Medical Complications of the Critically III Newborn: A Review for Early Intervention Professionals

Medical Complications of the Critically III Newborn: A Review for Early Intervention Professionals

Theresa C. McNab

Sophisticated technology in neonatal intensive care units (NICU) has resulted in remarkable improvements in the survival of the sickest and most premature newborn infants. Although fortunately the prevalence of disability among NICU graduates has not increased with such advances, the total number of these infants in the community has grown as a result of the improved survival. Many of these babies manifest complex residual health problems and are at risk for developmental difficulties. An understanding of the complications of prematurity and other neonatal illnesses as well as of their treatments can enhance the effectiveness of early intervention services, both in devising creative approaches aimed at promoting the optimal development of medically vulnerable infants and in supporting their families during prolonged periods of intense stress.

Over the past 30 years, neonatal intensive care has emerged as a distinct specialty within the field of pediatrics. Along with the development of intensive care units devoted exclusively to the care of premature infants and other critically ill newborns, an array of new technologies and problems has emerged that medical professionals and society as a whole must face. Extremely premature babies, who had previously been considered nonviable, are now surviving to be discharged home from the hospital to live with their families (Tudehope et al., 1995). Similarly, infants with diseases once considered impossible to treat are now being saved with medical technologies that a few years ago physicians only dreamed about. From 1985 to 1995, infant mortality (death during the first year of life) in the United States declined 31% for infants with birthweights of 500 to 749 grams (about 1 to 1 1/2 pounds). Similarly, for infants weighing 750 to 1,499 grams (about 1 1/2 to 3 1/2 pounds) at birth, the mortality rate decreased 53%; for infants with birthweights between 1,500 and 2,499 grams (about 3 1/2 to 5 1/2 pounds), mortality decreased 37%.

As of 1995, U.S. mortality rates for infants were as follows: Approximately 47% of infants weighing 500 to 749 grams at birth survived the first year of life, as did 80% of babies with birthweights between 750 and 999 grams. For infants weighing at least 1,000 grams, the survival rate was more than 90%; for babies weighing at least 1,500 grams it was more than 95%. Premature infants weighing less than 500 grams rarely survived, even with current technology (Guyer, Martin, MacDorman, Anderson, & Strobino, 1997).

A misconception exists that the saving of very-low-birthweight infants has resulted in a dramatic rise in the number of children with major disabilities. It is true that the smaller the infant, the higher the risk of disability. However, a concomitant improvement in outcomes for larger premature infants has offset this risk, so that the prevalence of children with disabilities who had a low birthweight has remained approximately the same in the last half-century (Lee et al., 1995). A study by LaPine, Jackson, and Bennett (1995) found that over a period of almost 15 years (1977-1990) there was a stable rate of about 20% of infants weighing less than 800 grams (just under 2 pounds) at birth who later manifested significant neurosensory impairments, such as cerebral palsy, below-average IQ, or permanent vision or hearing deficits. Similarly, researchers at Bowman Gray School of Medicine have shown that over the last 2 decades the increased survival of very-low-birthweight infants has not resulted either in a higher rate of major developmental problems identifiable at age 1 or in a greater prevalence of cerebral palsy among survivors (O’Shea, Klinepeter, Goldstein, Jackson, & Dillard, 1997; O’Shea, Preisser, Klinepeter, & Dillard, 1998). Still, because more premature and other sick infants are surviving, the absolute number of infants with or at significant risk for disabilities has increased.

Despite the ability of neonatologists to provide life-saving measures for very sick babies, allowing them to be discharged from the hospital, significant obstacles often face many of these infants and their families once they are at home. Ongoing health problems in these children can hamper and delay the normal course of neuromotor, cognitive, language, and social development. Community early intervention professionals such as infant educators; social workers; and physical, occupational, and speech therapists can improve these children’s long-term outcomes by being knowledgeable about these health problems and devising creative family-centered early intervention strategies.

The purpose of this article is to provide early intervention professionals with a basic familiarity and understanding of some of the newest technologies employed in the neonatal intensive care unit (NICU). We also explain some medical problems (e.g., chronic lung disease, visual impairment, and intracranial hemorrhage) that are commonly encountered in NICU babies, because they can have a profound effect on developmental progress following discharge from the hospital. Although a comprehensive review of the literature on interventions for premature infants or on specific complications is beyond the scope of this article, we will briefly discuss several notable studies that focus on these children. Our goal is to give early intervention professionals information about the types of medical problems facing these infants in order to enhance the developmental care of these children and the support of their families.


