RESPIRATORY

ABNORMALITY IN
NEONATES
Introduction

■ Signs and symptoms of respiratory distress = cyanosis, grunting, nasal flaring,

retractions, tachypnea, decreased breath sounds with or without rales and/or
rhonchi, and pallor
■ A wide variety of pathologic lesions may be responsible for respiratory disturbances,
including pulmonary, airway, cardiovascular, central nervous, and other disorders
Transition to Pulmonary Respiration

■ Successful establishment of adequate lung function at birth depends on airway patency,

functional lung development, and maturity of respiratory control.
■ Fetal lung fluid must be removed and replaced with gas.
– This process begins before birth as active Na transport across the pulmonary
epithelium drives liquid from the lung lumen into the interstitium with subsequent
absorption into the vasculature.
– Increased levels of circulating catecholamines, vasopressin, prolactin, and
glucocorticoids enhance lung fluid adsorption and trigger the change in lung
epithelia from a chloride-secretory to a sodium-reabsorptive mode.
■ Functional residual capacity (FRC) must be established and maintained in order to
develop a ventilation-perfusion relationship that will provide optimal exchange of oxygen
and carbon dioxide between alveoli and blood.
APNEA
■ Apnea 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.
These disorders produce apnea by
direct depression of the central
nervous system ’ s control of
respiration (hypoglycemia,
meningitis, drugs, hemorrhage,
seizures), disturbances in oxygen
delivery (shock, sepsis, anemia), or
ventilation defects (obstruction of
the airway, pneumonia, muscle
weakness).
Obstructive Apnea

■ Obstructive apnea (pharyngeal instability, neck flexion) is characterized by absence

of 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.
Central Apnea

■ 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 the hyperventilation observed after the 1st months of life.
Mixed Apnea

■ The most common pattern of idiopathic apnea in preterm neonates is (50-75% of

cases), with obstructive apnea preceding (usually) or following central apnea.
■ Short episodes of apnea are usually central, whereas prolonged ones are often
mixed.
■ Apnea depends on the sleep state; its frequency increases during active (rapid eye
movement) sleep.
Clinical Manifestation

■ The onset of idiopathic apnea can be during the 1st 1-2 weeks after birth but is
often delayed if there is RDS or other causes of respiratory distress.
■ Apneic episodes have been noted to be as frequent on day 1 as throughout the 1st
week in premature infants without respiratory disease.
■ In preterm infants, serious apnea = cessation of breathing for longer than 20 sec or
for any duration if accompanied by cyanosis and bradycardia.
Treatment

■ Infants at risk for apnea should be started on cardiorespiratory monitoring.

■ Gentle tactile stimulation is often adequate therapy for mild and intermittent
episodes.
■ Recurrent apnea of prematurity may be treated with theophylline or caffeine.
– Theophylline and caffeine are as effective, but caffeine has fewer side effects
(tachycardia, feeding intolerance).
– 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 IV route.
– Loading doses of 20 mg/kg of caffeine citrate are followed 24 hr later by
maintenance doses of 5 mg/kg/24 hr qd, either orally or IV.
■ Methylxanthines increase central respiratory drive by lowering the threshold of
response to hypercapnia as well as enhancing contractility of the diaphragm and
preventing diaphragmatic fatigue.
– Higher doses of methylxanthines are more effective, do not result in frequent
side effects, and tend to reduce major neurodevelopmental disabilities.
– Doxapram, known to be a potent respiratory stimulant, acts predominantly on
peripheral chemoreceptors and is effective in neonates with apnea of
prematurity that is unresponsive to methylxanthines.
■ Nasal continuous positive airway pressure (continuous positive airway pressure
[CPAP], 2-5 cm H 2 O) and high-flow humidifcation using nasal cannula (1-2.5
L/min) are therapies for mixed or obstructive apnea, but CPAP is preferred because
of its proven efficacy and safety.
Prognosis

