Apnea of Prematurity: Overview and Practice Questions (2024)

Apnea of Prematurity (AOP) is a common condition affecting preterm infants, characterized by pauses in breathing that last longer than 15-20 seconds and may be accompanied by a drop in heart rate and oxygen levels.

These episodes occur because the brain’s respiratory control center is not yet fully developed in premature babies. Understanding AOP is crucial for caregivers and medical professionals as it can lead to serious complications if not properly managed.

This article provides an overview of apnea of prematurity, its causes, diagnosis, and the treatment strategies used to ensure optimal outcomes for affected infants.

What is Apnea of Prematurity?

Apnea of Prematurity (AOP) is a condition commonly seen in premature infants, where they experience pauses in breathing that last for more than 15-20 seconds. This cessation of breathing may also be accompanied by a decrease in heart rate (bradycardia) and a drop in blood oxygen levels (desaturation).

AOP typically occurs because the part of the brain that controls breathing is not fully developed in premature infants. The condition is most common in babies born before 34 weeks of gestation and usually resolves as the infant’s brain matures, typically by the time they reach 37 weeks post-conceptional age.

Types

Apnea of prematurity (AOP) is categorized into three types:

• Central Apnea: No respiratory effort is made because the brain temporarily fails to send signals to the muscles that control breathing.
• Obstructive Apnea: The infant tries to breathe, but airflow is obstructed, usually due to the collapse of the soft tissues in the airway.
• Mixed Apnea: A combination of both central and obstructive apnea.

Note: Management of AOP may include monitoring in a neonatal intensive care unit (NICU), supportive treatments like continuous positive airway pressure (CPAP), and sometimes medication such as caffeine to stimulate the respiratory center in the brain.

Treatment and Management

The treatment and management of apnea of prematurity (AOP) are tailored to the severity and frequency of the apnea episodes. The main goal is to ensure that the infant maintains normal breathing patterns, stable heart rate, and adequate oxygenation.

Here are common strategies used for managing AOP:

• Continuous Monitoring: Infants with AOP are usually monitored in a neonatal intensive care unit (NICU), where their heart rate, breathing rate, and blood oxygen levels are continuously tracked using cardiorespiratory monitors. This helps healthcare providers quickly respond to any apnea episodes.
• Positioning: Keeping the infant in a prone (belly-down) or side-lying position may improve their breathing, though these positions are only recommended in the NICU under supervision to prevent other risks such as sudden infant death syndrome (SIDS).
• Gentle Stimulation: Tactile stimulation, such as gently rubbing the infant’s back or foot, can help restart regular breathing if an apnea episode occurs.
• Supplemental Oxygen: Some infants may need additional oxygen to maintain proper blood oxygen levels. This can be provided through nasal cannula or oxygen hoods, ensuring the baby gets enough oxygen without overstimulating the lungs.
• Nasal CPAP Therapy: CPAP provides a continuous flow of air through the nose, helping keep the airways open and reducing the chances of airway collapse. This therapy is beneficial, particularly for those with mixed or obstructive apnea.
• Caffeine Citrate: The most commonly used medication for AOP is caffeine citrate. It stimulates the central nervous system and improves respiratory drive, reducing the frequency of apnea episodes. Caffeine therapy is often started shortly after birth and can be continued until the risk of apnea episodes diminishes, typically around 34-37 weeks of post-conceptional age.
• Other Stimulants: In cases where caffeine is not effective, other medications like theophylline may be considered, although they are used less frequently due to potential side effects.
• Mechanical Ventilation: In severe cases where the infant has frequent, prolonged apnea episodes or experiences other respiratory issues, mechanical ventilation may be necessary to ensure proper breathing support.
• Education and Discharge Planning: Parents are educated on recognizing signs of apnea and what to do if an episode occurs. Some infants may be sent home with an apnea monitor if they are still experiencing occasional episodes.
• Follow-up Care: Infants who had AOP may require follow-up care after discharge to monitor their development and ensure that the apnea has resolved.

Apnea of Prematurity typically resolves as the infant matures. Most cases improve by 37 weeks of post-conceptional age as the brain develops further and gains better control over the breathing process.

