respiratory distress in newborn

Respiratory distress in neonates

Presenter- Dr. Aftab Ahmad Siddiqui

Moderators- Prof. S M Ali, Prof. F. K Beig, Dr. K Afzal, Dr. Kashif Ali,

Dr. Shaukat, Dr. Iraj Alam

Presence of at least 2 of the fallowing features are essential

1)Tachypnea (RR>60 PER MIN..)

2)Retractions (intercostal retractions and /or sub costal)

3) Expiratory grunt

Introduction

Clinical presentation of respiratory

distress in the newborn includes;

cyanosis,

grunting,

inspiratory stridor,

nasal flaring,

poor feeding,

tachypnea (more than

60 breaths per minute),

Lethargy.

retractions in the:

intercostal,

subcostal, or

suprasternal spaces.

Perinatal history

h/o of polyhydramnios -- congenital diaphragmatic hernia/TEF

h/o of oligohydramnios -- pulmonary hypoplasia

h/o of PROM -- congenital pneumonia

h/o of pretem delivery -- respiratory distress syndrome

h/o of MSAF -- meconium aspiration syndrome

Perinatal history

IUGR with Resp. distress -- Congenital infection/MAS

LGA with Resp. distress -- Decreased surfactant/

Polycythemia/CHD

Well baby for 1-2 days then resp. distress -- Sepsis/IEM

Obstruction of the airway Lung parenchymal disease

1- Choanal atresia

2- Congenital stridor

3- Tracheal or bronchial stenosis

1- Meconium aspiration

2- Respiratory distress syndrome

3- Pneumonia

4- Transient tachypnea of the newborn

(retained lung fluid)

5- Pneumothorax

6- Atelectasis

7- Congenital lobar emphysema

Non-pulmonary causes Miscellaneous

1- Heart failure

2- Intracranial lesions

3- Metabolic acidosis

1- Disorders of the diaphragm e.g.

(diaphragmatic hernia)

2- Pulmonary haemorrhage

3- Pulmonary hypoplasia

CAUSES OF RESPIRATORY DISTRESS

0 1 2

Cyanosis None In room air In 40% FIO2

Retractions None Mild Severe

Grunting NoneAudible with

stethoscope

Audible without

stethoscope

Air entry ClearDecreased or

delayedBarely audible

Respiratory

rateUnder 60 60-80 Over 80 or apnea

Score:

> 4 = Clinical respiratory distress; monitor arterial blood gases

> 8 = Impending respiratory failure

DOWNE’s SCORING OF RESPIRATORY DISTRESS

SILVERMAN- ANDERSON RETRACTION

SCORE FOR PRETERMS

SIL

VER

MA

N-

AN

DER

SO

N

RETR

AC

TIO

N S

CO

RE F

OR

PR

ETE

RM

S

A score of 7 or more is indicative of impending resp. failure.

SOME IMPORTANT CAUSES OF RESPIRATORY DISTRESS ARE DESCRIBED IN

SOME DETAIL

Choanal Atresia

Tracheoesophageal fistula

Transient tachypnea of newborn

Hyaline Membrane disease (RDS)

Meconium Aspiration Syndrome

Congenital pneumonia

Pneumothorax

Choanal Atresia

The back of the nasal passage (choana) is blocked, usually by

abnormal bony or soft tissue (membranous).

Bilateral choanal atresia is a serious life-threatening condition as babies

are obligate nasal breathers.

The distress may improve when the baby cries.

Choanal Atresia

Choanal atresia. Rhinogramdemonstrating blockage of

radiopaque dye at the posterior

choanae.

Oral airway which is the initial

treatment of choice can also be

seen.

Tracheo-esophageal fistula

A tracheoesophageal fistula (TEF) is a congenital communication between the

trachea and esophagus.


Clinical features-

Maternal polyhydramnios and absence of stomach gas on prenatal

ultrasound.

Copious, fine white frothy bubbles of mucus in the mouth and nose.

Secretions recur despite suctioning.

Episodes of coughing and choking in association with cyanosis esp. during

feeding.

Inability to pass a NG/OG tube.

TRANSIENT TACHYPNEA OF THE

NEWBORN (TTN)

A very common cause of neonatal respiratory distress,

constituting about 40 percent of cases.

Infants are usually full term/late preterm.

They are not at risk for other illnesses.

