Respiratory distress in newborn
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Transcript of Respiratory distress in newborn
Imp questions
Gestation : Term or Preterm?????
Weight : SGA or LGA????
Onset : at birth or hours or days after birth????
MEDICAL CAUSES
TTNB – transient tachypnea
RDS(HMD)
Aspiration syndromes
Pneumonia/sepsis
PPHN
CCF
Acidosis
SURGICAL CAUSES
Pneumothorax
Diaphragmatic hernia
TEF
Lobar emphysema
Phrenic nerve paralysis
Pleural effusion
Cystic lesions
Airway obstruction
Nasal –choanal atresia
nasal edema
Oral cavity –macroglossia.
micrognathia,
Glosoptosis
Laryngeal
obstruction –laryngeal web
Subglottic stenosis of larynx
Laryngomalacia
cord paralysis
Airway obstruction
Neck obstruction
Cystic hygroma
Congenital goiter
Tracheal obstruction
Tracheomalacia
TEF
Tracheal stenosis
Lung parenchyma
Aspiration syndrome (MAS)
Respiratory distress syndrome (HMD)
TTNB
Pneumonia
Pleural effusion
Pulmonary hemorrhage
Air leak – Pneumothorax,
Pneumomediastinm
Developmental defects
Agenesis of lung
Hypoplasia of lung
Diaphragmatic hernia
Tracheal agenesis
TEF
Clinical features
Newborn with respiratory distress
usually presents with
Tachypnoea
Chest retraction
Severe Grunting
Cyanosis
Apnoea
Approach to Evaluation
ANTENATAL H/o :
Polyhydramnios(TEF) or oligohydramnios(pulmonary hypoplasia).
Cervical incompetence.
Maternal Illness:
Diabetes(IDM).
PIH(intrauterine hypoxia).
Infections(pneumonia/sepsis).
Maternal medications.
Antenatal Steroids.
Antenatal Ultrasound suggestive of anomaly.
History of Sibling death / similar clinical presentation
in sibling.
DELIVERY
Prolonged / Premature rupture of membranes.
MSAF.
CLINICAL
Term or Preterm.
Time of presentation and progression of Respiratory
Distress.
External congenital anomalies, shape of the
chest(jeune’s syndrome).
Excessive oral secretions(TEF).
Hyperinflation of chest(MAS,CDH).
Position of cardiac apex, Breath sounds,
Transillumination (pneumothorax, CDH).
Normal passage of nasogastric tube
INVESTIGATION
Pulse oximetry :
SaO2.
Fluctuations of SaO2.
Differential SaO2.
Chest X-ray (with gastric tube in place).
Arterial Blood gas.
Echocardiography & CT scan if required.
Interpretation
Infants with RDS scores <4 for over 2 hours usually resolve without any problem.
Infants with scores of 4 to 6 have mild respiratory distress.
Infants with scores >6 will develop severe respiratory distress.
Higher scores correlate with decrease in oxygenation and pH.
These scores were studied in infants with respiratory distress syndrome, but they are useful in assessing any newborn with respiratory distress.
Interpretation
The parameters assessed by inspection or auscultation of
the upper and lower chest and nares on a scale of 0, 1 or
2.
The higher the score, the more severe the respiratory
distress.
Pneumothorax
Pneumothorax can occur in 1 % of all newborns.
Only 10 % of these are symptomatic.
15 – 20 % of pneumothoraces are bilateral.
An infant with lung disease like MAS & HMD, or those
given positive pressure ventilation are more to develop
a pneumothorax.
The compression of the underlying lung and progressive
mediastinal shift to the opposite side result in pulmonary
and hemodynamic changes.
A sudden increase in cerebral blood flow corresponding to
the changes systemic hemodynamics, could cause or
increase the bleed in to the germinal matrix or cerebral
ventricles, especially in premature infants.
The clinical presentation could varied.
It maybe dramatic with severe respiratory
distress, hyper-inflated chest, shift in cardiac
apex, unilateral decrease in breath sounds, and a
positive trans-illumination.
