Health issues in survivors of prematurity. (Featured CME Topic: Pediatrics).

As TECHNOLOGIC CAPABILITY INCREASES, so does the number of survivors of prematurity. By definition, a premature infant is one that is delivered before 37 completed weeks of gestation. More than 400,000 premature infants are born each year in the United States, an incidence of 11.6% of all live births. (1) As expected, the smallest and most immature infants have the greatest long-term problems. Table 1 lists the current mortality rate and expected birth weight associated with each level of gestation. (2) Long-term morbidity in these infants includes chronic lung disease, cerebral palsy, learning disabilities, and vision and hearing impairments.

RESPIRATORY SYSTEM

Every organ system is affected by prematurity. The primary concern after birth is respiratory distress syndrome or hyaline membrane disease, the deficiency of surfactant necessary to decrease alveolar surface tension and prevent alveoli from collapsing. Such infants are supported with oxygen, assisted ventilation, and surfactant replacement therapy when necessary. If the infant continues to require assisted ventilation with a high oxygen requirement (>80%) beyond 10 days of age, then further treatment with corticosteroids is considered.

Chronic lung disease (CLD) is defined as an oxygen requirement at corrected gestational age of 36 weeks. Chronic lung disease was formerly referred to as bronchopulmonary dysplasia, which was defined as clinical signs of respiratory distress with an abnormal chest radiograph consistent with Northway et al (3) stage 3 or 4, and an oxygen requirement after 28 days of age in children who had received assisted ventilation.

Some of the smallest infants may spend up to 3 months in the neonatal intensive care unit (NICU) before discharge, and may be sent home with CLD treated with oxygen, bronchodilators, and diuretics. It is imperative that these babies receive palivizumab, a monoclonal antibody against the respiratory syncytial virus (RSV). They should receive monthly injections during the RSV season (October through March, with regional variation) up to the age of 2 years. Our current policy is for all infants <32 weeks' gestation to receive palivizumab. The decision to administer palivizumab to infants at 32 to 35 weeks' gestation is based on risk factors such as CLD, siblings, day-care provision, and/or smoking in the home.

Predictions about infants in nurseries today must be limited by the fact that the long-term effects of many newer therapies are unknown. The effects of surfactant, corticosteroids, palivizumab, and other therapies, such as nitric oxide and extracorporeal membrane oxygenation, on the respiratory health in adulthood are undetermined. For example, reports indicate that corticosteroid therapy reduces alveolar septation. (4) The outcome of cohorts from eras in the immediate past is our best guide to predict the respiratory health of today's infants, however. Doyle et al (5) have reported changes in lung function for extremely low-birth-weight infants (ELBW, <1,000 g) at age 14 years compared with normal birth-weight (NBW) control subjects. Based on data collected between 1977 and 1982 at the Royal Women's Hospital in Melbourne, lung function in ELBW children in this study improved between 8 and 14 years of age. The rate of change in lung function between the ages of 8 and 14 years in ELBW children was the same wit h or without CLD. (5) It is notable that ELBW children with or without CLD had lung function mostly in the normal range at 14 years of age. They did, however, have some variables reflecting flow that were of potential concern. It has not been determined if their lung function may deteriorate at a faster rate as they approach adulthood. (5,6) Table 2 contrasts lung function alterations between premature and term infants, while Table 3 contrasts lung functions in ELBW children with and without CLD. (5)

CARDIOVASCULAR SYSTEM

The primary concern during the neonatal period is persistent patent ductus arteriosus (PDA). Premature infants frequently have failure of ductus closure after birth. Sequelae of a persistent PDA in premature infants include risk of intraventricular hemorrhage (IVH), CLD, necrotizing enterocoliltis (NEC), and retinopathy of prematurity. (7) Closure can be facilitated by treatment with intravenous indocin, a prostaglandin [E.sub.1] inhibitor. For infants who do not improve with indocin therapy, surgical ligation is recommended, with the only long-term effect being the potential scar from the ligation.

