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RADIOLOGY UNIVERSITY THEORY EXAM - MODEL ANSWERS

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Q.36 PNEUMATOSIS INTESTINALIS (30 Marks)

Definition

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Classification

• No identifiable underlying cause
• Gas-filled submucosal or subserosal cysts (Pneumatosis cystoides intestinalis)
• Usually benign, incidental finding
• Associated with COPD, obstructive lung disease (theory: alveolar rupture - air tracking along perivascular sheaths)

• Ischemic/Life-threatening (most important to exclude)
• Non-ischemic/Benign (majority of secondary causes)

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Etiopathogenesis - Three Theories

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Causes

• Mesenteric ischemia / bowel infarction
• Necrotizing enterocolitis (NEC) in neonates
• Bowel obstruction with strangulation
• Sepsis / toxic megacolon
• Graft-versus-host disease

• COPD, asthma, barotrauma
• Steroid therapy, immunosuppression
• Connective tissue diseases (scleroderma, SLE)
• Post-endoscopy / colonoscopy
• Inflammatory bowel disease (Crohn's, ulcerative colitis)
• Post bone marrow transplant
• HIV/AIDS
• Celiac disease

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Radiological Features

Plain Abdominal Radiograph (AXR)

• Mural gas: Linear or curvilinear lucencies running parallel to the bowel wall (submucosal); or rounded/oval lucent foci along serosal surface (subserosal cysts)
• Portal venous gas: Branching lucencies extending to the liver periphery (peripheral hepatic gas - highly ominous sign of ischemia; distinguishes from biliary gas which is central)
• Pneumoperitoneum: If perforation has occurred
• Dilated bowel loops: Indicating obstruction

Ultrasound

• Echogenic foci within bowel wall with "dirty" acoustic shadowing or ring-down artifact
• Portal venous gas: Bright echogenic foci moving in portal veins (highly specific)
• May show peritoneal free fluid

CT Scan (Gold Standard)

• Mural gas: Hypodense (gas density, ~-100 to -1000 HU) foci within the bowel wall
  • Bubbly pattern: Multiple small rounded foci in submucosa (more benign)
  • Linear pattern: Continuous linear gas along bowel wall (more ominous for ischemia)
• Portal venous gas: Branching hypodense foci in portal vein and intrahepatic portal branches extending to within 2 cm of liver capsule
• Bowel wall thickening / thinning (paper-thin wall = infarction)
• Lack of bowel wall enhancement after IV contrast = ischemia/necrosis
• Free peritoneal fluid, ascites
• Pneumoperitoneum if perforated
• Mesenteric fat stranding

MRI

• T1: Gas appears as signal void
• Less commonly used in acute setting
• Useful for chronic/follow-up cases

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Differentiating Benign from Ominous PI

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Portal Venous Gas vs Pneumobilia

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Management Implications

• Benign PI: Conservative management, treat underlying cause
• Ischemic PI: Surgical emergency - exploratory laparotomy, bowel resection
• The radiologist's role is to identify CT features that distinguish benign from life-threatening PI and communicate urgently

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Q.37 MECKEL'S DIVERTICULUM (30 Marks)

Definition

Rule of 2s

• Occurs in 2% of the population
• Located within 2 feet (~60 cm) of the ileocecal valve
• Approximately 2 inches (5 cm) in length
• 2:1 male to female ratio for symptomatic cases
• 2 types of ectopic mucosa: gastric (most common) and pancreatic
• Symptomatic in 2% of those who have it
• Most commonly presents before age 2 years

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Anatomy

• True diverticulum with all 3 layers (mucosa, muscularis, serosa)
• Arises from antimesenteric border of ileum
• Has its own blood supply from a remnant of the vitelline artery (branch of superior mesenteric artery)
• Contains ectopic mucosa in 50% of symptomatic cases:
  • Gastric mucosa (most common - 85%) - responsible for peptic ulceration and bleeding
  • Pancreatic tissue (second most common)
  • Colonic, duodenal mucosa

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Clinical Presentations

1. Hemorrhage (most common in children) - painless rectal bleeding (bright red to maroon), due to peptic ulceration of adjacent ileal mucosa by ectopic gastric acid
2. Intestinal obstruction - volvulus, intussusception, Littre's hernia (Meckel's in hernia sac)
3. Diverticulitis (most common in adults) - mimics acute appendicitis
4. Perforation - with peritonitis
5. Umbilical fistula / sinus - if duct remains patent

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Radiological Investigations

Plain X-ray

• Usually normal
• May show small bowel obstruction (dilated loops, air-fluid levels)
• Rarely, ectopic calcification (enterolith within MD)

Barium Small Bowel Studies (Enteroclysis/Follow-Through)

• MD is notoriously difficult to visualize with contrast radiology (Bailey & Love)
• May appear as a blind-ending sac off the antimesenteric border of distal ileum
• Barium may fill the lumen
• Limitations: Cannot detect ectopic mucosa

Ultrasound

• Limited role; may show tubular structure near terminal ileum
• May detect complications (inflammatory mass, intussusception)
• Doppler: blood flow in vitelline artery remnant

Technetium-99m Pertechnetate Scan (Meckel's Scan) - KEY INVESTIGATION

• Investigation of choice for suspected Meckel's diverticulum with bleeding
• Principle: 99mTc-pertechnetate is taken up by mucus-secreting cells of gastric mucosa (ectopic gastric tissue in MD)
• Technique: IV injection of 99mTc-pertechnetate; images at 5-minute intervals for 60 minutes
• Positive scan: Area of abnormal increased uptake in the right lower abdomen (not present normally) appearing simultaneously with gastric mucosa uptake
• Sensitivity: ~85% in children, lower in adults
• Specificity: ~95%
• Pharmacological enhancement:
  • Pentagastrin: Stimulates uptake (pretreatment)
  • H2-blockers (cimetidine/ranitidine): Block secretion but not uptake (increases target-to-background ratio) - preferred
  • Glucagon: Reduces peristalsis, prevents washout of tracer

CT Scan

• Cannot specifically diagnose MD unless it demonstrates:
  • Tubular structure arising from antimesenteric border of ileum
  • Inflammation (Meckel's diverticulitis) - inflamed blind-ending structure in RLQ with surrounding fat stranding
  • Complications: abscess, perforation, obstruction
• CT enterography improves detection
• Cannot detect ectopic mucosa

MRI / MR Enterography

• Increasing use in children (no radiation)
• May show diverticulum and inflammatory changes
• Cannot detect ectopic mucosa

Angiography

• For active hemorrhage when nuclear scan is equivocal
• May show vitelline artery, active bleeding blush

