APNEA, - University of Arizona Department of Pediatrics
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Transcript APNEA, - University of Arizona Department of Pediatrics
APNEA,
ALTE,
and SIDS
Valerie Vickers, RNC, BSN
Previous Apnea Program Coordinator
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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)
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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.
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PERIODIC BREATHING
•Thought to be benign
•PB Apnea SIDS???
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.
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APNEA
Cessation of respiratory airflow
CENTRAL (40-45%)
No respiratory effort, no nasal airflow
Developmental phenomenon
OBSTRUCTIVE
respiratory effort, no nasal airflow, HR
Caused by aspiration, laryngospasm or
poor airway control
MIXED
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(10-15%)
(40-45%)
Both obstructive and central
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:
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CNS immaturity - # of synaptic
connections sensitivity to CO2
activity of protective respiratory
reflexes (conserve, rather than breath)
minute ventilation
diaphragmatic fatigue
soft compliant chest
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)
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
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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
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Bacterial (GBS, staph. Proteus, Listeria, Coliforms
Viral (RSV, paraflu, herpes, CMV
Chlamydial
NEC
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
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blood viscosity and blood flow to CNS
begins at 2-4 hours of age
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
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Myelomeningocele
Meningitis
TREATMENT OF APNEA
Dependent on Etiology
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Least invasive
Treat underlying causes
Non-pharmacologic vs
pharmacologic
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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TREATMENT OF APNEA:
PHARMACOLOGIC
• May treat more severe AOP with
methylxanthines.
• Methylxanthines effect
neurotransmitters and increase
the transmission of impulses
across nerves and synapses.
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METHYLXANTHINES
CAFFEINE
2.5 - 5 mg /kg / day once per
day (therapeutic range 8-15
mcg/ml)
THEOPHYLLINE
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3-6 mg/kg/day divided in 2
doses per day
(therapeutic range 6-12 mcg/ml)
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
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ALTE
“APPARENT LIFE THREATENING EVENT”
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Frightening event to the observer
Combination of apnea
Color change
Marked change in muscle tone
Over 37 weeks conceptual age
Careful Evaluation of Episode
Indicators for Type of Treatment
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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
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:
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May discharge sooner than 5 days if
work-up negative and no events
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
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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
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
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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 only
Parents 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 STATISTICS
Currently, 0.5 death per 1000
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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
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
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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 FACTS
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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
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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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)
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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
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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