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Write full theory answers radiology university theory exam cover all topics related to it --each question of 30 Marks don't write in a short,add diagram and images of wherever possible and needed

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JUNE 2026 Paper 2 - Radiology Theory Exam

Full Model Answers (30 Marks Each)


QUESTION 1 (10 Marks Total)

1a. Pulmonary Imaging Findings in Immunocompromised Individual (2 Marks)

An immunocompromised patient includes those with HIV/AIDS, post-transplant, on chemotherapy, on long-term steroids, or with hematologic malignancies. The spectrum of pulmonary infections is wide and the imaging pattern depends on the type and degree of immunosuppression.
Approach to Imaging:
  • Chest X-ray (CXR) is the first line investigation
  • High Resolution CT (HRCT) chest is more sensitive, especially when CXR is normal
  • CT Pulmonary Angiography (CTPA) for suspected fungal angioinvasion
Key Imaging Patterns in Immunocompromised:
PatternTypical Organism
Bilateral interstitial/ground glassPCP, CMV, viral pneumonia
Nodules with halo signInvasive Aspergillosis
Cavitating nodulesTB, Aspergillus, Cryptococcus
Lobar/segmental consolidationBacterial (Strep, Pseudomonas)
Miliary patternTB, disseminated fungal
Pleural effusionKaposi sarcoma, bacterial, TB
LymphadenopathyTB, lymphoma, Kaposi
Tree-in-bud patternEndobronchial spread TB, atypical organisms
Diagram - Imaging Pattern Recognition:
IMMUNOCOMPROMISED CHEST - PATTERN APPROACH
 ┌─────────────────────────────────────────────┐
 │  CXR/CT Finding         → Likely Diagnosis  │
 │  ─────────────────────────────────────────  │
 │  Bilateral GGO (upper)  → PCP               │
 │  Halo sign nodule       → Aspergillus       │
 │  Miliary nodules        → TB / Fungal       │
 │  Consolidation + LAD    → Bacterial         │
 │  Diffuse nodules        → Kaposi / Lymphoma │
 │  Air crescent sign      → Aspergilloma      │
 └─────────────────────────────────────────────┘

1b. Imaging Findings of Infections in HIV+ and HIV- Individuals (4+4 Marks)

HIV POSITIVE (CD4-Dependent) Imaging Findings:

The type of infection correlates with CD4 count:
CD4 >500 cells/μL (near normal immunity):
  • Bacterial pneumonia: segmental/lobar consolidation, air bronchograms
  • Same spectrum as immunocompetent
CD4 200-500 cells/μL:
  • Pulmonary TB: upper lobe cavitary disease, lymphadenopathy, pleural effusion
  • Bacterial pneumonias more frequent
CD4 <200 cells/μL:
Pneumocystis jirovecii Pneumonia (PCP):
  • CXR: Bilateral perihilar interstitial infiltrates, "bat wing" distribution, progressing to ground glass opacification
  • HRCT: Bilateral ground glass opacification (GGO) - most characteristic
  • Crazy-paving pattern (GGO + interlobular septal thickening)
  • Upper lobe predominance
  • Pneumatoceles in ~35% (thin walled cysts - risk of pneumothorax)
  • Absent pleural effusion (distinguishing feature)
  • Absence of lymphadenopathy
CXR in PCP:
        Right          Left
  apex  ░░░░░░░░░░░░░░░░░░
  upper ░░░░░░░░░░░░░░░░░░  ← Bilateral symmetric
  mid   ▓▓▓▓▓▓▓▓▓▓▓▓▓▓▓▓    perihilar GGO
  lower ▓▓▓▓▓▓▓▓▓▓▓▓▓▓▓▓    (bat-wing pattern)
  base  ░░░░░░░░░░░░░░░░░░  ← Bases relatively spared

  ░ = clear   ▓ = infiltrates
CD4 <100 cells/μL - Additional organisms:
Cytomegalovirus (CMV) Pneumonitis:
  • CXR: Bilateral interstitial infiltrates, similar to PCP
  • HRCT: GGO with or without consolidation, nodules
  • Peribronchovascular distribution
Cryptococcosis:
  • CXR: Bilateral lower lobe nodules, interstitial pattern
  • May show miliary nodules
  • Lymphadenopathy (mediastinal/hilar) - more common in HIV+
  • Pleural effusion in ~30%
Non-Tuberculous Mycobacteria (MAC - Mycobacterium avium complex):
  • CD4 < 50
  • CXR: Diffuse reticulonodular pattern
  • Mediastinal lymphadenopathy (hallmark)
  • May be indistinguishable from TB
Kaposi Sarcoma (CD4 <150):
  • CXR: Peribronchovascular nodules along bronchovascular bundles, flame-shaped
  • HRCT: Peribronchovascular nodules, septal thickening, pleural effusion
  • Lymphadenopathy
  • "Cannonball" metastases in late disease
Pulmonary TB in HIV+:
  • Atypical presentation: lower lobe disease, hilar/mediastinal LAD, miliary pattern, no cavitation
  • Primary-type pattern even in reactivation (because immunity cannot wall off)
  • Pleural effusion common

HIV NEGATIVE (Immunocompromised by other causes):

This includes post-transplant, chemotherapy-induced neutropenia, long-term steroids.
Invasive Pulmonary Aspergillosis (IPA) - Most important in neutropenic:
  • CXR: Single or multiple nodules, poorly marginated
  • HRCT: Halo Sign (nodule surrounded by ground-glass halo of hemorrhage) - EARLY SIGN
  • Air crescent sign (crescent of air at periphery of nodule) - LATE SIGN (neutrophil recovery)
  • Wedge-shaped consolidation (infarction from angioinvasion)
CT - Halo Sign:
        ┌──────────────────┐
        │   GGO halo       │
        │  ┌──────────┐    │
        │  │ Dense    │    │
        │  │ nodule   │    │
        │  └──────────┘    │
        │                  │
        └──────────────────┘
  Nodule = fungal necrosis
  Halo = hemorrhagic infarction
Air Crescent Sign:
        ┌──────────────────┐
        │    ╭─────────╮   │
        │    │ Necrotic│   │
        │  ╭─┤ Ball    ├─╮ │
        │  │ ╰─────────╯ │ │
        │  ╰─────────────╯ │
        │   ↑ Air crescent │
        └──────────────────┘
Post-Transplant (Solid Organ / HSCT):
  • Early phase (<1 month): Bacterial pneumonia, pulmonary edema
  • Middle phase (1-6 months): CMV (bilateral GGO, peribronchovascular), PCP, fungal
  • Late phase (>6 months): Community-acquired, viral, Aspergillus
Nocardia:
  • CXR/CT: Consolidation, cavitation, multiple nodules
  • May mimic tumor or TB
Viral (CMV, RSV, Influenza):
  • Bilateral GGO, tree-in-bud, centrilobular nodules
Pulmonary Drug Toxicity (Methotrexate, Bleomycin):
  • Bilateral GGO
  • Organizing pneumonia pattern
  • Peribronchovascular distribution

QUESTION 2: Thoracic Findings in Connective Tissue Disorders (10 Marks)

Connective tissue disorders (CTDs) have significant thoracic manifestations affecting lungs, pleura, airways, vasculature, esophagus, and pericardium. The thorax is involved in virtually all major CTDs.

