Original Article
Late Pulmonary Sequelae of Bronchopulmonary Dysplasia
N Engl J Med 1990; 323:1793-1799December 27, 1990
- Abstract
- Abstract
Background.
Bronchopulmonary dysplasia is a chronic lung disease that often develops after mechanical ventilation in prematurely born infants with respiratory failure. It has become the most common form of chronic lung disease in infants in the United States. The long-term outcome for infants with bronchopulmonary dysplasia has not been determined.
Methods.
We studied the pulmonary function of 26 adolescents and young adults, born between 1964 and 1973, who had bronchopulmonary dysplasia in infancy. We compared the results with those in two control groups: 26 age-matched adolescents and young adults of similar birth weight and gestational age who had not undergone mechanical ventilation, and 53 age-matched normal subjects.
Results.
Sixty-eight percent of the subjects with bronchopulmonary dysplasia in infancy (17 of the 25 tested) had airway obstruction, including decreases in forced expiratory volume in one second, forced expiratory flow between 25 and 75 percent of vital capacity, and maximal expiratory flow velocity at 50 percent of vital capacity, as compared with both control groups (P<0.0001 for all comparisons). Twenty-four percent of the subjects with bronchopulmonary dysplasia in infancy had fixed airway obstruction, and 52 percent had reactive airway disease, as indicated by their responses to the administration of methacholine or a bronchodilator. Hyperinflation (an increased ratio of residual volume to total lung capacity) was more frequent in the subjects with a history of bronchopulmonary dysplasia than in either the matched cohort (P<0.0006) or the normal controls (P<0.0004). Six of the subjects who had bronchopulmonary dysplasia in infancy had severe pulmonary dysfunction or current symptoms of respiratory difficulty.
Conclusions.
Most adolescents and young adults who had bronchopulmonary dysplasia in infancy have some degree of pulmonary dysfunction, consisting of airway obstruction, airway hyperreactivity, and hyperinflation. The clinical consequences of this dysfunction are not known. (N Engl J Med 1990; 323:1793–9.)
Article Activity
- Article
BRONCHOPULMONARY dysplasia was first described in 1967 as a syndrome of chronic lung disease in prematurely born infants who had been treated for respiratory distress syndrome with supplemental oxygen and mechanical ventilation.1 The clinical diagnosis of this chronic lung disease is made at one month of age in prematurely born infants who have undergone mechanical ventilation for at least one week, who have symptoms of persistent respiratory distress, who are dependent on supplemental oxygen, and who have chest radiographs that show rounded radiolucent areas in the lung alternating with thinner strands of radiodensity. The lungs of infants with bronchopulmonary dysplasia who have died have histologic evidence of necrotizing bronchiolitis, alveolar fibrosis, emphysema, and arterial changes characteristic of pulmonary hypertension. The pathogenesis of bronchopulmonary dysplasia is believed to be multifactorial, with pulmonary oxygen toxicity and barotrauma having important roles. Bronchopulmonary dysplasia has become the most common form of chronic lung disease in infants in the United States; approximately 7000 new cases occur each year.2
About 40 percent of the infants who have bronchopulmonary dysplasia die, most during the initial hospitalizaron.3 , 4 Those who survive have increased morbidity due to respiratory disease at 4 and 12 months of age, as compared with infants with a similar neonatal course in whom bronchopulmonary dysplasia does not develop.5 The cardiopulmonary abnormalities that occur in infants with bronchopulmonary dysplasia in the first year or two of life include increased airway resistance, increased airway reactivity, increased functional residual capacity, high arterial carbon dioxide tension, low arterial oxygen tension, right or left ventricular hypertrophy (or both), and pulmonary and systemic hypertension.6 7 8 9 10 11 12 13 14 15 Although abnormalities of pulmonary function can improve with age,9 there is increasing evidence that they may persist into mid-childhood.16 17 18 19
It is not known to what degree these abnormalities and the abnormalities of growth and development associated with bronchopulmonary dysplasia in infancy4 , 5 , 20 are present in adolescents or young adults. In this study, we tested the hypothesis that the pulmonary function of adolescents and young adults 14 to 23 years old who had bronchopulmonary dysplasia in infancy was normal; the study population included the infants originally described in our 1967 report.1
Methods
Informed consent was obtained from all the subjects or their parents; the design of the study was reviewed and approved by the Medical Committee for the Use of Human Subjects in Research of the Stanford University Medical Center (SUMC).