Effective management includes a combination of monitoring, supportive care, and, if needed, pharmacological treatment to reduce apnea episodes and ensure the infant’s safety and development.

Apnea of Prematurity Practice Questions

1. What is characterized by cycles of hyperventilation followed by short apneic pauses of less than 3 seconds?
Periodic breathing

2. What is the purpose of central chemoreceptors?
To increase ventilation in response to a low pH in the cerebrospinal fluid.

3. How is apnea of prematurity defined clinically?
Apnea of prematurity is defined as a cessation of breathing lasting longer than 20 seconds, accompanied by bradycardia and hypoxemia lasting more than 10 seconds.

4. What are the detrimental consequences of apnea in neonates?
Hypoxemia, hypercarbia, and bradycardia.

5. What long-term treatments are available to treat or prevent apnea of prematurity?
Treatments include methylxanthine therapy, nasal cannula use, blood transfusions, NCPAP (nasal continuous positive airway pressure), and caffeine citrate.

6. At what age do most infants resolve apnea issues?
Most infants resolve apnea by 37 weeks postmenstrual age.

7. What risk factors increase the likelihood of more severe bronchopulmonary dysplasia?
Surfactant therapy and nosocomial infections are key risk factors.

8. What strategies should be considered for treating respiratory distress syndrome to minimize the risk of bronchopulmonary dysplasia?
Maintaining arterial oxygen tension above 90 mmHg, administering surfactant before mechanical ventilation, and extubating to NIPPV within the first month of life.

9. What is essential for optimal cell and tissue growth?
Vitamin A

10. What is the diuretic of choice for ventilator-dependent infants with evolving or established bronchopulmonary dysplasia (BPD)?
Thiazide diuretics

11. What is apnea of prematurity (AOP)?
A sudden cessation of breathing lasting at least 20 seconds, often accompanied by bradycardia or oxygen desaturation, occurring in infants younger than 37 weeks gestation.

12. What are the causes of apnea in premature infants?
Causes include improper neural signaling and airway obstruction.

13. What is periodic breathing?
A benign, abnormal breathing pattern characterized by cycles of hyperventilation followed by short apneic pauses of less than 3 seconds.

14. What two factors can stimulate apnea of prematurity?
High-humidity cannula and caffeine.

15. When is CPAP indicated?
CPAP is indicated for treating obstructions, such as those caused by enlarged tonsils.

16. What are the three classifications of apnea of prematurity (AOP)?
Central apnea, obstructive apnea, and mixed apnea.

17. What causes central apnea?
Central apnea is caused by a dysfunction in the brainstem’s nerve centers that send signals to the respiratory muscles, resulting in no observed effort to inspire.

18. How is central apnea treated?
It can be treated with caffeine.

19. What characterizes obstructive apnea?
It involves an attempt to ventilate, evidenced by chest wall movement but without gas entry, typically due to upper airway obstruction.

20. What is the condition of the airway in obstructive apnea, and what is the treatment?
The airway is floppy, and CPAP is the recommended treatment.

21. What is mixed apnea?
Mixed apnea involves obstructive respiratory efforts that typically follow central pauses and is considered the most common type of apnea in premature infants.

22. What is the treatment for mixed apnea?
Treatment includes caffeine administration and CPAP.

23. What is the primary role of the respiratory control system?
To regulate ventilation in order to meet the body’s oxygen requirements and expel carbon dioxide effectively.

24. Where does the control of ventilation occur?
Ventilation control takes place in the brainstem.

25. What is the dysfunction of the respiratory control system?
It is the main cause of the central apnea component in apnea of prematurity (AOP).

26. What medications are used to treat apnea of prematurity?
Methylxanthines, primarily caffeine.

27. What do methylxanthines do?
They stimulate respiratory drive, increase diaphragmatic activity and ventilation (VE), enhance chemoreceptor sensitivity to CO2, reduce periodic breathing, minimize hypoxic respiratory depression, elevate metabolic rate and oxygen consumption, and promote diuresis.

