Apnea of prematurity

kibaru
 is a common problem in preterm infants that may be due
to prematurity or an associated illness.

 In term infants, apnea is always worrisome and demands

immediate diagnostic evaluation.
 Periodic breathing must be distinguished from prolonged
apneic pauses because the latter may be associated with
serious illnesses.

 Apnea is a feature of many primary diseases that affect

neonates
 It may be idiopathic
 Many disorders produce apnea by
 A) direct depression of the central nervous system's control
of respiration
 (hypoglycemia
 meningitis
 drugs
 hemorrhage
 seizures
 B) disturbances in oxygen delivery
 shock
 sepsis
 anemia
 disturbances in oxygen delivery due ventilation defects
 Pneumonia
 RDS

 persistent pulmonary hypertension of the newborn [PPHN]

 muscle weakness
Idiopathic apnea of prematurity
occurs in the absence of identifiable
predisposing diseases.

disorder of respiratory control and may be

obstructive, central, or mixed.
 In central apnea, which is caused by decreased central nervous
system (CNS) stimuli to respiratory muscles, airflow and chest wall
motion are absent.

 Gestational age is the most important determinant of respiratory

control
 with the frequency of apnea being inversely related to gestational age.

 The immaturity of the brainstem respiratory centers is manifested by

an attenuated response to carbon dioxide and a paradoxical response
to hypoxia that results in apnea rather than hyperventilation.
 Obstructive apnea
(pharyngeal instability, neck flexion, nasal
occlusion) is characterized by absent airflow but
persistent chest wall motion.

 Pharyngeal collapse may follow the negative airway

pressures generated during inspiration, or it may
result from incoordination of the tongue and other
upper airway muscles involved in maintaining
airway patency.
 The most common pattern of idiopathic apnea in
preterm neonates has a mixed etiology (50–75%),
with obstructive apnea preceding (usually) or
following central apnea.

 Shortepisodes of apnea are usually central, whereas

prolonged ones are often mixed.
Apnea is sleep state dependent; the frequency
increases during active (rapid eye movement)
sleep.
CLINICAL MANIFESTATIONS
 incidence of idiopathic apnea of
prematurity varies inversely with
gestational age.
 In preterm infants, it is rare on the 1st day
of life
 apnea immediately after birth signifies
another illness.
 The onset of idiopathic apnea occurs on the 2nd–
7th day of life.

 In preterm infants, serious apnea is defined as

cessation of breathing for longer than 20 sec, or any
duration if accompanied by cyanosis and
bradycardia.
 The incidence of associated bradycardia increases with the length of
the preceding apnea and correlates with the severity of hypoxia.

 Short apnea episodes (10 sec) are rarely associated with bradycardia,
whereas longer ones (>20 sec) have a higher incidence of bradycardia.
 TREATMENT
 Gentle tactile stimulation is often adequate therapy for mild and
intermittent episodes.
 Infants with recurrent and prolonged apnea may require suctioning,
repositioning, and bag and mask ventilation.

 Oxygen should be administered to treat hypoxia.

 The onset of apnea in a previously well premature neonate after the

2nd wk of life or in a term infant at any time is a critical event that
warrants immediate investigation.
 Treatment of Recurrent apnea of prematurity
 Methylxanthines increase central respiratory drive by lowering the
threshold of response to hypercarbia, as well as enhancing
contractility of the diaphragm and preventing diaphragmatic fatigue.

 caffeine is a more potent centrally acting respiratory agent with fewer

side effects than theophylline.
 Loading doses of 5–7 mg/kg of theophylline (orally) or aminophylline (intravenously)
should be followed by doses of 1–2 mg/kg given every 6–12 hr by the oral or
intravenous routes.

 Loading doses of 20 mg/kg of caffeine citrate are followed 24 hr later by maintenance

doses of 5 mg/kg/24 hr qd orally or intravenously.
TREATMENT CONTINUES
 Nasal continuous positive airway pressure (CPAP, 2–5
cm H2O) and high-flow humidified nasal cannula (1–2.5
L/min) are effective therapies for mixed or obstructive
apnea.

 The efficacy of CPAP is related to its ability to splint the

upper airway and prevent airway obstruction.
PROGNOSIS.

 Unless severe, recurrent, and refractory to therapy, apnea of

prematurity does not alter an infant's prognosis.

 Associated problems of intraventricular hemorrhage (IVH),

bronchopulmonary dysplasia (BPD), and retinopathy of
prematurity are critical in determining the prognosis for apneic
infants.
PROGNOSIS
 Apnea of prematurity usually resolves by 36 wk PCA and does
not predict future episodes of sudden infant death syndrome.

 Some infants with persistent apnea are discharged as long as

cardiorespiratory monitoring can be performed at home.
PREVENTING APNOEA
• • Give caffeine citrate and aminophylline to prevent
apnoea in premature infants.
– Caffeine is preferred if it is available.
• The loading dose of caffeine citrate is 20 mg/kg orally
or IV (given slowly over 30 min).

• A maintenance dose of 5 mg/kg per day should be

prescribed 24 h later and can be increased by 5 mg/kg
every 24 h to a maximum of 20 mg/kg per day, unless
side-effects develop
• . Continue treatment for 4–5 days after cessation of
apnoea

• If caffeine is not available, give a loading dose of

aminophylline at 6 mg/kg
• IV over 20 min, followed by a maintenance dose of 2.5
mg/kg every 12 h
• • If an apnoea monitor is available, this should be used.

• • If an apnoea monitor is not available, a pulse oximeter

with the alarm turned on for hypoxaemia may help to
detect apnoea if the neonate is breathing room air