II.

LEARNING CONTENT

MECONIUM ASPIRATION SYNDROME

Meconium is present in the fetal bowel as early as 10 weeks’ gestation. If hypoxia occurs, a vagal reflex
is stimulated, resulting in relaxation of the rectal sphincter. This releases meconium into the amniotic
fluid.

Meconium staining occurs in approximately 10% to 12% of all pregnancies; in 2% to 9% of these

Meconium aspiration does not tend to occur in extremelylow-birth-weight infants because the
substance has not passed far enough in the bowel for it to be at the rectum in these infant

An infant may aspirate meconium either in utero or with the first breath at birth.

Can cause severe respi distree by: It causes inflammation of bronchioles because it is a foreign
substance; it can block small bronchioles by mechanical plugging; and it can cause a decrease in
surfactant production through lung trauma

Hypoxemia, carbon dioxide retention, and intrapulmonary and extrapulmonary shunting occur

A secondary infection of injured tissue may lead to pneumonia.

Assessment:

Tachypnea, retractions, and cyanosis occur.

Infant should be suctioned with a bulb syringe or catheter while at the perineum, before the birth of the
shoulders, to avoid meconium aspiration.

Do not administer oxygen under pressure (bag and mask) until an infant has been intubated and
suctioned, so that the pressure of the oxygen does not drive small plugs of meconium farther down into
the lungs, worsening the irritation and obstruction

Therapeutic Management:

Amnioinfusion can be used to dilute the amount of meconium in amniotic fluid and reduce the risk of
aspiration

Born by cesarean birth after deeply meconium-stained amniotic fluid becomes evident during labor.

Antibiotic therapy may be used to forestall the development of pneumonia as a secondary problem

Surfactant may be administered to increase lung compliance

Chest physiotherapy with clapping and vibration may be helpful to encourage removal of remnants of
meconium from the lungs

Assess fo cardiac distress and pulmunary compramise

Apnea is a pause in respirations longer than 20 seconds with accompanying bradycardia

Beginning cyanosis also may be present.

Many preterm infants have periods of apnea due to fatigue or immature respiratory mechanisms.

Babies with secondary stresses, such as infection, hyperbilirubinemia, hypoglycemia, or hypothermia,

Gently shaking an infant or flicking the sole of the foot often stimulates the baby to breathe again,
almost as if the child needed to be reminded to maintain this function.

If an infant does not respond to these simple measures, resuscitation is necessary.

Management:

maintain a neutral thermal environment and use gentle handling to avoid excessive fatigue

Always suction gently to minimize nasopharyngeal irritation, which can cause bradycardia because of
vagal stimulation

Using indwelling nasogastric tubes rather than intermittent ones can also reduce the amount of vagal
stimulation.

Never take rectal temperatures in infants prone to apnea; the resulting vagal stimulation can reduce the
heart rate (bradycardia), which can lead to apnea

Theophylline or caffeine sodium benzoate may be administered to stimulate respirations.

SUDDEN INFANT DEATH SYNDROME (SIDS)

SIDS is sudden unexplained death in infancy. It tends to occur at a higher-than-usual rate in infants of
adolescent mothers, infants of closely spaced pregnancies, and underweight and preterm infants. Also
prone to SIDS are infants with bronchopulmonary dysplasia, twins.

The peak age of incidence is 2 to 4 months of age

Although the cause of SIDS is unknown, in addition to prolonged but unexplained apnea, other possible
contributing factors include:

Viral respiratory or botulism infection

Pulmonary edema

Brain stem abnormalities

Neurotransmitter deficiencies

Heart rate abnormalities

Decreased arousal responses

Possible lack of surfactant in alveoli

Sleeping in a room without moving air currents (the infant rebreathes expired carbon dioxide)

Typically, affected infants are well nourished. Parents report that an infant may have had a slight head
cold. After being put to bed at night or for a nap, the infant is found dead a few hours later; they die
with laryngospasm

An autopsy often reveals petechiae in the lungs and mild inflammation and congestion in the respiratory
tract

Family counselling should be done, explain that its not their fault

APPARENT LIFE-THREATENING EVENT

Some infants have been discovered cyanotic and limp in their beds but have survived after mouth-to-
mouth resuscitation by parents.

For these infants as well as for preterm infants with a tendency toward apnea or new babies born to a
family whose child died from SIDS, apnea monitoring is available.

Because SIDS is a baffling disease, these parents will live in fear of SIDS until their child reaches at least 1
year of age.

HEMOLYTIC DISEASE OF THE NEWBORN

Lysis of red blood cells in the newborn leads to hyperbilirubinemia (an elevated level of bilirubin in the
blood)

Causes: Rh and ABO incompatibility

ABO Incompatibility:

the maternal blood type is O and the fetal blood type is A; it may also occur when the fetus has type B or
AB blood. A reaction in an infant with type B blood is often the most serious.

