NEONATAL RESPIRATORY DISEASES

BY

Dr.(Mrs) P. O. OBIAJUNWA

Introduction• Respiratory diseases usually present as

respiratory distress in the neonate. It has four main clinical features.

• Tachypnoea; resp rate >60c/min.• Recessions; indrawing of the sternum and

intercostals and subcostal regions.• Grunting.• Cyanosis.• All four symptoms may not be present in

every case, but the presence of 2 or more symptoms qualifies for respiratory distress.

• Causes of Neonatal Respiratory distress include;

• Respiratory distress syndrome (hyaline membrane disease),

• Pneumonias, Pneumothorax, aspiration syndrome (meconium, milk, blood, Amniotic squames), Congenital diaphragmatic hernia, Transient tachypnoea of the newborn, Tracheo-eosophageal fistula, cardiac failure, Pulmonary hypoplasia, Persistent fetal circulation (Primary pulmonary hypertension), Broncho-pulmonary dysplasia, chronic pulmonary insufficiency of prematurity, (CPIP).

• Respiratory distress syndrome (Hyaline membrane diseases)

• This is due to lack of Surfactant, which is a phospholipids that lowers the surface tension within the terminal airway. Surfactant is secreted by the type 2 pneumocytes situated within the alveolar membrane. They are present by 22 weeks of gestation but become functionally active by full term. Surfactant production can be switched on by stress, premature rupture of membrane, and exogenous steroid given to mother. Maternal diabetes suppresses development of surfactant so that their babies may have RDS even when term.

• The birth process squeezes out fluid from the lungs by compression of the chest wall. The infant’s first breath expands the alveoli. In the presence of surfactant, the alveoli remain expanded, but if absent, the alveoli collapse down to their foetal state, and the baby’s next breath is another massive one to re-expand the terminal airways. Surfactant molecules form a monolayer on the inside of the alveolar membrane. They are poorly compressible and maintain the alveolus in an expanded state. In RDS, each breath is like the first breath in effort, respiratory distress results and baby gets tired.

• About 1% of newborns infant have RDS. It is closely related to immaturity; 60-70% of infants born at<28 weeks and 20% of those born less than 34weeks have it.

• Risk factors for RDS are diadetes in mother, 2nd twin, ante partum haemorrhage, shock, maleness.

Pathology:

Hyaline membranes are seen within the alveoli of dead babies dying of RDS, and are part of the inflammatory response to the condition. The infant shows signs of respiratory distress soon after birth, progressing over the first day, peaks at 48 hours. The infant may be oliguric initially,and may become oedematous, diuresis occurring as the infant starts to recover.

Diagnosis

• Chest –ray Ground glass appearance showing airless alveoli with an air bronchogram, air-filled eosophagus may be seen too.

• Measuring directly or indirectly the amount of surfactant in the amniotic fluid or gastric aspirate. The lecithin: sphingomyelin (L:S) ratio reflects surfactant activity and a ratio of <1.5 predicts a high risk for RDS.

Management • It is self-limiting. The baby’s lungs recover

with endogenous production of surfactant. Management is directed towards supporting the infant during respiratory distress.

• In mild disease, give humidified oxygen supplements by headbox to maintain normal arterial blood oxygen tension.

• In more severe cases continuous positive airway pressure (CPAP) is used to provide constant positive pressure during expiration which limits collapse of the alveoli.

Management (contd)• Mechanical ventilation is indicated when

there is hypoxia, and there is hypercapnoae with a rising Pco2 >8 kpa(60mmHg with falling pH( <7.25) or there is apnoea.

• General supportive treatment are chest physiotherapy, early infection treatment, blood pressure monitoring, optimal environmental temperature.

• Exogenous surfactant replacement therapy can be given.

Complications of respiratory distress syndrome.

Pulmonary:• Air leak including Pneumothorax,• Pulmonary interstitial emphysema, • Pneumonia, atelectasis, Lobar collapse,

chronic lung disease.Extrapulmonary ones are; Patent doctus arteriosus, Intraventricular

haemorrhage, Retinopathy of prematurity, Subglottic stenosis.

Pneumonias

• Neonatal pneumonia could be early, within 24 hours of birth intrapartum that is through the birth canal, or later.

