PEDIATRIC TRACHEOSTOMIES IN THE EMERGENCY …
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Transcript PEDIATRIC TRACHEOSTOMIES IN THE EMERGENCY …
APNEA of Prematurity, SIDS
and ALTE
Pat Mathios,RN, MSN
Pediatric Pulmonary Educator
Historical perspective
Objectives
Define AOP, SIDS and ALTE
Discuss treatments for AOP
Describe the “triple-risk” theory for
SIDS
Identify an evidenced based
intervention for prevention of SIDS
Discuss the UAMC Apnea/CLD Clinic
Discuss the indications for use of an
apnea monitor
APNEA—what is it?
Apnea is a nonspecific indicator of
distress:
√Failure of a system
√Early indicator of deterioration
Many causes of apnea can be diagnosed
and treated.
Apnea of Infancy
Definition: “an unexplained episode of
cessation of breathing for 20 seconds or
longer, or a shorter respiratory pause
associated with bradycardia, cyanosis,
pallor, and/or marked hypotonia. The
term ‘apnea of infancy’ generally refers to
infants with a gestational age of 37 weeks
or more at the onset of apnea.”
American Academy of Pediatrics policy statement
PEDIATIRCS Vol. 111, No. 4 April 2003
Definition of Apnea of
Prematurity-AOP
Apnea of prematurity is cessation of
breathing that lasts longer than 20
seconds and is associated with
bradycardia (<100bpm), oxygen
desaturation, pallor/cyanosis in an
infant younger than 37weeks
gestational age.
American Academy of Pediatrics policy statement
PEDIATRICS, Vol 111, No. 4 April 2003
Periodic breathing
Periodic breathing is not apnea.
3 or more pauses for greater than 30
seconds duration with less than 20 seconds
of respiration between pauses.
Thought to be benign
Periodic breathingApneaSIDS????
Should not be considered linear events
They overlap, but one is not causative
to the next
Apnea of prematurity
Apnea and periodic breathing are
common in premature infants after
the first 24-48 hours of life.
Apnea only occurs during active sleep
Premature infants sleep 80% of the
time full term infants 50%.
Chronic Lung Disease past &
present
Surfactant
Annual deaths from RDS (respiratory distress
syndrome) in the US decreased from 1015,000 babies in the 1960’s to fewer than 1000
in 2002.
www.faseb.org/opar/break/. 2002
Types of Apnea
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
Factors contributing to
respiratory effort
CNS immaturity- # of synaptic
connectionssensitivity to CO2
activity of protective respiratory
reflexes (conserve rather than breathe)
minute ventilation
Diaphragmatic fatigue
Soft complaint chest
Therefore AOP:
Mixed apnea occurs frequently in premature
infants due to:
√ Increased CNS immaturity (central apnea)blunted response to 02 and CO2
√ Softer chest, weaker diaphragms (obstructive
apnea)
√ Immature immune system -viruses, infections
(obstructive apnea)
Usually resolves by 37 weeks PCA or persists
several weeks post term
Clinical conditions associated
with Apnea
Intraventricular bleed-may see
hypoventilation, apnea arrest
Subtle seizures
Sepsis
Congestive heart failure-due to
atelectasis WOB, fatigue
Anemia
Polycythemia
Other contributing factors to
AOP
Feeding problems:
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Over distention
Aspiration
GER (gastroesphogeal reflux) with or w/o aspiration
Due to laryngospasm
Stimulations of irritant receptors in lower esophagus
Metabolic conditions
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Hypoglycemia
Hypercalcemia
Hypernatremia
Other
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Myelomeningocele/meningitis
Treatment of Apnea
Dependent on Etiology
Least invasive-monitor, medication
Treat underlying causes
Non–pharmacologic vs pharmacologic
Treatment of Apnea
Mechanical CPAP/ ventilation
CPAP markedly apneic episodes
with an obstructive component
Improves patency of upper airways
by activation of dilator muscles by
passive splinting
Treatment of apnea
METHYLXANTHINES:
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May treat more severe AOP with
methylxlanthines
Methylxanthines effects neurotransmitters and
increase the transmission of impulses across
nerves and synapses
Caffeine preferred over Theophylline
Caffeine more centrally active, not metabolized
by liver-not all pharmacies carry
Caffeine- 2.5-5mg/kg/day once per day
(therapeutic range 6-20mcg/ml-toxic >40)
Treatment of Apneapharmocologic
Oxygen via nasal cannula-can go
home if no apnea or bradycardia for
at least 5 days and parents room in.
