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RADIOLOGY UNIVERSITY EXAM - COMPLETE ANSWERS

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Q1. INVESTIGATION OF SOLITARY PULMONARY NODULE (SPN)

Definition

Epidemiology and Significance

• ~1 million new SPNs detected annually in the USA
• 40-50% of SPNs are malignant
• Of malignant SPNs: adenocarcinoma (47%), squamous cell carcinoma (22%), small cell (4%)
• Of benign SPNs: ~80% are infectious granulomas
• Early detection is critical - lung cancer survival depends heavily on stage at diagnosis

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Step-by-Step Investigation

STEP 1: Plain Chest X-Ray (CXR)

• First-line investigation
• Assess: size, site, shape, density, calcification pattern, margins
• Benign calcification patterns on CXR:
  • Central "bull's eye" - histoplasmoma
  • Diffuse/solid - granuloma
  • Laminated/concentric rings - granuloma
  • "Popcorn" - hamartoma (chondroid matrix)
• Malignant features: irregular/spiculated margins, no calcification, lobulated contour
• Compare with old films: no change over 2 years = benign (doubling time of malignant nodule = 30-400 days)

STEP 2: MDCT (Multi-Detector CT) - KEY INVESTIGATION

• Spiculated/irregular margins ("corona radiata" sign)
• Size >15 mm
• Upper lobe location
• Eccentric or no calcification
• Pleural tethering
• Air bronchogram within solid nodule (adenocarcinoma)
• Vascular convergence sign
• Doubling time 30-400 days

• Smooth round margins
• Central/laminated/popcorn calcification
• Size <6 mm
• Satellite nodules
• Stability for >2 years

• Solid nodule: homogeneous soft tissue attenuation
• Ground glass opacity (GGO): hazy increase in attenuation, vessels still visible
• Part-solid: both GGO and solid components (highest malignancy risk)

• Enhancement >15 HU after IV contrast = suggestive of malignancy (sensitivity 98%, specificity 58%)
• Enhancement <15 HU = benign

STEP 3: PET-CT (FDG-PET)

• Indicated for solid nodules >8 mm where CT is inconclusive
• Malignancy: increased FDG uptake (SUV >2.5)
• Sensitivity: 82-97%, Specificity: 78-82%
• False positives: active TB, aspergillosis, sarcoidosis, histoplasmosis
• False negatives: carcinoid, bronchoalveolar carcinoma (now AIS/MIA), hyperglycemia, nodules <8 mm

STEP 4: Dynamic CT / CT Perfusion

• Sequential CT after contrast: enhancement >15 HU → likely malignant
• Useful when PET-CT not available

STEP 5: Transthoracic Needle Biopsy (TTNB) / CT-guided Biopsy

• Indicated when nodule >8 mm with intermediate/high probability of malignancy
• CT-guided biopsy: sensitivity 90%, specificity 97%
• Complication: pneumothorax (10-25%)
• Contraindicated: contralateral pneumonectomy, severe COPD, uncorrected coagulopathy

STEP 6: Bronchoscopy with BAL / Transbronchial Biopsy

• For central lesions with bronchus sign on CT
• Diagnostic yield 20-80% depending on size and location
• EBUS-guided biopsy increases yield

STEP 7: VATS (Video-Assisted Thoracoscopic Surgery)

• Both diagnostic and therapeutic
• For peripheral nodules where other methods failed
• If malignant, can proceed to lobectomy

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Fleischner Society Guidelines (Solid Nodules - Adults >35 years)

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Lung-RADS Classification (ACR)

• Lung-RADS 1: Negative
• Lung-RADS 2: Benign - 12-month follow-up
• Lung-RADS 3: Probably benign - 6-month CT
• Lung-RADS 4A/B/X: Suspicious - CT/PET/biopsy

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Q2. SEGMENTAL ANATOMY OF THE LUNG

Overview

• Segmental bronchus
• Pulmonary artery branch
• Lymphatics
• Autonomic innervation
• (Pulmonary veins are intersegmental)

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RIGHT LUNG - 10 Segments

Right Upper Lobe (3 segments):

1. Apical (S1) - apex of lung
2. Posterior (S2) - posterior surface upper lobe
3. Anterior (S3) - anterior surface upper lobe

Right Middle Lobe (2 segments):

1. Lateral (S4)
2. Medial (S5)

Right Lower Lobe (5 segments):

1. Superior (apical) (S6) - apex of lower lobe
2. Medial basal (S7) - medial surface adjacent to heart (cardiac segment)
3. Anterior basal (S8)
4. Lateral basal (S9)
5. Posterior basal (S10)

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LEFT LUNG - 8-10 Segments (S7 and S8 often fused = anteromedial basal)

Left Upper Lobe (4-5 segments):

1. Apicoposterior (S1+2) - equivalent of apical + posterior of right
2. Anterior (S3)
3. Superior lingular (S4) - lingulaequivalent of right middle lobe
4. Inferior lingular (S5)

Left Lower Lobe (4-5 segments):

1. Superior (apical) (S6) 7+8. Anteromedial basal (S7+8) - often fused
2. Lateral basal (S9)
3. Posterior basal (S10)

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DIAGRAM (Labeled Bronchopulmonary Segments)

RIGHT LUNG (Lateral View)        LEFT LUNG (Lateral View)

UPPER LOBE:                       UPPER LOBE:
  S1 - Apical                       S1+2 - Apicoposterior
  S2 - Posterior                    S3 - Anterior
  S3 - Anterior                     S4 - Superior lingular
                                    S5 - Inferior lingular
MIDDLE LOBE:
  S4 - Lateral
  S5 - Medial

