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APNEA, ALTE

, and SIDS

Valerie Vickers RNCApnea Program Coordinator, UMC

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APNEA is a nonspecific indicator of distress

Failure of a systemEarly indicator of

deterioration

Many known cause of apnea can be diagnosed and treated.

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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.

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APNEA Cessation of respiratory airflow

CENTRAL No respiratory effort, no nasal airflow Developmental phenomenon

OBSTRUCTIVE respiratory effort, no nasal airflow, HR Caused by aspiration, laryngospasm or

poor airway control

MIXED Both obstructive and central

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PERCENTAGE OF APNEA: Central 40-45% Obstructive 10-15% Mixed 40-45%

More premature = more mixed

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INCIDENCE OF APNEA:

•25 % of infants under 2500 grams at birth•80% of infants under 1000 grams at birth•25% of infants of all gestational ages (Rigatto)

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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.

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CNS Immaturity

number of synaptic connections and incomplete dendritic arborization - cause sensitivity of respiratory center to CO2

therefore in afferent traffic to reticular formation and reduction and fluctuation of respiratory center output

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Other factors contributing to decreased inspiratory effort:

activity of protective respiratory reflexes

minute ventilation diaphragmatic fatigue soft compliant chest

Therefore mixed apnea occurs

frequently in premies.

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PATHOLOGIC APNEA

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

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APNEA OF PREMATURITY (AOP)

Premature infants who never had AOP or whose AOP has resolved

ASYMPTOMATIC PREMATURE INFANTS

PB with pathologic apnea in a premature infant Diagnosis of exclusion Usually resolves by 37 weeks post conception but

occasionally persists for several weeks past term

SYPMTOMATIC PREMATURE INFANTS Premature infants who continue to have

pathologic apnea at the time when they otherwise would be ready for discharge

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If no other cause found, the diagnosis is AOP.

Diagnosis of exclusion Most common form of apnea in premies Developmental characteristics are primary

cause due to poor development of both CNS and airway control

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

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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

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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

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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

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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

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Careful Evaluation of Episode 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

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TREATMENT OF APNEA

Dependent on Etiology Least invasive Treat underlying causes Non-pharmacologic vs

pharmacologic

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TREATMENT: 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

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• May treat more severe AOP with methylxanthines.

• Methylxanthines effect neurotransmitters and increase the transmission of impulses across nerves and synapses.

TREATMENT: PHARMACOLOGIC

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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)

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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

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GOAL: HOME DRUG FREE

Goal is to discharge without methylxanthines

No apneic events for 5 days If discharge on methylxanthines,

standard in this community is also discharge with monitor

May discharge with monitor only and no medications (rare)

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HOME MONITORS

At Risk Group: Infants less than 1000 grams Infants who continue to apnea and

bradycardia Infants requiring methylxanthines to

control apnea Infants with severe reflux Infants with tracheostomies 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

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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!

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TERMINATION OF MONITOR USE

Usually by 6 months of age No significant apnea 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

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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

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SIDS STATISTICS1-2 deaths per 1000 live births per year

with Back to Sleep campaign in the US - by 40%

leading cause of death in infants older than one month

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 change in response to hypoxia

around 6 months of age

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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

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Research indicates that SIDS is more complex than a single abnormality in a single system.

SIDS PREVENTION

Failure of arousal mechanism

Ethnicity is a factor

Back to Sleep campaign

AAP discourages the use of monitors

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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 Research indicates SIDS is a malfunction in arousal CHIME study indicates that normal infants have

apnea, bradycardia and desaturations into the 70’s - question why they can recover and the infant who dies of SIDS does not

Tachycardia then bradycardia prior to fatal event - not necessarily proceeded by apneic event

Research indicates that SIDS is more complex than a single abnormality in a single system.