Apnea of prematurity

1. M.D .( Paed ) D.N.B . KIMSDU KARAD DR CHANDRASHEKHAR A UNDHAKAR

2. Apnea of Prematurity AOP is a developmental disorder that self-resolves . In most cases, AOP likely reflects a “physiological” rather than a “pathological” immature state of respiratory control . AOP is related inversely to gestational age. 7 % of neonates with GA of 34-35weeks 15% of neonates with GA of 32-33weeks 54% of neonates with GA of 30-31 weeks Nearly 100% neonates with GA of < 29 weeks or weight < 1000gm

3. Apnea of prematurity C essation of breathing in excess of 15-20 seconds’ duration T ypically accompanied by desaturation and bradycardia . In Infant less than 37 weeks gestational age.

4. Apnea of prematurity

5. Apnea of prematurity

6. Apnea is classified into three categories based on the presence or absence of upper airway obstruction: Central Obstructive Mixed apneas .

7. Central Apnea A pause in alveolar ventilation due to a lack of diaphragmatic activity . There is no signal to breathe being transmitted from the CNS to the respiratory muscles . This is due to immaturity of brainstem control of central respiratory drive. The premature infant also manifests an immature response to peripheral vagal stimulation .

8. Obstructive Apnea A pause in alveolar ventilation due to obstruction of airflow within the upper airway, particularly at the level of the pharynx. Once collapsed, mucosal adhesive forces tend to prevent the reopening of the airway during expiration . Neck flexion will worsen this form of apnea. Excessive secretions in the nasopharynx and hypopharynx may also cause obstructive apnea.

9. Mixed Apnea A combination of both types of apnea representing as much as 50% of all episodes. Mixed apnea consists of obstructed respiratory efforts usually following central pauses . Central apnea is either preceded or followed by airway obstruction.

10. Apnea of Prematurity Periodic Breathing regular , recurring cycles of breathing of 10 to 15 seconds’ duration that are interrupted by pauses of at least 3 seconds in duration . benign respiratory pattern for which no treatment is required the respiratory pauses appear to be self-limited, and ventilation does continue , albeit cyclically. Apnea of Prematurity infants who have prolonged apnea may fail to reinitiate ventilation entirely or do so ineffectively . the respiratory pauses during apnea are associated with swallowing movements

11. Causes of Apnea ( All Types) Infection - Sepsis, especially in the first day of life, and nosocomial infections and/or NEC in the first weeks of life Neurological - Intraventricular hemorrhage, intracranial hemorrhage, neonatal seizures, perinatal asphyxia Cardiovascular - Impairment of oxygenation from congestive heart failure and pulmonary edema (PDA, coarctation , etc.), or from shunting (cyanotic heart disease) Pulmonary - Impairment of oxygenation and ventilation from lung disease (surfactant deficiency disease, pneumonia, transient tachypnea of the newborn, meconium aspiration, etc.) Inborn Errors of Metabolism

12. Causes of Apnea ( All Types) Metabolic - Hypocalcemia , hypoglycemia, hyponatremia or acidosis Hematological - Anemia Gastrointestinal - NEC or gastroesophageal reflux Temperature Regulation - Hypothermia or hyperthermia Drugs - Prenatal exposure with transplacental transfer to the neonate of various drugs (narcotics, beta-blockers). Postnatal exposure to sedatives, hypnotics or narcotics.

13. Evaluation of a child with apnoea Investigations To exclude common causes of secondary apnea . Investigations that should be considered include blood glucose, hematocrit , electrolytes, septic screen, blood culture, arterial blood gas, chest x-ray, abdominal x-ray, ultrasound head and other investigations depending on the history and physical examination.

14. Treatment of apnoea General measures : · Maintain airway, breathing and circulation (ABC) · Avoid vigorous suctioning of the oro -pharynx · Avoid oral feeds for at least 24 hours. · Adjust environmental temperature. Avoid swings in environmental temperature. · Treatment of the underlying cause: sepsis, anemia , polycythemia , hypoglycemia , hypocalcemia , respiratory distress syndrome (RDS). · Transfuse packed cells if hematocrit <30%. Specific measures · Drugs including aminophylline, caffeine, doxapram Continuous positive airway pressure (CPAP) · Mechanical ventilation

15. Emergency treatment The neonate should be checked for bradycardia, cyanosis and airway obstruction. The neck should be positioned in slight extension; oro -pharynx gently suctioned Tactile stimulation should be given. Most apneic spells respond to tactile stimulation. Provide oxygen if patient is hypoxic (maintain saturation 92-95%) by head box or nasal cannula. If the newborn continues to remain apneic and does not respond to tactile stimulation, ventilation with bag and mask (BMV) using 100% oxygen should be initiated. If BMV fails to initiate spontaneous respiration in the newborn , then the infant should be managed with positive pressure ventilation.

16. Key determinants in choosing the appropriate drug . Ease of administration , rapid response, Minimal side effects , predictable plasma concentrations.

17. Methylxanthines These agents also work by competitively antagonizing the adenosine receptor or increasing catecholamine release by modulating the flux of calcium . Other effects include improving ventilation and neural impulses, reducing rapid eye movement (REM) sleep , improving oxygenation, and improving skeletal muscle contraction to prevent diaphragmatic fatigue

18. Maior Effects of Methylxanthines Regularized breathing pattern Increased ventilatoty drive Increased chemoreceptor sensitivity to carbon dioxide Decreased REM sleep Increased blood glucose Improved diaphragmatic contractility Stimulation of the CNS at all levels Antagonism of adenosine, a neurotransmitter Increased renal blood flow and diuresis Augmentation of the basal metabolic rate Stimulation of gastric secretion and decreased esophageal sphincter tone

19. Methylxanthines If administered orally, they are best given with feedings. Because the daily caffeine dose often disrupts the infant’s sleep pattern at night, it should not be given in the afternoon . Intake and output should be monitored because methylxanthines can cause mild diuresis . Stools should be checked for occult blood because these drugs (especially theophylline ) can cause gastric irritation and, in some cases , lead to necrotizing enterocolitis . Persistence of apnea is a sign that drug levels are not appropriate or that an underlying problem , (e.g., sepsis, reflux, or neurologic deficit) may exist.

20. Complications of AOP S pastic diplegia or quadriplegia Bilateral retrolental fibroplasia resulting in significant visual impairment S ensorineural deafness Varying degrees of mental retardation,

21. Surveillance AOP All newborns less than 34 weeks gestational age, or less than 1800 grams birth weight, should be monitored for both apnea and bradycardia. Bradycardia by itself is often a sign of obstructive apnea. No apnea alarm is sounded because the chest wall is moving even through air flow is absent. Also reflex apnea can lead to bradycardia within 2 seconds of onset thus setting off the cardiac alarm 10 to 15 seconds ahead of the apnea alarm.