Capsule Endoscopy

• Good for detecting ectopic mucosa
• Cannot differentiate MD from other causes of obscure GI bleed

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Complications Summary

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Treatment

• Symptomatic MD: Surgical diverticulectomy or segmental ileal resection
• Incidentally found MD: Controversial (resect if young, >2cm, ectopic mucosa suspected, broad neck)

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Q.38 ACUTE ABDOMEN IN A 50-YEAR-OLD FEMALE (30 Marks)

Definition

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Special Considerations in a 50-Year-Old Female

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Causes - Classification

1. Acute appendicitis (less common at 50, but still occurs)
2. Perforated peptic ulcer / gastric ulcer
3. Acute cholecystitis / biliary colic / choledocholithiasis
4. Acute pancreatitis
5. Intestinal obstruction (adhesions, hernia, volvulus, tumor)
6. Mesenteric ischemia / volvulus
7. Diverticulitis (sigmoid more common in 50+ age group)
8. Perforated viscus (from any cause)
9. Inflammatory bowel disease - Crohn's / UC
10. Intussusception (in adults, usually pathological lead point - tumor)

1. Ruptured ovarian cyst
2. Ovarian torsion
3. Ectopic pregnancy (unlikely at 50 but possible in perimenopause)
4. Fibroid degeneration / torsion
5. Tubo-ovarian abscess / pelvic inflammatory disease
6. Ovarian / uterine malignancy with complication

1. Renal/ureteric colic (calculus)
2. Pyelonephritis / perinephric abscess
3. Acute urinary retention

1. Ruptured abdominal aortic aneurysm (AAA)
2. Aortic dissection
3. Acute mesenteric ischemia (embolic, thrombotic, non-occlusive)
4. Splenic infarction

1. Hepatic abscess
2. Budd-Chiari syndrome
3. Splenic abscess / rupture

1. Adrenal hemorrhage
2. Rectus sheath hematoma
3. Referred pain (myocardial infarction, lower lobe pneumonia, pleuritis)

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Radiological Approach - Stepwise

Step 1: Plain Abdominal X-ray (AXR) + Erect Chest X-ray

• Free air under diaphragm = perforated viscus (needs >0.5 ml air to be visible)
• Basal pneumonia / empyema (referred pain)

Step 2: Ultrasound (US)

• Biliary tract disease (cholecystitis, choledocholithiasis)
• Gynecological causes (cysts, fibroids, torsion, ectopic)
• Renal tract (hydronephrosis, calculi)
• AAA screening
• Appendicitis (limited by gas)
• Free fluid detection

• Cholecystitis: Thickened gallbladder wall (>3mm), gallstones, pericholecystic fluid, positive Murphy's sign on US
• Ovarian torsion: Enlarged ovary with absent Doppler flow, peripheral follicles
• Ectopic: Empty uterus, adnexal mass, free fluid in Pouch of Douglas
• AAA: Aortic diameter >3 cm, aneurysm or dissection flap
• Renal calculi: Hydronephrosis, echogenic stone with shadowing
• Pancreatitis: Edematous pancreas, peripancreatic fluid

Step 3: CT Scan - Investigation of Choice for Acute Abdomen

• CECT abdomen and pelvis (arterial + portal venous phases) provides definitive diagnosis in most cases
• Sensitivity and specificity >90% for most causes

Step 4: Additional Modalities

• In pregnant patients (avoiding radiation)
• Unclear diagnosis on CT
• Pelvic masses, fibroids, ectopic
• Mesenteric ischemia

• Water-soluble enema for suspected large bowel obstruction or perforation
• Small bowel follow-through in partial obstruction

• HIDA scan for acute cholecystitis when US equivocal
• 99mTc WBC scan for occult septic focus

• Active GI bleeding (therapeutic: embolization)
• Mesenteric ischemia (selective angiography, thrombolysis)
• Ruptured AAA (EVAR)

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Summary Algorithm for 50-Year-Old Female Acute Abdomen

1. History and clinical exam
2. AXR + Erect CXR - exclude pneumoperitoneum, obstruction
3. Ultrasound - biliary, gynecological, renal (fast, no radiation)
4. CECT abdomen + pelvis - if US inconclusive or surgical emergency suspected
5. MRI - if pregnant, young, or pelvic pathology needs further evaluation
6. Interventional procedures as clinically indicated

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Q.39 INVESTIGATION OF A 40-YEAR-OLD MALE WITH HAEMOPTYSIS IN A FULLY EQUIPPED RADIO-IMAGING CENTRE (30 Marks)

Definition

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Causes of Haemoptysis

1. Pulmonary tuberculosis (TB) - most common in developing countries
2. Bronchogenic carcinoma (especially in 40-year male smoker)
3. Bronchiectasis
4. Acute bronchitis / pneumonia

• Bronchogenic carcinoma (squamous cell carcinoma most common)
• Tuberculosis
• Bronchiectasis

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Radiological Investigations - Sequential Approach

1. Plain Chest Radiograph (CXR) - PA and Lateral

2. High Resolution CT (HRCT) of Thorax

• Detects lesions invisible on CXR (small tumors, early bronchiectasis)
• Thin slices (0.5-1.5 mm) through entire thorax
• Multiplanar reconstruction (MPR), minimum intensity projection (MinIP) for airways

• Bronchiectasis: Signet ring sign (dilated bronchus > accompanying pulmonary artery), tram-track lines on AP view, absence of bronchial tapering, mucous plugging
• Bronchogenic carcinoma: Spiculated/lobulated mass, hilar/mediastinal adenopathy, pleural effusion, chest wall invasion
• TB: Upper/posterior lobe consolidation, cavity, satellite nodules, tree-in-bud pattern (endobronchial spread), calcified nodes (Ghon focus, Ranke complex)
• Aspergilloma: Dense rounded mass within a pre-existing cavity, surrounded by aircrescent (Monod sign/Halo sign), changes with posture (mobile ball)
• AVM: Feeding artery + draining vein + nidus (pulmonary aneurysm on plain film)
• Pulmonary infarction: Peripheral wedge-shaped density (Hampton's hump), pleurally-based

3. CT Pulmonary Angiography (CTPA)

• Investigation of choice for pulmonary embolism
• Findings: Filling defects in pulmonary arteries, peripheral wedge infarcts, pleural effusion
• Also evaluates pulmonary arterial anatomy for pre-embolization planning in massive haemoptysis

4. Contrast Enhanced CT (CECT) Thorax

• Arterial phase for vascular lesions, AVM
• Mediastinal window for lymph nodes, masses
• Bronchial artery anatomy (pre-interventional planning)