Respiratory Distress Syndrome

The most common disorder facing neonates in the first few hours to days of life is respiratory distress syndrome (RDS), formerly known as hyaline membrane disease. It may occur in up to 1% of all live births, with the greatest incidence in preterm infants who weigh less than 1,500 grams (about 3.3 pounds; Klaus & Fanaroff, 1993). Deficiency of a fatty biochemical substance known as surfactant in the baby’s lung is one of the primary causes of RDS. Surfactant, which is usually present in adequate amounts in healthy term infants, is responsible for helping the lungs to expand easily with each inhalation and preventing total lung collapse on exhalation. Because certain preterm infants lack both sufficient lung development and adequate amounts of surfactant, their lungs are stiff and unable to expand well with their own respiratory effort. These babies are unable to take in enough oxygen to sustain themselves and usually develop a need for mechanical breathing support (e.g., a respirator or ventilator; Klaus & Fanaroff, 1993). Two decades ago, mechanical ventilation was essentially all that could be done for an infant with RDS. Then in 1980, Fujiwara et al. demonstrated successful endotracheal (i.e., into the breathing tube) administration of surfactant to a baby with RDS. Since that time some studies have shown that giving surfactant to premature infants may reduce the morbidity and mortality of RDS (Gong et al., 1995; Haas & Rice, 1995). Furthermore, surfactant administration has been shown to shorten the time that a baby requires a respirator and to decrease the total number of hospital days, thereby saving health-care dollars (Bregman & Kimberlin, 1993). Also, Kraybill et al. (1995) showed that administration of surfactant decreased the number of infants who developed chronic lung disease in the first month of life. Determining the specific developmental effects of surfactant administration to premature neonates is difficult because of the frequent presence of confounding variables in these infants, such as intracranial hemorrhages. However, research has shown that surfactant administration had no detrimental effects on neurodevelopment (Kraybill et al., 1995; Saigal et al., 1995).

Unfortunately, although surfactant administration has markedly improved the survival of tiny preterm babies with RDS, these infants are still subject to the development of a chronic lung disease known as bronchopulmonary dysplasia (BPD). First described by Northway, Rosan, and Porter in 1967, BPD is thought to result from a combination of lung immaturity and oxygen toxicity, with resultant lung inflammation and pressure-induced damage to the baby’s lungs. BPD creates breathing difficulties that often require the infant to receive supplemental oxygen following NICU discharge. It also makes the baby more prone to fluid accumulation in the lungs and to complications from upper respiratory tract infections. Infants and young children with BPD often require treatment with medications, including oxygen as noted above, diuretics to help remove built-up fluid, inhaled medications to decrease wheezing and airway spasm, and corticosteroids to reduce lung inflammation. These children also require maximal nutritional support because of the greater caloric needs associated with the increased effort of breathing.

Infants with BPD require close medical supervision following their discharge from the intensive care unit. As a result of their chronic lung disease, these babies can have serious complications, including death, from respiratory infections–such as respiratory syncytial virus (RSV)–that would cause only a common cold in a healthy child. Therefore, care should be taken to avoid exposing these babies to other people who are sick, and at the first sign of increased breathing effort a visit to the infant’s doctor should be considered. Babies with BPD are also at risk for a condition called gastroesophageal reflux (GER). In GER, acidic stomach contents flow up the esophagus and can potentially be inhaled (aspirated) into the lungs, causing further lung injury. Infants who develop worsening lung disease, poor growth, frequent episodes of choking and spitting up, or refusal to eat may need medical evaluation for the treatment of gastroesophageal reflux (Hrabovsky & Mullett, 1986).

BPD is one of the clearest markers of biological risk in premature babies (Meisels, Plunkett, Roloff, Pasick, & Stiefel, 1986). Due to their very low birthweight and history of chronic illness, these children are likely to need early intervention services such as physical, occupational, and speech therapies. Although it is unclear exactly what role the chronic lung disease plays, babies with a history of BPD often demonstrate slower oral-motor development and have more feeding problems compared to their peers (Lifschitz et al., 1987; Spitzer, 1996). Specifically, these infants often have difficulty coordinating their oral-motor function with the increased effort of breathing. Speech therapy can be helpful in teaching these children to develop the ability to feed orally and thereby lay the groundwork for expressive language skills (Singer et al., 1996). Prolonged and recurrent hospitalizations, suboptimal nutrition, and varying degrees of brain injury due to oxygen deprivation or hemorrhage often result in delayed or disordered motor skills. The monitoring of motor skill development and direct intervention are often warranted.

When providing developmental services such as physical and occupational therapy to infants with BPD, early intervention professionals should be aware that these children often have poor exercise tolerance and tire easily. Also, many of these babies are best served by inhome, as opposed to facility-based, therapies because of their increased risk of infection when exposed to large numbers of people. In addition to providing home-based therapies, early intervention providers can also assist these children by offering emotional support to the family and by discouraging smoking in the home, which could exacerbate asthma-like symptoms in people with BPD (Spitzer, 1996).

