Meconium aspiration syndrome

• Meconium is the earliest stool of an infant.

• It is a thick, black-green, odorless material which results from the
accumulation of debris, including desquamated cells from the
intestine and skin, gastrointestinal mucin, lanugo hair, fatty material
from the vernix caseosa, amniotic fluid, and intestinal secretion.
• Meconium-stained amniotic fluid is found in 10–15% of births and
usually occurs in term or post term infants.
• Meconium aspiration syndrome (MAS) develops in 5% of such
infants; 30% require mechanical ventilation, and 3–5% die.
Meconium aspiration syndrome

• Usually, but not invariably, fetal distress occur before the passage of
meconium into amniotic fluid.
• The infants are meconium stained and may be depressed and require
resuscitation at birth.
• Infants with MAS are at increased risk of persistent pulmonary
hypertension
CLINICAL MANIFESTATIONS
• Either in utero or with the first breath, thick, particulate meconium is
aspirated into the lungs.
• The resulting small airway obstruction may produce respiratory distress
within the 1st hours, with tachypnea, retractions, grunting, and cyanosis
observed in severely affected infants.
• Partial obstruction of some airways may lead to pneumomediastinum,
pneumothorax, or both. Over distention of the chest may be prominent.
• The condition usually improves within 72 hr, but when its course requires
assisted ventilation, it may be severe with a high risk for mortality.
• Tachypnea may persist for many days or even several weeks.
• The typical chest radiograph is characterized by patchy infiltrates,
coarse streaking of both lung fields, increased anteroposterior
diameter, and flattening of the diaphragm.
• A normal chest radiograph in an infant with severe hypoxemia and no
cardiac malformation suggests the diagnosis of pulmonary
hypertension
incidence
• The incidence is 1 in 500-1,500 live births, with a wide variation
among clinical centers.
• Regardless of etiology of PPHN, profound hypoxemia from right-to-
left shunting and normal or elevated PaCO2 are present
PREVENTION

• The risk of meconium aspiration may be decreased by rapid

identification of fetal distress and initiation of prompt delivery in the
presence of late fatal heart rate deceleration or poor beat-to-beat
FHR variability.
TREATMENT

• Treatment of the MAS includes supportive care and standard

management for respiratory distress.
• The beneficial effect of mean airway pressure on oxygenation must be
weighed against the risk of pneumothorax.
• Administration of exogenous surfactant and/or iNO to infants with
MAS and hypoxemic respiratory failure, or pulmonary hypertension
Meconium aspiration. Serial radiographs in a newborn with uncomplicated meconium aspiration. Radiograph obtained shortly after birth shows
ill-defined, predominantly perihilar opacities in the lungs; these are more severe on the right than on the left. The lungs are hyperexpanded. The
neonate's heart size is within normal limits
Persistent pulmonary hypertension of the
newborn (PPHN)
• occurs most often in term and postterm infants.
• Predisposing factors include
• birth asphyxia,
• MAS,
• early-onset sepsis,
• RDS,
• hypoglycemia,
• polycythemia,
• maternal use of nonsteroidal anti inflammatory drugs with in utero constriction of the
ductus arteriosus,
• maternal late trimester use of selective serotonin reuptake inhibitors, and pulmonary
hypoplasia caused by diaphragmatic hernia, amniotic fluid leak, oligohydramnios, or pleural
effusions.
PATHOPHYSIOLOGY
• Persistence of the fetal circulatory pattern of right-to-left shunting
through the PDA and foramen ovale after birth is a result of
excessively high pulmonary vascular resistance (PVR).
• Fetal PVR is usually elevated relative to fetal systemic or postnatal
pulmonary pressure.
• This fetal state normally permits shunting of oxygenated umbilical
venous blood to the left atrium (and brain) through the foramen
ovale, from which it bypasses the lungs through the ductus arteriosus
and passes to the descending aorta.
• . Increased neonatal PVR may be
• (1) maladaptivefrom an acute injury (not demonstrating normal vasodilation
in response to increased and other changes after birth);
• (2) the result of increased pulmonary artery medial muscle thickness and
extension of smooth muscle layers into the usually nonmuscular, more
peripheral pulmonary arterioles in response to chronic fetal hypoxia;
• (3) a consequence of pulmonary hypoplasia(diaphragmatic hernia, Potter
syndrome); or
• (4) obstructiveas a result of polycythemia, total anomalous pulmonary venous
return (TAPVR), or congenital diffuse development disorders of acinar lung
development
CLINICAL MANIFESTATIONS
,
• PPHN usually manifests in the delivery room or within the 1st 12 hr
after birth.
• Idiopathic PPHN or PPHN related to polycythemiahypoglycemia, hypothermia, or
asphyxia may result in severe cyanosis and respiratory distress. In some cases,
however, initial signs of respiratory distress may be minimal.
• Infants who have PPHN associated with meconium aspiration, group B
streptococcal pneumonia, diaphragmatic hernia, or pulmonary hypoplasia usually
exhibit cyanosis, grunting, flaring, retractions, tachycardia, and shock.
• Multiorgan involvement may be present .Myocardial ischemia, papillary muscle
dysfunction with mitral and tricuspid regurgitation, and biventricular dysfunction
produce cardiogenic shock with decreases in pulmonary blood flow, tissue
perfusion, and O2delivery.
• Hypoxemia is often labile and out of proportion to the findings on
chest radiographs. In asphyxia-associated and idiopathic PPHN, chest
x-ray findings are often normal,
• whereas in PPHN associated with pneumonia and diaphragmatic
hernia, parenchymal opacification and bowel/liver in the chest,
respectively, are seen
DIAGNOSIS