GROWTH AND NUTRITION

Intrauterine and/or neonatal growth retardation is present in up to 50% of very-low-birth-weight (VLBW, <1,500 g) neonates who receive intensive care and require prolonged hospitalizations. For children born at weights appropriate for gestational age, poor neonatal growth is related to inadequate nutrition during the acute phase of neonatal disease, increased caloric requirements related to breathing in CLD, poor feeding in neurologically impaired children, and lack of parental care or an optimal environment for growth in the nursery. As these conditions gradually resolve and when an optimal home environment is provided, body growth may catch up during the first 2 to 3 years of life. Up to 20% of these infants remain subnormal in weight and height by their third year of life, however. (8)(p531)

Problems encountered with feeding and nutrition in the NICU include delay in feeding while awaiting development, at 32 weeks' gestation, of the suck and swallow reflexes. Gastroesophageal reflux disease has been reported to affect as many as 63% of premature infants born at or around 30 weeks' gestation when assessed using a pH probe test. (9) Necrotizing enterocolitis remains the major gastrointestinal cause of morbidity and mortality among the NICU population, however, occurring at the estimated rate of 22 per 1,000 admissions. (8)(p187) Necrotizing enterocolitis is a multifactorial disorder, with a delicate balance between bowel perfusion, enteric organisms, and nutritional intake. Necrotizing enterocolitis is managed either medically, with intravenous antibiotics, nasogastric suction, and bowel rest, or surgically, if the infant exhibits signs of bowel perforation or bowel death (prolonged metabolic acidosis, thrombocytopenia, hyponatremia, abdominal distention/erythema, pneumatosis intestinalis).

The sequelae of NEC for survivors of prematurity include long-term problems of strictures and short-bowel syndrome (SBS). Strictures occur in 20% of documented cases of NEC.'0 Symptoms include evidence of intestinal obstruction, such as feeding intolerance, abdominal distention, and bilious emesis. Management almost always involves surgical resection.

Approximately 20% of patients who have NEC and undergo surgical resection develop SBS. (10) In the past, SBS was defined as having <75 cm of residual small intestine after bowel resection." Currently, the definition is a functional one (ie, the presence of malabsorption after significant small-intestine resection) . (12) The major consequences of SBS are related to malabsorption, especially of carbohydrates, from decreased surface area of the small intestine, and loss of specific functions from removed segments, such as the ileum, which is the site of both vitamin [B.sub.12] and bile acid absorption. The presence of the ileocecal valve after resection is paramount to future complications, since the valve serves 2 important functions: regulation of transit and prevention of bacterial reflux into the small bowel. Lack of this valve can lead to decreased intestinal transit time (which exacerbates fluid and nutrient losses) and increased risk of small-bowel overgrowth. The development of cholestatic liver disease is frequent in infants with SBS who receive parenteral nutrition, (13,14) and, along with sepsis, is the leading cause of death in these patients. (13,15-17)

Potential new therapies include glucagon-like peptide 2, which stimulates intestinal mucosal growth and decreases small-bowel motility, (18) surgery, and small-intestine transplantation (SIT). Surgery may be an option for patients who are unable to tolerate full feedings. Small-intestine transplantation is an option for patients with SBS and progressive, severe, parenteral-nutrition-associated liver disease, recurrent sepsis, and threatened loss of central venous access, with the only absolute contraindication being acquired immunodeficiency syndrome (AIDS) or overwhelming sepsis. (19) Irreversible liver disease is suggested by hyperbilirubinemia persisting beyond the age of 3 to 4 months, combined with features of portal hypertension, such as splenomegaly, thrombocytopenia, or prominent superficial abdominal veins.

CENTRAL NERVOUS SYSTEM

The preterm infant is at high risk for a number of neurologic insults, most commonly intracranial/intraventricular hemorrhage, posthemorrhagic hydrocephalus, and periventricular leukomalacia.

