RADIOLOGY UNIVERSITY THEORY EXAM - FULL ANSWERS (30 Marks Each)

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Q20. HYPERTROPHIC PYLORIC STENOSIS (HPS)

Definition

Epidemiology

• Incidence: 2-4 per 1000 live births
• Male:Female ratio = 4:1 (males predominantly affected)
• Age of presentation: 2-8 weeks of life (peak at 3-6 weeks)
• First-born males most commonly affected
• Associated with macrolide antibiotic use (erythromycin) in early infancy

Pathophysiology

• Projectile, non-bilious vomiting (post-prandial)
• Hypochloraemic, hypokalaemic metabolic alkalosis
• Dehydration and weight loss
• "Hungry" infant who feeds again immediately after vomiting

Clinical Features

• Projectile non-bilious vomiting (olive-sized mass palpable in epigastrium)
• Visible gastric peristaltic waves (left to right)
• Electrolyte imbalance: low Na+, K+, Cl-, high HCO3-
• Jaundice in 2-5% (unconjugated - due to glucuronyl transferase deficiency)

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RADIOLOGICAL INVESTIGATIONS

1. Plain Abdominal Radiograph (AXR)

• Dilated stomach with paucity of gas distally
• "Caterpillar sign" - visible gastric peristaltic waves as indentations
• Gasless abdomen distal to pylorus
• Limited diagnostic value, mainly to exclude other causes

2. Barium Meal (Upper GI Study) - GOLD STANDARD (historically)

• "String sign" (Kangaroo sign): Thin line of barium passing through elongated, narrowed pyloric canal - most specific sign
• "Shoulder sign": Indentation of barium-filled antrum by pyloric mass, creating a "shoulder" or "mushroom" appearance at antroduodenal junction
• "Teat sign": Barium trapped in folds at pyloric entrance creates teat-like projection
• "Double track sign": Two parallel tracks of barium in compressed pyloric canal
• "Pyloric beak sign": Beak-like projection of barium into pyloric lumen
• Delayed gastric emptying
• Antrum narrowing and elongation of pyloric channel (>14 mm in length)
• "Umbrella" or "Mushroom" sign at base of pyloric canal

3. Ultrasound (USG) - CURRENT MODALITY OF CHOICE

• No radiation
• Highly accurate (sensitivity 97-99%, specificity 97-100%)
• Can directly measure pyloric muscle

• "Cervix sign" (Pseudokidney sign): Hypoechoic muscle ring around echogenic mucosa resembles cervix uteri on transverse scan
• "Antral nipple sign": Redundant mucosa prolapsing into antrum
• "Target sign": Bull's eye appearance on transverse section
• Failure of pyloric canal to open during real-time observation
• Absence of gastric emptying over extended observation period

4. MRI

• Not routinely used; reserved for inconclusive cases
• Accurate but expensive and time-consuming

5. Upper GI Endoscopy

• Can show "crowning" of folds at pylorus
• Not first-line; more useful to exclude other causes

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Differential Diagnosis

1. Pylorospasm (transient, not persistent)
2. Antral web/diaphragm
3. Gastroesophageal reflux
4. Overfeeding
5. Duodenal atresia (bilious vomiting - different)

Treatment

• Ramstedt pyloromyotomy (laparoscopic or open)
• Pre-operative correction of electrolyte imbalance is essential
• NOT a surgical emergency (medical optimization first)

Key Points for Exam

• USG is investigation of choice; barium meal if USG inconclusive
• Pyloric muscle thickness ≥4 mm is diagnostic
• String sign on barium - most specific radiological sign
• Non-bilious projectile vomiting in 3-6 week old male

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Q21. BARIUM FINDINGS IN COMMON INTESTINAL PATHOLOGIES

Introduction

• Barium swallow: Oesophagus
• Barium meal: Stomach and duodenum
• Small bowel follow-through (SBFT): Small intestine
• Barium enema: Large intestine
• Double contrast: Air + barium (better mucosal detail)

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A. OESOPHAGEAL PATHOLOGIES

1. Carcinoma Oesophagus

• Squamous cell carcinoma (middle third): Irregular shouldered narrowing ("rat-tail" or "apple core" appearance), mucosal destruction, shouldered margins (Carman's meniscus)
• Adenocarcinoma (lower third/GEJ): Asymmetric narrowing, mucosal irregularity
• Signs: "Rat tail" stricture, eccentric irregular filling defect, pre-stenotic dilatation

2. Achalasia Cardia

• Smooth tapering narrowing at lower oesophagus ("bird beak" or "champagne glass" sign)
• Dilated oesophagus (megaoesophagus)
• Food residue in oesophagus
• Failure of relaxation of lower oesophageal sphincter
• "Air-fluid level" in chest on plain film

3. Oesophageal Varices

• Worm-like/tortuous filling defects in lower oesophagus
• "Worm-eaten" or "rosary bead" appearance
• Best seen on prone swallow
• Collapse on Valsalva

4. Peptic Stricture

• Smooth, tapered, symmetric narrowing in lower third
• Associated hiatus hernia

5. Plummer-Vinson Syndrome (Paterson-Kelly)

• Thin web at pharyngo-oesophageal junction (post-cricoid)
• Associated with iron deficiency anaemia

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B. GASTRIC/DUODENAL PATHOLOGIES

1. Peptic Ulcer Disease

• Gastric ulcer:
  • "Niche" sign (barium-filled crater projecting beyond gastric wall)
  • Hampton's line (thin radiolucent line across ulcer neck)
  • Radiating mucosal folds from ulcer base
  • Carman's meniscus sign (meniscus-like filling defect - malignant ulcer)
  • Ulcer on lesser curvature most commonly
• Duodenal ulcer:
  • "Bull's eye" or "target" lesion
  • Deformity of duodenal cap ("clover leaf" deformity)
  • "Trefoil" or "Mickey Mouse ear" deformity

2. Gastric Carcinoma

• Scirrhous type (Linitis plastica): "Leather bottle" stomach - small, rigid, non-distensible stomach; loss of peristalsis
• Ulcerative type: Irregular, shouldered ulcer with Carman's meniscus sign
• Polypoid type: Lobulated filling defect
• Infiltrative type: Mucosal destruction, rigidity

3. Hypertrophic Gastritis (Menetrier's disease)

• Giant rugal folds (>1 cm) predominantly in fundus/body
• "Cerebriform" appearance of mucosa

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C. SMALL INTESTINAL PATHOLOGIES

1. Crohn's Disease (Terminal Ileum)

• "String sign of Kantor": Narrow string-like lumen due to spasm/fibrosis
• "Skip lesions" (discontinuous involvement)
• "Cobblestone" mucosa (longitudinal + transverse ulcers)
• "Rose thorn" ulcers (deep fissuring ulcers)
• Fistulae formation
• Pre-stenotic dilatation
• Separation of bowel loops (mesenteric thickening)
• "Creeping fat" sign on CT

2. Tuberculosis (Ileocaecal)

• Stierlin's sign: Rapid emptying of involved segment (caecum + terminal ileum), leaving "streak" of barium
• Pulled-up caecum (shortening of ascending colon)
• "Inverted umbrella" deformity of ileocaecal valve
• "Purse string" deformity
• Conical caecum

3. Coeliac Disease (Sprue)

• Moulage sign: Featureless, effaced small bowel loops (loss of valvulae conniventes)
• Flocculation and segmentation of barium column
• Jejunalisation of ileum (ileum develops fold pattern of jejunum)
• Dilated loops with thickened folds in severe disease

4. Small Bowel Obstruction

• Dilated loops of small bowel (>3 cm)
• Valvulae conniventes (plicae circulares) visible
• "Stack of coins" or "ladder" appearance
• Air-fluid levels (stepladder on erect film)
• Transition point identification

5. Intussusception

• "Coiled spring" appearance on barium enema (entrapped barium around intussusceptum)
• "Claw sign" (barium outlining head of intussusceptum)

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D. LARGE INTESTINAL PATHOLOGIES

1. Carcinoma Colon

• "Apple core" sign: Annular, circumferential narrowing with shouldered margins, mucosal destruction
• Most common in sigmoid and rectosigmoid
• Short segment (3-5 cm) involvement
• Shouldering ("rat-tail" ends)

2. Ulcerative Colitis

• "Lead pipe" colon: Loss of haustrations, shortened, rigid colon
• Granular/stippled mucosal pattern
• "Collar button" ulcers (flask-shaped, undermining)
• Continuous involvement from rectum proximally
• Pseudopolyps (inflammatory)
• "Backwash ileitis" involvement of terminal ileum

3. Diverticulosis

• Flask-shaped outpouchings outside bowel wall (mainly sigmoid)
• "Saw tooth" appearance on barium enema
• Complications: perforation (tracking extravasation), obstruction

4. Hirschsprung's Disease

• "Transition zone": Narrow aganglionic segment (rectum) with abrupt dilatation proximally
• Inverted rectosigmoid ratio (normal >1, reversed in Hirschsprung's)
• "Funnel" or "cone" at transition zone
• Delayed barium evacuation (>24 hours)

5. Volvulus

• Sigmoid volvulus: "Coffee bean" sign (omega-shaped distended loop), "bird beak" at site of twist
• Caecal volvulus: Distended caecum in left upper quadrant

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Q22. SONOGRAPHIC FINDINGS AND DIFFERENTIAL DIAGNOSIS OF PAEDIATRIC ABDOMINAL MASSES

Introduction

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A. WILMS' TUMOUR (Nephroblastoma)

• Large, well-defined solid renal mass
• Heterogeneous echogenicity (mixed solid-cystic due to necrosis/haemorrhage)
• Intrarenal origin - identifiable claw of normal renal tissue around mass ("claw sign")
• May contain calcification (10-15%, fine/stippled)
• Renal vein and IVC extension (25%) - Doppler shows tumour thrombus
• Bilateral in 5-10% cases
• Displacement of adjacent organs
• Lymphadenopathy assessment