5. Flexible Bronchoscopy

• Key procedure (not imaging, but complementary)
• Localizes bleeding site
• Samples lesion for histology/microbiology
• Virtual bronchoscopy from CT data

6. Bronchial Artery Angiography + Embolization (BAE)

• Bronchial arteries arise from descending aorta (T5-T6 level)
• Right bronchial artery often shares origin with right intercostal artery (intercostobronchial trunk - ICBT)
• Angiographic findings of active bleed: Hypervascularity, tortuous bronchial arteries, arteriovenous shunting, active extravasation of contrast
• Embolization with polyvinyl alcohol (PVA) particles, coils
• Success rate 75-90% for stopping acute bleed

7. MRI / MRA

• Limited role in acute haemoptysis (patient cannot hold breath, motion artifacts)
• Role: Vascular anomalies, cardiac causes (mitral stenosis - MRI for valvular disease, ventricular function)
• MR angiography for AVM characterization
• Useful when iodine contrast is contraindicated

8. Nuclear Medicine (V/Q Scan)

• Ventilation/Perfusion scan for PE when CTPA is contraindicated (renal failure, contrast allergy)
• Perfusion defect with normal ventilation = mismatch (positive for PE)

9. PET-CT

• For staging of confirmed bronchogenic carcinoma
• Differentiating benign from malignant lesions (FDG avidity)
• Detecting mediastinal, distant metastases

10. Fluoroscopy

• Screening for diaphragm movement, hilar masses
• Barium swallow if esophageal cause suspected

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Algorithm for 40-Year Male with Haemoptysis

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Comparison: HRCT vs Bronchoscopy

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Q.40 ROLE OF MDCT IN ACUTE ABDOMEN (30 Marks)

Introduction

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Technical Advantages of MDCT

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CT Protocol for Acute Abdomen

1. Non-contrast (Plain) phase: Detects calcification (stones, aortic wall), hemorrhage (hyperattenuating), gas patterns
2. Arterial phase (25-30 sec): Vascular injuries, active bleeding, bowel ischemia (non-enhancement), hepatic arterial phase, pancreatic parenchyma
3. Portal venous phase (60-70 sec): Standard phase for abdominal organs - liver, spleen, kidneys, bowel wall enhancement, peritoneal disease
4. Delayed / Excretory phase (3-5 min): Urinary tract, ureteric calculi, bladder injuries

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Role of MDCT in Specific Causes

1. Gastrointestinal Perforation

• Free air (pneumoperitoneum): Hypodense foci under diaphragm (more sensitive than AXR); as little as 1-2 ml detectable
• Site of perforation: Bowel wall defect, localized free air adjacent to specific organ
• Perforated peptic ulcer: Air near lesser sac, extraluminal fluid
• Perforated colon (diverticulitis, carcinoma): Pericolonic inflammation, pericolic air

2. Intestinal Obstruction

• Transition point: Abrupt change from dilated to collapsed bowel
• Cause identification: Adhesions (normal bowel at transition), hernia (bowel through defect), volvulus (whirl sign, X-marks-the-spot), tumor (mass at transition)
• Closed loop obstruction: C or U-shaped dilated segment with two adjacent transitions, high risk of strangulation
• Strangulation: Mural thickening, pneumatosis, portal venous gas, non-enhancement, mesenteric edema/haziness, ascites

• Carcinoma: Annular "apple-core" lesion
• Volvulus: Omega loop (sigmoid), coffee bean sign, whirl sign

3. Acute Appendicitis

• Dilated appendix > 6mm diameter with mural thickening
• Appendicolith (hyperattenuating)
• Periappendiceal fat stranding
• Free fluid in right iliac fossa
• Phlegmon or abscess formation
• Perforated: Discontinuity of appendiceal wall, pericecal abscess, free air

4. Acute Cholecystitis

• Distended gallbladder (> 5 cm width)
• Mural thickening (>3 mm)
• Pericholecystic fat stranding
• Gallstones (hyperattenuating)
• Subserosal edema (halo sign)
• Gangrenous cholecystitis: Irregular/absent wall enhancement, intramural gas (emphysematous cholecystitis), mural irregularity
• Mirizzi syndrome: Stone in Hartmann's pouch compressing common hepatic duct

5. Acute Pancreatitis

• CT Severity Index (Balthazar Score):
  • Grade A: Normal
  • Grade B: Enlargement alone
  • Grade C: Peripancreatic inflammation
  • Grade D: One fluid collection
  • Grade E: Two+ fluid collections
• Necrosis: Non-enhancing pancreatic parenchyma (black on CECT) - walled-off necrosis after 4 weeks
• CT Severity Index = Balthazar grade (0-4) + Necrosis score (0-4) - correlates with morbidity/mortality
• Complications: Pseudocyst, abscess, hemorrhage, vascular complications (splenic vein thrombosis, pseudoaneurysm)

6. Acute Mesenteric Ischemia

• Embolic: Filling defect in SMA (usually proximal, just beyond middle colic artery origin); spares proximal jejunal branches
• Thrombotic: SMA occlusion at origin; diffuse bowel involvement; atherosclerotic disease in adjacent vessels
• Non-occlusive (NOMI): Patent vessels, diffuse bowel changes, spasm of SMA branches
• Bowel wall: Thickening (early) or thinning (late ischemia/infarction), absent enhancement
• Pneumatosis intestinalis (submucosal/subserosal gas)
• Portal venous gas: Branching gas in portal veins; ominous sign
• Bowel dilation, ascites, peritoneal fluid
• "Whirl sign": Rotation of mesenteric vessels in volvulus
• Double halo / target sign: Concentric mural thickening in reperfusion edema or intramural hemorrhage

7. Diverticulitis

• Sigmoid (most common) or right colon
• Diverticula (outpouchings through bowel wall)
• Pericolonic fat stranding (hallmark)
• Mural thickening
• Complications: Abscess, fistula (colovesical: air in bladder), perforation, obstruction
• Modified Hinchey classification guides management

8. Abdominal Aortic Aneurysm (AAA) and Rupture

• Aortic diameter >3 cm = AAA
• Rupture: Retroperitoneal hematoma (periaortic high-density blood), loss of aortic wall definition
• "Draped aorta" sign: Aortic posterior wall not separable from vertebral body
• Active extravasation of contrast = life-threatening emergency (EVAR or open surgery)

9. Renal and Ureteric Colic

• Non-contrast CT urogram: Most sensitive for calculi
• Ureteric calculus: Hyperattenuating focus in ureter with proximal hydronephrosis, perinephric/periureteric fat stranding
• "Rim sign": Soft tissue rim around calculus

