Solitary Pulmonary Nodule

Overview & Definition

A solitary pulmonary nodule (SPN) — historically a "coin lesion" — is a single, well-defined, roughly spherical opacity 3 cm or less in greatest diameter, surrounded by aerated lung, with no associated atelectasis, mediastinal adenopathy, or pleural effusion. The size threshold is the central exam fact: a lesion larger than 3 cm is, by definition, a pulmonary mass, which is presumed malignant until proven otherwise and is investigated and staged as probable lung cancer rather than worked up as an SPN.[1][5]

The clinical importance of the SPN is not that it is dangerous in itself — most are benign — but that a minority represent early, surgically curable lung cancer. The whole apparatus of nodule management (risk models, surveillance intervals, PET, biopsy) exists to catch the curable stage IA cancer without over-investigating the great majority of nodules that are benign. Because chest CT use has exploded (incidental imaging, COVID-era CT, and most importantly organised low-dose CT lung cancer screening), SPNs are detected in over 1.5 million adults in the United States each year, making the algorithm one of the highest-yield topics in thoracic medicine.[1][6]

[1]

Classification

An SPN is classified along three axes that each change pre-test probability and drive the management pathway: (1) size, (2) radiographic density, and (3) aetiology. Density is the most examinable, because it tracks the underlying biology — a solid nodule behaves differently from a pure ground-glass nodule, and a part-solid nodule carries the highest malignant risk of all.[1]

By density (the most examinable axis)

By aetiology

Epidemiology & Risk Factors

The prevalence of SPNs and their malignant probability both depend entirely on the population being scanned. In an incidental-CT population the malignant rate is low (often 1-12 percent); in a lung cancer screening (LDCT) population it is higher (around 1 in 10 baseline nodules eventually proves malignant, with many more false positives); in a patient with prior cancer the rate rises sharply.[6]

Patient-level risk factors for malignancy are the backbone of every risk model and every examiner's first follow-up question. They are, in roughly descending weight: age (risk rises steeply after 50, and an SPN in a person under 35 is much more likely benign); smoking (the dominant modifiable risk; current over former, pack-years matter); personal history of extrathoracic cancer (especially melanoma, sarcoma, breast, colon, renal — raises the metastasis differential); family history of lung cancer; chronic lung disease (COPD and pulmonary fibrosis both raise lung cancer risk independently of smoking); and occupational exposure (asbestos, uranium, radon, silica, chromium, nickel).[2][4]

Nodule-level imaging features that raise malignant probability are the other half of every risk model: size (cancer probability tracks diameter roughly linearly — under 10 percent for a 5 mm nodule, around 50 percent at 2 cm, and over 80 percent at 3 cm in a smoker); spiculated or lobulated border; upper-lobe location (lung cancer is more common in upper lobes); growth on serial imaging; part-solid morphology; and cavitation with a thick, irregular wall (a wall over 15 mm favours malignancy or infection, under 5 mm favours benign).[1][4]

Pathophysiology

The malignant pathway: the adenocarcinoma sequence

A malignant SPN, in the modern CT era, is most often a pulmonary adenocarcinoma travelling along a defined histological and molecular sequence. The earliest lesion is atypical adenomatous hyperplasia (AAH) — a small (≤5 mm) ground-glass focus of Clara-cell/type-II-pneumocyte atypia. AAH can progress to adenocarcinoma in situ (AIS), a pure lepidic (along-alveolar-wall, non-invasive) growth that appears radiologically as a persistent pure ground-glass nodule. AIS can progress to minimally invasive adenocarcinoma (MIA) — a lepidic lesion with a small invasive component (≤5 mm) — and finally to invasive adenocarcinoma, where a solid component appears within the ground-glass as stroma-invasive tumour breaks through the alveolar wall. This sequence is the biological basis of the density axis: a pure ground-glass nodule sits early in the sequence and is slow, a part-solid nodule has developed an invasive component, and a solid nodule may have replaced the lepidic precursor entirely.[1]

The driver mutations are the examinable molecular detail. In non-smokers and women, EGFR mutations (and ALK / ROS1 rearrangements) are more common; in smokers, KRAS dominates. Each driver defines not only the biology but the systemic-therapy options (EGFR/ALK tyrosine-kinase inhibitors in advanced disease — relevant when an SPN turns out to be a more advanced cancer than hoped). [1]