Persistent Fetal Circulation

Although term infants usually do not have a deficiency of surfactant and therefore do not suffer from classical RDS, full-term babies can experience respiratory difficulties for a variety of reasons. Such reasons commonly include infections, such as pneumonia or bacteremia (bacteria growing in the blood), and meconium aspiration (a type of fetal distress in which the baby defecates prior to delivery and then inhales stool particles into his or her lungs with the first breaths). A less common cause of breathing difficulties in term infants is congenital diaphragmatic hernia (a condition in which abdominal organs escape into the chest cavity and compress the lungs). Severe respiratory difficulty in the full-term newborn is often associated with high pressure in the blood vessels of the lungs. This pulmonary hypertension, or persistent fetal circulation, as it is sometimes called by neonatologists, prevents blood from moving properly from the right side of the heart to the lungs, where it could pick up vital oxygen. Consequently, the infant’s health deteriorates as she or he is deprived of more and more oxygen (Klaus & Fanaroff, 1993).

To treat these critically ill newborns, neonatologists often have to resort to a technology known as extracorporeal membrane oxygenation (ECMO). ECMO is closely related to the heart-lung bypass machines used in open-heart surgery. In fact, it is just a very long course of heart-lung bypass (Spitzer, 1996). During ECMO, blood is removed from the patient through a tube placed in a large neck blood vessel (see Figure 1). The blood is then run through an apparatus called a membrane oxygenator (artificial lung), where oxygen can move into the blood and carbon dioxide can leave the blood, just as would have occurred inside the body had the blood been able to move properly through the lungs. After leaving the membrane oxygenator, the blood is gently warmed and then returned to the body of the infant, where it circulates through the arterial system and delivers oxygen and other nutrients to the tissues (Spitzer, 1996). Essentially, ECMO provides oxygen to these sick neonates while their lungs go through a growth and healing process that will eventually allow these infants to breathe normally without assistance. A baby may require ECMO for only a few days or up to a few weeks. Although ECMO is not a cure-alt for infants with severe respiratory difficulties, it has markedly improved the survival of babies with respiratory difficulties. Currently, it is estimated that approximately 80% of all infants treated with ECMO survive, with the greatest success rate occurring in infants with meconium aspiration syndrome (about 94% survival; Spitzer, 1996).


ECMO has clearly improved the mortality rates in infants with pulmonary hypertension. However, it is not without its associated complications. Although some of the complications seem to be closely related to the infant’s underlying diagnosis (e.g., diaphragmatic hernia or meconium aspiration), babies treated with ECMO are at risk for intracranial hemorrhage, chronic lung disease, feeding difficulties, gastroesophageal reflux, and possible developmental delays (Bernbaum et al., 1995). Follow-up studies of ECMO-treated infants have found an overall incidence of developmental problems of about 20% (Schumacher, Palmer, Roloff, LaClaire, & Bartlett, 1991; Wildin, Landry, & Zwischenberger, 1994). In a comparative follow-up study of children with a history of ECMO treatment and children who had been healthy newborns, Glass et al. (1995) showed that at age 5 the ECMO-treated babies as a group had mean IQs that were in the normal range but significantly lower than those of the healthy control children. (For ECMO-treated children M = 96; for the control group M = 115.) Overall, they concluded–based on a review of the literature–that the incidence of major disability in former ECMO babies was similar to that in other children who had been critically ill as neonates. They did note, however, that based on commonly used standardized measures of behavioral adjustment and an academic screening battery, the children who had received ECMO as infants were at increased risk of developing behavior problems and experiencing school failure. Consequently, a close follow-up of these children was recommended through kindergarten age (Glass et al., 1995). Early intervention professionals may have an important role to play in maximizing the developmental progress of these children prior to the start of school.

Retinopathy of Prematurity

With the growing numbers of very-low-birthweight infant survivors, there has also been an increasing number of children at risk for developing a disorder called retinopathy of prematurity (ROP), which can result in permanent visual impairment (Spitzer, 1996). This disease was originally known as retrolental fibroplasia when it was first recognized in the 1940s and 1950s as the cause of an epidemic of blindness in children who had been premature infants. Since that time, a great deal of information about ROP has been discovered, including more effective means of prevention and treatment (Phelps, 1995).

Retinopathy of prematurity is thought to be partially related to oxygen toxicity on the blood vessels of the retina in the eye. As indicated by its name, it primarily affects infants born too early. In fact, the risk of developing ROP is inversely related to both gestational age at birth and

birthweight. According to a study by Palmer, Flynn, and Hardy (1991), about 90% of infants weighing less than 750 grams (about 1.6 pounds) will develop some degree of ROP. Fortunately, most of these infants will experience spontaneous healing of their disease. For unclear reasons, White infants are more prone to ROP than their African-American peers (Palmer, Flynn, & Hardy, 1991).