It occurs due to delayed clearance of fetal lung fluid.

Change in hormonal milieu (surge in glucocorticoids and

catecholamines) near end of pregnancy and labor facilitates

fetal lung fluid clearance.

Risk for TTN increases if normal labor is bypassed

(Caessarian/Precipitate labor).

RISK FACTORS:

cesarean delivery

Precipitous labor

Preterm birth

Male sex

Macrosomia,

Maternal diabetes

Maternal Asthma

Multiple gestation

CLINICAL PICTURE- TTN

Tachypnea immediately after birth or within 6 hours with mild

respiratory distress.

A-P diameter of chest may be increased (barrel shape).

Usually responds to supplemental Oxygen @ FiO2 <40 %.

Respiratory failure and mechanical ventilation are rare.

Symptoms usually last 12 to 24 hrs but in severe cases it can last till

72 hours.

TTN

Radiological features of TTN-

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.

TREATMENT- TTN

It is supportive with close observation because the condition isusually self limited.

Low flow supplemental oxygen may be necessary for severalhours.

More severe cases- CPAP.

Oral furosemide (Lasix) has not been shown to significantlyimprove status and should not be given

23

Respiratory distress

syndrome

- RDS

(hyaline membrane

disease)

• Inadequate pulmonary surfactant due to preterm birth.

• Alveoli with low surfactant tend to collapse, leading to atelectasis,

VQ mismatching, hypoxemia and respiratory acidosis.

•Repetitive reopening & collapse of alveoli can damage the fragile

lung architecture leakage of protein-debris into the airways

(hyaline membranes).

•These debris impair the function of what little surfactant is present.

RDS- Introduction

Structure of lung surfactant

Major constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin),

phosphatidylglycerol, apoproteins (surfactant proteins SP-A, -B, -C, -D), cholesterol

RDS- Introduction

With advancing gestational age, increasing amounts of phospholipids

are synthesized and stored in type II alveolar cells .

Wk 20: start of surfactant production and storage. Does not reach lung

surface until later

Wk 28-32: maximal production of surfactant and appears in amniotic

fluid

Wk 34-35; mature levels of surfactant in lungs

Incidence of respiratory problems in preterms

RISK FACTORS-RDS

Prematurity

Maternal diabetes

Caesarean delivery without preceding labor

Precipitous labor

Foetal asphyxia

Genetic factors (white race, history of RDS in siblings, male

sex).

Thoracic malformations that cause lung hypoplasia, such as

diaphragmatic hernia

Secondary surfactant deficiency may occur in infants with the

following:

Pulmonary infections (eg, group B beta-hemolytic streptococcal

pneumonia)

Pulmonary hemorrhage

Meconium aspiration pneumonia

Oxygen toxicity along with barotrauma or volutrauma to the lungs

Prenatal Prediction-RDS

Assessment of fetal lung maturity (FLM)- testing amniotic fluid obtained by

amniocentesis.

Lecithin/Sphingomylin ratio- Risk is very low if the L/S ratio is >2

The TDx-FLM II- measures the surfactant-albumin ratio, >55mg

surfactant/gm albumin correlates with lung maturity.

Lamellar body counts- >50,000 lamellar bodies/microliter predicted lung

maturity.

Presence of Phosphatidyglycerol (PG)

Foam stability index (FSI)- stability foam when amniotic fluid is shaken

with ethanol.

CLINICAL COURSE-RDS

Signs of RDS start in minutes to hours after birth

Tachypnea, prominent (often audible) Grunting, Flaring, Retractions,

and Cyanosis relatively unresponsive to oxygen

Breath sounds normal or harsh bronchial

Crepitations esp over posterior lung bases

RDS tends to get worse over the first 1 to 3 days after birth, and then

usually improves gradually over a few days

Tachypnoea and grunting may decreases or disappear with fatigue and

apnoea may occur.

Initially, ABG or SpO2 may show only hypoxemia or desaturation. The

PaCO2 may be normal because of tachypnea.

Later, with fatigue, the PaCO2 will rise - respiratory acidosis. With

imminent respiratory failure, there may be metabolic acidosis due to

inadequate oxygen delivery to tissues. (Mixed acidosis)

If inadequately treated, hypotension, fatigue, cyanosis, and pallor

increase- MODS.

