Neonatal respiratory distress

Question 1

what is?

Answer 1

lung disorder in infants that is caused by a deficiency of pulmonary surfactant.
most common in preterm infants, with the incidence and severity decreasing with gestational age.
Surfactant deficiency causes the alveoli to collapse, resulting in impaired blood gas exchange. manifest shortly after birth and include tachypnea, tachycardia, increased breathing effort, and/or cyanosis.
The suspected diagnosis is based on clinical features and confirmed by evaluating the extent of atelectasis via chest x-ray.
Blood gases show respiratory and metabolic acidosis in addition to hypoxia.
Treatment: emergent resuscitative measures, including nasal CPAP and stabilizing blood sugar levels and electrolytes + intratracheal surfactant is administered if ventilation alone is unsuccessful.
Most cases resolve within 3–5 days of treatment. However, complications such as hypoxemia, tension pneumothorax, bronchopulmonary dysplasia, sepsis, and neonatal death may still occur.
NRDS can be prevented by administering antenatal glucocorticoids to the mother if premature delivery is expected.

Question 2

etiology

Answer 2

Impaired synthesis and secretion of surfactant
Risk factors
Premature birth
Cesarean section; results in lower levels of fetal glucocorticoids than vaginal delivery (uterine contractions during vaginal delivery increase fetal stress levels, which cause glucocorticoids to be released as a physiologic response to stress)
Maternal diabetes mellitus: leads to ↑ fetal insulin, which inhibits surfactant synthesis

Question 3

pathophysiology

Answer 3

Surfactant
Pulmonary surfactant is a mixture of phospholipids and proteins produced by lamellar bodies of type II alveolar cells. These phospholipids reduce alveolar surface tension, preventing the alveoli from collapsing.
Any infant born preterm is vulnerable to surfactant deficiency for the following reasons:
Surfactant production occurs at around 20 weeks’ gestation.
Distribution throughout the lungs begins around weeks 28–32 and does not reach sufficient concentration until week 35.
Surfactant deficiency → little or no reduction of alveolar surface tension → increased alveolar collapse → atelectasis → decreased lung compliance and functional residual capacity → hypoxemia and hypercapnia
Hypoxemia and hypercapnia → vasoconstriction of the pulmonary vessels (hypoxic vasoconstriction) and metabolic acidosis → intrapulmonary right-to-left shunt → increased permeability due to alveolar epithelial damage → fibrinous exudation within the alveoli → development of hyaline membranes in the lungs (hyaline membrane disease)

Question 4

clinical features

Answer 4

History of premature birth
Onset of symptoms: usually immediately after birth
Signs of increased breathing effort
Tachypnea
Nasal flaring and moderate to severe subcostal/intercostal and jugular retractions
Typical expiratory “grunting”
Auscultation: decreased breath sounds
Cyanosis due to peripheral hypoxic vasoconstriction

Question 5

Diagnostics

Answer 5

Chest x-ray: diffuse, fine, reticulogranular (ground-glass) densities with low lung volumes and air bronchograms
Amniocentesis for prenatal testing of NRDS: screening for markers of fetal lung immaturity
Lecithin-sphingomyelin ratio < 1.5 (≥ 2 is considered mature)
The amount of sphingomyelin in the amniotic fluid remains relatively consistent during pregnancy.
The amount of lecithin, which is the major component of surfactant, starts increasing after week 26 of gestation.
The lower the lecithin-sphingomyelin ratio, the more likely it is that the lungs are immature.
Foam stability index
Low surfactant-albumin ratio
Pathological findings [6]
Hyaline membranes lining the alveoli
Composed of fibrin, cellular debris, and red blood cells
Appear as eosinophilic, amorphous material lining the alveolar surface
Engorged and congested capillary vessels in the interstitium

Question 6

Treatment

Complications

Answer 6

Treatment
Ventilation
Nasal CPAP with a PEEP of 3–8 cm H2O
If respiratory insufficiency persists, start intubation with mechanical ventilation and O2 inhalation.
Endotracheal administration of artificial surfactant within 2 hours postpartum
Physiologic O2 saturation in neonates is around 90% instead of 100%. A saturation of 100% is considered toxic for neonates!

Complications
Bronchopulmonary dysplasia (BPD)
Definition: chronic lung disease primarily found in premature infants exposed to prolonged mechanical ventilation and oxygen therapy for neonatal RDS
Etiology: An immature lung with exposure to ventilation leads to barotrauma, oxygen toxicity, and inflammation.
Ventilation for more than 28 days
Clinical features
Seen in infants < 32 weeks
Persistence of symptoms similar to NRDS (e.g., tachypnea, grunting, nasal flaring); episodes of desaturation
Diagnostics
Chest x-ray: diffuse, fine, granular densities, areas of atelectasis interspersed with areas of hyperinflation
atelectasis

Pneumothorax

Patent ductus arteriosus (due to a persistently low partial pressure of oxygen in the blood)
Complications of O2 inhalation: retinopathy of prematurity, bronchopulmonary dysplasia, intraventricular hemorrhage

Baby oxen have RIBs: Babys receiving too much oxygen get Retinopathy of prematurity, Intraventricular hemorrhage, an

Question 7

Prevention

Answer 7

Prevent premature birth if possible.
Antenatal corticosteroid therapy administered to the mother (stimulates infant lung maturation) - Given 48 hours before delivery - 2 doses of IM betamethasone