Study Population
The group of subjects with a history of bronchopulmonary dysplasia in infancy comprised all 26 children born from 1964 to 1973 at SUMC who were given a diagnosis of respiratory distress syndrome at birth on the basis of the physical examination and chest radiograph, received mechanical ventilation and oxygen supplementation at SUMC, were dependent on oxygen and had a chest radiograph consistent with bronchopulmonary dysplasia at four weeks of age,1 and still lived in California. Two subjects who met these criteria were not studied. One could not be located, and the other chose not to participate. Infants who underwent mechanical ventilation but did not have radiographic evidence of bronchopulmonary dysplasia at four weeks of age were excluded because of the difficulty of identifying milder forms of bronchopulmonary dysplasia without histologic confirmation. To control for the effect of premature birth, we used a matched cohort control group, consisting of 26 children born at SUMC from 1964 through 1973 who were cared for in the intensive care nursery but did not receive mechanical ventilation, did not have bronchopulmonary dysplasia, had no major congenital anomalies, and lived nearby; these controls were matched for birth weight and sex with the subjects who had a history of bronchopulmonary dysplasia. A second control group of 53 normal subjects of the same age as the subjects with a history of bronchopulmonary dysplasia, who had no history of chronic lung disease, were nonsmokers, and were not born prematurely, was also studied (normal control group).
Evaluation of Pulmonary Function
A cardiorespiratory history was obtained with use of the American Thoracic Society cardiorespiratory epidemiology history form.21 A complete history was also obtained and a physical examination was performed.
Pulmonary-function tests were performed at the Pulmonary Physiology Laboratory of Children's Hospital at Stanford. The respiratory technologist was not blinded to the subject's diagnosis. The pulmonary-function studies included spirometry, flow—volume curves, measurements of functional residual capacity, single-breath carbon monoxide—diffusing capacity (DLCO), and single-breath nitrogen washout, low-density gas spirometry, and bronchial provocation with methacholine. Thoracic gas volume and airway resistance were measured by plethysmography in 75 of the 105 subjects.
Spirometry and measurements of forced expiratory volume were obtained with a Fleisch pneumotachometer, in which the flow signal was integrated with a computerized pulmonary-function—testing system (model 47804 Pulmonary Calculator System, Hewlett—Packard, Palo Alto, Calif). The functional residual capacity, single-breath nitrogen washout, and single-breath DLCO were measured and the results analyzed with the automated Hewlett-Packard pulmonary-function-testing system. The DLCO was measured twice; the results were corrected for the subject's actual hemoglobin value and then averaged.22 Thoracic gas volumes and airway resistance were measured with a computerized volume plethysmograph (model 1085, Medical Graphics, St. Paul, Minn.).
Low-density gas spirometry was performed with use of a gas isolator (Jones Medical Pulman Arm, Oak Brook, Ill.) incorporated with the Fleisch pneumotachometer. The subject initially performed forced expiratory maneuvers through the gas isolator after breathing room air. The forced maneuvers were then repeated after the subject had breathed a mixture of 80 percent helium and 20 percent oxygen for five minutes. The flow—volume curves were superimposed in the Hewlett—Packard system, and the percent change in flow at 25 percent and 50 percent of forced vital capacity was determined, as was the volume at isoflow (the volume at which the flow is equal when air or the helium—oxygen mixture is breathed).
The study subjects who had forced expiratory volumes in one second (FEV1) that were less than 80 percent of the predicted value were given 3.75 mg of aerosolized isoproterenol at a dilution of 1:400, and flow—volume curves were determined again. Those with base-line FEV1 values at least 80 percent of the predicted value underwent provocative bronchial-inhalation challenge with methacholine to evaluate bronchial hyperreactivity.23 The methacholine was administered with use of a Rosenthal-French nebulization dosimeter (model D-2A, Baltimore). The diagnosis of reactive airway disease was based on either a decrease of more than 20 percent in FEV1 in response to a cumulative dose of less than 8 mg of methacholine or an increase of more than 10 percent in FEV1 after the inhalation of isoproterenol. Oxygen saturation, determined by pulse oximetry (model N-100, Nelcor, Hayward, Calif), and arterialized capillary-blood gas values were measured under room-air conditions.