• "Claw sign" of renal origin
• Heterogeneous enhancement
• Lung metastases screening (most common site)

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B. NEUROBLASTOMA

• Suprarenal, retroperitoneal mass
• Heterogeneous echogenicity
• Coarse, irregular calcification (90%) - highly characteristic
• Encasement/displacement of adjacent vessels (aorta, IVC) - "vascular encasement" vs. Wilms' (vessel displacement)
• Crosses midline
• Lymphadenopathy
• Liver metastases (4S disease)
• Bone marrow involvement

• Stage 4S: special stage in infants <1 year with localized primary + liver/skin/marrow spread - can spontaneously regress

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C. HEPATOBLASTOMA

• Large solitary hepatic mass (often right lobe)
• Hyperechoic, heterogeneous
• May have calcification
• Increased vascularity on Doppler
• AFP markedly elevated (diagnostic marker)
• Portal vein invasion in advanced disease

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D. HEPATOCELLULAR CARCINOMA (HCC) in Children

• Older children (>5 years)
• Associated with hepatitis B, cirrhosis, tyrosinaemia
• USG: heterogeneous mass, often multifocal, portal vein thrombosis

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E. ADRENAL HAEMORRHAGE (Neonatal)

• Most common adrenal mass in neonates
• USG: Initially hyperechoic solid mass; becomes cystic and involutes over weeks
• Serial USG shows resolution (differentiates from neuroblastoma)
• Suprarenal location; calcification may develop later

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F. MULTICYSTIC DYSPLASTIC KIDNEY (MCDK)

• Most common renal mass in neonates
• USG: Multiple non-communicating cysts of varying sizes replacing renal parenchyma; no identifiable normal renal tissue; no renal sinus
• Differentiates from hydronephrosis: in hydronephrosis, cysts communicate with a central pelvis

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G. HYDRONEPHROSIS

• Most common cause of abdominal mass in neonates
• USG: Dilated renal pelvis and calyces communicating with each other; identifiable renal parenchyma around cysts
• Causes: PUJ obstruction (most common), VUR, posterior urethral valves

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H. OVARIAN CYSTS AND MASSES

• Simple ovarian cysts in neonate/infant (maternal hormonal stimulation)
• USG: Simple anechoic cyst, thin-walled, acoustic enhancement
• Complications: torsion (complex appearance, internal echoes)
• Malignant ovarian tumors (older girls): complex, solid-cystic, papillary projections

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I. MESENTERIC/OMENTAL CYSTS

• USG: Thin-walled, unilocular or multilocular cystic mass in mesentery; transilluminates; no flow on Doppler; moves freely

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J. LYMPHOMA (NHL/Hodgkin's)

• Older children
• USG: Multiple enlarged lymph nodes (>1 cm, rounded, hypoechoic, loss of hilum); may have mesenteric involvement
• "Sandwich sign" on CT (nodes surrounding mesenteric vessels)

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APPROACH TO USG EVALUATION

1. Determine organ of origin (renal, hepatic, adrenal, retroperitoneal, mesenteric)
2. Solid vs. cystic vs. mixed
3. Internal architecture (septa, calcification, vascularity)
4. Relationship to adjacent vessels (displacement vs. encasement)
5. Other organ involvement (liver, lymph nodes, IVC)
6. Follow with CT/MRI for staging

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Q23. INTUSSUSCEPTION

Definition

Epidemiology

• Most common cause of intestinal obstruction in infants 6 months to 3 years
• Peak: 5-9 months of age
• Male > Female (2:1)
• 90% ileocolic (terminal ileum into caecum) in children
• Adults: 90% have a pathological lead point

Causes / Lead Point

• Children (<3 years): 90% idiopathic (likely enlarged Peyer's patches post-viral infection)
• Lead points (more common in older children and adults):
  • Meckel's diverticulum (most common lead point requiring surgery)
  • Intestinal polyp (Peutz-Jeghers)
  • Lymphoma (Burkitt's in Africa)
  • Duplication cyst
  • Appendix
  • Lipoma

Clinical Features (Classic Triad)

1. Colicky abdominal pain (intermittent, severe, drawing up of legs)
2. "Redcurrant jelly" stools (blood-stained mucus - late sign indicating ischemia)
3. Palpable "sausage-shaped" mass in right upper quadrant

• Vomiting (initially non-bilious, later bilious)
• Dance's sign: emptiness in right iliac fossa

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RADIOLOGICAL INVESTIGATIONS

1. Plain Abdominal X-Ray

• Often first investigation
• Signs:
  • Soft tissue density mass (intussusceptum visible as soft-tissue opacity)
  • Paucity of gas in right iliac fossa (where caecum normally is)
  • Signs of obstruction (dilated loops, air-fluid levels)
  • Target sign (occasionally) - concentric soft tissue densities
  • "Crescent sign": gas trapped around intussusceptum in periphery
  • Normal in up to 25% of cases

2. Ultrasound - PRIMARY DIAGNOSTIC MODALITY

• "Doughnut sign" / "Target sign": Hyperechoic central mass (intussusceptum with its mesentery) surrounded by hypoechoic ring (edematous outer intussuscipiens wall)
• Multiple concentric rings ("Onion skin" appearance)

• "Pseudokidney sign" / "Sandwich sign": Layers of bowel resembling kidney on sagittal section
• Identified layers: outer intussuscipiens wall, intussusceptum with trapped mesentery

• Bowel wall thickening
• Free peritoneal fluid (suggests ischemia/perforation)
• Lead point identification (lymph node, polyp)
• Doppler: absent vascularity = bowel ischemia (poor prognostic sign)
• Lymphadenopathy (Peyer's patch enlargement as lead point)

• Absent Doppler flow
• Large amount of free fluid
• Visible lead point other than lymph node

3. Contrast Enema (Fluoroscopic / Air) - DIAGNOSTIC AND THERAPEUTIC

• "Claw sign": Barium outlining the apex (intussusceptum) within intussuscipiens
• "Coiled spring sign": Barium trapped in mucosal folds between intussusceptum and intussuscipiens creating coil-spring pattern
• "Cup" sign: Cup-shaped filling defect at leading edge

• Air insufflated per rectum under fluoroscopic/USG guidance
• Pressure maintained at <120 mmHg
• Success rate: 70-90% for first presentation
• Signs of successful reduction:
  • Disappearance of mass
  • Free reflux of air into terminal ileum
  • Resolution of mass on USG

• Saline enema under USG monitoring
• Preferred in centres with USG expertise
• Success rate comparable to pneumatic

• Peritonitis / perforation
• Shock, unresuscitated
• Free pneumoperitoneum
• Evidence of bowel ischemia (absent Doppler flow, prolonged symptoms >48 hours)

4. CT Scan

• For complex/atypical cases or adults
• Identifies lead point
• CT Signs: "Target sign" on cross-section, "sausage sign" on longitudinal section
• Bowel wall enhancement assessment for ischemia
• Adults: almost always identifies pathological lead point

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Complications

• Bowel ischemia and necrosis
• Perforation
• Peritonitis
• Recurrence after reduction (5-10%)

Treatment Summary

1. Resuscitation
2. Pneumatic/hydrostatic enema reduction (if no contraindication) - first line
3. Surgical reduction / resection if enema fails or contraindicated

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Q24. SMA SYNDROME (Superior Mesenteric Artery Syndrome)

Definition

Anatomy

• The third/transverse part of the duodenum (D3) crosses the midline between:
  • Posteriorly: Abdominal aorta and vertebral column
  • Anteriorly: SMA (arising from aorta at L1 at an angle of 38-65 degrees normally)
• Normally, the aortomesenteric angle is 38-65° and distance is 10-28 mm
• In SMA syndrome: Angle reduced to <22-25°; distance <8-10 mm
• The narrow angle compresses the duodenum

Pathophysiology

• Rapid weight loss (most common cause)
• Anorexia nervosa
• Prolonged supine immobilization/body cast application ("cast syndrome")
• Scoliosis correction surgery
• Burns
• Malabsorption states
• Cachexia from malignancy
• High-riding SMA origin

Clinical Features

• High intestinal obstruction symptoms
• Postprandial epigastric pain
• Nausea and bilious vomiting (bile-stained)
• Early satiety
• Weight loss (worsening the condition - vicious cycle)
• Relief in left lateral decubitus, prone, or knee-chest position
• Chronic intermittent symptoms common

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RADIOLOGICAL INVESTIGATIONS

1. Plain X-Ray Abdomen

• Distended stomach and duodenum (D1, D2) with air
• "Double bubble" sign (dilated stomach + duodenum)
• Air-fluid levels

2. Barium Meal / Upper GI Study (Upper GI Series)

• Dilatation of first and second parts of duodenum
• Abrupt, linear, oblique cut-off of barium at D3 (at the level of L1-L2 vertebra, crossing the midline)
• "Pulsatile extrinsic compression" at D3 - the impression corresponds to aortic pulsation
• "Reverse 3 sign" or "to and fro" peristalsis (barium oscillates back and forth across compressed segment)
• Delay in gastric emptying
• Relief of obstruction in left lateral decubitus position (diagnostic and therapeutic test within the study)

3. Ultrasound

• Identification of SMA and measurement of aortomesenteric angle
• Dilated duodenum proximal to compression point
• Assessment of retroperitoneal fat

4. CT Scan (Investigation of Choice for Diagnosis)

• Aortomesenteric angle <22-25° (normal 38-65°)
• Aortomesenteric distance <8-10 mm (normal 10-28 mm)
• Compression of D3 between aorta and SMA
• Dilated proximal duodenum and stomach
• Absence of retroperitoneal fat
• High origin of SMA
• CT angiography shows SMA-aortic angle precisely