Intraventricular Hemorrhage

Intraventricular hemorrhage (IVH) is reported in 35% to 50% of infants <32 weeks' gestation or weighing <1,500 g at birth. (20,21) There is an inverse relationship between gestational age and incidence of IVH, due in part to the increasing fragility of capillaries and the poorer support of the vascular bed associated with decreasing gestational age. The 4 grades of IVH originally defined by Papile are described in Table 4, (22) with the higher grades showing more extensive hemorrhagic involvement and greater potential for long-term sequelae. Rarely are grade 1 hemorrhages associated with long-term morbidity, as opposed to the almost uniform morbidity with grade 4 hemorrhages. Recently, low-dose indocin therapy has been used as a preventive measure against IVH. (23)

Posthemorrhagic Hydrocephalus

Posthemorrhagic hydrocephalus is defined as progressive ventricular dilatation after an IVH, either acute (caused by either a blood clot that impairs the normal flow of cerebral spinal fluid [CSF], or obstruction to the absorption of CSF at the level of the arachnoid villi), or chronic (due to obliterative arachnoiditis or blockage from necrotic debris, reactive gliosis, or disrupted ependyma that interferes with flow of the CSF). (24) Progressive hydrocephalus associated with increased intracranial pressure (ICP) may require removal of CSF by serial lumbar punctures or permanent ventroperitoneal (VP) shunt. Long-term care of VP shunts includes close monitoring for infection and mechanical obstruction. Signs and symptoms of a shunt infection include fever, irritability, stiff neck, lethargy, erythema overlying the shunt, and ascites. The diagnosis is supported by culture and Gram stain of the CSF. Treatment includes appropriate broad spectrum antibiotics and possible removal and replacement of the existing sh unt. Mechanical obstruction presents with signs and symptoms of increased ICP. Treatment requires intervention by a neurosurgeon. The number and severity of shunt complications is a major contributing factor to long-term neurologic morbidity.

Periventricular Leukomalacia

The CNS lesions of greatest importance to prognosis in childhood and adulthood involve the white matter. Periventricular leukomalacia (P\FL) is an ischemic infarction of the white matter adjacent to the lateral ventricles, as its name suggests. Periventricular leukomalacia is reported to occur in up to 25% of infants with birth weights of <1,500 grams. (20,25,26) Risk factors for PVL are included in Table 5.

Cerebral Palsy

Cerebral palsy (CP) refers to a "group of non-progressive, but often changing, motor impairment syndromes due to lesions or anomalies of the brain arising in the early stages of its development." (27) Extremely low-birth-weight infants face a risk of CP, predominantly the spastic forms, that is at least 70 times that of NBW infants. (28) Numerous factors are implicated in the development of CP in VLBW infants. In the first week of life, VLBW infants often have low thyroxine levels compared with term infants (transient hypothyroxinemia of prematurity), (29) which have been associated with increased risk of CP. (30) Among pregnancy complications that account for a substantial proportion of VLBW infants, preeclampsia is the only one associated with a decreased risk of CP, with an odds ratio of 0.4. (31-37) There is, however, a strong association between intrauterine infection and CP. This is due to a proinflammatory cytokine cascade triggered by bacterial invasion of the uterine cavity. (38-41) Placental abrupti on has also been identified as a risk factor for CP, with an odds ratio of 1.6 (95% confidence interval, 1.1-2.3). (31,33,35,42,43) Antenatal corticosteroid therapy is used routinely to advance fetal lung maturity and reduce neonatal mortality and has been reported to decrease the risk of brain injury and CP by inhibiting the proinflammatory cytokine cascade. (38,44-46) The use of repeated doses has now been implicated in retarding brain growth, however. (47) Therefore, the use of steroids requires caution and judicious use, weighing risks and benefits of therapy. When addressing labor and delivery characteristics, the most important factor may be site of delivery. The risk of CP was increased sixfold among infants delivered at hospitals without specialized perinatal services. (42) A reasonable biologic explanation is that physiologic stability is enhanced by the efforts of specialized nurses and physicians at tertiary-care hospitals.

Appropriate neurodevelopmental follow-up is necessary to detect those areas of deficiency as early as possible to allow for appropriate referral to intervention services. This follow-up in childhood should also be corrected for the normal variations seen due to gestational age.