The blood vessels on the retina are not completely formed until 40 to 44 weeks after conception. While these vessels are developing, they are extremely susceptible to injury (Phelps, 1995). It has been shown that prolonged exposure of these fledgling blood vessels to excessive levels of oxygen can cause constriction of the vessels, with subsequent disruption of vessel growth. Later, new blood vessels, which are very fragile and prone to leakage or hemorrhage, start to grow out from the retina into the vitreous space (interior of the eyeball). The growth of these new, weak vessels can set off a cascade of events that culminates in blindness in the most severe cases. It is a difficult balance to provide a premature infant–who most likely also has immature lungs–with just the right amount of oxygen without providing too much. However, excess oxygen exposure is probably just one of several factors, some of which are yet to be identified, that are causally related to ROP (Klaus & Fanaroff, 1993). Other factors that may influence the development of ROP include lack of oxygen, poor nutrition, and excess light exposure.

When the body’s repair mechanisms are working well, the new, fragile vessel growth recedes spontaneously before traction on the retina develops. The eye can then develop in a normal fashion with minimal problems. Unfortunately, this does not always occur, and scars (called cicatrices) may form that often lead to retinal detachment in infancy or as late as the adult years. Other consequences of ROP may include myopia (nearsightedness), strabismus (crossed eyes), or other visual difficulties. Sometimes ROP progresses quickly in the affected infants to a very severe stage with immediate risk of retinal detachment. In these cases surgical intervention by an ophthalmologist is required, either with a technique called cryotherapy (“freezing” of the vessels) or most recently with laser therapy. The goal of these techniques is to encourage the abnormally proliferating vessells to regress, increasing the chances of a favorable outcome. Even so, up to 2% to 4% of infants with a birthweight of less than 2 pounds suffer total vision loss (Phelps, 1995).

Infants and children with a diagnosis of ROP require close ophthalmologic follow-up, depending on the severity of their disease. Even patients with regression of their ROP are at risk for nearsightedness, which is very severe in 5% of cases. Many of these infants require glasses to aid appropriate development and to prevent amblyopia (vision loss due to inadequate brain stimulation). Children with residual ROP scars should be seen by an ophthalmologist at least annually because., of the increased risk of retinal detachment (Phelps, 1995). Unfortunately, children who do undergo surgery for retinal detachment generally have a poor visual outcome, and additional complications such as cataracts and glaucoma may occur (Knight-Nanan, Algawi, Bowell, & O’Keefe, 1996).

An important issue to be considered by early intervention professionals is the risk of visual impairment in infants who have been treated for retinopathy of prematurity. This visual impairment can range from mild nearsightedness in minimally affected babies to total blindness in infants who have sustained retinal detachments. Implications for early intervention include supporting the parents and teaching them techniques that can be used to stimulate their visually challenged child. Specifically, early intervention programming might include special adaptations for the visually impaired that promote maximal integration of the other sensory areas such as hearing, touch, and taste (Holbrook, 1996). Another important role for early intervention providers is to help ensure that these infants attend scheduled follow-up appointments with their ophthalmologists. These follow-up visits need to occur regularly until the retina becomes fully vascularized and the ophthalmologist believes that the child is no longer at risk for the complications of ROP.

Intraventricular Hemorrhage

Another common problem in premature infants is the occurrence of bleeding in the brain, usually intraventricular hemorrhages, so called because of their location. The ventricles are the cavities in the brain that act as containers for the cerebrospinal fluid (CSF) that is produced by an organ called the choroid plexus. Lying very close to the ventricles in infants of less than 32 to 34 weeks’ gestation is a structure called the germinal matrix, which is a remnant of early brain development. The germinal matrix consists of a rich capillary bed that is very fragile and prone to leakage or bleeding. When a preterm infant suffers from oxygen deprivation (hypoxia) or has rapid fluctuations in’ blood pressure, the vessels in the germinal matrix can easily rupture, leading to intraventricular hemorrhage (IVH; Watt, 1994).

Approximately 40% to 45% of infants with a birthweight of less than 1,500 grams (about 3.3 pounds) or a gestational age of less than 35 weeks sustain an IVH. Although these hemorrhages are most frequently seen in babies of less than 32 weeks’ gestation, they do occasionally occur in full-term infants. Most IVH happens in the first 3 days of life and can be detected by ultrasound through the anterior fontanel (the large soft spot on the top of a baby’s head; Watt, 1994).

Intraventricular hemorrhages are graded in four levels, with Grade IV having the worst prognosis. Grade I bleeds are limited to the germinal matrix itself, but Grade II hemorrhages extend into the ventricles. Grades I and II usually resolve without significant neurodevelopmental abnormalities. Unfortunately, in extremely premature infants these low-grade IVHs often progress into Grades III or IV. A Grade III IVH involves bleeding into the ventricle with swelling of that ventricle (ventriculomegaly), and a Grade IV IVH involves swelling of the ventricle plus bleeding into the substance of the brain itself (Watt, 1994; see Figure 2).


