Neonatal Resource Services Clinical Guideline Apnea and ...

Neonatal Resource Services Clinical Guideline  Guideline 

Apnea and Bradycardia 

Purpose/Goal: To provide guidelines to determine the optimal course of treatment and subsequent case
management of the neonate with neonatal apnea.

Background  For decades investigators have tried to understand the complex developmental
Definitions neuropathology involved in apnea of prematurity (AOP) in an effort to interrupt or
treat apnea and remove its impact on Apparent Life Threatening Events (ALTE’s),
apnea spell sequelae, and death from Sudden Infant Death Syndrome (SIDS).

 The AAP policy statement from 2003 serves as the main source of clinical advice
and as a resource from which to adapt guidelines that address SIDS, ALTE’s,
apnea, home apnea monitors (HAM) and their use. The bibliography also includes
research completed in the last decade on apnea, use of monitors, and treatments
for apnea.

 The clinical goal is establishment of regular breathing patterns in infants to
facilitate a safe discharge from the NICU and, in select patients, outpatient follow
up until they “outgrow” their respiratory control immaturity.

 Recurrent apnea events are a frequent manifestation of general problems in term
and preterm infants often resulting in a loss of effective breathing that can lead to
severe hypoxemia and bradycardia requiring resuscitation.

 Supportive as well as pharmacological treatments are incorporated into clinical
practice to diminish the frequency and severity of central apneas.

 The challenge with neonates is determining when to safely remove treatment
medically and/or monitoring electronically and let the infant mature and self-
regulate his or her own breathing.

 Management of apnea and bradycardia requires observation in the hospital before
discharge for several days (margin of safety) after physiologic maturity is reached
and/or medical treatment has had a chance to stabilize regular breathing (Darnall
1997 and Lorch 2011).

Apnea of prematurity (AOP) is defined as sudden cessation of breathing that lasts for
at least 20 seconds or less than 20 seconds and accompanied by bradycardia or
oxygen desaturation (with or without cyanosis) in an infant younger than 37 weeks’
gestational age. It usually ceases by 37 weeks’ gestational age but may persist for
several weeks or even months beyond term, especially in infants born before 28
weeks’ gestation. (AAP Policy Statement, Sudden Infant Death Syndrome, and Home
Monitoring).

 Note: An O2 saturation level of less than 85% is considered pathologic in this
age group, as is a decrease in O2 saturation should it persist for 5 seconds or
longer.

Apnea of infancy (AOI) is defined as “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 gestational age of 37 weeks or more at the onset of
apnea (AAP Policy Statement Apnea, Sudden Infant Death Syndrome, and Home
Monitoring).

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Apparent Life Threatening Event (ALTE) is characterized by some combination of
apnea (central or occasionally obstructive), color change (cyanosis and/or pallor, but
occasionally erythematous and plethoric), marked change in muscle tone (limpness),
choking, and or gagging.

Client Target Periodic breathing
Population  Periods of regular respiration for up to 20 seconds followed by apneic periods
of 10 seconds or less that occur at least 3 times in succession.
Clinical  Periodic breathing may be observed for 2-6% of the breathing time in healthy
Management term neonates and as much as 25% of the breathing time in preterm
neonates. The occurrence of periodic breathing is directly proportional to the
degree of prematurity.
 Periodic breathing typically does not occur in neonates during their first 2 days
of life.
 Periodic breathing most frequently occurs during active sleep, but it can also
occur when neonates are awake or lightly sleeping. This pattern, commonly
observed in patients at high altitudes, is eliminated with supplemental
oxygenation and/or with the use of continuous positive airway pressure
(CPAP).
 Because the prognosis is excellent and because the infant is usually not
compromised, frequently no treatment is required.

Neonates with the following diagnosis(es):
 Apnea: with co-existing bradycardia, and/or significant hypoxemic
desaturations.

