A premature infant is an infant born before 34 wk gestation.
Full-term gestation is 40 wk (range 37 to 42 wk). Infants born before 37 wk are preterm and have an increased incidence of complications and mortality roughly proportional to the degree of prematurity. Infants born < 34 wk are considered moderate premature and those born ≥ 34 wk and < 37 wk gestation are considered late preterm (see Late Preterm Infant). Infants born < 32 wk are considered very premature, and those < 28 wk are considered extremely premature.
The rate of preterm birth was 11.7% in 2011; 8.3% were late preterm and 3.4% were [premature], including 2% who were very premature.
Previously, any infant weighing <2.5 kg was termed premature. This definition is inappropriate because many infants weighing < 2.5 kg are mature or postmature but small for gestational age; they have a different appearance and different problems. Infants < 2.5 kg at birth are considered low-birth-weight infants, and those < 1500 g are considered very low-birth-weight infants (VLBW).
In a given patient, the specific cause of premature labor and delivery, whether preceded by premature rupture of the membranes (see Premature Rupture of Membranes (PROM)) or not, is usually unknown. There are many known maternal risk factors, which may involve
Past obstetric history
Prior premature births (see Risk Factors for Complications During Pregnancy : Prior Preterm Delivery)
Prior multiple pregnancies
Current pregnancy-related factors
Pregnancy achieved by in vitro fertilization (see Assisted Reproductive Techniques : In vitro fertilization (IVF))
Little or no prenatal care
Poor nutrition during gestation (and perhaps before)
Multiple gestation (eg, twins, triplets—see Risk Factors for Complications During Pregnancy : Multifetal (Multiple) Pregnancy)
Cervical insufficiency (formerly cervical incompetence—see Cervical Insufficiency)
Preeclampsia (see Preeclampsia and Eclampsia)
Placental abruption (see Abruptio Placentae)
However, most women who give birth preterm have no known risk factors.
The premature infant is small, usually weighing < 2.5 kg, and tends to have thin, shiny, pink skin through which the underlying veins are easily seen. Little subcutaneous fat, hair, or external ear cartilage exists. Spontaneous activity and tone are reduced, and extremities are not held in the flexed position typical of term infants. In males, the scrotum may have few rugae, and the testes may be undescended. In females, the labia majora do not yet cover the labia minora. Reflexes develop at different times during gestation. The Moro reflex begins by 28 to 32 wk gestation and is well established by 37 wk. The palmar reflex starts at 28 wk and is well established by 32 wk. The tonic neck reflex starts at 35 wk and is most prominent at 1 mo postterm.
Most complications relate to dysfunction of immature organ systems. In some cases, complications resolve completely; in others, there is residual organ dysfunction.
The most common cardiac complication is
The ductus arteriosus is more likely to fail to close after birth in premature infants. The incidence of PDA (see Patent Ductus Arteriosus (PDA)) increases with increasing prematurity; PDA occurs in almost half of infants < 1750 g birth weight and in about 80% of those < 1000 g. About one third to one half of infants with PDA have some degree of heart failure. Premature infants ≤ 29 wk gestation at birth who have respiratory distress syndrome have a 65 to 88% risk of a symptomatic PDA. If infants are ≥ 30 wk gestation at birth, the ductus closes spontaneously in 98% by the time of hospital discharge.
CNS complications include
Infants born before 34 wk gestation have inadequate coordination of sucking and swallowing reflexes and need to be fed intravenously or by gavage. Immaturity of the respiratory center in the brain stem results in apneic spells (central apnea—see Apnea of Prematurity). Apnea may also result from hypopharyngeal obstruction alone (obstructive apnea). Both may be present (mixed apnea).
The periventricular germinal matrix (a highly cellular mass of embryonic cells that lies over the caudate nucleus on the lateral wall of the lateral ventricles of a fetus) is prone to hemorrhage, which may extend into the cerebral ventricles (intraventricular hemorrhage—see Intracranial Hemorrhage : Intraventricular and/or intraparenchymal hemorrhage). Infarction of the periventricular white matter (periventricular leukomalacia) may also occur for reasons that are incompletely understood. Hypotension, inadequate or unstable brain perfusion, and BP peaks (as when fluid or colloid is given rapidly IV) may contribute to cerebral infarction or hemorrhage. Periventricular white matter injury is a major risk factor for cerebral palsy and neurodevelopmental delays.