5. MRI / MR Enterography

• Multiplanar assessment of duodenum and mesenteric vessels
• No radiation; useful in young patients

6. Upper GI Endoscopy

• Pulsatile extrinsic compression at D2-D3 junction
• Confirms location, excludes intrinsic pathology
• Limited in showing dynamic compression

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Differential Diagnosis

• Duodenal web/atresia
• Annular pancreas
• Duodenal tumor
• Periduodenal adhesions
• Retroperitoneal fibrosis
• Duodenal hematoma

Treatment

1. Conservative: nutritional support, nasojejunal feeding, prone/left lateral positioning, weight gain
2. Surgical: Duodenojejunostomy (Strong's procedure) - bypasses obstruction; Laparoscopic approach preferred

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Q25. EVALUATION OF ANEURYSM OF ABDOMINAL AORTA AND ITS COMPLICATIONS BY RADIO-IMAGING

Definition

Classification

• Fusiform (most common - 95%): Symmetrical dilatation involving entire circumference
• Saccular: Asymmetric outpouching of one wall
• True aneurysm: All three layers of vessel wall involved
• False aneurysm (pseudoaneurysm): Contained haematoma outside vessel wall (usually post-traumatic/iatrogenic)
• Inflammatory AAA (5-10%): Thick periaortic fibrosis, associated with retroperitoneal fibrosis

• Infrarenal (95%): Below renal arteries - most common
• Juxtarenal, Pararenal, Suprarenal

• AAA: >3 cm
• Significant/large: >5 cm (surgical threshold - rupture risk high)
• Risk of rupture doubles for every 0.5 cm increase above 5 cm
• Annual rupture risk: 5 cm = 5-10%; 6 cm = 10-20%; >7 cm = >20%

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RADIOLOGICAL INVESTIGATIONS

1. Plain X-Ray Abdomen

• Curvilinear "eggshell" calcification outlining aortic wall (calcification of intima/media)
• Widened aortic silhouette
• "Draped aorta" sign (aneurysm lying in prevertebral fossa)
• Loss of psoas margin suggests retroperitoneal haematoma
• Vertebral body erosion in large aneurysms
• Limitations: Cannot measure diameter accurately; misses non-calcified aneurysm

2. Ultrasound (USG) - SCREENING AND SURVEILLANCE MODALITY OF CHOICE

• Most cost-effective screening tool; no radiation; highly accurate for size measurement
• Sensitivity 98-100% for diagnosis; accurate sizing (within ±2 mm)

• Dilated aorta >3 cm
• Mural thrombus (hypoechoic/heterogeneous material lining aortic wall)
• Calcified plaques
• Residual lumen identification with colour Doppler
• Extent of aneurysm (supra vs. infrarenal)
• Colour Doppler: Swirling flow pattern ("yin-yang sign") in lumen; absent flow in thrombus
• Power Doppler/CEUS: Endoleak detection post-EVAR

• One-time screening with USG in all men aged 65 years
• If aorta <3 cm: no further surveillance
• 3-4.4 cm (small AAA): annual USG
• 4.5-5.4 cm (medium AAA): 3-monthly USG
• ≥5.5 cm: referral for surgical/endovascular repair

3. CT Angiography (CTA) - GOLD STANDARD FOR PRE-OPERATIVE PLANNING

• Investigation of choice for pre-operative evaluation, complications, and emergency rupture

• Non-contrast phase: detect thrombus, calcification, retroperitoneal blood
• Arterial phase (CTA): contrast-enhanced, 3D reconstructions (MPR, MIP, VR, CPR)

• Accurate diameter measurement (true lumen + mural thrombus)
• Aortic neck anatomy (length, angulation, diameter) for EVAR planning
• Iliac artery assessment (occlusive disease, tortuosity)
• Renal artery involvement
• Visceral vessel origins
• Mural thrombus (concentric, eccentric)
• Calcification pattern
• Retroperitoneal/periaortic inflammation (inflammatory AAA: "mantle sign" - soft tissue collar)

• Retroperitoneal haematoma (hyperdense blood in retroperitoneum)
• "Draped aorta sign": Posterior aortic wall not definable, aneurysm drapes over vertebral body
• "Crescent sign": Hyperdense crescent within mural thrombus (sentinel bleed - impending rupture)
• Active extravasation of contrast
• Loss of retroperitoneal fat planes
• Free intraperitoneal blood (worst prognosis)

4. MR Angiography (MRA)

• No ionizing radiation or iodinated contrast
• Excellent for renal function-impaired patients
• Gadolinium-enhanced MRA with 3D reconstruction
• Black blood MRI: Aortic wall assessment (mural thrombus, wall haematoma)
• Limitations: Overestimates length, less accurate than CTA, longer scan time

5. Conventional Angiography (DSA)

• Historical gold standard - now superseded by CTA/MRA
• Shows only residual lumen (not total diameter including thrombus)
• Used intra-procedurally during EVAR
• Intra-operative angiography guides endograft deployment and detects endoleaks

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COMPLICATIONS OF AAA AND THEIR IMAGING

1. Rupture (Most Feared Complication)

• Mortality: untreated >90%; emergency surgery 40-50%
• Types: Retroperitoneal (most common), Intraperitoneal (worst), Aortocaval, Aortoduodenal
• CT Signs: Retroperitoneal haematoma, crescent sign, draped aorta sign, active extravasation
• USG: Useful in haemodynamically unstable patients; identifies AAA but limited for retroperitoneal bleed

2. Thrombosis and Embolism

• Mural thrombus fragments embolize distally
• "Blue toe syndrome": Digital ischemia from microembolism
• CT shows absent peripheral vessels; USG shows absent Doppler flow

3. Aortoduodenal Fistula

• Communication between aorta and duodenum (usually D2/D3)
• Massive GI bleeding (herald bleed)
• CT: gas within aortic thrombus/wall, duodenal thickening, loss of fat plane between aorta and duodenum

4. Aortocaval Fistula

• Communication between aorta and IVC
• High-output cardiac failure, lower limb venous hypertension, haematuria
• CT/Doppler: early opacification of IVC, dilated IVC

5. Inflammatory AAA

• 5-10% of AAAs
• Periaortic fibrosis entrapping ureters (hydronephrosis)
• CT: thick soft tissue "mantle" around anterior/lateral aortic wall; spares posterior wall ("mantle sign")
• Elevated ESR, CRP

6. Infection (Mycotic Aneurysm)

• Rapid expansion, saccular morphology, gas in aortic wall
• CT: periaortic gas/fluid, adjacent vertebral erosion, irregular/lobulated outline

7. Endoleak (Post-EVAR Complication)

• CTA post-EVAR: enhancement outside graft within aneurysm sac = endoleak

Treatment

• Endovascular repair (EVAR): For anatomically suitable aneurysms; less invasive; requires surveillance
• Open surgical repair: For young patients, ruptured AAA, unsuitable anatomy
• Threshold for repair: ≥5.5 cm, rapid expansion (>1 cm/year), symptomatic

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Q26. COMPLICATIONS OF PANCREATITIS

Introduction

Severity Classification (Atlanta 2012)

• Mild: No organ failure, no local complications
• Moderately severe: Transient organ failure (<48 hr) and/or local complications
• Severe: Persistent organ failure (>48 hr) - single or multi-organ

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A. LOCAL COMPLICATIONS

1. Acute Peripancreatic Fluid Collections (APFC)

• Timing: First 4 weeks of interstitial oedematous pancreatitis
• Imaging: Non-encapsulated, homogeneous fluid, follows fascial planes, no debris
• CT: Peripancreatic fluid without defined wall; low attenuation; no internal septations
• Outcome: 50% resolve spontaneously

2. Pseudocyst

• Timing: >4 weeks after onset (wall matures over 4 weeks)
• Definition: Encapsulated peripancreatic fluid collection with well-defined inflammatory wall; no solid component
• CT Findings:
  • Well-defined, rounded/oval cystic collection
  • Thick fibrous/inflammatory wall
  • Homogeneous low attenuation contents (Hounsfield ~0-20)
  • No internal septations or solid components
  • Communication with main pancreatic duct (in ~50%)
  • Peripancreatic location (lesser sac most common)
• USG: Anechoic/hypoechoic collection with posterior acoustic enhancement; well-defined wall
• MRCP/EUS: Assess ductal communication - critical for management
• Complications: Infection, rupture, haemorrhage, gastric/biliary obstruction
• Treatment: Endoscopic cystogastrostomy (if >6 cm, symptomatic, failing to resolve), EUS-guided drainage

3. Acute Necrotic Collection (ANC)

• Timing: First 4 weeks of necrotizing pancreatitis
• CT Findings:
  • Non-enhancing pancreatic parenchyma (necrosis = no contrast enhancement)
  • Heterogeneous collection with solid and liquid components
  • No encapsulating wall
  • May involve peripancreatic tissues

4. Walled-Off Necrosis (WON)

• Timing: >4 weeks; mature encapsulated collection in necrotizing pancreatitis
• CT Findings:
  • Well-defined thick enhancing wall
  • Heterogeneous contents (solid necrotic material + fluid) - distinguishes from pseudocyst
  • Gas bubbles within (if infected)
  • "Non-liquefied solid components" within cystic collection
• MRI: Better than CT for characterizing solid necrotic debris
• Treatment: Endoscopic step-up approach (drainage, necrosectomy)

5. Pancreatic Necrosis

• Definition: Non-viable pancreatic parenchyma
• CT Criteria (best at 48-72 hours after onset):
  • CT Severity Index (Balthazar Score + Necrosis Score)
  • Non-enhancing pancreatic parenchyma on contrast-enhanced CT
  • <30% necrosis = mild; 30-50% = moderate; >50% = severe

