Neonatology - Apnoea of Prematurity.pptx

Apnoea of prematurity - an important topic to study in Neonatology.

1. Apnoea of Prematurity Dr.K.Kalaniti .

2. Definition Cessation of breathing for >20 seconds or a shorter respiratory pause - if associated with hypoxemia and/or bradycardia in infants < 37 weeks’ gestation. Apnea that lasts for <10 seconds is considered “significant” if it is associated with a decrease in oxygen saturation (SpO 2 ) to ≤80% or 85 %.

3. Types of Apnea Central apnea - immaturity of the central nervous system → ↓CNS stimulation to the respiratory muscles → total cessation of inspiratory effort. Obstructive apnea - cessation of airflow in the presence of continued respiratory efforts → especially at the level of the pharynx. Neck flexion will worsen obstructive apnea. Mixed apnea - Consists of both obstructive and central apnea. Periodic breathing - Periodic breathing is a normal breathing pattern.

4. Incidence The incidence ↑ with decreasing gestational age. born at <29 weeks → 100% develop apnea , by 30 weeks → 85 % and at 34 weeks → 20 % . Mixed is the most common type of apnea (50%), followed by central (40%) and then obstructive (10%).

5. Pathophysiology AOP is a developmental disorder and generally resolves by 36 to 37 weeks in infants born beyond 27 weeks’ gestation . reflects a “physiologic” rather than “pathologic” immature state of respiratory control .

6. Fetal to neonatal transition – chemoreceptors which are set to low O2 levels in Fetal life → when given 100% oxygen before resetting to postnatal life→ delay in spontaneous breathing Ventilatory response to hypoxia - Ventilatory response to laryngeal chemo reflex- Neurotransmitters and apnea-

7. Genetic variability and apnea Sleep-related apnea Siblings of infants with sudden infant death Gastroesophageal reflux and apnea

8. Risk factors AOP - Physiologic immaturity of the respiratory center → usually presents after 1 to 2 days of life. AOP diagnosis must be done after excluding Secondary Causes of Apnea.

9. B. Secondary causes : - Neurologic: Meningitis, ICH Pulmonary: Surfactant deficiency Cardiac: Cyanotic congenital heart diseases Gastrointestinal: Necrotizing enterocolitis (NEC). Hematologic: Anemia. Hypothermia or hyperthermia. Metabolic: Acidosis, hypoglycemia, hypocalcaemia, and hypo- or hypernatremia. Inborn errors of metabolism. Sepsis

10. Management - Pharmacologic management: Methylxanthines – block inhibitory adenosine A 1 receptors with resultant excitation of respiratory neural output. Caffeine citrate has replaced theophylline → once a day regimen / no monitoring of blood levels. Doxapram - potent nonspecific respiratory stimulant of peripheral chemoreceptors at low dose and central chemoreceptors at high dose → administered as a continuous intravenous infusion → effective in reducing apnea when refractory to Methylxanthines.

11. Management – contd. Nonpharmacologic management :- Evidence based :- 1. Prone head-elevated positioning 2. Continuous positive airway pressure 3. Synchronized nasal ventilation

12. Other interventions with unclear efficacy: Orogastric versus nasogastric feeding tube placement Kangaroo mother care Stable environmental temperature Tactile stimulation Red blood cell transfusion Oxygen administration Treating gastroesophageal reflux

13. Prognosis. AOP resolves with maturation. Physiologic basis for resolution of apnea is believed to be myelination of the brainstem . Poor neurodevelopmental outcome is associated with a delay in myelination in infants with AOP. Otherwise , in most infants, apnea resolves without the occurrence of long-term deficiencies.