Neonatal Diseases

common causes of respiratory distress in the neonate are : - 1. Hyaline Membrane Disease (HMD) 2. Meconium Aspiration Syndrome (MAS) 3. Transient Tachypnoea of the Newborn (TTNB) 4. Congenital or acquired pneumonia 5. Persistent Pulmonary Hypertension of the Newborn (PPHN) 6. Air leaks

Cont.. 7. Congenital anomalies of upper airway (choanal atresia), gut (tracheoesophageal fistula, congenital diaphragmatic hernia) or lungs (lobar emphysema, cysts) 8. Cardiac shock or Congenital Heart Disease (CHD). 9. Haematological causes (severe anaemia, polycythaemia) 10. Neurological ( seizures ) 11. Metabolic causes- metabolic acidosis

Clinical Examination Clues to the likely aetiology on examination of the neonate : 1. A preterm baby weighing <1500 gms with retractions and grunt is likely to have HMD. 2. A term baby born through meconium stained amniotic fluid with an increase in the anteriorposterior diameter of the chest (full chest) is likely to be suffering from MAS. 3. A depressed baby with poor circulation is likely to have neonatal sepsis with or without congenital pneumonia. 4. A near term baby with no risk factors and mild distress may have TTNB. 5. An asphyxiated baby may have PPHN.

Cont.. 6. A growth retarded baby with a plethoric look may have polycythaemia. 7. A baby with respiratory distress should be checked for an air leak by placing a cold light source over the chest wall in a darkened room. 8. A baby presenting with tachypnoea and a cardiac murmur may have a congenital heart disease. 9. Inability to pass catheter through the nostril of a term baby is suggestive of choanal atresia.

Cont.. For babies presenting later with distress ask for : a) Is the distress associated with feed refusal and lethargy? (sepsis, pneumonia) b) Is there a family history of early neonatal deaths? (CHD).

Respiratory Distress Syndrome (RDS) Synonym: hyaline membrane disease Caused by the inadequate production of surfactant in the lungs. produced by type II pneumocytes (reduce surface tension). surfactant is produced after 30 weeks gestation. Inadequate surfactant production causes air sacs to collapse on expiration and greatly increases the energy required for breathing. The development of interstitial oedema makes the lung less compliant. This leads to hypoxia and retention of carbon dioxide. Right-to-left shunting occurs: - - in collapsed lung (intrapulmonary) or, - if pulmonary hypertension is severe, across the ductus arteries and the foramen ovale (extrapulmonary).

Risk factors Premature delivery Infants delivered via caesarian section without maternal labour. Hypothermia Perinatal asphyxia Multiple pregnancy Family history of RD

Clinical features . Usually preterm delivery. - tachypnoea, expiratory grunting, subcostal and intercostal retractions diminished breath sounds, cyanosis and nasal flaring. May rapidly progress to fatigue, apnoea and hypoxia

Investigations Blood gases: respiratory and metabolic acidosis along with hypoxia. Pulse oximetry should be maintained at 90-95%. Chest x-ray (ground glass opacity ) Monitor full blood count, electrolytes, renal and liver function Echocardiogram diagnosing PDA determine the direction and degree of shunting, Cultures to rule out sepsis

Respiratory Distress Syndrome (RDS) Also known as Hyaline Membrane Disease (HMD)

Occurrence 1-2% of all births 10% of all premature births Greatest occurrence is in the premature and low birth weight infant

Etiology & Predisposing Factors Prematurity Immature lung architecture and surfactant deficiency Fetal asphyxia & hypoxia Maternal diabetes Increased chance of premature birth Possible periods of reflex hypoglycemia in the fetus causing impaired surfactant production

The cycle continues until surfactant levels are adequate to stabilize the lung Symptoms usually appear 2-6 hours after birth Why not immediately? Disease peaks at 48-72 hours Recovery usually occurs 5-7 days after birth

Clinical findings: Physical Tachypnea (60 BPM or >) Retractions Nasal flaring Expiratory grunting Helps generate autoPEEP Decreased breath sounds with crackles Cyanosis on room air Hypothermia Hypotension

Clinical Findings: Lab ABGs: initially respiratory alkalosis and hypoxemia that progresses to profound hypoxemia and combined acidosis Increased Bilirubin Hypoglycemia Possibly decreased hematocrit

CXR: Normal

RDS CXR: Ground Glass Effect

RDS CXR: Air Bronchograms & Hilar Densities

Time constant is decreased since elastic resistance is so high Increased elastic resistance means decreased compliance!