6. Infected Necrosis

• Timing: After first week; peak at 2-4 weeks
• CT Findings:
  • Gas bubbles within necrotic collection - PATHOGNOMONIC of infection
  • CT-guided aspiration confirms infection (Gram stain + culture)
  • "Bubbly" appearance within necrotic area

7. Pancreatic Ascites

• Disruption of pancreatic duct with fistula into peritoneal cavity
• High amylase-rich ascitic fluid
• CT: free peritoneal fluid + ductal disruption on MRCP/ERCP

8. Pancreatic Abscess

• Walled-off collection with pus and minimal necrosis (distinct from infected necrosis)
• Late complication (>4 weeks)
• CT: loculated collection with thick wall and gas; rim enhancement

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B. VASCULAR COMPLICATIONS

1. Splenic Vein Thrombosis

• Most common vascular complication
• Causes segmental portal hypertension
• CT/Doppler: Non-filling of splenic vein; collateral vessels in gastric wall (gastric varices)
• CT: filling defect in splenic vein, splenomegaly

2. Pseudoaneurysm

• Enzymatic digestion of arterial wall
• Most common: splenic artery (45%), gastroduodenal artery (18%), hepatic artery, pancreaticoduodenal arteries
• CT Angiography: Round/oval contrast-filled structure adjacent to pancreas; communicates with artery
• USG Doppler: "Yin-yang" or swirling colour flow; turbulent pulsatile waveform
• Complication: Massive haemorrhage (into pseudocyst = "haemorrhagic pseudocyst", GIT, peritoneum)
• Treatment: Transcatheter arterial embolization (TAE) - first line; surgery if fails

3. SMV/Portal Vein Thrombosis

• Extension of splenic vein thrombosis
• CT: filling defect in SMV/portal vein; bowel ischemia if extensive

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C. SYSTEMIC COMPLICATIONS

1. ARDS (Acute Respiratory Distress Syndrome)

• Inflammatory mediators damage pulmonary capillaries
• CXR/CT: bilateral pulmonary infiltrates, "white out", ground-glass opacities
• Left-sided pleural effusion most common (from diaphragmatic lymphatics)

2. Pleural Effusion

• Left-sided > bilateral > right-sided
• CT: pleural fluid; elevated amylase in pleural fluid (pancreatopleural fistula)

3. Colon/Bowel Complications

• Colonic necrosis: most common bowel complication; splenic flexure most commonly affected
• CT: bowel wall thickening, lack of mucosal enhancement, pneumatosis

4. Renal Failure, Cardiac Failure, DIC

• Part of multi-organ failure in severe pancreatitis
• Imaged with relevant modalities

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D. ROLE OF IMAGING IN PANCREATITIS

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Q27. CYSTIC OMENTAL AND MESENTERIC MASSES

Introduction

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MESENTERIC CYSTS

Classification (de Perrot, 2000)

1. Cysts of lymphatic origin (most common)
2. Cysts of mesothelial origin
3. Cysts of enteric origin
4. Cysts of urogenital origin (remnants)
5. Mature cystic teratoma (dermoid)
6. Pseudocysts (non-neoplastic, secondary to trauma/haemorrhage/infection)

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A. LYMPHATIC CYSTS (Lymphangioma / Chylous Cyst)

Pathology

• Arise from sequestered lymphatic tissue that fails to communicate with lymphatic system
• Chylous cysts: contain milky fluid (chyle) from lymphatic drainage of small bowel
• Most common mesenteric cyst in children

Clinical Features

• Soft, non-tender abdominal mass
• Freely mobile (transilluminates)
• Symptoms: abdominal pain, distension; complications: torsion, rupture

USG Findings

• Large, thin-walled, multilocular cystic mass
• Anechoic or low-level echoes (chylous fluid)
• Multiple thin septations
• No solid components or internal vascularity on Doppler
• Displaces adjacent bowel but does not invade
• Characteristic: moves freely on real-time scan (mesenteric origin)
• Mesentery of small bowel or right colon most common location

CT Findings

• Low attenuation content (0-20 HU for serous; negative HU = fat in chylous)
• Thin enhancing wall and septations
• No solid component
• "Fluid-fluid level" in chylous cysts
• No invasion of adjacent structures
• Location: between leaves of mesentery

MRI

• T1: low signal (serous) or high signal (chylous/haemorrhagic)
• T2: high signal (bright) - cystic fluid
• STIR: chylous fluid may suppress

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B. ENTERIC CYSTS (Duplication Cysts)

Pathology

• Congenital; remnant of alimentary tract development
• Lined by gut epithelium (gastric, intestinal, or respiratory)

USG Findings

• Well-defined cystic structure adjacent to bowel
• "Gut signature": Double wall layer (inner hyperechoic mucosa + outer hypoechoic muscularis propria) - characteristic
• May have peristalsis visible
• Can be tubular or spherical

CT Findings

• Low attenuation cystic mass
• Smooth wall with two distinct layers
• May show calcification
• Closely related to bowel loop (mesenteric side)

Complications

• Hemorrhage (hyperdense on CT if recent)
• Infection
• Peptic ulceration (if gastric mucosa present)
• Obstruction

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C. MESENTERIC PSEUDOCYST

Causes

• Post-traumatic haematoma
• Mesenteric panniculitis
• Post-operative complication

USG/CT Findings

• Variable wall thickness
• Heterogeneous contents (blood/debris)
• History of trauma
• Calcification in chronic cases
• No epithelial lining

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D. CYSTIC MESOTHELIOMA (Multilocular Peritoneal Inclusion Cyst)

• Rare, predominantly in premenopausal women
• Usually on peritoneal surfaces around pelvic organs
• USG/CT: Multiple thin-walled cysts in clusters; drapes around organs; no solid components; no peritoneal thickening
• MRI: Multilocular cystic mass following peritoneal surfaces

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E. MATURE CYSTIC TERATOMA (Dermoid Cyst) - Mesenteric

• Rare in mesentery (more common in ovary)
• CT Findings: Fat density (-100 to -20 HU), calcification, Rokitansky nodule (soft tissue component), "floating ball" of fat

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OMENTAL CYSTS

Types

• Lymphangioma of omentum
• Omental pseudocysts (post-inflammatory, traumatic)
• Parasitic cysts (hydatid)

USG

• Mobile, freely moving cystic mass (changes position with breathing)
• Located anterior to viscera
• No peristalsis

CT

• Anterior abdominal location, between anterior abdominal wall and bowel
• Omental fat visible around cyst
• "Omental cake" pattern if peritoneal disease

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F. HYDATID CYST (Echinococcal)

• Echinococcus granulosus
• Most common in liver (60-70%) but can involve mesentery/omentum
• USG Findings:
  • "Water lily sign": Detached endocyst floating in cyst (pathognomonic)
  • "Double-line sign": Pericyst (outer) + endocyst (inner)
  • "Snowstorm sign": Rupture with scolices filling cyst
  • Daughter cysts (peripheral smaller cysts within main cyst)
  • Calcified wall (dead cyst)
• CT: Hypodense cyst, daughter cysts (lower density than mother cyst), rim calcification

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DIFFERENTIAL DIAGNOSIS OF CYSTIC ABDOMINAL MASSES - Summary Table

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Q28. HIATUS HERNIA

Definition

Anatomy of Oesophageal Hiatus

• Oesophageal hiatus: opening in right crus of diaphragm at T10 level
• Phrenoesophageal ligament (membrane): attaches oesophagus to diaphragm
• Normal: gastro-oesophageal junction (GOJ) lies 2 cm below hiatus
• GEJ held in place by phrenoesophageal membrane, gastric cardia fat pad, and oesophageal muscle

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CLASSIFICATION

Type I - Sliding Hiatus Hernia (Axial) - 95%

• GOJ and fundus of stomach slide through hiatus into mediastinum
• GOJ lies above diaphragm
• Most commonly associated with GORD (gastro-oesophageal reflux disease)
• Reducible (returns to normal position)
• The hernia ring = hiatus = GOJ location

Type II - Rolling (Paraesophageal) Hernia - 5%

• Fundus of stomach herniates through hiatus alongside (lateral to) oesophagus
• GOJ remains in normal subdiaphragmatic position
• Oesophagus does not move
• Risk of gastric volvulus, strangulation, incarceration
• Serious complication risk

Type III - Mixed Hernia

• Combined sliding and rolling components
• Both GOJ and fundus herniate into thorax
• Most common paraesophageal hernia type

Type IV - Giant Paraesophageal Hernia

• Entire stomach + other organs (colon, small bowel, omentum) herniate through hiatus
• "Upside down stomach" - gastric volvulus within hernia

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RADIOLOGICAL INVESTIGATIONS

1. Chest X-Ray (CXR)

• Retrocardiac mass: Soft tissue mass with/without air-fluid level behind cardiac shadow
• Air-fluid level in mediastinum (posterior mediastinum)
• Double contour of cardiac border (right side)
• Gas bubble in posterior mediastinum
• Widened mediastinum
• Type IV: large portion of bowel shadow in chest

2. Barium Swallow / Meal (MOST INFORMATIVE)

• GOJ above diaphragmatic hiatus (>2 cm above)
• Gastric folds (rugae) seen above diaphragm
• "A ring" (muscular ring): Corresponds to GOJ/lower oesophageal sphincter; normally below diaphragm
• "B ring" (Schatzki ring): Mucosal ring at GOJ; associated with reflux and dysphagia; <13 mm = symptomatic
• Hiatal ring: the narrowing at diaphragm level
• Wide gastric cardia visible above diaphragm
• Reflux of barium from stomach to oesophagus (demonstrates GORD)
• "Pseudo-Schatzki" ring