The benign granuloma: a walled-off infection

The commonest benign SPN worldwide is the healed granuloma — a fibro-calcified scar of an old inhaled infection. The mechanism is the classic cell-mediated immune response: inhaled Mycobacterium tuberculosis (or, in endemic regions, Histoplasma capsulatum, Coccidioides immitis, or Blastomyces) is phagocytosed by alveolar macrophages, processed and presented to CD4+ T-helper-1 cells, which release interferon-γ and IL-2, recruiting and activating more macrophages. Activated macrophages fuse into epithelioid and Langhans giant cells and organise into a granuloma that walls off the organism. Over months to years the centre undergoes caseous necrosis and dystrophic calcification, producing the radiologically dense, central, laminated ("target") or diffuse calcification that is the exam hallmark of a benign healed granuloma. Importantly, this calcification is metabolically inactive — which is why a benign granuloma can still be mildly FDG-avid on PET (active inflammatory cells) but is negative for the high-SUV uptake of cancer.[4]

The hamartoma: a benign mesenchymal neoplasm

A pulmonary hamartoma is the commonest benign tumour of the lung. It is a disordered but mature mixture of cartilage, fat, smooth muscle and epithelial clefts. The radiological signature is fat within a nodule (negative Hounsfield units, −40 to −120 HU) with or without 'popcorn' chondroid calcification. When fat or popcorn calcification is present, no follow-up is required — the diagnosis is radiological and benign.[5]

Growth dynamics: the doubling-time rule

A tumour grows by exponential cell division, and the examinable metric is the volume doubling time — the time for a nodule to double its volume. A malignant nodule doubles in volume every 30 to 400 days; faster than 30 days is too quick for cancer and suggests infection or inflammation (e.g. a round pneumonia); slower than 400 days is too slow for most cancers and suggests benign disease (the lepidic adenocarcinomas are an important exception — they can be very slow).[1][5]

[1]

Why part-solid is the highest-risk morphology

A part-solid nodule's ground-glass component is the lepidic (in-situ) tumour spreading along alveolar walls; its solid component is the invasive adenocarcinoma breaching those walls. Because invasion is what makes a cancer a cancer, the solid-component size (not the total nodule size) drives risk — a part-solid nodule with a solid component of 6 mm or more is high-risk even if the overall lesion is modest. This is why the Fleischner and BTS guidelines key off the solid component for subsolid lesions.[1]

Clinical Presentation

An SPN is almost always asymptomatic — that is the whole point of its detection by imaging. It is found in one of three contexts: (1) incidentally, on a CT done for another reason (trauma, cardiac work-up, COVID suspicion, abdominal pathology with chest slices); (2) on organised low-dose CT lung cancer screening in a high-risk smoker; or rarely (3) on a chest X-ray (the historic "coin lesion"), where thin-section CT is then mandatory to characterise it. [1]

The history is therefore not a symptom history but a risk-factor history, and it is where the marks are won in a viva or long case. Elicit, specifically and quantitatively: smoking (current vs former, pack-years, and for ex-smokers the time since quitting — recent quitters carry near-current risk and the "quitter's cough / cancer after quitting" pattern is classic); personal history of cancer (and for the Mayo/Herder models, whether it was extrathoracic and more than 5 years ago); family history of lung cancer; occupational exposure (asbestos, uranium mining, radon, silica, chromium, nickel); travel and residence in TB- or histoplasmosis-endemic regions; and constitutional symptoms (haemoptysis, weight loss, anorexia, bone pain, hoarseness from recurrent laryngeal nerve involvement) — any of which signals advanced or alternative disease rather than an incidental nodule.[4][5]

Symptoms, when present, change the question entirely. Haemoptysis with a nodule implies either a central endobronchial lesion (consider bronchoscopy), cavitation, or advanced disease. Weight loss, bone pain, jaundice, or neurological symptoms indicate metastatic disease and move the nodule from "incidental" to "the tip of the iceberg". Paraneoplastic syndromes (SIADH in small-cell, hypercalcaemia from PTHrP in squamous, hypertrophic pulmonary osteoarthropathy with clubbing) are rare but exam-favourite clues that a nodule is malignant.[5]