LOWER LOBE:                       LOWER LOBE:
  S6 - Superior                     S6 - Superior
  S7 - Medial basal                 S7+8 - Anteromedial basal
  S8 - Anterior basal               S9 - Lateral basal
  S9 - Lateral basal                S10 - Posterior basal
  S10 - Posterior basal

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Radiological Importance

• Localizing collapse/consolidation to a specific segment
• Surgical planning for segmentectomy
• S6 (superior lower lobe) - most common site of aspiration in supine patients
• S1, S2, S6 - apices and superior segments - most common for TB
• Right middle lobe syndrome - involves S4 and S5
• Lingula is the left equivalent of the right middle lobe

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Q3. CP ANGLE SPACE OCCUPYING LESIONS (SOL) - CLASSIFICATION AND DESCRIPTION

Definition

• Anteriorly: posterior surface of petrous bone
• Posteriorly: anterior cerebellar surface
• Medially: pons and medulla
• Contains: CN V, VI, VII, VIII, IX, X, XI, AICA

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Classification of CP Angle SOL

A. Extraaxial (Most common - 90%)

1. Acoustic neuroma / Vestibular schwannoma - 75-80%
2. Meningioma - 10-15%
3. Epidermoid cyst - 5%
4. Arachnoid cyst - 1%
5. Lipoma
6. Trigeminal schwannoma

B. Intraaxial

1. Astrocytoma/Cerebellar glioma
2. Metastases
3. Hemangioblastoma
4. Ependymoma (from 4th ventricle)

C. Vascular

1. Vertebrobasilar aneurysm
2. Vascular malformation (AVM)
3. AICA aneurysm

D. Infectious/Inflammatory

1. Neurocysticercosis
2. Tuberculoma
3. Abscess

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4 CP Angle Lesions in Detail

1. ACOUSTIC NEUROMA (Vestibular Schwannoma) - Most Common (75-80%)

• Widening and erosion of internal acoustic meatus (IAM)
• Normal IAM: height 4-5 mm; width 2-3 mm

• Iso-/slightly hypodense mass
• Expands and erodes IAM ("ice cream cone" appearance)
• Moderate to intense enhancement
• No calcification (helps differentiate from meningioma)
• Central low attenuation = cystic degeneration in large tumours

• T1: Hypointense
• T2/CISS/FIESTA: Hyperintense - "filling defect" in IAM
• T1+Gd: Intense enhancement (solid component)
• DWI: No restricted diffusion (differentiates from epidermoid)
• May show "ice cream cone" - larger CPA component + intracanalicular component
• Can be purely intracanalicular (enhanced MRI essential)

• Grade I: intracanalicular
• Grade II: into CPA, no brainstem contact
• Grade III: contacts brainstem
• Grade IV: displaces brainstem

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2. MENINGIOMA (10-15%)

• Hyperdense lesion (due to calcification and vascularity)
• Calcification seen in 20-25%
• Broad dural base (eccentric to IAM)
• "En plaque" meningioma - flat along petrous surface
• Hyperostosis of adjacent bone
• Avid, homogeneous enhancement

• T1: Isointense to brain
• T2: Iso- to hyperintense
• T1+Gd: Intense homogeneous enhancement; dural tail sign (pathognomonic)
• DOES NOT enter IAM (key differentiator from schwannoma)
• CSF cleft between tumour and brain
• No restricted diffusion on DWI

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3. EPIDERMOID CYST (5%)

• Hypodense (near CSF density, -10 to 0 HU)
• No enhancement
• May encase vessels and nerves (insinuating, lobulated margins)
• "Cauliflower" or "bone-like" irregular margins

• T1: Hypointense (like CSF)
• T2: Hyperintense (like CSF) - hard to distinguish from arachnoid cyst
• FLAIR: Heterogeneous - incomplete suppression (KEY differentiator from arachnoid cyst which fully suppresses)
• DWI: RESTRICTED DIFFUSION (bright on DWI, dark on ADC) - PATHOGNOMONIC
• No enhancement
• Does not follow shape of cistern, insinuates along structures

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4. ARACHNOID CYST (1%)

• Perfectly CSF-density lesion (-5 to 5 HU)
• Sharp, smooth margins
• No internal structure or enhancement
• Scallops/remodels adjacent bone

• T1: CSF hypointense
• T2: CSF hyperintense
• FLAIR: Complete suppression (CSF signal nulled) - KEY differentiator from epidermoid
• DWI: No restricted diffusion - KEY differentiator from epidermoid
• Phase contrast cine MRI: non-communicating cyst

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Q4 & Q12. INVESTIGATION OF HEMOPTYSIS (50-YEAR-OLD PATIENT)

Definition

Classification by Volume

• Scant: Blood-streaked sputum
• Mild: <100 mL/24h
• Moderate: 100-200 mL/24h
• Massive/Life-threatening: >200-600 mL/24h (various definitions; implies immediate danger)

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Causes of Hemoptysis

• Bronchogenic carcinoma - HEAD OF LIST
• Tuberculosis and post-TB sequelae
• Bronchiectasis
• Chronic bronchitis (most common overall cause)
• Pulmonary embolism
• Aspergilloma (in old cavity)
• Mitral stenosis (hemoptysis from pulmonary venous hypertension)
• Lung abscess

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INVESTIGATION ALGORITHM for 50-Year-Old

FIRST STEP: Clinical Assessment

• History: smoking (pack-years), duration, amount of blood, fever, weight loss, travel (TB endemic area)
• Examination: respiratory rate, SpO2, signs of consolidation, lymphadenopathy

SECOND STEP: Basic Investigations

1. Complete Blood Count (CBC) - anemia (chronic blood loss), thrombocytopenia
2. Coagulation profile - PT, aPTT, INR
3. Sputum for AFB (3 specimens) - mandatory in this age group
4. Sputum culture and sensitivity
5. Sputum cytology - malignant cells
6. Urine examination - RBC casts (Goodpasture's, vasculitis)
7. Serum ANCA, anti-GBM antibody (if vasculitis suspected)
8. LFT, KFT