• Fundal herniation lateral to oesophagus
• GOJ at normal subdiaphragmatic level
• Pouch of stomach beside lower oesophagus in chest

• Stomach in inverted position (greater curve up) = "Organoaxial volvulus"
• "Upside-down stomach" pattern
• Beak at pylorus or GOJ depending on type of volvulus

• Cameron ulcers (linear erosions at hiatus level)
• Oesophageal stricture (peptic stricture from chronic GORD)
• Barrett's mucosa (irregular mucosal pattern, irregular Z-line)

3. CT Scan

• Identifies GOJ position relative to diaphragm
• Posterior mediastinal herniation of stomach
• "Hook sign": Hernia sac curves around diaphragmatic hiatus
• Assessment of other herniated organs in Type IV
• Volvulus: rotation of stomach, beak-like narrowing at pylorus/cardia
• Strangulation: thickened wall, lack of wall enhancement, pneumatosis

4. MRI

• Multi-planar capability - excellent for diaphragm assessment
• No contrast needed
• Dynamic MRI can assess hernia reducibility and GEJ mobility

5. Endoscopy

• Not primarily imaging but important: identifies oesophagitis, Barrett's, Cameron ulcers, Schatzki ring
• Z-line location relative to diaphragmatic pinch (normal: at pinch)

6. pH Monitoring / Manometry

• Functional assessment
• Combined with imaging for complete evaluation

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Complications

• GORD (commonest, especially Type I)
• Oesophagitis, stricture, Barrett's oesophagus
• Cameron ulcers (Type I - at the hernial rim)
• Volvulus (Type II, III, IV) - organoaxial or mesenteroaxial
• Incarceration and strangulation (Type II-IV)
• Bleeding
• Obstruction

Treatment

• Type I: Medical (PPI), surgery if GORD complications
• Type II-IV: Surgical repair (Nissen fundoplication + hernia reduction)

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Q29. CARCINOID TUMOR OF GIT

Definition

Epidemiology

• Most common GI neuroendocrine tumor
• Most common site: Small intestine (ileum, 45%), then appendix (26%), rectum (15%), stomach, colon
• Appendiceal carcinoid: most common tumor of appendix; benign behavior if <2 cm
• Carcinoid syndrome: Only occurs when liver metastases present (5-HT bypasses hepatic metabolism)

Classification (WHO 2019)

• G1 (Well-differentiated): Ki-67 <3%, <2 mitoses/10 HPF
• G2: Ki-67 3-20%, 2-20 mitoses/10 HPF
• G3: Ki-67 >20%
• Poorly differentiated NEC (large/small cell)

Carcinoid Syndrome (occurs with liver metastases)

• WDHA: Watery diarrhoea, flushing, wheezing, right-sided heart disease (carcinoid heart disease - fibrosis of tricuspid/pulmonary valves), abdominal pain
• Biochemical: elevated urinary 5-HIAA (5-hydroxyindoleacetic acid), serum CgA (chromogranin A)

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RADIOLOGICAL INVESTIGATIONS

1. Plain X-Ray

• Calcification visible in some cases (mesenteric mass)
• Bowel obstruction patterns if large
• "Sunburst" calcification pattern in mesenteric metastases

2. Barium Studies

• Small mucosal polyp/nodule (primary lesion)
• Submucosal location: smooth, sessile filling defect with intact overlying mucosa
• "Tethering" or "spoke-wheel" pattern of adjacent bowel loops (from fibrotic mesenteric reaction)
• Kinking, angulation, obstruction of ileal loops (due to desmoplastic reaction)
• Multiple primary lesions (20% multifocal)

3. Ultrasound

• Primary GI tumor: difficult to detect (small, submucosal)
• Liver metastases: Variable appearance - hyperechoic (most common), hypoechoic, "bull's eye" pattern
• CEUS: hypervascular metastases (arterial enhancement)
• Mesenteric mass with echogenic center and hypoechoic halo (desmoplastic reaction)

4. CT Scan - PRIMARY CROSS-SECTIONAL MODALITY

• Submucosal nodule/mass in terminal ileum (small, often <2 cm)
• Hypervascular (avidly enhances on arterial phase)
• Calcification within tumor (25%)

• "Spiculated/stellate mesenteric mass" - soft tissue mass with radiating spicules (desmoplastic fibrosis pulling bowel loops)
• Calcification in mesenteric mass (50%)
• "Sunburst" or "spoke-wheel" pattern of radiating fibrotic strands
• Bowel loop tethering and kinking
• Mesenteric vessel encasement
• "Christmas tree" pattern: multiple liver metastases

• Hypervascular: best seen on arterial phase
• Variable size, number
• Calcification within metastases

5. MRI

• Superior to CT for liver metastases
• T1: Hypointense lesion
• T2: Hyperintense metastases (bright)
• DWI: Restricted diffusion
• DOTANOC/DOTATATE PET-MRI: Functional-anatomical fusion (see below)
• Fibrotic mesenteric mass: T2 hypointense (fibrous)

6. Nuclear Medicine - MOST SPECIFIC

Somatostatin Receptor Scintigraphy (Octreoscan/OctreoScan)

• 111-Indium-DTPA-pentetreotide (Octreoscan)
• Most common functional imaging (being replaced by PET)
• Sensitivity 75-95% for well-differentiated NETs
• Detects primary, lymph nodes, metastases

DOTANOC/DOTATATE PET/CT (68Ga-DOTATATE PET)

• 68Gallium-DOTATATE (or DOTANOC/DOTANOC) PET/CT - CURRENT GOLD STANDARD
• Superior sensitivity to Octreoscan (95% vs. 75%)
• Detects somatostatin receptor-positive tumors
• Staging, restaging, response assessment
• Determines eligibility for PRRT (Peptide Receptor Radionuclide Therapy)
• "Doughnut sign" in carcinoid heart disease: pericardial/endocardial uptake

18F-FDG PET/CT

• Less sensitive for well-differentiated G1/G2 tumors (low metabolism)
• Useful for G3/high-grade tumors
• "Flip-flop" phenomenon: FDG+ = worse prognosis; DOTANOC+ = better (receptor positive)

MIBG Scan (123I or 131I-MIBG)

• Less used now; lower sensitivity than Octreoscan for carcinoids

7. EUS (Endoscopic Ultrasound)

• Detects small submucosal lesions
• Accurate assessment of wall layer invasion (T-staging)
• EUS-guided FNA for tissue diagnosis
• Rectal carcinoids: T-staging accuracy >90%

8. Capsule Endoscopy

• Detects primary small bowel tumors invisible to conventional endoscopy
• High sensitivity for mucosal/submucosal lesions

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STAGING AND PROGNOSIS

• T1 (<1 cm, mucosa/submucosa only): excellent prognosis
• T2 (1-2 cm or muscularis propria): good prognosis
• T3 (>2 cm or subserosa): intermediate
• T4 (perforation, adjacent organs): poor

• Localized: 97%
• Regional lymph nodes: 79%
• Distant metastases: 47%

Treatment

• Surgical resection (primary + mesenteric lymph nodes)
• Liver metastases: resection, ablation (RFA), TACE, embolization
• Somatostatin analogues (octreotide, lanreotide): symptom control + anti-proliferative
• PRRT (177Lu-DOTATATE): radionuclide therapy for receptor-positive disease
• Everolimus, Sunitinib: targeted therapy

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Q30. DISCUSS ANATOMY AND PHYSIOLOGY OF OESOPHAGUS. ENUMERATE CAUSES OF DYSPHAGIA. DESCRIBE THE ROLE OF IMAGING IN NON-OESOPHAGEAL CAUSES OF DYSPHAGIA IN ANY FOUR CONDITIONS

PART A: ANATOMY OF OESOPHAGUS

Extent and Length

• Extends from the lower border of cricoid cartilage (C6) to the cardiac orifice of the stomach (T11)
• Length: 25-30 cm (adults)
• Divided into: Cervical (5 cm), Thoracic (20 cm), Abdominal (2-3 cm)

Regions

Anatomical Narrowings (Physiological Constrictions - 4 narrowings)

1. Pharyngo-oesophageal junction (Killian's mouth / cricopharyngeus) - C6, 15 cm from incisor - most common site for foreign body and Zenker's diverticulum
2. Aortic arch crossing - T4, 23 cm from incisor
3. Left main bronchus crossing - T5-T6, 27 cm from incisor
4. Diaphragmatic hiatus - T10, 40 cm from incisor

• Foreign body impaction
• Stricture formation
• Carcinoma development

Layers of Oesophageal Wall

• Outer adventitia (no serosa - unlike rest of GIT; important in carcinoma spread)
• Outer longitudinal muscle
• Inner circular muscle
• Submucosa (contains oesophageal glands)
• Mucosa: non-keratinized stratified squamous epithelium (except distal 2 cm - columnar in Barrett's)

Blood Supply

• Cervical: inferior thyroid artery
• Thoracic: bronchial arteries, aortic branches, right intercostal arteries
• Abdominal: left gastric artery (branch of coeliac), inferior phrenic arteries
• Venous drainage: to thyroid, hemi-azygos, azygos; lower 1/3 to left gastric vein (portal system) - site of portosystemic anastomosis (varices)

Lymphatic Drainage

• Cervical: deep cervical (internal jugular) nodes
• Thoracic: posterior mediastinal, paratracheal, subcarinal nodes
• Abdominal: left gastric, coeliac nodes
• Note: Skip metastases common due to extensive submucosal lymphatics

