Anemia of Prematurity - Portal Neonatal

Comparisons of the nutrient content and source of macronutrients of these fortifiers have been
published. Potential complications of human milk fortifiers include nutrient imbalance, increased
osmolarity, and bacterial contamination. A number of specially formulated preterm formulas are
available that have been shown to promote proper growth, as well. Caloric density usually is
increased when a full feeding volume is achieved and the infant is no longer on intravenous
supplementation.
Hyperbilirubinemia
Most ELBW infants develop clinically significant typically unconjugated or indirect hyperbilirubinemia
requiring treatment. Hyperbilirubinemia develops as a result of increased red blood cell turnover and
destruction, an immature liver that is impaired during conjugation and elimination of bilirubin, and
reduced bowel motility, which delays elimination of bilirubin-containing meconium. These
manifestations of extreme prematurity in addition to typical conditions that cause jaundice (eg, ABO
incompatibility, Rh disease, sepsis, inherited diseases) place these infants at higher risk for
kernicterus at levels of bilirubin far below those in more mature infants. Kernicterus occurs when
unconjugated bilirubin crosses the blood-brain barrier and stains the basal ganglia, pons, and
cerebellum. Infants with kernicterus who do not die may have sequelae such as deafness, mental
retardation, and cerebral palsy.
Phototherapy is used to decrease bilirubin levels to prevent the elevation of unconjugated bilirubin to
levels that cause kernicterus. Phototherapy, which uses special blue lamps with wavelengths of 420-
475 nm, breaks down unconjugated bilirubin to a more water-soluble product via photoisomerization
and photooxidation through the skin. Then, this product can be eliminated in bile and urine. The
fluorescent bulbs are positioned at 50 cm above the infant with a resulting intensity of 6-12 μW/cm 2 .
Tan has shown that the rate of bilirubin reduction is proportional to the light intensity. Phototherapy
causes an increase in insensible water loss, so the amount of fluid intake typically should be
increased. The infant's eyes are covered with patches to avoid exposure to blue light.
While phototherapy is initiated at birth of ELBW infants at some institutions, others start phototherapy
when the bilirubin value approaches 50% of the birth weight value (eg, 4 mg/dL in an 800-g infant). If
the level of bilirubin does not decrease satisfactorily with phototherapy, exchange transfusion is
another option. If the level of bilirubin approaches 10 mg/dL (or 10 mg/dL/kg), exchange transfusion
can begin to be considered in ELBW infants. In otherwise healthy term infants, exchange transfusion
is not considered until the bilirubin level approaches 25 mg/dL.
In exchange transfusions, almost 90% of the infant's blood is replaced with donor blood, and the
bilirubin level falls to 50-60% of the preexchange level. Complications include electrolyte
abnormalities (hypocalcemia, hyperkalemia), acidosis, thrombosis, sepsis, and bleeding.
Respiratory distress syndrome
An early complication of extreme prematurity is respiratory distress syndrome (RDS), which is
caused by surfactant deficiency. Clinical signs include tachypnea (>60 breaths/min), cyanosis, chest
retractions, nasal flaring, and grunting. Untreated RDS results in increased difficulty in breathing and
an increased oxygen requirement over the first 24-72 hours of life. Chest radiographs reveal a
uniform reticulogranular pattern with air bronchograms. Since the incidence of RDS correlates with
the degree of prematurity, most ELBW infants are affected. As a result of surfactant deficiency, the
alveoli collapse, causing a worsening of atelectasis, edema, and decreased total lung capacity.
Surfactants decrease the surface tension of the smaller airways so that the alveoli or the terminal air
sacs do not collapse, which results in less need for supplemental oxygen and ventilatory support.
Common complications include air leak syndromes, CLD, and retinopathy of prematurity (ROP).
Surfactant agents may be administered as prevention or prophylactic treatment or as rescue
intervention after hyaline membrane disease (HMD) is established. Synthetic surfactants lack the
proteins found in animal-derived surfactants and may not be as effective as the latter.