10. Gynecological Emergencies

• Ovarian torsion: Enlarged ovary, edematous stroma, peripheral follicles, absent enhancement
• Ruptured ectopic: Adnexal mass, tubal ring, free pelvic blood
• Fibroids: Well-defined hypodense or calcified uterine masses

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Advantages of MDCT over Other Modalities

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Limitations of MDCT

• Radiation exposure (especially in young patients, pregnancy)
• Iodinated contrast: Nephrotoxicity, anaphylaxis
• False negatives in early/subtle disease
• Requires patient cooperation (motion artifacts)
• Cost

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Q.41 ELASTOGRAPHY IN LIVER LESIONS (30 Marks)

Introduction

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Principle

• Soft tissue deformation (strain) in response to an applied force is measured
• Stiff tissue deforms less than soft tissue
• Liver stiffness is expressed as kPa (kiloPascals) or m/s (velocity of shear wave)
• Normal liver: 2-6 kPa; Cirrhotic liver: >12-14 kPa

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Types of Elastography

A. Ultrasound-Based Elastography

• Most established method
• A mechanical vibration (50 Hz) creates a shear wave propagating through liver
• The shear wave velocity is measured by pulse-echo ultrasound
• Velocity correlates with liver stiffness
• Probe placed intercostally (right lobe)
• Result: LSM (Liver Stiffness Measurement) in kPa
• Limitations: Cannot be performed in ascites, obesity (XL probe available), cannot guide to specific region, no imaging

• Focused acoustic pulse displaces tissue → generates shear waves
• Measures velocity at a specific point of interest
• Can be combined with real-time B-mode imaging
• Advantage over TE: Can be performed with ascites, targets specific region

• Generates color elastogram overlaid on B-mode image
• Real-time 2D map of liver stiffness
• Advantage: Targets specific lesions, larger sampling area, real-time visualization
• Can differentiate focal liver lesions

• Manual compression of tissue → measures strain
• Qualitative (color map) - not quantitative
• Limited hepatic use; better for superficial lesions (breast, thyroid)

B. MR Elastography (MRE)

• Mechanical driver applied to liver (60-80 Hz vibrations)
• Phase-contrast MRI sequences detect wave propagation through liver
• Generates quantitative stiffness maps (elastograms)
• Advantages over US-based: Not affected by obesity, ascites, iron overload; images entire liver; higher accuracy
• Disadvantage: Expensive, less available, longer acquisition time
• Can accurately assess stiffness of fatty livers (unlike transient elastography which is affected by steatosis)
• Role in assessing portal hypertension: Spleen stiffness correlates with portal pressure

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Liver Fibrosis Staging

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Elastography in Focal Liver Lesions

Benign Lesions

• Simple cysts: Very soft (low stiffness) - cannot propagate shear wave (no solid components)
• Hemangioma: Variable; typically soft; may appear blue (soft) on color maps
• FNH (Focal Nodular Hyperplasia): Slightly stiffer than normal liver but softer than malignancy
• Hepatic adenoma: Soft to intermediate stiffness

Malignant Lesions

• Hepatocellular Carcinoma (HCC): Stiff lesion; higher stiffness compared to surrounding cirrhotic liver
• Metastases: Generally stiff (especially from colorectal, breast cancers)
• Cholangiocarcinoma: Very stiff (desmoplastic reaction)

Key Role: Characterizing Focal Liver Lesions

• 2D-SWE and pSWE can target focal lesions:
  • Stiffness > 34.5 kPa: Suggests malignancy
  • Lower stiffness: More likely benign
  • Not yet replacing other modalities but adds functional information

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Clinical Applications of Liver Elastography

1. Staging hepatic fibrosis in chronic liver disease (hepatitis B, C, NAFLD/NASH, alcohol) - replacing liver biopsy in many cases
2. Monitoring treatment response (antiviral therapy, alcohol abstinence) - decrease in stiffness
3. Predicting portal hypertension and esophageal varices (spleen stiffness > 54 kPa predicts varices)
4. Detecting cirrhosis and its complications
5. Guiding biopsy - sampling from areas of highest stiffness (most severe disease)
6. Differentiating benign from malignant focal lesions (supplementary role)
7. Liver transplant assessment - donor evaluation, post-transplant fibrosis

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Advantages Over Liver Biopsy

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Limitations of Elastography

• Cannot distinguish cause of fibrosis
• High stiffness in acute hepatitis (inflammation, not fibrosis)
• Affected by: Ascites (TE), high BMI, bile duct obstruction (overestimates fibrosis), cardiac congestion
• Operator-dependent (US methods)
• Cannot characterize all focal lesions definitively

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Q.42 SEGMENTAL ANATOMY OF LIVER BY CT + CECT PHASES + FOCAL LIVER LESIONS (30 Marks)

Part A: Segmental Anatomy of Liver by CT Scan

Couinaud Segmental Anatomy

• Right and Left Liver: Divided by the Middle Hepatic Vein (MHV) and the plane through the gallbladder fossa to IVC (Cantlie's line)
• Left Liver Lobes: Further divided by the left hepatic vein (LHV) and round ligament (falciform ligament)
• Right Liver Lobes: Divided by the right hepatic vein (RHV) into anterior and posterior sectors

The 8 Segments

• Posteriorly between IVC and left portal vein
• Has dual portal supply and drains directly into IVC via short hepatic veins
• Seen posterior to hepatoduodenal ligament on CT

CT Identification Method

• Three hepatic veins (LHV, MHV, RHV) seen draining into IVC
• Segments II, VII, VIII visible at this level

• Right and left portal veins visible
• All 8 segments partially visible

• Segments III, IVb, V, VI, I visible

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Part B: Enhancement Phases of Liver on CECT

Why Multiphase CT?

