Neonatal Respiratory Failure Flashcards
What are the five stages of fetal lung development?
- Embryonic (weeks 4-7)
- Pseudoglandular (weeks 5-17)
- Canalicular (weeks 16-25)
- Saccular (weeks 24-birth)
- Alveolar (week 36 to age 8)
What occurs in the embryonic stage (weeks 4-7) of lung development?
Lung bud forms, develops into trachea, bronchial buds, and mainstem bronchi. Errors can lead to tracheoesophageal fistula.
What occurs in the Pseudoglandular (weeks 5-17) of lung development?
- Endodermal tubules transition to terminal bronchioles.
- Surrounded by modest capillary network.
At what stage do pneumocytes start developing?
Week 20 in the canalicular phase.
At what week is respiration viable?
Around week 25, when alveolar ducts and primitive air sacs start forming (saccular phase) where alveolar ducts and terminal sacs begin to develop. The terminal sacs are separated by 1° septae.
What major changes occur at birth to transition from fetal to neonatal respiration?
Air replaces lung fluid, leading to a decrease in pulmonary vascular resistance.
What are the cardinal symptoms for respiratory distress in newborns?
- Tachypnea
- Grunting
- Nasal flaring
- Subcostal and intercostal retractions
What is bronchopulmonary dysplasia (BPD)?
A chronic lung disease of premature infants characterized by prolonged oxygen dependence and lung injury.
What are the highest risk factors for developing bronchopulmonary dysplasia?
Prematurity, low birth weight, mechanical ventilation, and oxygen toxicity.
How does bronchopulmonary dysplasia typically present in neonates?
Tachypnea, retractions, rales, and persistent oxygen requirement beyond 28 days after birth.
What imaging finding is characteristic of bronchopulmonary dysplasia?
Diffuse lung opacities with areas of atelectasis and hyperinflation on chest X-ray.
What is the primary management strategy for bronchopulmonary dysplasia?
Keep oxygen levels LOW, mechanical ventilation with minimal settings, fluid restriction, and diuretics if necessary.
How does lung function change in bronchopulmonary dysplasia patients as they age?
Lung function improves over months to years, with complete development by 8 years old.
What causes neonatal respiratory distress syndrome (NRDS)?
Insufficient surfactant production leading to alveolar collapse (atelectasis). What is deficient are lamellar bodies.
What are the risk factors for neonatal respiratory distress syndrome?
Prematurity, C-section delivery, and maternal diabetes.
What is the pathognomonic chest X-ray finding in neonatal respiratory distress syndrome?
Diffuse ground-glass opacities and low lung volumes.
What is the treatment for neonatal respiratory distress syndrome?
CPAP, supplemental oxygen, surfactant administration, and mechanical ventilation if severe.
What are the complications of neonatal respiratory distress syndrome?
PDA and bronchopulmonary dysplasia.
How can neonatal respiratory distress syndrome be prevented in premature infants?
Antenatal corticosteroids (e.g., betamethasone) given to mothers before preterm delivery.
What causes transient tachypnea of the newborn (TTN)?
Delayed clearance of alveolar fluid leading to mild pulmonary edema.
What are the risk factors for transient tachypnea of the newborn?
TTN is a condition caused by retained fetal lung fluid after delivery. Prematurity, C-section delivery, maternal diabetes are the main risk factors. Newborns have respiratory distress and the imaging findings consistent with transient tachypnea of the newborn (TTN). Patients born prematurely or by cesarean section are at increased risk, as typical resorptive mechanisms are activated at term and during labor. TTN also occurs more frequently in infants born to mothers with diabetes due to impaired fluid clearance in the diabetic fetal lung. TTN presents shortly after birth with tachypnea, increased work of breathing (eg, retractions, nasal flaring), and often cyanosis. However, breath sounds are usually clear on examination.
What chest X-ray finding is seen in transient tachypnea of the newborn?
Bilateral perihilar linear streaks. Hyperinflation (ie, flattened diaphragm), mild cardiomegaly, prominent vascular markings, fluid in the interlobar fissures, and pleural effusions may be seen on chest x-ray.
How is transient tachypnea of the newborn managed?
Supportive care with supplemental oxygen; self-resolves in 24-72 hours. The symptoms usually resolve spontaneously within 72 hours with no long-term complications.
What is the pathophysiology of persistent pulmonary hypertension of the newborn (PPHN)?
Failure of normal pulmonary vascular resistance decline, leading to persistent right-to-left shunting.
What are the risk factors for persistent pulmonary hypertension of the newborn?
Meconium aspiration, perinatal asphyxia, congenital diaphragmatic hernia.
What is the unique clinical sign of persistent pulmonary hypertension of the newborn?
Differential cyanosis: oxygen saturation is higher in the right hand than in the lower extremities.
What is the treatment for persistent pulmonary hypertension of the newborn?
100% oxygen, inhaled nitric oxide, sildenafil, or ECMO in severe cases.
What causes meconium aspiration syndrome?
Aspiration of meconium-stained amniotic fluid causing airway obstruction and chemical pneumonitis.
What is the hallmark chest X-ray finding in meconium aspiration?
Patchy infiltrates with hyperinflation.
How is meconium aspiration syndrome managed?
Intubation with suction avoidance, oxygen support, antibiotics for possible secondary infection.
What is a significant long term complication of meconium aspiration syndrome?
Permanent neurocognitive impairment is a severe complication of birth asphyxia due to meconium aspiration syndrome, which presents at delivery with respiratory distress from meconium-stained amniotic fluid.
What is apnea of prematurity?
Cessation of breathing for >20 sec in a premature infant due to an immature respiratory drive.
How is apnea of prematurity managed?
Supportive care, CPAP, caffeine therapy (methylxanthines).
How do you differentiate a pulmonary cause from a cardiac cause of neonatal respiratory failure?
If supplemental oxygen improves saturation, the cause is pulmonary; if not, it is likely cardiac (e.g., congenital heart disease with right-to-left shunting).
What is the first-line treatment if a congenital heart defect is suspected?
Prostaglandin E1 to keep the ductus arteriosus open.
