Respiratory distress syndrome (RDS)

• Caused by surfactant deficiency in immature lungs. Surfactant lowers alveolar surface tension; without it, alveoli collapse at the end of each expiration (atelectasis), so every breath must reopen them.
• Result: low lung compliance, increased work of breathing, ventilation–perfusion mismatch, hypoxemia, hypercapnia, and combined respiratory and metabolic acidosis (anaerobic metabolism). Hypoxia and acidosis constrict pulmonary vessels and further reduce surfactant production — a vicious cycle.
• Surfactant production begins in the late second trimester and becomes adequate in most fetuses by about 35 weeks. Risk rises with lower gestational age; other risk factors are maternal diabetes, male sex, cesarean birth without labor, perinatal asphyxia, and a sibling with RDS. Late preterm infants (34–36 weeks) remain at risk.
• Course: signs start at or within hours of birth, worsen over the first 48–72 hours, then improve as the infant produces its own surfactant (often heralded by diuresis).

Transient tachypnea of the newborn (TTN) — delayed clearance of fetal lung fluid, typically in near-term or term infants after cesarean birth. Tachypnea with mild oxygen need that resolves within 24–72 hours. It is included here because it must be distinguished from RDS and pneumonia.

Apnea of prematurity (AOP)

• Caused by an immature brainstem respiratory center (blunted response to CO₂ and hypoxia) and an easily collapsible upper airway.
• Definition: a pause in breathing of 20 seconds or longer, or a shorter pause accompanied by bradycardia (heart rate below 100/min), oxygen desaturation, or cyanosis/pallor.
• Types: central (no respiratory effort), obstructive (effort against a blocked airway), and mixed (most common in preterm infants).
• Periodic breathing — 5- to 10-second pauses followed by rapid breaths, without color or heart-rate change — is a normal immature pattern, not apnea.
• AOP is a diagnosis of exclusion: apnea may also signal sepsis, hypoglycemia, hypothermia or overheating, anemia, intraventricular hemorrhage, seizures, electrolyte disturbance, or drug exposure.
• Frequency is inversely related to gestational age; most episodes resolve by 36–37 weeks postmenstrual age (PMA), but in extremely preterm infants they may persist to about 43–44 weeks PMA.

Meconium aspiration syndrome (MAS)

• Fetal hypoxic stress causes passage of meconium into amniotic fluid; gasping in utero or at birth draws it into the airways. Most common in term and post-term infants and those with fetal distress.
• Mechanisms: airway obstruction (complete → atelectasis; partial → ball-valve air trapping → hyperinflation and pneumothorax), chemical pneumonitis, surfactant inactivation, and persistent pulmonary hypertension of the newborn (PPHN), in which high pulmonary vascular resistance causes right-to-left shunting through the foramen ovale and ductus arteriosus.

Signs of neonatal respiratory distress (all three conditions)

• Tachypnea (above 60/min), expiratory grunting (the infant closes the glottis to keep alveoli open), nasal flaring, retractions (subcostal, intercostal, substernal), see-saw breathing
• Cyanosis, decreased breath sounds, fine crackles
• Increasing oxygen requirement

Condition-specific clues

• RDS: preterm, progressive worsening over the first 1–3 days
• Apnea: alarms for pauses with bradycardia and desaturation; check color, tone, and temperature during events
• MAS: meconium-stained skin, nails, and cord; barrel-shaped (hyperinflated) chest; possibly post-term appearance
• PPHN: marked cyanosis out of proportion to lung disease; preductal saturation (right hand) higher than postductal (foot)
• Pneumothorax (RDS on ventilation, after surfactant, MAS): sudden deterioration, unequal breath sounds, shifted heart sounds, hypotension, bradycardia

For apnea: cardiorespiratory monitoring with event review; glucose, CBC, blood culture, electrolytes, and cranial ultrasound as indicated to exclude secondary causes.

RDS — prevention and treatment

• Antenatal corticosteroids to the mother when preterm birth is expected, most strongly between 24 and 34 weeks (betamethasone 2 IM doses 24 hours apart, or dexamethasone). They accelerate lung maturity and reduce RDS, IVH, NEC, and death. Maternal hyperglycemia is the main adverse effect.
• CPAP from birth for spontaneously breathing preterm infants — keeps alveoli open (maintains functional residual capacity).
• Exogenous surfactant (e.g., poractant alfa, beractant, calfactant) instilled into the trachea via an endotracheal tube or a thin catheter (less invasive techniques) when oxygen needs rise on CPAP. Adverse effects: transient bradycardia and desaturation, tube obstruction, pulmonary hemorrhage, and air leak as compliance suddenly improves — ventilator pressure and oxygen are weaned promptly. Avoid endotracheal suctioning for a period after dosing per protocol.
• Mechanical ventilation if CPAP fails; gentle ventilation strategies limit lung injury.
• Oxygen targeting: for preterm infants, SpO₂ targets of about 90–95% balance the risks of hypoxia (death) against hyperoxia (retinopathy of prematurity, BPD). Delivery-room resuscitation of preterm infants starts with low oxygen (21–30%) and titrates to minute-specific targets.
• Careful fluids: excess fluid worsens pulmonary edema and promotes a symptomatic patent ductus arteriosus.