Rheumatoid Arthritis (RA)

ILD (most common thoracic complication):
  • Usual Interstitial Pneumonia (UIP) pattern: Most common
    • Bibasal subpleural honeycombing
    • Traction bronchiectasis
    • Reticulation
  • Non-Specific Interstitial Pneumonia (NSIP): Bilateral GGO, basal predominance
Pleura:
  • Pleural effusion (exudate, low glucose)
  • Pleural thickening
Airways:
  • Bronchiectasis (particularly lower lobes)
  • Follicular bronchiolitis
  • Constrictive bronchiolitis (BO)
Necrobiotic (Rheumatoid) Nodules:
  • Well-defined lung nodules, may cavitate
  • Peripheral subpleural
  • Caplan syndrome: Large nodules in coal miners + RA
Cardiovascular:
  • Pericardial effusion
RA Thoracic Findings - HRCT Pattern:
Upper lobes → Nodules, bronchiectasis
Middle       → Interstitial changes
Lower lobes  → UIP/NSIP: Honeycombing, GGO, traction bronchiectasis
Pleura       → Effusion, thickening

Systemic Lupus Erythematosus (SLE)

Pleuritis / Pleural Effusion:
  • Most common thoracic manifestation
  • Bilateral, exudative
  • "Shrinking lung syndrome" - diaphragmatic dysfunction
Lupus Pneumonitis (Acute):
  • Bilateral airspace consolidation, GGO
  • Lower lobe predominance
Chronic ILD:
  • NSIP pattern: bilateral basal GGO with reticulation
Pulmonary Hemorrhage:
  • Bilateral consolidation/GGO, rapid change
Pulmonary Hypertension:
  • Enlarged central pulmonary arteries
Cardiovascular:
  • Pericardial effusion (common)
  • Libman-Sacks endocarditis (CT may show valve thickening)

Systemic Sclerosis (Scleroderma / SSc)

ILD - Most significant cause of morbidity:
  • NSIP pattern (most common): Bilateral basal GGO, reticulation, traction bronchiectasis
  • UIP pattern (less common)
  • Subpleural sparing (distinguishes NSIP from UIP)
Pulmonary Arterial Hypertension (PAH):
  • Dilated central pulmonary arteries
  • Enlarged right heart
  • May be severe even with mild ILD
Esophageal Dilatation:
  • Characteristic finding on CT chest
  • Dilated air-filled esophagus seen behind heart/trachea
  • Aspiration pneumonia as consequence
Pericardial Effusion
Scleroderma on CT:
  - Dilated esophagus (behind heart)
  - Bilateral basal NSIP pattern
  - Enlarged main pulmonary artery (PAH)
  - Pericardial effusion

Dermatomyositis / Polymyositis (DM/PM)

  • ILD: NSIP most common pattern
  • Organizing Pneumonia (OP): Peribronchovascular consolidation
  • Acute interstitial pneumonia (AIP) in rapidly progressive disease
  • "Mechanic's hands" association - anti-Jo-1 antibody
  • Aspiration pneumonia (due to esophageal/pharyngeal muscle weakness)

Sjogren Syndrome

  • Lymphocytic Interstitial Pneumonia (LIP): Bilateral GGO, thin-walled cysts
  • NSIP pattern
  • Follicular bronchiolitis
  • Multiple pulmonary cysts (characteristic): Thin-walled, scattered, random distribution
  • B-cell lymphoma (a complication)
Sjogren LIP on CT:
  - Bilateral GGO (diffuse)
  - Multiple thin-walled cysts (scattered)
  - Occasional consolidation
  - Lower lobe and peribronchovascular predominance

Mixed Connective Tissue Disease (MCTD)

  • Features overlap SLE, SSc, PM
  • PAH: Most serious manifestation (similar to SSc)
  • Pleuritis, ILD (NSIP)

Summary Table - CTD Thoracic Manifestations

CTDILD PatternPleuraAirwayVascularOther
RAUIP/NSIPEffusionBronchiectasis, BO-RA nodules, Caplan
SLENSIPEffusion, shrinking lung-PAHPneumonitis, hemorrhage
SScNSIP > UIPEffusion-PAH (severe)Dilated esophagus
DM/PMNSIP, OP---Aspiration
SjogrenLIP, NSIP-Follicular bronchiolitis-Cysts, lymphoma

QUESTION 3 (10 Marks Total)

3a. Enumerate Causes of Pulmonary Arterial Hypertension (PAH) (2 Marks)

Definition: PAH is defined as mean pulmonary artery pressure (mPAP) ≥20 mmHg at rest.
WHO/DANA POINT Classification (Updated Nice 2022):
Group 1 - Pulmonary Arterial Hypertension (PAH):
  • Idiopathic PAH (IPAH) - most common in young women
  • Heritable PAH (BMPR2 gene mutation - most common)
  • Drug and toxin-induced (anorexigens, methamphetamine, dasatinib)
  • Associated with:
    • Connective tissue disease (SSc, SLE, RA)
    • HIV infection
    • Portal hypertension (porto-pulmonary)
    • Congenital heart disease (L→R shunts)
    • Schistosomiasis
    • Pulmonary veno-occlusive disease (PVOD)
Group 2 - PH due to Left Heart Disease:
  • Heart failure with reduced EF, preserved EF
  • Valvular disease (mitral stenosis, aortic stenosis)
Group 3 - PH due to Lung Disease / Hypoxia:
  • COPD, Interstitial lung disease
  • Sleep-disordered breathing
  • High altitude
Group 4 - Chronic Thromboembolic PH (CTEPH):
  • Organized thrombus in pulmonary arteries
Group 5 - Unclear/Multifactorial:
  • Hematologic (myeloproliferative, splenectomy)
  • Systemic (sarcoidosis, histiocytosis)
  • Metabolic (Gaucher, thyroid)

3b. CXR and CT Findings of PAH (4+4 Marks)

CXR Findings of PAH:

Central Pulmonary Arteries:
  • Enlarged main pulmonary artery (MPA): >29 mm in diameter at level of right PA
  • Right descending pulmonary artery >17 mm (men) or >15 mm (women)
  • Left pulmonary artery enlargement
  • "Pruning" of peripheral vessels: Peripheral vascularity reduced while central vessels dilated - sharp tapering/cut-off
Cardiac Changes:
  • Right ventricular enlargement: Filling of retrosternal space on lateral CXR
  • Right atrial enlargement: Bulging right heart border
  • Cardiomegaly
  • Loss of normal pulmonary artery notch
Lung Parenchyma:
  • Peripheral oligemia (decreased vascularity)
  • In chronic CTEPH: May show wedge-shaped infarcts
CXR Diagram - PAH:
         ←←← enlarged ←←←←←←←←
   ┌──────────────────────────────┐
   │    ╭───────────╮             │
   │    │ Trachea   │             │
   │   ╭╰───────────╯╮            │
   │   │   Aorta     │            │
   │  ┌┴─────────────┴┐           │
   │  │  ENLARGED MPA │           │
   │  └┬─────────────┬┘           │
   │  ╭╯             ╰╮           │
   │ ╭╯               ╰╮ enlarged │
   │ │ RA enlarged →→  │ RV       │
   │ ╰─────────────────╯          │
   │   ↑ Peripheral pruning ↑     │
   └──────────────────────────────┘
Criteria on CXR:
  • Main pulmonary artery diameter > 29 mm
  • Right descending PA diameter > 16 mm
  • PA to trachea ratio > 1.0 (normal < 0.7)

CT Findings of PAH:

CT Pulmonary Angiography (CTPA) is the key modality
Direct Signs - Pulmonary Vessels:
  • Main pulmonary artery (MPA) diameter >29 mm - most reliable
  • MPA to ascending aorta ratio >1.0 (sensitivity 70%, specificity 92%)
  • Bilateral pulmonary artery enlargement
  • Pruning / abrupt tapering of peripheral pulmonary arteries
CT Cross-section at PA level:
     Ascending Ao
       ┌──────┐
       │      │   ← Ao diameter
       └──────┘
         ≈ 35mm
     Main PA
       ╭──────╮
       │      │   ← PA diameter > 29mm = PAH
       ╰──────╯       PA:Ao ratio > 1.0 = PAH
Cardiac Changes on CT:
  • Right ventricular hypertrophy/dilation: RV:LV ratio >1 in short axis
  • Interventricular septal bowing (D-shaped LV): Leftward septal deviation at end-systole
  • Right atrial dilation
  • Tricuspid regurgitation (contrast reflux into IVC and hepatic veins)
  • Pericardial effusion (severe PAH)
Normal:               PAH (D-sign):
   ┌────┐ ┌────┐         ┌────┐  ╔════╗
   │ RV │ │ LV │         │    │  ║    ║
   └────┘ └────┘         │ RV │  ║ LV ║
   RV:LV = 0.6           └────╯  ╚════╝
                         RV:LV > 1, LV D-shaped
                         ↑ RV pressure flattens IVS
Parenchymal Changes on CT:
  • Mosaic attenuation: Geographic areas of high and low attenuation (air trapping)
  • Peripheral oligemia (hypovascular areas)
  • In CTEPH: Wedge-shaped parenchymal scarring, linear bands
Mediastinum/Lymph Nodes:
  • Dilated central pulmonary veins (Group 2/PVOD)
CTEPH Specific Signs:
  • Web, band, pouch defects in pulmonary arteries
  • Mural thrombus (eccentric filling defect)
  • Abrupt vessel cutoffs
  • Bronchial artery enlargement (collateral supply)
  • Mosaic perfusion on CT (best seen on expiratory scans)
PVOD Specific Signs:
  • Centrilobular GGO nodules
  • Interlobular septal thickening
  • Pleural effusion
  • Lymphadenopathy
  • Dilated pulmonary veins

QUESTION 4: Pediatric Fractures and Non-Accidental Injury (5+5 Marks)

Part A: Specific Features of Fractures in Pediatrics (5 Marks)

Pediatric bone has unique properties that produce fracture patterns distinct from adults:
  • Periosteum is thicker and more vascular
  • Bone is more porous and plastic (deforms before breaking)
  • Growth plates (physes) are present and are weaker than ligaments
  • Remodeling capacity is greater

Unique Pediatric Fracture Types:

1. Torus (Buckle) Fracture:
  • Most common fracture in children
  • Compression force → cortex buckles (kinks) on one side without breaking
  • Metaphyseal location
  • Distal radius most common site
  • X-ray: Subtle cortical buckling/angulation, no displaced fracture line
  • Inherently stable
Torus Fracture:
    ─────────── Normal cortex
    ─────╮╭──── Buckle (cortical kink)
    ─────╯╰──── 
    ─────────── 
2. Greenstick Fracture:
  • Incomplete fracture (like green stick breaking)
  • Cortex breaks on tension side, remains intact on compression side
  • Bowing with cortical breach on one side
  • Shaft of long bone most common
Greenstick Fracture:
         ────────────
        /  Angulated 
       /   
      ╱  ← Fracture line through one cortex only
     ────────────
     (Compression side intact)
3. Plastic (Bowing) Deformity:
  • Multiple microfractures along the bone - bone bends without discrete fracture line
  • Ulna and fibula most common
  • X-ray: Bowed cortex without visible fracture line
  • Easy to miss!
4. Physeal (Salter-Harris) Fractures:
  • Involve the growth plate (physis)
  • Physis is weakest link in pediatric skeleton
Salter-Harris Classification:
TypeDescriptionX-rayMnemonic
IFracture through physis onlyWidened physisStraight through
IIPhysis + metaphysisMetaphyseal fragment (Thurston Holland)Above (metaphysis)
IIIPhysis + epiphysisEpiphyseal fragmentLower (epiphysis)
IVMetaphysis + physis + epiphysisComplete fracture through all threeThrough all
VCrush injury to physisMay appear normal, growth arrest laterRammed/Crush
Salter-Harris Types (diagrammatic):
      Epiphysis
      ═══════════  ← Physis (growth plate)
      Metaphysis

Type I:    Type II:   Type III:   Type IV:   Type V:
  ══║══      ══╝══      ╔══════     ╔══╗══     ══╬══
  ══║══      ══╝══      ║══════     ║══╝══     (Crush)
5. Apophyseal Avulsion Fractures:
  • Traction through apophysis at muscle/tendon insertion
  • Common in adolescent athletes
  • Anterior inferior iliac spine (AIIS) - rectus femoris
  • Anterior superior iliac spine (ASIS) - sartorius
  • Ischial tuberosity - hamstrings
6. Other Pediatric Characteristics:
  • Callus formation is rapid and exuberant
  • Periosteal reaction more pronounced than adults
  • Toddler's fracture: Spiral/oblique non-displaced tibial fracture from minor trauma in toddlers
  • Clavicle and forearm are most common fracture sites overall

Part B: Imaging Findings in Non-Accidental Injury (NAI) in Infants (5 Marks)

Non-Accidental Injury (NAI), also called Child Abuse or Battered Child Syndrome, is a medical and social emergency. Radiology plays a key role in detection and documentation.
Skeletal Survey is Mandatory (AP skull, lateral skull, full spine, chest AP/oblique, pelvis, extremities).

Classic/Specific NAI Fractures:

1. Posterior Rib Fractures (MOST SPECIFIC for NAI):
  • Result from squeezing the chest
  • Hands grip around chest and thumbs/fingers fracture posterior ribs near costovertebral junction
  • X-ray: Fractures at posterior rib angle (medial 1/3)
  • "Buckle handle" appearance
  • New and old fractures in same child = pathognomonic
  • Often only seen on oblique views or bone scan
Posterior Rib Fractures (squeezed chest):
         ┌──────────────────┐
         │  Spine           │
     ←─← │ ←← Force ←←     │
     Hands grip thorax      │
         │  ╲╲╲╲ Posterior  │
         │   fractures here │
         └──────────────────┘
2. Classic Metaphyseal Lesions (CML) / Corner Fractures:
  • Highly specific for NAI
  • Result from traction/rotational forces (gripping and twisting)
  • Avulsion of cartilaginous metaphysis
  • X-ray: Bucket-handle or corner fragment at metaphysis
  • Distal femur, proximal and distal tibia most common
Classic Metaphyseal Lesion:
    ┌──────────────────────┐
    │   Shaft              │
    ╞══════════════════════╡  Metaphysis
    ↑╰──corner fragment ──╯↑
    (bucket handle or corner chip)
3. Multiple Fractures of Different Ages:
  • Fractures at different stages of healing
  • Periosteal reaction age:
    • Soft callus: 10-14 days
    • Hard callus: 14-21 days
    • Remodeling: >3 weeks
4. Subperiosteal New Bone Formation:
  • Along diaphyses (gripping and twisting the baby)
5. Spiral/Oblique Fractures in Non-ambulatory Infants:
  • Spiral humeral fracture in child <18 months WITHOUT adequate explanation
  • "Toddler's fracture" of tibia from walking is explained, but spiral humerus in infant is suspicious
6. Skull Fractures:
  • Multiple, bilateral, branching, crossing sutures, complex = suspicious for NAI
  • Simple linear skull fractures alone may be accidental
  • Intracranial injuries (subdural hematoma especially) are key finding
7. Subdural Hematoma (SDH) - Shaken Baby Syndrome:
  • CT/MRI: Subdural collections of DIFFERENT AGES (mixed density on CT)
  • Bilateral SDH in infant = highly suspicious
  • Diffuse axonal injury
  • Retinal hemorrhages (fundoscopy)
CT Head - Shaken Baby:
    ┌─────────────────────┐
    │  Bilateral subdural │
    │  ╭──────────╮       │
    │  │  Brain   │       │
    │  ╰──────────╯       │
    │ ↑                 ↑ │
    │ SDH (crescent sign) │
    │ (Mixed density =    │
    │  different ages)    │
    └─────────────────────┘
8. Bruised/Soft Tissue Injuries visible on MRI:
  • Deep soft tissue bruising not visible on X-ray

