APNEA,

1. APNEA, ALTE, and SIDS Valerie Vickers, RNC, BSN Previous Apnea Program Coordinator

2. OBJECTIVES At the completion of this talk, the learner will be able to: • Define apnea • Name the most common form of apnea in the premature infant • Distinguish three conditions of an infant that may cause apnea • Recognize two characteristics of an apparent life threatening event (ALTE) • Identify an evidenced-based intervention for the prevention of sudden infant death syndrome (SIDS)

3. APNEA is a nonspecific indicator of distress • Failure of a system • Early indicator of deterioration Many known causes of apnea can be diagnosed and treated.

4. Thought to be benign PB Apnea  SIDS??? PERIODIC BREATHING These should not be considered linear events. They overlap but one is not causative to the next. Definition of Periodic Breathing: 3 or more pauses for greater than 30 seconds duration with less than 20 seconds of respiration between pauses.

5. APNEACessation of respiratory airflow • CENTRAL (40-45%) • No respiratory effort, no nasal airflow • Developmental phenomenon • OBSTRUCTIVE (10-15%) •  respiratory effort, no nasal airflow,  HR • Caused by aspiration, laryngospasm or poor airway control • MIXED (40-45%) • Both obstructive and central

6. Reflex Effects of APNEA • sinus bradycardia • drop in blood pressure • change in cerebral blood flow Apnea and periodic breathing are common in premature infants after the first 24 to 48 hours of life. Premature infants sleep 80% of the time, term infants 50%. Apnea only occurs with active sleep.

7. Factors contributing to decreased inspiratory effort: • CNS immaturity -  # of synaptic connections   sensitivity to CO2 •  activity of protective respiratory reflexes (conserve, rather than breath) •  minute ventilation • diaphragmatic fatigue • soft compliant chest

8. THEREFORE: Mixed apnea occurs frequently in premature infants due to: • increased CNS immaturity (central apnea) • softer chest, weaker diaphragms (obstructive apnea)

9. PATHOLOGIC APNEA Apnea > 20 seconds with cyanosis, abrupt, marked pallor or hypotonia, or bradycardia < 100 bpm

10. APNEA OF PREMATURITY (AOP) AOP is probably caused by abnormality in the central control for breathing: Decreased inspiratory effort and blunted response to CO2 and O2 plus prolonged brainstem conduction times result in hypoventilation and hypercarbia • Developmental characteristics are the primary cause due to poor development of both CNS and airway control • Most common form of apnea in premies • Diagnosis of exclusion • Usually resolves by 37 weeks post conception but occasionally persists for several weeks past term

11. Apnea is Associated with Many Clinical Conditions: • Intraventricular bleed May see hypoventilation, apnea or respiratory arrest • Subtle seizures Along with fluttering eyelids, drooling or sucking, tonic posturing • Sepsis • Bacterial (GBS, staph. Proteus, Listeria, Coliforms • Viral (RSV, paraflu, herpes, CMV • Chlamydial • NEC

12. Congestive Heart Failure • PDA and CHD • Due to decreased lung compliance • Respiratory muscle fatigue • Chest wall distortion • Hypoxemia • Respiratory Distress Syndrome • Due to atelectasis,  work of breathing, fatigue • May lead to chronic lung disease • Anemia • oxygen carrying capacity of blood  • Arterial pressure perfusing CNS  • Polycythemia •  blood viscosity and  blood flow to CNS • begins at 2-4 hours of age

13. High temperature of environment • Feeding problems • overdistention of stomach • aspiration • GER (gastroesphogeal reflux) with or without aspirations • due to laryngospasm • stimulation of irritant receptors in lower esophagus causing ‘reflux apnea’ • some reflux is common (laundry issue only?) • Metabolic conditions • Hypoglycemia • Hypocalcemia • Hypernatremia • Alkalosis • Others • Myelomeningocele • Meningitis

14. TREATMENT OF APNEA • Dependent on Etiology • Least invasive • Treat underlying causes • Non-pharmacologic vs pharmacologic

15. TREATMENT OF APNEA: NON-PHARMACOLOGIC • Tactile stimulation •  neutral ambient temperature • Address feeding issues / GER • Oxygen • Mechanical CPAP / ventilation • CPAP markedly reduces apneic episodes with an obstructive component • Improves patency of upper airway by activation of dilator muscles or by passive splinting

16. TREATMENT OF APNEA: PHARMACOLOGIC • May treat more severe AOP with methylxanthines. • Methylxanthines effect neurotransmitters and increase the transmission of impulses across nerves and synapses.