CLINICAL COURSE-RDS

Investigations-RDS

ABG/Capillary blood gas – low PaO2, high PaCO2, respiratory/mixed

acidosis.

Chest X-ray (AP&Lat) – Reticulogranular (ground-glass) pattern and air

bronchograms, lungs are diffusely and homogeneously dense due to

widespread collapse of alveoli with low lung volume.

Blood glucose, Electrolytes, RFT

Complete blood count

Blood culture

X-Ray RDS

Management-RDS

1. Warmth - radiant warmer/ incubator

2. Maintain Hydration

3. Nutrition

a) Initially D5W or D10W (with protein, if

possible)

b) NPO if RR > 60 or moderate/severework of breathing

c) Gavage feeds if stable

d) Consider parenteral nutrition if

enteral feeds are delayed

4. Antibiotics if at risk for pneumonia/sepsis

5. Supplemental oxygen

6. SpO2 monitoring, with appropriate target

for infants at risk for ROP.

7. Exogenous surfactant

8. CPAP or mechanical ventilation, asneeded.

Management-RDS

Oxygen Therapy

Target SpO2

<30 weeks or wt< 1.250gm – 88 to 92 %

>30 weeks or wt > 1.250gm- 88 to 95%

Blood gas monitoring- Frequent measurements during acute

stage, do ABG after 30 min of changes in FiO2/ventilator setting.

Management-RDS

CPAP

Indication- In infants with RDS start CPAP as soon as possible.

The most common cause of failed CPAP is ???

Starting pressure 5 to 7 cm H2O, at flow of 5 to 10 L/min, FiO2

titrated to target SpO2.

Use OG tube to decompress swallowed air.

As the infant improves, start tapering FiO2, when FiO2 requirement

is 0.3 bring CPAP to 5 cm H2O.

Discontinue CPAP if no distress and FiO2 remains <0.3.

Bubble CPAP

Management-RDS

Problem encountered with CPAP

Decreased venous return.

Raised pulmonary vascular resistance – increased Rt to Lt. shunt.

Hypercarbia- if CPAP is too high with low tidal volumes.

Nasal prongs may fail to generate pressure if crying or mouth

opening.

Pulmonary air leak syndromes

Damage to nasal septum

Management-RDS

Surfactant Therapy

Indicated for all diagnosed cases of RDS.

“Early rescue” (before 2 hours of age) is preferable to delayed

treatment.

Prophylactic surfactant can be given in very premature (<27

weeks) neonates.

Repeated doses (upto 4) can be given, most infants require only

one or two doses.

Management-RDS

Administration of Surfactant –

Given through endotracheal tube – If not on ventilator use ‘INSURE’

technique (INtubate SURfactant Extubate).

Given as bolus through ET tube as rapidly as tolerated.

Neonates posture can be changed to allow better distribution of

Surfactant (though no evidence supports this practice).

If intubation is difficult/risky LMA can be used.

Surfactant Preparations and their sources

Doses (*use package insert)

Curosurf - 2.5 mL/kg (200 mg/kg

phospholipid)

Infasurf - 3 mL/kg (105 mg/kg

phospholipid)

Survanta - 4 mL/kg (100/kg mg

phospholipid)

Exosurf - 5 ml/kg

SURFACTANT

Surfactant therapy reduces mortality rates most effectively in infants

<30 weeks and those of birth weight <1250 gm

45

Management-RDS

Mechanical Ventilation

Indications-

Respiratory acidosis with a

PaCO2 >55 mm Hg or rapidly

rising,

PaO2 <50 mm Hg or SPO2 <90%

with an Fio2 above 0.50.

Severe Apnoea

Ventilator settings-

Rapid rates

Moderate Peep (4-6 cm H2O)

Low PIP

Short Ti 0.24-0.4 sec

Low tidal volume 3-6 ml/kg

Early extubation to nasal CPAP


Pneumonia that presents within the first 24 hours after birth.

The 3 categories of congenital pneumonia are as follows:

True congenital pneumonia - already established at birth, infection occursby Hematogenous, Ascending or Aspiration.

Intrapartum pneumonia - acquired during passage through the birth

canal.

Postnatal pneumonia - originates after the infant has left the birth canal

*Pneumonia in association with sepsis presenting beyond 24 hrs is well known

and not discussed here.


