ABO incompatibility

ABO incompatibility disease afflicts newborns whose mothers are blood type O, and who have a baby with type A, B,
or AB.

Ordinarily, the antibodies against the foreign blood types A and B that circulate in mother's bloodstream remain there,
because they are of a type that is too large to pass easily across the placenta into the fetal circulation. Some fetal red
cells always leak into mother's circulation across the placental barrier (mother and fetal blood theoretically do not mix,
but in actuality, they do to a small degree).

These fetal red cells stimulate the formation of a smaller type of anti-A or anti-B antibody which can pass into the
baby's circulation and there cause the destruction of fetal red cells. The increased rate of destruction of red cells
causes a subsequent increase in waste product production. This excess waste product, bilirubin, can overwhelm the
normal waste elimination processes and lead to jaundice, the presence of excess bilirubin.

This condition is one of the hemolytic anemias. Jaundice is the most common problem encountered, which may
require phototherapy or even exchange transfusion.

Diagnosis

Routine antenatal antibody screening blood tests (indirect Coombs test) do not screen for ABO HDN. If IgG anti-A or
IgG anti-B antibodies are found in the pregnant woman's blood, they are not reported with the test results, because
they do not correlate well with ABO HDN. Diagnosis is usually made by investigation of a newborn baby who has
developed jaundice during the first day of life.

Treatment

Neonatal jaundice caused by ABO HDN is usually successfully treated with phototherapy, unless the ABO HDN is
uncommonly severe. Treatment of moderate or severe HDN caused by ABO antibodies is similar to that for Rh
disease.

Infant respiratory distress syndrome (IRDS), also called neonatal respiratory distress syndrome[1] or
respiratory distress syndrome of newborn, previously called hyaline membrane disease, is a syndrome caused
in premature infants by developmental insufficiency of surfactant production and structural immaturity in the lungs. It
can also result from a genetic problem with the production of surfactant associated proteins. RDS affects about 1% of
newborn infants and is the leading cause of death in preterm infants.[2] The incidence decreases with advancing
gestational age, from about 50% in babies born at 26–28 weeks, to about 25% at 30–31 weeks. The syndrome is
more frequent in infants of diabetic mothers and in the second born of premature twins.

IRDS is distinct from pulmonary hypoplasia, another leading cause of neonatal death that involves respiratory
distress.

Treatment

Oxygen is given with a small amount of continuous positive airway pressure ("CPAP"), and intravenous fluids are
administered to stabilize the blood sugar, blood salts, and blood pressure. If the baby's condition worsens, an
endotracheal tube (breathing tube) is inserted into the trachea and intermittent breaths are given by a mechanical
device. An exogenous preparation of surfactant, either synthetic or extracted from animal lungs, is given through the
breathing tube into the lungs. One of the most commonly used surfactants is Survanta, derived from cow lungs, which
can decrease the risk of death in hospitalized very-low-birth-weight infants by 30%.[4] Such small premature infants
may remain ventilated for months. A line of research shows that an aerosol of perfluorocarbon can reduce
inflammation in piglets.[5] Chronic lung disease including bronchopulmonary dysplasia are common in severe RDS.
The etiology of BPD is problematic and may be due to oxygen, overventilation or underventilation. The mortality rate
for babies greater than 27 weeks gestation is less than 10%.
Preterm birth refers to the birth of a baby of less than 37 weeks gestational age. The cause for preterm birth is in
many situations elusive and unknown; many factors appear to be associated with the development of preterm birth,
making the reduction of preterm birth a challenging proposition.

Premature birth, commonly used as a synonym for preterm birth, refers to the birth of a baby before its organs
mature enough to allow normal postnatal survival, and growth and development as a child. Premature infants are at
greater risk for short and long term complications, including disabilities and impediments in growth and mental
development. Significant progress has been made in the care of premature infants, but not in reducing the prevalence
of preterm birth.[1] Preterm birth is by far the most common cause of prematurity, and is the major cause of neonatal
mortality in developed countries. Premature children may commonly be referred to throughout their life as being born
a "preemie" or "preemie baby"

Diagnosis

Helpful clinical test should predict a high risk for preterm birth during the early and middle part of the third trimester,
when their impact is significant. Many women experience false labor (not leading to cervical shortening and
effacement) and are falsely labelled to be in preterm labor. The study of preterm birth has been hampered by the
difficulty in distinguishing between "true" preterm labor and false labor.[11] These new test are used to identify women
at risk for preterm birth.

Prevention

Historically efforts have been primarily aimed to improve survival and health of preterm infants (tertiary intervention).
Such efforts, however, have not reduced the incidence of preterm birth. Increasingly primary interventions that are
directed at all women, and secondary intervention that reduce existing risks are looked upon as measures that need
to be developed and implemented to prevent the health problems of premature infants and children

Transient Tachypnea of the New Born

Before birth, a fetus' lungs are filled with fluid. While inside the mother, a fetus does not use the lungs to breathe —
all oxygen comes from the blood vessels of the placenta.