• Hepatic artery: 25% of blood supply, 50% of oxygen
• Portal vein: 75% of blood supply, 50% of oxygen

The Four Enhancement Phases

• Baseline attenuation
• Detects: Calcification, fat, hemorrhage (hyperattenuating blood), biliary stones
• Normal liver: 50-70 HU
• Fat: -20 to -80 HU (suggests steatosis)
• Hemorrhage: 50-80 HU

• Hepatic artery and its branches are opacified
• Portal vein just beginning to opacify
• Normal liver parenchyma: 70-80 HU (moderately enhanced)
• Hypervascular lesions light up: HCC, FNH, hepatic adenoma, hemangioma (peripheral nodular enhancement), hypervascular metastases (carcinoid, RCC, thyroid, breast)
• Celiac, SMA, hepatic artery anatomy assessment

• Optimal phase for normal liver parenchyma (highest liver enhancement ~120-130 HU)
• Portal vein fully opacified
• Liver reaches peak enhancement
• Hypervascular lesions may "washout" - become iso/hypodense (HCC washout appearance)
• Hypovascular lesions best seen: Most metastases, cholangiocarcinoma, abscesses
• Hepatic veins and IVC opacified

• Contrast redistributes to extravascular space
• Most lesions become isodense to liver (equilibration)
• Persistent enhancement (enhancement on delayed phase):
  • Hemangiomas: Progressive centripetal fill-in, complete fill-in on delayed
  • Cholangiocarcinoma: Peripheral washout, central/delayed enhancement (fibrous stroma)
  • Fibrotic scars (FNH): Central scar enhances on delayed
• Hepatobiliary phase (with hepatocyte-specific agents like Gd-EOB-DTPA / Primovist): 20 minutes post-injection; hepatocytes take up agent → HCC and metastases appear dark (no uptake)

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Part C: Causes of Focal Liver Lesions

Benign Focal Liver Lesions

Malignant Focal Liver Lesions

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Q.43 CROHN'S DISEASE (30 Marks)

Introduction

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Pathological Features (Basis of Radiological Findings)

• Transmural inflammation (all layers - mucosa to serosa)
• Skip lesions - alternating diseased and normal segments
• Granuloma formation (non-caseating)
• Mucosal ulceration - aphthous ulcers → longitudinal ulcers → cobblestone mucosa → deep fissuring ulcers
• Fibrosis and strictures (from chronic inflammation)
• Fistula and sinus tract formation (due to transmural ulceration)
• Creeping fat (mesenteric fat wrapping around bowel)
• Lymphoid aggregates - cobblestone appearance

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Sites of Involvement

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Radiological Investigations

1. Plain X-Ray / AXR

• Dilated small bowel (in obstruction)
• Air-fluid levels
• Fecal loading (colonic disease)
• Toxic megacolon (rare in Crohn's)
• Bowel wall thickening (hazy outer margin of bowel)

2. Small Bowel Barium Studies (Enteroclysis / Small Bowel Follow-Through)

• Aphthous ulcers: Small target lesions - central barium dot surrounded by lucent halo (earliest mucosal change)
• Cobblestone appearance: Network of longitudinal and transverse ulcers surrounding islands of edematous mucosa
• String sign of Kantor: Long narrow stricture in terminal ileum (most characteristic) due to fibrosis/spasm; normal mucosa cannot be seen
• Skip lesions: Normal bowel between diseased segments
• Terminal ileal thickening and narrowing
• Fistulae: Sinus tracts between bowel loops, between bowel and bladder (colovesical fistula), bowel and skin (enterocutaneous)
• Widened ileocecal junction
• Rose-thorn ulcers: Deep penetrating ulcers into thickened wall
• Thumbprinting: Submucosal edema in acute colonic disease

3. CT Enterography (CTE) - Current Gold Standard

• Mural thickening (>3-4 mm; normal <3 mm)
• Mural stratification - "target sign" / "double halo sign":
  • Inner ring: Hyperenhancing mucosa
  • Middle ring: Submucosal edema (fat density)
  • Outer ring: Muscularis
• Mucosal hyperenhancement: Active inflammation (increased vascularity)
• Mesenteric fat stranding: Perilesional inflammation
• "Comb sign": Engorgement of vasa recta (mesenteric vessels) perpendicular to bowel wall - indicates active inflammation
• Creeping fat: Mesenteric fat proliferating around bowel
• Strictures: Wall thickening + luminal narrowing
• Fistulae: Tracts connecting bowel loops or to other structures
• Abscesses: Rim-enhancing collections
• Lymphadenopathy: Mesenteric nodes
• Skip lesions: Diseased segments with normal intervening bowel

4. MR Enterography (MRE)

• Equal sensitivity and specificity to CTE for small bowel Crohn's
• Better for:
  • Perianal fistulae (MRI is gold standard)
  • Assessing disease activity (T1 post-contrast enhancement, T2 mural edema)
  • Repeated follow-up (no radiation)
• MRI activity score: MaRIA (Magnetic Resonance Index of Activity)
• Wall thickening, mural hyperenhancement, perimural edema, ulcers on MRE

• SSFSE/HASTE (T2): Bowel wall edema, fluid collections
• T1 + contrast: Mucosal enhancement, fistulae
• DWI: Restricted diffusion in active inflammation

5. Ultrasound

• Bowel wall thickening >3 mm
• Loss of normal bowel wall stratification
• Increased Doppler flow (active disease)
• Mesenteric fat echogenicity
• Abscesses, fistulae
• Limited by gas and obesity

6. Capsule Endoscopy

• Most sensitive for mucosal disease (aphthous ulcers, subtle changes)
• Cannot be used in strictures (risk of retention)
• Used in suspected small bowel Crohn's with negative cross-sectional imaging

7. Nuclear Medicine

• 99mTc-HMPAO leukocyte scintigraphy / 18F-FDG PET:
  • Assess extent and activity of disease
  • Useful when contrast is contraindicated

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Complications and Their Radiological Findings

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Differentiating Crohn's from Ulcerative Colitis

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Q.44 EXPLAINING EACH PHASE (CECT Liver Enhancement Phases - Detailed) (30 Marks)

Introduction to CECT Liver Phases

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Pharmacokinetics of Iodinated Contrast

• Administered IV (100-120 ml at 3-4 ml/sec)
• Distributes first in intravascular space, then extravascular extracellular space
• Not taken up by hepatocytes (unlike MRI hepatobiliary agents)
• Excreted by glomerular filtration
• Peak liver enhancement depends on timing of acquisition

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Phase 1: Non-Contrast (Plain) CT

• Baseline liver attenuation: Normal 50-70 HU (higher than spleen)
• Steatosis: Liver attenuation < 48 HU or liver-spleen ratio < 0.9 (fatty infiltration appears dark)
• Hemosiderosis/Iron overload: Very high attenuation liver (>75 HU)
• Calcification: Gallstones, calcified granulomas, old hemangioma, parasitic cysts (Echinococcus)
• Hemorrhage: Hyperattenuating fresh blood (50-80 HU) in HCC, hepatic adenoma rupture
• Biliary stones
• Gas: Pneumobilia, hepatic abscess gas

• Cysts: 0-20 HU (very dark - water density)
• Hemangiomas: 35-45 HU (slightly hypodense)
• HCC: Variable, may contain fat (10-15 HU areas), calcification rare

