Metastatic Lung Disease - Radiology (10 Marks)

Definition & Routes of Spread

1. Haematogenous - most common; tumour cells lodge in pulmonary capillaries and grow as discrete nodules
2. Lymphatic - gives lymphangitic carcinomatosis
3. Direct extension - from hilar nodes, pleura, or a primary bronchial carcinoma into adjacent tissue
4. Endobronchial - rare; submucosal deposits cause airway obstruction

Radiological Patterns

1. Discrete Pulmonary Nodules (Haematogenous Metastases)

• With multiple non-calcified nodules on plain CXR: probability of metastases >90% (near 100% in non-endemic areas).
• For CT-only visible nodules <1 cm: probability may fall to 50%, depending on community prevalence of infectious granulomas.

Fig. 8.33 from Grainger & Allison - Irregular pulmonary metastases, metastatic adenocarcinoma; note irregular outlines and large left pleural effusion.

2. Cannon-ball Metastases

• Term used for large, round, well-defined bilateral pulmonary nodules
• Classically associated with: renal cell carcinoma, testicular germ cell tumours, choriocarcinoma
• Easily visible on plain CXR

3. Lymphangitic Carcinomatosis

• Bilateral symmetric pattern - from haematogenous emboli spreading via vessel walls into perivascular interstitium
• Unilateral/localised pattern - from direct hilar node extension or pleural invasion

Fig. 8.34 - Unilateral lymphangitic carcinomatosis, bronchial carcinoma. Thickened septal lines and nodules confined to right lung.

Fig. 8.35 - Bilateral lymphangitic carcinomatosis. Bilateral thickened septal lines and widespread nodulation. Primary: bronchial carcinoma on sputum cytology.

Fig. 8.36 - HRCT: variable thickening of interlobular septa and bronchovascular bundle enlargement in lymphangitic carcinomatosis.

4. Miliary Metastases

• Innumerable tiny nodules mimicking miliary tuberculosis throughout both lungs
• No large masses, no lymphatic obstruction
• Rarest pattern of metastatic spread
• Primary tumours: thyroid carcinoma, renal carcinoma, bone sarcomas, choriocarcinoma

5. Endobronchial Metastases

• Rare; submucosal deposits cause airway obstruction as dominant radiological feature
• Leads to collapse, consolidation, or obstructive pneumonitis distal to the deposit
• Primary tumours: melanoma, renal, colorectal, breast carcinoma

6. Tumour Emboli

• Radiologically recognisable pulmonary arterial hypertension from tumour emboli blocking small pulmonary arteries
• Tumours: hepatoma, breast, kidney, stomach, prostate, choriocarcinoma
• Rare but high-yield PG MCQ association

7. Pleural Effusion

• Pleural effusion may accompany any pattern
• Especially common with lymphangitic spread (~30%)
• May also result from lymphatic obstruction, direct pleural seeding, or hypoalbuminaemia

Summary Table - High-Yield for PG Exam

Role of Imaging Modalities

• CXR (PA + lateral, high-kV): First-line; detects nodules >1 cm; misses lesions behind cardiac shadow, diaphragm, hilum
• MDCT: Detects lesions >3 mm; gold standard for staging and follow-up; essential for lymphangitic pattern (HRCT)
• PET-CT: FDG uptake; best for detecting distant metastases and monitoring treatment response
• MRI: Not routine for pulmonary metastases; useful for chest wall/pleural invasion assessment

Solitary Pulmonary Nodule in a Known Malignancy

• Smooth, round borders on CT
• Temporal proximity to the primary lesion
• History of RCC, sarcoma, germ cell tumour

• Spiculated edge
• History of head and neck (94%), lung (92%), bladder (89%), or uterine (74%) carcinoma - these carry highest risk of new primary

• Grainger & Allison's Diagnostic Radiology, Chapter 8 (Lung Metastases, Lymphangitic Carcinomatosis, Unusual Patterns)
• Schwartz's Principles of Surgery, 11e, Chapter 19 (Metastatic Lesions to the Lung)

HRCT: Definition, Technique, Role in Diffuse Lung Disease & Diagnostic Features of SPN

PART 1: DEFINITION OF HRCT

PART 2: HRCT TECHNIQUE

1. Thin Collimation (Section Thickness)

• Usually 1 to 2 mm slice thickness
• Reducing below 1 mm gives no significant further improvement in spatial resolution but increases image noise (reduces signal-to-noise ratio)
• Eliminates partial volume averaging that obscures fine lung detail on conventional CT

