, abdominal distension
 Jaundice
 Glucose intolerance
 Temperature instability
 Cyanosis
 crepitations or reduced breath sound over the affected side
Lab investigations

 FBC
 CRP
 Blood culture
 Arterial blood gas
 Chest Xray

 Lobar consolidation
 Diffuse, streaky or
patchy infiltrates
 Air bronchogram
 Increased interstitial
markings
Management

 Initiate IV ampicillin (50-100mg/kg/dose) 6H and IV gentamicin

(4mg/kg/dose) 24H or IV cefotaxime (50mg/kg/dose) 12H
 Oxygen therapy
 Chest physiotherapy
 IV fluids
 3) Transient Tachypnea of Newborn

 Most common cause of neonatal respiratory distress (more than 40 percent of cases)
 A benign condition
 Occurs when residual pulmonary fluid remains in fetal lung tissue after delivery.
 Tachypnea immediately after birth or within 6 hrs after delivery, mild to moderate
respiratory distress.
 Usually persist for 12-24 hrs, but can last up to 72 hrs
 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 fetal

lung lumen decreases before birth, most during labour

 The mechanism for fluid absorption is triggered by neuroendocrine

hormones (Prostaglandins), which cause lymphatic vessel
dilatation

 As the lung pulmonary circulation increases following the first

breath, the fluid in the lungs is cleared
 Interruption of this process of clearing fluid from the lungs may
result in respiratory distress.
 Radiological features

 Retained lung fluid with characteristic

prominent perihilar streaking (sun-burst pattern)

 Coarse fluffy densities may reflect alveolar

edema

 Hyperinflation with widening of intercostal

spaces.

 Fluid filled interlobar fissure.

 Management

 Supportive with close observation because the condition is usually self

limited.
 Oxygen therapy
 Low flow supplemental oxygen may be necessary for several hours.
 More severe cases- CPAP.
 Continuously monitor with pulse oximeter.
 Obtain a chest radiograph.
 Correct metabolic abnormalities (acidosis,hypoglycemia).
 Obtain a blood culture & begin an antibiotic coverage (ampicillin +
gentamicin) - if persistent (consider other associated condition e.g. sepsis)
 4) Respiratory distress syndrome

 Also called Hyaline Membrane Disease

 Primarily affects preterm infants; its incidence is inversely related to
gestational age
 Develops in 30-60% in infant 28-32 W. 15-30% of those between 32-36
weeks‘ gestation, in about 5% beyond 37 weeks' gestation
 Occurred after the onset of breathing and is associated with an
insufficiency of pulmonary surfactant
 Pathophysiology

 Lining of alveolus consists 90% type 1 and 10% type II

pneumocytes

 Surfactant produced by type II pneumocytes of alveolar

epithelium (differentiate and produce surfactant at 34-38w)

 Surfactant prevents atelectasis and contributes to the lung

recoil by manipulates the surface tension of the lungs

 Surfactant deficiency  widespread alveolar collapse

&inadequate gaseous exchange.
 Other risk factors:
Decreased risk (increased production)
 Delivery of previous preterm infant with
RDS,  Chronic intrauterine stress (PIH, IUGR)
 Maternal diabetes  Prolonged rupture of membranes
 Multiple pregnancy  Antenatal steroid prophylaxis
 Elective cesarean section without labor
 Perinatal asphyxia Increased risk (decreased production)
 Genetic disorders  Hypoxia, acidemia, cold
 The incidence is approximately six times in  Fetal hyperinsulinemia
infants whose mothers have diabetes because
of delayed pulmonary maturity despite
macrosomia.
 Radiological features

 Grade 1 (mild cases): diffuse granular / fine  Grade 2: widespread air bronchogram become
homogenous ground glass shadowing visible
 Radiological features