As opposed to the usually benign course of the lower grade IVHs, Grade III and IV bleeds require treatment in about 80% of cases. The problem that sometimes arises and may require treatment in babies with Grades III or IV is hydrocephalus (water on the brain). Hydrocephalus develops in infants with high-grade IVH because the flow of the CSF through the ventricles is disrupted and the CSF is being produced by the choroid plexus faster than it can leave the ventricles. This results in excess pressure on the brain cells, which can be damaging. Because Grade III and IV bleeds are prone to the development of hydrocephalus, the infant may need medication such as diuretics to help decrease the production of fluid in the brain. If medical management fails, the infant may require placement of a permanent ventriculo-peritoneal (VP) shunt (Watt, 1994). A VP shunt is a surgically placed conduit that drains CSF from the ventricle of the brain down into the abdominal cavity, where it is absorbed and excreted by the body. This shunt prevents the buildup of fluid and excess pressure on the brain. Unfortunately, VP shunts are prone to malfunction and infection that often requires medical and surgical treatment. Symptoms associated with VP shunt malfunction or infection that early intervention professionals may find helpful to know include the following:

* fever

* vomiting

* excessive sleepiness

* seizures

* prominent scalp veins

* swelling or redness along the shunt path

* bulging of the fontanel

* loss of previous developmental milestones

* balance or coordination problems

* visual difficulties

(Madikians & Conway, 1997).

In the long term, Grades I and II are often free of significant neurodevelopmental problems. However, about 40% of infants with Grade III IVH and at least 65% of babies with Grade IV IVH develop neurodevelopmental disabilities such as cerebral palsy (Watt, 1994).

Periventricular Leukomalacia

Another brain disorder seen in premature infants that can be associated with neurodevelopmental abnormalities is periventricular leukomalacia (PVL). PVL is characterized by the appearance of cysts (fluid-filled holes) in the brain tissue surrounding the ventricles. Like IVH, it is thought to be related to a disruption of brain blood flow in the premature infant with subsequent injury of the nearby brain cells. PVL usually occurs on both sides of the brain and tends to result in problems such as spastic diplegia or quadriplegia, impairment of speech and vision, and general developmental delays, which can be severe (Weindling, 1995). However, a study by Blackman, McGuinness, Bale, and Smith (1991) found that the developmental outcome for infants who had developed cysts in their brain tissue may have been better than previously suspected. In this study, although 81% of the children had developed spastic cerebral palsy by the age of 33 months, only 19% of the children demonstrated moderate to severe cognitive deficits with developmental or intelligence quotients lower than 52.

Given the high incidence of developmental disabilities such as cerebral palsy in babies with high-grade IVH or PVL, early interventionists can play an important role. Physical and occupational therapy is important to maximize motor function. Because cognitive impairments may be present as well, parent-infant educators should monitor the infant’s general development and be vigilant for possible associated deficits in vision or speech.


The improved survival rates of extremely low-birthweight infants and other critically ill newborns have been brought about by advances in neonatal intensive care. However, the improved survival of these children is not without a price. This article has sought to familiarize early intervention professionals with some of the medical and developmental problems encountered by NICU graduates. Because smaller and sicker babies are surviving to be discharged to live with their families, the number of NICU graduates requiring specialized developmental support services has increased. This raises questions about the potential benefits of early intervention for this population.

It is not the purpose of this article to provide a comprehensive review of efficacy studies related to premature and other high-risk infants. These babies constitute a heterogeneous group whose care must be individualized depending on their specific needs. An excellent reference in which specific interventions and their merits are reviewed is provided by Guralnick (1997). However, other relevant work should be cited here.

Als et al. (1994) examined the effectiveness of early intervention in the NICU itself. Infants weighing less than 1,250 grams (2.75 pounds) at birth were randomized either to a treatment group that received a personalized, developmentally oriented care plan or to a control group that received the usual care. The relationship-based developmental care plan was based on an assessment of the individual infant’s current strengths, vulnerabilities, and threshold to disorganization. The goal was to enhance the infant’s strengths and to reduce the stressors.