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Phase 2: Arterial Phase

• Hepatic artery and its branches: Brilliant enhancement (300-400 HU)
• Abdominal aorta: Peak enhancement
• Early portal vein: Beginning to opacify (~50-70 HU)
• Liver parenchyma: Mild enhancement (70-90 HU) from arterial supply

• Early arterial: Only artery opacified (portal not yet visible) - best for vascular anatomy
• Late arterial (hepatic arterial dominant phase): Hepatic artery branches opacified, portal vein just becoming visible - BEST PHASE for hypervascular liver tumors

• HCC: Bright arterial enhancement (fed by abnormal hepatic arteries - neovascularity)
• FNH: Intense homogeneous enhancement (central scar remains dark)
• Hepatic adenoma: Peripheral arterial enhancement, heterogeneous (may contain hemorrhage/fat)
• Hemangioma: Peripheral nodular enhancement (globular pattern matching aorta/IVC)
• Hypervascular metastases: RCC, carcinoid, neuroendocrine tumor, thyroid, melanoma, choriocarcinoma
• HCC in cirrhosis: Classic arterial hyperenhancement is hallmark

• Hepatic artery aneurysm / pseudoaneurysm
• Arteriovenous fistulae (hepatic artery to portal vein - triangular or wedge-shaped enhancement near capsule)
• Active arterial hemorrhage (contrast extravasation)
• Hepatic trauma (laceration, contusion, active bleed)

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Phase 3: Portal Venous Phase

• Liver parenchyma reaches peak enhancement (~120-140 HU) - due to portal venous inflow (75% of blood supply)
• Portal vein: Fully opacified (90-120 HU)
• Hepatic veins: Beginning to opacify
• Spleen: Complete and uniform enhancement (no more "tiger" stripe artifact)
• Bowel wall: Good mucosal and mural enhancement
• Kidneys: Nephrographic phase

• Overall liver parenchyma assessment
• Detection of hypovascular lesions (appear dark against bright liver):
  • Most metastases (colorectal, pancreatic, gastric, lung)
  • Cholangiocarcinoma
  • Liver abscesses
  • Biliary cystadenocarcinoma
• Portal vein: Thrombosis, tumor thrombus (enhancing = tumor; non-enhancing = bland thrombus)
• Splenomegaly, splenic lesions
• Bowel wall pathology (ischemia, inflammation)
• IVC patency

• HCC that was bright in arterial phase becomes relatively hypodense in portal venous phase = "washout"
• Arterial hyperenhancement + portal venous washout = LI-RADS 4/5 for HCC

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Phase 4: Delayed / Equilibrium Phase

• Contrast equilibrates between intravascular and extravascular extracellular spaces
• Liver attenuation falls back towards baseline
• Most lesions become isodense (no longer visible)
• Only specific lesions retain contrast

• Progressive centripetal fill-in from arterial phase
• Complete or near-complete fill-in on delayed phase
• Remains isodense to blood pool (compare with aorta/IVC density)
• Key: Isodense to aorta on all phases (blood pool lesion)

• "Progressive delayed enhancement" / "central fill-in"
• Due to desmoplastic fibrous stroma - contrast enters fibrous tissue slowly
• Becomes MORE DENSE on delayed phase (unlike HCC)
• Peripheral washout, central progressive enhancement

• Central stellate scar: Hypodense on plain and arterial; enhances on delayed (scar contains myxomatous stroma and vessels)
• Lesion itself becomes isodense on delayed (rapid washout)

• Areas of fibrosis retain contrast on delayed (progressive fibrotic enhancement)

• Fibrous components may show delayed enhancement

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Phase 5: Hepatobiliary Phase (MRI specific - Gd-EOB-DTPA / Primovist)

• Hepatocyte-specific contrast agent taken up by normal hepatocytes via OATP1B1/B3 transporters and excreted into bile
• Normal liver and FNH: Bright (uptake)
• HCC, metastases, adenoma (except in rare cases): Dark (no uptake)
• Bile ducts: Visualized (biliary anatomy)
• Focal biliary strictures, leaks visible

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Summary Table: Lesion Enhancement Pattern

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Q.45 CAUSES OF ACUTE ABDOMEN IN ADULT + FIVE COMMON CONDITIONS WITH RADIOLOGICAL FINDINGS (30 Marks)

Definition

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Classification of Causes

1. Acute appendicitis
2. Acute cholecystitis / acute cholangitis
3. Acute pancreatitis
4. Diverticulitis
5. Peritonitis (primary / secondary)
6. Pelvic inflammatory disease
7. Liver/splenic abscess
8. Meckel's diverticulitis

1. Small bowel obstruction (adhesions, hernia, volvulus, intussusception)
2. Large bowel obstruction (carcinoma, volvulus, fecal impaction)
3. Biliary colic / choledocholithiasis
4. Renal/ureteric colic

1. Perforated peptic ulcer
2. Perforated appendix
3. Perforated diverticulum
4. Perforated carcinoma
5. Boerhaave syndrome (esophageal rupture)

1. Acute mesenteric ischemia
2. Ruptured AAA
3. Ischemic colitis
4. Splenic infarction
5. Ovarian / testicular torsion

1. Ruptured ectopic pregnancy
2. Ruptured ovarian cyst (hemorrhagic)
3. Spontaneous hepatic / splenic rupture
4. Anticoagulant-related hemorrhage (rectus sheath hematoma)

1. Ectopic pregnancy (ruptured / unruptured)
2. Ovarian torsion
3. Severe endometriosis

1. Acute urinary retention
2. Perinephric abscess
3. Renal vein thrombosis

1. Acute myocardial infarction (inferior MI)
2. Lower lobe pneumonia / empyema
3. Diabetic ketoacidosis
4. Sickle cell crisis
5. Herpes zoster

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Five Common Conditions with Radiological Findings

1. ACUTE APPENDICITIS

• Usually normal
• Fecalith (calcified appendicolith) in RIF in 15% (strongly suggestive)
• Localized ileus / sentinel loop
• Obliteration of psoas margin
• Soft tissue mass if abscess

• Noncompressible blind-ending tubular structure >6 mm diameter (outer-to-outer)
• Target sign in cross-section (concentric rings)
• Appendicolith: Echogenic focus with acoustic shadow
• Periappendiceal fat echogenicity (inflammation)
• Free fluid in RIF
• Absent peristalsis in appendix
• Power Doppler: Hyperemia (active inflammation)
• Perforation: Loss of wall integrity, loculated fluid

