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Diagnostic Imaging in Children (Chest) (MAS– meconium aspiration syndrome,…
Diagnostic Imaging in Children (Chest)
Minimizing the radiation dose to children
exposure should be as low as reasonably achievable (ALARA)
Children are more sensitive to radiation than adults
Children have longer life expectancy, resulting in a higher opportunity for expressing radiation damage.
Compared with a 40-year old, the same radiation dose given to a neonate is several times more likely to produce a cancer over the child's lifetime
Focus Film Distance FFD at least 1m
Protect gonads by using thick lead rubber sheet
Needs for using fluoroscopy are limited
Consider other modalities such as US or MRI, that do not use X ray.
MR or CT imaging needs sedation that may last from few to 20 minutes
Interpreting a chest x-ray in the neonate
symmetry of the patient positioning
inspiratory film or expiratory film
examine the entire film, and not just the chest
appearance of lungs, heart , thymus and bones, abdomen - bowel gas pattern
positioning of the endotracheal tube (ETT), nasogastric tube (NGT), feeding tube (FT), umbilical arterial catheter (UAC), and umbilical venous catheter (UVC) tips
Normal Newborn Chest
has a trapezoid shape in AP films
On normal inspiration the hemidiaphragmas in an AP chest film are at the level of the sixth rib anteriorly and the eighth or ninth rib posteriorly.
Newborns’ lungs are more radiolucent than those of older children
heart is more spherical in shape compare to older children
cardiothoracic ratio of newborns has a wide range.
The upper limit is about 0,6 beyond which cardiomegaly should be considered.
The aorta and pulmonary arteries are difficult to identify because of the thymic shadow
The thymus is usually seen in newborns.
Sometimes the thymus has an inferior margin with an sharp angle which produces a sail sign.
If chest is rotated in films of patients with a sail sign, the thymus may appear shifted laterally, which may be incorrectly interpreted as upper lobe pneumonia
RDS – respiratory distress syndrome (hyaline membrane disease HMD)
incidence and severity of RDS are related to the infant gestational age
Infants born at 28-32 weeks' gestation are of high risk of developing RDS.
deficiency of surfactant leads to collapse of alveoli (during expiry) and producing hyaline membranes from proteins that penetrate into the alveoli
the increased use of antenatal steroids ( improving pulmonary maturity), early postnatal surfactant therapy ( replacing surfactant deficiency) , and gentler techniques of ventilation ( using lower pressure) minimize damage to the immature lungs.
the hyaline membrane formation is a consequence, not a cause, of this disease.
radiographic features
Low lungs volume
Air bronchograms
Fine, granular lung pattern usually symmetrical
Ground glass appearance
These features are progressive but may be altered by ventilation strategy or surfactant therapy.
Mild disease is seen as a diffuse, linear, granular pattern which is usually uniform.
Moderate disease shows „ground glass” appearance of peripheral air bronchograms with cardiac border blurred
Severe disease-the lungs fields are completely opaque and indistinguishable from the cardiac shadow (white-out).
TTN - transient tachypnoea of the newborn, „wet lung”
results from delayed absorption of foetal lung fluid following delivery.
TNN commonly is observed following birth by caesarean delivery because infants do not receive the thoracic compression that accompanies vaginal delivery, in neonates of mothers suffering from diabetes, also in very small preterm infants
Abnormalities resolve within the first 72 hours of life in cases of TTN.
radiographic features
Plane chest x-ray is the diagnostic standard for TTN.
features are:
prominent perihilar streaking, which correlates with the overloading of the lymphatic system with retained lung fluid
fluid in the fissures.
Patchy infiltrates may be visible
A follow-up CXR may be necessary if the clinical history suggests meconium aspiration syndrome or neonatal pneumonia. In these cases, the CXR shows persistent infiltrates
Supine chest radiograph of a newborn demonstrating mild cardiomegaly and bilateral reticulonodular densities that radiate from the hila. There is atelectasis in the upper lobes.
Supine chest radiograph in the same patient taken one day later showing interval clearance of the reticulonodular densities.
MAS– meconium aspiration syndrome
In utero meconium passage results from neural stimulation of a mature GI tract due to foetal hypoxia
As the fetus approaches term, the GI tract matures, and vagal stimulation from head or cord compression may cause peristalsis and relaxation of the rectal sphincter leading to meconium passage.