Overall, the babies participating in the special care group required fewer days on the breathing machine and showed a lower incidence of both intraventricular hemorrhage and severe bronchopulmonary dysplasia. The babies in the special care group also demonstrated better weight gain and achieved full intestinal feedings sooner than those in the control group. The treatment group on average had a shorter hospitalization time and a less expensive bill at the end of the study. Moreover, the special care babies achieved a more favorable developmental outcome, demonstrating more organized abilities in the areas of motor function, interaction, and self-regulation (Als et al., 1994). The particular importance of this work is its emphasis on the neurobehavioral organization of infants. Some infants that leave the NICU still lack a well-organized central nervous system, which results in less control of sleep, arousal, alerting, attention, fussing, and feeding. Traditional hands-on interventions may be contraindicated because many of these infants are not stabilized at a neurophysiological level that would allow them to effectively process the sensory input of therapies offered.

It should be noted that studies of developmental care that was based on the NIDCAP (Neonatal Individualized Developmental Care Plan) model developed by Als and Gilkerson (1997) have shown mixed results. Ariagno et al. (1997) found that premature infants who experienced the NIDCAP model were not at a greater developmental advantage at the time of discharge from the hospital than those who did not use the model. Still, there seems to be convincing evidence of benefits from the NIDCAP approach in other domains.

The benefits of combining early child development and family support services with pediatric follow-up to reduce the incidence of health and developmental problems among low-birthweight premature infants were evaluated in the Infant Health and Development Program (IHDP; Infant Health and Development Program Consortium, 1990). In this study, low-birthweight infants were randomly assigned to receive either early intervention services or routine medical, developmental, and social follow-up with specific referral for services only as needed. The children and families in the early intervention group participated in regular home visits, educational programs that were specially designed for low-birthweight babies, and frequent parent group meetings. At age 3, higher IQ scores were noted for the intervention group; however, at age 5 this advantage was lost for the children who had been the smallest premature infants (Brooks-Gunn et al., 1994; Infant Health and Development Program Consortium, 1990). Similarly, at age 8, there was an attenuation of the favorable effects for the early intervention group that had been seen at 3 years of age (McCarton et al., 1997). Barring serious complications, the effect of biological risk factors on development diminishes beyond the first several years of life (Wilson, 1985) regardless of intervention. Early intervention programs should focus on developmental surveillance among high-risk populations, amelioration of specific developmental problems as they emerge, preservation of developmental skills in the face of ongoing medical complications, and preventive community-wide environmental enrichment.


After hospital discharge, interventions should be tailored to the individual child and family rather than to a specific risk factor. The fact that an infant was premature or critically ill in the first days of life is not as relevant as whether she or he now has residual visual impairment, muscle tone abnormalities, or language delays. However, the knowledge that an infant had retinopathy of prematurity or intraventricular hemorrhage or required ECMO therapy should alert one to the heightened likelihood of specific problems that require more intensive developmental monitoring or intervention. Furthermore, it is important to recognize the impact that the NICU environment has had on the parents of these children. A better understanding of the medical complications and developmental issues facing NICU graduates can be a valuable tool used by early intervention professionals to help achieve the best outcomes for these children.


(1.) For an excellent resource on medical and developmental disabilities terminology, see Accardo, P. J., & Whitman, B. Y. (1996). Dictionary of developmental disabilities terminology. Baltimore: Brookes.

(2.) The authors wish to thank Dr. Robert Boyle, University of Virginia Department of Pediatrics, Division of Neonagology, for his help in reviewing this article and Michael P. McNab for his help in preparing Figure 1.


Als, H., Lawhon, G., Duffy, F. H., McAnulty, G. B., Gibes-Grossman, R., & Blickman, J. G. (1994). Individualized developmental care for the very low-birth-weight preterm infant: Medical and neurofunctional effects. Journal of the American Medical Association, 272, 853-858.

Als, H., & Gilkerson, L. (1997). The role of relationship-based developmentally supportive newborn intensive care in strengthening outcome of preterm infants. Seminars in Perinatology, 21, 178-189.

Ariagno, R. L., Thoman, E. B., Boeddiker, M. A., Kugener, B., Constantinou, J. C., Mirmiran, M., & Baldwin, R. B. (1997). Developmental care does not alter sleep and development of premature infants [99, 1026, e9]. Pediatrics fen-line serial]. Available

Bernbaum, J., Schwartz, I. P., Gerdes, M., D’Agostino, J. A., Coburn, C. E., & Polin, R. A. (1995). Survivors of extracorporeal membrane oxygenation at 1 year of age: The relationship of primary diagnosis with health and neurodevelopmental sequelae. Pediatrics, 96, 907-913.

Blackman, J. A., McGuinness, G. A., Bale, J. E, & Smith, W. L. (1991). Large postnatally acquired cysts: Unexpected developmental outcomes. Journal of Child Neurology, 6, 58-64.

Bregman, J., & Kimberlin, L. V. S. (1993). Developmental outcome in extremely premature infants–impact of surfactant. Pediatric Clinics of North America, 40, 937-951.