Diagnostic(s)

Apnea is typically observed by the bedside caregiver (i.e., nurse). An infant should be
placed on a cardiorespiratory monitor to identify further episodes of apnea and
associated bradycardia and desaturations. Caregivers should attempt to define the
type, severity, associated activity (such as feedings) and the etiology of apnea. It is
important to remember that AOP is a diagnosis of exclusion.

 There is a lack of evidence regarding the management and treatment of
feeding-related apnea and bradycardia events. If these feeding-related events
do not cause significant physiologic changes and are easily corrected by
feeding interruption, they may not warrant prolonged hospitalization.
Consideration should be given to providing the caregiver feeding education
and training with appropriate discharge follow-up.

 Gastroesophageal Reflux (GER): GER is rarely associated with apnea. The
pH probe is not as reliable as manometry to establish the diagnosis of GER.
An episode of 20 or more seconds of continuous apnea can be documented
via a 3-channel pneumogram, or via 4- or 5-channel sleep studies. The 5-
channel sleep study adds a measurement of esophageal pH (< 4), to diagnose
GER, which occasionally mimics AOP.

 Routine screening of all asymptomatic preterm infants with
pneumocardiograms (PCGs) is not indicated.

 PCGs are not recommended in the management of AOP because they have a
high false-positive rate, cannot predict with accuracy the occurrence of severe
apnea or death, and are not beneficial in identifying which patients should be
discharged with a home monitor, therefore, its use is not appropriate to delay

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discharge from the hospital.

Medication Therapy
 Methylxanthines (caffeine, aminophylline and theophylline) may help to reduce
the frequency of events in infants with central apnea, though apnea in
approximately 15% of infants does not respond to methylxanthines.
 Caffeine is the only FDA approved treatment for AOP and the preferred drug
of choice for this indication. Theophylline is not recommended due to its side
effects, including the increased risk for seizures.
 Caffeine has a long half-life, is well tolerated in IV or oral forms, and also
stimulates midbrain CNS activity to cause more regular breathing in neonates.
 There is no current evidence of short or long-term significant side effects.
 Home apnea monitoring might be considered for infants discharged home on
caffeine.

Home Monitoring

The common consensus is that apnea monitors do not prevent or reduce the incidence
of the incidence of SIDS.

 Avoid using home monitoring to prevent SIDS.
 Home respiratory monitoring “may be warranted for premature infants who are

at high risk of recurrent episodes of apnea, bradycardia, and hypoxemia.”
(AAP)
 Home apnea monitors may be warranted for neonates who have experienced
an ALTE and who are technology-dependent (ventilator, tracheostomy with
collar, gastrostomy, etc.), have unstable airways, have rare medical conditions
affecting regulation of breathing, or have symptomatic chronic lung disease.
 The main caregiver(s) or parent(s) as well as ancillary caregivers must pass
CPR training, and should be trained on home monitoring equipment and
durable medical equipment (DME) prior to discharge.
 Parents are encouraged to room in overnight x 1 night to familiarize
themselves with the baby’s habits on the monitor the evening before discharge
home.
 Parents should be advised that home apnea monitoring has not been proven
to prevent SIDS in infants.
 Home monitors are usually ordered for 1 to 3 months. The AAP (2003)
recommends monitoring until 43 weeks post-conceptual age or after the
cessation of extreme episodes, whichever comes later. Data from “smart”
monitors can be downloaded for serial analysis. The download results can
direct the physicians when to stop caffeine treatment or the monitor itself.
 An apnea “countdown” of 5 days is a reasonable period to demonstrate cardio-
respiratory stability before a safe hospital discharge. However, for babies born
at < 30.6 weeks' gestation there is some literature to suggest that a 7-day
countdown is more appropriate (Lorch 2011). According to Darnall’s survey of
neonatologists (1997) the “margin of safety” ranges from 2 to 8 days.
 If an infant fails two apnea countdowns, consideration should be given to
discharge on a home monitor, or initiation or restart of caffeine, or a search for
other etiologies.
 Pediatricians should continue to promote proven practices that decrease the
risk of SIDS—supine sleep position, safe sleeping environments, and

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Medical elimination of prenatal and postnatal exposure to tobacco smoke.
Director
Escalation Goal of Therapy
 Resolution of abnormal breathing pattern, cessation of apnea spells and
Best Practices associated desaturations/bradycardia.
 Discontinuation of medication if appropriate and no need for an apnea monitor
to treat AOP.
 Symptom-free for 7 days after discontinuing caffeine.
 Caffeine can safely be withdrawn when patient shows no recurrent apnea for
5-7 days into therapy and a corrected gestational age (CGA) of 32-34 weeks
has been reached.

