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1.
Pediatr Pulmonol ; 29(5): 341-50, 2000 May.
Article in English | MEDLINE | ID: mdl-10790245

ABSTRACT

We performed a prospective observational study to define the clinical course and the prognostic factors of 31 patients with postinfectious bronchiolitis obliterans. All patients presented with an episode of acute bronchiolitis in the first 2 years of life, and respiratory symptoms and signs persisted since then. Other diseases which may cause chronic airflow obstruction were excluded. The patients were followed after their inclusion in the study and the clinical findings were recorded in a standardized questionnaire and form. Repeated chest radiographs and lung perfusion scans were obtained in all 31 patients and semiannual spirometry was performed in 8 older patients. Eight patients had lung biopsies. The clinical course varied in the 31 patients during a mean of 3.5 years of follow-up. The outcome of the patients included clinical remission (22.6%), persistence of respiratory symptoms and signs (67.7%), and death (9.7%). An older age at onset of illness and presence of atopy as suggested by an elevated serum IgE appeared to predispose to a poor prognosis.


Subject(s)
Bronchiolitis Obliterans/pathology , Bronchiolitis, Viral/complications , Acute Disease , Age of Onset , Atrophy , Female , Follow-Up Studies , Humans , Immunoglobulin E/analysis , Infant , Male , Prognosis , Prospective Studies
2.
J Pediatr ; 108(5 Pt 1): 756-9, 1986 May.
Article in English | MEDLINE | ID: mdl-3701524

ABSTRACT

Idiopathic persistent pulmonary hypertension of the newborn infant (PPHN) is characterized by intrauterine structural remodeling of the pulmonary arterial bed, consisting of precocious development of muscle in intraacinar arteries, proliferation of adventitial connective tissue, and sometimes medial hypertrophy of preacinar arteries. To evaluate whether gestational hypoxemia causes these changes, we studied pulmonary arterial structure in two groups of newborn rats: one control, the other exposed to hypoxemia produced by maternal hypoxia during the second half of gestation. Morphometric analysis of the pulmonary arterial bed was performed after barium injection into the pulmonary arteries and formol saline expansion of the air spaces. Birth weight was similar in each group. Hematocrit was elevated in the hypoxemia group (51% +/- 1.0% vs 46% +/- 0.8%, P less than 0.005). The structure of preacinar and intraacinar arteries was similar and normal in both groups. Chronic fetal hypoxemia in the rat does not produce the pulmonary arterial structural changes identified in fatal cases of PPHN in human infants.


Subject(s)
Hypoxia/pathology , Pulmonary Artery/pathology , Animals , Birth Weight , Female , Hematocrit , Humans , Hypertension, Pulmonary/etiology , Hypoxia/blood , Infant, Newborn , Male , Pregnancy , Pulmonary Artery/embryology , Pulmonary Veins/pathology , Rats , Rats, Inbred Strains
3.
J Pediatr ; 107(3): 457-64, 1985 Sep.
Article in English | MEDLINE | ID: mdl-4032138

ABSTRACT

Some infants with congenital diaphragmatic hernia who die after surgical correction have a transient postoperative period during which systemic oxygenation is adequate (honeymoon period), whereas others have persistent hypoxemia. Using morphometric techniques, we analyzed lung structure, especially the arterial bed, in seven infants who died within 1 week of surgical repair. Three infants comprised the honeymoon group, the PaO2 transiently being greater than 150 mm Hg in the descending aorta (FiO2 1.0); four infants comprised the no-honeymoon group and never had PaO2 greater than 85 mm Hg. All lungs were hypoplastic for age; with one exception, infants in the no-honeymoon group had smaller lungs. Arterial structure in the no-honeymoon group contributed to a greater reduction in pulmonary arterial cross-sectional area. Each infant in the no-honeymoon group had muscularization of intra-acinar arteries and failure of perinatal increase in compliance of small preacinar arteries, features not seen in the honeymoon group or in the normal newborn infant. In addition, compared with the honeymoon group, luminal area of preacinar and intra-acinar arteries in the no-honeymoon group was decreased by reduced external diameter or increased medial thickness. Clinical deterioration in the honeymoon group is based on a vasoconstrictive response of the hypoplastic vascular bed. Persistent hypoxemia in the no-honeymoon group is based on both severity of pulmonary hypoplasia and structural remodeling of the pulmonary arteries.


Subject(s)
Hernia, Diaphragmatic/surgery , Hypertension, Pulmonary/etiology , Lung/blood supply , Arteries/pathology , Female , Hernia, Diaphragmatic/physiopathology , Hernias, Diaphragmatic, Congenital , Humans , Hypertension, Pulmonary/pathology , Infant, Newborn , Lung/pathology , Lung Volume Measurements , Male , Organ Size , Postoperative Complications , Pulmonary Alveoli/blood supply , Pulmonary Alveoli/pathology , Time Factors
4.
J Pediatr ; 104(5): 758-62, 1984 May.
Article in English | MEDLINE | ID: mdl-6716223

ABSTRACT

Although not proved, it is generally accepted that pulmonary vasospasm is responsible for the persistent pulmonary hypertension frequently associated with meconium aspiration. We have studied the pulmonary vasculature in 11 consecutive infants with fatal meconium aspiration, applying morphometric techniques to pulmonary arteries distended with barium gelatin before fixation. In 10 of the 11 infants, persistent pulmonary hypertension was evident clinically, with right-to-left shunting through the foramen ovale or ductus arteriosus. In all but one, severe structural abnormal muscularization of the smallest intra-acinar arteries was present. These changes must have developed before birth. In only one infant was the structure of the intra-acinar precapillary arteries virtually normal, as would be expected if vasospasm alone had caused the hypertension. The persistent pulmonary hypertension associated with fatal meconium aspiration may be the result of a structurally abnormal pulmonary microcirculation.


