1. V Vickers 2005 APNEA, ALTE, and SIDS Valerie Vickers RNC Apnea Program Coordinator UMC

2. V Vickers 2005 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.

3. V Vickers 2005 PERIODIC BREATHING Thought to be benign PB  Apnea  SIDS??? Definition of Periodic Breathing: 3 or more pauses for greater than 30 seconds duration with less than 20 seconds of respiration between pauses. These should not be considered linear events. They overlap but one is not causative to the next.

4. V Vickers 2005 APNEA Cessation of respiratory airflow CENTRAL (40-45%) l No respiratory effort, no nasal airflow l Developmental phenomenon OBSTRUCTIVE (10-15%) l  respiratory effort, no nasal airflow,  HR l Caused by aspiration, laryngospasm or poor airway control MIXED (40-45%) l Both obstructive and central

5. V Vickers 2005 Reflex Effects of APNEA l sinus bradycardia l drop in blood pressure l 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.

6. V Vickers 2005 Factors contributing to decreased inspiratory effort: l CNS immaturity -  # of synaptic connections   sensitivity to CO 2 l  activity of protective respiratory reflexes (conserve, rather than breath) l  minute ventilation l diaphragmatic fatigue l soft compliant chest

7. V Vickers 2005 THEREFORE: Mixed apnea occurs frequently in premature infants due to: l increased CNS immaturity (central apnea) l softer chest, weaker diaphragms (obstructive apnea)

8. V Vickers 2005 PATHOLOGIC APNEA Apnea > 20 seconds with cyanosis, abrupt, marked pallor or hypotonia, or bradycardia < 100 bpm

9. V Vickers 2005 APNEA OF PREMATURITY (AOP) 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 AOP is probably caused by abnormality in the central control for breathing: Decreased inspiratory effort and blunted response to CO 2 and O 2 plus prolonged brainstem conduction times result in hypoventilation and hypercarbia

10. V Vickers 2005 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 l Bacterial (GBS, staph. Proteus, Listeria, Coliforms l Viral (RSV, paraflu, herpes, CMV l Chlamydial l NEC

11. V Vickers 2005 Congestive Heart Failure l PDA and CHD l Due to decreased lung compliance l Respiratory muscle fatigue l Chest wall distortion l Hypoxemia Respiratory Distress Syndrome l Due to atelectasis,  work of breathing, fatigue l May lead to chronic lung disease Anemia l oxygen carrying capacity of blood  l Arterial pressure perfusing CNS  Polycythemia l  blood viscosity and  blood flow to CNS l begins at 2-4 hours of age

12. V Vickers 2005 High temperature of environment Feeding problems l overdistention of stomach l aspiration l 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 l Hypoglycemia l Hypocalcemia l Hypernatremia l Alkalosis Others l Myelomeningocele l Meningitis

13. V Vickers 2005 ALTE “APPARENT LIFE THREATENING EVENT” l Frightening event to the observer l Combination of apnea l Color change l Marked change in muscle tone l Over 37 weeks conceptual age

14. V Vickers 2005 Careful Evaluation of Episode l Obtain accurate report including feeding and sleeping history l Physical exam, vital signs l Temperature of isolette l CBC, lytes, ABG’s, pulse ox l Blood and viral cultures l Chest xray l Cranial ultrasound l Echocardiogram l pH probe, barium swallow l Placement of feeding tubes (OG/NG) l Computer monitor reports if available l Sleep study

15. V Vickers 2005 TREATMENT OF APNEA OR ALTE Dependent on Etiology l Least invasive l Treat underlying causes l Non-pharmacologic vs pharmacologic

16. V Vickers 2005 TREATMENT OF APNEA: NON-PHARMACOLOGIC l Tactile stimulation l  neutral ambient temperature l Address feeding issues / GER l Oxygen l 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

17. V Vickers 2005 May treat more severe AOP with methylxanthines. Methylxanthines effect neurotransmitters and increase the transmission of impulses across nerves and synapses. TREATMENT OF APNEA: PHARMACOLOGIC

18. V Vickers 2005 METHYLXANTHINES CAFFEINE l 2.5 - 5 mg /kg / day once per day (therapeutic range 8-15 mcg/ml) THEOPHYLLINE l 3-6 mg/kg/day divided in 2 doses per day (therapeutic range 6-12 mcg/ml)

19. V Vickers 2005 Caffeine is often preferable: l More centrally active l Not metabolized by the liver l However - many pharmacies do not carry it METHYLYXANTHINES (cont.) NOTE: Neither drug has had controlled study for efficacy Methylxanthines can exacerbate GER - use the right drug for treatment

20. V Vickers 2005 GOAL FOR HOME For AOP/Apnea: l No apneic events for 5 days l If discharge on methylxanthines, standard in this community is also discharge with monitor l May discharge with monitor only if no other treatment indicated For ALTE: l May discharge sooner than 5 days if work-up negative and no events Goal is to discharge without methylxanthines or monitor

21. V Vickers 2005 HOME MONITORS At Risk Group: l Infants with BW less than 1000 grams l Infants with continued apnea and bradycardia l Infants requiring methylxanthines to control apnea l Infants with severe gastroesophageal reflux l Infants with tracheostomies l 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

22. V Vickers 2005 CRITERIA FOR SUCCESS OF HOME MONITORING Training is crucial! l Apnea class including CPR l Caregivers have adequate time to use equipment prior to discharge Support is imperative! l Support system includes: medical, technical, psychosocial, community support Choose the right monitor!

23. V Vickers 2005 TERMINATION OF MONITOR USE Usually by 6 months of age No significant apnea or repeat of ALTE event for 2 months If on methylxanthines, 1-2 weeks after discontinuation of medications and not significant apnea Resolution of primary problem MONITORING CANNOT GUARANTEE SURVIVAL

24. V Vickers 2005 MONITORS l Monitors heart rate and respirations l Common settings: Low HR 70 bpm for premie, 60 for term; high HR off; apnea delay 20 seconds l Has a memory, can be printed/analyzed l ON/OFF switch: child-proof, sometimes nurse proof l Belt must be tight – pad touches skin always l Clean pads with water only Parents are the best monitor; use only when the baby is not observed.

25. V Vickers 2005 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

26. V Vickers 2005 SIDS STATISTICS Currently, 0.6 death per 1000 l 1-2 deaths per 1000 live births per year until the Back to Sleep campaign in the US -  by 40%. l leading cause of death in infants older than one month Most common age for SIDS is 2-4 months l 99% of deaths before 6 months l 1 % of deaths 6-12 months l extremely rare in the 1st month of life l infants have a change in response to hypoxia around 6 months of age

27. V Vickers 2005 SIDS FACTS l SIDS risk for an infant with AOP or who has had an ALTE is at no greater risk than the general population l Premature infants have a slightly greater risk which increases as their gestational age decreases l Home monitoring of infants has NOT decreased the incidence of SIDS l The SIDS sibling is not at greater risk of SIDS than the general population

28. V Vickers 2005 SIDS RESEARCH Research findings : l Supine sleeping position most protective, side lying better than prone but not protective as supine l Overheating contributory l Smoking contributory l Any breastfeeding is protective l Pacifier use is protective l Sleeping in the same place every night is protective l Research indicates SIDS is a malfunction in arousal l 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)

29. V Vickers 2005 Research indicates that SIDS is more complex than a single abnormality in a single system. 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

30. V Vickers 2005 SIDS PREVENTION Failure of arousal mechanism Ethnicity is a factor (  in blacks) Back to Sleep campaign AAP discourages the use of monitors