SIDS Flashcards

1
Q

What is Sudden Infant Death Syndrome (SIDS)?

A

SIDS is the sudden, unexplained death of an infant, often occurring during sleep.

It may occur in infants experiencing an apparent life-threatening event (ALTE) and premature infants with apnea.

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2
Q

What does ALTE stand for?

A

Acute Life-Threatening Events

ALTE is defined as an episode that is frightening to the observer, characterized by apnea, color change, marked change in muscle tone, choking, or gagging.

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3
Q

What is BRUE?

A

Brief Resolved Unexplained Event

BRUE refers to an event in an infant under 1 year characterized by sudden, brief, and now resolved episodes of specific symptoms.

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4
Q

List the symptoms that define a BRUE.

A
  • Cyanosis or pallor
  • Absent, decreased, or irregular breathing
  • Marked change in tone (hypertonia or hypotonia)
  • Altered level of responsiveness
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5
Q

What is the difference between BRUE and ALTE?

A

BRUE is defined as both brief and resolved, while ALTE does not have this requirement.

Events that have not returned to baseline health do not qualify as BRUE.

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6
Q

What is the incidence of ALTE?

A

0.6 and 4.1 per 1000 live births

The true incidence of ALTEs is unknown, but they account for 0.6%–1.7% of ER visits for children under 1 year.

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7
Q

What are the low-risk criteria for diagnosing BRUE?

A
  • Age more than 60 days
  • Gestational age ≥32 weeks and postconceptional age ≥45 weeks
  • First BRUE
  • Duration of event less than 1 minute
  • No CPR required
  • No concerning historical features
  • No concerning physical examination findings
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8
Q

What is Laryngeal ChemoReflex Apnea (LCRA)?

A

A reflex that occurs in infants triggered by stimuli in the larynx, leading to prolonged apnea and bradycardia.

It involves sensory nerve endings that respond to irritants or changes in fluid composition.

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9
Q

What are the clinical features of an apparent life-threatening event?

A
  • Majority of infants are asymptomatic
  • History of the event including timing, nature, and caregiver actions
  • Physical exam findings are often normal
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10
Q

What are common physical exam findings in infants presenting with ALTE?

A

Vital signs may show fever, tachypnea, hypotension, or hypoxemia, indicating underlying illness.

Growth parameters and neurological findings may also provide clues to underlying issues.

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11
Q

What is the management guideline for BRUE?

A

Guidelines apply only to low-risk infants who have returned to baseline health.

Any abnormal findings should warrant further investigation.

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12
Q

What are the recommendations for imaging and laboratory findings in BRUE?

A

Minimal testing for low-risk infants; routine tests such as blood cultures or imaging are discouraged unless criteria are exceeded.

Tests may include hemoglobin, WBC count, and cultures for RSV and pertussis.

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13
Q

What are the indications for home apnea monitors in infants?

A
  • Family history of SIDS
  • Apnea of prematurity
  • History of previous ALTE
  • Choking episodes
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14
Q

What is the AAP’s stance on home monitoring for infants with ALTE?

A

Routine monitoring is NOT recommended for infants with an ALTE or siblings of SIDS victims.

The recommendation remains controversial despite common practice.

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15
Q

What defines Apnea of Prematurity (AOP)?

A

Cessation of airflow for 10–20 seconds or longer, or shorter pauses associated with desaturation.

This occurs in premature infants and may require interventions.

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16
Q

What is Apnea of Prematurity (AOP)?

A

Cessation of airflow for 10–20 seconds or longer, or shorter pauses in respiration associated with desaturation <90% or bradycardia <100

AOP is common in premature infants and often requires monitoring and intervention.

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17
Q

What percentage of premature infants weighing <1500 g will require interventions due to apnea?

A

50%–100%

This indicates the high prevalence of apnea in this vulnerable population.

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18
Q

List some differential diagnoses of Apnea of Prematurity.

A
  • Immaturity of ventilatory control
  • Intracranial hemorrhage
  • Sedation crossing the placenta
  • Sepsis with or without meningitis
  • Heat or cold stress
  • PDA
  • Hypoglycemia
  • Electrolyte abnormalities
  • Anemia
  • Necrotizing enterocolitis
  • Feeding-related apnea
  • Heart block or heart failure
  • Excessive sedation given to the infant directly

These conditions can complicate the diagnosis of AOP.

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19
Q

What is the primary etiology of apnea in premature infants?

A

Idiopathic, attributed to immaturity of ventilatory control

This immaturity significantly impacts respiratory function.

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20
Q

What types of apnea are described in preterm infants?

A
  • Central apnea
  • Obstructive apnea
  • Mixed apnea

Mixed apnea is the most common type among premature infants.

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21
Q

What is the most common type of apnea among premature infants?

A

Mixed apnea

Mixed apnea often involves both central and obstructive components.

