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• Prematurity can lead to several complications at birth
• These include Respiratory Distress Syndrome (RDS), Apnea of Prematurity (AOP), Bronchopulmonary Dysplasia (BPD), Patent Ductus Arteriosus (PDA), Necrotizing Enterocolitis (NEC), Intraventricular Hemorrhage (IVH), and Retinopathy of Prematurity (ROP).

Respiratory Distress Syndrome (RDS)

• RDS is characterized by severely impaired respiratory function in immature lungs due to a lack of surfactant, leading to low alveolar compliance.
• Symptoms include abnormal breathing patterns, substernal retractions, grunting, nasal flaring, and respiratory acidosis.
• RDS was first characterized as hyaline membrane disease (HMD) in the early 20th century, thought of as rare pneumonia
• A decrease in surfactant production causes low alveolar compliance, which is the biggest issue in RDS
• Pathophysiology includes increased distance between alveolar spaces and capillaries, overly compliant chest wall, and lung hypoplasia.
• Interventions include ensuring trained personnel, maintaining a room temperature between 23°C−26°C, use of a chemically activated warming pad or prewarmed radiant warmer, and placing the newborn in a food-grade polyethylene bag immediately after birth to maintain thermal stability.
• Transport newborns in a transport incubator and administer oxygen using an air-oxygen blender, continuously monitoring oxygenation with pulse oximetry.
• Handle infants gently to minimize stress and prevent complications, avoid the Trendelenburg position, and prevent rapid fluid infusions.
• Provide noninvasive CPAP at 5-6 cmH2O, initiate PPV at 20–25 cm H2O if necessary, and administer surfactant early
• CPAP provides alveolar stability and increases FRC for babies with surfactant deficiency
• PPV is needed if CPAP can't provide adequate oxygenation using 20-25 cmH2O
• PEEP is provided at 5 cmH2O if intubated

Apnea of Prematurity (AOP)

• AOP is a sudden cessation of breathing for at least 20 seconds, or is accompanied by bradycardia or oxygen desaturation lasting ≥ 4 seconds, in an infant younger than 37 weeks gestational age (WGA).
• Apnea for at least 10 seconds with a HR < 100BPM or SpO2 < 80% is also considered AOP
• This is usually caused by immature neurological and chemical receptor systems.
• Types include central, obstructive, and mixed apnea.
• Untreated AOP can lead to neurodevelopmental outcomes.
• AOP Can be identified as a sign of underlying pathology such as sepsis
• Periodic breathing is a common but benign form of abnormal breathing, with cycles of hyperventilation followed by short apneic pauses of <3 seconds
• Central apnea is caused by a dysfunction of the nerve centers in the brainstem.
• Obstructive apnea is characterized by some attempt to ventilate, with chest wall movement but without gas entry.
• Mixed apnea consists of obstructed respiratory efforts following central pauses and is the most common type of apnea.
• Low FRC coupled with relatively high metabolic rates will cause a rapid onset of hypoxemia following cessation of breathing
• The immature respiratory-control system is centered in the brainstem, leading to central apnea and contributing to episodes of hypoxemia and hypercapnia.
• Monitoring includes abdominal pressure sensors to detect movement cessation and transthoracic impedance pneumonography to measure respiratory changes via chest electrodes.
• Methylxanthines, like caffeine citrate, are stimulant medications used to treat AOP
• A caffeine citrate is safer with a lower risk of toxicity, and reduces the risk of BPD, Surgical intervention for PDA, and long-term neurodevelopmental impairments compared to theophylline
• Tactile and kinesthetic stimulation are immediate interventions for apnea.
• Blood transfusions may reduce apnea episodes in anemic preterm infants by improving O2-carrying capacity.
• Nasal CPAP (NCPAP) prevents upper-airway collapse and is more effective for obstructive apnea.
• Body positioning (proning) can improve thoraco-abdominal synchrony and stabilize the chest wall, but is not recommended at home to reduce the risk of SIDS
• AOP typically resolves by 37 weeks PMA, some can remain present until 43-44 PMA
• Families of infants learn stimulation techniques and are reassured AOP does not increase SIDS risk
• Long term Prolonged apnea & bradycardia can lead to cerebral hypoperfusion and hypoxic-ischemic injury
• Caffeine citrate has a clear benefit in helping to reduce BPD

Bronchopulmonary Dysplasia (BPD)

• Babies are diagnosed with BPD by their need for an FiO2 >28% for at least 28 days
• Diagnosed in neonates needing supplemental oxygen for at least 28 days after birth, or assessed when the baby is close to their estimated full-term age.
• Severity is assigned based on FiO2 needs and/or positive pressure ventilation (PPV) or nasal continuous positive airway pressure (NCPAP) at the time of evaluation:
  • Mild if no supplemental oxygen is required at the time of evaluation
  • Moderate if with FiO2 ≤ 30% and/or PPV or NCPAP
  • Severe if FiO2 ≥ 30% and/or PPV or NCPAP
• Risk factors include prematurity (≤ 28 WGA), low birth weight (≤ 1000g), hypothermia, hypotension, and hypercarbia
• New BPD is caused by abnormal lung development from birth, leading to alveolar hypoplasia, arrested airway/alveolar growth and impaired pulmonary vascularization.
• In preterm infants ≤ 30 WGA, normal alveolar and capillary growth is interrupted, leading to reduced overall gas exchange capacity.
• The only guaranteed method of prevention is to prevent premature birth, as BPD develops due to lung immaturity

Patent Ductus Arteriosus (PDA)

• PDA occurs when the ductus arteriosus, a fetal blood vessel connecting the aorta and pulmonary artery, remains open after birth.
• This leads to abnormal blood flow between the aorta and pulmonary artery.
• Characterized by allowing abnormal blood flow between the aorta and pulmonary artery
• Normally the ductus arteriosus functionally closes within 24-48 hr after birth, but may take up to 2-3 months in preterm infants
• In utero PDA shunts the blood away from the lungs in a right-to-left shunt and stays open from low PaO2 and high prostaglandins
• In premature infants, the DA remains open due to immature vascular tissue and higher circulating prostaglandin levels.
• The DA tissue itself is highly sensitive to prostaglandin-induced relaxation, making closure more difficult.
• If PVR remains elevated, a right-to-left shunt may develop, causing hypoxia and worsening oxygenation instability.

Necrotizing Enterocolitis (NEC)

• NEC is a serious complication of prematurity affecting the GI tract.
• Preterm infants have immature host defenses and impaired inflammatory regulation, resulting to a higher risk of NEC.
• Can be transferred through breast milk to the baby
• Despite being a complication of prematurity, full-term infants can also develop this complication.
• Premature infants are prone to NEC due to immature host defenses and impaired inflammatory regulation
• Early signs include mild feeding intolerance, and severe symptoms include GI symptoms, temperature instability, and tachypnea

Intraventricular Hemorrhage (IVH)

• IVH is bleeding within the brain's ventricles, primarily occurring in the germinal matrix
• Premature infants (23-25 weeks WGA) are at the highest risk due to fragile blood vessels and rapid fluctuations in cerebral blood flow.
• Causes of altered cerebral blood flow include sepsis, acidosis, and hypoxemia
• Management includes adjusting PIP to maintain a pH of 7.25-7.35 and a PaCO2 of 45-55mmHg

Retinopathy of Prematurity (ROP)

• ROP is a complication caused by disruption of normal retinal vessel development from premature birth.
• Risk factors include early gestational age, low birth weight, and duration of mechanical ventilation.
• Safe oxygen delivery practices are critical in preventing ROP progression.