DME will bring home oxygen
Follow-up will be in the Apnea CLD
clinic in 2-4 weeks
Weaning Oxygen in the
Outpatient setting
Growing is important!-consider weight gain
Any apnea events/viral illness
Pulse ox on current setting
Consider altitude where the baby lives
Discontinue if good weight gain is pulse ox is
96+,
Oxygen at night if pulse ox 93-95 with good
growth
Pulse ox < 92 and RR and wt-keep 02
Keep oxygen in home for another 2-4 weeks
and check weight gain
Treatment of apnea
Non -pharmacologic
Tactile stimulation
Neutral ambient temperature
Address feeding issues
Monitor
Parent instruction
Apparetn Life Threatening
Event-ALTE
Definition: “an episode that is frightening
to the observer and is characterized by
some combination of apnea (central or
occasionally obstructive), color change
(usually cyanotic, pallid), marked change
in muscle tone (usually marked limpness)
choking or gagging”
American Academy of Pediatrics policy statement
Pediatrics Vol 111,No. 4 April 2003
ALTE-Apparent Life Threatening
Event
Frigententing to the observer
Combination of apnea
Color change
Marked change in muscle tone
Over 37 weeks of PCA
Usually awake
ALTE treatment condierations
History of event including feeding &
sleeping history
Physical exam, VS, overheated?
CBC, lytes, ABG, pulse ox,
Blood and viral cultures
CXR, Cranial US, Echocardiogram
Ph probe, barium swallow
Sleep study
Goals for Discharge to Home
Prefer to discharge without monitor and/or
methylxanthines
For AOP:
• No apneic episodes for 5 days
• If dc on methylxanthines - in this community is
with a monitor
• May discharge with only monitor or only
oxygen with follow up in Apnea/CLD clinic
For ALTE:
• May discharge < 5days if work up negative and
no events
Indications for Home Apnea
monitoring (or not)
Infants with BW < 1000grams
Infants with continued apnea and bradycardia
Infant requiring methylxanthines
Infants with severe GER
Infant with tracheostomies/or tech dependent
Family peace of mind severe CLD with 02,
sibling of SIDS, non–repeating ALTE with no
cause
American Academy of Pediatrics does not
recommend apnea monitors to reduce the
incidence of SIDS
Caregiver Monitor Training
Essential!!!!!!
Pulmonary consult required
Case manager arranges with DME for
equipment
Apnea nurse makes arrangement to teach
parents/ caregivers prior to discharge &
nesting/rooming in
Documented in EHR that parents were
successfully trained
Home Monitor Training
Parents instructed about signs symptoms of
apnea and respiratory distress
How to use the monitor and troubleshoot
Infant CPR & infant choking (American Heart
Association Friends and Family program)
Contacts to call for medical or equipment
concerns
Support via phone call, clinic, community
Event log-? Increase in alarms? Download
monitor.
Monitors
Prescription from MD with setting parameters:
Alarm
Record
Apnea: 20 seconds
15 seconds
HR
60 for term
70 seconds
70 for preterm 80 seconds
HR
off
Childproof on/off
Parents are the best monitor: use only when the
baby is not observed
Termination of Monitor use
Resolution of primary problem
If off caffeine for 1-2 weeks and no
significant apnea
No significant apnea or repeat ALTE
event for 1-2 months
AAP states by 43 weeks PCA or
“cessation of extreme events”
Parent comfort level
SIDS- Sudden Infant Death
Syndrome
The sudden death of an infant younger
than one year of age that remains
unexplained after a thorough case
investigation, including performance of a
complete autopsy, examination of the
death scene, and review of the infant’s and
family's clinical histories.