• Appendix > 6 mm in diameter with mural thickening
• Appendicolith (90% if seen = appendicitis)
• Periappendiceal fat stranding (haziness)
• Periappendiceal free fluid
• Appendiceal wall enhancement
• Loss of appendiceal wall integrity = perforation
• Abscess: Rim-enhancing collection in RIF/pelvis
• Phlegmon: Inflammatory soft tissue mass

• T2: Edematous dilated appendix with periappendiceal T2 signal

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2. ACUTE CHOLECYSTITIS

• Gallstones (echogenic with posterior acoustic shadow)
• Distended GB (length >9 cm, width >4 cm)
• Mural thickening (>3 mm) - especially anteriorly
• Pericholecystic fluid
• Murphy's sign on US (maximum tenderness when probe over GB)
• Subserosal edema ("halo sign")
• Gangrenous cholecystitis: Intraluminal membrane, irregular thickened wall, absent peristalsis of mobile stones
• Emphysematous cholecystitis: Echogenic foci in GB wall with ring-down artifact (gas)

• Distended GB with mural thickening
• Pericholecystic fat stranding
• Gallstones (calcified)
• Hyperenhancing inflamed GB wall
• Complications: Gangrenous change (absent enhancement), empyema (milk of calcium bile), perforation (discontinuous wall, pericholecystic abscess), cholecystoenteric fistula

• Technetium-99m HIDA injected IV - taken up by hepatocytes, excreted into bile
• Positive scan: GB NOT visualized by 60-90 minutes (cystic duct obstruction)
• 99% sensitivity for acute cholecystitis

• Choledocholithiasis (stones as dark filling defects in bright bile duct)
• Biliary anatomy

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3. ACUTE PANCREATITIS

• "Sentinel loop" (dilated proximal jejunum/duodenum due to local ileus)
• "Colon cutoff sign" (gas stops at splenic flexure due to transverse mesocolon inflammation)
• Loss of psoas shadow
• Pancreatic calcification (chronic pancreatitis)

• Edematous/hypoechoic pancreas
• Peripancreatic fluid
• Gallstones (identify biliary cause)
• CBD dilatation
• Limited by overlying bowel gas

• 0-3: Mild (low morbidity/mortality)
• 4-6: Moderate
• 7-10: Severe (morbidity >17%, mortality up to 17%)

• Pancreatic edema, enlargement
• Peripancreatic fat stranding
• Necrosis: Non-enhancing parenchyma (black areas on CECT) - >30% = severe
• Fluid collections: Acute peripancreatic fluid collection (APFC) - no defined wall; becomes pseudocyst after 4 weeks (defined wall)
• Walled-off necrosis (WON): After 4 weeks, encapsulated necrotic collection
• Complications: Splenic vein thrombosis, hepatic artery pseudoaneurysm, biliary obstruction

• Better for: Stone detection, ductal communication with fluid collection, no radiation
• MRCP: Pancreatic duct disruption / leakage
• Superior for characterizing fluid collections (debris vs pure fluid)

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4. SMALL BOWEL OBSTRUCTION (SBO)

• Multiple dilated small bowel loops (>2.5-3 cm) with air-fluid levels (Stepladder pattern)
• Central distribution (jejunum) vs peripheral (ileum)
• Valvulae conniventes (folds across entire bowel width) = small bowel
• Haustral folds (partial width) = large bowel
• Absent or minimal gas in colon (if complete obstruction)
• String of beads sign: Tiny air bubbles trapped between valvulae conniventes (seen in complete SBO with fluid-filled loops)

• Air-fluid levels at different heights in same loop = small bowel
• Air-fluid levels at same height = large bowel

• Transition point: Abrupt change from dilated to collapsed bowel (key finding)
• Cause at transition: Adhesions (no mass), hernia (loops through defect), tumor (mass), volvulus (whirl sign)
• Closed loop obstruction: C/U-shaped loop with two transition points, radial mesenteric vessels, high risk of strangulation
• Strangulation signs: Mural thickening, abnormal wall enhancement, pneumatosis, portal venous gas, mesenteric haziness, ascites, hyperattenuating bowel wall (hemorrhage)
• "Whirl sign": Twisted mesentery in volvulus
• "Beak sign": Tapered bowel at transition

• Used in younger patients
• Useful for Crohn's stricture, radiation enteropathy

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5. RUPTURED ABDOMINAL AORTIC ANEURYSM (AAA)

• Rapid bedside assessment (FAST/EFAST)
• Aortic diameter >3 cm = aneurysm
• Thrombus lining the aneurysm sac
• Cannot reliably detect retroperitoneal rupture
• Free intraperitoneal blood (anechoic fluid)

• Non-contrast CT: Aortic diameter measurement (outer wall to outer wall); retroperitoneal hematoma (hyperdense blood); aortic wall calcification
• CECT (Arterial phase):
  • Active contrast extravasation = active rupture
  • "Draped aorta" sign: Posterior aortic wall not separated from vertebral body (posterior rupture/periadventitial hematoma)
  • Hyperattenuating periaortic hematoma
  • Extent: Suprarenal or infrarenal (surgically important)
  • Iliac arteries: Extension of aneurysm
• CECT findings:
  • Intraluminal thrombus (low attenuation lining)
  • Luminal flow channel (enhancing)
  • Periaortic inflammatory changes (inflammatory AAA)
  • IVC compression (large AAA)
  • Aortoenteric fistula (erosion into duodenum - rare)

• For EVAR (endovascular aortic repair): Measure neck length, iliac anatomy, access vessel diameter
• 3D reconstruction for stent graft sizing

• Non-urgent cases; chronic aneurysm follow-up
• Better soft tissue characterization of inflammatory AAA
• No radiation

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Q.46 LIVER MRI SEQUENCES (30 Marks)

Introduction

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Basic Principles

• T1-weighted imaging: Signal proportional to T1 relaxation; fat, blood (subacute), proteinaceous material appear bright; fluid appears dark
• T2-weighted imaging: Signal proportional to T2 relaxation; fluid (cysts, bile) appears bright; fibrous tissue appears dark
• Gradient Echo (GRE): Fast acquisition, used for dynamic contrast; susceptible to field inhomogeneity (susceptibility effect)
• Echo Planar Imaging (EPI): Very fast, used for DWI
• Parallel imaging (SENSE/GRAPPA): Reduces acquisition time

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Complete Liver MRI Protocol - Sequences

1. T2-Weighted Sequences

• Breath-hold single shot; fast
• Fluid: Bright; Solid lesions: Variable
• Best for: Cysts (very bright T2), hemangiomas (moderately bright T2 "light bulb" sign)
• Detects: Bile duct dilatation, ascites, pleural effusion