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THIRD STEP: IMAGING INVESTIGATIONS

• First line imaging
• Look for:
  • Mass lesion - central or peripheral (carcinoma)
  • Cavitary lesion - TB, abscess, aspergilloma
  • Consolidation - pneumonia, TB, alveolar hemorrhage
  • Hilar adenopathy - carcinoma, TB, sarcoidosis
  • Bronchiectasis - cystic/tram-track opacities
  • Pleural effusion
  • Cardiomegaly + pulmonary venous hypertension - mitral stenosis
  • Rib erosion - malignancy
  • Normal CXR - 30% of hemoptysis cases (cryptogenic hemoptysis)

• Bronchiectasis detection: cylindrical, varicose, cystic; signet ring sign; tram-track opacities
• Airway assessment: endobronchial lesion, thickening
• Ground glass haemorrhage: peribronchovascular distribution
• Parenchymal findings: nodules, masses, cavities
• Aspergilloma: "crescent sign" (air crescent), "Monad sign", dependent movement of fungal ball

• Evaluation of hilar and mediastinal adenopathy
• Vascular causes: CTPA for pulmonary embolism
• Identifies bronchial artery hypertrophy (branches >2 mm tortuous = abnormal)
• CT Bronchoscopy / Virtual bronchoscopy

• If pulmonary embolism suspected
• Also demonstrates bronchial artery abnormalities (for pre-embolization planning)

• For massive hemoptysis - pre-procedure planning for BAE (Bronchial Artery Embolization)
• Identifies hypertrophied, tortuous, or anomalous bronchial arteries

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FOURTH STEP: ENDOSCOPIC INVESTIGATION

• Mandatory in: any adult >40 years, smoker, with hemoptysis
• Performed early (within 24-48 hours of bleeding if possible)
• Can localize bleeding to a specific bronchopulmonary segment
• Identifies endobronchial lesion - biopsy, brushings, BAL
• Can perform bronchial blocker for temporary hemostasis
• Rigid bronchoscopy for massive hemoptysis + airway control

• Bronchogenic carcinoma: mucosal irregularity, endobronchial mass, submucosal infiltration
• TB: granulomatous lesions, narrowing
• Bronchiectasis: dilated, inflamed bronchi

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FIFTH STEP: NUCLEAR MEDICINE

• V/Q Scan: if CTPA contraindicated (renal failure, contrast allergy) for PE
• Gallium scan: sarcoidosis, vasculitis

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SIXTH STEP: INTERVENTIONAL RADIOLOGY

• Bronchial Artery Embolization (BAE):
  • Treatment of choice for massive hemoptysis
  • 90% short-term success rate
  • Principle: bronchial arteries (systemic, high pressure) are main source in 90% of massive hemoptysis
  • Technique: femoral approach, catheter into descending aorta, selective bronchial arteriography, embolize with PVA particles/coils
  • Contraindication: anterior spinal artery arising from bronchial artery (risk of spinal cord ischemia)

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Summary Algorithm

HEMOPTYSIS (50-year-old)
→ CXR + CBC + Sputum (AFB, cytology)
→ HRCT Thorax (best overall evaluation)
→ If mass: CECT + PET-CT + Bronchoscopy + Biopsy
→ If bronchiectasis/infection: HRCT + Sputum culture + FOB
→ If massive: CTPA/DSA → BAE
→ If normal imaging: FOB mandatory

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Q5. RIB NOTCHING

Definition

Classification

A. INFERIOR RIB NOTCHING (Common - "classic rib notching")

1. Coarctation of Aorta - MOST COMMON CAUSE
2. Neurofibromatosis type 1 (NF-1) - superior surface notching also
3. Arteriovenous malformation (intercostal AVM)
4. Subclavian artery obstruction (unilateral notching on same side)
5. Superior vena cava obstruction
6. Takayasu's arteritis
7. Idiopathic (isolated)

B. SUPERIOR RIB NOTCHING

1. Rheumatoid arthritis - most common cause
2. Systemic lupus erythematosus (SLE)
3. Scleroderma
4. Sjögren's syndrome
5. Hyperparathyroidism
6. Marfan syndrome
7. Osteogenesis imperfecta
8. Neurofibromatosis (may affect either surface)

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COARCTATION OF AORTA - Detailed

• Coarctation (narrowing) at or just distal to ductus arteriosus / left subclavian origin
• Blood bypasses via collateral pathway: subclavian → internal mammary → intercostal arteries → descending aorta (distal to coarctation)
• Enlarged, tortuous intercostal arteries under pressure erode inferior rib surface
• Typically ribs 3-8 bilaterally (1st and 2nd ribs usually spared - different intercostal supply)

• Rib notching (appears by age 5-6 years, most evident by adulthood)
• "Figure of 3" sign / "Reverse 3" or "E" sign on barium swallow:
  • Upper bulge: aortic knuckle proximal to stenosis
  • Middle indentation: coarctation site
  • Lower bulge: post-stenotic dilatation
• Left ventricular enlargement (pressure overload)
• Prominent ascending aorta
• Dilated left subclavian artery

• Shows site, extent, and degree of coarctation
• Collateral vessels
• Pre- and post-stenotic dilatation

• Right-sided only: coarctation distal to left subclavian origin (right side still gets collaterals)
• Left-sided only: coarctation proximal to left subclavian origin
• Unilateral also with subclavian artery stenosis/occlusion

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Rib Notching in Neurofibromatosis (NF-1)

