Chapter 17
Solitary pulmonary nodule
Khalid M. Amer
1 | What is a solitary pulmonary nodule? |
• | A solitary pulmonary nodule (SPN) is a discrete radiological lesion less than 3cm in diameter, surrounded completely by normal lung parenchyma, in the absence of a pleural effusion, enlarged mediastinal lymph nodes or atelectasis. |
• | This excludes multinodular disease and lesions with smaller satellite nodules. |
• | By definition, an SPN is diagnosed on a chest X-ray (Figure 1) or computed tomography (CT) scan (Figure 2). |
• | It is an incidental finding in 0.09-0.2% of all chest X-rays (150,000 chest X-rays or CTs/per annum in the United States). |
2 | What is the aetiology of an SPN? |
| Benign conditions |
• | Congenital: |
a) | arteriovenous malformations (AVM), hereditary haemorrhagic telangiectasia (Osler-Weber-Rendu syndrome); |
b) | mucocoele within atretic bronchi. |
• | Acquired: |
a) | infection or abscess: |
i) | acute bacterial or viral infections; |
ii) | bronchiolitis obliterans organising pneumonia (BOOP); |
iii) | fungal, such as aspergillosis, histoplasmosis, coccidioidomycosis or actinomycosis; |
b) | inflammatory: |
i) | intrapulmonary enlarged lymph node or lymphoid tissue; |
c) | granulomatous: |
i) | Mycobacterium tuberculosis; |
ii) | histiocytoma (plasma cell granuloma or plasmacytoma) – which is the commonest benign cause in the USA; |
iii) | collagen vascular disease, such as rheumatoid nodules (Figure 3), granulomatosis with polyangiitis or systemic lupus erythematosus (SLE); |
iv) | autoimmune or idiopathic granulomas, such as sarcoidosis, amyloidosis and histiocytosis X; |
d) | pseudotumours – round atelectasis caused by enfolded lung rotating on a fixed point of pleural disease, chronic scarring or asbestos-related plaque (Blesovsky syndrome, Figure 4). The benign nodule usually gives no symptoms; |
ischaemic – lung infarction; | |
f) | developmental: |
i) | chondroid hamartoma (15%); |
ii) | sclerosing haemangioma; |
iii) | bronchogenic cyst; |
iv) | lung sequestration. |
| Malignant conditions (approximately 50% of all SPN are malignant) |
• | Primary lung carcinoma: |
a) | non-small cell carcinoma, such as adenocarcinoma, squamous cell carcinoma, adenosquamous carcinoma, large cell carcinoma (Figure 5) and primary pulmonary lymphoma; |
b) | small cell carcinoma; |
c) | carcinoid neuroendocrine pulmonary tumours. |
• | Secondary lesions, metastasising from the colon (commonest site, accounting for 30-40% of all metastatic SPN), kidney (Figure 6), breast, prostate, thyroid, endometrium, skin melanomas and long bone sarcomas. |
3 | What are the important features in the clinical history of a patient with an SPN? |
• | Symptom status – although an SPN is usually asymptomatic, any symptomatic SPN should be considered malignant until proven otherwise and should be investigated further. |
• | Age – primary lung cancer is unlikely in non-smokers below the age of 40. |
• | Smoking – increases the risk of primary lung cancer by 3.5 times and is proportional to the number of pack years. In ex-smokers, the risk of adenocarcinoma remains elevated for up to 30 years. |
• | Haemoptysis – is highly suggestive of malignancy in a smoker, over 40 years of age. Benign causes for haemoptysis include pneumonia (Klebsiella), tuberculosis (TB), bronchiectasis, AVMs, lung sequestration and sclerosing haemangioma (Figure 7). |
• | Constitutional symptoms – including fever, night sweats, malaise, weight loss, arthralgia and myalgia, generally point to an inflammatory or infectious aetiology, such as lung abscesses, TB or vasculitis. |
• | Drug history – especially of immunosuppressive medications. |
• | Acquired immune deficiency status. |
• | Travel history – including a recent exposure to TB or histoplasmosis. |
• | Occupational risk factors – including exposure to asbestos or toxic fumes. |
• | History of extrapulmonary malignancy – especially colon, breast, kidney, thyroid, uterus, prostate, seminoma, removed skin lesion (melanoma) and long bone sarcoma. |