The results of the pulmonary-function tests were reported as both absolute values and percentages of predicted values, according to standardized values for normal children and adults; we applied a 15 percent race-correction factor when appropriate.24 25 26 27 28 29 30 31 32 33
Other Assessments of Cardiopulmonary Function
Standard posteroanterior and lateral chest radiographs, obtained during full inspiration, were used to detect cardiomegaly and persistent parenchymal abnormalities in the lung. The chest radiographs were scored from 0 to 2 (normal = 0, mild abnormality = 1, and moderate-to-severe abnormality = 2) for each of eight variables, and the eight scores were totaled. The radiographs were assessed in random order by one of the investigators, who was unaware of the subject's study group, with use of a modification of the method developed by Toce et al.34 Each subject also underwent electrocardiography and echocardiography with Doppler ultrasound.
Determination of Atopic Status
Atopic status was determined by measuring serum total IgE and IgE antibodies to a screening panel of 10 major allergens with the paper-disk enzyme-linked immunosorbent assay in the Allergy Reference Laboratory at Children's Hospital at Stanford.35
Statistical Analysis
The results of the pulmonary-function tests were first analyzed by one-way analysis of variance and then by two-sample t-tests comparing the pulmonary-function results for the three groups of subjects (subjects with bronchopulmonary dysplasia, matched cohort controls, and normal controls). The numerical data from the physical examination were handled in the same way. The other findings from the history and physical examination were graded numerically for yes-or-no or normal-versus-abnormal responses and were analyzed by chi-square test. All reported P values are two-tailed.
Postnatal clinical and x-ray data were available for the subjects with bronchopulmonary dysplasia; these data included gestational age, birth weight, duration of intermittent positive-pressure breathing, the total time intubated, duration of inspired oxygen at a concentration of 21 to 39 percent, 40 to 79 percent, and 80 to 100 percent, peak ventilator pressure, duration of peak ventilator pressure, initial radiographically determined severity of respiratory distress syndrome, presence or absence of pneumothorax, and age at discharge. Possible significant relations between these variables and abnormal results on pulmonary-function tests were assessed by simple and multiple regression analysis.
Results
There was no significant difference between the birth weights and gestational ages of the subjects with bronchopulmonary dysplasia and those of the matched cohort controls who had not had bronchopulmonary dysplasia (Table 1Table 1
Characteristics of the Study Population.*). The three groups did not differ in current age. There were more males among the subjects with bronchopulmonary dysplasia and the matched cohort controls than among the normal controls. Correcting the study results for this sex difference had no effect on the statistical analyses of the results but did narrow the difference between the means in some instances.Clinical Findings
Six subjects in the bronchopulmonary-dysplasia group had current respiratory symptoms, but only four of the subjects with symptoms had moderate or severe pulmonary-function abnormalities. According to the history, the subjects with bronchopulmonary dysplasia had had more wheezing, episodes of pneumonia, limitation of exercise capacity, and long-term medication use than the matched cohort controls or the normal controls (P = 0.047 to 0.0001). Physical examination of the chest showed that the subjects with bronchopulmonary dysplasia more often had pectus excavatum (P = 0.041), overexpansion (P = 0.012), and wheezing (P = 0.041) than the normal controls, but there was no difference between the bronchopulmonary-dysplasia group and the matched cohort controls.
There were no significant differences among the three groups with regard to family history of allergy, bronchitis or asthma in the mother or father, or frequency of attacks of hay fever. The prevalence of atopy was not significantly different in the three groups.
Only one subject in the bronchopulmonary-dysplasia group had evidence of right ventricular hypertrophy on the electrocardiogram. Echocardiography with Doppler ultrasound showed no abnormalities in the bronchopulmonary-dysplasia group other than mitral-valve prolapse in one subject. None of the subjects with bronchopulmonary dysplasia had hypertension.
The chest x-ray score (see Methods) was significantly higher (P<0.002) in the bronchopulmonary-dysplasia group (mean [±SE], 2.2±0.4) than in either the matched cohort control group (0.7±0.2) or the normal control group (0.6±0.1). The changes seen on the chest radiograph consisted of mild hyperexpansion, blebs, interstitial thickening, peribronchial cuffing, and pleural thickening. These radiologic changes, when present, were generally subtle.