Atypical presentations are deliberately tested. In the elderly or immunocompromised patient a granuloma, an active fungal or mycobacterial infection, and a primary lung cancer can coexist — a single nodule cannot be assumed benign just because the patient is "well". In a patient with a prior extrathoracic cancer, an SPN is a solitary metastasis until tissue proves otherwise (especially melanoma, sarcoma, renal, breast, colon). In the Indian / TB-endemic patient, an apparently classic "spiculated growing nodule" can be an active tuberculoma — tissue (and AFB) is needed before staging as cancer. [1]

Differential Diagnosis

The differential of an SPN is wide, but a structured approach using imaging morphology collapses it rapidly. The exam answer requires at least three named differentials, each with at least three distinguishing features.[5]

[1]

Clinical & Bedside Assessment

The clinical assessment of an SPN is a focused history and a directed examination aimed at refining pre-test probability and finding signs of advanced or alternative disease — most patients have a completely normal examination, which does not exclude malignancy. [1]

The history must quantify, in this order: (1) smoking — current or former, pack-years ((cigarettes per day ÷ 20) × years smoked), and for ex-smokers the years since quitting (the NLST and most screening programmes treat quitting within 15 years as still screen-eligible); (2) prior malignancy — site, histology, time since diagnosis, and treatment; (3) family history of lung cancer in a first-degree relative; (4) occupational and environmental exposure — asbestos, uranium/radon, silica, chromium, nickel, arsenic, and indoor biomass-fuel smoke (a recognised lung-cancer risk in parts of India); (5) travel and residence in TB- or fungal-endemic regions; and (6) symptoms — haemoptysis, weight loss, anorexia, bone pain, hoarseness, headache, jaundice.[4]

The physical examination is directed at finding signs of: advanced local disease (wheeze or unilateral reduced breath sounds from obstruction, dullness from effusion, SVC syndrome from a right upper-lobe mass); metastatic spread (cervical and supraclavicular lymphadenopathy, hepatomegaly, bone tenderness, neurological signs, skin deposits); a primary extrathoracic cancer that has metastasised (breast examination, skin examination for melanoma, abdominal examination for renal or colorectal primary); and paraneoplastic signs (finger clubbing and hypertrophic pulmonary osteoarthropathy, gynaecomastia from hCG-secreting tumours, Cushingoid features from ectopic ACTH in small-cell).[5]

[1]

Investigations

The investigative principle of the SPN is characterise first, then estimate probability, then choose surveillance, further imaging, or tissue. The single most important investigation is a thin-section (1 mm) CT of the nodule, ideally with prior imaging for comparison.[1]

[1]

Step 1 — Characterise on thin-section CT

Thin-section CT defines the six features that drive every risk model and every guideline interval: [1]

• Size — the greatest diameter on axial, sagittal or coronal images (for subsolid nodules, volume is preferred because small diameter changes mean large volume changes).
• Density — solid, part-solid (a ground-glass nodule with a solid component), or pure ground-glass; presence of fat (−40 to −120 HU → hamartoma); presence of calcification and its pattern.
• Border — smooth (favours benign), lobulated (suggests uneven growth), spiculated (the classic malignant "sunburst" sign), with or without a halo (ground-glass — haemorrhage in invasive aspergillosis or angioinvasive tumour).
• Calcification pattern — the four benign patterns are central, laminated ("target"), diffuse, and "popcorn" (chondroid, hamartoma); the malignant-associated patterns are eccentric or stippled calcification (scarred cancer or tumour engulfing a granuloma).
• Cavitation and wall thickness — a wall over 15 mm favours malignancy or infection; under 5 mm favours benign.
• Location — upper lobe slightly raises malignant probability (lung cancer is upper-lobe predominant). [1]

Step 2 — Compare with prior imaging (the 2-year rule)

If a nodule has been stable in size for two years on serial CT (or, with caveats, on chest X-ray), it is benign by the stability rule and needs no further investigation. This single fact — having an old CT — can end the work-up; always hunt for prior imaging before PET or biopsy.[5]

Step 3 — Quantify pre-test probability with a validated risk model

This is the most examinable step. Three validated clinical prediction models are in active use, and the modern British Thoracic Society (BTS) 2015 algorithm chains the first two together.[2][3][4]

[1]

Step 4 — Further functional imaging

Step 5 — Tissue diagnosis

Tissue is required when the post-imaging probability is intermediate-high and the result will change management. The route depends on nodule location and patient fitness:[5]