Meconium usually isn’t found in the amniotic fluid prior to 34 weeks' gestation
It affects term and post term infants
Meconium-stained amniotic fluid may be aspirated during labour and delivery
Meconium aspiration may lead to MAS with pulmonary effects as: airway obstruction (atelectasis), chemical pneumonitis and surfactant dysfunction
The radiographic findings of meconium aspiration syndrome vary with the severity of aspiration. They may be normal if the meconium is largely tracheal and has been removed. Mild cases may simply manifest overaeration with small streaks or patches. In more severe cases there are overaerated lungs with asymmetric, coarse, patchy infiltrates due to subsegmental atelectasis. Pneumothorax and pneumomediastinum may result from sudden attempts to clear bronchi of meconium
Airway obstruction may lead to foci of atelectasis, Complete obstruction of the airways by meconium results in atelectasis.
Partial obstruction (ball-valve effect) causes air trapping and hyperdistention of the alveoli- hyperinflation of the lung
The air that is trapped, hyperinflating the lung, may rupture into the pleura (pneumothorax), mediastinum (pneumomediastinum), pericardium (pneumopericardium) or may penetrate along vessels and bronchioli resulting in pulmonary interstitial emphysema
Chemical pneumonitis- enzymes, bile salts, and fats in meconium irritate the airways and parenchyma of lungs causing a diffuse pneumonia that may begin within a few hours after aspiration.
Surfactant dysfunction -several constituents of meconium, especially the free fatty acids (eg, palmitin, stearic, oleic) destroy surfactant resulting in diffuse atelectasis.
Although meconium is sterile, its presence in the air passages can predispose the infant to pulmonary infection.
Enzymes, bile salts, and fats in meconium irritate the airways and parenchyma of lungs causing a diffuse pneumonia that may begin within a few hours after aspiration.
radiographic features
Bilateral, coarse patchy infiltrations
The radiographic findings of meconium aspiration syndrome vary with the severity of aspiration. They may be normal if the meconium is largely tracheal and has been removed. Mild cases may simply manifest overaeration with small streaks or patches. In more severe cases there are overaerated lungs with asymmetric, coarse, patchy infiltrates due to subsegmental atelectasis. Pneumothorax and pneumomediastinum may result from sudden attempts to clear bronchi of meconium
bronchopulmonary dysplasia
Chronic pulmonary disease
Complication due to oxygen therapy (hyperoxia) in neonates receiving mechanical ventilation
Hyperinflation is present, with multiple fine, lacy densities spreading to the periphery and with areas of lucency similar to bullae of the lung.
Clinical Presentation: Premature infant who had severe lung disease (usually hyaline membrane disease) and was treated with ventilatory and oxygen therapy.
Etiology/Pathophysiology: BPD is an end stage lung disease due primarily to oxygen toxicity from chronic ventilatory support. Other contributing factors include the effects of intermittent positive pressure ventilation, patent ductus arteriosus, and problems with pulmonary toilet. It is most commonly seen as a sequelae to hyaline membrane disease, but can also be seen as a sequelae to meconium aspiration, persistent fetal circulation, and congenital heart disease.
Pathology: Initially generalized capillary leak and mucosal necrosis is seen. At 1-2 weeks exudative alveolar and airway necrosis is seen along with hyaline membrane formation, mucosal squamous metaplasia and interstitial edema. At 2-3 weeks overdistended alveoli and scarred lung is seen. At several months large lung cysts and progressive interstitial and alveolar septal fibrosis is seen.
Imaging Findings:As ventilation techniques change, the classic radiographic stages of BPD are rarely seen. Classically, over time, the imaging findings progress. Initially the typical "ground glass" pattern of hyaline membrane disease is seen. At 1-2 weeks complete opacification of the lungs ("white out") is seen. At 2-3 weeks multiple small cystic lucencies of relatively uniform size and distribution are seen giving the lung a bubbly appearance. By several months of age, lung volume is increased, and the small cystic lucencies have coalesced into larger ones surrounded by fibrotic stranding. In most survivors, clinical and radiologic signs of BPD clear within 2-3 years.
Congenital pneumonia
Neonates are born with or show symptoms after delivery
Diffuse alveolar or interstitial disease that is usually asymmetric and localized also may be diffuse
Foci of atelectasis may occur
Group B streptococcal pneumonia can appear similar to HMD.