Etiology

Group B Streptococcus (GBS)

Escherichia coli

Haemophilus influenza

Other gram-negative bacilli

Listeria monocytogenes

Enterococci

Occasionally, Staphylococcus aureus

Rarely, Mycoplasma pneumonia/Ureaplasma urealyticum


Etiology- Atypical organisms

Cytomegalovirus

Treponema pallidum

Toxoplasma gondii

Rubella

Neisseria gonorrhoeae

Congenital tuberculosis

Congenital candidiasis


Etiology – Developing countries

Escherichia coli

Enterobacter aerogenes

Group B streptococci

Klebsiella

Pseudomonas

Staphylococcus

AP X ray in an infant born at 28 weeks‘ was performed following apnea and

profound birth depression. Subtle reticulogranularity and prominent distal air

bronchograms were consistent with respiratory distress syndrome, promptingexogenous surfactant and antimicrobial therapy. Initial smear of endotracheal

aspirate revealed few neutrophils but numerous, small, gram-negative

coccobacilli. Culture of blood and tracheal aspirate yielded florid growth ofnontypeable Haemophilus influenzae.

Case 1

Full-term infant with progressive respiratory distress from birth following delivery to a

febrile mother through thick, particulate, meconium-containing fluid and recovery

of copious meconium from the trachea. Right clavicle is fractured without

displacement. Note the coarse dense infiltrates obscuring the cardiothymicsilhouette bilaterally with superimposed prominent air bronchograms. Listeria

monocytogeneswas recovered from the initial blood culture.

Case 2


Work up-

CBC, CRP

Blood gases, B. Glucose, Electrolytes, RFT, Blood culture

Imaging- X-ray, USG, CT

Tracheal aspirate

Bronchoscopy


Treatment

Supportive measures (oxygen, warmth, hydration, nutrition

etc)

Antimicrobial therapy

Respiratory support ( airway patency, CPAP, Ventilation)

Maintain optimal hemoglobin (13-16 g/dL)

Meconium aspiration syndrome(MAS)

Acute or chronic hypoxia and/or infection can result in the passage of

meconium in utero.

5% of neonates born through MSAF develop meconium aspiration

syndrome (MAS).

Meconium itself, or the resultant chemical pneumonitis, mechanically

obstructs small airways, causes atelectasis and a “ball-valve” effect.

Meconium aspiration syndrome

MAS classification-

Mild MAS- requiring <40% oxygen for <48 hours.

Moderate MAS- requiring >40% oxygen for >48 hours without air leak.

Severe MAS- requiring assisted ventilation for >48 hours, often

associated with PPHN.

There are bilateral course interstitial markings and widespread

alveolar opacification.

MAS- Treatment

Supportive measures, Oxygen, Antibiotics

Respiratory Support

CPAP- consider CPAP if FiO2 requirement is > 0.40

Mechanical ventilation- if excessive carbon dioxide retention (Paco2 >60

mm Hg) or persistent hypoxemia (Pao2 <50 mm Hg).

PIP requirement is high (30-35 cm H2O), PEEP selected 3-6 cm H2O,

Adequate expiratory time should be permitted (I:E=1:2 or 1:3).

MAS- Treatment

Surfactant –

Endogenous surfactant activity may be inhibited by meconium.

Used in infants with deteriorating course and who require escalating

support.

Washing meconium from the lungs with bronchioalveolar surfactant

lavage is not recommended.

Pneumothorax

Spontaneous pneumothorax occurs in 0.07% of otherwise healthy

appearing neonates.

One in ten of these infants is symptomatic.

More common in newborns treated with mechanical ventilation.

There is a large right pneumothorax demonstrated on AP and lateral films

with a pig-tail catheter in situ with its tip at the apex.

http://radiopaedia.org/articles/pneumothorax

Pneumothorax

Treatment-

Conservative therapy – if no underlying lung disease or complicating therapy

(ventilator), no significant respiratory distress, and have no continuous air leak.

The extrapulmonary air will usually resolve in 24 to 48 hours.

Needle aspiration- Thoracentesis with a “butterfly” needle or intravenouscatheter. Needle aspiration may be curative in infants not receivingmechanical ventilation.

Chest tube drainage- needed esp. in those on ventilator. These air leaks are

continuous and will result in severe hemodynamic compromise if left untreated

Thank you

respiratory distress in newborn

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