The subjects with bronchopulmonary dysplasia were significantly shorter and weighed less than the normal controls and the matched cohort controls (Fig. 1Figure 1
Mean Height and Weight Percentiles for the Subjects with Bronchopulmonary Dysplasia (BPD) in Infancy, the Matched Cohort Controls, and the Normal Controls.). According to the history, the subjects with bronchopulmonary dysplasia had an increased incidence of delayed progression into the next grade in school as compared with the two control groups (P<0.02). They had taken more special classes in school than the normal controls (P<0.0001), but there was no difference in participation in special classes between the subjects with bronchopulmonary dysplasia and the matched cohort controls. More subjects with bronchopulmonary dysplasia than control subjects had abnormalities of coordination, gait, and muscle tone (P<0.04). Five of the subjects with bronchopulmonary dysplasia had some degree of cerebral palsy, three had hearing loss and required hearing aids, and one had retrolental fibroplasia. None of the matched cohort controls had any of these problems.Results of Pulmonary-Function Tests
One of the 26 subjects with bronchopulmonary dysplasia could not be tested because she had cerebral palsy. Seventy-six percent (19 of 25) of the subjects in this group who were tested had pulmonary dysfunction, as defined by results on pulmonary-function tests that differed from the mean values in the normal control subjects by more than 2 SD, the presence of reactive airway disease, or both. The pulmonary-function abnormalities consisted of airway obstruction, airway hyperreactivity, and hyperinflation (Table 2Table 2
Results of Pulmonary-Function Tests in Subjects with Bronchopulmonary Dysplasia (BPD) in Infancy, Matched Cohort Controls, and Normal Controls.* and Fig. 2Figure 2
Reactive Airway Disease in the Subjects with Bronchopulmonary Dysplasia (BPD) in Infancy, the Matched Cohort Controls, and the Normal Controls.).Airway obstruction, present in 68 percent (17 of 25) of the subjects in the bronchopulmonary-dysplasia group, was manifested by statistically significant decreases in peak expiratory flow rate, forced vital capacity, FEV1, forced expiratory flow between 25 and 75 percent of vital capacity (FEF25–75), and maximal expiratory flow velocity at 50 percent of vital capacity (Vmax50), as compared with the matched cohort control group and the normal controls (Table 2). The subjects with bronchopulmonary dysplasia also had evidence of airway obstruction in the results of tests performed while they were breathing the mixture of 80 percent helium and 20 percent oxygen (Table 3Table 3
Results of Special Small-Airway Pulmonary-Function Tests in Subjects with Bronchopulmonary Dysplasia (BPD) in Infancy, Matched Cohort Controls, and Normal Controls.*). They had significantly smaller increases in the maximal expiratory flow velocity at 25 percent and 50 percent of vital capacity (ΔV̇max25 and ΔV̇max50) and an increase in the volume at isoflow, as compared with the normal controls. The differences in pulmonary-function indexes, with the exception of ΔV̇max50, were similar when the subjects with bronchopulmonary dysplasia were compared with the matched cohort controls. Tracheal stenosis was not apparent in any subject on examination, on radiography, or on inspection of flow—volume loops.Twenty-four percent (6 of 25) of the subjects with bronchopulmonary dysplasia had fixed airway obstruction, and 52 percent (13 of 25) had reactive airway disease, as indicated by their response to either methacholine or isoproterenol (Fig. 2). Two subjects with bronchopulmonary dysplasia had positive responses at cumulative doses of 5.4 mg and 2.9 mg of methacholine, respectively. Four subjects with bronchopulmonary dysplasia had increases of 10 to 15 percent in FEV1 after the administration of isoproterenol, three had increases of 15 to 20 percent, and four had increases of more than 20 percent.
Hyperinflation (an increased ratio of residual volume to total lung capacity in comparison with the ratio for controls) was more frequent in the subjects with bronchopulmonary dysplasia, although there was no difference among the three groups in total lung capacity (Table 2). The DLCO was slightly lower in the subjects with bronchopulmonary dysplasia than in the normal controls.