As the due date nears, the baby's lungs begin to clear the fluid in response to hormonal changes. Some fluid may
also be squeezed out during the birth, as a baby passes through the birth canal. After the birth, as a newborn takes
those first breaths, the lungs fill with air and more fluid is pushed out of the lungs. Any remaining fluid is then coughed
out or gradually absorbed into the body through the bloodstream and lymphatic system.

In infants with TTN, however, extra fluid in the lungs remains or the fluid is cleared too slowly. So it is more difficult for
the baby to inhale oxygen properly, and the baby breathes faster and harder to get enough oxygen into the lungs.

Causes of TTN

TTN, also called "wet lungs" or type II respiratory distress syndrome, usually can be diagnosed in the hours after
birth. It's not possible to detect before the birth whether a child will have it.

TTN can occur in both preemies (because their lungs are not yet fully developed) and full-term babies.

Newborns at higher risk for TTN include those who are:

 delivered by cesarean section (C-section)

 born to mothers with diabetes
 born to mothers with asthma
 small for gestational age (small at birth)

During vaginal births, especially with full-term babies, the pressure of passing through the birth canal squeezes some
of the fluid out of the lungs. Hormonal changes during labor may also lead to absorption of some of the fluid.
Babies who are small or premature or who are delivered via rapid vaginal deliveries or C-section don't undergo the
usual squeezing and hormone changes of a vaginal birth. So they tend to have more fluid than normal in their lungs
when they take their first breaths.

Diagnosis

Because TTN has symptoms that are initially similar to more severe newborn respiratory problems (such as
pneumonia or persistent pulmonary hypertension), doctors may use chest X-rays in addition to physical examination
to make a diagnosis.

Other indicators used to make a diagnosis of TTN:

 If an infant has TTN, the X-ray picture of the lungs will appear streaked and fluid may be seen. The X-ray will
otherwise appear fairly normal.
 Pulse-oximetry monitoring, which is when a small piece of tape containing an oxygen sensor is placed
around a baby's foot or hand and connected to a monitor. This tells doctors how well the lungs are sending
oxygen to the blood and is also useful in monitoring TTN. Sometimes oxygen levels need to be checked with
a blood test.
 A complete blood count (CBC) may also be drawn from one of the baby's veins or a heel to check for signs
of infection.

Meconium aspiration syndrome (MAS, alternatively "Neonatal aspiration of meconium") is a medical condition
affecting newborn infants. It occurs when meconium is present in their lungs during or before delivery. Meconium is
the first stool of an infant, composed of materials ingested during the time the infant spends in the uterus.

 Meconium is normally stored in the infant's intestines until after birth, but sometimes (often in response to
fetal distress) it is expelled into the amniotic fluid prior to birth, or during labor. If the baby then inhales the
contaminated fluid, respiratory problems may occur.

Treatment

Amnioinfusion, a method of thinning thick meconium that has passed into the amniotic fluid through pumping of sterile
fluid into the amniotic fluid, has not shown a benefit in treating MAS. Until recently it had been recommended that the
throat and nose of the baby be suctioned by the delivery attendant as soon as the head is delivered. However, new
studies have shown that this is not useful and the revised Neonatal Resuscitation Guidelines published by the
American Academy of Pediatrics no longer recommend it. When meconium staining of the amniotic fluid is present
and the baby is born depressed, it is recommended by the guidelines that an individual trained in neonatal intubation
use a laryngoscope and endotracheal tube to suction meconium from below the vocal cords

Small for gestational age (SGA) babies are those whose birth weight, length, or head circumference lies below the
10th percentile for that gestational age

Diagnosis

The condition is generally diagnosed by measuring the mother's uterus, with the fundal height being less than it
should be for that stage of the pregnancy. If it is suspected, the mother will usually be sent for an ultrasound to
confirm.

Treatment

Possible treatments include the early induction of labour, though this is only done if the condition has been diagnosed
and seen as a risk to the health of the fetus.

Large for gestational age (LGA) babies are those whose birth weight (or length, or head circumference) lies above
the 90th percentile for that gestational age.[1] Macrosomia, also known as big baby syndrome, is sometimes used
synonymously with LGA, or is otherwise defined as a fetus that weighs above 4000 grams (8 lb 13 oz) or 4500 grams
(9 lb 15 oz) regardless of gestational age.
Treatment

Depending upon the relative size of the head of the baby and the pelvic diameter of the mother vaginal birth may
become complicated. One of the most common complications is shoulder dystocia. Such pregnancies often end in
caesarean sections in order to safely deliver the baby and to avoid birth canal lacerations. Upon birth, early feeding is
essential to prevent fetal hypoglycemia. Early diagnosis of individual problems is required.

Necrotizing enterocolitis (NEC) is a medical condition primarily seen in premature infants,[1] where portions of the
bowel undergo necrosis (tissue death).