28. How can anemia, which can cause irregular breathing in preterm infants, be alleviated?
Blood transfusions, as they improve oxygen-carrying capacity.

29. How is a nasal cannula used to prevent obstructive apnea?
It provides mild positive pressure in the upper airway to prevent collapse.

30. How does a nasal cannula help prevent central apnea?
It stimulates the nares tactically, reducing the incidence of central apnea.

31. What role does noninvasive ventilation play in treating apnea of prematurity?
NCPAP and NIPPV deliver positive pressure, reducing the likelihood of upper airway collapse.

32. How can body positioning help with apnea of prematurity?
Prone positioning can improve thoraco-abdominal synchrony and stabilize the chest wall, aiding in breathing.

33. What kind of stimulation can help in cases of apnea of prematurity?
Both tactile and kinesthetic stimulation can be beneficial.

34. What are the treatments for apnea of prematurity?
Treatments include blood transfusions, nasal cannula use, noninvasive ventilation, body positioning, and stimulation.

35. What is the NICU’s observation period before discharge for an apnea-free time?
Typically 3–8 days after discontinuing caffeine citrate.

36. Can premature infants be sent home with caffeine citrate?
Yes, it is provided alongside a home cardiorespiratory monitor.

37. What is essential before discharging a baby with apnea of prematurity?
Family education and training, including a basic life support course, are crucial.

38. What is bronchopulmonary dysplasia (BPD)?
A chronic lung disease defined as the need for supplemental oxygen for at least 28 days after birth, evaluated at discharge or near the infant’s estimated full-term age.

39. What impact does intubation have on lung development?
Intubation can slow lung development.

40. What constitutes mild bronchopulmonary dysplasia?
No requirement for supplemental oxygen at the time of evaluation (28 days after birth).

41. What constitutes moderate bronchopulmonary dysplasia?
Requiring FiO2 <30% and/or positive pressure ventilation (PPV) or NCPAP at the time of evaluation.

42. What constitutes severe bronchopulmonary dysplasia (BPD)?
Requiring FiO2 >30% and/or PPV or NCPAP at the time of evaluation.

43. What does dysplasia mean in the context of lung development?
It refers to abnormal growth or development of the airways.

44. What factors contribute to the development of new BPD?
Gestational age <28 weeks, birth weight <1000 grams, hypothermia at admission, hypotension at admission, respiratory distress syndrome (RDS), prolonged mechanical ventilation, hypercarbia, surfactant therapy, higher fluid intake, nosocomial infections, more than two blood transfusions, and maternal preeclampsia.

45. What are the characteristics of severe BPD?
Severe BPD is associated with acidosis at admission, the need for surfactant therapy, nosocomial infections, PDA, oligohydramnios, and an Apgar score of <6 at 5 minutes.

46. What is the management and treatment for bronchopulmonary dysplasia (BPD)?
Key strategies include preventing premature birth, minimal oxygen use, administration of exogenous surfactant, open lung ventilation, gentle ventilation techniques, corticosteroids, caffeine citrate, mast cell stabilizers, inositol, antioxidants, inhaled nitric oxide, treating pulmonary edema, fluid restriction, diuretics, and bronchodilators.

47. What is the prognosis for individual patients with BPD?
The prognosis is unpredictable and can vary widely between patients.

48. What do infants with BPD exhibit?
They often show some degree of obstructive lung disease that can persist into adolescence and young adulthood.

49. What challenges do BPD patients often face?
Frequent hospitalizations, abnormal pulmonary function test (PFT) results, and the need for supplemental oxygen at home.

50. How are spirometry values in BPD survivors?
Spirometry values in BPD survivors are consistently lower than normal.

51. What common issues do infants with BPD experience?
They frequently have respiratory exacerbations, recurrent respiratory symptoms, and infections.

52. What medications are used for BPD management?
Common medications include oxygen, diuretics, and respiratory drugs.

53. What is neurocognitive dysfunction in the context of BPD?
BPD is a major predictor of poor neurodevelopmental outcomes, including an increased risk of cerebral palsy, developmental delays, and poor neuromotor function at 6 months of age.