• Early onset pneumonia is said to be mainly caused by Group B beta haemolytic Stretococcus acquired from mother (10% of women are carriers.) It causes pneumonia or meningitis. Presents as respiratory distress or apnoae. The child could have septicaemia and shock.

Chest X-ray may be similar to RDS.• Management includes respiratory support with

oxygen supplement, mechanical ventilation, presumptive antibiotic management (ampicillin with gentamicin, 3rd generation cephalosporin). Change antibiotic according to sensitivity pattern.

• Later onset pneumonias could be due to damaged lungs in ventilated babies, or acquired from those around the babies. Causative germs include Pseudomonas, Staph aureus. E-coli, Klebsiella, Mycoplasma, Chlamydia, unusually candida or viruses.

• X-ray shows patchy opacities.

• Treatment is with appropriates antibiotics, oxygen if needed.

• Manage congestive cardiac failure if present.• Vigorous physiotherapy.• Air leak from the alveoli can occur. If the

leakage is into lung interstium it is called pulmonary interstitial emphysema. Air can track along the perivascular spaces and rupture into the mediastinum causing Pneumomediastinum, into the pleural space resulting in Pneumothorax, and when air leaks into the pericardial space, it is pneumopericardium.

• Pneumothorax may be spontaneous, but mostly following resuscitation especially with bag and mask.Risk afctors include RDS, meconium aspiration, and lung hypoplasiain conjuction with diaphragmatic hernia.

• Diagnosis-suspect when there is a sudden deterioration in infant’s condition. There is a reduction of breath sounds over the affected lung. Left-sided tension pneumothorax may displace the heart to the right side with heart sounds.

• Confirm by chest x-ray which shows a hyperlucency of the side affected with no air bronchogram. Treament involves placing a tube in the2nd intercostal space at the mid-clavicular line. Place the other end of the tube into a container of water below the infant.

• Meconium aspiration syndrome. Intrapartum asphyxia may cause the foetus to pass meconium which baby can aspirate into the small bronchi when gasping. During resuscitation at birth, the meconium is further driven into terminal airway. Meconium is very irritant and causes an inflammatory reaction, Meconium plugs some airways causing a “ball valve” effect of the with some hyperinflation, and air leak. An intense inflammatory exudates develop and secondary bacterial infection occurs. Ventillation/ perfusion inequality develops causing the infant to become more hypoxic and in severe cases pulmonary hypertension commonly develops.

• Diagnosis is suggested when there is the presence of meconium in the liquor, in the airway with respiratory distress.

• Chest X-ray shows hyperinflation with diffuse patchy opacities throughout the lung fields.

• Management involves the use of Oxygen, antibiotics, and steroids.

• Prevention; careful evaluation of the child with meconium-stained liquor and sucking it out from mouth. If meconium is seen below the vocal cords, remove it and lavage the

• Trachea with normal saline through an endotracheal tube.

• Milk aspiration is common in infants with gastro-eosophageal reflux, those with apnoae and tetanus patients. Naso-duodenal feeding may be useful in these. Total parenteral nutrition may be considered.

Congenital diaphragmatic hernia.

• Occurs I 1 in 2500 births. There is a defect in the postero-lateral part of the diaphragm in 80% of cases. Severity depends on the defect size, amount of bowel in chest and timing of herniation. Bowel in the chest causes lung compression and hypolasia. Large bilateral defects is not compartible with life. development.

• Their severe respiratory distress present from birth in severe cases.

• Suggestive features are scaphoid abdomen, and apparent dextrocardia if defect is left-sided. Diagnosis is confirmed by chest x-ray showing loops of bowel in the thorax.

Management: Patient can be delayed a few days to stabilize

before surgery. The bowel is returned to the abdomen and defect is repaired.

• Medical treatment: adequate ventilation, shock treatment, calories.

• Prognosis depends on lung hypoplasia. Mortality of 60-70% in early presentation <6 hours.

• Transient tachypnoae of new born is diagnosed in retrospect and is due to delayed clearance of fluid from the lungs in term infants especially born by C/S soon after birth.

• X-ray shows streakiness due to interstitial fluid and fluid in horizontal fissure.