 Grade 3: confluent alveolar shadowing  Grade 4: complete white lung fields with obscuring
of the cardiac shadow
 Management
1) Prevention:
 Tocolytics to delay labor.
 Antenatal corticosteroid therapy (IM deamethasone 12mg 2
doses12H apart)
► They induce surfactant production and accelerate fetal lung
maturation.
► Are indicated in pregnant women 24-34 weeks' gestation at high
risk of preterm delivery within the next 7 days.
► Optimal benefit begins 24 hrs after initiation of therapy and lasts
seven days.
 Lung maturity testing: lecithin/sphingomyelin (L/S) ratio
 Management
2) Surfactant:
 Surfactant therapy reduces mortality rates most effectively in infants
<30 weeks and those of birth weight <1250 gm
 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.
 Management
Surfactant:
 Indications:
 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
goodtone 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
 Severe RDS in more mature/larger infant
 Severe MAS with Type 2 respiratory failure
 Management

3) Oxygen and ventilatory support

 Begin NIV (CPAP) – minimize damage to immature lungs
 Reserve intubation for infant requiring 35-45% oxygen concentration to keep
Pao2> 50mmHg
4) Antibiotics
 Start antibiotic and take septic workup for 48-72 hrs (difficult to differentiate
sepsis, pneumonia from RDS)
 Iv ampicillin 50-100mg/kg/dose
 Iv gentamicin 4mg/kg/dose
Complications

• Patent ductus arteriosus

• Bronchopulmonary dysplasia
• Pulmonary interstitial
Acute emphysema Chronic • Subglottic stenosis
• Recurrent lung infection
• Pulmonary hemorrhage
5) Persistent Pulmonary Hypertension Of Neonate

 Failure of pulmonary vascular resistance to fall after birth thus reducing

pulmonary blood flow
 Incidence 1/1000-1500 live birth
 Causes: idiopathic (20%), MAS (50%), RDS (5%), CDH, asphyxia, maternal
diabetes, polycythemia
Presentation

 Respiratory distress (tachypnoea, grunting, nasal flaring, chest

recessation)
 Central cyanosis
 Loud second heart sound
 discrepancy between pre and post ductal arterial oxygen saturation
>10%
 CXR: cardiomegaly due to right atrial or ventricular enlargement
 Echo: increased pulmonary arterial pressure, right to left shunt at
foramen ovale and ductus arteriosus
 Mild breathlessness, acidosis, hypotension
Hyperoxia Test

 100% oxygen for 10 minutes, then take ABG

 May closes ductus arteriosus
PaO2 SPO2
PPHN 100-150mmHg Up to 95%
CHD (TGA), severe <100mmHg <80%
pulmonary outflow
obstruction

 Differentiation: Congenital cyanotic heart disease seldom critically ill,

bradycardia usually due to hypoxia, infants with cyanotic lesions usually do
not have respiratory distress, PPHN usually had some perinatal hypoxia and
handles poorly, cyanosed baby usually happy but blue
Management

 Prevent and treat: hypoglycaemia, hypothermia, hypovolemia, anaemia,

hypocalcaemia
 Sedation: morphine 10-20mcg/kg/hr
 Ventilation: aim PCO2 45-55mmHg, PO2 60-80mmHg; hypocabia cause
periventricular leokomalacia, hyperoxia leads to chronic oxygen
dependency and bronchopulmonary dysplasia,
 Vasodilators: inhaled nitric oxide, prostacycline, sildenafil
 Circulatory support: keep MAP> 50 by help of dopamine, dobutamine,
adrenaline
6) Congenital Diaphragmatic Hernia
Presentation

 Occurs 1/2400
 Antenatal: fluid filled stomach or bowel with/without liver in the left chest
cavity
 Respiratory distress with cyanosis
 Apparent dextrocardia
 Bowel sounds in chest, scaphoid abdomen
 Cxr: bowel loops within the chest and minimal bowel in abdomen
 Late presentation: bowel obstruction, recurrent resporatory infections
 PPHN
Management

 Intubation and ventilation

 Try to avoid face-mask ventilation
 Orogastric tube for gastric decompression, aspirate 4H and free flow
 Pre and post ductal pulse oximetry to detect PPHN
 Refer to paediatric surgeon when stabilised
Good Outcome

 Birth weight >2kg

 Apgar score at 5 minutes 7-10
 Primary repair achieved – 97% survival
 Without cardiac lesions – 70% survival
 Late presentation >30 days – 100% survival