Pulmonary-function testing with the body plethysmograph became available after the start of the study. The mean value for airway resistance was higher (P<0.0006) and the specific conductance of the airways was significantly lower in the subjects with bronchopulmonary dysplasia than in the matched cohort controls or the normal controls (Table 4Table 4
Results of Pulmonary-Function Tests with the Body Plethysmograph in Subjects with Bronchopulmonary Dysplasia (BPD) in Infancy, Matched Cohort Controls, and Normal Controls.*). The values for total lung capacity determined by plethysmography and by the nitrogen-washout technique were closely correlated (r = 0.92).Most abnormalities in pulmonary function in the subjects with bronchopulmonary dysplasia were mild to moderate (Table 5Table 5
Severity of Pulmonary Dysfunction in Subjects with Bronchopulmonary Dysplasia in Infancy.*). Six of the 25 subjects with bronchopulmonary dysplasia who had pulmonary-function tests had one or more abnormalities that could be considered severe.The number of current cigarette smokers (those who had smoked cigarettes during the month before the examination) was not significantly different in the bronchopulmonary-dysplasia group (n = 3) and the matched cohort control group (n = 6). Omitting cigarette smokers from the comparisons of the results of pulmonary-function tests in the three groups had no effect on statistical significance, except for the results of three tests in the bronchopulmonary-dysplasia and matched cohort control groups (functional residual capacity, from P = 0.08 to P = 0.07 [Table 2]; ΔV̇max25, from P = 0.01 to P = 0.1; the volume at isoflow (Visov), from P = 0.05 to P = 0.24 [Table 3]). On the basis of the history, passive smoking (exposure to environmental tobacco smoke) was more prevalent in both the bronchopulmonary-dysplasia group (P = 0.03) and matched cohort control group (P = 0.003) than in the normal control group, but the extent of this exposure could not be quantified.
We attempted to correlate the neonatal variables with the degree of current pulmonary dysfunction in the subjects who had bronchopulmonary dysplasia in infancy. Using simple and multiple regression analysis, we found a positive association between the ratio of residual volume to total lung capacity and both the duration of postnatal endotracheal intubation (F = 5.22, P = 0.03) and the duration of intermittent positive-pressure breathing (F = 11.59, P = 0.0024), and between the functional residual capacity and both the duration of postnatal intermittent positive-pressure breathing (F = 9.33, P = 0.0056) and exposure to oxygen levels above 80 percent (F = 9.78, P = 0.0047). Given the limited number of subjects and the number of analyses performed, these relations must be regarded as only suggestive. No significant correlations were found between the postnatal variables and the current measures of airway flow rates.
Discussion
We found that most adolescents and young adults with a history of bronchopulmonary dysplasia in infancy had pulmonary dysfunction, consisting of airway obstruction, airway hyperreactivity, and hyper-inflation. The pulmonary dysfunction was usually asymptomatic and not physiologically severe, although we did not assess exercise tolerance. Previous studies have demonstrated airway obstruction, airway hyperreactivity, hyperinflation, and abnormal blood gas values in 6-to-12-year-old children with a history of bronchopulmonary dysplasia.16 17 18 19 Thirteen of the 63 children in these earlier studies also had abnormalities in pulmonary function documented during the first year of life.
Although we found significant correlations between some neonatal variables and hyperinflation, we found none between current measures of reduced airflow and neonatal variables. Bader et al.18 found significant correlations between both gestational age and the duration of mechanical ventilation and FEV1 and FEF25–75 in a study of 10 children with a history of bronchopulmonary dysplasia. Andreasson et al.19 found a correlation between the duration of mechanical ventilation and FEV1 in 11 children with a history of bronchopulmonary dysplasia and 29 without such a history, all of whom had received mechanical ventilation during the neonatal period. The presence of pulmonary dysfunction in infants, children, and young adults with bronchopulmonary dysplasia in infancy, the persistence of this dysfunction from the first year of life to the age of 10 years in some children with a history of bronchopulmonary dysplasia, and the correlations between late pulmonary dysfunction and neonatal variables, though limited, suggest that lung injury resulting from bronchopulmonary dysplasia in infancy has a role in the pathogenesis of later pulmonary dysfunction.
In our study, tests of airway function demonstrated a significant reduction in flow and increase in resistance in the subjects with bronchopulmonary dysplasia (Tables 2 through 4). The pathological features of the conducting airways in patients with bronchopulmonary dysplasia include marked squamous metaplasia of the bronchial and bronchiolar mucosa, peribronchial and bronchiolar fibrosis, obliterating fibroproliferative bronchiolitis, and prominent hypertrophy of peribronchiolar smooth muscle.1 , 37 These pathological changes in the airways occur in newborn animals with pulmonary oxygen toxicity, which also inhibits DNA synthesis in the lung.38 , 39 Reduction of alveolar growth has been demonstrated in a child who survived bronchopulmonary dysplasia in infancy but died at 33 months of age.40 Reduction of airway growth during the rapid postnatal phase of lung growth could contribute to a disproportionate undergrowth of the luminal diameter of the airways and result in a persistent increase in airway resistance.