• | Previous mediastinal radiotherapy – which may result in post-radiation fibrosis and scar adenocarcinoma. |
• | Paraneoplastic syndromes – including hyperpigmentation and Cushingoid features that may suggest lung carcinoid. |
• | Previous radiology – increase in size over time is highly suggestive of malignancy, although a sclerosing haemangioma, may also increase in size (Figure 8). |
What are the important features in the clinical examination of a patient with an SPN? | |
• | Clubbing – which is found in lung cancer, chronic inflammatory conditions (such as bronchiectasis and lung abscess) and congenital AVMs. |
• | Cyanosis, clubbing, skin naevi, lip telangiectases and a pulmonary murmur might suggest a pulmonary AVM or familial haemorrhagic telangiectasia (Osler-Weber-Rendu syndrome). |
• | Heart murmur in a drug abuser might suggest tricuspid valve endocarditis, septic emboli and subsequent lung abscess formation. |
• | Weight loss and cachexia may indicate underlying malignancy. |
• | Epistaxis and skin lesions, such as a purpuric rash over the hands or legs, may suggest vasculitis. |
• | Metastases from previous malignancy may be suggested by scars of a previous operation, such as mastectomy, or the presence of a leg prosthesis following long bone sarcoma. |
5 | What are the important radiological characteristics of an SPN? |
| Based on the Fleischner Society glossary of terms for thoracic imaging: |
• | Size – with lesions subdivided into those <8mm (which are managed by surveillance) and those between 8-30mm (which are managed by further investigation). |
• | Shape – usually rounded (coin lesion) or oblong but can be lobulated. |
• | Margins – smooth, irregular or spiculated (suggestive of cancer until proven otherwise). |
• | Radiodensity – which can be radiodense (white) or radiolucent (grey or black) with high, low or indeterminate attenuation. |
• | CT density – which is measured in Hounsfield Units, where the density of air is -1000 HU (black), fat -80 HU, water 0 HU, calcification >+165 HU and bone +700 HU. |
• | Enhancement (with iodine contrast): |
a) | benign diseases – which normally show an absence of enhancement (≤15 HU); |
b) | malignant diseases – which usually ‘light up’ 5 minutes after injecting the contrast. |
• | Rim enhancement (or ring enhancement sign) – an area of decreased radiodensity surrounded by an enhanced ring is suggestive but not conclusive of a benign pathology. The enhancing rim is due to fibrotic inflammatory tissue surrounding a necrotic centre. |
PET activity – which is referred to as ‘FDG avidity’ and measured in SUVmax (maximum standard uptake value). An SUV ≥2.5 is considered ‘hypermetabolic’ and indicative of malignancy (lesion ‘lights up’). It should be emphasised that the absence of FDG avidity does not mean the lesion is definitely benign. | |
• | Calcification – which is the only finding that reliably indicates a benign lesion. |
6 | What is a ground-glass opacity? |
• | A ground-glass opacity (GGO) is defined as a hazy focal density, with ill-defined margins, but preserved bronchial and vascular markings. |
• | The differential diagnosis of GGO ranges from inflammatory lesions to early primary lung cancer, with around 60% of GGOs being malignant. |
• | Histologically, the ground-glass component typically corresponds to a lepidic pattern and the solid component to invasive patterns. Solid components usually arise from the airways. Bubble-like, cystic lucencies and bronchograms can appear within the GGO and are associated with well-differentiated adenocarcinoma. |
• | GGOs are classified as: |
a) | part-solid GGO (Figure 9A) – which is seen with mixed mucinous and non-mucinous adenocarcinoma; |
b) | pure GGO (non-solid, Figure 9B) – which is seen in pre-invasive lesions, such as adenocarcinoma in situ (AIS) and atypical adenomatous hyperplasia (AAH). |