PREMATURITY
DEFINITIONS
Premature infant: Live-born newborn delivered prior to 37 weeks from the first day of last menstrual period.
Low birth weigh (LBW): < 2500 g.
Very low birth weight (VLBW): 1500 g.
Extremely low birth weight (ELBW): < 1000 g.
Extremely low gestational age neonate (ELGAN): < 750 g and/or gestational age 26 weeks.
ETIOLOGY
Most premature births have no identifiable causes.
Identifiable contributors include maternal, fetal, and obstetric:
Maternal:
Low socioeconomic status.
Preeclampsia.
Infections (urinary tract infections, group B streptococcus, etc).
Chronic medical illness (hypertension, renal disease, diabetes, cyanotic heart disease, etc).
Drug use.
Fetal:
Multiple gestation.
Fetal distress (from hypoxia, etc).
Congenital anomalies.
Obstetric:
Incompetent cervix.
Polyhydramnios.
Chorioamnionitis.
Premature rupture of membranes.
Placenta previa and abruptio placenta.
Placing a healthy premature neonate in a neutral thermal environment reduces calories burned.
COMMON PROBLEMS IN PREMATURE NEWBORNS
Respiratory Distress Syndrome (RDS; Hyaline Membrane Disease of the Newborn)
ETIOLOGY/PATHOPHYSIOLOGY
Occurs secondary to insufficiency of lung surfactant due to immaturity of surfactant producing type 2 alveolar cells.
Alveoli are small, inflate with difficulty, and do not remain gas-filled between inspirations.
Rib cage is weak and compliant.
High surface tension and propensity for alveolar collapse.
Alveolar collapse results in progressive atelectasis, intrapulmonary shunting, hypoxemia, and cyanosis.
EPIDEMIOLOGY
Usually seen in infants < 32 weeks’ gestational age, but has been seen in full-term infants, especially when the mother has maternal diabetes.
The incidence of RDS is inversely proportional to gestational age.
SIGNS AND SYMPTOMS
Seen within the first 4 hours of life.
Tachypnea.
Grunting.
Cyanosis.
Production of surfactant can be accelerated by maternal steroid (betamethasone) administration; best if given 24–48 hours prior to delivery.
DIAGNOSIS
Chest x-ray with fine, diffuse reticulogranular or “ground glass” pattern and air bronchograms (see Figure 3-1).
TREATMENT
Aggressive respiratory support, including oxygen, continuous positive airway pressure (CPAP), intubation, and mechanical ventilation.
To ↓ barotrauma, novel methods of ventilation are sometimes used—high-frequency oscillation, jet ventilation, and liquid ventilation.
Exogenous surfactant replacement (instillation via endotracheal tube) has dramatically reduced mortality in infants with RDS.
Most of these neonates also receive antibiotics because clinically and radiographically RDS and congenital pneumonia are indistinguishable.
Bronchopulmonary Dysplasia (BPD)
DEFINITION
Chronic lung disease that develops in preterm neonates treated with oxygen and positive-pressure ventilation.
Need for supplemental oxygen beyond 28 days of life.
Characterized by squamous metaplasia and hypertrophy of small airways.
Antenatal steroids have shown to reduce the incidence of RDS.
FIGURE 3-1. Chest x-ray demonstrating “ground glass” infiltrates consistent with respiratory distress syndrome (with a more focal area of infiltrate or atelectasis in the medial right lung base).
ETIOLOGY
Multifactorial.
Lung immaturity.
Prolonged mechanical ventilation.
Barotrauma (from mechanical ventilation).
Oxygen toxicity to the lungs.
Infants with bronchopulmonary dysplasia can be wheezing; remember, “not all that wheezes is asthma!”
DIAGNOSIS
Chest x-ray with hyperaeration and atelectasis.
TREATMENT
Supplemental oxygen as needed.
Oral steroids.
Bronchodilators.
BPD occurs in neonates:
Born at 22–32 weeks
< 1000 g at birth.
Necrotizing Enterocolitis (NEC)
A 32-week-gestation female infant was doing well and advanced to full enteral feeds at 14 days of life. At day 15 of life she was noted to have significant abdominal distention and bloody stools. X-ray of the abdomen is shown in the figure. What is the likely diagnosis and management of the condition shown in this x-ray?
X-ray of this infant is consistent with necrotizing enterocolitis with evident pneumatosis (free air within the bowel wall) in the descending colon area. Management includes serial x-rays to detect perforation of the bowel wall, which requires immediate surgery to seal the bowel. Medical management before perforation includes NPO, IV fluids, and IV antibiotics for a period of 14 days.
Necrotizing enterocolitis carries a mortality of up to 20%.
The most common gastrointestinal emergency in the premature infants.
ETIOLOGY
Seen primarily in premature infants, but can occur in full-term neonates (5–25%).
Caused by bowel ischemia and bacterial invasion of intestinal wall.
More common in premature infants treated with indomethacin for patent ductus arteriosus. Indomethacin may cause splanchnic vasoconstriction.