• Intercostal neurofibromas enlarge the intercostal foramen and notch ribs
• "Ribbon ribs" - twisted, thin ribs
• Superior as well as inferior surface affected
• Associated: scoliosis, posterior vertebral body scalloping, posterior mediastinal neurofibroma

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Q6. DIFFERENTIAL DIAGNOSIS OF UNILATERAL OPAQUE HEMITHORAX

Definition

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KEY DIAGNOSTIC CLUE: TRACHEAL AND MEDIASTINAL SHIFT

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Differential Diagnoses

1. MASSIVE PLEURAL EFFUSION (Most Common)

• CXR: Homogeneous opacity, absent costophrenic angle, mediastinal shift contralateral
• Hydrothorax (CCF), exudate (infection, malignancy), hemothorax, chylothorax
• USG: Anechoic (transudate), internal echoes (exudate/empyema), septations
• CT: Fluid density (0-20 HU), rim of enhancement (empyema has enhancing split pleura)

2. MASSIVE CONSOLIDATION / PNEUMONIA

• CXR: Opaque hemithorax, NO mediastinal shift, air bronchograms visible
• Usually right lung (right main bronchus more vertical)
• Examples: lobar pneumonia, multilobar TB, necrotizing pneumonia

3. TOTAL COLLAPSE / MASSIVE ATELECTASIS

• CXR: Complete opacity + mediastinal shift TOWARD the opaque side
• Elevated ipsilateral diaphragm, rib crowding
• Causes: foreign body (children), large endobronchial carcinoma, mucus plug
• Air bronchograms ABSENT

4. MESOTHELIOMA

• CXR: Unilateral opacity, often associated with "rind-like" pleural thickening
• Mediastinal shift contralateral (pleural effusion) or ipsilateral (fibrothorax component)
• History of asbestos exposure
• CT: Circumferential pleural thickening >1 cm, nodular, involving mediastinal pleura and diaphragm; loss of normal fat planes
• "Frozen chest" - no volume change

5. DIAPHRAGMATIC HERNIA

• Large eventration or hernia (Bochdalek on left, Morgagni on right)
• CXR: Contains bowel loops (air/fluid levels), no air bronchogram, hemithorax opacification
• On left: stomach in chest (fundal bubble visible in chest)

6. FIBROTHORAX

• Post-infectious (TB, empyema), post-hemothorax
• CXR: Opacity, ipsilateral mediastinal shift, calcified pleural rind
• Rib crowding, elevated diaphragm
• "Vanishing lung" syndrome

7. PULMONARY AGENESIS/APLASIA

• Congenital
• CXR: Complete opacity, ipsilateral mediastinal shift, no aerated lung, hyperlucent contralateral lung (compensatory)
• CT: Absent main bronchus (agenesis) or present bronchus but no lung (aplasia)

8. LARGE TUMOUR (Benign/Malignant)

• Large lung cancer, lymphoma
• Heterogeneous opacity, may show air bronchogram

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Radiological Approach Summary

1. Assess mediastinal shift (most important first step)
2. Look for air bronchogram (present = parenchymal; absent = pleural/collapse)
3. USG to confirm effusion vs. solid
4. CECT for characterization

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Q7. ROLE OF RADIOLOGY IN INDUSTRIAL LUNG DISEASE (OCCUPATIONAL LUNG DISEASE)

Introduction

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ILO Classification System (International Labour Office)

• Used for standardized radiographic classification of pneumoconiosis
• Based on profusion, type, size, and distribution of opacities
• Small opacities:
  • Round: p (<1.5 mm), q (1.5-3 mm), r (3-10 mm)
  • Irregular: s, t, u
• Large opacities: A (<1 cm), B (1-5 cm), C (>5 cm or >1/3 hemithorax)
• Profusion: 0/1, 1/0, 1/1, 1/2, 2/1, 2/2, 2/3, 3/2, 3/3, 3/4
• Zones: upper (U), middle (M), lower (L)

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Major Industrial Lung Diseases

1. SILICOSIS (Quartz dust - mines, sandblasters, ceramics)

• Small round opacities (q/r) in upper and middle zones
• Hilar and mediastinal lymphadenopathy
• Eggshell calcification of lymph nodes (pathognomonic, also seen in sarcoidosis)
• Progressive Massive Fibrosis (PMF): large upper lobe masses migrating toward hila, peripheral traction emphysema

• Well-defined centrilobular and subpleural micronodules
• Upper and posterior lung predominance
• Subpleural pseudo-plaques
• PMF: large masses with low attenuation necrotic centres
• Eggshell nodal calcification

2. COAL WORKER'S PNEUMOCONIOSIS (CWP) (Coal dust)

• Similar to silicosis but nodules smaller (p type)
• Simple CWP: small rounded opacities, predominantly upper/mid zones
• PMF (progressive massive fibrosis): same as silicosis
• Caplan syndrome: rheumatoid + CWP → large well-defined nodules (Caplan's nodules), peripheral, may cavitate

3. ASBESTOSIS (Asbestos fibres - ship-building, insulation)

• Pleural plaques (most common finding): calcified, bilateral, on parietal pleura, diaphragm; "Halo sign" on CT
• Pleural effusion (benign asbestos effusion)
• Diffuse pleural thickening
• Mesothelioma (malignant; latency 20-40 years)
• Rounded atelectasis (Blesovsky syndrome): pleural-based mass, comet tail sign, associated pleural thickening

• Irregular/linear opacities, lower zone predominance
• Subpleural curvilinear lines
• Honeycombing (advanced)
• HRCT: subpleural lines, reticular opacities, traction bronchiectasis, ground glass

4. BYSSINOSIS (Cotton dust)

• Chest tightness on first day of work week ("Monday feeling")
• CXR usually normal early; may show hyperinflation