Brooks-Gunn, J., McCarton, C. M., Casey, P. H., McCormick, M. C., Bauer, C. R., Bernbaum, J. C., Swanson, M., Bennett, F. C., & Scott, D. T. (1994). Early intervention in low-birth-weight premature infants. Results through age 5 years from the Infant Health and Development Program. Journal of the American Medical Association, 272, 1257-1262.

Fujiwara, T., Maeta, H., Chida, S., Morita, T., Watabe, Y., & Abe, T. (1980) Artificial surfactant therapy in hyaline membrane disease. Lancet, 1(8159), 55-59.

Glass, P., Wagner, A. E., Papero, P. H., Rajasingham, S. R., Civitello, L. A., Kjaer, M. S., Coffman, C. E., Getson, P. R., & Short, B. L. (1995). Neurodevelopmental status at age 5 years of neonates treated with extracorporeal membrane oxygenation. Journal of Pediatrics, 127, 447-457.

Gong, A., Anday, E., Bores, S., Bucciarelli, R., Burchfield, D., Zucker, J., & Long, W. (1995). One-year follow-up of 260 premature infants with respiratory distress syndrome and birth weights of 700 to 1350 grams randomized to two rescue doses of synthetic surfactant or air placebo. American exosurf national study group I. Journal of Pediatrics, 126, S68-S74.

Guralnick, M. J. (1997). The effectiveness of early intervention. Baltimore: Brookes.

Guyer, B., Martin, J. A., MacDorman, M. F., Anderson, R. N., & Strobino, D. M. (1997). Annual summary of vital statistics–1996. Pediatrics, 100, 905-918.

Haas, M., & Rice, W. R. (1995). Respiratory distress syndrome for the practicing pediatrician. Pediatric Annals, 24, 572-579.

Holbrook, K. (1996). Children with visual impairments: A parents’ guide. Bethesda, MD: Woodbine.

Hrabovsky, E. E., & Mullett, M. D. (1986). Gastroesophageal reflux and the premature infant. Journal of Pediatric Surgery, 21, 583-587.

Infant Health and Development Program Consortium. (1990). Enhancing the outcomes of low-birth-weight, premature infants. A multisite, randomized trial. The Infant Health and Development Program. Journal of the American Medical Association, 263, 3035-3042.

Klaus, M. H., & Fanaroff, A. A. (1993). Care of the high risk neonate. Philadelphia: W. B. Saunders.

Knight-Nanan, D. M., Algawi, K., Bowell, R., & O’Keefe, M. (1996). Advanced cicatricial retinopathy of prematurity: Outcome and complications. British Journal of Ophthalmology, 80, 343-345.

Kraybill, E. N., Bose, C. L., Corbet, A. J., Garcia-Prats, J., Asbill, D., Edwards, K., & Long, W. (1995). Double-blind evaluation of developmental and health status to age 2 years of infants weighing 700 to 1350 grams treated prophylactically at birth with a single dose of surfactant or air placebo. Journal of Pediatrics, 126, S33-S42.

LaPine, T. R., Jackson, J. C., & Bennett, F. C. (1995). Outcome of infants weighing less than 800 grams at birth: 15 years’ experience. Pediatrics, 96, 479-483.

Lee, K., Kim, B., Khoshnood, B., Hsieh, H., Chen, T., Herschel, M., & Mittendorf, R. (1995). Outcome of very low birth weight infants in industrialized countries: 1947-1987. American Journal of Epidemiology, 141, 1188-1193.

Lifschitz, M., Seilheimer, D., Wilson, G., Williamson, W., Thurber, S., & Desmond, M. (1987). Neurodevelopmental status of low birth weight infants with bronchopulmonary dysplasia requiring prolonged oxygen supplementation. Journal of Perinatology, 7, 127-132.

Madikians, A., & Conway, E. E. (1997). Cerebrospinal fluid shunt problems in pediatric patients. Pediatric Annals, 26, 613-620.

McCarton, C. M., Brooks-Gunn, J., Wallace, I. E, Bauer, C. R., Bennett, E. C., Bernbaum, J. C., Broyles, R. S., Casey, P. H., McCormick, M. C., Scott, D. T., Tyson, J., Tonascia, J., & Meinert, C. L. (1997). Results at age 8 years of early intervention for low-birth-weight premature infants. The Infant Health and Development Program. Journal of the American Medical Association, 277, 126-132.

Meisels, S. J., Plunkett, J. W., Roloff, D. W., Pasick, P. L., & Stiefel, G. S. (1986). Growth and development of preterm infants with respiratory distress syndrome and bronchopulmonary disease. Pediatrics, 77, 345-352.

Northway, W. H., Rosan, R. C., & Porter, D. Y. (1967). Pulmonary disease following respirator therapy of hyaline-membrane disease. Bronchopulmonary dysplasia. New England Journal of Medicine, 276, 357-368.