■ Apnea of prematurity does not alter an infant ’ s prognosis unless it is severe,

recurrent, and refractory to therapy.
■ Apnea of prematurity usually resolves by 36 wk of postconceptional age (PCA) and
does not predict future episodes of sudden infant death syndrome (SIDS).
– Avoidance of cigarette smoking exposure and of overheating the infant are also
important in the prevention of SIDS.
■ Some infants with persistent apnea are discharged as long as cardiorespiratory
monitoring can be performed at home.
RESPIRATORY DISTRESS
SYNDROME
(HYALINE MEMBRANE
DISEASE)
Incidence and Risk Factor

■ Occurs primarily in premature infants; its incidence is inversely related to gestational

age and birthweight.
■ Occurs in 60-80% of infants < 28 wk of gestational age, in 15-30% of those between
32 and 36 wk, and rarely in those > 37 wk.
■ The risk for development of RDS increases with maternal diabetes, multiple births,
cesarean delivery, precipitous delivery, asphyxia, cold stress, and a maternal history
of previously affected infants.
Etiology and Pathophysiology

■ Surfactant deficiency (decreased production and secretion) is the primary cause of

RDS.
■ The failure to attain an adequate FRC and the tendency of affected lungs to become
atelectatic correlate with high surface tension and the absence of pulmonary
surfactant.
■ Because of immaturity, the amounts produced or released may be insufficient to
meet postnatal demands.
■ Surfactant is present in high concentrations in fetal lung homogenates by 20 wk of
gestation, but it does not reach the surface of the lungs until later.
■ It appears in amniotic fluid between 28 and 32 wk. Mature levels of pulmonary
surfactant are present usually after 35 wk.
Contributing factors in the
pathogenesis of hyaline
membrane disease.
The potential “ vicious circle
” perpetuates hypoxia and
pulmonary insufficiency.
Clinical Manifestation

■ Usually appear within minutes of birth, although they may not be recognized for several
hours in larger premature infants until rapid, shallow respirations have increased to 60
breaths/min or greater.
■ Some patients require resuscitation at birth because of intrapartum asphyxia or initial
severe respiratory distress (especially with a birthweight < 1,000 g).
■ Characteristically, tachypnea, prominent (often audible) grunting, intercostal and
subcostal retractions, nasal flaring, and cyanosis are noted.
■ In most cases, the symptoms and signs reach a peak within 3 days, after which
improvement is gradual.
■ Improvement is often heralded by spontaneous diuresis and improved blood gas values
at lower inspired oxygen levels and/or lower ventilator support.
Diagnosis

■ The clinical course, chest radiographic findings, and blood gas and acid-base values
help establish the clinical diagnosis.
■ On radiographs, the lungs may have a characteristic but not pathognomonic
appearance that includes a fine reticular granularity of the parenchyma and air
bronchograms, which are often more prominent early in the left lower lobe because
of superimposition of the cardiac shadow.
– The initial radiographic appearance is occasionally normal, with the typical
pattern developing at 6-12 hr.
■ Laboratory findings are characterized initially by hypoxemia and later by progressive
hypoxemia, hypercapnia, and variable metabolic acidosis.
Prevention

■ Avoidance of unnecessary or poorly timed cesarean section, appropriate management of

high-risk pregnancy and labor, and prediction of pulmonary immaturity with possible in
utero acceleration of maturation.
■ Administration of antenatal corticosteroids to women between 24 and 34 wk of gestation
reduces the incidence and mortality of RDS as well as overall neonatal mortality.
– Do not affect postnatal growth or increase the risk of maternal death or puerperal
sepsis.
– Antenatal steroids also reduce:
■ (1) the need for and duration of ventilator support and admission to a neonatal
intensive care unit (NICU) and
■ (2) the incidence of severe IVH, necrotizing enterocolitis, early-onset sepsis, and
developmental delay.
Treatment