54. What is apnea of prematurity (AOP)?
AOP is a sudden cessation of breathing lasting at least 20 seconds, often accompanied by bradycardia or oxygen desaturation, in an infant younger than 37 weeks gestation.

55. What are the causes of apnea in premature infants?
The main causes are improper neural signaling and upper airway obstruction.

56. What is AOP caused by?
AOP results from the physiological immaturity of the neurological and chemical receptor systems responsible for regulating respiration and responding to hypoxemia and hypercapnia.

57. What is periodic breathing?
A benign, abnormal breathing pattern characterized by cycles of hyperventilation followed by short apneic pauses of less than 3 seconds.

58. How can AOP be classified?
It can be classified as central, obstructive, or mixed apnea.

59. What is central apnea?
Central apnea is caused by a dysfunction in the brainstem’s nerve centers, preventing signals from reaching the respiratory muscles, with no attempt at inspiration observed.

60. What is obstructive apnea?
Obstructive apnea involves an attempt to breathe, with chest wall movement but no gas entry, typically due to upper airway obstruction.

61. What is mixed apnea?
Mixed apnea features obstructed respiratory efforts that usually follow central pauses and is considered the most common type of apnea.

62. What is the primary role of the respiratory control system?
The primary role is to regulate ventilation to meet the body’s oxygen needs and remove carbon dioxide.

63. Where does the control of ventilation occur?
Ventilation control occurs in the brainstem, with contributions from central and peripheral chemoreceptors.

64. What is the primary cause of the central apnea component of AOP?
The primary cause is a dysfunction of the respiratory control system.

65. What is a nasal cannula used for?
A nasal cannula provides mild positive pressure in the upper airway to prevent obstructive apnea and serves as tactile stimulation in the nares to prevent central apnea.

66. What is noninvasive ventilation?
Noninvasive ventilation, including NCPAP and NIPPV, provides positive pressure that helps prevent upper airway collapse.

67. How does body positioning help in managing apnea of prematurity?
Prone positioning can enhance thoraco-abdominal synchrony and stabilize the chest wall, aiding in better breathing patterns.

68. What is a significant developmental milestone for premature infants?
The resolution of apnea and the establishment of a normal respiratory pattern.

69. How long is the required observation period in the NICU before discharge?
Typically 3 to 8 days, after discontinuation of caffeine citrate.

70. What can premature infants be sent home with to manage apnea?
Caffeine citrate and a home cardiorespiratory monitor.

71. What role does family play in the discharge process of a preterm infant?
Family education and training are crucial, including a basic life support course prior to discharge.

72. What is bronchopulmonary dysplasia (BPD)?
BPD is a chronic lung disease defined as the need for supplemental oxygen for at least 28 days after birth, assessed either at discharge or when the infant reaches an estimated full-term age.

73. When is BPD evaluated?
At 36 weeks postmenstrual age or discharge to home (whichever comes first), or between 28 and 56 days postnatal age or discharge (whichever comes first).

74. What characterizes mild BPD?
No supplemental oxygen requirement at the time of evaluation.

75. What defines moderate BPD?
The need for FiO2 ≤ 0.30 and/or positive pressure ventilation (PPV) or NCPAP at the time of evaluation.

76. What defines severe BPD?
The requirement for FiO2 > 0.30 and/or PPV or NCPAP at the time of evaluation.

77. What are the risk factors for developing BPD?
Gestational age ≤ 28 weeks, birth weight ≤ 1,000 grams, hypothermia or hypotension at admission, RDS, prolonged mechanical ventilation, hypercarbia (PaCO2 > 50 mmHg), exogenous surfactant therapy, high fluid therapy, nosocomial infection, multiple blood transfusions, chorioamnionitis, preeclampsia, admission acidosis, PDA, oligohydramnios, and an Apgar score < 6 at 5 minutes.

78. What are the airway characteristics of BPD?
Features include fibroproliferative injury, smooth muscle hyperplasia, variable muscle amounts, and minimal damage.

79. What are the alveolar characteristics of BPD?
Alveolar fibrosis, emphysematous changes, heterogeneous atelectasis, overinflation, hypoplasia, fewer and larger alveoli, and limited direct damage evidence.