Subject(s)
Meconium , Pneumonia, Aspiration/etiology , Vascular Diseases/etiology , Female , Humans , Hypertension, Pulmonary/etiology , Infant, Newborn , Lung/blood supply , Microcirculation/pathology , Pregnancy , Pulmonary Artery/pathology
5.
J Pediatr ; 98(6): 962-7, 1981 Jun.
Article in English | MEDLINE | ID: mdl-7229803

ABSTRACT

Six neonates of 35 to 42 weeks' gestation had findings of persistent pulmonary hypertension and died between one and 6 days of age despite intensive medical therapy. Each patient had pulmonary artery pressure near or above systemic level, with a right-to-left shunt via the foramen ovale and/or ductus arteriosus. At postmortem, morphometric analysis of the peripheral pulmonary vascular bed revealed extension of muscle into small arteries, which was severe in five of six patients; all alveolar duct and wall arteries (less than 30 micrometers external diameter), normally nonmuscular, were fully muscularized. In these five patients medial wall thickness of the normally muscular intra-acinar arteries was doubled; arterial size and number, however, were normal in all. This striking structural maldevelopment of the peripheral pulmonary arterial bed occurred or was initiated in utero and does not merely represent a failure of the fetal pattern to regress. We suggest that this particular group of patients remained refractory to all current modes of therapy because of these severe structural pulmonary vascular changes.


Subject(s)
Hypertension, Pulmonary/mortality , Infant, Newborn, Diseases/mortality , Humans , Hypertension, Pulmonary/pathology , Infant, Newborn , Infant, Newborn, Diseases/pathology
6.
J Pediatr ; 97(2): 282-7, 1980 Aug.
Article in English | MEDLINE | ID: mdl-7400899

ABSTRACT

We report the clinical, general postmortem, and pulmonary morphometric features of a unique case of pulmonary hypoplasia resulting from phrenic nerve agenesis and diaphragmatic amyoplasia. The lungs showed a marked reduction in the number of bronchial branches with relatively normal intra-acinar growth, indicating interference with lung development before the sixteenth week of gestation. The pulmonary abnormalities arose early in gestation, suggesting that normal diaphragmatic neuromuscular development is essential for maintaining thoracic volume and permitting lung growth even before the fetus is capable of regular respiratory movements. The infant also had remodeling of the pulmonary circulation, causing persistent pulmonary hypertension. This case clarifies the interrelationship of diaphragmatic innervation, thoracic volume, fetal respiration, and lung development.


Subject(s)
Abnormalities, Multiple , Diaphragm/abnormalities , Lung/abnormalities , Phrenic Nerve/abnormalities , Abnormalities, Multiple/pathology , Autopsy , Humans , Infant, Newborn , Lung/pathology , Male
7.
J Pediatr ; 95(5 Pt 2): 836-41, 1979 Nov.
Article in English | MEDLINE | ID: mdl-490260

ABSTRACT

The term bronchopulmonary dysplasia has much to commend it. It does not declare the etiology of this disease, which seems to be an advantage. Another advantage is that it presents the idea of disturbance of growth as well as scarring. The premature lung responds at birth somewhat differently from the mature lung, not just in respect to surfactant but from the point of view of the blood vessels' size and compliance. But treatment must also be considered. The administration of steroids to the mother in the antenatal period probably favors maturation in the fetus, rather than growth of size and cell multiplication, which will also influence the behavior of the lung postnatally. This is probably a critical feature to look for in clinical assessment and follow-up of these patients.


Subject(s)
Infant, Newborn, Diseases/pathology , Lung Diseases/pathology , Lung/pathology , Humans , Hyaline Membrane Disease/pathology , Infant, Newborn , Infant, Premature, Diseases/pathology
8.
J Pediatr ; 88(4 Pt 1): 614-20, 1976 Apr.
Article in English | MEDLINE | ID: mdl-1255323

ABSTRACT

Three infants died with pulmonary hypertension of unknown cause during the first three months of life. Their lungs were examined using quantitative morphologic techniques. In all three cases the intra-acinar pulmonary arteries were more muscular than normal, as shown both by an increase in thickness of the muscle coat in arteries which are normally muscular, and by extension of muscle into smaller and more peripheral intra-acinar arteries not normally muscular at this age. It is suggested that "persistent pulmonary hypertension" of the newborn infant is, in some infants, due to a structural abnormality of the pulmonary circulation which is present at birth.


Subject(s)
Infant, Newborn, Diseases/etiology , Pulmonary Artery/abnormalities , Blood Pressure , Carbon Dioxide/blood , Humans , Infant, Newborn , Muscle, Smooth/abnormalities , Oxygen/blood , Pulmonary Circulation
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