Premature infants, particularly those with a history of sepsis (see Neonatal Sepsis), necrotizing enterocolitis (see Necrotizing Enterocolitis), hypoxia, and intraventricular or periventricular hemorrhages, are at risk of developmental and cognitive delays. These infants require careful follow-up during the first year of life to identify auditory, visual, and neurodevelopmental delays. Careful attention must be paid to developmental milestones, muscle tone, language skills, and growth (weight, length, and head circumference). Infants with identified delays in visual skills should be referred to a pediatric ophthalmologist. Infants with auditory and neurodevelopmental delays (including increased muscle tone and abnormal protective reflexes) should be referred to early intervention programs that provide physical, occupational, and speech therapy. Infants with severe neurodevelopmental problems may need to be referred to a pediatric neurologist.
Ocular complications include
Retinal vascularization is not complete until near term. Preterm delivery may interfere with the normal vascularization process, resulting in abnormal vessel development and sometimes defects in vision including blindness (ROP—see Retinopathy of Prematurity). Incidence of ROP is inversely proportional to gestational age. Disease usually manifests between 32 wk and 34 wk gestational age.
Incidence of myopia and strabismus (see Strabismus) increases independently of ROP.
GI complications include
Feeding intolerance is extremely common because premature infants have a small stomach, immature sucking and swallowing reflexes, and inadequate gastric and intestinal motility. These factors hinder the ability to tolerate both oral and NGT feedings and create a risk of aspiration. Feeding tolerance increases over time, particularly when infants are able to be given some enteral feedings.
Necrotizing enterocolitis (see Necrotizing Enterocolitis) usually manifests with bloody stool, feeding intolerance, and a distended, tender abdomen. Necrotizing enterocolitis is the most common surgical emergency in the premature infant. Complications of neonatal necrotizing enterocolitis include bowel perforation with pneumoperitoneum, intra-abdominal abscess formation, stricture formation, short bowel syndrome, septicemia, and death.
Infectious complications include
Sepsis (see Neonatal Sepsis) or meningitis (see Neonatal Bacterial Meningitis) is about 4 times more likely in the premature infant, occurring in almost 25% of VLBW infants. The increased likelihood results from indwelling intravascular catheters and endotracheal tubes, areas of skin breakdown, and markedly reduced serum immunoglobulin levels (see Perinatal Physiology : Neonatal immunologic function).
Renal complications include
Renal function is limited, so the concentrating and diluting limits of urine are decreased. Late metabolic acidosis (see Metabolic Acidosis) and growth failure may result from the immature kidneys’ inability to excrete fixed acids, which accumulate with high-protein formula feedings and as a result of bone growth. Na and HCO3 are lost in the urine.
Pulmonary complications include
Surfactant production is often inadequate to prevent alveolar collapse and atelectasis, which result in respiratory distress syndrome (see Respiratory Distress Syndrome in Neonates). Surfactant replacement therapy is used to both prevent and treat respiratory distress syndrome. In spite of this therapy, many premature infants develop a chronic form of lung disease known as bronchopulmonary dysplasia (see Bronchopulmonary Dysplasia (BPD)) with a prolonged need for ventilator therapy and supplemental O2 therapy beyond 36 wk.
Palivizumab prophylaxis for respiratory syncytial virus is important for infants with chronic lung disease (see Respiratory Syncytial Virus (RSV) and Human Metapneumovirus Infections : Prevention).
Metabolic complications include
Hyperbilirubinemia (see also Neonatal Hyperbilirubinemia) occurs more commonly in the premature as compared to the term infant, and kernicterus may occur at serum bilirubin levels as low as 10 mg/dL (170 μmol/L) in small, sick, premature infants. The higher bilirubin levels may be partially due to inadequately developed hepatic excretion mechanisms, including deficiencies in the uptake of bilirubin from the serum, its hepatic conjugation to bilirubin diglucuronide, and its excretion into the biliary tree. Decreased intestinal motility enables more bilirubin diglucuronide to be deconjugated within the intestinal lumen by the luminal enzyme β-glucuronidase, thus permitting increased reabsorption of unconjugated bilirubin (enterohepatic circulation of bilirubin). Conversely, early feedings increase intestinal motility and reduce bilirubin reabsorption and can thereby significantly decrease the incidence and severity of physiologic jaundice. Uncommonly, delayed clamping of the umbilical cord increases the risk of significant hyperbilirubinemia by allowing the transfusion of a large RBC mass, thus increasing RBC breakdown and bilirubin production.
The most common temperature regulation complication is
Premature infants have an exceptionally large body surface area to volume ratio. Therefore, when exposed to temperatures below the neutral thermal environment (see Hypothermia in Neonates), they rapidly lose heat and have difficulty maintaining body temperature.
Findings on physical examination correlate with gestational age (see Figure: Assessment of gestational age—new Ballard score.). Estimated date of delivery and prenatal ultrasonography, if done, also determine gestational age.
