The document discusses respiratory distress in neonates. It describes the clinical presentation of respiratory distress and various scoring systems used to assess severity. It then covers the major causes of respiratory distress including transient tachypnea of the newborn, respiratory distress syndrome, meconium aspiration syndrome, pneumonia and others. For each cause, it discusses risk factors, clinical features, investigations and management. The management sections provide details on oxygen therapy, CPAP, surfactant administration and mechanical ventilation.
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Respiratory distress in newborn
1. 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
2. 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
3. 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.
4. 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
5. 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
6. 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
7.
8. 0 1 2
Cyanosis None In room air In 40% FIO2
Retractions None Mild Severe
Grunting None
Audible with
stethoscope
Audible without
stethoscope
Air entry Clear
Decreased or
delayed
Barely audible
Respiratory
rate
Under 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
11. 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
12. 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.
13. Choanal Atresia
Choanal atresia. Rhinogram
demonstrating blockage of
radiopaque dye at the posterior
choanae.
Oral airway which is the initial
treatment of choice can also be
seen.
14. Tracheo-esophageal fistula
A tracheoesophageal fistula (TEF) is a congenital communication between the
trachea and esophagus.
15. Tracheo-esophageal fistula
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.
17. 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.
18. 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).
20. 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.
21. 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.
22. TREATMENT- TTN
It is supportive with close observation because the condition is
usually self limited.
Low flow supplemental oxygen may be necessary for several
hours.
More severe cases- CPAP.
Oral furosemide (Lasix) has not been shown to significantly
improve status and should not be given
24. • 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
25.
26.
27. Structure of lung surfactant
Major constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin),
phosphatidylglycerol, apoproteins (surfactant proteins SP-A, -B, -C, -D), cholesterol
28. 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
30. 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
31. 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
32. 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.
33. 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
34. 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
35. 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
37. 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/severe
work 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, as
needed.
38. 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.
39. 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.
41. 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
42. 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.
43. 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.
46. 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
47. Congenital pneumonia
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 occurs
by 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.
50. Congenital pneumonia
Etiology – Developing countries
Escherichia coli
Enterobacter aerogenes
Group B streptococci
Klebsiella
Pseudomonas
Staphylococcus
51. 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, prompting
exogenous 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 of
nontypeable Haemophilus influenzae.
Case 1
52. 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 cardiothymic
silhouette bilaterally with superimposed prominent air bronchograms. Listeria
monocytogeneswas recovered from the initial blood culture.
Case 2
55. 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.
56. 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.
57. There are bilateral course interstitial markings and widespread
alveolar opacification.
58. 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).
59. 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.
60. 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.
61. 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.
62. 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 intravenous
catheter. Needle aspiration may be curative in infants not receiving
mechanical 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
These causes helps to differenciate between pulmonary causes and cardiac causes or acidosis
Grunting occurs when the child expires against a closed glottice to generate auto PEEP
These perinatal histories are imp these point towards cause of respiratory distress
IUGR <10 percentile wt , LGA commonly occurs in infant of diabetic mothers where polycythemia causes sluggish flow which result in resp. distress CHD are PDA ,VSD ,Cardiac coushion defect ,
Incidence
Min score is 0 and max 10 , these scoring helps in grading improvement or deterioration on cpap
Baby is present with severe resp. distress in delivery room itself in case of B/L chonal atresia baby impoves on crying
Dye in nose reveling posterior nasal block so gudal airway is inserted
Upper part of esophagous developed from retropharyngeal segment and lower part from pregastric segment
Presence of maternal polyhydramnios and single umbilical artery should alert dr ,
Complication is aspiration pneumonia
A stiff red rubber catheter can not passed into stomach as it get coiled 7 to 10 cm from mouth
This is benign self limiting disease
Fio2 < 40 % required
In the absence of surfactant surface tension increases so alveoli tends to collapse during expiration and more negative pressure is required during inspiration to open alveoli
CLD or BPD occurs because of barotrauma and O2 toxicity that causes damage to alveolar cells
Surfactant is produced by type 2 alveolar cells
L/S ratio and TDx-FLM2 the presence of blood and meconium interfere with interpretation with the test
Lamellar bodies are packages of phospholipids produced by type 2 alveolar cells
PG tests major advantage is blood and meconium is not interfere in interpretation and disadvantage is sensitivity of this test is low
Reticulogranular pattern and air bronchogram
Adequate hydration is to be maintained because of increase of insensible losses but avoid overhydration because it can cause pulmonary edema and symptomatic PDA