Biomedical subjects
Publications and source records attributed to K S Oh.
There are many intrinsic and extrinsic, and congenital or acquired lesions that cause aeration disturbances in infants and children. The radiographic diagnosis of these entities and the pathophysiologic mechanisms by which they produce overinflation or underinflation are discussed. Longstanding airway compression may have serious effects on the developing lung and its vascular supply.
Recent technical advancements allow us to better evaluate the diaphragm and juxtadiaphragmatic lesions. Plain radiographs demonstrate morphology of the diaphragm in most cases. Function of the diaphragm can easily be evaluated by ultrasonography and fluoroscopy. Ultrasonography can be performed at bedside and should be used before fluoroscopy in infants and children. Ultrasonography can also demonstrate congenital anomalies of the diaphragm in utero. CT clearly discloses the underlying pathology and the extent of most juxtadiaphragmatic lesions. The newest modality, MRI, is quite promising and may become the procedure of choice for evaluation of diaphragmatic as well as juxtadiaphragmatic lesions in the very near future.
Abnormal size and/or number of the pulmonary and bronchial vessels and lymphatics may mimic pulmonary parenchymal lesions (pseudofibrosis). Abnormalities of the central pulmonary artery, pulmonary vein, thoracic aorta, and brachiocephalic branches may mimic intrathoracic mass lesions (pseudomass lesions). Radiologists should interpret these radiographic findings in the light of other accompanying radiographic findings and the clinical presentation.
"What is growth anyway? Can one talk about positive growth in childhood, neutral growth in maturity, and negative growth in old age?" Our goal is to help promote normal positive growth in infants and children. To achieve this, we must be cognizant of the morphologic changes of both normal and abnormal bone formation as they are reflected in the radiographic image of the skeleton. The knowledge of the various causes and the pathophysiologic mechanisms of the disturbances of bone growth and development allows us to recognize the early radiographic manifestations. Endocrine and metabolic disorders affect the whole skeleton, but the early changes are best seen in the distal ends of the femurs, where growth rate is most rapid. In skeletal infections and in some vascular injuries two-or three-phase bone scintigraphy supercedes radiography early in the course of the disease. MRI has proved to be very helpful in the early detection of avascular bone necrosis, osteomyelitis, and tumor. Some benign bone tumors and many bone dysplasias have distinct and diagnostic radiographic findings that may preclude further studies. In constitutional diseases of bone, including chromosomal aberrations, skeletal surveys of the patient and all family members together with biochemical and cytogenetic studies are essential for both diagnosis and genetic counseling. Our role is to perform the least invasive and most informative diagnostic imaging modalities that corroborate the biochemical and histologic findings to establish the definitive diagnosis. Unrecognized, misdiagnosed, or improperly treated disturbance of bone growth can result in permanent deformity usually associated with disability.
Of 270 children with Legg-Calvé-Perthes (LCP) disease, roentgenographic evidence of chondrolysis was noted in 12 (4.5%) within one year after diagnosis and appropriate management. Only in six hips of these 12 patients did the retrospective clinical, histological, and orthopedic findings fulfill the diagnostic requirements for chondrolysis. Sequential roentgenographic findings included initial periarticular osteoporosis and subchondral cortical irregularities, subsequent narrowing of the joint space, premature fusion of the growth plate, and eventual development of degenerative arthritis. The early roentgenographic recognition of chondrolysis is emphasized because it has an untoward effect on the prognosis of LCP and should therefore prompt a different orthopedic approach.
Blunt and penetrating chest trauma in children results from many causes but the major cause is motor vehicle accidents. The trauma induces a variety of injuries to the bony thorax, the pulmonary parenchyma, and mediastinal structures. In recent years, a disturbing increase in iatrogenic chest trauma has occurred in patients, particularly small infants, receiving intensive hospital care. Radiologic evaluation plays an important role in documenting and diagnosing these traumatic and iatrogenic injuries. The various radiologic manifestations of these injuries are described and discussed.
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Retrocardiac pneumomediastinum was encountered in two premature infants; one had a tracheal perforation and one an esophageal perforation. Contrast studies showed communication between the sites of perforation and the retrocardiac air. Clinical signs suggestive of such perforation include abnormal course of tubes on plain chest films and bloody aspirates.