Retinopathy of Prematurity

Retinopathy of prematurity (ROIP) is a potentially blinding condition affecting premature infants with incompletely vascularized retinas. It is a disorder that disrupts the normal progression of retinal vascular development in the preterm infant and results in the abnormal proliferation of blood vessels in the developing retina. Retinopathy of prematurity can lead to refractive errors, amblyopia, strabismus, or, as already noted, blindness due to retinal detachment. The severity of ROP is inversely proportional to the gestational age at the time of birth. Retinopathy of prematurity is classified by stage and zone. Stage refers to the severity of the disease. Zone refers to the area of the retina involved, based on the distance from the optic disk. Prethreshold disease and threshold disease are terms used to reflect severity of disease. If untreated, 50% of infants with threshold ROP will become blind.48 Even with treatment, 20% to 25% of infants will become blind. Treatment using laser photocoagulation is dir ected at the avascular retina in an attempt to decrease the stimulus for abnormal vessel development. One side effect is loss of peripheral vision at the site of the laser therapy; however, this is a worthwhile trade-off to deter retinal detachment and eventual blindness. A study of 108 patients aged 15 years or older with a history of ROP (with up to 23 years of follow-up) showed that eyes with minimal changes from ROP were still at high risk for retinal tears and detachments. Eighty percent of eyes with retinal tears and 60% of eyes with a detachment that started with vision >20/60 maintained that level of vision at final examination. (49)

HEARING LOSS

Universal hearing screening of all newborns is now recommended, especially for NICU graduates. The preterm infant with an immature auditory system is at higher risk of auditory damage. Environmental noise, hypoxia, fluctuations in blood pressure, ototoxic drugs, hyperbilirubinemia, and neonatal infections are common problems in the NICU. The average incidence of hearing loss in the preterm infant population is 2% to 6%. (20)

LEARNING DISABILITIES

The preterm infant faces several insults, as described. As a result, these children may have long-term developmental difficulties, compared with the full-term population. Table 6 lists the incidence of neurosensory and developmental outcomes of VLBW infants. (51-54) Table 7 is a compilation of studies from 1987 to 1999 evaluating the disability status outcomes of VLBW and ELBW children. Some children without major neurologic handicaps present at school age with learning problems. Reports related to learning problems estimate that these exist in from 11% to 45% of the preterm population.53 Learning disabilities are found in children with average intelligence and normal sensory acuity, and cannot be diagnosed before the child's entrance into school and academic learning. The diagnosis of learning disability is usually completed by the school system. Hack et al, (55) at Case Western Reserve University School of Medicine, compared 242 survivors of LBW babies born between 1977 and 1979 with 233 control subjects wi th NBW from the same population in Cleveland. The study found fewer individuals in the premature group had graduated from high school and that they had lower academic achievement, higher rates of neurosensory impairments, and subnormal height. Very-low-birth-weight individuals had significantly lower mean IQ scores than controls (87 vs 92), and had a higher frequency of subnormal IQ (defined as lower than 70) and borderline IQ (70 to 84). Fifty-one percent of the VLBW individuals had an IQ in the normal range (85), compared with 67% of the control subjects. These differences remained significant when the comparisons were restricted to participants without neurosensory impairment. On the encouraging side, the study found that the premature group reported less alcohol and drug use, had less contact with the police, and had lower rates of sexual activity and pregnancy at 20 years of age. The report did hint at higher rates of bipolar disorder among the group who had been premature (2%) than among control subject s (1%). Hack et a1 (55) noted that evidence in the medical literature suggests that the presentation of attention-deficit/hyperactivity disorder may differ among premature infants. Premature infants with ADHD have a more marked presentation of attention problems, but less hyperactivity.

CONCLUSION

As a result of the increasing number of ELBW patients surviving over the past 25 years, these patients are now entering the purview of continuing medical care by providers who care for adults. It is critical that the primary care physician be aware of the unique problems some of these patients may manifest. In addition, the primary caretaker must also be acutely aware of the resources needed for the continued optimal outcome of this specific group of patients. Fortunately, several centers continue to collect information on these patients as they progress through adulthood, and other outcome and management issues may well be identified.

Appendix 1

Information and Support Organizations

Easter Seals--National headquarters

230 W Monroe St, Suite 1800

Chicago, IL 60606

800-221-6827

312-726-6200

National Association for the Deaf

814 Thayer Ave

Silver Spring, MD 20910

301-587-1788

National Association for Parents of the Visually Impaired

PO Box 317

Watertown, MA 02272

800-562-6265

National Association for the Visually Handicapped

22 W 21st St

New York, NY 10010

212-889-3141

National Information Center for Children and Youth with Disabilities

PO Box 1429

Washington, DC 20013-1492

800-695-0285

National Organization--United Cerebral Palsy

1660 L St NW, Suite 700

Washington, DC 20036

202-776-0406

Appendix 2

Internet Resources

Ability On-Line Support Network

http://www.ablelink.org

Connects young people with disabilities and chronic illnesses to peers and mentors with and without disabilities