■ The basic defect requiring treatment in RDS is inadequate pulmonary exchange of

oxygen and carbon dioxide  metabolic acidosis and circulatory insufficiency are
secondary manifestations.
■ Therapy requires careful and frequent monitoring of heart and respiratory rates,
oxygen saturation, Pa o 2 , Pa co 2 , pH, serum bicarbonate, electrolytes, glucose,
and hematocrit, blood pressure, and temperature.
■ Because most cases of RDS are self-limited  the goal of treatment is to minimize
abnormal physiologic variations and superimposed iatrogenic problems.
■ Best carried out in the NICU.
■ To avoid hypothermia and minimize oxygen consumption, the infant should be
placed in an incubator or radiant warmer, and core temperature maintained
between 36.5 and 37 ° C.
– Use of an incubator is preferable in very LBW (VLBW) infants owing to the high
insensible water losses associated with radiant heat.
■ Calories and fluids should initially be provided intravenously.
– For the 1st 24 hr, 10% glucose and water should be infused through a
peripheral vein at a rate of 65-75 mL/kg/24 hr.
– Electrolytes should be added on day 2 in the most mature infants and on days
3 to 7 in the more immature ones.
– Fluid volume is increased gradually over the 1st week.
■ Excessive fluids ( > 140 mL/kg/day) contribute to the development of patent
ductus arteriosus (PDA) and BPD.
■ Surfactant deficiency is the primary pathophysiology of RDS.
– Immediate effects of surfactant replacement therapy = improved alveolar-
arterial oxygen gradients, reduced ventilator support, increased pulmonary
compliance, and improved chest radiograph appearance
– Treatment is initiated as soon as possible in the hours after birth.
– Repeated dosing is given via the endotracheal tube every 6-12 hr for a total of
2 to 4 doses, depending on the preparation.
– Exogenous surfactant should be given by a physician who is qualified in
neonatal resuscitation and respiratory management and who is able to care
for the infant beyond the 1st hr of stabilization.
– Synthetic surfactant = Exosurf.
– Natural surfactants = Survanta (bovine), Infasurf (calf), Curosurf (porcine).
■ Natural surfactants are superior because of their surfactant-associated protein
content, their more rapid onset, and their lower risk of pneumothorax and improved
survival.
Treatment: Pharmacologic

■ Vitamin A supplementation given largely to infants < 1,000 g resulted in a decrease

in death and/or BPD at 36 wk (from 66% to 60%) and trends for less nosocomial
sepsis and retinopathy of prematurity.
■ Systemic corticosteroids have been used to treat infants with RDS, to selectively
treat infants who continue to require respiratory support, and to treat those in whom
BPD develops.
– Short-term adverse effects = hyperglycemia, hypertension, GI bleeding,
gastrointestinal perforation, hypertrophic obstructive cardiomyopathy, poor
weight gain, poor growth of the head  routine use for the prevention or
treatment of BPD is not recommended
■ Metabolic acidosis in RDS may be a result of perinatal asphyxia and hypotension
and is often encountered when an infant has required resuscitation.
– Sodium bicarbonate 1-2 mEq/kg, may be administered over 15-20 min through
a peripheral or umbilical vein, followed by an acid-base determination within
30 min, or it may be administered over several hours.
Treatment: of BPD
■ Nutritional support, fluid restriction, drug therapy, maintenance of adequate
oxygenation, and prompt treatment of infection.
– Growth must be monitored because recovery depends on the growth of lung
tissue and remodeling of the pulmonary vascular bed.
– Nutritional supplementation to provide added calories (24-30 calories/30 mL
formula), protein (3-3.5 g/kg/24 hr), and fat (3 g/kg/24 hr) is needed for
growth.
– Diuretic therapy results in a short-term improvement in lung mechanics and
may lead to decreased oxygen and ventilatory requirements.
■ Treatment of choice: Furosemide (1 mg/kg/dose IV twice daily [bid] or 2
mg/kg/dose orally bid) for acute fluid overload in infants with BPD.
Reference

■ Nelson Textbook of Pediatrics, 19th Editon- Kliegman