Nerve Supply

• Sympathetic: thoracic sympathetic chain (T5-T12)
• Parasympathetic: vagus nerve (CN X) - left vagus (anterior), right vagus (posterior)
• Myenteric (Auerbach's) plexus
• Lower oesophageal sphincter (LOS): Maintained by intrinsic circular muscle + right crus of diaphragm; normal resting pressure 15-30 mmHg

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PART B: PHYSIOLOGY OF OESOPHAGUS

Deglutition (Swallowing) - Three Phases

• Food bolus formed, pushed posteriorly by tongue
• Duration: <1 second

• Triggered when bolus reaches posterior pharynx
• Soft palate closes nasopharynx
• Vocal cords adduct, larynx elevates, epiglottis deflects
• Cricopharyngeus relaxes (UOS opens)
• Duration: ~1 second
• Coordinated by swallowing center (medulla oblongata)

• Primary peristalsis: sequential contraction wave from UOS to LOS
• Speed: 2-4 cm/second (esophageal body)
• Secondary peristalsis: triggered by distension (clearance function)
• Tertiary contractions: non-propulsive (pathological/ageing)
• LOS relaxes 2-3 seconds after swallow (vasoactive intestinal peptide, NO mediated)
• Normal transit time: 8-20 seconds

Upper Oesophageal Sphincter (UOS)

• Cricopharyngeus muscle + inferior pharyngeal constrictor
• Resting pressure: 60-120 mmHg
• Prevents regurgitation and aspiration

Lower Oesophageal Sphincter (LOS)

• High pressure zone: 15-30 mmHg above gastric pressure
• Prevents GORD
• Relaxes with swallowing (VIP and NO mediated)
• Achalasia: Failure of LOS relaxation (loss of inhibitory neurons)
• GORD: LOS pressure <10 mmHg or inappropriate relaxations

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PART C: CAUSES OF DYSPHAGIA

I. OESOPHAGEAL CAUSES

• Foreign body
• Food bolus impaction
• Bezoar

1. Neuromuscular/Motility Disorders:
   • Achalasia (primary, idiopathic)
   • Diffuse oesophageal spasm
   • Nutcracker oesophagus
   • Scleroderma
   • Chagas disease
2. Inflammatory/Stricture:
   • Peptic stricture (GORD)
   • Caustic stricture (acid/alkali)
   • Radiation stricture
   • Eosinophilic oesophagitis
   • Plummer-Vinson syndrome
3. Tumours:
   • Squamous cell carcinoma
   • Adenocarcinoma
   • Benign tumours (leiomyoma, polyp)
4. Diverticula:
   • Zenker's (pharyngeal)
   • Mid-oesophageal (traction)
   • Epiphrenic
5. Vascular anomalies:
   • Dysphagia lusoria (aberrant right subclavian artery)
   • Aortic aneurysm
   • Vascular rings

• Mediastinal lymphadenopathy
• Bronchogenic carcinoma
• Retrosternal goitre
• Lung carcinoma

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II. NON-OESOPHAGEAL CAUSES

• Neurological: stroke, MND, Parkinson's, MS, pseudobulbar palsy
• Muscular: myasthenia gravis, polymyositis, dermatomyositis
• Structural: pharyngeal cancer, tonsil abscess, goitre

• Lymphadenopathy
• Thyroid mass/goitre
• Aneurysms
• Spinal osteophytes (cervical spondylosis)

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PART D: ROLE OF IMAGING IN NON-OESOPHAGEAL CAUSES OF DYSPHAGIA (4 Conditions)

1. STROKE (Neurological Dysphagia)

• DWI (Diffusion-Weighted Imaging): Restricted diffusion (bright DWI, dark ADC) in acute infarct
• Cortical infarcts (fronto-parietal) affecting swallowing area
• Brainstem infarcts (medullary, Wallenberg syndrome - lateral medullary syndrome)
• Wallenberg syndrome: dysphagia, Horner's, ipsilateral ataxia, contralateral pain/temperature loss
• MRA (Circle of Willis assessment): vertebrobasilar arterial occlusion

• Gold standard for functional assessment of dysphagia
• Demonstrates oral, pharyngeal and oesophageal phases
• Identifies: premature spillage, reduced tongue propulsion, delayed pharyngeal trigger, laryngeal penetration/aspiration, residue in vallecula/pyriform sinuses
• Aspiration (before, during, after swallow) - "silent aspiration" identified
• Guides rehabilitation and diet modification

• Bedside assessment
• Identifies pharyngeal pooling, penetration, aspiration

2. MEDIASTINAL LYMPHADENOPATHY (Extrinsic Compression)

• Widened mediastinum
• Hilar lymphadenopathy (bilateral in sarcoidosis/lymphoma)
• Mass effect displacing trachea/oesophagus
• "Potato node" calcification in TB/sarcoidosis

• Homogeneous enlarged nodes (lymphoma - >1 cm short axis in mediastinum)
• Necrotic nodes (TB, metastatic)
• Ring enhancement (TB)
• Matted nodes with periadenitis (TB)
• "Bulky" mediastinal disease
• Compression/displacement of oesophagus
• Surrounding infiltration in aggressive disease
• Distribution: paratracheal, subcarinal, hilar - helps in differential
• Sarcoidosis: bilateral symmetric hilar + right paratracheal ("pawnbroker's sign")

• FDG-avid nodes in lymphoma, metastases
• Confirms metabolic activity, staging
• Guides biopsy site

• Extrinsic smooth compression with intact mucosa
• "Rat-bite" impression
• Displacement without mucosal irregularity (differentiates from primary oesophageal carcinoma)

3. CERVICAL SPONDYLOSIS / ANTERIOR CERVICAL OSTEOPHYTES

• Large anterior osteophytes visible at C3-C7 level
• Most commonly C5-C6
• Posterior displacement of larynx/trachea
• "Teardrop" or "candle drip" osteophytes

• 3D reconstruction shows extent and projection of osteophytes
• Cross-sectional narrowing of hypopharynx/oesophagus
• Measures residual lumen
• Adjacent soft tissue oedema/inflammatory changes
• CT Myelogram if associated cord compression

• No radiation; multiplanar
• Shows associated disc disease, cord compression
• T2: spinal canal narrowing, myelomalacia
• Soft tissue posterior to osteophyte (retropharyngeal swelling)

• Smooth extrinsic compression/posterior indentation of cervical oesophagus
• Barium column displaced anteriorly at level of osteophyte
• Intact mucosa
• Pharyngeal pooling above obstruction
• VFSS: demonstrates functional impact on swallowing

4. THYROID GOITRE (Retrosternal Goitre)

• Superior mediastinal widening
• Tracheal deviation (usually away from larger lobe)
• "Reverse 3 sign" (tracheal deviation)
• Calcification within goitre
• Compression of trachea ("rat-tail" tracheal narrowing)

• Multinodular goitre: multiple nodules with heterogeneous echogenicity
• Calcification, cystic areas
• Colour Doppler: vascularity
• Cannot assess retrosternal extension adequately
• TI-RADS classification for malignant nodules

• Extent of goitre (from neck into superior mediastinum)
• Tracheal/oesophageal compression and displacement
• Retrosternal component below thoracic inlet
• Relationship to great vessels
• Calcification pattern
• CT characteristics suggesting malignancy: irregular margins, extrathyroidal extension, necrosis, lymph nodes

• Heterogeneous goitre (T1 varying, T2 hyperintense areas)
• Multiplanar assessment of vascular encasement
• No ionizing radiation
• Better soft tissue detail for surgical planning

• "Cold nodule" (malignancy risk), "Hot nodule" (toxic adenoma)
• Confirms functioning thyroid tissue in mediastinum
• Substernal extension of functioning thyroid

• Extrinsic, smooth compression with posterior/lateral displacement of oesophagus
• Intact mucosa
• "Cervical oesophageal displacement" sign

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Q31. INTESTINAL OBSTRUCTION IN INFANT (SMALL BOWEL) - ROLE OF RADIOLOGY

Introduction

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CLASSIFICATION BY LEVEL AND AGE

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A. DUODENAL ATRESIA

Pathology

• Failure of recanalization of duodenum (8-10 weeks gestation)
• 50% associated with Down syndrome (Trisomy 21)
• Other associations: cardiac defects, malrotation, biliary atresia

Clinical Features

• Bilious vomiting within hours of birth (80% below Ampulla of Vater)
• Polyhydramnios on antenatal USG

Radiological Findings

• "Double bubble" sign: Two gas-filled structures (stomach + dilated duodenal cap) with NO gas distal
• The two bubbles separated by the pyloric muscle
• Gasless abdomen below duodenum (no gas passage)
• Classic sign: pathognomonic

• "Double bubble" sign visible in utero
• Polyhydramnios
• Diagnosis possible from 20 weeks gestation

• Confirms obstruction level
• Identifies web vs. atresia
• Rules out malrotation (rotation of duodenojejunal flexure)

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B. JEJUNOILEAL ATRESIA

Pathology

• Vascular accident in utero (mesenteric vascular insufficiency)
• Types: I (membrane), II (cord), IIIa (gap), IIIb (apple peel), IV (multiple)

Radiological Findings

• Multiple dilated loops of small bowel (number of dilated loops suggests level - more loops = lower obstruction)
• "Ladder pattern": Multiple air-fluid levels in stepladder fashion on erect view
• No gas in colon/rectum
• "Gasless colon" (distal to obstruction)
• Calcification = meconium peritonitis (intrauterine bowel perforation)

• Microcolon (unused/hypoplastic colon): Small caliber colon (not used in utero due to proximal obstruction)
• Confirms obstruction level; identifies atresia
• Differentiates from meconium ileus (may clear ileal plug)