17. METHYLXANTHINES • CAFFEINE • 2.5 - 5 mg /kg / day once per day (therapeutic range 8-15 mcg/ml) • THEOPHYLLINE • 3-6 mg/kg/day divided in 2 doses per day (therapeutic range 6-12 mcg/ml)

18. METHYLYXANTHINES (cont.) • Caffeine is often preferable: • More centrally active • Not metabolized by the liver • However - many pharmacies do not carry it • Methylxanthines can exacerbate GER - use the right drug for treatment NOTE: Neither drug has had controlled study for efficacy

19. ALTE “APPARENT LIFE THREATENING EVENT” • Frightening event to the observer • Combination of apnea • Color change • Marked change in muscle tone • Over 37 weeks conceptual age

20. Careful Evaluation of EpisodeIndicators for Type of Treatment • Obtain accurate report including feeding and sleeping history • Physical exam, vital signs • Temperature of isolette • CBC, lytes, ABG’s, pulse ox • Blood and viral cultures • Chest xray • Cranial ultrasound • Echocardiogram • pH probe, barium swallow • Placement of feeding tubes (OG/NG) • Computer monitor reports if available • Sleep study

21. GOAL FOR HOME Goal is to discharge without methylxanthines or monitor • For AOP/Apnea: • No apneic events for 5 days • If discharge on methylxanthines, standard in this community is also discharge with monitor • May discharge with monitor only if no other treatment indicated • For ALTE: • May discharge sooner than 5 days if work-up negative and no events

22. HOME MONITORS At Risk Group: • Infants with BW less than 1000 grams • Infants with continued apnea and bradycardia • Infants requiring methylxanthines to control apnea • Infants with severe gastroesophageal reflux • Infants with tracheostomies or technology dependent • Less risk but for family’s peace of mind • Infants with severe BPD requiring oxygen • SIDS sibling or twin of SIDS • Infants with non-repeated ALTE, no cause found

23. CRITERIA FOR SUCCESS OF HOME MONITORING • Training is crucial! • Apnea class including CPR • Caregivers have adequate time to use equipment prior to discharge • Support is imperative! • Support system includes: medical, technical, psychosocial, community support • Choose the right monitor!

24. TERMINATION OF MONITOR USE • AAP says by 43 weeks post conception or “cessation of extreme events” • No significant apnea or repeat of ALTE event for 1-2 months • If on methylxanthines, 1-2 weeks after discontinuation of medications with no significant apnea • Resolution of primary problem MONITORING CANNOT GUARANTEE SURVIVAL

25. MONITORS • Monitors heart rate and respirations • Common settings: Low HR 70 bpm for premie, 60 for term; high HR off; apnea delay 20 seconds • Has a memory, can be printed/analyzed • ON/OFF switch: child-proof, sometimes nurse proof  • Belt must be tight – pad touches skin always • Clean pads with water only Parents are the best monitor; use only when the baby is not observed.

26. SUDDEN INFANT DEATH SYNDROME (SIDS) Sudden death of any infant or young child which is unexplained by history and in which a thorough post mortem fails to demonstrate and adequate cause of death.* *Definition taken from the NIH Consensus Development Conference on Infantile Apnea and Home Monitoring

27. SIDS STATISTICS • Currently, 0.5 death per 1000 • 1.2 deaths per 1000 live births per year 1992 • Back to Sleep campaign in the US • 1994 endorsed side or supine • 1996 endorsed supine only • 0.6 deaths per 1000 in 20

28. SIDS STATISTICS • Ranked 3rd in cause of death in infants older than one month • Congenital anomalies is 1st • Prematurity or low birth weight is 2nd • Most common age for SIDS is 2-4 months • 99% of deaths before 6 months • 1 % of deaths 6-12 months • extremely rare in the 1st month of life • infants have a change in response to hypoxia around 6 months of age

29. SIDS FACTS • SIDS risk for an infant with AOP or who has had an ALTE is at no greater risk than the general population • Premature infants have a slightly greater risk which increases as their gestational age decreases • Home monitoring of infants has NOT decreased the incidence of SIDS • The SIDS sibling is not at greater risk of SIDS than the general population

30. SIDS RESEARCH Research findings: • Supine sleeping position most protective, side lying better than prone but not protective as supine • Overheating contributory • Smoking contributory • Any breastfeeding is protective • Pacifier use is protective • Sleeping in the same place every night is protective • Research indicates SIDS is a malfunction in arousal • CHIME study indicates that normal infants have apnea, bradycardia and desaturations into the 70’s (question then is why they can recover and the infant who dies of SIDS does not)

31. SIDS RESEARCH CONCLUSIONS Research indicates that SIDS is more complex than a single abnormality in a single system. • According to the triple-risk hypothesis, SIDS occurs when three events happen to an infant simultaneously: • “an underlying vulnerability in homeostatic control, • a critical developmental period in state-related homeostatic control • an exogenous stressor(s) that exacerbates the infant’s underlying vulnerability” National Institute of Child Health & Human Development (NICHD)

32. SIDS PHYSIOLOGICAL CHARATERISTICS • tachycardia then bradycardia prior to fatal event – not necessarily proceeded by apneic event • diminished # of breathing pauses •  heart rate variation related to respirations • profuse sweating

33. SIDS PREVENTION • Failure of arousal mechanism • Ethnicity is a factor • Back to Sleep campaign • AAP continues to discourage the use monitors in its 2005 policy statement • includes recommendations regarding pacifier use and sleep environments, some of which is controversial Pediatrics Vol 116, No. 5, November 2005 AWHOON website http://www.awhonn.org/awhonn/?pg=873-8010-18770