NAI Imaging Protocol:

  1. Skeletal Survey (full): Initial + repeat at 2 weeks
  2. CT Head: All suspected head injury
  3. MRI Brain: Better characterization of brain injury
  4. Bone scan (scintigraphy): Detects early/healing fractures missed on X-ray
  5. Ophthalmology: Retinal hemorrhage

Differential Diagnosis of NAI:

  • Osteogenesis imperfecta (OI): Blue sclerae, wormian bones, osteopenia
  • Rickets: Metaphyseal irregularity, cupping, fraying
  • Metabolic bone disease of prematurity
  • Scurvy: Periosteal hemorrhage, Pelkan spurs

QUESTION 5 (10 Marks Total)

5a. Lines/Tubes/Catheters in ICU Patient and Their Correct Position on CXR (6 Marks)

Portable chest X-ray is the most commonly performed investigation in the ICU. Correct positioning of lines and tubes is critical for patient safety.

1. Endotracheal Tube (ETT)

Purpose: Airway management, mechanical ventilation
Correct Position:
  • Tip should be 5 cm above carina (mid-trachea)
  • Alternatively: at T3-T4 vertebral level
  • 2-5 cm above carina is acceptable range
  • With neck in neutral position
Common Errors:
  • Too deep: Right mainstem intubation (right is more vertical) → left lung collapse
  • Too superficial: Tip in larynx or pharynx → inadequate ventilation
CXR - ETT Position:
    Carina at T4-T5
    ┌──────────────────┐
    │   Trachea        │
    │     │            │
    │     │ ← ETT tip  │  ← Should be here (5cm above carina)
    │     │            │
    │   Carina ───────→│  T4-T5 level
    │   /     \        │
    │  L.main  R.main  │
    └──────────────────┘

2. Central Venous Catheter (CVC) / Central Line

Purpose: CVP monitoring, IV access, vasopressors, TPN
Insertion sites: Internal jugular vein, subclavian vein, femoral vein
Correct Position:
  • Tip at cavoatrial junction (junction of SVC and right atrium)
  • Radiologically: At level of right tracheobronchial angle / T4-T5
  • Should NOT be in right atrium (arrhythmia risk)
  • Should NOT be in right ventricle
CVC Position:
    SVC
     │
     │ ← Correct: cavoatrial junction
     │   (right tracheobronchial angle)
    RA
     │
    RV  ← Too deep (arrhythmia risk)

3. Pulmonary Artery Catheter (Swan-Ganz Catheter)

Purpose: Hemodynamic monitoring (PCWP, CO)
Correct Position:
  • Tip in right or left main pulmonary artery
  • Should NOT be in peripheral pulmonary artery (wedged position at rest = risk of PA rupture)
  • Should be within 2 cm of hilum

4. Nasogastric Tube (NGT)

Purpose: Gastric decompression, feeding, drug delivery
Correct Position:
  • Tip should be below left hemidiaphragm
  • Ideally in stomach, at least 10 cm below gastroesophageal junction
  • Distal side hole below GEJ
Common Errors:
  • Coiled in esophagus
  • Tip in right bronchus → lung placement (DANGEROUS - infusion into lung)
  • Loop in nasopharynx
NGT Position Check on CXR:
    ─────── Carina level
    │ NGT → must cross midline at carina level
    │       then descend to left
    │
    ─────── Diaphragm
    
    ✓ Correct: tip below diaphragm, leftward stomach position
    ✗ Wrong: tip right of spine below carina = right bronchus

5. Intra-Aortic Balloon Pump (IABP)

Purpose: Cardiac assist device, counterpulsation
Correct Position:
  • Tip 2-3 cm distal to origin of left subclavian artery
  • At level of aortic knuckle / T4-T5
  • NOT in aortic arch (too proximal - risk of cerebral emboli)
  • NOT too distal (below renal arteries - renal ischemia)

6. Chest Drains

Purpose: Draining pneumothorax, pleural effusion, hemothorax
Correct Position for pneumothorax:
  • Anterior, apical - 2nd intercostal space midclavicular line (anterior)
  • Or in 4th-5th ICS mid-axillary line
Correct Position for pleural effusion:
  • Posterior basal - 4th-5th ICS posterior-lateral
X-ray Check:
  • All side holes should be within pleural cavity (beyond chest wall)
  • Track should not cross midline

7. Pacemaker / Implantable Defibrillator Leads

RA lead: Tip in right atrial appendage (anterior-superior RA, "J" curve on lateral) RV lead: Tip at right ventricular apex (over cardiac apex on PA, pointing anteriorly on lateral) LV lead (CRT): In coronary sinus, lateral/postero-lateral wall

Summary Table:

DeviceCorrect Tip PositionCXR Level
ETTMid-tracheaT2-T4
CVCCavoatrial junction (SVC)T4-T5
NGTStomach (below GEJ)Below diaphragm
Swan-GanzMain PA (within hilum)Hilar level
IABPDescending Ao, below L subclavianT4 (aortic knuckle)
Chest drainApex (pneumothorax) / Base (effusion)2nd ICS / 5th ICS

5b. Difference Between Cardiogenic and Non-Cardiogenic Pulmonary Edema (4 Marks)

Pathophysiology:

  • Cardiogenic: Elevated left atrial pressure → hydrostatic pressure overwhelms oncotic pressure → fluid leaks into interstitium and alveoli
  • Non-Cardiogenic (ARDS): Inflammation/injury to alveolar-capillary membrane → increased permeability → fluid leaks regardless of hydrostatic pressure

Radiological Differences:

FeatureCardiogenicNon-Cardiogenic (ARDS)
Heart sizeEnlarged (cardiomegaly)Normal
DistributionCentral, perihilar ("bat wing")Peripheral, diffuse, bilateral
Interstitial linesKerley B lines (septal)Absent or minimal
Pleural effusionPresent (bilateral)Absent or minimal
Vascular redistributionPresent (upper lobe diversion)Absent
Air bronchogramsAbsent (early)Prominent
Response to treatmentRapid improvement with diureticsSlow, poor response
Onset radiologicallyGradual (can track stages)Rapid, within 24h of insult
CVP/PCWPElevated (>18 mmHg)Normal (<18 mmHg)
Stages of Cardiogenic Pulmonary Edema (radiological):
Stage 1 (PCWP 12-18 mmHg): Vascular redistribution
    Upper > Lower zone vessels (upright CXR)
    "Stag's antler" pattern

Stage 2 (PCWP 18-25 mmHg): Interstitial edema
    Peribronchial cuffing
    Kerley B lines (horizontal lines at bases, < 2cm)
    Kerley A lines (from hilum outward)
    Hilar blurring

Stage 3 (PCWP >25 mmHg): Alveolar edema
    Bilateral airspace consolidation
    "Bat wing" / perihilar distribution
    Air bronchograms

CXR - Kerley B Lines:
   ─────────────────── 
   |                 |
   |─────            |
   |─────  ← Kerley B│  (<2cm, horizontal, peripheral, base)
   |─────            |
   └─────────────────┘

QUESTION 6: 25-Year Female with Gangrene in Fingers - Causes, Differentials and Imaging Features (10 Marks)

Clinical Context

A 25-year-old young female with digital gangrene. In this age group, inflammatory/autoimmune causes dominate over atherosclerosis (which would be atypical).

