The hilum encompasses the root of the lung and consists of the major pulmonary vessels, bronchial walls, and lymph nodes. Hilar enlargement in children may be due to a general increase in hilar markings, usually reflecting peribronchial thickening such as occurs in viral lower respiratory tract infection, CF, and asthma. True hilar enlargement represents either hilar lymphadenopathy or hilar pulmonary arterial enlargement. Adenopathy is characterized by a lobulated outline to the hilum, often with filling in of the hilar point at the junction of the superior pulmonary vein with pulmonary artery. Arterial enlargement demonstrates retained vascular contours, often with a dilated main pulmonary artery. Distinction between arterial enlargement and adenopathy is best achieved with cross-sectional imaging.
In children, the lymph nodes will only be seen if they are enlarged and thus pathologic in size. For a detailed evaluation of the hilum, contrast-enhanced CT or MRI should be used.
Although the hilum can be visualized on the lateral film, it is not common practice to obtain routine lateral films in children; as radiation protection, this is essential (image gently).
Table 1.54 Bilateral hilar enlargement due to lymphadenopathy
Bronchiolitis, reactive airway disease (RAD), viral infections of the lower airways
Minimal interstitial prominence, peribronchial thickening, hyperinflation (especially in viral infections). The hilar lymph nodes are increased in size rather than density; the outline is hazy.
Episodes of coughing, possibly febrile, signs of infection.
Seasonal occurrence of RSV infections, mainly in autumn and winter.
Hila are dense, with prominent bronchovascular markings. In the exanthematous phase of measles pneumonia, the hila are widened and more dense, and lung markings are increased; miliary nodules are also present adjacent to the hila.
Nowadays rare as a result of vaccination programs.
The increased dense hilar markings and perihilar signs (“shaggy heart”) reflect bronchitis in the cartarrhal stage. Increased pulmonary density occurs mainly in the basal segments.
Diagnosed by the typical episodes of coughing in the convulsive stage, previously known as “catarrhal bronchitis.”
Densely enlarged hila, initially moderate and increasing over ensuing years. Increasing pulmonary involvement with chronic infilitrative changes. Secondary hyperinflation and barrel chest deformity. Late findings resemble bronchiectasis.
Onset in infancy, increasing and progressing in childhood. All signs of chronic infection with dyspnea and cough.
Neoplastic mediastinal enlargement is mostly due to bilateral lymph node enlargement, particularly the paratracheal nodes.
Diagnosed on bone marrow biopsy. Hematologic changes. Peripheral lymphadenopathy, hepatosplenomegaly. Bruises. Hilar involvement in Hodgkin disease in 50%, more common than in NHL.
Hilar enlargement accompanied by segmental pneumonia, particularly in the lower lobes (may even be unilateral). Radiographic appearance commonly resembles TB.
Mild leucocytosis or normal white cell count. Organism must be positively proven. Bronchoalveolar lavage.
LCH, malignant histiocytosis
Mild, rarely marked hilar enlargement with sharp outlines. Evolves into interstitial pulmonary changes with small patches and confluent densities mainly in the bases. Emphysematous blebs, honeycomb lungs.
Combination of bilateral hilar enlargement with multiple disseminated small patchy pulmonary densities.
May be unilateral. Perihilar and occasional mediastinal lymph node involvement. Caution: air-space disease.
Characteristically symmetric lobulated lymph nodes; no pulmonary changes in stage 1, later (stage 2) there are small patchy densities in the lungs. Other lymph nodes can also become involved (tracheobronchial, paratracheal).
This classic adult presentation is extremely rare in preteenaged children.
Vascular causes: increased hilar and pulmonary vascular markings—active: left-to-right shunt
Peribronchial thickening, increased pulmonary vascular markings. Effacement of the mediastinal contour at the level of the hilum, more commonly bilateral.
Fever, cough, wheezing.
TB (primary infection)
Nodular density leads to increasing hilar size. Primary complex in the lungs. Loss of the mediastinal contour. Usually right-sided. Often associated subcarinal ± paratracheal lymphadenopathy. May cause air t rapping or collapse (see Fig. 1.17c). Rim enhancement with low central density on CT. Calcification rare in primary infection. Primary focus may or may not be visible.
Small children to young school age. Gradual onset, with or without cough. Rarely febrile. PPD positive. May also be asymptomatic.
Other granulomatous infection
Bacterial, mycoplasma, and fungal pneumonias
Disease correlates with the radiographic appearance. Unilateral more common than bilateral.
Signs of acute infection, cough, moderate dyspnea.
Enlarged main pulmonary segment and apparent enlargement of proximal left pulmonary artery. Proximal right pulmonary artery dilatation concealed on frontal radiograph.
Pulmonary hypertension with absent contralateral pulmonary artery
Small, oligemic contralateral lung.
For example, in unilateral pulmonary hypoplasia.
Simulated Hilar Enlargement
Apparent hilar enlargement, and particularly an increase in hilar density without enlargement, may be due to superimposed densities on the frontal projection. This is usually clarified by a lateral projection or CT examination.
Table 1.58 Pitfalls with unilateral hilar enlargement or density
Segmental pneumonia in the superior segments of the lower lobes
Frontal view: projects over the hilar region.
Lateral view: posterior in position. Hilum unremarkable.
Signs of pneumonia.
Atelectasis of the RUL, one of the segments, or partial atelectasis of the middle lobe