V Vickers 2005

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 causes 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.

These should not be considered linear events. They overlap but one

is not causative to the next.

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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

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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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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

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THEREFORE:

Mixed apnea occurs frequently in premature infants due to:

increased CNS immaturity (central apnea)

softer chest, weaker diaphragms (obstructive apnea)

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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)

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

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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 OR ALTE

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

pharmacologic

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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

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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 OF APNEA: 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 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

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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 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

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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 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

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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.

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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 STATISTICSCurrently, 0.6 death per 1000

1-2 deaths per 1000 live births per year until the 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 a 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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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)

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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

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SIDS PREVENTION

Failure of arousal mechanism

Ethnicity is a factor ( in blacks)

Back to Sleep campaign

AAP discourages the use of monitors