Causes and Differentials:

1. Systemic Sclerosis (Scleroderma) - MOST LIKELY

Mechanism: Digital artery vasospasm (Raynaud's) + intimal fibrosis + thrombosis
Clinical: Sclerodactyly, tight skin, Raynaud's phenomenon (white-blue-red)
Imaging Features:
  • Doppler Ultrasound: Absent/markedly reduced or absent flow in digital arteries, severely reduced resistive index
  • Digital subtraction angiography (DSA) / CT Angiography:
    • Bilateral smooth tapered occlusions of digital arteries
    • "Corkscrew" collateral arteries (tortuous corkscrew collaterals pathognomonic)
    • Abrupt cut-off of palmar arches and digital vessels
    • Proximal vessels (radial/ulnar) relatively spared initially
  • X-ray hands: Calcinosis cutis (subcutaneous calcifications), acro-osteolysis (resorption of distal phalanges), soft tissue calcification
  • Chest CT: Dilated esophagus, NSIP pattern ILD, enlarged PA
Corkscrew Vessels (Scleroderma):
    Normal:  ─────────────────
    SSc:    ~~~~~~~~~~~~~~~~~  (tortuous collaterals)
                   ↓ (occlusion)
             (no flow beyond)

2. Thromboangiitis Obliterans (Buerger's Disease)

Mechanism: Inflammatory thrombotic occlusion of small/medium vessels - strongly associated with smoking
Imaging Features (DSA/CTA):
  • Normal proximal vessels (aorta, femoral, brachial)
  • Abrupt occlusion of distal small vessels (digital, palmar, plantar)
  • "Corkscrew collaterals" are also characteristic (similar to SSc)
  • Segmental occlusions with normal intervening segments
  • No calcification of vessel walls (unlike atherosclerosis)

3. Raynaud's Phenomenon (Primary and Secondary)

Primary: No underlying cause, younger women, episodic, symmetric, no tissue loss Secondary: Associated with CTD, medications
Imaging: Doppler shows functional vasospasm, reverses with warmth
  • Digital plethysmography: Diminished waveforms

4. Antiphospholipid Antibody Syndrome (APS)

Mechanism: Hypercoagulable state → thrombosis in small and large vessels
Clinical: Young woman, recurrent miscarriages, stroke, DVT, livedo reticularis
Imaging Features:
  • Digital artery thrombosis on DSA/CTA
  • Multiple occlusions at different vascular levels
  • May show embolic occlusions
  • CT/MRI brain: Multiple ischemic infarcts (different ages)
  • Echocardiography: Valve thickening (Libman-Sacks)

5. Vasculitis

a) Giant Cell Arteritis (GCA): Unlikely at 25 years (>50 yo)
b) Takayasu Arteritis:
  • Young Asian women
  • Large vessel vasculitis
  • CT Angiography: Wall thickening and enhancement of aorta and branches, stenosis/occlusion of subclavian (causing arm claudication), dilated aorta
  • Digital involvement possible as downstream effect
c) Small Vessel Vasculitis (ANCA-associated):
  • Microscopic polyangiitis, Wegener's, Churg-Strauss
  • Imaging: Renal infarcts, pulmonary infiltrates, digital ischemia

6. Embolism (Cardiac origin)

  • Atrial fibrillation, left atrial thrombus, infective endocarditis, atrial myxoma
  • Echocardiogram: Thrombus in LA/LV, valve vegetations
  • DSA: Embolic occlusion (filling defect), clean vessel walls

7. Ergotamine Toxicity / Drug-induced

  • Vasospasm from vasoconstricting drugs
  • DSA: Smooth, elongated bilateral narrowing of multiple vessels (rat-tail appearance)

8. Cryoglobulinemia

  • Cold-induced precipitation of immunoglobulins → thrombosis
  • Associated with hepatitis C
  • Imaging: Digital artery occlusions, purpura

Imaging Approach for This Patient:

Step 1: Plain X-rays hands/wrists
         → Calcinosis (SSc), Acro-osteolysis, Joint disease

Step 2: Doppler USS of upper limb arteries
         → Assess flow, resistive index

Step 3: CT Angiography (CTA) or MR Angiography
         → Map extent of disease

Step 4: DSA (if intervention planned)
         → Gold standard

Step 5: Echocardiogram
         → Cardiac source of embolus

Step 6: CT Chest
         → ILD (CTD), aortic disease (Takayasu)

QUESTION 7: 50-Year-Old Male with Massive Hemoptysis - Approach to Imaging and Management (10 Marks)

Definition

Massive hemoptysis: >200-600 mL/24h (definitions vary, but "life-threatening" is more useful clinically - any bleed that compromises airway or hemodynamic stability).

Causes of Massive Hemoptysis:

CategoryCause
InfectiousTB (most common worldwide), bronchiectasis, lung abscess, aspergilloma
NeoplasticBronchogenic carcinoma (most common in older smokers)
VascularPulmonary AVM, Dieulafoy lesion
IatrogenicSwan-Ganz catheter, transbronchial biopsy
CardiovascularMitral stenosis, pulmonary infarction
MiscellaneousGoodpasture, Wegener's, SLE
In this 50-year-old male: TB (if endemic area), bronchogenic carcinoma, and aspergilloma are top differentials.

Imaging Approach:

Step 1: Chest X-Ray (CXR)

  • Immediate, bedside
  • May show:
    • Opacification of bleeding lung
    • Cavitary lesion (TB, abscess, aspergilloma)
    • Mass (carcinoma)
    • Consolidation (pneumonia, infarction)
    • Bronchiectasis (tram-track lines)

Step 2: CT Chest (Multidetector MDCT) - MOST IMPORTANT

  • CTPA (CT Pulmonary Angiography): Maps vascular anatomy, identifies bleeding site
  • Multiplanar reconstruction helps localize
  • Identifies: Cavities, fungus ball, tumor, bronchiectasis
CT Findings by Etiology:
CauseCT Finding
TBFibrocavitary upper lobe disease, tree-in-bud, lymphadenopathy
AspergillomaFungus ball (mobile, gravity-dependent) in pre-existing cavity, "Monod sign"
Bronchogenic CaEndobronchial mass, hilar/mediastinal LAD, atelectasis
BronchiectasisDilated bronchi, "signet ring sign," cystic spaces
PAVMFeeding artery + draining vein + nidus
Aspergilloma (Fungus Ball) on CT:
    ╭──────────────────╮
    │    Cavity        │
    │  ╭────────╮      │
    │  │ Fungus │      │
    │  │  ball  │      │ ← Dependent position
    │  ╰────────╯      │
    │                  │
    ╰──────────────────╯
    Air crescent between ball and wall (Monod sign/halo)
    Ball changes position with posture

Step 3: Bronchoscopy

  • Localize side of bleeding (right vs left)
  • May be therapeutic (tamponade, coagulation, blockers)
  • Limitation: Cannot identify bleeding vessel, limited in massive hemoptysis

Step 4: Bronchial Artery Angiography (DSA) - Definitive for Intervention

Bronchial Artery Anatomy:
  • Arise from descending thoracic aorta at T5-T6
  • Right intercostobronchial trunk (most common variant)
  • 1-3 on right, 1-2 on left
Angiographic Findings of Active/Recent Bleeding:
  • Bronchial artery hypertrophy (>2 mm = abnormal)
  • Tortuous, dilated bronchial arteries
  • Systemic-pulmonary collaterals
  • Active contrast extravasation (hemorrhage into bronchi)
  • Hypervascularity / tumor blush
  • Pseudoaneurysm
  • Bronchopulmonary shunts
Bronchial Arteriogram - Abnormal:
    Aorta
      │
      ├──→ Dilated bronchial art.
      │         │
      │         ├──→ Hypervascularity
      │         │
      │         └──→ Active bleed (contrast in bronchus)
      │
      └──→ Collateral from intercostal aa.