Commonly an infant under treatment for other
cause of respiratory distress would develop a
pneumothorax.
An unexplained increase in heart rate, or gradual drop in
blood pressure in an infant with respiratory distress should
arouse the suspicion of pneumothorax, More so if the
infant is on mechanical ventilator support or required
positive pressure resuscitation.
Screening for pneumothorax by trans-illuminating the
chest of an at-risk infant at regular intervals may be
helpful.
A chest-Xray would confirm the diagnosis.
Incidentally detected asymptomatic
pneumothorax requires no treatment other than
close observation.
Immediate decompression is the rule in all
symptomatic patients.
Aspiration thru a 21G or 22 G scalp-vein needle inserted in
to the 2nd intercostals space in the mid-clavicular line or
5th/6th inercostal space in the mid-axillary line would
temporarily abate symptoms.
Insertion of the intercostals catheter under local
anesthesia in the 6th intercostals space in the mid-axillary
line, connected to an under water sealed drain would
satisfactorily drain out the airleak.
If the infant continues to be symptomatic, despite a
bubbling ICD, think of a pneumothorax on the opposite
side.
If all the clinical features are
exclusively due to the
pneumothorax, the recovery
would also be quite dramatic.
In the presence of an underlying
lung disease, improvement in
symptoms are significantly
influenced by the extent of the
primary disease.
The catheters are clamped when
the ICD has not bubbled for 24
hours.
If there is no clinical worsening,
the infant is observed for a 6 -12
hr period and the clamped
catheters are removed.
Choanal atresia
A infant who is normal and pink when it cries but rapidly develops
respiratory distress becomes cyanosed when it stops crying should be
evaluated for bilateral choanal atresia.
As neonates are obligate nasal breathers, bilateral choanal
obstruction results in their becoming cyanosed when they stop
crying.
An oral airway would often immediately alleviate the symptoms.
Occasionally the presentation would be as respiratory distress while
attempting to breast feed.
Diagnosis is suspected when one is unable to
introduce a nasopharyngeal catheter.
CT scan would confirm the diagnosis.
Surgical intervention to alleviate the membranous
or bony obstruction to the choanae would have to
be undertaken with out delay.
Tracheo-esophageal fistula(TEF)
Antenatal history of polyhydroamnios may be available.
Clinical suspicion of TEF must be aroused in an infant who
continues to pour out oral secretion, warranting repeated
oral suction.
There is a high chance of the infant aspirating these
oropharyngeal secretion & aspiration of gastric secretion
through the lower tracheoesophageal communication and
resultaning in pneumonia.
If undetected at the time of delivery presentation could
be as cyanotic episodes associated with feeding,
respiratory distress, abdominal distension in the presence
of fistula, and a scaphoid abdomen in the presence of
pure esophageal atresia.
Prenatal diagnosis of congenital TEFs:
Prenatal ultrasound may reveal polyhydramnios, absence of fluid-filled stomach, small abdomen, distended esophageal pouch.
Postnatal diagnosis of congenital TEFs :
Plain chest radiographs may reveal tracheal compression and deviation.
Absence of a gastric bubble indicates esophageal atresia without a TEF or esophageal atresia with a proximal TEF.
Chest radiography leads to the diagnosis of TEF in most cases of congenital TEF.
Aspiration pneumonia in the posterior segments of the upper lobes may occur secondary to aspiration of the contents from the esophageal pouch or stomach. Recurrent or massive aspiration may lead to acute lung injury in some patients.
Insertion of a nasogastric tube may show coiling in the mediastinum of patients who have concomitant esophageal atresia. This finding is diagnostic of TEFs associated with esophageal atresia.
Contrast studies are seldom required to confirm the diagnosis.
These studies have the risk of aspiration pneumonitis and pulmonary
injury.