American Academy of Pediatrics , Pediatrics (1992) 11201126
SIDS statisitcs
Currently 0.5 (0.49) per 1000 live
births
1.2 deaths per 1000 in 1992
Back to Sleep campaign in the US
• 1994 endorsed side or supine
• 1996 endorsed supine only
Understanding SIDS
Leading cause of death in infants from
one month to one year of age
Most deaths occur between 2-4 months
(99% before 6 months, 1% 6 months to
a year)
Infants have a change in response to
hypoxia at 6 months
Associated with sleep and little or no
signs of suffering
Understanding SIDS
SIDS risk for an infant with AOP or had
an ALTE is at no greater risk than the
general population
Premature infants have a slightly
greater risk as their gestational age
decreases
The SIDS sibling/twin is not at greater
risk than general population
Home monitoring if infants has NOT
decreased the incidence of SIDS
SIDS Research
SIDS is not entirely preventable, but the risk can
be reduced:
• Supine sleeping on a firm sleep surface
covered with a fitted sheet
• Keep soft objects, toys and loose bedding out
of baby’s sleep area
• Overheating is contributory
• Smoking is contributory
• Any breastfeeding is protective
• Pacifier use is protective
Preventing SIDS
Sleeping in the same place every night is
protective
Keep baby’s sleep area close to but separate
from where you sleep and others sleep
Avoid products that claim to reduce the risks
SIDS
Reduce the chance that flat spot will develop
on the baby’s head by providing ‘tummy time”
Back to Sleep-Safe Sleeping
SIDS research
CHIME (Collaborative Home Infant
Monitoring Evaluation)study indicates
that normal infants can have apnea,
bradycardia and desaturations into the
70’s-why do they recover and some
infants die of SIDS-How do they arouse?
Research indicates that SIDS is
more complex than a single
abnormality in a single system
In conclusion
Questions???
References to follow or contact Pat
Mathios, Pediatric Pulmonary Nurse at
VM #4-7133 for additional
information
Thank you
References
Eunice Kennedy Shriver National Institute of Child
Health and Human Development (NICHD)
Back to Sleep campaign
http://www.nichid.nih.gov/SIDS
American Academy of Pediatrics (AAP)
http://www.aap.org/healthtopics/Sleep.cfm
References
Willinger, M., James, L.S. & Catz, C (1991) Defining the
Sudden Infant Death Syndrome (SIDS): Deliberations of
an expert panel convened by The National Institute of
Child Health and Human Development. Pediatric
Pathology 11(5) 677-684
Esani, N. Hodgman, J. E., Ehsani, N., Toke, H. (March
2008) Apparent Life Threatening Events and Sudden
Infant Death Syndrome: Comparison of Risk Factors,
Journal of Pediatrics Vol. 152, issue 3
Halbower, A.C., (August 2008),Pediatric Home Apnea
Monitors, Chest, Vol. 134, issue 2.
Silvestri, J.M. (March 2009), Indications for Home Apnea
Monitoring (or Not), Clinics in Perinatology, Vol.36 Issue
1
References
Darnall. R.A., (March 2009), ALTE’s: Still a Puzzle after
all These Years, Journal of Pediatrics, Vol. 154. Issue 3
Eichenwald, E.C., Zupancic, J.A., Wen-Yang, M.,
Richardson, D.K., McCormick, M.C., Escobar, G.J.,
(January 2011) pediatrics, Vol. 127, No. 1
Adams, S.M. , Good, M.W., Defranco. G.M., Sudden
Infant Death Syndrome, (May 2008) American Family
Physician, Vol. 79, Issue 10
Ralston, S., and Hill, V. (November 2009) Incidence of
Apnea in Infants Hospitalized with Respiratory Syncytial
Virus Bronchiolitis, Journal of Pediatrics, Vol. 155, Issue
5
References
Weese-Meyer, D.E., Berry-Kravis, E.M., Ceccherini,
I., Keens, T.G., Loughmanee, D.A., Trang, H. on
behalf of the American Thoracic Society (ATS)
Congenital Central Hypoventilation Syndrome
Subcommittee, (March 2010), American Journal of
Respiratory and Critical Care Medicine, Vol. 181, No.
6 626-644
Task force on Sudden Infant Dear Syndrome, (online
October 17, 2011) Pediatrics (American Academy of
Pediatrics)
Sexton, S. and Natale, R. (April 2009) Risk and
Benefits of Pacifiers, American Family Physician, Vol.
79, Issues 8
References
Committee on Fetus and Newborn, American Academy of
Pediatrics Policy Statement, (April 2003) Apnea, Sudden
Infant Death Syndrome, and Home Monitoring,
Pediatrics, Vol. 111, No. 4
Federation of American Societies for Experimental
Biology, Bubbles, Babies, and Biology: The Story of
Surfactant, 2004