5. BERYLLIOSIS (Beryllium - aerospace, ceramics)

• Identical to sarcoidosis radiologically
• Bilateral hilar adenopathy, diffuse nodular opacities
• History of exposure differentiates

6. EXTRINSIC ALLERGIC ALVEOLITIS (EAA) / Hypersensitivity Pneumonitis

• Farmer's lung (Micropolyspora faeni), Bird fancier's lung
• Acute: bilateral GGO, air-space consolidation
• Subacute: centrilobular nodules, GGO, head-cheese sign (mixed attenuation)
• Chronic: fibrosis, honeycombing, traction bronchiectasis (upper/mid predominance - unlike IPF)

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Role of HRCT in Industrial Lung Disease

1. Earlier detection than CXR
2. Better characterization of nodule type, distribution, and profusion
3. Detection of complications (PMF, emphysema, fibrosis)
4. Detection of associated malignancy
5. Guidance for biopsy
6. Monitoring disease progression

Role of Nuclear Medicine

• V/Q scan for pulmonary function assessment pre-surgery
• Gallium-67 scan for activity in EAA/sarcoidosis

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Q8. ROLE OF ULTRASOUND (USG) IN PLEURAL PATHOLOGIES

Advantages of Pleural USG

• Real-time, bedside, no radiation
• Superior to CXR for small effusions (detects as little as 3-5 mL)
• Differentiates free vs. loculated effusion
• Guides thoracocentesis and pleural biopsy
• Monitors treatment response

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USG Findings in Pleural Pathologies

1. PLEURAL EFFUSION

• Semi-upright position at the base
• Effusion volume estimation: V (mL) = 20 × maximum depth (cm) at base

• Flapping sign: atelectatic lung moving in large effusion
• Sinusoid sign (on M-mode): floating hyperechoic line synchronous with respiration
• Quad sign: 4 hyperechoic lines surrounding anechoic fluid

2. EMPYEMA

• Complex echogenic fluid with floating echogenic debris ("snowstorm" pattern)
• Thick, hyperechoic peel (cortex) over visceral pleura
• Split pleura sign on CECT: enhancing thickened parietal and visceral pleura separated by complex fluid - pathognomonic for empyema
• Septa and loculations
• May show gas (from anaerobes): hyperechoic foci with dirty shadowing

3. HEMOTHORAX

• Acutely: anechoic (fresh blood)
• Later: echogenic with fibrinous debris
• Organised: complex septated echogenic
• History of trauma / procedure

4. PLEURAL THICKENING

• Normal pleura: <3 mm
• Pathological: >3 mm
• Irregular, nodular, or diffuse thickening
• Cannot reliably differentiate benign from malignant on USG alone
• CECT/MRI needed for full evaluation

5. PNEUMOTHORAX

• Absence of lung sliding (M-mode: "barcode sign" / "stratosphere sign" - horizontal lines only)
• Normal: M-mode shows "seashore sign" (granular pattern below pleural line)
• Lung point sign: specific for pneumothorax - the exact point where collapsed lung meets pneumothorax
• Absence of B-lines
• Used in POCUS (ICU and emergency) - more sensitive than supine CXR

6. PLEURAL TUMOURS

• Malignant mesothelioma: hypoechoic pleural thickening, nodular
• Pleural metastases: nodular deposits, irregular thickening
• USG-guided biopsy of pleural nodule/thickened pleura

7. CHEST DRAINAGE GUIDANCE

• Identifies safe window for thoracocentesis
• Avoids solid organs, vasculature
• Marks best site (usually one intercostal space above the upper border of marked area)
• Real-time guidance during procedure reduces complications

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B-Line Protocol (Lung USG)

• B-lines ("comet tail artifacts"): arise from thickened subpleural interlobular septa

• 3 B-lines per intercostal space = interstitial syndrome

• Bilateral B-lines = pulmonary oedema / cardiogenic or non-cardiogenic
• Used in cardiac ICU and emergency medicine to differentiate ACUTE PULMONARY OEDEMA from COPD exacerbation

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Q9 & Q15. PULMONARY OEDEMA AND ROLE OF RADIOLOGY

Definition

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Classification by Mechanism

1. CARDIOGENIC (Hydrostatic/Haemodynamic)

• Increased pulmonary venous pressure (>18 mmHg) → fluid transudation
• Causes: LVF, mitral stenosis, fluid overload, renal failure, cardiomyopathy

2. NON-CARDIOGENIC (Increased Permeability)

• Acute Lung Injury (ALI) / ARDS (Acute Respiratory Distress Syndrome)
• Fluid rich in protein (high permeability membrane injury)
• Causes: sepsis, aspiration, trauma, pancreatitis, near-drowning, drugs

3. NEUROGENIC PULMONARY OEDEMA

• Post-subarachnoid hemorrhage, head injury
• Massive sympathetic discharge → capillary injury

4. HIGH ALTITUDE PULMONARY OEDEMA (HAPE)

• Non-cardiogenic; hypoxic pulmonary vasoconstriction → elevated pulmonary artery pressure

5. RE-EXPANSION PULMONARY OEDEMA

• After rapid drainage of large pneumothorax or pleural effusion

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RADIOLOGY OF PULMONARY OEDEMA

CHEST X-RAY (CXR) - Sequential Stages

• Cephalization / Upper lobe blood diversion
• Normal vessels taper toward apex; in pulmonary hypertension, upper lobe vessels become prominent (>3 mm)
• Redistribution of pulmonary blood flow
• Enlarged hilar shadows