• More detailed; multiple breath-holds or respiratory gating
• Better for lesion characterization
• Fibrotic lesions (cholangiocarcinoma, scarring): Dark on T2 (short T2)
• Hemangioma: Very bright (follows fluid)
• HCC: Moderately bright T2 (higher T2 than surrounding liver)
• Metastases: Variable T2 (bright if mucinous, hemorrhagic)

• Heavily T2-weighted (TR/TE very long)
• Only fluid remains bright → bile ducts visualized
• Biliary anatomy: Primary and intrahepatic ducts
• Choledocholithiasis: Dark stones (filling defects) in bright bile
• Primary sclerosing cholangitis (PSC): Beading, strictures
• Biliary strictures, cholangiocarcinoma
• Pancreatic duct assessment

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2. T1-Weighted Sequences

• Exploits chemical shift between water and fat protons
• In-phase (TE ~4.8 ms at 1.5T / ~2.4 ms at 3T): Water + fat signals add
• Out-of-phase (TE ~2.4 ms at 1.5T / ~1.2 ms at 3T): Water - fat signals cancel

• Hepatic steatosis: Liver signal drops on out-of-phase (India ink artifact at organ interface)
• India ink / etching artifact: Black rim around liver (fat-water interface)
• Drop in SI on out-of-phase compared to in-phase = fat content (diffuse or focal steatosis)
• HCC: May contain fat (drop in signal) - supports HCC diagnosis
• Hepatic adenoma: Often contains fat

• Volumetric interpolated breath-hold examination
• Isotropic voxels; MPR capability
• Used for dynamic contrast-enhanced series (pre-contrast + multiphase post-contrast)
• Fat-saturated version: Suppresses fat background, improves lesion-to-liver contrast

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3. Dynamic Contrast-Enhanced MRI (DCE-MRI)

• Baseline; identifies intrinsic T1 bright lesions (fat, blood, protein)
• HCC: May have T1 bright foci (fat, copper, glycogen)
• Hemangioma: T1 dark (fluid)
• Adenoma: T1 bright (fat, blood)

• Gadolinium-based contrast agent (GBCA): Standard extracellular agents (Gd-DTPA, Gd-DOTA, Gadobutrol) OR hepatocyte-specific agents (Gd-EOB-DTPA/Primovist, Gd-BOPTA/Multihance)
• Hypervascular lesions bright: HCC, FNH, adenoma, hemangioma (peripheral nodular)

• Liver parenchyma peak enhancement
• Hypovascular lesions visible: Metastases, cholangiocarcinoma

• Hemangioma: Complete fill-in
• FNH: Central scar enhances
• Cholangiocarcinoma: Progressive enhancement
• HCC: Washout appearance (hypointense)

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4. Hepatobiliary Phase (HBP) - Unique to MRI

• Gd-EOB-DTPA (Primovist/Eovist): 50% hepatic excretion; stronger HBP signal
• Gd-BOPTA (MultiHance): 3-5% hepatic excretion; weaker HBP

• Normal liver / FNH: Bright (uptake) - FNH contains functional hepatocytes
• HCC: Usually dark (poorly differentiated - OATP downregulated); well-differentiated HCC may show uptake
• Hepatic adenoma: Dark (no uptake) - exception: HNF1a-mutated adenoma sometimes shows faint uptake
• Metastases: Dark (no hepatocytes)
• Cysts, hemangiomas: Dark (no hepatocytes)
• Bile ducts: Bright (contrast excreted into bile) → dynamic cholangiography possible
• Biliary anatomy: Leak, fistula, stricture

• Detects additional HCC nodules invisible on other phases
• Differentiates FNH from adenoma (FNH = bright; adenoma = dark on HBP)
• Biliary mapping pre-surgery

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5. Diffusion-Weighted Imaging (DWI)

• Measures Brownian motion (random movement) of water molecules in tissue
• Restricted diffusion = tightly packed cells (malignancy, abscess) = bright on high b-value DWI
• Free diffusion = cysts, necrosis = dark on high b-value DWI

• b-values: 0, 50, 400, 800 s/mm² (higher b = more diffusion weighting)
• ADC map (Apparent Diffusion Coefficient): Calculated from multiple b-values
  • Low ADC = restricted diffusion = malignancy
  • High ADC = free diffusion = cyst, hemangioma

• Detection of focal liver lesions (especially metastases) - comparable to CECT for liver mets
• Characterization: Benign vs malignant
• Fibrosis assessment (liver stiffness correlates with lower ADC)
• Treatment response monitoring (successful ablation → ADC increases)
• Hepatocellular carcinoma - detection and staging

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6. Susceptibility Weighted Imaging (SWI) / GRE T2*

• Detects paramagnetic substances: Iron, calcium, blood, air
• Iron overload (hemosiderosis, hemochromatosis): Liver very dark (T2* signal loss) - quantitative MRI for iron
• Hemangiosarcoma: Hemorrhagic areas dark
• Calcification in echinococcal cyst wall
• Pneumobilia: Air appears dark

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7. Magnetic Resonance Elastography (MRE)

• Mechanical driver applies external vibrations (60 Hz)
• Phase-contrast MRI sequence captures wave propagation
• Generates stiffness maps (elastograms) of entire liver
• Values:
  • Normal: 2-3 kPa
  • F2 fibrosis: ~3.5 kPa
  • Cirrhosis: >5 kPa
• More accurate than US elastography; not affected by ascites or obesity
• Can assess steatotic livers accurately

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8. Fat Quantification Sequences (MRI-PDFF)

• Proton Density Fat Fraction (PDFF): Most accurate non-invasive fat quantification
• Multi-echo Dixon method: Separates fat and water signals
• PDFF > 5.5% = hepatic steatosis
• Grades: S1 (5-17%), S2 (17-33%), S3 (>33%)
• Important in NAFLD/NASH management

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9. MR Angiography (MRA)

• Phase-contrast MRA or CE-MRA (gadolinium)
• Hepatic arterial anatomy (pre-TACE, transplant planning)
• Portal vein patency, Budd-Chiari (hepatic vein thrombosis)
• IVC involvement

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Standard Liver MRI Protocol Summary

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LI-RADS Classification (Liver Imaging Reporting and Data System)

• LR-1: Definitely benign
• LR-2: Probably benign
• LR-3: Intermediate probability for HCC
• LR-4: Probably HCC
• LR-5: Definitely HCC (arterial hyperenhancement + washout on portal/delayed + capsule)
• LR-M: Probably/definitely malignant, not HCC specific
• LR-TR: Treated lesion

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What Was Covered - Summary