With birth, progressive jaundice, usually occurring within the first 24 hours of life, will begin, indicating
in both Rh and ABO incompatibility that a hemolytic process is at work.

The jaundice occurs because as red blood cells are destroyed, indirect bilirubin is released. Indirect
bilirubin is fat soluble and cannot be excreted from the body.

Liver will relase an enzyme glucuronyl transferase converts indirect bilirubin to direct bilirubin to make it
water soluble and be excreted in urine( yellow in color urine)
In preterm infants or those with extreme hemolysis, the liver cannot convert indirect to direct bilirubin,
so jaundice becomes extreme.

An increasing indirect bilirubin level is dangerous because if the level rises above 20 mg/dL in a term
infant or 12 mg/dL in a preterm infant, brain damage from bilirubin-induced neurologic dysfunction
(BIND) or a wide spectrum of disorders caused by increasingly severe hyperbilirubinemia that range
from mild dysfunction to kernicterus (invasion of bilirubin into brain cells) can occur.

Therapeutic Management:

Initiation of Early Feeding-Bilirubin is removed from the body by being incorporated into feces.
Therefore, the sooner bowel elimination begins, the sooner bilirubin removal begins.

Phototherapy-With birth, exposure to light triggers the liver to assume this function and Additional light
supplied by phototherapy appears to speed the conversion potential of the liver.

In phototherapy, an infant is continuously exposed to specialized light such as quartz halogen, cool
white daylight, or special blue fluorescent light. The lights are placed 12 to 30 inches above the
newborn’s bassinet or incubator

An infant must continuously wear eye patches and a diaper during phototherapy to protect the retinas
and the ovaries or testes

The stools of an infant under bilirubin lights are often bright green because of the excessive bilirubin
that is excreted as the result of the therapy. Urine may be dark-colored from urobilinogen formation.

Assess skin turgor and intake and output to ensure that dehydration is not occurring from the warm
environment.

Exchange Transfusion-The umbilical vein is catheterized as the site for transfusion. The procedure
involves alternatively withdrawing small amounts (2–10 mL) of the infant’s blood and then replacing it
with equal amounts of donor blood. The blood is exchanged slowly this way to prevent alternating
hypovolemia and hypervolemia. This can make an exchange transfusion a lengthy procedure of 1 to 3
hours.

AN INFANT OF A WOMAN WHO HAS DIABETES MELLITUS

An infant of a woman who has diabetes mellitus whose illness was poorly controlled during pregnancy is
typically longer and weighs more than other babies (macrosomia).

baby also has a greater chance of having a congenital anomaly such as a cardiac anomaly.

Most such babies have a cushingoid (fat and puffy) appearance. They tend to be lethargic or limp in the
first days of life as a result of hyperglycemia.

They are prone with: Immature, RDS , small colon

Therapeutic Management:
To avoid a serum glucose level from falling this low, infants of diabetic women are fed early with
formula or administered a continuous infusion of glucose

AN INFANT OF A DRUG-DEPENDENT MOTHER

Infants of drug-dependent women tend to be SGA. If the woman is dependent on a drug, an infant will
show withdrawal symptoms (neonatal abstinence syndrome)

Irritability

Disturbed sleep pattern

Constant movement, possibly leading to abrasions on the elbows, knees, or nose

Tremors

Frequent sneezing

Shrill, high-pitched cry

Possible hyperreflexia and clonus (neuromuscular irritability)

Convulsions

Tachypnea (rapid respirations), possibly so severe that it leads to hyperventilation and alkalosis

Vomiting and diarrhea, leading to large fluid losses and secondary dehydration

In newborns experiencing opiate withdrawal, signs usually begin 24 to 48 hours after birth, but in some
infants they may not appear for up to 10 days.

Infants of drug-dependent women usually seem most comfortable when firmly swaddled. Keep them in
an environment free from excessive stimuli (a small isolation nursery, not a large, noisy one). Some quiet
best if the room is darkened.

Specific therapy for an infant is individualized according to the nature and severity of the signs

AN INFANT WITH FETAL ALCOHOL EXPOSURE

Alcohol crosses the placenta in the same concentration as is present in the maternal bloodstream. This
results in fetal alcohol exposure and fetal alcohol syndrome

The newborn with fetal alcohol syndrome has several possible problems at birth. Characteristics that
mark the syndrome include prenatal and postnatal growth restriction; central nervous system
involvement such as cognitive challenge, microcephaly, and cerebral palsy; and a distinctive facial
feature of a short palpebral fissure and thin upper lip.

The most serious long-term effect is cognitive challenge.