Escalate for infant:
 Who has more than one countdown with extended length of stay
 Who is on a 7 day countdown when 5 day countdown is indicated
 Who has feeding-related events characterized by no significant physiologic
changes and resolution with interruption of feedings that is extending hospital
stay
 Who can potentially be discharged to home on caffeine with no significant
events

N/A

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Bibliography

American Academy of Pediatrics Committee on Fetus and Newborn. Hospital discharge of the high-risk neonate.
Pediatrics. 2008;122:1119-1126.

American Academy of Pediatrics Task Force on Sudden Infant Death Syndrome: Expansion of Recommendations for
a Safe Infant Sleeping Environment: Policy Statement: SIDS and Other Sleep-Related Infant Deaths. Pediatrics 2011:
128 (5): 1030-1039.

American Academy of Pediatrics Task Force on Sudden Infant Death Syndrome. The changing concept of sudden
infant death syndrome: Diagnostic coding shifts, controversies regarding the sleeping environment, and new
variables to consider in reducing risk. Pediatrics. 2005; 116(5):1245-1255.

Archives of Pediatric and Adolescent Medicine. 2005; 159(1):18-24.

Darnall RA, Kattwinkel J, et al. Margin of safety for discharge after apnea in preterm infants. Pediatrics. 1997; 100:
795-801. (1997)

Darnall, RA, Ariagno, RL, Kinney HC. The late preterm infant and the control of breathing, sleep, and brainstem
development: a review. Clin Perinatology. 2006; 33: 883-914.

Eichenwald, EC, et al. Inter-Neonatal Intensive Care Unit Variation in Discharge Timing: Influence of Apnea and
Feeding Management. Pediatrics. 2001; 108:928-933.

Eichenwald EC, Zupancic JA, Mao WY, et al. Variation in diagnosis of apnea in moderately preterm infants predicts
length of stay. Pediatrics. 2011 Jan;127(1):e53-8.

Finer, N, Higgins, R, Kattwinkel, J, Martin, R. Summary of Proceedings from the Apnea-of-Prematurity Group.
Pediatrics 2006; 117; S47.

Henderson-Smart DJ, De Paoli AG. Methylxanthine treatment for apnoea in preterm infants. Cochrane Database Syst
Rev. Dec 8 2010.

Henderson-Smart DJ, Steer PA. Caffeine versus Theophylline for apnea in the preterm infant. Cochrane Database
Syst Rev. Jan 20 2010.

Lorch SA, Srinivasan L, Escobar GJ. Epidemiology of apnea and bradycardia resolution in premature infants.
Pediatrics. 2011; 128:e366-e373.

Matthew OP. Apnea of Prematurity: Pathogenesis and management of Strategies. J Perinatol. 2011 May;31(5):302-
10. doi: 10.1038/jp.2010.126

Schmidt B, et al. Caffeine for apnea of prematurity trial group. New England Journal of Medicine. 2006; 354: 2112-21.

Schmidt B, Roberts R, Davis P, et al. Long-term effects of caffeine therapy for apnea of prematurity. New England
Journal of Medicine.2007; 357(19):1893-1902.

Silvestri J, Lister G, Corwin M, et al. Collaborative home infant monitoring evaluation study group. Factors that
influence use of a home cardiorespiratory monitor for infants: The collaborative home infant monitoring evaluation.

Silvestri J. Indications for home apnea monitoring (or not). Clinics in Perinatology. 2009; 36(1):87-99.

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