O’Shea, T. M., Klinepeter, K. L., Goldstein, D. J., Jackson, B. W., & Dillard, R. G. (1997). Survival and developmental disability in infants with birth weights of 501-800 grams, born between 1979 and 1994. Pediatrics, 100, 982-986.

O’Shea, T. M., Preisser, J. S., Klinepeter, K. L., & Dillard, R. G. (1998). Trends in mortality and cerebral palsy in a geographically based cohort of very low birth weight neonates born between 1982 and 1994. Pediatrics, 101, 642-647.

Palmer, E. A., Flynn, J. T., & Hardy, R. J. (1991). Incidence and early course of retinopathy of prematurity. Ophthalmology, 98, 1628-1640.

Phelps, D. L. (1995). Retinopathy of prematurity. Pediatrics in Review, 16, 50-56.

Saigal, S., Robertson, C., Sankaran, K., Bingham, W., Casiro, O., MacMurray, B., Whitfield, M., & Long, W. (1995). One-year outcome in 232 premature infants with birth weights of 750 to 1249 grams and respiratory distress syndrome randomized to rescue treatment with two doses of synthetic surfactant or air placebo. Canadian exosurf neonatal study group. Journal of Pediatrics, 126, S61-S67.

Schumacher, R. E., Palmer, T. W., Roloff, D. W., LaClaire, P. A., & Bartlett, R. H. (1991). Follow-up of infants treated with extracorporeal membrane oxygenation for newborn respiratory failure. Pediatrics, 87, 451-457.

Singer, L. T., Davillier, M., Preuss, L., Szekely, L., Hawkins, S., Yamashita, T., & Baley, J. (1996). Feeding interactions in infants with very low birth weight and bronchopulmonary dysplasia. Journal of Developmental and Behavioral Pediatrics, 17, 69-76.

Spitzer, A. R. (1996). Intensive care of the fetus and neonate. Baltimore: Mosby-Year Book.

Tudehope, D., Burns, Y., Gray, P., Mohay, H., O’Callaghan, M., & Rogers, Y. (1995). Changing patterns of survival and outcome at 4 years of children who weighed 500-999 g at birth. Journal of Paediatrics and Child Health, 31, 451-456.

Watt, T. J. (1994). Intraventricular hemorrhage in the premature infant. Nebraska Medical Journal, 79, 322-325.

Weindling, M. (1995). Periventricular haemorrhage and periventricular leukomalacia. British Journal of Obstetrics and Gynecology, 102, 278-281.

Wildin, S. R., Landry, S. H., & Zwischenberger, J. B. (1994). Prospective, controlled study of developmental outcome in survivors of extracorporeal membrane oxygenation: The first 24 months. Pediatrics, 93, 404-408.

Wilson, R. S. (1985). Risk and resilience in early mental development. Developmental Psychology, 21, 795-805.


The Organization

The Winston School was established in 1975 as an educational institution dedicated to realizing the extraordinary potential of bright students who learn differently. Winston’s mission is to encourage each student to become an independent learner through individualized learning strategies that prepare graduates for college-level work and the challenges of the future. The Winston School is located in an attractive North Dallas neighborhood in a new and renovated facility that will accommodate 230 students.


Reporting to the Board of Trustees, the Head of School will have overall responsibility for the academic quality, institutional strength, and community involvement of The Winston School. Key to this person’s role will be communicating with all of the school’s internal and external constituencies. Specific duties will include the following: continue the School’s tradition of academic innovation and real-world learning strategies, direct involvement in broad-based fund-raising activities, develop and implement effective business management systems, devise improved programs that will facilitate student transition to traditional academic environments, and broaden community awareness of Winston. The new Head of School will assume responsibilities no later than July of 1999.

Candidate Qualities

A leadership style that emphasizes listening, creativity, and collaboration. Sufficient background in and knowledge of learning differences to have demonstrated expertise and credibility in the field. Experience in senior administrative roles that require broad-based communication, empowering faculty and staff, implementing change, and exercising independent thought. Ideally, background in fund-raising and development. Demonstrated competence in establishing educational policy, curriculum development, and program creation.

May now be: Head of School or senior administrative position with a school that specializes in the holistic and individualized education of students with learning differences; a senior administrator in a traditional school that strongly supports students with learning differences; or an individual trained in learning differences who is presently in an academic institution, diagnostic center, or social agency.

Address: Theresa C. McNab, 1603 Pinewood Drive, Smithfield, RI 02917

For further information or to submit a resume, please contact L. Lincoln Eldridge, Kristina Dorsey, Brigham Hill Consultancy, 2909 Cole Ave., Suite 301, Dallas, TX 75204, FAX 214/871-6004.

Theresa C. McNab,

Brown University, and

James A. Blackman,

University of Virginia


COPYRIGHT 2004 Gale Group