2. High Spatial Frequency ("Sharp" / "Lung") Reconstruction Algorithm

• A "sharp" or "bone" algorithm is used instead of the standard smooth algorithm
• Reduces image smoothing, making structures visibly sharper
• Image noise becomes more visible but this is acceptable and expected
• Enhances detection of: thickened interlobular septa, ground-glass opacification, abnormal subsegmental airways

3. Single Breath-Hold Imaging (Full Inspiration)

• Images obtained at full inspiration, supine position, apices to lung bases
• Eliminates respiratory motion artefact that degrades fine lung detail
• With MDCT (multi-detector CT): volumetric acquisition in a single breath-hold is now standard, even in tachypnoeic patients

Additional Technical Points

Post-Processing Techniques

Fig. 1.2 - Unenhanced (A) vs IV-enhanced (B) HRCT in NSIP: contrast enhancement mimics new parenchymal opacification - key reason IV contrast is avoided in HRCT.

PART 3: ROLE OF HRCT IN DIFFUSE LUNG DISEASE (DLD)

Key HRCT Patterns in DLD

1. Ground-Glass Opacification (GGO)

• Hazy increased attenuation; vessels still visible through it
• Represents alveolar filling or interstitial thickening that does not fill alveoli completely
• Conditions: NSIP, DIP, alveolar haemorrhage, oedema, PCP, acute HP, drug toxicity

2. Reticulation

• Network of fine lines; represents thickened interlobular septa or intralobular interstitium
• In UIP/IPF: bilateral, basal, subpleural reticulation + honeycombing + traction bronchiectasis

3. Honeycombing

• Clustered cystic air spaces (3-10 mm), thick well-defined walls, in subpleural distribution
• Represents end-stage fibrosis; pathognomonic of UIP pattern
• Key finding in IPF

4. Traction Bronchiectasis / Bronchiolectasis

• Irregular airway dilatation due to fibrotic traction
• Indicates established fibrosis; part of UIP and fibrotic NSIP

5. Nodules - Distribution on HRCT is Diagnostic

6. Mosaic Attenuation Pattern

• Regional attenuation differences with well-defined interlobular septal borders
• Three causes:
  • Small airways disease (air trapping): "black" areas abnormal; accentuated on expiratory CT; vessels small in black zones
  • Chronic occlusive vascular disease (CTEPH): "black" areas abnormal; no air trapping
  • Infiltrative lung disease: "grey" (increased attenuation) areas abnormal

7. Consolidation

• Complete alveolar filling; vessels obscured
• Alveolar pattern: pneumonia, cryptogenic organising pneumonia (COP), BAC/adenocarcinoma in situ, alveolar haemorrhage

HRCT Patterns in Specific Diffuse Diseases

Clinical Role of HRCT in ILD

• Diagnosis without biopsy: Typical UIP pattern on HRCT eliminates need for surgical lung biopsy in the right clinical context (ATS/ERS guidelines)
• Pattern recognition: Guides multidisciplinary discussion (pulmonologist + radiologist + pathologist)
• Prognostication: UIP pattern = worse prognosis even when not idiopathic
• Disease activity: GGO = active, potentially reversible; honeycombing = irreversible fibrosis
• Biopsy site selection: Identifies areas of active disease (GGO > fibrosis)
• Treatment monitoring: Serial HRCT tracks progression or drug response

PART 4: DIAGNOSTIC FEATURES OF SOLITARY PULMONARY NODULE (SPN)

Definition

Epidemiology

• Found in 0.2% of CXRs incidentally; ~1 million/year in the USA
• 40-50% of SPNs are malignant (Fishman's Pulmonary)
• 80% of benign SPNs are infectious granulomas; hamartoma is the next most common benign cause (~10%)
• Most common malignant type: adenocarcinoma (47%), squamous cell (22%), small cell (4%)

CT Features Suggesting MALIGNANCY

CT Features Suggesting BENIGNITY

Nodule Classification by Composition (CT)

Role of Imaging Modalities in SPN

Summary Table - High-Yield for PG Exam

• Grainger & Allison's Diagnostic Radiology - Chapter 1 (HRCT Technique), Chapter 9 (Diffuse Lung Disease HRCT patterns)
• Schwartz's Principles of Surgery, 11e - Chapter 19 (SPN CT features)
• Fishman's Pulmonary Diseases & Disorders - Chapter 30 (Evaluation of SPN, FDG-PET)
• Goldman-Cecil Medicine - Chapter 177 (SPN evaluation algorithm)

Key Decision Points Summarised

Fleischner Society 2017 - Complete Reference Table

Applies to: Incidental nodules in immunocompetent patients ≥35 years, without prior cancer. NOT for lung cancer screening programmes.