Management:

1. Initial Stabilization (ABC):

  • Position: Bleeding lung DOWN (protective position)
  • Supplemental oxygen
  • IV access, blood products
  • Intubation if needed (selective bronchial intubation of healthy side)

2. Bronchial Artery Embolization (BAE) - Treatment of Choice

Procedure:
  • Femoral artery approach
  • Catheterize bronchial arteries
  • Super-selective catheterization of feeding vessels
  • Embolization: PVA particles (350-500 μm), coils, gelfoam
Precaution: Spinal artery of Adamkiewicz (arises from intercostal/bronchial trunk at T9-T12 on left) - must avoid embolization → paraplegia risk
Success rate: 70-90% initial control
Re-bleeding rate: 10-30% at 1 year (treat underlying cause)

3. Surgery

  • Indication: BAE failure, PAVM, localized resectable disease
  • Options: Lobectomy, pneumonectomy, wedge resection

4. Endovascular - Pulmonary Artery

  • For rare cases (PAVM, Rasmussen aneurysm in TB)
  • Coil embolization of PAVM

Rasmussen Aneurysm (TB-related):

  • Pseudoaneurysm of pulmonary artery within TB cavity
  • Treatment: Coil embolization of pulmonary artery aneurysm

QUESTION 8: AV Fistula Mapping and Complications and Imaging Features (5+5 Marks)

Part A: AV Fistula Mapping (5 Marks)

Arteriovenous (AV) fistula for hemodialysis access is created surgically by anastomosing an artery to a vein (usually in forearm or upper arm).
Common Types:
  • Radiocephalic (Cimino-Brescia): Radial artery to cephalic vein (wrist) - gold standard
  • Brachiocephalic: Brachial artery to cephalic vein (elbow)
  • Brachiobasilic: Brachial artery to basilic vein (arm)
  • AV Graft: Synthetic (PTFE) graft connecting artery to vein

Pre-operative Mapping (Vascular Access Planning):

Purpose: Identify suitable artery and vein for fistula creation
Modality: Duplex Ultrasound (First Line)
Arterial Assessment:
  • Radial artery diameter ≥ 1.5-2.0 mm at wrist
  • Peak systolic velocity (PSV) > 50 cm/s
  • Absence of stenosis, calcification, obstruction
  • Assessment of palmar arch patency (Allen's test + Doppler)
Venous Assessment:
  • Cephalic vein diameter ≥ 2.5-3.0 mm at wrist/forearm
  • Tourniquet applied to distend vein
  • Continuous lumen without gaps or stenosis
  • Course/tortuosity mapped for surgical planning
  • Absence of valves in critical segments
Duplex Findings in Mature AVF:
  • Fistula flow rate > 500-600 mL/min for hemodialysis adequacy
  • Dilated, thickened vein with arterial waveform
  • Increased flow velocity in feeding artery
CT/MR Angiography:
  • Used when US inconclusive or central vein obstruction suspected
  • Central vein mapping (subclavian, brachiocephalic, SVC)
  • 3D reconstruction shows entire outflow pathway
AV Fistula Anatomy:
    Radial Artery → Anastomosis → Cephalic vein
    ─────────────→ ╔══╗ ←─────────────────
                   ║  ║  Fistula
    Anastomosis   ╚══╝
    (end-to-side or side-to-side)
    
    Blood flow: Artery → Fistula → Dilated vein → AV site
MR Angiography for Central Veins:
  • No radiation
  • Excellent for subclavian, brachiocephalic, SVC stenosis
  • Used pre-transplant or when CTA contraindicated

Part B: AV Fistula Complications and Imaging Features (5 Marks)

1. Stenosis (Most Common - 50-80% of failures)

Location:
  • Juxta-anastomotic (within 2 cm of anastomosis) - most common
  • Outflow vein stenosis
  • Central vein stenosis (subclavian/SVC)
Imaging:
  • Duplex USS:
    • Focal velocity increase at stenosis (PSV > 400 cm/s or PSV ratio > 2.0)
    • Post-stenotic turbulence
    • Reduced fistula flow rate (<500 mL/min)
    • Vein diameter narrowing
Stenosis on Doppler:
    Normal:   ─────────── (laminar flow, PSV ~200 cm/s)
    Stenosis:  ──╮╭───── (focal narrowing)
                 ╰╯
    Post-stenotic: turbulence, high PSV (>400)
Fistulogram (DSA): Gold standard - shows % stenosis, guides intervention

2. Thrombosis

  • Complete occlusion of fistula
  • Clinical: Non-palpable thrill, no bruit
  • Duplex USS: No flow on color Doppler, echogenic thrombus in lumen
  • Management: Pharmacomechanical thrombolysis (alteplase), surgical thrombectomy

3. Aneurysm / Pseudoaneurysm

  • True aneurysm: Fusiform dilatation of venous segment (>3x normal diameter)
  • Pseudoaneurysm: Pulsatile hematoma with extravascular blood, develops after needle puncture
  • Duplex USS: Swirling flow in pseudoaneurysm ("yin-yang" sign on color Doppler)
  • Risk of rupture or skin ulceration
Pseudoaneurysm - Yin-Yang Sign:
    ╭────────────────╮
    │  ╭──╮   ╭──╮  │
    │  │→→│   │←←│  │  Color Doppler:
    │  ╰──╯   ╰──╯  │  Red and Blue swirling
    ╰────────────────╯
       (yin-yang appearance)

4. Steal Syndrome

  • Reversal of flow in distal artery (away from hand)
  • Mechanism: High-flow fistula "steals" blood from distal hand → ischemia, hand pain, paresthesia, gangrene
  • Duplex USS:
    • Reversed diastolic flow in radial artery distal to anastomosis
    • Absent/reduced palmar arch flow
    • PSV in distal radial artery is negative (reversal)
  • Management: DRIL procedure (Distal Revascularization with Interval Ligation), banding
Steal Syndrome Flow Pattern:
    Radial artery:
    Proximal → → → → Anastomosis
                        ↓ (fistula)
    Distal   ← ← ← ← (reverse flow!)
                        ↑ Flow steals from hand

5. High-Output Cardiac Failure

  • Very high fistula flow (> 2 L/min)
  • Causes volume overload → cardiac failure
  • Echo: Dilated LV, pulmonary hypertension
  • Management: Banding/ligation

6. Venous Hypertension / Arm Swelling

  • Central vein obstruction (subclavian/SVC stenosis)
  • Arm edema, distended collateral veins on chest wall
  • CT/MR Venography: Central vein stenosis
  • Fistulogram: Central stenosis, collateral veins

7. Infection

  • Rare in native AVF, more common in grafts
  • USS: Perigraft fluid, abscess, pseudoaneurysm
  • CT: Air in graft, fluid collection

8. Non-Maturation (Failed Fistula)

  • Fistula fails to dilate adequately for dialysis use
  • Criteria for maturation: Diameter ≥ 6mm, flow ≥ 600 mL/min
  • USS: Outflow vein diameter < 6mm, stenosis
  • Fistulogram: Identifies correctable lesions

QUESTION 9: 35-Year Male with RTA and Hematuria - Imaging Approach and Management (10 Marks)

Introduction

Road Traffic Accident (RTA) with hematuria indicates possible urological trauma. Hematuria (gross or microscopic) following trauma suggests injury to kidneys, ureters, bladder, or urethra.