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22
Q

What physiological mechanism is suggested to explain mixed apnea in premature infants?

A
  • Upper airway obstruction
  • Inability to compensate for increased CO2
  • Asynchronous activity of diaphragm and genioglossus

These mechanisms perpetuate the cycle of apneic events.

23
Q

What is Laryngeal ChemoReflex Apnea (LCRA)?

A

A type of mixed apnea that may play a role in AOP, where swallowing interrupts the reflex

Premature infants swallow more frequently during apnea.

24
Q

What is the prognosis of Apnea of Prematurity?

A

Natural history is unclear; apneic pauses longer than 5 seconds are common in early days of life

The resolution of apnea and bradycardia is age-dependent.

25
What is the first-line treatment for Apnea of Prematurity?
Methylxanthines (aminophylline, theophylline) ## Footnote Caffeine has replaced theophylline as the preferred methylxanthine.
26
What is the mechanism of action of caffeine in treating apnea?
Blocks brainstem inhibitory adenosine A1 receptors, leading to increased respiratory neural output ## Footnote This enhances respiratory drive in premature infants.
27
How does nasal continuous positive airway pressure (NCPAP) help in treating apnea?
Stabilizes respiratory mechanics and treats AOP ## Footnote NCPAP is used for infants who do not respond to methylxanthines.
28
What is the relationship between blood transfusion and apnea in premature infants?
Apnea is less frequent for 3 days after a transfusion; long-term effects are unclear ## Footnote Infants may have more apnea with lower hematocrit levels.
29
What is the definition of Sudden Infant Death Syndrome (SIDS)?
The sudden death of an infant < 1 y/o, which remains unexplained after thorough investigation ## Footnote SIDS remains a significant concern in infant mortality.
30
What framework is used to study SIDS?
The triple-risk model ## Footnote This model considers susceptibility, environmental stressors, and developmental stage.
31
What are potentially lethal mechanisms linked to sleep position and environment in SIDS?
* Interaction between sleep position and soft bedding * Rebreathing of CO2-depleted air * Thermal stress ## Footnote These factors can increase the risk of SIDS.
32
What is the significance of sleep position in SIDS?
Prone position is critical and linked to increased risk of death ## Footnote Supine sleep interventions have been successful in reducing SIDS rates.
33
True or False: Monitoring premature infants at home is not recommended.
False ## Footnote Monitoring is recommended until infants reach 43 weeks PMA.
34
What is the challenge regarding rebreathing in infants?
Understanding when rebreathing can be or is likely to be lethal
35
How do infants thermoregulate when exposed to dangerous thermal stress?
Effectively and predictably
36
What is the significance of the 50% fall in SIDS deaths from the early 1990s through 2004?
It is labeled a success story for epidemiology
37
What has continued at a rate near 1.0 per 1000 live births after 2004?
Total sudden unexpected deaths
38
What percentage of deaths attributed to SIDS can be explained by postmortem findings?
Approximately 1 in 6
39
What were the primary causes of SIDS deaths explained by autopsy?
* Congenital heart disease * Acute infections * Fatty acid oxidation deficiencies
40
What is a prominent theory regarding programmed cell death in SIDS?
Apoptosis triggered by CNS hypoxia
41
What role do specific receptors within the CNS play in SIDS?
They are needed for the excitatory function of serotonergic networks
42
What are the known deficiencies in infants with SIDS regarding the arcuate nucleus?
* Hypoplasia of the arcuate nucleus * Reduced functional activity of cholinergic receptors * Reduced serotonin binding in multiple brainstem structures
43
What condition is the most common inborn error of beta oxidation?
Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency
44
What environmental triggers may lead to lethal cardiac arrhythmias in SIDS victims?
Fever or overheating
45
What is the role of autopsy in diagnosing causes of sudden infant death?
Important for diagnosing nonaccidental trauma
46
What physiological characteristics may make infants more vulnerable to SIDS?
* Abnormal arousal * Hypoxic drive * Airway protective reflexes
47
What can be a consequence of arousal deficits in infants?
Increased risk for obstructive apnea
48
How does prone sleeping on soft bedding affect an infant's gas exchange?
Increases CO2 concentration and decreases O2 concentration
49
What factors increase the risk of SUID when bed sharing?
* Increased risk for suffocation * Increased relative thermal stress * More likely to sleep on their sides
50
What is the triple-risk model related to sudden infant death?
* Infant susceptibility * Developmental vulnerability * Exogenous stressors of varying magnitude
51
Fill in the blank: The most well-known defects causing pediatric cardiomyopathies are associated with _______.
fatty acid oxidation deficiencies
52
True or False: Infants sleeping prone are less likely to experience ventilatory instability.
False
53
What percentage of SIDS deaths might be caused by lethal cardiac arrhythmias according to Schwartz's theory?
~2%–5%