Please pay attention to the state of the patient immunocompetence and if there was a preexisting cystic or cavitary lung disease in a previous CT. As a matter of fact, invasive aspergillosis should be suspected in any patient with neutropenia who develops a fever and presents the air crescent sign inside a consolidation or mass (Patient A). On the contrary, the air crescent sign of mycetoma, also referred to as the Monad sign, is seen in an immunocompetent host with preexisting cystic or cavitary lung disease, usually from tuberculosis or sarcoidosis (Patient B).

Air crescent sign is recognized as a crescent-shaped or circumferential area of radiolucency within a parenchymal consolidation or nodular opacity. This sign is often seen in two types of Aspergillus infection: angioinvasive and mycetoma.

Pathogenesis of air crescent sign in angioinvasive Aspergillus infection. It is caused by parenchymal cavitation, which typically occurs 2 weeks after the detection of the initial radiographic abnormality. The nodules are composed of infected hemorrhagic and infarcted lung tissue. As the neutrophil count recovers and the patient mounts an immune response, peripheral reabsorption of necrotic tissue causes the retraction of the infarcted center, and air fills the space in between. This creates an air crescent within the nodules and is a good prognostic finding because it marks the recovery phase of the infection. This sign is seen in approximately 50 % of patients. Angioinvasive Aspergillus infection is often fatal.

Pathogenesis of air crescent sign in mycetoma (aspergilloma). It is caused by the presence of a fungus ball inside a cavity separated from the wall of the cavity by an airspace of variable size. Air crescent sign in mycetoma, also referred to as the Monad sign, was first described in 1954 by Pesle and Monod. It is seen in an immunocompetent host with preexisting cystic or cavitary lung disease, usually from tuberculosis or sarcoidosis. The radiographic appearance is often that of a gravity-dependent mass within a preexisting cavity.

In our patient air trapping is not associated with bronchiectasis but with interstitial lung disease (nodules) displaying solid density and random distribution. The presence of random nodules rules out the diagnosis of sarcoidosis or hypersensitivity pneumonitis.

The coexistence of patchy areas of air trapping with solid random nodules supports the diagnosis of constrictive bronchiolitis in diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH).

DIPNECH, when associated with bronchiolar fibrosis, is also known as Aguayo–Miller syndrome after the name of the authors who first published a clinical series of six cases in 1992. The majority of patients presenting with DIPNECH are middle-aged females with symptoms of cough and dyspnea, obstructive abnormalities on pulmonary function testing, and radiographic imaging showing pulmonary nodules, air trapping, and mild bronchiectases. In general, the clinical course remains stable; however, progression to respiratory failure does occur. Long-term follow-up and treatment remain unclear. Transbronchial biopsy in search of a specific etiology is often a first step. If this remains negative, then a video-assisted thoracoscopic surgical biopsy may be necessary. Please also refer to DIPNECH in the Dark Lung Diseases chapter.

Please note that the consolidation presents a mass-like aspect without bronchogram sign. The vessels inside the lesion (angiogram sign) appear thinned and stretched. This feature suggests the presence of material that occupies the alveoli with mass effect.

In our case the mass-like consolidation with angiogram sign is associated with a nodule. These imaging features are nonspecific and may resemble a variety of benign and malignant chest disorders including adenocarcinoma. However, the diagnosis of pulmonary MALT lymphoma should be considered in patient with the imaging features described above and with a history of autoimmune disorder.

Lymphangitic carcinomatosis (LC)

Small and dense nodules beaded some septa (see above, left) but also the subpleural space with the so-called perilymphatic distribution (“avid of pleura”). This pattern is most typical of sarcoidosis, lymphangitic spread of carcinoma or other neoplasms, and lymphoproliferative disease.

Note that a grouping of small subpleural nodules adjacent to the costal margins coexists. They are due to agglomerates of nodules and arranged linearly along the pleural surfaces, thus mimicking focal thickening (pseudoplaques ➨). Pseudoplaques are thought to be most commonly seen in association with granulomatous disease and in particular with sarcoidosis.

The distribution of the enlarged lymph nodes is a key sign for diagnosis of some diseases. Bilateral hilar lymph node enlargement may be a feature of infection (particularly fungal or mycobacterial infection) or malignancy (e.g., lymphoma), but sarcoidosis is the most common cause of bilateral lymph node enlargement.

Calcifications are often present in chronic sarcoidosis.

In our case the beaded septum sign, together with perilymphatic micronodules, pseudoplaques, and the symmetric lymphadenopathy with punctate calcifications are highly suggestive of sarcoidosis.

The presence of hyperlucencies within a consolidation or within a subsolid nodule should not always be considered as a synonym of necrosis or cavitation. Small, rounded, or oval hyperlucencies, similar to bubbles (bubble-like lucencies), may be the expression of ectatic bronchioles (); in this last case, therefore, they are pseudocavitations.

The association between persistent opacities (“non-resolving pneumonia”) with bubble-like hyperlucencies and extended halo sign () is suggestive of primary pulmonary adenocarcinoma, more frequently of the mucinous type.

Infectious disease (mainly, secondary tuberculosis), pulmonary infarction, organizing pneumonia (OP), and BALT lymphoma are other possible etiologies, more rarely encountered.

Diffuse parenchymal opacification, either with GGO or consolidations, constitute the alveolar pattern, which encompasses a wide range of diagnostic hypotheses. Consequently, it is very useful to consider the “time” factor: distinguishing acute from chronic opacification is very helpful in reducing the differential diagnoses (please see the tables at the end of Alveolar Pattern).

The presence of Bat’s wing or butterfly pulmonary opacities without pleural effusion, and of other signs of pulmonary venous hypertension, makes the hypothesis of hydrostatic pulmonary edema unlikely.