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V Vickers 2006
APNEA, ALTE
, and SIDS
Valerie Vickers, RNC, BSN
Previous Apnea Program Coordinator
V Vickers 2006
OBJECTIVESAt 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)
V Vickers 2006
APNEA is a nonspecific indicator of distress
Failure of a systemEarly indicator of
deterioration
Many known causes of apnea can be diagnosed and treated.
V Vickers 2006
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.
V Vickers 2006
APNEA Cessation 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
V Vickers 2006
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.
V Vickers 2006
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
V Vickers 2006
THEREFORE:
Mixed apnea occurs frequently in premature infants due to:
increased CNS immaturity (central apnea)
softer chest, weaker diaphragms (obstructive apnea)
V Vickers 2006
PATHOLOGIC APNEA
Apnea > 20 seconds with cyanosis, abrupt, marked pallor or hypotonia, or bradycardia < 100 bpm
V Vickers 2006
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 CO2 and O2 plus prolonged brainstem conduction times result in hypoventilation and hypercarbia
V Vickers 2006
Apnea is Associated with Many Clinical Conditions:
Intraventricular bleedMay see hypoventilation, apnea or respiratory
arrest
Subtle seizuresAlong with fluttering eyelids, drooling or
sucking, tonic posturing
Sepsis Bacterial (GBS, staph. Proteus, Listeria,
Coliforms Viral (RSV, paraflu, herpes, CMV Chlamydial NEC
V Vickers 2006
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
V Vickers 2006
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
V Vickers 2006
TREATMENT OF APNEA
Dependent on Etiology Least invasive Treat underlying causes Non-pharmacologic vs
pharmacologic
V Vickers 2006
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
V Vickers 2006
• May treat more severe AOP with methylxanthines.
• Methylxanthines effect neurotransmitters and increase the transmission of impulses across nerves and synapses.
TREATMENT OF APNEA:
PHARMACOLOGIC
V Vickers 2006
METHYLXANTHINESCAFFEINE
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)
V Vickers 2006
Caffeine is often preferable: More centrally active Not metabolized by the liver 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
V Vickers 2006
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
V Vickers 2006
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
V Vickers 2006
GOAL FOR HOME
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
Goal is to discharge without methylxanthines or monitor
V Vickers 2006
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
V Vickers 2006
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!
V Vickers 2006
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
V Vickers 2006
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 onlyParents are the best monitor; use only when the baby is not observed.
V Vickers 2006
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
V Vickers 2006
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
V Vickers 2006
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
SIDS STATISTICS
V Vickers 2006
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
V Vickers 2006
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)
V Vickers 2006
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”
Research indicates that SIDS is more complex than a single abnormality in a single system.
SIDS RESEARCH CONCLUSIONS
National Institute of Child Health & Human
Development (NICHD)
V Vickers 2006
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
V Vickers 2006
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
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