A premature infant is an infant born before 37 wk gestation.
Full-term gestation is 40 wk. Infants born before 37 wk have an increased incidence of complications and mortality roughly proportional to the degree of prematurity. Preterm delivery occurs in about 12.5% of pregnancies in the US and is one of the chief causes of neonatal morbidity and mortality. The rate of prematurity for black infants is 17.9%.
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.
The cause of premature labor and delivery, whether preceded by premature rupture of the membranes or not, is usually unknown. However, maternal history commonly shows low socioeconomic status; inadequate prenatal care; poor nutrition; poor education; unwed state; previous preterm birth; and intercurrent, untreated illness or infection (eg, bacterial vaginosis). Other risk factors include placental abruption, preeclampsia, multiple pregnancies, cervical incompetence, and multiple abortions.
Symptoms and Signs
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 post term.
Findings on physical examination correlate with gestational age (see Fig. 1: Approach to the Care of Normal Infants and Children: 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, 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.
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.
Most complications relate to dysfunction of immature organ systems. In some cases, complications resolve completely; in others, there is residual organ dysfunction.
Surfactant production is often inadequate to prevent alveolar collapse and atelectasis, which result in respiratory distress syndrome (see Respiratory Disorders in Neonates, Infants, and Young Children: Respiratory Distress Syndrome). 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 with a prolonged need for ventilator therapy and supplemental O2 therapy. Palivizumab prophylaxis for respiratory syncytial virus is important for infants with chronic lung disease (see Respiratory Disorders in Neonates, Infants, and Young Children: Prognosis).
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 Respiratory Disorders in Neonates, Infants, and Young Children: Apnea of Prematurity). Apnea may also result from hypopharyngeal obstruction alone (obstructive apnea). Both may be present (mixed apnea).
The periventricular germinal matrix (a mass of embryonic cells on the lateral wall of the lateral ventricles and present only in the fetus) is prone to hemorrhage, which may extend into the cerebral ventricles (intraventricular 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, 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.
Sepsis (see Infections in Neonates: Neonatal Sepsis) or meningitis (see Infections in Neonates: Neonatal Bacterial Meningitis) is about 4 times more likely in the premature infant. The increased likelihood results from indwelling intravascular catheters and endotracheal tubes, areas of skin breakdown, and markedly reduced serum immunoglobulin levels (see Perinatal Physiology: Immunologic function).
The ductus arteriosus is more likely to fail to close after birth in premature infants. The incidence of patent ductus arteriosus (PDA—see Congenital Cardiovascular Anomalies: 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 < 1200 g. About 1/3 to ½ of those 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.
Premature infants have an exceptionally large body surface area to volume ratio. Therefore, when exposed to temperatures below the neutral thermal environment (see Perinatal Problems: Hypothermia in Neonates), they rapidly lose heat and have difficulty maintaining body temperature.
The small stomach and immature sucking and swallowing reflexes hinder oral or NGT feedings and create a risk of aspiration. Necrotizing enterocolitis (see Gastrointestinal Disorders in Neonates and Infants: 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, and short bowel syndrome.
Renal function is limited, so the concentrating and diluting limits of urine are decreased. Late 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.
Retinal vascularization is not complete until near term. Preterm delivery may interfere with this process, resulting in abnormal vessel development and sometimes defects in vision (retinopathy of prematurity—(see Perinatal Problems: Retinopathy of Prematurity). Incidence of myopia and strabismus increases independently of retinopathy of prematurity.
Hypoglycemia (see Metabolic, Electrolyte, and Toxic Disorders in Neonates: Neonatal Hypoglycemia) and hyperglycemia (see Metabolic, Electrolyte, and Toxic Disorders in Neonates: Neonatal Hyperglycemia) are discussed elsewhere.
Hyperbilirubinemia (see also Metabolic, Electrolyte, and Toxic Disorders in Neonates: Neonatal Hyperbilirubinemia) occurs more commonlyn 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.
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 Table 4: Perinatal Problems: Survival Estimates for Premature 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.
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.
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, a 10% glucose solution with maintenance electrolytes is given IV to prevent dehydration and undernutrition. Continuous breast milk or formula feeding via NGT or nasojejunal tube 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. If 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 until full enteral feedings can be tolerated.
The risk of preterm delivery can be reduced by ensuring that all women, especially those in high-risk groups, have access to early and appropriate prenatal care, including advice on the importance of avoiding alcohol, tobacco, and illicit drugs. The use of tocolytics to arrest premature labor and provide time for prenatal administration of corticosteroids to hasten lung maturation is discussed elsewhere (see Abnormalities and Complications of Labor and Delivery: Preterm Labor).
Last full review/revision March 2007 by James W. Kendig, MD
Content last modified February 2012