• Kerley B lines: horizontal lines, 1-2 cm long, perpendicular to pleural surface, best seen at costophrenic angles (thickened interlobular septa)
• Kerley A lines: long (2-6 cm) oblique lines radiating from hila (thickened deep septa)
• Kerley C lines: fine reticular pattern throughout lung (thickened septa in all orientations)
• Peribronchial cuffing: thickened bronchial walls seen end-on
• Perihilar haze ("bat wing" or "butterfly" distribution)
• Pleural effusions (bilateral, more on right)
• Blurring of pulmonary vessels
• Subpleural oedema: filling of fissures (thickening of horizontal fissure)

• Air space consolidation - confluent alveolar filling
• "Bat wing" / "Butterfly" pattern: bilateral perihilar, central consolidation with relatively clear periphery
• Air bronchogram
• May be asymmetric (especially with gravitational distribution)

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HRCT/CT FINDINGS

• Bilateral, symmetrical, dependent distribution
• Ground glass opacity (GGO) - predominantly central/perihilar
• Interlobular septal thickening (smooth) - "crazy paving" in severe cases
• Peribronchovascular thickening
• Cardiomegaly (CTR >0.5)
• Bilateral pleural effusions
• Dilated pulmonary veins

• Bilateral, diffuse, heterogeneous GGO and consolidation
• Peripheral/dorsal predominance (unlike cardiogenic)
• No cardiomegaly, no prominent pulmonary veins
• May show "crazy paving" pattern
• CT density gradient in dependent lung

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ECHOCARDIOGRAPHY

• Distinguishes cardiogenic from non-cardiogenic
• Assesses LVEF, wall motion, valvular pathology

ULTRASOUND (POCUS)

• B-lines: 3 or more per intercostal space bilaterally = interstitial oedema
• Absence of lung sliding + B-lines = possible ARDS

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Differentiating Cardiogenic vs. Non-Cardiogenic on CXR

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Q10. FELSON'S CLASSIFICATION OF MEDIASTINUM + POSTERIOR MEDIASTINAL LESIONS

Felson's Compartmental Classification

• Anterior mediastinum: from sternum to anterior wall of trachea/posterior border of heart
• Middle mediastinum: from anterior trachea/posterior heart to posterior tracheal wall/anterior margin of vertebral bodies
• Posterior mediastinum: posterior tracheal wall/anterior vertebral body margin to posterior chest wall (vertebral bodies)

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Felson's 3-Compartment Model (Lateral CXR)

ANTERIOR         |    MIDDLE        |     POSTERIOR
-----------------|------------------|------------------
Sternum          |                  |
to anterior      |  Trachea, heart, |  Vertebral column
pericardium      |  great vessels,  |  to posterior chest
                 |  hila, pericardium|  wall

Anterior Mediastinal Lesions (4 T's):

1. Thymoma (most common anterior mediastinal mass in adults)
2. Teratoma / Germ cell tumour
3. Terrible lymphoma
4. Thyroid (retrosternal goitre)

• Parathyroid adenoma, lipoma, vascular lesions

Middle Mediastinal Lesions:

• Lymphadenopathy (lymphoma, sarcoidosis, TB, metastases)
• Bronchogenic cyst
• Pericardial cyst
• Tracheal tumours
• Oesophageal lesions

Posterior Mediastinal Lesions:

• Neurogenic tumours (most common)
• Oesophageal lesions
• Descending aortic aneurysm
• Vertebral body lesions
• Thoracic duct cyst (lymphangioma)
• Lateral meningocele (NF-1)
• Extramedullary haematopoiesis

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POSTERIOR MEDIASTINAL LESIONS IN DETAIL

Neurogenic Tumours (Most Common Posterior Mediastinal Mass - 75%)

1. Schwannoma (Neurilemmoma): most common; arises from Schwann cells of dorsal nerve root
   • Encapsulated, benign
   • CT: well-defined oval mass, homogeneous, posterior mediastinum, paravertebral, +/- calcification, cystic areas
   • MRI T1: iso-hypointense; T2: hyperintense; enhancement variable
   • "Dumbbell" tumour: extends through neural foramen into spinal canal - seen in 10-15%
   • MRI spinal canal mandatory if dumbbell configuration suspected
2. Neurofibroma: plexiform in NF-1; not encapsulated
   • Similar imaging; may have "target sign" on MRI T2 (central low T2 with peripheral high T2)
   • Malignant transformation risk in NF-1
3. MPNST (Malignant Peripheral Nerve Sheath Tumour)
   • Heterogeneous, irregular, invasive
   • Associated with NF-1

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Radiological Features of Posterior Mediastinal Neurogenic Tumours

• Paravertebral, posterior mediastinal mass
• Sharp, well-defined oval/round opacity
• May widen the posterior mediastinum
• Rib erosion / splaying (slow-growing benign tumours cause smooth pressure erosion)
• Vertebral body erosion/scalloping
• Neural foraminal widening (dumbbell tumour)
• Calcification (neuroblastoma, ganglioneuroma)

• Well-defined, homogeneous/heterogeneous mass
• Located in the costovertebral sulcus (paravertebral region)
• Bony changes: foraminal widening, vertebral erosion, rib erosion
• Enhancement: moderate and homogeneous (schwannoma)
• Calcification: 10-20%

• Defines intraspinal extension (dumbbell tumour)
• T1: hypointense
• T2: hyperintense (neurofibromas may show target sign)
• Post-Gd: moderate enhancement
• Spinal cord displacement/compression assessment
• Multiplanar capability essential for surgical planning

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Oesophageal Lesions (Posterior Mediastinum)

• Oesophageal carcinoma: irregular wall thickening on CT; barium swallow: irregular mucosal destruction
• Achalasia: dilated oesophagus with air-fluid level - posterior mediastinal widening
• Hiatus hernia: retrocardiac mass with air-fluid level