Initial Assessment: ABCs and Clinical Triage

Indications for mandatory imaging:
  • Gross hematuria
  • Microscopic hematuria + hypotension (SBP < 90 mmHg)
  • Mechanisms: High-speed deceleration, flank contusion, direct impact
  • Pediatric trauma (image even microscopic hematuria)
  • Significant mechanism without hematuria (possibility of renal pedicle injury)

Imaging Approach:

Step 1: FAST Ultrasound (Focused Assessment with Sonography in Trauma)

  • Immediate bedside
  • Detects free fluid in: perihepatic (Morison's pouch), perisplenic, pericardial, pelvic (pouch of Douglas)
  • Limitations: Cannot grade renal injury, operator-dependent
  • Positive FAST → immediate CT or surgery

Step 2: CT Abdomen and Pelvis with IV Contrast - GOLD STANDARD

Protocol (Triple Phase CT):
  1. Non-contrast phase: Detect hematoma, calculi, baseline attenuation
  2. Arterial/Nephrographic phase (100 seconds): Parenchymal enhancement, vascular injuries, lacerations
  3. Delayed excretory phase (5-10 min): Urinary extravasation, collecting system injury, ureteric injury
Note: Both arterial and delayed phases are essential to completely evaluate renal trauma.
CT Protocol - Renal Trauma:
    ┌──────────────────────────────────────┐
    │  Non-contrast → Nephrographic →      │
    │  Excretory phase                     │
    │                                      │
    │  Non-contrast: hematoma density      │
    │  Nephrographic: laceration depth     │
    │  Excretory: urine leak (contrast     │
    │             in collecting system)    │
    └──────────────────────────────────────┘

AAST Renal Trauma Grading (American Association for Surgery of Trauma):

GradeDescriptionCT Finding
IContusion or non-expanding subcapsular hematomaParenchymal bruising, subcapsular hematoma
IILaceration < 1 cm depth, no collecting systemLaceration, perirenal hematoma, contained
IIILaceration > 1 cm depth, no collecting systemDeeper laceration, hematoma
IVLaceration through collecting system / vascular injuryUrinary extravasation, segmental infarct
VShattered kidney / renal pedicle avulsionFragmented kidney, non-enhancing kidney, devascularized
AAST Renal Trauma Grades:

Grade I:   ╭────╮           Grade II:  ╭──╮╭──╮
           │╰──╯│ Contusion            │Lac│  │ Hematoma
           ╰────╯                      ╰──╰╯──╯

Grade III: ╭──╮ ╭──╮       Grade IV:  ╭──╮  ←extravasation
           │  laceration│             │  │→→ urine leak
           ╰──╯ ╰──╯                  ╰──╯

Grade V:   ╭──╭─╮╮  Shattered / Non-enhancing (pedicle avulsion)
CT Findings of Specific Injuries:
Renal Laceration:
  • Hypodense linear defect through renal parenchyma
  • Perirenal hematoma (crescentic hyperdense collection)
  • Hematoma in Gerota's fascia
Vascular Injury (Grade IV-V):
  • Non-enhancing kidney (renal artery avulsion/thrombosis)
  • Active contrast extravasation (pseudoaneurysm or arteriovenous fistula)
  • Segmental infarcts (wedge-shaped non-enhancement)
Collecting System Injury:
  • Medial urinary extravasation on delayed phase → pelvicalyceal or ureteric injury
  • Lateral extravasation → fornical rupture (minor, usually benign)
Ureteric Injury:
  • Rare, high-energy trauma
  • Delayed CT: Medial extravasation without distal opacification
  • "Megaureter" above injury site

Step 3: Retrograde Urethrogram (RUG) - if urethral injury suspected

Indication: Blood at urethral meatus, inability to pass catheter, perineal hematoma, scrotal bruising
Procedure: Inject contrast at external urethral meatus, screen for extravasation
Injury Classification:
  • Type 1: Stretch (intact mucosa, no extravasation)
  • Type 2: Partial tear (extravasation, contrast reaches bladder)
  • Type 3: Complete tear (no contrast in bladder)

Step 4: Cystogram - for bladder injury

Indication: Gross hematuria, pelvic fracture (15% have bladder injury)
CT Cystogram:
  • Fill bladder with 350 mL dilute contrast
  • Assess for extravasation
Injury Types:
  • Intraperitoneal rupture: Contrast surrounds bowel loops, fills peritoneal space (requires surgery)
  • Extraperitoneal rupture: Contrast in pelvic soft tissues, "flame-shaped" (most managed conservatively with catheter drainage)
Bladder Injury on CT Cystogram:
    Intraperitoneal:              Extraperitoneal:
    ╭─────────────────╮           ╭──────────────╮
    │ Contrast around │           │ Flame-shaped │
    │ bowel loops     │           │ extravasation│
    │  ↕              │           │ in pelvis    │
    │  Bladder rupture│           │              │
    ╰─────────────────╯           ╰──────────────╯

Management:

Conservative (Non-operative) Management - Grade I, II, III:

  • Bed rest, IV fluids, monitoring
  • Serial CT for monitoring
  • Urological consultation
  • Grades I-III: >95% managed non-operatively

Endovascular Management:

  • Angioembolization: For Grade IV-V with active arterial bleeding (contrast blush on CT)
    • Selective catheterization of renal artery
    • Embolize with coils or gelfoam
    • Preserves renal parenchyma
    • Success rate 70-90%
  • Endovascular stenting: For renal artery dissection

Surgical Management:

  • Indications: Hemodynamic instability, failed embolization, expanding hematoma (>25%), Grade V injury
  • Options: Renorrhaphy (repair), partial nephrectomy, nephrectomy

Urinary Extravasation:

  • Most resolve spontaneously (70-80%)
  • Persistent: JJ ureteric stent or percutaneous nephrostomy

QUESTION 10 (10 Marks Total)

10a. Anatomy of Pericardium (3 Marks)

The pericardium is a fibroserous sac surrounding the heart and the roots of the great vessels.

Layers:

1. Fibrous Pericardium (Outer Layer):
  • Tough fibrous sac
  • Composed of dense collagen
  • Attached to: Diaphragm (inferiorly), sternum (sternopericardial ligaments), great vessels (superiorly)
  • Prevents overdistension of heart
  • Fused with adventitia of great vessels
2. Serous Pericardium (Inner Layer) - Two layers:
  • Parietal Layer: Lines inner surface of fibrous pericardium
  • Visceral Layer (Epicardium): Adherent to heart surface
  • Between parietal and visceral layers: Pericardial cavity with 15-35 mL of fluid (lubricant)
Pericardium - Cross Section:
    ┌───────────────────────────────────┐
    │  Fibrous Pericardium (outer)      │
    │  ┌────────────────────────────┐   │
    │  │ Parietal serous pericardium│   │
    │  │ ┌──────────────────────┐  │   │
    │  │ │ Pericardial cavity   │  │   │
    │  │ │ (15-35 mL fluid)     │  │   │
    │  │ │ ┌──────────────────┐ │  │   │
    │  │ │ │ Visceral layer   │ │  │   │
    │  │ │ │  (Epicardium)    │ │  │   │
    │  │ │ │ ┌──────────────┐ │ │  │   │
    │  │ │ │ │ Myocardium   │ │ │  │   │
    │  │ │ │ └──────────────┘ │ │  │   │
    │  │ │ └──────────────────┘ │  │   │
    │  │ └──────────────────────┘  │   │
    │  └────────────────────────────┘   │
    └───────────────────────────────────┘

Pericardial Recesses and Sinuses:

Transverse Pericardial Sinus:
  • Between ascending aorta/pulmonary trunk anteriorly and superior pulmonary veins/LA posteriorly
  • Accessible by finger behind aorta during surgery
  • Appears on CT as fluid-containing space posterior to aorta, anterior to right PA
Oblique Pericardial Sinus:
  • Behind left atrium, surrounded by pulmonary veins and IVC
  • Blind ending (J-shaped)
  • Important: Fluid here does NOT communicate readily with main pericardial space
Pericardial Ligaments:
  • Sternopericardial
  • Phrenicopericardial (to central tendon of diaphragm)
  • Vertebropericardial

Normal CT/MRI Anatomy:

  • CT: Pericardium appears as thin hyperdense line (1-2 mm) between pericardial fat (inside and outside)
  • Normal pericardial thickness on CT: < 2 mm
  • Fluid in pericardial cavity: fluid density (0-20 HU)

10b. CT and MRI Findings of Constrictive Pericarditis (7 Marks)

Pathophysiology:

Constrictive pericarditis (CP) results from fibrosis and calcification of the pericardium following inflammation. The thickened, inelastic pericardium restricts diastolic filling of all chambers equally → equalization of diastolic pressures → venous congestion.
Causes: TB (most common worldwide), idiopathic/viral, post-cardiac surgery, radiation therapy, uremia, bacterial pericarditis

CT Findings:

1. Pericardial Thickening (Most Important Finding):
  • Pericardial thickness > 4 mm is abnormal (normal < 2 mm)
  • Focal or diffuse
  • May be circumferential or localized (especially over RV and AV groove)
  • CT can measure precisely
2. Pericardial Calcification:
  • PATHOGNOMONIC feature for CP (when combined with symptoms)
  • Eggshell calcification encasing the heart
  • Irregular, dense calcification visible on non-contrast CT
  • Distribution: AV groove, right heart border, diaphragmatic surface most common
CT - Pericardial Calcification (Non-contrast):
    ┌────────────────────────────────┐
    │                                │
    │    ████████████████████        │
    │   █                  █        │
    │  █  Right heart       █       │
    │  █  left heart         █      │
    │   █  (encased)        █       │
    │    ████████████████████        │
    │   ↑ Dense calcium (HU >400)   │
    └────────────────────────────────┘
3. Cardiac Chamber Changes:
  • Tubular/conical right ventricle: Compressed RV (flattening)
  • Dilation of right atrium and left atrium (backpressure from restricted filling)
  • Enlarged IVC and SVC (venous hypertension)
  • Small right and left ventricles (restricted filling)
  • Normal left ventricular ejection fraction
4. Interventricular Septal Motion:
  • Septal bounce / paradoxical septal motion on dynamic CINE MRI
5. Signs of Venous Congestion:
  • Dilated IVC and hepatic veins (IVC > 21 mm)
  • Hepatic congestion (heterogeneous liver parenchyma, mosaic pattern)
  • Pleural effusion (bilateral, right > left)
  • Ascites
  • Peripheral edema (clinical, not CT)
6. Pericardial Tethering:
  • Obliteration of pericardial sinuses
  • Tethering of epicardium to pericardium
CT Summary - Constrictive Pericarditis:
    ┌─────────────────────────────────┐
    │  1. Pericardial thickening >4mm │
    │  2. Calcification (eggshell)    │
    │  3. Tubular/conical RV          │
    │  4. Dilated RA, LA              │
    │  5. Dilated IVC, hepatic veins  │
    │  6. Bilateral pleural effusions │
    │  7. Ascites                     │
    └─────────────────────────────────┘

MRI Findings:

Advantages of MRI over CT:
  • No radiation
  • Superior soft tissue contrast
  • Functional assessment (CINE MRI)
  • Can distinguish constrictive pericarditis from restrictive cardiomyopathy
1. Pericardial Thickening:
  • 4 mm on MRI is pathological
  • Appears as:
    • Low signal (dark) on T1 and T2: Fibrous/calcified pericardium
    • High signal on T2: Active inflammation/edema
2. Signal Characteristics:
  • Fibrous pericardium: Low T1, Low T2 (hypointense on both)
  • Inflammatory/active pericarditis: High T2 signal (edema)
  • Late gadolinium enhancement (LGE): Enhancing pericardium = active inflammation (responds to anti-inflammatory treatment)
  • No enhancement: Calcified/fibrotic = surgical pericardiectomy required
MRI Signal - Pericardium:
    T1 weighted:   Dark pericardium (fibrous)
    T2 weighted:   Dark = fibrosis; Bright = inflammation
    T1+Gd (LGE):  Enhancement = active inflammation
                  No enhancement = calcified/fibrotic
3. CINE MRI (Functional - KEY FEATURE):
  • Septal bounce: Abrupt paradoxical interventricular septal motion in early diastole
    • Septum moves toward LV in early diastole, then back
    • "Septal bounce" or "diastolic septal flattening"
  • Respirophasic septal shift (enhanced with respiratory maneuvers)
  • Ventricular interdependence: Right heart expands at expense of left with inspiration
CINE MRI - Septal Bounce:
    Inspiration:    Expiration:
    ╭─────────────╮  ╭─────────────╮
    │ RV ↑  → LV │  │ RV ↓  ← LV │
    │    ╲        │  │       ╱     │
    │     ╲ IVS  │  │      ╱ IVS  │
    │      ╲      │  │     ╱       │
    ╰─────────────╯  ╰─────────────╯
    
    Septal movement: ← → ← → (bouncing)
4. Ventricular Filling Pattern:
  • Abrupt halt of ventricular filling in mid-diastole (dip-plateau / square root sign on pressure tracing)
  • Corresponding to pericardial restraint
5. Pericardial Tethering:
  • Pericardium adherent to epicardium
  • No normal pericardial sliding on CINE
6. Associated Findings:
  • Dilated IVC, hepatic veins
  • Pleural effusions
  • Hepatic congestion

CP vs Restrictive Cardiomyopathy (Important Differential):

FeatureConstrictive PericarditisRestrictive Cardiomyopathy
Pericardial thicknessIncreased (>4 mm)Normal
CalcificationMay be presentAbsent
Septal bouncePresentAbsent
Ventricular interdependencePresentAbsent
LGE pericardiumPresent (if active)Absent
Myocardial LGEAbsentMay be present (amyloid, sarcoid)
TreatmentPericardiectomyMedical management

SUPPLEMENTAL IMAGING DIAGRAMS

Schematic: Pulmonary Artery Hypertension - CXR vs CT

CXR:                          CT:
  ┌─────────────────┐           ┌─────────────────┐
  │   PA            │           │ MPA > 29mm      │
  │  ╭──────╮       │           │ PA:Ao > 1.0     │
  │ ╭╯ MPA  ╰╮      │           │ RV:LV > 1.0     │
  │ │enlarged│      │           │ D-sign (IVS)    │
  │ ╰╮      ╭╯      │           │ Mosaic          │
  │  ╰──────╯       │           │ attenuation     │
  │  ↑ Pruning      │           │ Pericardial eff │
  └─────────────────┘           └─────────────────┘

Schematic: Cardiogenic vs Non-Cardiogenic Pulmonary Edema

Cardiogenic:                Non-Cardiogenic (ARDS):
  ┌────────────────┐          ┌────────────────┐
  │ Big heart      │          │ Normal heart   │
  │ Perihilar dens │          │ Peripheral dens│
  │ Kerley B lines │          │ No Kerley B    │
  │ Effusions      │          │ No effusions   │
  │ Upper lobe     │          │ Air bronchograms│
  │ diversion      │          │ (diffuse)      │
  └────────────────┘          └────────────────┘

These answers cover all topics from JUNE 2026 Paper 2. Each question has been addressed comprehensively with pathophysiology, imaging findings, differentials, and management where applicable, along with schematic diagrams for key imaging concepts.
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