Although more adolescents and young adults with a history of bronchopulmonary dysplasia than control subjects had hyperreactive airways in our study, this increase was not associated with a more frequent family history of asthma. Nickerson and Taussig41 reported a high incidence of asthma in first- and second-degree relatives of children with bronchopulmonary dysplasia, but other investigators found no correlation between bronchopulmonary dysplasia and a family history of asthma.16 , 18 , 19 Moreover, airway hyperreactivity was not related to an increased prevalence of atopy in our study. The increase in airway reactivity may instead have been due to prematurity,42 hypertrophy of smooth muscle in the small airways,1 , 37 or the late effects of infections in the lower respiratory tract in infancy and early childhood.43
The pulmonary dysfunction observed in the adolescents and young adults who had bronchopulmonary dysplasia in infancy may not reflect solely the effects of neonatal bronchopulmonary dysplasia. Other investigators have demonstrated that infants who recover from bronchopulmonary dysplasia are more susceptible to lower respiratory illnesses in childhood than normal infants.3 , 5 , 20 , 44 The hypothesis that lower respiratory illnesses in early childhood may be related to chronic airflow obstruction in adulthood has been reviewed by Samet et al.45 The common feature of the respiratory illnesses during the first two years of life that was most strongly associated with the subsequent development of chronic airflow obstruction was injury to the small airways. Viral respiratory illnesses, such as respiratory syncytial virus infection, could exaggerate the increase in small-airway resistance in infants with bronchopulmonary dysplasia and contribute to its persistence.44
We found no correlation between the chest x-ray score and abnormalities identified in the physical examination, respiratory symptoms, or pulmonary function. Although the chest radiograph tends to be abnormal in young people with a history of bronchopulmonary dysplasia, it is not useful in identifying an adult as having had bronchopulmonary dysplasia, since the findings are subtle and not always present.
Infants with bronchopulmonary dysplasia may have substantial retardation of growth and development.4 , 20 , 46 , 47 We found significant differences in both height and weight between the subjects with bronchopulmonary dysplasia and the normal controls, although the mean values for height and weight were at the 37th and 42nd percentiles, respectively — that is, they were not severely reduced. The relation of reduced height and weight in the adolescents and young adults with bronchopulmonary dysplasia in infancy to the late pulmonary dysfunction is not clear.
Our results indicate that pulmonary dysfunction is common in adolescents and young adults with a history of bronchopulmonary dysplasia. Although most such persons are leading normal lives, the measurable pulmonary dysfunction in this group causes concern about their susceptibility to progressive obstructive pulmonary disease as older adults. Cigarette smoking by young adults with a history of bronchopulmonary dysplasia should be strongly discouraged. It seems likely that infants born since 1973 in whom bronchopulmonary dysplasia developed also have persistent pulmonary dysfunction. Such infants, who were generally smaller at birth and more premature than our study subjects, may be even more susceptible to pulmonary oxygen toxicity, barotrauma, and lower respiratory infection.
Supported by a grant (HL36796) from the National Heart, Lung, and Blood Institute.
We are indebted to Ms. Roslyn Bienenstock, Jerry Halpern, Ph.D., Ms. Kusum Kumar, Norman Lewiston, M.D., Ms. Natalie Malachowski, Judy Palmer, M.D., Mr. Terrence Tye, and John Van Wye, M.D., for their help with the study, and especially to David Edward, M.D., for his help with the data from the neonatal period.
Source Information
From the Departments of Diagnostic Radiology and Nuclear Medicine (W.H.N., B.R.P., R.L.L.), Pediatrics (R.B.M., P.T.P.), Medicine (R.L.P.), and Health Research and Policy (B.W.B.), Stanford University Medical Center, and the Children's Hospital at Stanford (K.B.C., I.E.), Stanford, Calif. Address reprint requests to Dr. Northway at the Department of Diagnostic Radiology and Nuclear Medicine, Stanford University Medical Center, Stanford, CA 94305.
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