Most common site: Terminal ileum and proximal ascending colon.
SIGNS AND SYMPTOMS
Intolerance of oral feeding (vomiting, bilious aspirates, and large volume residue in stomach).
Abdominal distention.
Temperature instability.
Respiratory distress.
Acidosis, sepsis, shock.
Serious sequelae of NEC include intestinal strictures, malabsorption, fistulae, and short bowel syndrome (in case of surgery).
DIAGNOSIS
Distended loops of bowel.
Abdominal x-ray with “pneumatosis intestinalis”—air bubbles within the bowel wall (see Figure 3-2).
An absolute indication for operative intervention in NEC is pneumoperitoneum.
Most common complication is stricture.
FIGURE 3-2. Necrotizing enterocolitis.
Distended loops of bowel and pneumatosis intestinalis.
Air in portal vein.
Free air under diaphragm (in case of perforation).
Occult blood in stool.
TREATMENT
Discontinue feeds.
Nasogastric decompression.
Intravenous fluids.
Antibiotics.
Surgery (bowel necrosis, intestinal perforation, pneumoperitoneum, failure of medical treatment).
Currently, severe retinopathy of prematurity is rare due to judicious use of oxygen.
Retinopathy of Prematurity (ROP)
Disease that affects immature vasculature in the eyes of premature infants.
ETIOLOGY
Caused by proliferation of immature retinal vessels due to excessive use of oxygen.
Can → retinal detachment and blindness in severe cases.
Multifactorial; the number one cause has been noted to be hyperoxia.
Characterized by neovascularization of retina and vascular congestion that can → retinal detachment and ↓ visual acuity in severe cases.
All infants < 1500 g birth weight or younger than 32 weeks’ gestational age at birth are at risk of developing ROP.
DIAGNOSIS
All very-low-birth-weight infants should be screened for ROP with an ophthalmoscopic exam.
An ophthalmology evaluation is necessary in all premature infants < 1500 g, < 32 weeks’ gestation.
First eye exam:
At 27–28 weeks (for 23–24 weeks’ gestational age).
At 4th or 5th week (> 25–28 weeks’ gestational age).
Before discharge (> 29 weeks’ gestational age).
TREATMENT
Laser surgery may be needed in severe cases.
Intraventricular Hemorrhage (IVH)
DEFINITION
Rupture of germinal matrix blood vessels due to hypoxic or hypotensive injury.
Most IVHs occur within 72 hours after birth.
All premature, very-low-birth-weight infants should have a cranial ultrasound in the first week of life to look for intraventricular hemorrhage.
PREDISPOSING FACTORS
Prematurity.
RDS.
Hypo- or hypervolemia.
Shock.
Bleeding disorders.
SIGNS AND SYMPTOMS
Most are asymptomatic.
Apnea.
Hypertension or hypotension.
Changes in muscle tone.
Lethargy.
Poor suck.
Seizure.
Bulging fontanelle.
DIAGNOSIS
Cranial ultrasound (through anterior fontanelle).
TREATMENT
Directed toward correction of underlying conditions (RDS, shock, etc).
In cases of associated hydrocephalus, placement of ventriculoperitoneal shunt may be required.
Prognosis is dependent on the grade of IVH:
Grades I and II: Good outcome.
Grade III: Significant cognitive impairment.
Grade IV: Major neurologic problems.
SURVIVAL OF PREMATURE NEONATES
Disorders related to prematurity and low birth weight (BW) are the leading cause of neonatal death.
Only 20% of neonates with BW of 500–600 g survive.
Survival of infant with BW of 1250–1500 g is ~ 90%.
There is no worldwide, universal gestational age that defines viability.
In the United States, chance of normal survival is 50% after 24 weeks.
Ex-preemies can receive RSV prophylaxis with RSV monoclonal antibodies during RSV season (IM injections once a month).
SPECIAL NEEDS OF EX-PREEMIES
Heat loss: ↑ susceptibility to heat loss (high body surface area-to-body weight ratio, ↓ brown fat stores, nonkeratinized skin, and ↓ glycogen supply). Minimize heat loss by:
Warmed blankets or cellophane wrap.
Plastic film over the baby immediately after drying.
Hypoglycemia.
Fluid and electrolyte imbalance.
Hyperbilirubinemia.
Due to their bronchopulmonary dysplasia, ex-preemies can experience recurrent wheezing episodes and severe course of respiratory infections, especially respiratory syncytial virus (RSV).
Due to ↑ work of breathing and “catch-up” growth, ex-preemies should receive high-calorie diet to allow for this additional caloric expenditure.
Routine vaccination should be given based on postnatal (not gestational) age.
Early identification and intervention is needed for infants with developmental problems.
Premature infants have proportionally more fluid in the extracellular fluid compartment than the intracellular compartment and are at risk for fluid and electrolyte imbalance.
Optimal parenteral nutrition can be achieved by total parenteral nutrition (TPN)—specialized solution consisting of amino acids, dextrose, minerals, and electrolytes.
Breast milk is the best choice for enteral feeding for premature infants.