American Association for Premature Infants

http://www.aapi-online.org

Advocacy organization dedicated to improving the quality of health, developmental, and educational services for premature infants and their families

ARCH National Resource Center for Respite & Crisis Care

http://www.chtop.com/archbroc.htm

Information to support service providers and families through training, technical assistance, evaluation, and research

Caring for a Child Dependent on Technology

http://kidshealth.org/parent/healthy/machine.html

Resource for caring for technology-dependent children

Cochrane Neonatal Group

http://www.cochrane.org/cochrane/revabtr/g030index.htm

Lists abstracts of Cochrane reviews from the Cochrane Library

Federation for Children with Special Needs

http://www.fcsn.org

Support for families with special-needs families

National Parent Network on Disabilities

http://www.npnd.org

Provides up-to-date information on the activities of all 3 branches of government that impact individuals with disabilities and their families

Neonatology on the Web

http://www.neonatology.org

Resource for health care professionals including practice guidelines, consensus statements, Internet resources for neonatal-perinatal medicine

NICU Special Needs Forum

www.geocities.com/RainForest/Canopy/37/forum1.htm

Offers a message board with several topics available concerning premature babies and special needs

NICU-Web

http://neonatal.peds.washington.edu

University of Washington Academic Medical Center's Web site that includes common neonatal diagnoses, procedures/interventions, neonatal resources

Parents of Preemies

http://www2.medsch.wisc.edu/childrenshosp/parents_of_preemies/toc.htm l

Provides detailed table of contents for topics of interest to parents of premature infants

PreemieParents.com

http://www.preemieparents.com

Lists Web sites for recommended reading and parent resources

TABLE 1.

Mortality Rate and Expected Birth Weight (50th Percentile) at 23 to 30
Weeks' Gestation

Gestational Age  Mortality  Birth Weight
    (weeks)         (%)         (g)

      23           <97           500
      24           50-90         700
      26           10-50         900
      28            5-10       1,100
      30           <5          1,350
TABLE 2.

Variation in Lung Function by Birth Weight


Lung Function          ELBW ([+ or -]SD)       NBW ([+ or -]SD)
   Variable                (n = 72)                (n = 39)

FVC                  100.6 ([+ or -] 13.3)  104.8 ([+ or -] 12.0)
[FEV.sub.1]           93.1 ([+ or -] 14.9)  104.6 ([+ or -] 13.21)
[FEV.sub.1]/FVC (%)   81.9 ([+ or -] 10.6)   87.0 ([+ or -] 7.0)
[FEF.sub.25%-75%]     77.0 ([+ or -] 26.8)   99.1 ([+ or -] 23.4)
[V'.sub.EMAX75%]      93.1 ([+ or -] 24.0)  110.7 ([+ or -] 22.1)
[V'.sub.EMAX50%]      89.8 ([+ or -] 30.5)  113.0 ([+ or -] 25.7)
[V'.sub.EMAX25%]      87.5 ([+ or -] 37.1)  110.7 ([+ or -] 35.1)
RV                   112.1 ([+ or -] 43.3)  117.4 ([+ or -] 30.8)
TLC                   98.9 ([+ or -] 16.0)  102.5 ([+ or -] 13.9)
RV/TLC (%)            27.5 ([+ or -] 9.2)    26.8 ([+ or -] 6.3)

                       Mean Difference
Lung Function             (95 % CI)
   Variable             Between Groups

FVC                   -4.2 (-9.3 to 0.9)
[FEV.sub.1]          -11.6 (-17.9 to -5.2) *
[FEV.sub.1]/FVC (%)   -5.1 (-8.9 to -1.4) *
[FEF.sub.25%-75%]    -22.1 (-32.2 to -12) *
[V'.sub.EMAX75%]     -17.6 (-26.9 to -8.2) *
[V'.sub.EMAX50%]     -23.2 (-34.7 to -11.7) *
[V'.sub.EMAX25%]     -23.2 (-37.6 to -8.7) *
RV                    -5.2 (-21 to 10.5)
TLC                    3.5 (-9.6 to 2.5)
RV/TLC (%)             0.7 (-2.6 to 4)