SOLID NODULES

SUBSOLID NODULES

Key Changes from 2005/2013 Guidelines (High-Yield MCQ Points)

Risk Factors (High vs Low Risk)

• Smoking history (current or ex-smoker)
• Upper lobe location
• Spiculated margin
• Family history of lung cancer
• Occupational exposure (asbestos, radon)
• Age >40

Malignancy Risk by Nodule Type (Henschke et al.)

• Part-solid nodules: 63% malignant (highest)
• Pure GGO: 18% malignant
• Solid nodules: 7% malignant

Reference: MacMahon H et al. Guidelines for Management of Incidental Pulmonary Nodules Detected on CT Images: From the Fleischner Society 2017. Radiology 2017;284(1):228-243. [PMID: 28240562]

The Master Memory Framework

STEP 1 - Remember the "6-8-MORE" Rule for SOLID nodules

< 6 mm   →  GREEN  = GO (no follow-up needed)
6-8 mm   →  YELLOW = WAIT (follow-up CT)
> 8 mm   →  RED    = ACT (CT / PET / Biopsy)

• Below Six = Fine (no routine follow-up)
• Above Eight = Late (act now - CT/PET/biopsy at 3 months)
• Between = Wait (CT at 6-12 months)

STEP 2 - Remember the Follow-up Intervals with "3-6-12-18-24"

• Bigger = earlier scan

• 8 mm solid = 3 months (most urgent)

• Part-solid ≥6mm = 3-6 months (high malignancy risk 63%)
• 6-8 mm solid = 6-12 months (intermediate)
• Pure GGO ≥6 mm = 6-12 months (slow growing)

STEP 3 - Subsolid: Remember "6 is the Magic Number"

< 6 mm  →  NO follow-up (same as solid)
≥ 6 mm  →  Follow-up required

"Confirm it exists at 3-6 months, then watch the solid bit - if the solid component hits 6, it's suspicious"

• Solid component < 6 mm = annual CT × 5 years
• Solid component ≥ 6 mm = HIGHLY SUSPICIOUS → act (PET/biopsy/surgery)

STEP 4 - Multiple Nodules: "Halve the Interval"

STEP 5 - The "63-18-7" Malignancy Risk Triplet

Part-solid   =  63%  malignant  ← MOST DANGEROUS (looks innocent but isn't)
Pure GGO     =  18%  malignant  ← Moderate risk
Solid        =   7%  malignant  ← Lowest risk per nodule

STEP 6 - What Changed in 2017 (The "RAISE" Mnemonic)

STEP 7 - Visual Story to Anchor It All

Imagine a traffic cop standing at the lung gate:

• Nodule comes up - he measures it.
• Under 6? "You're small, move along" ✅
• 6 to 8? "Wait here, I'll check on you in 6-12 months" 🕐
• Over 8? "Stop right there - scan, PET, or biopsy in 3 months" 🚨
• Part-solid ≥6 with solid bit ≥6? "Surgeon, NOW" 🔴

Quick Recall Card (Write this on your palm before the exam)

SOLID:   <6 = none  |  6-8 = 6-12mo  |  >8 = 3mo/PET/biopsy
GGO:     <6 = none  |  ≥6 = 6-12mo → 2yr×5yr
PART-SOLID: <6 = none | ≥6 = 3-6mo → solid<6: annual×5yr | solid≥6: SURGERY
MULTIPLE: halve the first interval, manage worst nodule
RISK: Part-solid 63% > GGO 18% > Solid 7%
2017 CHANGES: threshold ↑ to 6mm, follow-up 5yr, ranges not fixed

Imaging of Interstitial Lung Disease (ILD)

Definition

Imaging Modalities

1. Chest Radiograph

• Part of initial assessment but non-specific, considerable observer variation, and low sensitivity for early ILD
• Useful for:
  • Detecting gross abnormality
  • Establishing disease distribution (zonal predominance)
  • Tracking progression by comparison with prior films

• Early: diffuse ground-glass pattern
• Progressive: reticular (linear) infiltrates → reticulonodular infiltrates
• Alveolar filling: ill-defined nodules (acinar rosettes) with air bronchograms

