Solitary pulmonary nodules (SPNs) are defined as focal, round, or oval areas of increased opacity in the lung with diameters of ≤3 cm [1] (Fig. 1.1). The lesion is not associated with pneumonia, atelectasis, or lymphadenopathy.

Particularly when the nodule is less than 10 mm in diameter, it may be called small nodule (Fig. 1.2). With its diameter less than 3 mm, it may be called micronodule [2].

The most common cause is malignant tumor including lung cancer (Fig. 1.3), carcinoid (Fig. 1.4), bronchus–associated lymphoid tissue (BALT) lymphoma (Fig. 1.5), and a solitary metastasis to the lung. Benign tumors are granuloma (Fig. 1.6), hamartoma (Fig. 1.7), sclerosing hemangiomas (Fig. 1.8), inflammatory myofibroblastic tumor (IMT, inflammatory pseudotumor) (Fig. 1.9), rheumatoid nodule (Fig. 1.2), parasitic infection (Paragonimus westermani), and nodule in antineutrophil cytoplasmic antibody (ANCA)-associated granulomatous vasculitis (former Wegener’s granulomatosis) (Fig. 1.10) (Table 1.1).

Likelihood ratio for malignancy in upper and middle lobe nodule is 1.22 as compared with 0.66 in lower lobe nodule [3].

The hierarchy of radiologic and clinical likelihood ratios for malignancy includes, in decreasing rank, a cavity of 16 mm in thickness, irregular or speculated margin on CT scans, patient complaints of hemoptysis, a patient history of malignancy, patient age >70 years, nodule size of 21–30 mm in diameter, nodule growth rate of 7–464 days, an ill-defined nodule on chest radiographs, a currently smoking patient, and nodules with indeterminate calcification on CT scans [3].

Adenocarcinoma is the most common histologic type of lung cancer in many countries. Adenocarcinoma is a malignant epithelial tumor with glandular differentiation or mucin production, showing lepidic, acinar, papillary, solid, and micropapillary pattern or a mixture of these patterns [11] (Figs. 1.1 and 1.3).

Patients with lung cancer presenting with an SPN are usually asymptomatic. Physical examination shows no specific abnormality. In most cases, the SPN is detected by routine chest imaging.

The characteristic CT finding of solid adenocarcinoma consists of a solitary nodule or mass with a lobulated or spiculated margin. On multivariate analysis, lobulated or spiculated margin and the absence of a satellite nodule appear to be independently associated with malignant nodule with high odd ratio [7]. The nodules enhance following intravenous administration of contrast medium. The enhancement of >25 HU plus morphologic malignant features on dynamic CT appears to be the most efficient method for characterizing a malignant SPN [9].

The histopathologic correlation of spiculated margin is variable and may correspond to the strands of fibrous tissue that extend from the tumor margin into the lung, to the direct infiltration of tumor into the adjacent parenchyma, to the small foci of parenchymal collapse as a result of bronchiolar obstruction by the expanding tumor, or to the spread of tumor cells into the lymphatic channels and interstitial tissue of adjacent vessels, airways, or the interlobular septa [12]. The enhancement of nodules presumably reflects the vascular stroma of the tumor [13].

In solitary adenocarcinomas with part-solid and solid nodule, the prognosis depends on nodal and distant metastasis. Solid tumors exhibit more malignant behavior and have a poorer prognosis than part-solid tumors [14].

Carcinoids are slow-growing neuroendocrine tumors characterized by their growth patterns (organoid, trabecular, insular, palisading, ribbon, rosette-like arrangements). They consist of typical carcinoids and atypical carcinoids according to mitotic count or presence of necrosis. Carcinoid is a distinct disease entity, discriminated from other pulmonary neuroendocrine tumors such as large cell neuroendocrine carcinoma or small cell carcinoma [15] (Fig. 1.4).

Typical carcinoid may be accompanied with hormone-related manifestations. Fewer than 5 % have the carcinoid syndrome (cutaneous flushing, bronchospasm, diarrhea). Cushing’s syndrome can also occur. Atypical carcinoid, one on the contrary, may cause lymph node and distant metastasis in half of the cases.

The most common imaging finding of carcinoid is a lung nodule or a mass. The CT features of a peripheral carcinoid presenting as SPN include a lobulated nodule of high attenuation on contrast-enhanced CT; nodule that densely enhances with IV contrast-medium administration; the presence of calcification (approximately 30 % of cases have calcification on CT) (Fig. 1.4); subsegmental airway involvement on thin-section analysis; and nodules associated with distal hyperlucency, bronchiectasis, or atelectasis [16]. Typical carcinoid tends to be smaller (average diameter 2 cm) than atypical carcinoid (average diameter 4 cm) [17]. Secondary effects on distal lung parenchyma such as distal hyperlucency are uncommon in atypical carcinoids.

The neoplastic cells of carcinoids are grouped in small nests or trabeculae separated by a prominent vascular stroma (Fig. 1.4). Because of their vascular stroma, most carcinoids show marked enhancement following intravenous administration of contrast [18]. Segmental or lobar atelectasis, obstructive pneumonitis, and segmental oligemia are related to complete or partial obstruction of airway.

Since typical carcinoids are extremely slow growing, the long-term prognosis is excellent if completely resected. However, all carcinoids are malignant although indolent. Nodal involvement clearly affects survival [19]. The 5-year survival of patients with atypical carcinoids is only 57 %.