If the contrast study is performed, 1-2 mL of barium is instilled through an
8F catheter placed into the esophagus. Chest radiographs are taken in the
lateral decubitus position as well as the anteroposterior position to detect
spilling of the contrast into the trachea.
Use of multidetector-row CT scans have made 3-dimensional (3D) displays
of many organs and structures.
Presence of TEF is correctly diagnosed with CT esophagography.
Treatment
The infant should be kept nil by mouth.
Nutrition, fluid and electrolytes requirements being maintained intravenously.
The baby should be nursed in a 15 – 30 degrees head elevated prone or lateral
position.
The upper pouch should be continuously drained, preferably with minimal
continuous suction.
Once stabilized the infant must be transferred to the surgical team for further
management.
Surgical managment
In healthy Newborn – primary repair.
In Newborn with comorbidities like pneumonia, low birth
weight or respiratory distress syndrome staging of surgery
is done.
1st stage –
Tracheostomy
Gastrostomy tube.
Feeding jejunostomy.
Exteriorisation of upper pouch and minimal continuous suction.
2nd stage –
Definitive surgery for fistula – division & closure.
Approach –
Right side thoracotomy in lateral decubitus position.
Thoracoscopy.
Congenital diaphragmatic hernia(CDH)
• Antenatal USG is helpful in identifying CDH.
• Rule out “diaphragmatic hernia” in all neonates presenting
with respiratory distress at birth with a cardiac impulse
better felt in the right hemithorax.
• Scaphoid abdomen.
• Radiograph of the chest would confirm the diagnosis.
Management
If warranting resuscitation at the time of delivery, positive pressure ventilation
through a mask is discouraged and ventilation is commenced after directly
intubating the infant.
The associated hypoplasia of the ipsilateral lung, compression of the contralateral
lung, and the associated hypoxemia, acidosis and hypercapnia result in these
infants having a significant degree of PPHN.
Immediate emergency surgery is no longer recommended.
Instead a period of stabilization with adequate fluid support, maintenance of
blood pressure, control of PPHN and ventilatory stability have ensured better
surgical outcome.
The primary aim of respiratory management is to ensure adequate
oxygenation and avoiding acidosis.
Various strategies of conventional and high frequency ventilation are
adapted for attaining this.
Aim is to try and lower the PaCO2 to acceptable low values by
hyperventilation, providing adequate FiO2 and Mean Airway pressure (MAP)
for oxygenation.
An oxygenation index (OI) greater than 20 at 6 hrs of life, was associated
with higher mortality.
Surgical correction is mandatory.
Approach for surgical repair :
Abdominal subcostal.
Thoracotomy.
Thoracoscopy.
The major determinants of the final out come would be prenatal factors that
affect the development of pulmonary parenchyma, pulmonary vascular bed
and surfactant system.
Postoperative care would involve continued ventilator support, strategies to
manage the associated PPHN and if warranted extracorporeal membrane
oxygenation (ECMO).
Follow-up of the survivors is necessary to evaluate and manage respiratory
problems and tackle issues of those of feeding, growth and development.
Congenital lobar emphysema
This is a rare but well recognized cause for an infant presenting with respiratory
distress anytime within the neonatal period.
The infant would present with tachypnea, recessions, cyanosis and hyperinflation of
the affected side.
Breath sounds on the affected side may be diminished.
A differential diagnosis of pneumothorax may be considered.
A chest X-ray would show hyperinflation of the affected lobe, mediastinal shift to
the opposite side and on closer examination would reveal the lung markings --- thus
differentiating this from pneumothorax.
Definitive surgical treatment - lobectomy.
Intranasal tumours, laryngeal webs, laryngeal cysts,
laryngomalacia are few of the anomalies of the upper
airway that could present as respiratory distress in the
neonatal period.
Rare developmental anomalies like cystic adenomatoid
malformation of the lung, congenital pulmonary
lymphangectasia etc. could present as neonatal
respiratory distress, requiring surgical intervention .
The outcome of these conditions depends on the extent of
lung involvement and association of other congenital
anomalies.