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Ten full-term newborn infants with transient myocardial ischemia developed radiographic evidence of cardiomegaly and pulmonary venous congestion within the first few hours of life. In five patients, radiographic findings returned to normal during the first week of life. In the remaining five patients, radiographic findings improved within the second week and eventually became normal. Echocardiography done on six patients demonstrated left ventricular dysfunction in all six patients. Those infants with documented perinatal insults tend to have a protracted clinical course with eventual recovery. Pathophysiology and clinical course are discussed.
Clinical and radiographic observations in 34 infants and children with congenital stenosis of the oesophagus are reported. (1) Congenital stenosis of the oesophagus occurs more frequently than the previous literature suggests. (2) A congenital stenosis most commonly affects the lower oesophagus at the junction of its middle and distal thirds. (3) High oesophageal stenosis is less common, usually producing respiratory distress. Low oesophageal stenosis is more frequent, usually producing vomiting and oesophageal obstruction at the time the patients begin eating solid foods. (4) Oesophageal stenosis persists into adult life although its clinical course is benign. (5) An infant who vomits undigested food should have an oesophagram for evaluation of possible congenital oesophageal stenosis. (6) A child who impacts a foreign body in the oesophagus, particularly in the distal half of the oesophagus, should have a follow-up oesophagram after removal of the foreign body to assess the possibility of congenital oesophageal stenosis.
Expectoration of large, branching, bronchial casts, termed plastic bronchitis, is an uncommon condition in children. Asthma or allergy often is the cause of cast production, but in some instances no etiology is found. Five children produced large, obstructing bronchial casts that either were expectorated or were extracted at bronchoscopy. Four of the children had asthma or allergies and the fifth had congenital tricuspid atresia and chronic pericardial and pleural effusions. In two patients, expectorated casts initially were thought to be aspirated food material. Radiographic findings during periods of cast formation included atelectasis, obstructive emphysema, bronchiectasis, pleural effusion, and pneumomediastinum. Cast formation may be self-limited but generally ceases with appropriate treatment of the causative disorder. Bronchoscopic extraction of casts may benefit some patients.
Four new cases of calcified mediastinal lymph nodes in Hodgkin's Disease in children are reported. Calcifications appeared 13 months to 3 years 11 months following radiotherapy. One of the four cases continued to show a widened mediastinum despite remission. It is still to be determined if the presence of calcified mediastinal nodes in Hodgkin's disease represents a favourable prognostic sign.
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Spontaneous pneumothorax as the initial manifestation of cystic adenomatoid malformation of the lung is rare. Only four cases have been reported in the English literature. We add one more case, and review the clinical and roentgenographic findings. All the patients presented later in infancy or childhood and the cyst type appear to belong to Madewell's dominant cyst type.
Clinical and radiological findings of hepatogenic pulmonary angiodysplasia are reported in two cases. Myriad spidery pulmonary blood vessels are seen on plain radiographs and verified with right to left intrapulmonary shunting on pulmonary angiogram and pulmonary isotopic perfusion scan. Pathophysiology and differential diagnosis are discussed. We propose that the term "pulmonary angio-dysplasia" should include: 1) Pulmonary telangiectasia 2) Hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber syndrome) 3) Classical discrete pulmonary arteriovenous fistula 4) Hepatogenic pulmonary angiodysplasia: pulmonary arteriovenous communications with right to left shunting secondary to hepatic cirrhosis.
Three patients with late-onset Bochdalek's hernia are presented. All three had obstruction of the herniated bowel and, in two patients, this was complicated by strangulation and necrosis. The spectrum of roentgenographic manifestation included obvious findings of bowel in the chest in one patient; in another, the findings simulated pneumonia associated with reflex bowel ileus in the abdomen. The third patient had a massive pleural effusion, with what appeared to be associated bowel ileus. In spite of the misleading presentation it is imperative that the correct diagnosis be made early since the incidence of strangulation and severe morbidity is high.
Two sequential nasopharyngeal radiographs (the initial image with the mouth open and the second image with the mouth closed) of 100 randomly selected patients were obtained. Based on this series and a fluoroscopic study of two adult volunteers, the authors conclude that optimal visualization of the nasopharyngeal airway is achieved when the film is exposed during the latter phase of inspiration with the patient's mouth closed.