• Percutaneous transthoracic needle biopsy (TTNB) — best for peripheral nodules under CT or fluoroscopic guidance. Sensitivity ~90 percent for malignancy; principal complication is pneumothorax (~20 percent, ~5 percent requiring chest tube), plus pulmonary haemorrhage and rare systemic air embolism. Avoid in the fully anticoagulated or in patients with severe emphysema and a deep lesion.
• Bronchoscopic biopsy — best for central nodules or those reachable by radial endobronchial ultrasound (r-EBUS) or electromagnetic navigation bronchoscopy (ENB) / robotic bronchoscopy, which can reach small peripheral lesions. Lower pneumothorax risk than TTNB; allows rapid on-site cytology and staging of mediastinal nodes in the same sitting.
• Surgical biopsy — when a nodule is high-risk and resectable, the diagnosis and treatment can be combined: a video-assisted thoracoscopic (VATS) wedge resection with intra-operative frozen section, proceeding to anatomic lobectomy + mediastinal lymph node dissection if malignant. This is both diagnostic and therapeutic and is preferred when pre-operative probability is very high.[5]

[1]

Management — Resuscitation

An SPN is rarely a time-critical emergency — the work-up spans weeks, not minutes. The "resuscitation" step is therefore a safety-net assessment, asking three questions at the first encounter: [1]

1. Is the lesion actually a mass? A lesion over 3 cm is, by definition, a pulmonary mass presumed malignant — work it up and stage it as lung cancer, not as an SPN. This is the single most important reclassification at triage.[1]
2. Is there an acute complication needing urgent care? Look for haemoptysis (especially with a central or cavitating lesion), post-obstructive pneumonia, SVC obstruction, hypercalcaemia (PTHrP), SIADH, or haemodynamic instability from a ruptured AVM or abscess. Any of these escalates the nodule from an outpatient CT pathway to an urgent inpatient one.
3. Is the patient already symptomatic from advanced disease? Weight loss, bone pain, jaundice, neurological symptoms, or a palpable mass indicate metastatic disease and shift the pathway to urgent staging CT-PET and tissue diagnosis within two weeks (UK "2-week-wait" / suspected-cancer pathway).[5]

In the absence of any of these, the SPN enters the risk-stratified outpatient pathway below. [1]

Management — Definitive & Stepwise

The overarching principle is risk-stratified, guideline-driven management, designed to minimise the harm of over-treatment (unnecessary PET, biopsy, surgery, anxiety, cost — the great majority of nodules are benign) while never delaying the curable early lung cancer. The two operating guideline families are Fleischner Society 2017 (incidental nodules, global) and British Thoracic Society 2015 (algorithmic, model-driven, UK), with ACCP (Gould 2013) used in North America.[1][3][5]

The four-step algorithm

Fleischner Society 2017 — incidental solid nodules (low-risk adults)

Fleischner Society 2017 — incidental subsolid nodules

Subsolid nodules follow longer surveillance because the lepidic biology is slow but the malignant potential is real, and the rules key off the solid component.[1]

British Thoracic Society (BTS) 2015 — the model-driven algorithm

The BTS algorithm is explicitly chained on the risk models, and is the cleanest single examinable pathway:[2][3]

Lung cancer screening (NLST / NCCN / Lung-RADS) — the third pathway

When the nodule is found on organised low-dose CT screening in a high-risk smoker, neither Fleischner nor BTS applies — instead use the Lung-RADS scheme. Screening is offered to adults aged 55-80 (USPSTF) / 55-74 (NCCN) who have 30 pack-years or more of smoking and quit within 15 years, with annual low-dose CT. The National Lung Screening Trial (NLST, NEJM 2011) showed a 20 percent reduction in lung-cancer mortality and a 6.7 percent all-cause mortality reduction with three rounds of annual LDCT vs chest X-ray.[6]

Surgical treatment of the malignant SPN

Once a malignant SPN is confirmed (or a high-risk nodule is resected diagnostically), the standard operation is anatomic lobectomy with mediastinal lymph node sampling or dissection, which provides both cure and accurate pathological staging.[5]

• Sublobar resection (segmentectomy or wedge) — acceptable for small (under 2 cm), peripheral stage IA tumours, especially in patients with limited pulmonary reserve. Sublobar must achieve a 2 cm or greater margin or a margin-to-tumour ratio of 1 or more and include hilar and mediastinal node sampling (CALGB 140503 and JCOG0802/WJOG4607L showed non-inferior survival vs lobectomy for small peripheral tumours; segmentectomy preferred over wedge for adequate margins and nodal yield).
• VATS / robotic lobectomy — minimally-invasive approach is now standard for early-stage disease, with lower morbidity, shorter stay, equivalent oncologic outcome to thoracotomy.
• SBRT (stereotactic body radiotherapy) — for medically inoperable early-stage (T1-2aN0) lung cancer; delivers a biologically potent dose in a few fractions; local control over 90 percent and 3-year survival ~50-60 percent in unfit patients who would otherwise receive best supportive care. [1]