Apnea of prematurity

• Caffeine citrate (a methylxanthine) is first-line: it stimulates the respiratory center, increases CO₂ sensitivity, and improves diaphragm function. Label dosing: loading 20 mg/kg caffeine citrate IV or oral, then maintenance 5 mg/kg once daily starting 24 hours later; many units use up to 10 mg/kg/day (caffeine citrate 2 mg = caffeine base 1 mg; verify doses against a neonatal reference).
  • Adverse effects: tachycardia, irritability/jitteriness, feeding intolerance, vomiting; overdose can cause seizures. A possible association with necrotizing enterocolitis is noted in labeling — monitor the abdomen. Hold and notify for tachycardia per unit parameters. Its long half-life means routine levels are usually unnecessary.
  • Benefits beyond apnea: caffeine therapy reduced BPD and improved neurodevelopmental outcomes in trials.
  • Usually stopped around 33–35 weeks PMA once apnea-free; infants are observed for several days off caffeine before discharge.
• Theophylline and aminophylline are older alternatives with a narrow therapeutic range (toxicity: tachycardia, dysrhythmias, seizures).
• CPAP or high-flow nasal cannula reduces obstructive and mixed apnea; ventilation for refractory apnea.
• Treat secondary causes (sepsis, anemia, hypoglycemia, temperature instability).

Meconium-stained amniotic fluid and MAS

• Current resuscitation guidance: a vigorous infant (good tone, breathing or crying) receives routine care. A nonvigorous infant receives the initial steps and positive-pressure ventilation without delay. Routine intubation and tracheal suctioning are no longer recommended, for vigorous or nonvigorous infants; suction under direct view only if the airway is obstructed. Older exam items that require tracheal suctioning of every nonvigorous infant reflect outdated practice.
• Oxygen and ventilation to avoid hypoxia and acidosis (which worsen PPHN), surfactant for severe disease, inhaled nitric oxide for PPHN (selective pulmonary vasodilator; monitor methemoglobin and wean gradually — abrupt stop causes rebound hypoxemia), high-frequency ventilation, and ECMO for refractory cases.
• Minimal handling and sedation per order (agitation raises pulmonary vascular resistance); antibiotics if infection cannot be excluded; therapeutic hypothermia if criteria for hypoxic-ischemic encephalopathy are met.

Listed in priority order.

1. Airway and ventilation
   • Continuous cardiorespiratory monitoring and pulse oximetry; keep alarm limits set appropriately
   • Position with the neck neutral or slightly extended; avoid flexion; suction only as needed (excess suctioning causes hypoxia, bradycardia, and pressure swings)
   • For an apnea event: observe color and heart rate → gentle tactile stimulation (rub back or soles) → reposition airway and clear secretions → increase oxygen as ordered → bag-mask ventilation if no response; document duration, heart rate, SpO₂, and interventions
2. CPAP care
   • Correct prong or mask size and position; alternate prongs and mask and inspect the nasal septum and nares for pressure injury frequently
   • Keep the circuit and humidifier functioning; maintain the seal; an open orogastric tube vents swallowed air
3. Oxygen safety — titrate to the ordered SpO₂ range, avoiding both hypoxia and hyperoxia; analyze delivered FiO₂
4. Recognize air leak — sudden desaturation, unequal breath sounds, hypotension → notify immediately; prepare for needle aspiration or chest tube
5. Thermoregulation and glucose — cold stress increases oxygen consumption and acidosis
6. Fluids and nutrition — strict intake and output, daily weight, parenteral nutrition then gavage feeds; human milk with fortifier once stable
7. Minimal stimulation and clustered care, especially in PPHN
8. Medication monitoring — caffeine: heart rate, feeding tolerance, abdomen; surfactant: vital signs and SpO₂ during and after dosing
9. Family support and education

• Explain equipment and alarms; encourage touch and skin-to-skin care when stable
• Most apnea of prematurity resolves before the baby's due date or soon after; the baby goes home when events have stopped for a safe period
• At home: back to sleep, every sleep; smoke-free environment; avoid overheating
• Home apnea monitors do not prevent SIDS and are used only for specific medical reasons
• Learn infant CPR before discharge
• Report breathing pauses, color change, fast or labored breathing, or poor feeding
• Keep follow-up for eyes, lungs, and development

• RDS = surfactant deficiency → alveolar collapse; signs: tachypnea, grunting, nasal flaring, retractions, cyanosis
• RDS X-ray: ground-glass pattern with air bronchograms; ABG: respiratory + metabolic acidosis
• Prevention: antenatal corticosteroids; treatment: CPAP and surfactant
• After surfactant, watch for pneumothorax and wean ventilator support promptly
• Preterm SpO₂ targets about 90–95% — hyperoxia contributes to ROP and BPD
• Apnea = pause 20 seconds or more, or shorter with bradycardia or desaturation; periodic breathing is normal
• Apnea first action: gentle tactile stimulation, then airway, then bag-mask ventilation
• Caffeine citrate is first-line: watch for tachycardia, irritability, feeding intolerance
• Always rule out sepsis and hypoglycemia in new or worsening apnea
• MAS: term/post-term, hyperinflation with patchy infiltrates, air trapping, PPHN
• Nonvigorous infant with meconium: start ventilation; no routine tracheal suctioning