2. HRCT - The Cornerstone of ILD Imaging

• Early detection before CXR becomes abnormal
• Histo-specific diagnosis in select cases (e.g. typical UIP pattern = no biopsy needed)
• Assessment of disease reversibility and prognosis (GGO = potentially reversible; honeycombing = irreversible)
• Biopsy site selection (sample active GGO, not fibrotic areas)

HRCT Patterns in Diffuse Lung Disease

Pattern 1: Reticular Pattern

• Network of fine lines representing thickened intralobular or interlobular septa, or honeycombing
• Intralobular thickening: often appears as faint GGO rather than distinct reticulation (below spatial resolution)
• Numerous thickened interlobular septa = extensive interstitial abnormality (fluid in oedema; cells in lymphangitis; fibrosis in UIP)
• Honeycombing: clustered cystic spaces 3-10 mm with thick well-defined walls; subpleural; represents end-stage fibrosis

Pattern 2: Nodular Pattern

Pattern 3: Mosaic Attenuation Pattern

Pattern 4: Cystic Pattern

• Thin-walled air-containing spaces
• Key: assess morphology (smooth wall = cyst vs. irregular = emphysema) and geometry
• LAM: Diffuse, thin-walled, round, bilateral uniform distribution
• LCH (Langerhans): Upper lobe, bizarre-shaped cysts + nodules
• LIP: Cysts + GGO + centrilobular nodules (often in HIV/Sjögren's)
• DIP: Lower zone cysts + GGO

Idiopathic Interstitial Pneumonias (IIPs) - HRCT Patterns

The 2013 ATS/ERS Classification and HRCT Correlation

UIP/IPF in Detail - The Most Important Pattern

Typical UIP Pattern (Virtually Pathognomonic = No Biopsy Needed)

• Subpleural bibasal reticulation with honeycombing
• Traction bronchiectasis within areas of fibrosis
• Temporal heterogeneity (areas of fibrosis at different stages of maturity)
• Progressive "propeller blade distribution" - creeps around periphery toward anterior upper lobes

Fleischner Society UIP CT Categories (2018 Guidelines)

Key exam point: Typical UIP on HRCT in appropriate clinical context = no surgical biopsy required (ATS/ERS/JRS/ALAT 2018 guidelines)

Other Key ILDs and Their HRCT Features

Sarcoidosis

Fig. 9.13 from Grainger & Allison - (A) perilymphatic nodules at fissures, (B) Galaxy sign, (C) upper lobe fibrosis with traction bronchiectasis in sarcoidosis.

• Well-defined 2-4 mm nodules in perilymphatic distribution (fissures, bronchovascular bundles, interlobular septa)
• Upper lobe predominant
• Bilateral hilar + mediastinal lymphadenopathy (hallmark)
• Galaxy sign: micronodules clustering into larger opacity with peripheral satellite nodules
• Fibrotic stage: upper lobe honeycombing, volume loss, bronchiectasis, fissural displacement

Hypersensitivity Pneumonitis (HP / Extrinsic Allergic Alveolitis)

Langerhans Cell Histiocytosis (LCH)

• Smokers
• Upper lobe nodules (early) → nodules cavitate → bizarre-shaped irregular cysts (late)
• Lower lobe and costophrenic angles spared (distinguishes from LAM)

Lymphangioleiomyomatosis (LAM)

• Young women of childbearing age
• Diffuse, bilateral, uniform thin-walled round cysts throughout all zones
• No nodules, no GGO
• Associated with pneumothorax and chylous effusion

NSIP (Non-Specific Interstitial Pneumonia)

• Favoured over UIP if:
  • Central rather than peripheral predominance
  • Subpleural sparing (key distinguishing feature from UIP)
  • More uniform fibrosis; honeycombing usually absent
  • Extensive bilateral symmetrical GGO ± reticulation
• Most commonly associated with CTD (especially SSc, polymyositis/dermatomyositis)

Cryptogenic Organising Pneumonia (COP)

• "Reverse halo" (atoll) sign: central GGO surrounded by rim of consolidation - characteristic but not pathognomonic
• Subpleural or peribronchial patchy consolidation
• Perilobular pattern: arcs of consolidation outlining secondary pulmonary lobule
• Migratory/recurrent infiltrates
• Responds to steroids

Acute Interstitial Pneumonia (AIP) / Diffuse Alveolar Damage

• Idiopathic form of ARDS
• HRCT: Patchy or diffuse GGO + consolidation (dependent predominant)
• Traction bronchiectasis + reticulation after several days
• Temporal homogeneity (unlike UIP)

Zonal Distribution - High-Yield Table

Role of Other Modalities