Biomedical subjects
Publications and source records attributed to H M Chambers.
A case is reported of an extreme form of intrauterine pulmonary maldevelopment in a term infant characterized by almost total failure of development of terminal respiratory units with arrest of pulmonary growth early in the second trimester. This is believed to be only the second reported case of this condition.
Explore the source record for details and available documents.
Ventilator-related lung pathology in 83 very low birth weight infants was analyzed from autopsy material obtained over a 5-year period. A consistent evolving pattern of change appeared in all infants who died after 10 days or more of ventilation. This included the persistence of simple, evenly distributed terminal air spaces lined by undifferentiated cuboidal epithelium and separated by evenly widened septa with hypercellular fibrous stroma and increased amounts of subepithelial elastic tissue. Radial alveolar counts confirmed arrested development of terminal respiratory units. Changes in small airways were conspicuously absent, in contrast to the classical descriptions of bronchopulmonary dysplasia in larger infants. A high proportion of babies with evolving disease had severe acute pulmonary interstitial emphysema of relatively late onset with a lethal course suggesting increased susceptibility of immature mesenchyme to barotrauma. The distinct histologic pattern and clinical course leads to the conclusion that this is a parenchymal variant of bronchopulmonary dysplasia with the pathology restricted to the terminal respiratory unit.
The incidence of nephrocalcinosis in very low birthweight (less than 1500 g) premature infants was assessed by ultrasound scan and analysis of urine. Three of 36 infants had nephrocalcinosis. All had been receiving long term frusemide for bronchopulmonary dysplasia with simultaneous fluid restriction. Urinary investigations showed no consistent findings in babies with nephrocalcinosis.
Data of nuclear cardiology studies are acquired on a computer and transmitted by telephone from a community hospital to a computer at a teaching hospital for analysis. Interpretations of the studies are dictated into a RTAS radiology reporting system. The referring physician and transcriptionists from the sending hospital may hear the interpretations by calling into RTAS on the same day as the studies were performed.
Explore the source record for details and available documents.
In sick preterm neonates receiving intensive care a spectacular rise in monocyte count has frequently been observed in sequential full blood examinations. The etiology of this has not previously been investigated and this study examines clinical factors that may contribute to this finding. Thirty (5.1%) of the 587 neonates who required intensive care during the study period had significant monocytosis (absolute count greater than 1700/mm3). Their mean gestation was 29 weeks (range 26-32 weeks). Monocytic response occurred at an age of 5.5 +/- 3 (mean +/- S.D.) days with 20% occurring at birth, 57% in the first week and 23% in the second week of life and lasted for 19.8 +/- 16 days (mean +/- S.D.). Most reached peak levels within two weeks and these ranged between 2,170 and 7176 per mm3. Analysis of the clinical variables against 37 controls revealed lower mean birth weight and gestational age, and higher incidence of leukocytosis, multiple transfusions, albumin infusions and theophylline therapy in the study group in comparison to the controls (P less than 0.001). No significant difference was found in maternal risk factors (pre-eclampsia, diabetes and amnionitis), birth asphyxia, respiratory disease, parenteral nutrition, proven infection and antibiotic therapy. An unexpected association with maternal steroid therapy was demonstrated. It is speculated that monocytosis represents a physiological though immature response of the marrow of small premature infants to a variety of exogenous stimuli including drugs and foreign protein infusions.