Descending Aortic Aneurysm

• Enlarging left paraspinal opacity
• Curvilinear calcification in wall
• CT confirms diagnosis

Extramedullary Haematopoiesis

• In chronic haemolytic anaemias (thalassaemia, hereditary spherocytosis)
• Bilateral, lobulated, smooth paraspinal masses
• Lower thoracic level (T8-T12)
• No bony erosion
• CT: homogeneous soft tissue, enhances moderately

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Q11. PRINCIPLES AND INDICATIONS OF HRCT (HIGH RESOLUTION CT)

Definition

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Technical Principles

1. Slice Thickness

• Thin slices: 0.5-2 mm (conventional CT: 5-10 mm)
• Thin slices reduce volume averaging (each voxel more representative of actual tissue)
• Allows secondary pulmonary lobule to be resolved

2. Reconstruction Algorithm

• High spatial frequency (bone/detail) kernel: enhances edge sharpness and interfaces
• Produces sharper image of vessel walls, bronchial walls, septa
• Increases image noise compared to soft tissue algorithm - acceptable trade-off

3. Field of View (FOV)

• Targeted/small FOV (25-30 cm): zooms into each lung, maximising pixel resolution
• Full lung FOV used for mediastinal evaluation

4. kVp and mAs

• High kVp (120-140 kVp): better penetration
• Normal mAs or reduced mAs (dose reduction possible as noise is acceptable)

5. Multiplanar Reconstruction (MPR)

• Coronal and sagittal reconstructions from volumetric thin-slice data
• Newer MSCT: isotropic resolution - equal quality in any plane

6. Window Settings

• Lung window: W 1500 HU, L -700 HU - displays lung parenchyma
• Mediastinal window: W 400 HU, L 40 HU - displays soft tissues
• Bone window: W 1500 HU, L 400 HU

7. Inspiration vs. Expiration

• Inspiratory scans: standard assessment
• Expiratory scans: air trapping (mosaic attenuation), small airways disease (bronchiolitis)

8. Prone Scans

• Used to differentiate posterior gravity-dependent atelectasis from true fibrosis
• Gravity-dependent opacities resolve in prone position (normal)

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HRCT Pattern Recognition

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Secondary Pulmonary Lobule (SPL) on HRCT

• Smallest independently functioning lung unit
• Polyhedral, 1-2 cm
• Bounded by connective tissue septa containing pulmonary veins and lymphatics
• Core: centrilobular artery + bronchiole
• HRCT shows normal SPL anatomy - basis for pattern description

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INDICATIONS OF HRCT

A. Diffuse Interstitial Lung Disease (ILD)

1. UIP/IPF (usual interstitial pneumonia/idiopathic pulmonary fibrosis)
2. NSIP (non-specific interstitial pneumonia)
3. DIP (desquamative interstitial pneumonia)
4. COP (cryptogenic organising pneumonia)
5. AIP (acute interstitial pneumonia)
6. RB-ILD (respiratory bronchiolitis-ILD)
7. LIP (lymphoid interstitial pneumonia)

B. Pneumoconioses / Occupational Lung Disease

• Silicosis, CWP, asbestosis (earlier detection than CXR)

C. Emphysema

• Centrilobular (smoking), panlobular (alpha-1 antitrypsin), paraseptal
• Quantification of emphysema extent

D. Bronchiectasis

• Gold standard investigation for bronchiectasis
• Signet ring sign, tram-track opacities, mucus plugging
• Better than bronchography (old method)

E. Pulmonary Hypertension

• Assess underlying cause (ILD, emphysema)
• Mosaic perfusion in CTEPH

F. Hypersensitivity Pneumonitis (EAA)

• Acute, subacute, chronic phases
• Centrilobular nodules, GGO, mosaic attenuation

G. Small Airways Disease

• Expiratory HRCT: air trapping
• Constrictive and proliferative bronchiolitis

H. Malignancy

• Characterisation of SPN (see Q1)
• Ground glass nodules (adenocarcinoma spectrum)
• Lymphangitic carcinomatosis (beaded septa)

I. Immunocompromised Patients

• PCP (Pneumocystis jirovecii): GGO + crazy paving
• Fungal (Aspergillus): halo sign (early), air crescent sign (late)
• CMV, others

J. Sarcoidosis

• Perilymphatic nodules, bilat hilar adenopathy, fibrosis

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Q13 & Q14. RADIOLOGICAL FINDINGS IN PLEURAL PATHOLOGIES / CT AND USG FINDINGS

Pleural Space - Normal

• Thin potential space between visceral and parietal pleura
• Normal pleural fluid: <15 mL
• Pleura: <3 mm thick on CT

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1. PLEURAL EFFUSION

• Costophrenic angle blunting (>200-300 mL needed)
• Meniscus sign (fluid level curves up laterally)
• Homogeneous opacity in lower zone
• Shifting with position (decubitus view confirms free effusion)
• Lateral decubitus CXR: confirms free vs. loculated; detects as little as 50 mL
• Subpulmonary effusion: elevated "diaphragm" with lateral peak, >500 mL

• Anechoic (transudate) or echogenic/septated (exudate/empyema)
• Thickened visceral/parietal pleura = exudate
• Guidance for aspiration

• Attenuation: 0-15 HU = transudate; >15 HU = exudate/hemorrhagic
• Homogeneous crescentic opacity in dependent pleural space
• Lenticular (biconvex) shape: loculated effusion
• Enhanced split pleura sign: empyema

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2. EMPYEMA

• Loculated opacity, may have meniscus or no meniscus
• May be bilateral
• Often associated with underlying pneumonia

• Complex echogenic fluid with septa and debris
• Thick pleural rind
• "Snowstorm" appearance
• Guides pigtail catheter insertion

