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RESPIRATORY DISEASES
OF THE NEWBORN

Early Development

Fetal Lung Development


Week 4: the laryngotracheal groove forms on the floor

foregut
Week 5: the left and right lung buds push into the
pericardioperitoneal canals (primordial of pleural cavity)
Week 6: the descent of heart and lungs into the thorax.
Pleuroperitoneal foramen closes

Fetal Lung Development


Week 7: the lung buds divide into secondary and tertiary

bronchi
Week 24: the bronchi divide 14 more times and the
respiratory bronchioles develop
By birth, there will be an additional 7 divisions of bronchi

Fetal Lung Histology

STAGE 1: Pseudoglandular Period (5-17 weeks) all


the major elements of the lungs have formed except
for those involved with gas exchange

STAGE 2: Canalicular Period (16-25 weeks) bronchi


and terminal bronchioles increase in lumen size and
the lungs become vascularized

Fetal Lung Histology

STAGE 3: Terminal Sac Period (24 weeks to birth)


more terminal sacs develop and interface with
capillaries lined with Type I alveolar cells or
pneumocytes
--Also have Type II pneumocytes which secrete
surfactant thereby decreasing the surface tension
forces and aids in expansion of the terminal sacs

STAGE 4: Alveolar
Period (late fetal
period to 8 years)
95% of mature
alveoli develop after
birth. A newborn
has only 1/6 to 1/8
of the adult number
of alveoli and lungs
appear denser on xray

Respiratory Distress in the


Newborn
Transient Tachypnea of the Newborn (TTN)
Surfactant Deficiency (HMD,RDS)
Meconium Aspiration Syndrome (MAS)
Pneumonia/ Sepsis
Pneumothorax or other air leaks

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Respiratory Distress in the Newborn


Respiratory Causes
Congenital Abnormalities of the Lung/Thorax
Congenital Heart Disease (CHD)
Congenital Diaphragmatic Hernia (CDH)
Congenital Cystic Adenomatiod Malformation (CCAM)
Tracheal Abnormalities
Esophageal Atresia
Pulmonary Hypoplasia
Persistent Pulmonary Hypertension of the Newborn (PPHN)

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Transient Tachypnea of the Newborn


(TTN)
Also known as wet lung
Most common diagnosis of respiratory distress in the

newborn
Relatively mild, self limited disorder, usually affecting
infants who are born at or near term gestation.
Ineffective clearance of amniotic fluid from lungs with
delivery
Most often seen at birth or shortly after

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Transient Tachypnea of the Newborn


Caused by conditions that elevate CVP, leading to

delayed clearance of fluid by the thoracic duct or


pulmonary lymphatic system.
Retained fluid accumulates in peribronchiolar lymphatics
and bronchovascular spaces, causing compression and
bronchiolar collapse with areas of air trapping and
hyperinflation.
These causes decrease lung compliance, leading to
tachypnea to counter the resultant increased respiratory
work.

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Transient Tachypnea of the


Newborn
History
Common with C-Section delivery and precipitous birth
Delayed cord clamping or cord milking
Maternal asthma
Maternal analgesia
Maternal anesthesia during labor
Maternal fluid administration
Maternal diabetes, bleeding
Perinatal asphyxia
Prolapsed cord

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TTN presents:
Respiratory Assessment (usually within 6H of life)

Tachypnea >80 bpm


Nasal flaring
Grunting
Retracting
Fine Rales (crackles)
Cyanotic
Increased Antero-posterior diameter of

chest secondary to air trapping

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TTN
X-Ray findings
Prominent Perihilar streaking
Mild to moderate cardiomegaly
Coarse, fluffy density
Hyperinflation with flattening of diaphragm
Fluid in fissure
Labs
FBC within normal limits
ABG/CBG showing mild to moderate hypercapnia, hypoxemia with
a respiratory acidosis

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TTN

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TTN
Have delayed reabsorption of fetal lung fluid which

eventually will clear over several hours to days


Signs usually persist for 12-24 hours but can last up to
48-72 hours
Treatment: Mainly supportive. Treat signs and symptoms.
Support infant, may need supplemental O2, is probably
too tachypneic to PO feed so start IV fluids. If mild
tachypnea, may be fed with orogastric tube.
Prognosis: Self limited process. No residual pulmonary
effects.