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C. MALROTATION AND VOLVULUS

Pathology

• Failure of normal 270° counterclockwise rotation of midgut
• Duodenojejunal flexure (DJF) fails to move to left of midline; caecum stays in midline/right upper quadrant
• Narrow mesenteric base predisposes to midgut volvulus (clockwise rotation around SMA)
• Most dangerous cause of intestinal obstruction: can lose entire midgut in hours

Clinical Features

• Bilious vomiting (acute presentation - emergency)
• May present at any age but 80% in first month of life

Radiological Findings

• Variable: often normal early or shows dilated stomach/duodenum
• "Double bubble" sign: if Ladd's bands obstruct duodenum
• "Gasless abdomen": Volvulus with ischemia (gas absorbed)
• "Duodenal cut-off": Loss of gas at DJF
• Dilated small bowel loops may be present

• Malrotation (without volvulus):
  • Duodenojejunal flexure (DJF) lies to the RIGHT of midline (normal: left of vertebral pedicles at L1-L2)
  • "Z-shaped" or "corkscrew" duodenum (doesn't cross midline)
  • Caecum in unusual position (midline, right upper quadrant)
• Volvulus:
  • "Corkscrew" or "barber pole" sign: Twisted configuration of duodenum/proximal jejunum
  • "Bird's beak" sign: Tapering spiral obstruction
  • Duodenum fails to cross midline
  • Obstruction at 2nd-3rd part of duodenum

• "Whirlpool sign": Clockwise wrapping of mesenteric vessels and bowel around SMA axis - pathognomonic of midgut volvulus
• Reversal of SMA/SMV relationship (SMV to LEFT of SMA = malrotation; normal = SMV to right)
• Dilated fluid-filled duodenum
• Absent/decreased bowel peristalsis
• Free ascites (ischemia)

• "Whirlpool sign" of mesenteric vessels
• Duodenum failing to cross retroperitoneally
• Ischemic bowel: pneumatosis intestinalis, portal venous gas

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D. MECONIUM ILEUS

Pathology

• Inspissated (thick) meconium obstructing distal ileum
• 90% associated with cystic fibrosis (pancreatic exocrine insufficiency - abnormal meconium)

Types

• Simple: No complication
• Complicated: Volvulus, atresia, perforation, pseudocyst formation (meconium peritonitis)

Radiological Findings

• Dilated small bowel loops with absent air-fluid levels (meconium too thick to form fluid levels) - distinguishes from other obstructions
• "Ground glass" or "soap bubble" appearance (Neuhauser sign): Gas mixed with thick meconium in right lower quadrant - PATHOGNOMONIC
• No rectal/colonic gas
• Calcification if meconium peritonitis (scattered)

• Microcolon (unused): Narrow throughout colon
• Obstructing pellets of meconium in terminal ileum
• Gastrografin (hyperosmolar, water-soluble): draws fluid into bowel, softens meconium
• Therapeutic enema: 50-60% success in uncomplicated cases
• Multiple enemas may be needed

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E. HIRSCHSPRUNG'S DISEASE

Pathology

• Absence of ganglion cells (Auerbach's + Meissner's plexus) in distal bowel
• Most common: rectosigmoid (75%)
• Failure of neural crest cell migration

Clinical Features

• Failure to pass meconium within 48 hours
• Abdominal distension
• Bilious vomiting

Radiological Findings

• Dilated bowel loops (proximal to aganglionic segment)
• No gas in rectum
• "Soap bubble" pattern if complicated enterocolitis (gas-filled dilated bowel + mucosal edema)

• Transition zone: Narrow aganglionic rectum (or distal colon) with abrupt dilatation of normal proximal ganglionic bowel
• "Cone" or "funnel" at transition zone
• Inverted rectosigmoid ratio (normal rectum wider than sigmoid; reversed in Hirschsprung's)
• Delayed evacuation: Barium retained at 24-48 hours (normal if barium evacuated at 24 hrs)
• Irregular mucosal pattern (in enterocolitis)
• Important technique: No rectal preparation; water-soluble contrast preferred in neonates; lateral view essential to see rectum

• Limited role; may show dilated proximal colon
• Transrectal USG: increased muscularis propria in aganglionic segment

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F. INTUSSUSCEPTION (already described in Q23)

• Most common cause of intestinal obstruction in 6 months - 2 years age group

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SUMMARY: ROLE OF RADIOLOGY IN INFANTILE SMALL BOWEL OBSTRUCTION

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Q32. (Question 32 was blank/not visible in the image - No question available to answer)

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Q33. LYMPHATIC DRAINAGE OF STOMACH WITH DIAGRAM AND IMAGING OF GASTRIC CARCINOMA

PART A: LYMPHATIC DRAINAGE OF STOMACH

Four Main Drainage Areas / Territories

• Left gastric nodes (along left gastric artery) → Coeliac nodes
• Right gastric nodes (along right gastric artery) → Hepatic nodes → Coeliac

• Right gastroepiploic nodes (along right gastroepiploic artery) → Subpyloric nodes → Hepatic nodes
• Left gastroepiploic nodes (along left gastroepiploic artery) → Splenic nodes

• Left gastroepiploic nodes → Splenic hilar nodes → Splenic artery nodes → Coeliac

• Subpyloric/infrapyloric nodes → Superior mesenteric/hepatoduodenal nodes → Coeliac

Final Common Pathway

• All lymphatics ultimately drain to coeliac lymph nodes at coeliac axis (T12/L1)
• Coeliac nodes → Para-aortic lymph nodes → Thoracic duct → Left subclavian vein

Japanese Classification (N1-N4)

• N1: Perigastric nodes (within 3 cm of stomach wall - stations 1-6)
  • Stations 1-6: right/left cardiac, lesser curvature, greater curvature, suprapyloric, infrapyloric, short gastric, left gastroepiploic
• N2: Regional nodal stations along named vessels (stations 7-11)
  • Left gastric, common hepatic, coeliac, splenic hilar, splenic artery
• N3: Para-aortic, retropancreatic, root of SMA nodes (stations 12-14)
• N4: Distant nodes (para-aortic at renal vessels, paraoesophageal)

Important Routes of Spread / Special Nodes

• Virchow's node: Left supraclavicular node (Troisier's sign) - via thoracic duct
• Sister Mary Joseph node: Periumbilical nodule (direct spread via falciform ligament)
• Irish node: Left axillary node
• Krukenberg tumor: Ovarian metastases (transcoelomic spread)

Diagram (Schematic Description)

STOMACH
├── Cardia/Fundus → Left gastric (N1) → Coeliac → Para-aortic
│                → Short gastric (N1) → Splenic hilar → Splenic artery → Coeliac
├── Body (Lesser) → Left gastric (N1) → Coeliac (N2)
│   (Greater)     → L.gastroepiploic (N1) → Splenic (N2)
└── Antrum/Pylorus → Subpyloric (N1) → Hepatic (N2) → Coeliac → Para-aortic → Thoracic duct

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PART B: IMAGING OF GASTRIC CARCINOMA

Types of Gastric Carcinoma (Borrmann Classification)

Lauren Classification

• Intestinal type: well-differentiated, glandular; H. pylori related; distal stomach; older patients
• Diffuse type: poorly differentiated, signet ring cells; linitis plastica; younger patients, genetic

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RADIOLOGICAL INVESTIGATIONS

1. Barium Meal (Double Contrast) - Useful for Detection

• Carman's meniscus sign: Semilunar filling defect within ulcer; concave face toward lumen (malignant)
• Irregular, shaggy ulcer base
• Surrounding mucosal rigidity, destruction of folds
• Abrupt cut-off of folds at ulcer margin ("meniscus" or "guillotine")
• No Hampton's line (present in benign ulcers)
• Non-projection beyond gastric wall (unlike benign ulcers)

• Linitis plastica (Type IV): "Leather bottle stomach" - diffusely contracted, rigid, non-distensible stomach; loss of peristalsis; narrowed lumen throughout; thick rigid wall; diffuse mucosal irregularity
• Polypoid carcinoma: Irregular lobulated filling defect within stomach
• Scirrhous carcinoma: Narrowed gastric antrum or entire stomach

2. Endoscopy + Biopsy (Definitive Diagnosis)

• Not imaging per se, but essential for tissue confirmation
• Endoscopic ultrasound (EUS) for T-staging

3. CT Scan (Investigation of Choice for Staging)

• Gastric wall thickening (normal <5 mm; >10 mm = suspicious)
• Irregular mucosal enhancement pattern
• Focal or diffuse loss of normal layered architecture
• Hypoenhancing or heterogeneous enhancement
• Ulceration within mass
• Linitis plastica: concentric wall thickening, reduced distensibility, loss of layers

• Nodes >1 cm (short axis) considered abnormal
• Central necrosis, loss of hilum = highly suspicious
• N1-N4 stations assessed systematically
• Perigastric nodes, coeliac axis, hepatoduodenal, para-aortic
• CT: 65-70% accuracy for nodal staging (EUS superior for N1)

• Liver: Hypovascular metastases (best seen on portal venous phase)
• Peritoneal metastases: Peritoneal thickening, omental caking, ascites
• "Omental cake": Sheet-like soft tissue replacing omentum
• Lung metastases: CT chest
• Adrenal, bone: Less common

• Gastric carcinoma is staged by TNM (AJCC/UICC 8th edition)
• Resectability criteria: No distant metastases, no encasement of great vessels (coeliac, SMA, hepatic arteries), no T4b invasion

4. Endoscopic Ultrasound (EUS) - Best for T and N1 Staging

• High-frequency ultrasound (7.5-12 MHz) via endoscope
• Visualizes all 5 layers of gastric wall
• Most accurate for T-staging (accuracy 85-90%)
• EUS-guided FNA for suspicious lymph nodes
• Limited for distant metastases