• Thickened, enhancing parietal AND visceral pleura
• Fluid between them (typically >20 HU, occasionally with gas bubbles from anaerobes)
• Extrapleural fat proliferation (increased density)
• Split pleura sign: PATHOGNOMONIC for empyema
• Adjacent compressive atelectasis

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3. PLEURAL PLAQUES (Asbestos)

• Bilateral, irregular calcified densities on parietal pleura
• Diaphragmatic surface, posterolateral chest wall
• "Holly leaf" pattern of calcification
• Para-spinal region ("en face" view)
• NOT on mediastinal pleura (mediastinal pleural involvement = mesothelioma)

• Discrete plaques on parietal pleural surface
• Calcified or non-calcified
• "Halo sign": thin non-calcified zone around calcified plaque
• Do NOT extend into fissures (helps distinguish from mesothelioma)
• Associated with rounded atelectasis / Blesovsky tumour

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4. MALIGNANT MESOTHELIOMA

• Unilateral pleural effusion (usually right > left due to greater asbestos exposure from right-sided work)
• Pleural thickening (lobulated, irregular)
• "Frozen chest" - ipsilateral volume loss despite effusion
• Rib destruction in advanced cases

• Hypoechoic lobulated pleural thickening
• Associated effusion
• Guides biopsy

• Circumferential/rind-like pleural thickening (encases lung)
• Nodular, irregular pleural masses
• Mediastinal pleural involvement (hallmark - distinguishes from plaques)
• Fissural involvement
• Pleural thickening >1 cm = suspicious for mesothelioma
• Invasion of chest wall, diaphragm, mediastinum
• Extension to pericardium
• Contraction of hemithorax (fibrous type) or expansion (with effusion)
• Nodal metastases: ipsilateral hilar, subcarinal

• Better for diaphragm/chest wall invasion assessment
• T1: heterogeneous
• T2: intermediate-hyperintense
• Predicts resectability better than CT

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5. PNEUMOTHORAX

• Visceral pleural line (thin line parallel to chest wall, lung edge)
• Absence of lung markings beyond this line
• Deep sulcus sign (supine): lucency at lateral/inferior costophrenic angle
• Tension pneumothorax: mediastinal shift away, ipsilateral diaphragm depression, rib space widening
• Size classification: Light index = (hemithorax diameter - lung diameter) / hemithorax diameter × 100%

• Confirms clinically ambiguous pneumothorax
• Identifies underlying cause (blebs, bullae, metastases, lymphangioleiomyomatosis)
• Measures size accurately

• Absent lung sliding + absent B-lines
• "Barcode/stratosphere sign" on M-mode
• Lung point = junction of pneumothorax and residual lung contact

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Q16. SILICOSIS (Detailed)

Definition

Sources of Exposure

• Mining (gold, coal, copper, lead)
• Quarrying, stone cutting
• Sandblasting (highest risk)
• Ceramics, pottery manufacture
• Glass manufacture
• Tunneling, construction

Types

1. Chronic/Classic Silicosis: 10-20 years exposure to low concentration; most common
2. Accelerated Silicosis: 5-10 years, higher concentration; rapid progression
3. Acute Silicosis (Silicoproteinosis): weeks to 5 years, very high concentration; resembles alveolar proteinosis; rapidly fatal

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Pathology

• Silica particles phagocytosed by alveolar macrophages
• Macrophages die and release silica → re-phagocytosis cycle
• Cytokine release → fibroblast activation → collagen deposition
• Hyaline silicotic nodule: concentric lamellae of collagen around dust-laden macrophages (whorled appearance)
• Upper lobe predominance
• PMF: progressive coalescence of nodules → massive upper lobe fibrosis

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Radiological Features

CXR (ILO Classification)

• Small round nodules (p, q, or r type)
• Upper and mid zone predominance
• Bilateral, symmetrical
• Hilar adenopathy, may show eggshell calcification
• ILO profusion ≥1/1 in Zone U = diagnostic

• Large opacity (>1 cm) - ILO A, B, or C
• Bilateral upper lobe masses
• "Wing-like" densities migrating toward hila
• Peripheral traction emphysema
• Upper lobe fibrosis, cicatrization atelectasis
• Bulla formation in peripheral emphysema

• Peripheral rim calcification of hilar/mediastinal nodes
• Seen in 5% but pathognomonic when present
• Also seen in sarcoidosis (post-radiation), post-radiation fibrosis

HRCT Findings (Grainger & Allison's - Diagnostic Radiology)

• Well-defined centrilobular and subpleural micronodules
• Upper and posterior lung predominance
• Subpleural pseudo-plaques (confluent subpleural micronodules)
• Hilar/mediastinal lymphadenopathy ± eggshell calcification
• PMF: upper lobe masses with central low density (necrosis)
• Associated panlobular emphysema (lower zones)
• Cavitation in PMF (DDx: TB reactivation)

Complications on Imaging

• Tuberculosis: silicosis increases risk of TB 30-fold (silicotuberculosis)
  • Cavitation within PMF mass
  • New consolidation/infiltrate
• Lung cancer: increased risk (though disputed); heterogeneous opacity
• Pneumothorax: from bullae rupture
• Cor pulmonale: right heart enlargement, pulmonary hypertension signs
• Progressive systemic sclerosis (Erasmus syndrome): silicosis + scleroderma

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Nuclear Medicine in Silicosis

• PET-CT: PMF can show mild FDG uptake (false positive for malignancy - caveat)
• Gallium scan: active inflammation in nodules

Medicolegal Role of Radiology

• ILO standardized classification used for compensation assessment
• Comparison with ILO standard films (pneumoconiosis panel)
• Pre-employment and periodic surveillance CXR mandatory in high-risk industries
• HRCT more sensitive but not standard for ILO classification

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