Escalation and de-escalation triggers

The triggers to step up from surveillance to biopsy/surgery are: growth on serial CT (especially a diameter rise consistent with volume doubling — recall the 26 percent diameter rule); rising or new FDG avidity on PET; positive biopsy; or a Herder/Mayo probability crossing the high-risk threshold in a fit patient. The trigger to step down is a definite benign pattern (fat, popcorn calcification, dense central/laminated calcification, stability over 2 years) or a patient who is not fit for any treatment even if the nodule is malignant (in whom surveillance is appropriate and invasive work-up is futile).[1][5]

Specific Subtypes & Scenarios

Pure ground-glass nodule (the lepidic spectrum)

A persistent pure ground-glass nodule (GGN) of 6 mm or more sits along the AAH → AIS → MIA pathway and grows slowly (often over years). Management is long surveillance (Fleischner: CT at 6-12 months then every 2 years to 5 years). Surgery (sublobar resection) is reserved for a growing lesion, a developing solid component (transition to part-solid = invasion), or a lesion that persists and grows beyond 5 years. PET and contrast-CT are often negative in pure GGN because the lesion is lepidic and low-metabolic — a negative PET does not exclude AIS/MIA.[1]

Part-solid nodule

The highest-risk morphology. The solid component size drives risk: a solid component of 6 mm or more (or any growth of the solid component) is high-risk and warrants PET ± tissue. The ground-glass component is the lepidic part; the solid component is the invasive part.[1]

Hamartoma

Fat (−40 to −120 HU) ± 'popcorn' calcification in a smooth, well-defined nodule = radiological diagnosis, no follow-up required, no treatment. The commonest benign lung tumour; typically in patients under 50 and non-smokers.[5]

Carcinoid tumour

A well-defined, often central, intensely FDG-avid (or rather, DOTATATE-avid) nodule in a younger, non-smoking patient. May cause central obstruction, haemoptysis, or carcinoid syndrome. Surgical resection (lobectomy or sleeve resection) is curative for typical carcinoid; excellent prognosis (5-year survival over 90 percent for typical carcinoid). Atypical carcinoid behaves more aggressively.[5]

Solitary metastasis from an extrathoracic primary

In a patient with a known extrathoracic cancer (especially melanoma, sarcoma, renal, breast, colon), an SPN is a solitary metastasis until proven otherwise. Tissue histology decides (compare with the primary). Pulmonary metastasectomy is curative in selected cases (single lesion, controlled primary, long disease-free interval, no extrathoracic disease).[5]

Nodule in a TB-endemic region (the Indian context)

In TB/histoplasmosis-endemic regions, the pre-test probability of a benign granuloma is much higher and PET specificity drops sharply (granulomas are FDG-avid). The approach is: correlate with IGRA / tuberculin test, send sputum for AFB, mycobacterial culture and Xpert MTB-RIF, and have a lower threshold for tissue biopsy with stains for AFB and fungi before assuming cancer and embarking on staging.[1]

Screening-detected nodule (Lung-RADS)

Use Lung-RADS categories (1-4) rather than Fleischner. A solid nodule of 15 mm or more (or 8 mm or more new/growing at annual screening) is Lung-RADS 4B (suspicious) and warrants PET-CT and/or biopsy. The baseline round of screening generates more false positives than annual rounds.[6]

Complications & Pitfalls

Prognosis & Disposition

Most SPNs are benign and need no treatment — the goal of management is to catch the curable early lung cancer among them. A resected stage IA lung cancer detected as a nodule has a 5-year survival of over 80-90 percent, compared with under 20 percent for symptomatic late-stage disease — this survival gap is the entire justification for the surveillance-and-tissue apparatus, and is the one-liner to give the examiner.[5][6]

Outcome is driven by four factors: (1) malignant vs benign (the dominant determinant); (2) histological subtype and stage (adenocarcinoma, squamous, small-cell, carcinoid, metastasis); (3) fitness for surgery (comorbidity, pulmonary reserve, age); and (4) the timeliness of detection (whether caught at stage IA or allowed to progress).[5]

