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ETIOLOGY
BASICS An underlying diagnosis is identified in only 50% of DIAGNOSIS
cases (∼50% are idiopathic):
DESCRIPTION r GI: HISTORY
r According to the NIH, an infant apparent Detailed accounts from witnesses (caretaker) and
– Gastroesophageal reflux
life-threatening event (ALTE) is an unexpected, emergency prehospital personnel may provide
– Intussusception
frightening episode that is characterized by some important insight on nature of event:
– Volvulus r Condition:
combination of (1): – Swallowing incoordination
– Apnea (central, obstructive, or mixed) r Neurologic: – Awake, asleep, crying, position (prone vs. supine)
– Color change (cyanosis, pallor, redness, or r Activity during event:
– Seizure
plethora) – CNS hemorrhage – Coughing, feeding, vomiting, gagging
– Marked change in muscle tone (limpness or r Respiratory effort:
– Hydrocephalus
rigidity) – Chiari malformation – Fast, slow, shallow, stridor, gasping, choking, none
– Choking or gagging – Central hypoventilation syndrome r Color:
– Fear (in some cases) that the infant has died – Vasovagal syncope – Red, blue, purple, pale
r An ALTE may prompt the caregiver to stimulate or r Respiratory: r Tone and movement:
resuscitate the infant before recovery. – Laryngotracheomalacia – Limp, rigid, convulsions
EPIDEMIOLOGY – Vocal cord dysfunction r Duration:
Incidence – Vascular ring – Time to recovery (eg, normal respiratory pattern or
Unknown, though estimates range from 0.5–6% – Obstructive sleep apnea tone)
(2): – Foreign body aspiration r Interventions (and duration):
r Most occur in infants <1 yr of age, peaking at 1 wk – Congenital airway anomalies – None, gentle or vigorous stimulation, artificial
– Stimulation of laryngeal chemoreceptors respirations, CPR
to 2 mo of age (3).
– Breath-holding spell r Recent illnesses
RISK FACTORS r Cardiac: r Past medical history:
r Prematurity
– Congenital heart disease (eg, ductal-dependent – Prenatal care
r Infection with respiratory syncytial virus (RSV) lesion) – Prematurity
r Male gender – Dysrhythmia (eg, long QT, Wolff-Parkinson-White – Developmental history
r Prone sleeping position syndrome) – Feeding history
r Feeding difficulties – Cardiomyopathy – Sleep habits
r History of apnea, cyanosis, or pallor – Myocarditis – Prior events
r Metabolic/Endocrine: r Family/Social history:
PATHOPHYSIOLOGY – Inborn error of metabolism – Siblings with sudden infant death syndrome (SIDS)
r The pathophysiology of ALTE in infants is unclear.
– Endocrine disorder – Dysrhythmias
r Apnea (1): r Infection:
– Medications in home
– Cessation of respiratory airflow for any reason: – Sepsis or meningitis – Smoking, alcohol, or substance abuse
◦ In central apnea, respiratory pauses may be – RSV
caused by CNS immaturity, seizures, or tumors. – Pertussis PHYSICAL EXAM
◦ In obstructive apnea, breathing may be r Infants may appear well without any signs or
– Croup
obstructed by a laryngeal web, vascular ring, – Pneumonia symptoms of pathology:
tracheoesophageal fistula, or foreign body. r Child abuse: – In 1 study, 83% of infants evaluated by
– In pathologic apnea, there is a respiratory pause paramedics had unremarkable physical exams
– Physical abuse
>20 sec accompanied by bradycardia, cyanosis, – Munchausen by proxy (eg, suffocation, intentional
after an ALTE (4).
pallor, hypotonia, or other signs of compromise. poisoning, head trauma)
– In apnea of infancy, there is an unexplained r Normal:
respiratory pause >20 sec, or <20 sec when – Respiratory pauses
accompanied by bradycardia, cyanosis, pallor, – Periodic breathing
hypotonia, or other signs of compromise.
– Periodic breathing is a normal respiratory pattern
involving ≥3 brief pauses interrupted by <20 sec
of normal respirations in between (no bradycardia,
cyanosis, or hypotonia).
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P1: OSO/OVY P2: OSO/OVY QC: OSO/OVY T1: OSO
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