Along with appropriate testing for any identified problems or disorders, routine evaluations include pulse oximetry, serum Ca and electrolytes, CBC, bilirubin level, blood culture, serum alkaline phosphatase and phosphorus levels (to screen for osteopenia of prematurity), hearing evaluation, cranial ultrasonography to screen for intraventricular hemorrhage and periventricular leukomalacia, and screening by an ophthalmologist for retinopathy of prematurity. Weight, length, and head circumference should be plotted on an appropriate growth chart at weekly intervals.
If initial laboratory testing was done before the infant was taking full enteral feedings, some of the tests for metabolic disorders may be false-positive and should be repeated. In particular, positive screening tests for thyroid function and congenital adrenal hyperplasia (eg, 17-hydroxyprogesterone) should be confirmed.
Preterm infants must be monitored for apnea and bradycardia until they are 34.5 to 35 wk adjusted age. Before discharge from the hospital, premature infants should undergo a car seat monitoring evaluation using pulse oximetry to make sure that they can maintain a patent airway and good O2 saturation while positioned in the car seat. After discharge, premature infants should receive careful neurodevelopmental follow-up and appropriate early referral to intervention programs as needed for physical, occupational, and language therapy.
Prognosis varies with presence and severity of complications, but usually mortality and likelihood of complications decrease greatly with increasing gestational age and birth weight (see Figure: Survival and survival without severe impairment in extremely low-birth-weight infants.).
Survival and survival without severe impairment in extremely low-birth-weight infants.
Disability rates of singleton vs multiple births in preterm infants.
Specific disorders are treated as discussed elsewhere in The Manual. General supportive care of the premature infant is best provided in a neonatal ICU or special care nursery and involves careful attention to the thermal environment, using servo-controlled incubators. Scrupulous adherence is paid to handwashing before and after all patient contact. Infants are continually monitored for apnea, bradycardia, and hypoxemia until 34.5 or 35 wk gestation.
Parents should be encouraged to visit and interact with the infant as much as possible within the constraints of the infant’s medical condition. Skin-to-skin contact between the infant and mother (kangaroo care) is beneficial for infant health and facilitates maternal bonding. It is feasible and safe even when infants are supported by ventilators and infusions.
Preterm infants should be transitioned to the supine sleeping position before hospital discharge. Parents should be instructed to keep cribs free of fluffy materials including blankets, quilts, pillows, and stuffed toys, which have been associated with an increased risk of SIDS (see Sudden Infant Death Syndrome (SIDS)).
Feeding should be by NGT until coordination of sucking, swallowing, and breathing is established at about 34 wk gestation, at which time breastfeeding is strongly encouraged. Most premature infants tolerate breast milk, which provides immunologic and nutritional factors that are absent in cow’s milk formulas. However, breast milk does not provide sufficient Ca, phosphorus, and protein for very low-birth-weight infants (ie, < 1500 g), for whom it should be mixed with a breast milk fortifier. Alternatively, specific premature infant formulas that contain 20 to 24 kcal/oz (2.8 to 3.3 joules/mL) can be used.
In the initial 1 or 2 days, if adequate fluids and calories cannot be given by mouth or NGT because of the infant’s condition, IV parenteral nutrition with protein, glucose, and fats is given to prevent dehydration and undernutrition. Breast milk or preterm formula feeding via NGT can satisfactorily maintain caloric intake in small, sick, premature infants, especially those with respiratory distress or recurrent apneic spells. Feedings are begun with small amounts (eg, 1 to 2 mL q 3 to 6 h) to stimulate the GI tract. When tolerated, the volume and concentration of feedings are slowly increased over 7 to 10 days. In very small or critically sick infants, total parenteral hyperalimentation via a peripheral IV or a percutaneously or surgically placed central catheter may be required for a prolonged period of time until full enteral feedings can be tolerated.
Although early and appropriate prenatal care is important overall, there is no good evidence that such care or any other interventions decrease the incidence of premature birth.
The use of tocolytics to arrest premature labor and provide time for prenatal administration of corticosteroids to hasten lung maturation is discussed elsewhere (see Preterm Labor).
There are many risk factors for premature birth but they are not present in most cases.
Complications include hypothermia, hypoglycemia, respiratory distress syndrome, apneic episodes, intraventricular hemorrhage, developmental delay, sepsis, retinopathy of prematurity, hyperbilirubinemia, necrotizing enterocolitis, and poor feeding.
Mortality and likelihood of complications decrease greatly with increasing gestational age and birth weight.
Treat disorders and support body temperature and feeding.
There is no evidence that improved prenatal care or other interventions decrease the incidence of premature birth.