* Statistically significant difference between groups. ELBW = Extremely
low birth weight, NBW = normal birth weight, SD = standard deviation, CI
= confidence interval, FVC = forced vital capacity, [FEV.sub.1] = forced
expiratory volume in 1 second, [FEF.sub.25%-75%] = forced midexpiratory
expiratory flow, [V'.sub.EMAX75%] = flow rate at 75% of vital capacity,
[V'.sub.EMAX50%] = flow rate at 50% of vital capacity, [V'.sub.EMAX25%]
= flow rate at 25% of vital capacity, RV = residual volume, TLC = total
lung capacity.
TABLE 3.

Variation in Lung Function of Children With or Without Chronic Lung
Disease Born at Extremely Low Birth Weight


Lung Function          CLD ([+ or -]SD)      No CLD ([+ or -]SD)
   Variable                (n = 30)               (n = 42)

FVC                   99.7 ([+ or -] 12.7)  101.2 ([+ or -] 13.9)
[FEV.sub.1]           90.4 ([+ or -] 15.8)   95.0 ([+ or -] 14.1)
[FEV.sub.1]/FVC (%)   79.3 ([+ or -] 9.9)    83.7 ([+ or -] 10.8)
[FEF.sub.25%-75%]     73.0 ([+ or -] 29.1)   79.9 ([+ or -] 25.0)
[V'.sub.EMAX75%]      89.1 ([+ or -] 22.5)   95.7 ([+ or -] 24.9)
[V'.sub.EMAX50%]      86.9 ([+ or -] 34.5)   91.8 ([+ or -] 27.8)
[V'.sub.EMAX25%]      79.1 ([+ or -] 35.6)   93.5 ([+ or -] 37.4)
RV                   103.2 ([+ or -] 38.5)  118.3 ([+ or -] 45.7)
TLC                   97.4 ([+ or -] 13.3)  100.0 ([+ or -] 17.7)
RV/TLC (%)            25.4 ([+ or -] 9.0)    29.0 ([+ or -] 9.1)

                       Mean Difference
Lung Function             (95 % CI)
   Variable             Between Groups

FVC                   -1.5 (-7.9 to 4.9)
[FEV.sub.1]           -4.6 (-11.7 to 2.4)
[FEV.sub.1]/FVC (%)   -4.4 (-9.4 to 0.6)
[FEF.sub.25%-75%]     -6.9 (-19.7 to 5.8)
[V'.sub.EMAX75%]      -6.6 (-18.6 to 5.4)
[V'.sub.EMAX50%]      -4.9 (-20.2 to 10.3)
[V'.sub.EMAX25%]     -14.4 (-32.2 to 3.5)
RV                   -15.1 (-36.2 to 6)
TLC                   -2.6 (-10.5 to 5.3)
RV/TLC (%)            -3.7 (-8.1 to 0.8)

CLD = Chronic lung disease, SD = standard deviation, CI = confidence
interval, FVC= forced vital capacity, [FEV.sub.1] = forced expiratory
volume in 1 second, [FEF.sub.25%-75%] = forced midexpiratory expiratory
flow, [V'.sub.EMAX75%] = flow rate at 75% of vital capacity,
[V'.sub.EMAX50%] = flow rate at 50% of vital capacity, [V'.sub.EMAX25%]
= flow rate at 25% of vital capacity, RV = residual volume, TLC = total
lung capacity.
TABLE 4.

Grading of Intraventricular Hemorrhage

Grade  Description

I      Isolated germinal matrix hemorrhage
       with no extension to the
       ventricles

II     Intraventricular hemorrhage with
       normal ventricular size; blood
       occupies up to 50% of ventricular
       volume

III    Intraventricular hemorrhage with
       ventricular dilatation; blood
       occupies more than 50% of
       ventricular volume

IV     Intraventricular hemorrhage with
       parenchymal involvement;
       ventricles often dilated
TABLE 5.

Risk Factors for Development of Periventricular Leukomalacia


Extreme prematurity
Severe hypoxemia/ischemia/shock
Sepsis/meningitis
Seizures
Intraventricular hemorrhage
Cardiorespiratory arrest
Significant apnea
Bronchopulmonary dysplasia
TABLE 6.