• Independent of the prenatal history, PPHN should be suspected in all

term infants who have cyanosis
• .Hypoxemia is universal and intermittently unresponsive to 100%
O2given by oxygen hood. A transient improvement may occur in
response to hyperoxic hyperventilation administered by positive
pressure ventilation.
• A PaO2or SaO2gradient between a preductal (right radial artery) and
a postductal (umbilical artery) site of blood sampling suggests right-
to-left shunting through the ductus arteriosus.
Treatment
• Therapy for PPHN is directed toward correcting any predisposing
condition (e.g., hypoglycemia, polycythemia) and improving poor
tissue oxygenation.
• The response to therapy is often unpredictable, transient, and
complicated by the adverse effects of drugs or mechanical ventilation.
Initial management includes O2administration and correction of
acidosis, hypotension, and hypercapnia.
• Persistent hypoxemia should be managed with intubation and
mechanical ventilation because of their instability and ability to fight
the ventilator, newborns with PPHN usually require sedation
• Inotropic therapyis frequently needed to support blood pressure and
perfusion.
• Whereas dopamine is frequently used as a first-line agent, other
agents, such as dobutamine, epinephrine, and milrinone, may be
helpful when myocardial contractility is poor.
• Inhaled NO is an endothelium-derived signaling molecule that relaxes
vascular smooth muscle and can be delivered to the lung by
inhalation . Use of iNO reduces the need for ECMO support by
approximately 40%.The optimal starting dose is 20 ppm
• ECMOis a form of cardiopulmonary bypass that augments systemic
perfusion and provides gas exchange. Most experience has been with
• venoarterial bypass, which requires carotid artery ligation and the
placement of large catheters in the right internal jugular vein and
carotid artery.
• Venovenous bypassavoids carotid artery ligation and provides gas
exchange, but it does not support cardiac output. Blood is initially
pumped through the ECMO circuit at a rate that approximates 80% of
the estimated cardiac output, 150-200 mL/kg/mi
Transient Tachypnea of the Newborn
• Transient tachypnea of the newborn (TTN) is a clinical syndrome of
self-limited tachypnea associated with delayed clearance of fetal lung
fluid.
• Although the actual incidence is likely underreported, it is estimated
at 3-6 per 1,000 term infant births, making TTN the most common
etiology of tachypnea in the newborn.
• Twin gestation, maternal asthma, late prematurity , precipitous
delivery , gestational diabetes, and cesarean delivery without labor
are common associated risk factors.
.
• Clearance of fetal lung fluid occurs through increased expression of
epithelial sodium channels (ENaC) and sodium-potassium adenosine
triphosphatase (Na+ ,K+ -A TPase) that drive active sodium (and
thereby fluid) reabsorption.
• TTN is believed to result from ineffective expression or activity of
ENaC and Na,K+-A TPase, which slows absorption of fetal lung fluid
and results in decreased pulmonary compliance and impeded gas
exchange.
• TTN is characterized by the early onset of tachypnea (>60 breaths/min), sometime
with retractions or expiratory grunting and occasionally with cyanosis that is relieved
by minimal O2 supplementation (<40%).
• The chest generally sounds clear without crackles or wheeze, and the chest
radiograph shows prominent perihilar pulmonary vascular markings, fluid in the
intralobar fissures, and rarely small pleural effusions.
• Hypercapnia and acidosis are uncommon. Respiratory failure requiring positive
pressure support (either with nCpAP or mechanical ventilation) also is uncommon,
but when it occurs usually resolves rapidly (<12-24 hr).
• Most infants recover with supportive care alone, and over the first 24-72 hours the
tachypnea and O2 requirements slowly resolve
• Treatment for TTN is supportive.
Pulmonary Hemorrhage

• occurs in about 10% of extremely preterm infants. Autopsy demonstrates

massive pulmonary hemorrhage in 15% of neonates who die in the 1st 2 wk
of life. The reported incidence at autopsy varies from 1-4 per 1,000 live
births.
• Approximately 75% of affected patients weigh <2,500 g at birth.
• The onset may occur at birth or may be delayed several days.
• Hemorrhagic pulmonary edema is the source of blood in many cases and is
associated with significant ductal shunting and high pulmonary blood flow
or severe left-sided heart failure resulting from hypoxia. ducal In severe
cases, sudden cardiovascular collapse, poor lung compliance, profound
cyanosis, and hypercapnia may be present.
• The risk of pulmonary hemorrhage is increased in association with acute
pulmonary infection, severe asphyxia,RDS, assisted ventilation, PDA,
Congenital heart disease, erythroblastosis fetalis, hemorrhagic disease of
the newborn, thrombocytopenia, inborn errors of ammonia metabolism,
and cold injury .
• Pulmonary hemorrhage is the only severe complication in which the rate
is increased with surfactant treatment.
• Pulmonary hemorrhage is seen with all surfactants; the incidence ranges
from 1–5% of treated infants and is higher with natural surfactant.
Bleeding is predominantly alveolar in approximately 65% of cases and
interstitial in the rest.
• Patients present with acute, severe respiratory failure requiring
mechanical ventilation. Chest radiographs usually demonstrate
bilateral alveolar infiltrates. The condition usually responds to
intensive supportive treatment
treatment
• treatment of pulmonary hemorrhage includes blood replacement,
suctioning to clear the airway ,
• intratracheal administration of epinephrine, and tamponade with
increased mean airway pressure (often requiring HFV).
• Although surfactant treatment has been associated with the
development of pulmonary hemorrhage, administration of exogenous
surfactant after the bleeding has occurred can improve lung
compliance, because the presence of intra alveolar blood and protein
can inactivate surfactant.