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Surfactant Deficiency
(RDS, HMD)
One of the most common problems associated with a

premature infant
Decreased surfactant production in lungs of pre-term
infants
Manifestation caused by diffuse alveolar atelectasis,
edema and cell injury.
With decreased surfactant production, alveoli collapse,
become atelectatic, yielding poor lung function and
increasing signs of respiratory distress

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RDS
History
Gestational age < 38 weeks
Prenatal care
Diabetes (controlled vs uncontrolled)
Perinatal infection

Problems during pregnancy/delivery


Asphyxia
Stress to fetus
Hypothyroidism
Multiple births
Surfactant protein B deficiency
- a genetic disorder of surfactant production, causing congenital alveolar

proteinosis that in its early stages resembles RDS

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RDS - Prenatal Prediction


Assesment of fetal lung prematurity by testing amniotic fluid by

amniocentesis
Lecithin-sphingomyelin (L/S) ratio risk of RDS low if ratio >2.0
TDx-Fetal Lung Maturity (FLM II) measures surfactant-albumin ratio

Antenatal corticosteroid therapy


Given to pregnant women 24-36 weeks gestation with intact membrane

or with preterm rupture of membrane who are at high risk of preterm


delivery within the next 7 days.
Induces surfactant production and accelerates maturation of lung.
Treatment should consist of either
2 doses of 12 mg of betamethasone, IM, given 24 hours apart; or
4 doses of 6 mg of dexamethasone, IM, given 12 hours apart.
The optimal benefit begins 24 hours after initiation of therapy and last 7 days.

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RDS presents:
Respiratory Assessment
Tachypnea > 60 bpm
Nasal flaring
Grunting
Retracting
Apnea/ irregular respiratory pattern
Rales (crackles)
Diminished breath sounds
Cyanosis

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RDS
X-Ray
Loss of volume
Reticulogranular pattern or ground glass appearance
Air bronchograms
Bell shaped thorax
Air leak, pulmonary interstitial emphysema
Loss of heart borders/ atelectasis
White out

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RDS

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RDS

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RDS
Laboratory Results
ABG/VBG
Hypoxia
Hypercarbia
Acidosis

FBC with Differential


Culture & sensitivity - Used to rule out other causes of respiratory

distress
Always check electrolytes, especially glucose, potassium and
calcium

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Treatment for RDS


Goals
1.To prevent hypoxemia and acidosis
2.Optimize fluid management
3.Reduce metabolic demands
4.Prevent worsening atelectasis and pulmonary edema
5.Minimize oxidant lung injury

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Treatment for RDS


Surfactant replacement therapy
Prophylactic treatment
Within minutes of birth
Usually in labour room

Selective or rescue treatment


After symptoms and signs of RDS are present

Several types
Survanta (bovine lung extract)
Infasurf (calf lunf extract)
Curosurf (porcine lung extract)

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Treatment for RDS


Usually administered within 1 2 H of age. The earlier the

administration the better the effect.


Method of survanta administration
Dose : 4 cc/kg through ETT
Administered during brief disconnection from ventilator, in quarter

dose via a feeding tube that is cut to a length just slightly longer
than that of the ETT
Baby is ventilated for at least 30 seconds, or until stable between
quarter doses.
Changes in positioning of the infant are routine and intended to
facilitate distribution.
Careful observation is necessary. Desaturation, bradycardia and
apnea are common adverse effects.
Subsequent doses of survanta, if needed, are given at 6H intervals

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Treatment for RDS


Oxygen Support
CPAP / Mechanical Ventilation
Should be sufficient to maintain arterial tensions at 50-80 mm HG.
Higher than necessary FiO2 should be avoided due to risk of lung
injury and retinopathy of prematurity.
Blood gases monitoring is important. Frequent sampling may be
required to maintain ABG within appropriate ranges.
Blood gases should be measured 30 mins after changes in
respiratory therapy settings.
Weaning is done as the infant improves.

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Treatment for RDS


Supportive therapy
Temperature
Fluids and nutrition
Circulation
Cover for possible infection

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RDS complication
Acute
Air leak Pneumothorax, Pneumomediastinum,
penumopericardium, interstitial emphysema
Infection from catheters, respiratory equipment
Intracranial hemorrhage
Patent Ductus Arteriosus
Long term
Bronchopulmonary dydplasia

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MECONIUM ASPIRATION SYNDROME


Most often found in post date infants > 40 weeks,

but may occur in infants >34 weeks


Infant passes meconium due to varying degrees
of asphyxia in utero
Obstruction of large and small airways with
aspirated meconium
Aspiration may occur:
in utero
intrapartum
postpartum period

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MAS
Composition of meconium
Epithelial cells
Fetal hair
Mucus
Bile

Color of amniotic fluid


Light Thinly stained amniotic fluid (watery)
Moderate opaque without particles
Thick pea soup with particles

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MAS-Risk factors for MAS

Maternal HT
Maternal DM
Maternal heavy cigarette smoking
Maternal chronic respiratory or Cardio vascular disease
Post term pregnancy
Pre-eclampsia/eclampsia
Oligohydramnios
IUGR
Abnormal fetal HR pattern