Incidence of Neurosensory and Developmental Outcomes of Very-
Low-Birth-Weight Infants *

                              Incidence in  Incidence in  Incidence in
                              <1,500 g BW   <1,000 g BW    <800 g BW
Disability                        (%)           (%)           (%)

Mental retardation                 5             12            22
Cerebral palsy                     3              6             9
Sensory impairment                 3              9            25
Use of any special education      30             50            50

                                Incidence in
                              Total Population
Disability                          (%)

Mental retardation                  2.3
Cerebral palsy                      0.5
Sensory impairment                  0.5
Use of any special education        23

* Birth weight <1,500 grams.

BW = Birth weight.
TABLE 7.

Severity of Disabilities Resulting From Very Low * and Extremely Low +
Birth Weight

                                              Mild ++ to
                                  Severe **   Moderate ss      No
Author                    No.     Disability  Disability   Disability
(Publication Year)"     Subjects     (%)          (%)         (%)

Kitchen (1987)             83        19.0         9.0         72.0
Veen (1991)               927         6.6        13.0         80.0
Scottish LBW Study
  Group (1992)            611        17.5        12.8         67.5
Johnson (1993)            153        23.0        42.0         35.0
Cooke (1994)              441         9.0        19.0         72.0
LaPine (1995)             132        11.0        11.0         78.0

Lee (1995)                251        18.0        21.0        616.0
Tudehope (1995)           154        15.0         8.0         77.0
Hack (1996)                88        16.0        23.0         61.0
Monset-Couchard (1996)     84         6.0        57.0         37.0
Dar]ow (1997)              77         9.1        19.5         71.1
Piecuch (1997)            446        12.0        26.0         61.0

Emsley (1998)              64        13.0        44.0         44.0
Ment (1999)               257         8.0        11.0         81.0



Author                         Birth Year(s)/
(Publication Year)"            Study Location

Kitchen (1987)          1979-1980/Australia
Veen (1991)             1983/Netherlands
Scottish LBW Study
  Group (1992)          1984/Scotland
Johnson (1993)          1984-1986/Oxfbrd, England
Cooke (1994)            1980-1989/United Kingdom
LaPine (1995)           1977-1980 and 1983-1990/
                          Seattle, Washington
Lee (1995)              International review
Tudehope (1995)         1977-1983/Australia
Hack (1996)             1990-1992/Cleveland, Ohio
Monset-Couchard (1996)  1981-1991/Paris, France
Dar]ow (1997)           1986/New Zealand
Piecuch (1997)          1979-1971/San Francisco,
                          California
Emsley (1998)           1984-1995/United Kingdom
Ment (1999)             1989-1992/New England

All groups had extremely low birth weights, except those of Veen, the
Scottish LBW Study Group and Lee, which comprised a mixture of very low
and extremely low birth weights.

* Very low birth weight = <1,500 g.

+ Extremely low birth weight = <1,000 grams or <29 weeks' gestation.

** Severe disability = mental retardation with an IQ<50, cerebral palsy
with inability to walk, blindness, or deafness.

++ Mild disability = combinations of slow learning (IQ 70-84),
coordination, communication, and learning and perceptual disorders.

(ss) Moderate disability = cognitive disabilities of mild mental
retardation (IQ 50-70), hearing loss, or cerebral palsy with the ability
to walk.

LBW = Low birth weight

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(4.) Sahebjami H, Domino M: Effects of postnatal dexamethasone treatment on development of alveoli in adult rats. Exp Lung Res 1989; 15:961-973

(5.) Doyle LW, Chavasse R, Ford CW, et al: Changes in lung function between age 8 and 14 years in children with birth weight of less then 1501 g. Pediatr Pulmonol 1999; 27:185-190

(6.) Weiss ST: Early life predictors of adult chronic obstructive lung disease. Eur Respir Rev 1995; 5:303-309

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From the Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tenn, and the Department of Pediatrics, East Tennessee State University College of Medicine, Johnson City.

Reprint requests to Jackie York, MD, East Tennessee State University, Department of Pediatrics, PO Box 70578, Johnson City, TN 37614-1708.