Diagnosis

The diagnosis is usually suspected clinically but often requires the aid of diagnostic imaging modalities. Radiographic
signs of NEC include dilated bowel loops, paucity of gas, a "fixed loop" (unaltered gas-filled loop of bowel),
pneumatosis intestinalis, portal venous gas, and pneumoperitoneum (extraluminal or "free air" outside the bowel
within the abdomen). The pathognomic finding on plain films is pneumatosis intestinalis. More recently
ultrasonography has proven to be useful as it may detect signs and complications of NEC before they are evident on
radiographs. Diagnosis is ultimately made in 5-10% of very low-birth-weight infants (<1,500g)

Treatment

Treatment consists primarily of supportive care including providing bowel rest by stopping enteral feeds, gastric
decompression with intermittent suction, fluid repletion to correct electrolyte abnormalities and third space losses,
support for blood pressure, parenteral nutrition, and prompt antibiotic therapy. Monitoring is clinical, although serial
supine and left lateral decubitus abdominal roentgenograms should be performed every 6 hours. Where the disease
is not halted through medical treatment alone, or when the bowel perforates, immediate emergency surgery to resect
the dead bowel is generally required, although abdominal drains may be placed in very unstable infants as a
temporizing measure. Surgery may require a colostomy, which may be able to be reversed at a later time. Some
children may suffer later as a result of short bowel syndrome if extensive portions of the bowel had to be removed.

Hyperbilirubinemia/Jaundice, (also known as icterus, attributive adjective: icteric) is a yellowish pigmentation of

the skin, the conjunctival membranes over the sclerae (whites of the eyes), and other mucous membranes caused by
hyperbilirubinemia (increased levels of bilirubin in the blood). This hyperbilirubinemia subsequently causes increased
levels of bilirubin in the extracellular fluids. Typically, the concentration of bilirubin in the plasma must exceed 1.5
mg/dL[1] ( > 35 micromoles/L), three times the usual value of approximately 0.5 mg/dL[1], for the coloration to be easily
visible. Jaundice comes from the French word jaune, meaning yellow.

One of the first tissues to change color as bilirubin levels rise in jaundice is the conjunctiva of the eye, a condition
sometimes referred to as scleral icterus. However, the sclera themselves are not "icteric" (stained with bile pigment)
but rather the conjunctival membranes that overlie them. The yellowing of the "white of the eye" is thus more properly
conjunctival icterus.

Retinopathy of prematurity (ROP), previously known as retrolental fibroplasia (RLF), is an eye disease that
affects prematurely born babies. It is thought to be caused by disorganized growth of retinal blood vessels which may
result in scarring and retinal detachment. ROP can be mild and may resolve spontaneously, but may lead to
blindness in serious cases. As such, all preterm babies are at risk for ROP, and very low birth weight is an additional
risk factor. Both oxygen toxicity and relative hypoxia can contribute to the development of ROP.

Treatment

The retina (red) is detached at the top of the eye.

The silicone band (scleral buckle, blue) is placed around the eye. This brings the wall of the eye into contact with the
detached retina, allowing the retina to re-attach.

 Peripheral retinal ablation is the mainstay of ROP treatment. The destruction of the avascular retina is
performed with a solid state laser photocoagulation device, as these are easily portable to the operating
room or neonatal ICU. Cryotherapy, an earlier technique in which regional retinal destruction was done
using a probe to freeze the desired areas, has also been evaluated in multi-center clinical trials as an
 effective modality for prevention and treatment of ROP. However, cryotherapy is no longer preferred for
routine avascular retinal ablation in premature babies, due to the side effects of inflammation and lid
swelling.
 Scleral buckling and/or vitrectomy surgery may be considered for severe ROP (stage 4 and 5) for eyes that
progress to retinal detachment. Few centers in the world specialize in this surgery, because of its attendant
surgical risks and generally poor outcomes.
 Intravitreal injection of bevacizumab (Avastin) has been reported as a supportive measure in aggressive
posterior retinopathy of prematurity.

Apnea of prematurity is defined as cessation of breathing by a premature infant that lasts for more than 15 seconds
and/or is accompanied by hypoxia or bradycardia. Apnea is traditionally classified as either obstructive, central, or
mixed. Obstructive apnea may occur when the infant's neck is hyperflexed or conversely, hyperextended. It may also
occur due to low pharyngeal muscle tone or to inflammation of the soft tissues, which can block the flow of air though
the pharynx and vocal cords. Central apnea occurs when there is a lack of respiratory effort. This may result from
central nervous system immaturity, or from the effects of medications or illness. Many episodes of apnea of
prematurity may start as either obstructive or central, but then involve elements of both, becoming mixed in nature

Treatment

Medications

Methylxanthines (theophylline and caffeine) have been used for almost three decades to treat apnea of prematurity.[2]

Respiratory support

Simple tactile stimulation by touching the skin or patting the infant may stop an apneic episode by raising the infant's
level of alertness. Increasing the environmental oxygen level by placing the infant in a tent of hood with supplemental
oxygen can diminish the frequency of AOP, and may also help the infant maintain adequate oxygenation during short
episodes of apnea. Increased oxygen at low levels can also be delivered using a nasal cannula, which additionally
may provide some stimulation due to the tactile stimulation of the cannula. CPAP (continuous positive airway
pressure) is sometimes used for apnea when medications and supplemental oxygen are not sufficient. Usually as a
last resort, mechanical ventilation is used to support infants whose apnea cannot be controlled sufficiently by other
methods and where the potential risk of harm from recurrent hypoxia is felt to outweigh the risks of injury from
ventilation.