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MAS
Ball-valve effect

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MAS
Management on delivery
Determine whether infant is vigorous (HR>100, Spontaneous
respiration, good tone)
If vigorous, continue routine care regardless of meconium
consistency (clear mouth and nose of secretions, dry, stimulate and
reposition)
If not vigorous, intubate infant under direct laryngoscopy, perform
intratracheal suctioning with meconium aspirator or large bore
suction catheter. Apply continuous suction as tube is withdrawn.
Repeat as necessary until little additional meconium is recovered,
or until resuscitation needs to be initiated.
In questionable cases, it is safer to intubate and suction as MAS
can occur in infants delivered through thinly stained amniotic fluid.
PPV should be avoided until tracheal suctioning is accomplished if
possible

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MAS
Meconium aspirator

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MAS
Postnatal Management

Apparently well child born through MSAF


Most of them do not require any interventions besides close

monitoring for respiratory distress.


Most infants who develop symptoms will do so in the first 12 hours
of life.

Approach to the ill newborns:


Transfer to NICU.
Monitor closely.

Full range of respiratory support should be given.


Sepsis w/up and broad spectrum ABx indicated. (Ampicillin and

Gentamicin)

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MAS
Respiratory Assessment
Tachypnea
Nasal flaring
Grunting
Retracting
Apnea/ irregular respiratory pattern
Decreased breath sounds/ wet/ rhonchi

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MAS
Clinical Assessment
Color
Pale/gray
Cyanotic
Stained skin

X-Ray
Increased AP diameter
Hyperinflation
Atelectasis
Course irregular patchy infiltrate
Pneumothorax

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MAS
Areas of opacification due to atelectasis bilaterally

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MAS
Coarse irregular patchy infiltrate with emphysema

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MAS Treatment in NICU


Goals:
Increased oxygenation while minimizing the barotrauma
(may lead to air leak).
Prevent pulmonary hypertension.
Successful transition from intrauterine to extrauterine life
with a drop in pulmonary arterial resistance and an
increase in pulmonary blood flow.

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MAS Treatment in NICU


Ventilatory support depends on the amount of

respiratory distress:
O2 head box
CPAP
Mechanical ventilation

HFV should reduce air leaks.


High-frequency ventilators may slow the progression of meconium

down the tracheobronchial tree and allow more time for meconium
removal.

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MAS
Surfactant
Endogenous surfactant activity may be inhibited by meconium.
Surfactant therapy may improve oxygenation and reduce
pulmonary complications.
It is not routinely indicated, however it may be helpful in those
infants whose clinical status continues to deteriorate.
Inhaled Nitric oxide (NO)
Selective pulmonary vasodilation.
Activate guanylate cyclase and increases cyclic GMP and acting
directly on the vascular smooth muscle
ECMO
Extracorporeal membrane oxygenation (ECMO) is a treatment that
uses a pump to circulate blood through an artificial lung back into
the bloodstream of a very ill baby. This system provides heart-lung
bypass support outside of the baby's body.

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MAS
Acute Complication
Air Leak Pneumothorax or pnuemopericardium
PPHN
Chronic lung disease may result from prolong mechanical
ventilation

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Persistent Pulmonary
Hypertension (PPHN)
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.

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PPHN
Idiopathic - 20%

Associated with a variety of lung diseases:

Meconium aspiraton syndrome (50%)


Pneumonia/sepsis (20%)
RDS (5%)
Congenital diaphragmatc hernia (CDH)
Others: Asphyxia, Maternal diabetes, Polycythemia

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PPHN
History

- Precipitating factors during antenatal, intrapartum,


postnatal periods
Respiratory signs
- Signs of respiratory distress (tachypnoea, grunting,
nasal faring, chest retractions)
- Onset at birth or within the frst 4 to 8 hours of life
- Marked lability in pulse oximetry

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Cardiac signs

- Central cyanosis (differential cyanosis between the upper and


lower body may be noted clinically, by pulse oximetry and blood
gasses)
- Prominent praecordial impulse
- Low parasternal murmur of tricuspid incompetence
Radiography
- Lung fields
Normal, parenchymal lesions if lung disease is present, oligaemia
- Cardiac shadow
Normal sized-heart, or cardiomegaly (usually right atrial or
ventricular enlargement).

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Echocardiography - important to:

- Exclude congenital heart disease.

- Define pulmonary artery pressure using tricuspid incompetence,


ductal shunt velocities.

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


foramen ovale.

- Define the ventricular output.

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PPHN - Management
General measures:
Preventing and treating
- Hypothermia
- Hypoglycaemia
- Hypocalcaemia
- Hypovolaemia
- Anaemia
Avoid excessive noise, discomfort and agitation.
Minimal handling
Sedation
Morphine given as an infusion at 10-20 mcg/kg/hr. Morphine is a safe
sedative and analgesic even in the preterm infants.
Midazolam not recommended for preterms < 34 weeks gestational
age, associated with adverse long term neurodevelopmental outcomes.