Pneumatoceles (air-filled lung cysts) can occur with staphylococcal pneumonia.
Pleural effusions or empyema may occur with any bacterial pneumonia.
Clinical Presentation
Associated with premature rupture of the membranes (PROM) during labor. The disease may have an early onset with septicemia and fulminant progression to severe respiratory distress, shock and respiratory failure within 24 hours; or a late onset 1 to 12 weeks after birth with this more insidious onset frequently associated with meningitis. Neonatal pneumonia can closely mimic hyaline membrane disease clinically, and is the most frequent cause of septicemia in neonate.
Etiology/Pathophysiology
There are three ways for the baby to acquire a neonatal pneumonia. First is infection acquired prior to birth by an ascending route or transplacental route. Classically this is Group B Streptococcus in the mother's vagina which passes to the infant during birth, particularly in cases with prolonged rupture of membranes and prolonged labor. Other normal inhabitants of the birth canal - staph, strep, diphtheroids, anaerobes, E. coli and Listeria - are other pathogens that may cause neonatal pneumonia. Second is infection acquired by aspiration during delivery, with the pathogens remaining the same. Third is via infection acquired after birth.
Pathology: There is a less uniform distribution of hyaline membranes in collapsed alveoli than is seen in hyaline membrane disease. There are cocci in the alveolar membrane and in the interstitial inflammatory exudate.
Imaging Findings: Ascending infection may resemble hyaline membrane disease very closely, especially in smaller infants. Most commonly seen are extensive granular confluent infiltrates whose distribution is often less uniform than that of hyaline membrane disease
Chylothorax
Clinical Presentation: Respiratory distress. Fifty percent present in first 24 hours of life, and 70% present within one week of birth.
Ethiology/Pathophysiology: Chylothorax is the accumulation of lymphatic fluid in the pleural space. Abruptly elevated venous pressure during delivery can lead to thoracic duct rupture which leads to intrapleural accumulation of lymph fluid. Initially the fluid is serous, but turns chylous after milk feedings. This is the most frequent cause of a large pleural effusion in newborn. It is rarely bilateral, and is rarely associated with generalized lymphangiomatosis. It is diagnosed and usually managed successfully via thoracenteses
Imaging Findings: Usually unilateral and usually on right side (60%). It is difficult to find the exact site of lymph extravasation with contrast studies.
Air leak syndromes
Pneumopericardium. Air surrounds the heart,
Pneumomediastinum A hyperlucent rim of air is present lateral to the cardiac border and thymus. This rim may displace the thymus superiorly away from the cardiac silhouette (angel wing sign)
Pneumothorax. The lung is typically displaced away from the lateral chest wall by a radiolucent zone of air. The adjacent lung may be collapsed with larger pneumothoraces.The small pneumothorax may be very difficult to identify. There is only a subtle zone of air peripherally, a diffusely hyperlucent hemithorax, unusually sharply defined cardiothymic margins, or a combination of these.
Tension pneumothorax. The diaphragm on the affected side is depressed, the mediastinum is shifted to the contralateral hemithorax, and collapse of the ipsilateral lobes is evident
Pulmonary interstitial emphysema (PIE) Single or multiple circular radiolucencies with well-demarcated walls are seen in a localized or diffuse pattern. The volume of the involved portion of the lung is usually increased, often markedly so.
Generalized PIE: coarse, irregular air densities (dark areas) throughout the lung fields with bubbly appearance, oriented towards the hilum. The air density is unlike the „finer” air bronchogram and granularity of HMD
Air leak syndromes may be complications due to RDS, MAS and mechanical ventilation
Persistent Foetal Circulation (PFC)
Clinical Presentation: Profound progressive hypoxemia that is usually out of proportion to the radiographic evidence of pulmonary disease.
Ethiology/Pathophysiology: Persistent or recurrent pulmonary artery hypertension with right to left shunting through a patent foramen ovale and patent ductus arteriosus in a patient with pulmonary disease. Factors that increase pulmonary vascular resistance include acidosis, hypoglycaemia, hypothermia, and polycythemia.
Imaging Findings: The CXR may be normal or can show changes of the underlying lung disease such as hyaline membrane disease, meconium aspiration syndrome, etc. A slightly enlarged heart may be seen along with slightly decreased pulmonary vascularity.