80. What are the pulmonary vasculature characteristics of BPD?
Basement membrane thickening, increased alveolar-capillary (A-C) membrane distance, reduced vasculature, and lower A-C membrane area.

81. What is the management and treatment for BPD?
Strategies include preventing premature birth, minimal oxygen use, exogenous surfactant, open lung and gentle ventilation strategies, corticosteroids, caffeine citrate, mast cell stabilizers, vitamin A, inositol, antioxidants, inhaled nitric oxide, treating pulmonary edema, fluid restriction, diuretics, and bronchodilators.

82. What is the prognosis for BPD patients?
The prognosis can be unpredictable and varies widely among patients.

83. What symptoms do infants with BPD exhibit?
They often show obstructive lung disease that may persist into adolescence and adulthood.

84. What common medical needs do BPD patients have?
Frequent hospitalizations, abnormal pulmonary function tests, and the requirement for home supplemental oxygen.

85. What spirometry results are typically lower in BPD patients?
Lower FEV1, FVC, and forced expiratory flow at 25-75% of FVC, indicating substantial airway obstruction and alveolar hyperinflation.

86. Do BPD patients often need home oxygen?
Yes, studies show around 40% of preterm infants diagnosed with BPD require home oxygen.

87. What are respiratory exacerbations in BPD patients?
Frequent and recurring respiratory symptoms and infections, requiring specialized care from pulmonologists and neonatologists, as well as treatment with oxygen, diuretics, and respiratory medications.

88. What is neurocognitive dysfunction related to BPD?
BPD is a significant predictor of poor neurodevelopmental outcomes, including higher rates of cerebral palsy, developmental delays, and poor neuromotor performance at 6 months of age.

89. What is the economic impact of BPD on families?
Chronic health issues related to BPD can significantly impact a family’s quality of life and finances due to costs associated with prescriptions and respiratory care.

90. What additional symptoms may accompany apnea of prematurity?
Hypoxemia and bradycardia.

91. What factors contribute to the development of apnea of prematurity?
Prematurity, underdeveloped central nervous system, immature respiratory muscles, and inadequate response to hypoxia and hypercapnia.

92. How does hypoxia influence apnea of prematurity?
Hypoxia can suppress the respiratory drive, leading to episodes of apnea in premature infants.

93. Why is caffeine citrate commonly used for treating apnea of prematurity?
Caffeine citrate acts as a central nervous system stimulant that increases respiratory drive and enhances diaphragmatic function.

94. How does oxygen therapy help in managing apnea of prematurity?
Supplemental oxygen can help maintain adequate oxygen levels and reduce the frequency of apneic episodes.

95. What is the role of continuous positive airway pressure (CPAP) in apnea of prematurity?
CPAP provides positive airway pressure to keep the upper airway open, preventing obstructive apnea and stabilizing breathing patterns.

96. How does thermal regulation impact apnea of prematurity?
Maintaining an optimal body temperature can help prevent metabolic stress and reduce apneic events.

97. What non-pharmacological interventions are used for managing apnea of prematurity?
Tactile stimulation, appropriate positioning, and optimizing environmental conditions such as temperature and noise levels.

98. How is apnea of prematurity diagnosed?
Diagnosis is based on clinical observation of cessation of breathing for >20 seconds, often accompanied by bradycardia and/or oxygen desaturation.

99. What monitoring is essential for infants with apnea of prematurity?
Continuous cardiorespiratory monitoring to detect apneic episodes, bradycardia, and oxygen desaturation.

100. Why is it important to differentiate between central, obstructive, and mixed apnea in premature infants?
Differentiating between the types helps guide appropriate treatment strategies, such as the use of CPAP for obstructive apnea or caffeine for central apnea.

Final Thoughts

Apnea of Prematurity, while concerning, is a condition that typically resolves as an infant’s brain matures. Through comprehensive monitoring, supportive care, and targeted treatments like caffeine therapy, most infants overcome AOP without long-term complications.

Advances in neonatal care have significantly improved the management of this condition, enhancing survival rates and developmental outcomes for preterm infants.