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Ventilation

Conventional ventilation adopt gentle ventilator approach by


- Avoidance of hyperventilation (i.e. hypocarbia and hyperoxia).
Hypocarbia is associated with periventricular leukomalacia. Aim for a
PCO2of 45-55mmHg.
Hyperoxia leads to chronic oxygen dependency and bronchopulmonary
dysplasia. Keep PO2 within normal limits of 60 -80 mmHg.
- Ventilating to achieve a tidal volume of 3 to 5mls/kg.
- Short inspiratory time (0.2-0.3 sec) to prevent alveolar over distension
- Inadvertently increasing ventilator settings may lead to overdistention
of the lungs and high mean airway pressures compromising venous
return to the heart which further aggravates systemic hypotension as
cardiac output is compromised.
High Frequency Oscillatory ventilation / High Frequency Jet Ventilation
Effective in new-borns with PPHN secondary to a pulmonary pathology.

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Circulatory support
Inotropes for circulatory support improve cardiac output and enhances

systemic oxygenation.
Its use is poorly substantiated in PPHN, especially with the use of inhaled
nitric oxide (iNO), which through its pulmonary vasodilating effect helps to
improve cardiac output and the systemic blood pressure.
Aim to keep the mean arterial pressure > 50 mmHg in term infants.

However, inotropes are still recommended in institutions without facilities


for iNO:
Dopamine
5 20 mcg/kg/min
Dobutamine 5 20 mcg/kg/min
Adrenaline
0.1 1.0 mcg/kg/min

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Vasodilators
Inhaled nitric oxide (iNO)- selective pulmonary vasodilator.

- In term and near term infants (>34 weeks gestational age) reduces
need for Extra Corporeal Membrane Oxygenation (ECMO)(Dose: 5-20 ppm).

- insufficient evidence to support use in preterm infants < 34 weeks age.

Prostacycline and Sildenafil. These are not recommended for routine use

as their safety and efficacy had not been tested in large randomized
trials.

Sildenafil in the treatment of PPHN has significant potential especially in


resource limited settings.

Extracorporeal membrane oxygenation (ECMO)

ECMO is effective in PPHN. It is expensive as it requires trained personnel,


specialized equipment and a good nursing-cot ratio.

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Neonatal Pneumonia
Intrauterine infection or during delivery
Most are bacterial in origin
Pneumonia that becomes clinically evident

within 24 hours of birth may originate at 3


different times.
The 3 categories of congenital pneumonia are
as follows:
True congenital pneumonia
Intrapartum pneumonia
Postnatal pneumonia

True congenital pneumonia


True congenital pneumonia is already established at birth.

Transmission of congenital pneumonia usually occurs via

1 of 3 routes:
Hematogenous
Ascending
Aspiration

Intrapartum pneumonia
Intrapartum pneumonia is acquired during passage

through the birth canal.


It may be acquired via hematogenous or ascending
transmission:
from aspiration of infected or contaminated maternal fluids

from mechanical or ischemic disruption of a mucosal surface that

has been freshly colonized with a maternal organism

Postnatal pneumonia
Postnatal pneumonia in the first 24 hours of

life originates after the infant has left the birth


canal.
It may result from some of the same
processes described above, but infection
occurs after the birth process.

Etiology
Group B Streptococcus (GBS)

Nontypable Haemophilus influenzae


cytomegalovirus, Treponema pallidum, Toxoplasma

gondii,
Enterococci

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Causes
Prematurity

Prolonged rupture of membranes (> 18 - 24H)


Prolonged delivery
Maternal temp > 38C
Foul smelling amniotic fluid

Meconium
Maternal hx of STDs

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Respiratory Assessment
Tachypnea

Apnea, irregular breathing pattern


Grunting
Retractions
Nasal flaring

Colorful secretions
Rales, rhonchi
Cyanosis

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Clinical Assessment
Gray, pale color

Lethargy
Temperature instability
Skin rash-pettechia
Tachycardia

Glucose issues
Hypoperfusion
Oliguria
Changed in behaviour

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X-Ray
Patchy infiltrates (aspiration)

Bilateral diffuse granular pattern


Streaky
Loss of volume
Densities

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Pneumonia

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Pneumonia
Lab
FBC
Cultures
CRP
Management
Start antibiotic immediately when diagnosis is suspected (IV C-penicillin /
Ampicillin & Gentamicin)
Adjust Antibiotics according to culture & sensitivity result
Supportive therapy
Respiratory: ensure adequate oxygenation
CVS: support BP and perfusion
Fluid and nutrition support