RDS Treatment: Primarily supportive until lung stabilizes Maintain perfusion, maintain ventilation and oxygenation O2 therapy, CPAP or mechanical ventilation May require inverse I:E ratios if oxygenation can not be achieved with normal I:E ratio Surfactant instillation!!! May cause a sudden drop in elastic resistance!

Prognosis/Complications Prognosis is good once infant makes it past the peak (48-72 hours) Complications possible are: Intracranial Bleed BPD (Bronchopulmonary Dysplasia) PDA (Patent Ductus Arteriosus)

Meconium Aspiration Syndrome -MAS- Syndrome of respiratory distress that occurs when meconium is aspirated prior to or during birth

Occurrence 10-20% of ALL births show meconium staining 10-50% of stained babies may be symptomatic More common in term and post-term babies

Etiology & Predisposing Factors Intra-uterine hypoxic or asphyxic episode Post-term Cord compression

Pathophysiology: Check Valve Effect Causes gas trapping (obstruction) If complete obstruction, then eventually atelectasis occurs Irritating to airways, so edema and bronchospasm Good culture ground for bacteria, so pneumonia possible

Pathophysiology (cont.) V/Q mismatch leads to hypoxia and acidosis which increases PVR TC increases because it increases airway resistance Meconium is usually absorbed in 24-48 hours; there are still many possible complications

Clinical Signs Respiratory depression or distress at birth Hyperinflation Pallor Meconium stained body Possible cyanosis on room air Moist crackles ABGs – hypoxemia with combined acidosis CXR – coarse, patchy infiltrates with areas of atelectasis and areas of hyperinflation May see flattened diaphragms if obstruction is severe

Management Surfactant replacement therapy (endotracheal tube). Oxygen: infants with mild RDS. Continuous positive airway pressure (CPAP). CPAP may be administered via an endotracheal tube, nasal prongs, or nasopharyngeal tubes. Assisted ventilation at fast rates (more than 40 breaths per minute)

Supportive therapy includes the following : . . Temperature regulation: prevent hypothermia. Fluids, metabolism, and nutrition: monitor and maintain blood glucose, electrolytes, acid balance, renal function, and hydration. Once the infant is stable, intravenous nutrition with amino acids and lipid. After the respiratory status is stable, initiate small volume gastric feeds (preferably breast milk) via a tube to initially stimulate gut development.

Cont.. Circulation and anaemia: monitor heart rate, peripheral perfusion, and blood pressure. Blood or volume expanders may be required. Antibiotics: start antibiotics in all infants who present with respiratory distress at birth after obtaining blood cultures. Discontinue antibiotics after three to five days if blood cultures are negative. Support of parents and family: keep the parents well informed. Encourage parents to frequently visit and stay with their baby.

Treatment schedule Inj. Betamethasone 12 mg IM every 24 hours , 2 doses Inj. Dexamethasone 6 mg IM every 12hours , 4 doses Timing of effect : Opitimal effect occurs after 24 hours of initiating treatment Effect of one course lasts for 7 days.

Prevention Antenatal corticosteroids (dexamethasone) accelerate foetal surfactant production and lung maturation. They have been shown to reduce respiratory distress syndrome, intraventricular haemorrhage and mortality by 40%. Delaying premature birth. Tocolytics, e.g.nifedipine or ritodrine, may delay delivery by 48 hours and therefore enable time for antenatal corticosteroids to be given. Avoid hypothermia in the neonate.

M.A.S. Treatment NaHCO3 if severe metabolic acidosis Broad spectrum antibiotics Bronchial hygiene May need mechanical ventilation Slow rates and wide I:E ratios because of increased TC Low level of PEEP may help prevent check valve effect May need HFO Amnioinfusion – artificial amniotic fluid infused into uterus to dilute meconium Proper resuscitation at birth(clear meconium from trachea before stimulating respiration) Oro-gastric tube NTE O2

Prognosis & Complications Good prognosis if there are no complications Complications: Pneumonia Pulmonary baro/volutrauma Persistent Pulmonary Hypertension (PPHN)

CXR: Pneumothorax