Pulmonary marginal zone B-cell lymphoma of bronchus-associated lymphoid tissue (BALT) is an extranodal lymphoma, which is thought to arise in acquired MALT secondary to inflammatory or autoimmune processes. The neoplastic cells infiltrate the bronchiolar epithelium, forming lymphoepithelial lesion [20] (Fig. 1.5).

BALT lymphoma of SPN rarely causes pulmonary symptoms. Weight loss and night sweating may be found. Extrapulmonary symptoms and signs of connective tissue diseases such as Sjögren’s syndrome, systemic lupus erythematosus, and rheumatoid arthritis may occur.

Typical CT findings of BALT lymphoma include solitary (Fig. 1.5) or multifocal nodules or masses and areas of airspace consolidation with an air bronchogram [20, 21]. Less common findings include ground-glass opacity (GGO) lesion, interlobular septal thickening, centrilobular nodules, and bronchial wall thickening and pleural effusion.

CT findings of BALT lymphoma showing solitary or multifocal nodules or masses and areas of airspace consolidation are related to proliferation of tumor cells within the interstitium such that the alveolar airspaces and transitional airways are obliterated [22] (Fig. 1.5). Because the bronchi and membranous bronchioles tend to be unaffected, an air bronchogram is common. Interlobular septal thickening, centrilobular nodules, and bronchial wall thickening on CT images are related to perilymphatic interstitial infiltration of tumor cells.

BALT lymphoma shows the indolent clinical course. The estimated 5- and 10-year overall survival rates have been reported to be 90 and 72 %, respectively [23]. Age and performance status are the prognostic factors.

Tuberculoma is a parenchymal nodular histologic reaction which is primarily granulomatous and necrotizing with frequent cavitation. The granulomas may have palisading histiocytes, prominent epithelioid cells, or Langerhans-type giant cells. These necrotizing granulomas can progress to fibrosis and calcification [24] (Fig. 1.6).

In active tuberculoma, constitutional symptoms (fever, malaise, night sweating, weight loss, and anorexia) as well as respiratory symptoms (cough, blood-tinged sputum) occur infrequently. Most patients with inactive tuberculoma are asymptomatic.

Tuberculoma is seen as a sharply marginated round or oval lesion measuring 0.5–4.0 cm in diameter [10, 25]. However, fibrosis related to vessels, interlobular septa, or lung parenchyma adjacent to the nodule may result in a spiculated margin. Calcification within the nodule is present in 20–30 % of cases. Satellite nodules around the tuberculoma may present in as many as 80 % of cases [26]. Following intravenous administration of contrast medium, tuberculomas usually show no or little enhancement although sometimes show ringlike enhancement [27] (Fig. 1.6).

The central part of tuberculoma consists of caseous material and the periphery of epithelioid histiocytes and multinucleated giant cells and a variable amount of collagen. Ringlike enhancement corresponds histologically to the granulomatous inflammatory tissue capsule, whereas the non-enhancing area corresponds to the central necrotic material [27].

It has been reported that a majority of pulmonary tuberculomas show decrease in size with antituberculous treatment. Over 15 % did not show a decrease in size even after the medical treatment [28].

Hamartomas are benign neoplasms composed of varying proportions of mesenchymal tissues, such as cartilage, fat, smooth muscle, and connective tissue, typically combined with entrapped respiratory epithelium. Genetic studies indicate a neoplastic rather than hamartomatous origin [29] (Fig. 1.7).

Pulmonary hamartomas are usually asymptomatic and found incidentally when imaging the chest for other reasons. It can occasionally present with hemoptysis, bronchial obstruction, and cough (especially endobronchial types) [30].

The characteristic CT findings of hamartomas are comprised of a lesion of 2.5 cm or smaller in diameter, of a smooth margin, and of focal areas of fat (CT attenuation values between −40 and −120 HU) or calcification [8]. However, these findings are present in only 30–50 % of the tumors (Fig. 1.7). Recent MRI and dynamic CT studies demonstrate septal or cleft-like enhancements of pulmonary hamartomas [31, 32].

Hamartomas are composed of mature cartilage and fat, which are often surrounded by a thin layer of loose mesenchymal tissue. Recent MRI and dynamic CT studies demonstrated septal or cleft-like enhancement of pulmonary hamartomas [31, 32]. Pathologically, these structures were found to represent variable mesenchymal tissue components arrayed along respiratory epithelial cells lining the cleft and show richer vascularity than main cartilaginous portion of pulmonary hamartoma.

Surgical resection is curative. Recurrence or malignant transformation is rare.

Although sclerosing hemangiomas (SHs) were originally termed as a variant of hemangiomas, now there is a consensus that they are epithelial tumors. SH comprises a mixture of four histologic patterns, such as papillary, sclerotic, solid, and hemorrhagic [33] (Fig. 1.8).

Most patients are asymptomatic at the time of diagnosis.

On CT scans, SH appears as a well-defined, round- or oval-shaped, homogeneous mass with smooth margin in subpleural area [34]. On dynamic CT, it has strong and rapid enhancement [35] (Fig. 1.8). Unusual manifestations of SH include mediastinal mass, tumor with a cystic appearance, air trapping around the tumor, multiple tumors, or a tumor surrounded by multiple daughter nodules in the same lobe; it can also be accompanied by hilar lymph node metastasis [36–40].

On CT–pathology comparisons, dynamic characteristics of sclerosing hemangioma depend on the levels of hemangiomatous or papillary (early and strong enhancement) and solid or sclerotic (slow and persistent enhancement and little washout) components present [35] (Fig. 1.8).

Regardless of surgical resection, the prognosis of patients with sclerosing hemangioma is excellent in cases manifesting as SPN.