Disposition follows the risk band: low-risk nodules return to primary care with a structured CT surveillance plan and reassurance; intermediate-risk nodules are referred to the respiratory / lung-cancer multidisciplinary team (MDT) for PET ± biopsy; high-risk nodules are referred to the thoracic surgery / lung-cancer MDT for tissue diagnosis and resection (or SBRT if inoperable). The safety-net is a clear, written surveillance plan with named CT dates and a named responsible clinician — patients lost to follow-up during surveillance are the classic preventable failure.[1]

Special Populations

Evidence, Guidelines & Regional Differences

The SPN literature is built on a small number of landmark prediction models and trials that every examiner rewards.[2][3][4][6]

Guideline landscape and regional deltas

• Fleischner Society 2017 (MacMahon, Radiology 2017) — the global default for incidental solid and subsolid nodules; simplified and reduced follow-up versus the 2005 version; does not apply to screening, immunocompromised, or known-cancer patients.[1]
• British Thoracic Society (BTS) 2015 (Callister, Thorax 2015) — the UK algorithm; model-driven (Brock → Herder), with explicit risk thresholds (under 10, 10-70, over 70 percent).
• ACCP (Gould 2013) — the US/North American guideline; uses the Mayo/VA models and clinical judgement; thresholds similar to BTS.[5]
• NCCN / Lung-RADS — for screening only; categorises nodules 1-4 and drives biopsy thresholds.
• ICMR / Indian context — no single national SPN guideline; in practice Fleischner/BTS is applied with regional calibration because the high prevalence of TB and granulomatous disease lowers PET specificity and raises the benign pre-test probability.[1]

Controversies

The two live controversies are overdiagnosis of indolent ground-glass / lepidic adenocarcinomas (treating AIS/MIA that may never have harmed the patient — the downside of sensitive CT) and PET false-positives in TB-endemic regions (treating a tuberculoma as cancer). Both push toward structured, model-driven, biopsy-before-staging pathways rather than reflex PET-CT or reflex surgery.[1][3]

Exam Pearls

[1]

Exam application bank (NEET-PG / INICET)

One-line answer

A solitary pulmonary nodule (SPN) is a single, well-defined, roughly spherical opacity 3 cm or less in diameter, surrounded by aerated lung, with no associated atelectasis, adenopathy or pleural effusion — most often found incidentally on CT or on low-dose CT lung cancer screening. The clinical task is to distinguish benign from malignant using size, density (solid, part-solid, ground-glass), border (smooth vs spiculated), growth rate, calcification, and patient risk (age, smoking, prior cancer). Benign features favour a smooth border, dense central/popcorn calcification, and no growth over two years; malignant features are a spiculated or part-solid nodule that grows in an older smoker. A validated risk model (Brock, then Herder; Mayo/Swensen as the classical model) quantifies cancer probability and drives management — low risk: CT surveillance (Fleischner or BTS intervals); intermediat

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. [1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Solitary Pulmonary Nodule.

References

1. [1]MacMahon H, Naidich DP, Goo JM, et al. Guidelines for Management of Incidental Pulmonary Nodules Detected on CT Images: From the Fleischner Society 2017 Radiology, 2017.PMID 28240562
2. [2]McWilliams A, Tammemagi MC, Mayo JR, et al. Probability of cancer in pulmonary nodules detected on first screening CT N Engl J Med, 2013.PMID 24004118
3. [3]Herder GJ, van Tinteren H, Golding RP, et al. Clinical prediction model to characterize pulmonary nodules: validation and added value of 18F-fluorodeoxyglucose positron emission tomography Chest, 2005.PMID 16236914
4. [4]Swensen SJ, Silverstein MD, Ilstrup DM, et al. The probability of malignancy in solitary pulmonary nodules. Application to small radiologically indeterminate nodules Arch Intern Med, 1997.PMID 9129544
5. [5]Gould MK, Donington J, Lynch WR, et al. Evaluation of individuals with pulmonary nodules: when is it lung cancer? Diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines Chest, 2013.PMID 23649456
6. [6]National Lung Screening Trial Research Team; Aberle DR, Adams AM, Berg CD, et al. Reduced lung-cancer mortality with low-dose computed tomographic screening N Engl J Med, 2011.PMID 21714641