5. MRI

• Alternative when CT contraindicated (iodinated contrast allergy, pregnancy)
• T2: hyperintense tumor mass within stomach
• DWI: restricted diffusion (bright DWI, low ADC)
• Superior to CT for liver metastases and peritoneal deposits
• MRI-based T-staging less established than EUS/CT

6. PET/CT (18F-FDG)

• Used for:
  • Detecting occult metastases (peritoneal, distant nodes, liver)
  • Recurrence surveillance
  • Response assessment (after chemotherapy)
• Limitation: Signet ring cell and mucinous carcinomas have low FDG uptake (false negative)
• FDG PET cannot replace CT for local staging

7. Staging Laparoscopy

• Identifies peritoneal metastases not visible on CT/PET (20% of "resectable" tumors found to have peritoneal disease)
• Mandatory before curative resection in most centres

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TNM Staging Summary (AJCC 8th)

• Stage I: T1-2, N0-1
• Stage II: T1-3 with regional nodes or T3N0
• Stage III: T3-4 with nodes or T4N0
• Stage IV: Any T, any N, M1 (distant metastases) - unresectable

Radiological Markers of Unresectability

1. Distant metastases (liver, lung, bone, peritoneum)
2. Para-aortic lymph node involvement (N4)
3. T4b invasion (hepatic artery, coeliac axis, SMA, portal vein encasement)

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Q34. PHEOCHROMOCYTOMA

Definition

• 10% bilateral
• 10% malignant
• 10% extra-adrenal (paraganglioma)
• 10% in children
• 10% familial
• 10% incidental (Modern data: malignancy ~15-25%; bilateral up to 20% in familial; extra-adrenal ~15-20%)

Biochemistry

• Secretes: noradrenaline (norepinephrine) most commonly, adrenaline (epinephrine), dopamine
• Diagnosis: 24-hour urinary catecholamines and metanephrines (metanephrine + normetanephrine); plasma metanephrines (most sensitive)
• Elevated urinary VMA (vanillylmandelic acid)

Clinical Features (classic triad)

1. Episodic/paroxysmal hypertension (spells: headache, palpitations, diaphoresis)
2. Headache
3. Diaphoresis (sweating)

• Also: tremor, pallor, anxiety, weight loss
• Hypertensive crisis can be triggered by drugs (beta-blockers, tricyclics), surgery, stress

Associations / Genetic Syndromes

• MEN2A: Pheochromocytoma + medullary thyroid carcinoma + parathyroid hyperplasia
• MEN2B: Pheochromocytoma + MTC + mucosal neuromas + Marfanoid habitus
• Von Hippel-Lindau (VHL): Pheochromocytoma + haemangioblastoma + RCC + retinal angioma
• NF1 (Neurofibromatosis): Pheochromocytoma (1-5%)
• SDH mutations (SDHB, SDHC, SDHD): Familial paraganglioma-pheochromocytoma syndrome

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RADIOLOGICAL INVESTIGATIONS

1. Ultrasound (USG)

• First-line screening tool
• Adrenal mass identification
• USG Features:
  • Oval/round, well-defined mass in adrenal region
  • Echotexture: heterogeneous (due to haemorrhage, necrosis, cystic areas)
  • Variable echogenicity (mixed solid-cystic)
  • Calcification (15-20%)
  • Colour Doppler: peripheral or internal vascularity
  • May reach large size (>3 cm)
• Limitations: Cannot characterize adrenal mass definitively; operator dependent; left adrenal obscured by bowel gas

2. CT Scan (Primary Anatomical Modality - FIRST CHOICE for localisation)

• Non-contrast (Unenhanced CT - important): attenuation measurement
• Arterial phase (35-40 seconds)
• Portal venous phase (70 seconds)
• Delayed phase (10-15 minutes): washout calculation

• Adrenal mass (usually >3 cm at diagnosis; often 5-10 cm)
• Non-contrast CT attenuation >10 HU (lipid-poor lesion - does NOT appear as adenoma which is <10 HU)
• Heterogeneous, mixed solid-cystic mass
• Marked enhancement on contrast-enhanced CT (hypervascular tumor)
• Necrosis and cystic areas within (central necrosis common)
• Calcification (15-20%)
• Absolute CT washout <60% (compared to adenoma >60%)
• Bilateral in MEN2, VHL
• Extra-adrenal sites: organ of Zuckerkandl (aortic bifurcation), bladder wall, carotid body, paravertebral ganglia

3. MRI (Investigation of Choice for Pheochromocytoma)

• Young patients (no radiation)
• Pregnancy
• Iodinated contrast allergy
• Suspected paraganglioma (multiple locations)
• Biochemically confirmed but CT-negative (extra-adrenal search)

• T1: Hypointense or isointense to liver
• T2: Markedly hyperintense ("Light bulb sign") - CLASSICAL - very bright on T2
  • However, not specific; malignant pheochromocytoma may be less T2-bright
• Chemical shift imaging (in-phase/out-of-phase): No signal loss on out-of-phase (no intracellular lipid; differentiates from adenoma which drops signal)
• Post-contrast: heterogeneous, marked enhancement with areas of necrosis
• DWI: restricted diffusion in malignant lesions
• MRI superior for:
  • Para-spinal paragangliomas
  • Detecting multiple synchronous lesions (in MEN/VHL)
  • Spinal/medullary extension

4. Nuclear Medicine - FUNCTIONAL IMAGING

MIBG Scintigraphy (131I or 123I-MIBG)

• Meta-iodobenzylguanidine - structural analogue of noradrenaline - taken up by chromaffin cells
• 123I-MIBG: Preferred for diagnosis (better image quality, lower radiation)
• 131I-MIBG: Therapeutic
• Sensitivity: Pheochromocytoma 83-90%; paraganglioma 56-75%
• Whole-body imaging: detects primary + metastases
• Indications:
  • CT/MRI-negative biochemically positive case
  • Malignant pheochromocytoma (staging)
  • Recurrence
  • Pre-therapeutic assessment for 131I-MIBG therapy

68Ga-DOTATATE PET/CT

• Somatostatin receptor-based imaging
• Sensitivity: 85-97% for head-neck paragangliomas
• Superior to MIBG for SDH-mutated paragangliomas (SDHB, SDHD)
• Whole-body staging

18F-FDG PET/CT

• Useful for malignant/metastatic pheochromocytoma
• Less specific than MIBG for benign pheochromocytoma
• High grade or FDG-avid lesions = worse prognosis

18F-DOPA PET/CT

• Highly sensitive for sporadic pheochromocytoma and paraganglioma
• Better than FDG for extra-adrenal localisation

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MALIGNANT PHEOCHROMOCYTOMA

• 15-25% incidence (SDHB mutation highest risk)
• Metastases to: lymph nodes, liver, lung, bone (most common bone mets)
• No histological criteria for malignancy - malignancy defined by presence of metastases in non-chromaffin tissue
• Large size (>6 cm), extra-adrenal, SDHB mutation = risk factors
• CT: local invasion, lymph node involvement, distant spread
• MIBG/FDG PET for staging

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ADRENAL INCIDENTALOMA vs. PHEOCHROMOCYTOMA

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PRE-OPERATIVE MANAGEMENT

• Alpha-blockade first: phenoxybenzamine (irreversible) OR doxazosin (reversible)
  • At least 10-14 days pre-operatively
• Beta-blockade: ONLY after alpha-blockade is established (to avoid hypertensive crisis)
• High salt diet + fluids (volume expansion)
• Surgical: laparoscopic adrenalectomy (procedure of choice)

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Q35. GENERALISED SPLENOMEGALY

Definition

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CAUSES OF GENERALISED SPLENOMEGALY

I. HAEMATOLOGICAL (Most common overall)

1. Haemolytic anaemias:
   • Hereditary spherocytosis
   • Sickle cell disease (early - later auto-infarction → "autosplenectomy")
   • Thalassaemia major (massive splenomegaly)
   • Haemolytic anaemia (immune, microangiopathic)
2. Leukaemias:
   • CML (chronic myeloid leukaemia) - MOST COMMON cause of MASSIVE splenomegaly
   • CLL (chronic lymphocytic leukaemia)
   • Acute leukaemias
3. Lymphomas:
   • Hodgkin's lymphoma
   • Non-Hodgkin's lymphoma
4. Myeloproliferative disorders:
   • Myelofibrosis (primary) - massive splenomegaly (extramedullary haematopoiesis)
   • Polycythaemia vera
   • Essential thrombocythaemia
5. Myeloma (rarely)

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II. INFECTIVE

1. Viral:
   • Infectious mononucleosis (EBV) - commonest infectious cause of acute splenomegaly
   • CMV, HIV
   • Viral hepatitis
2. Parasitic:
   • Malaria (Plasmodium vivax - most common cause worldwide)
   • Visceral leishmaniasis / Kala-azar (Leishmania donovani) - massive splenomegaly
   • Schistosomiasis
   • Toxoplasmosis
3. Bacterial:
   • Infective endocarditis (septic emboli)
   • Typhoid fever (Salmonella typhi)
   • Brucellosis
   • Splenic abscess
4. Mycobacterial: TB (miliary TB)

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III. CONGESTIVE (Portal Hypertension)

1. Liver cirrhosis (hepatic cause)
2. Portal vein thrombosis (prehepatic)
3. Budd-Chiari syndrome (posthepatic)
4. Right heart failure (systemic venous hypertension)
5. Constrictive pericarditis

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IV. STORAGE DISORDERS

1. Gaucher disease (glucocerebrosidase deficiency) - massive splenomegaly
2. Niemann-Pick disease
3. Mucopolysaccharidoses (Hurler's syndrome)
4. Amyloidosis (systemic)
5. Lipid storage diseases

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V. AUTOIMMUNE / CONNECTIVE TISSUE

1. Rheumatoid arthritis + splenomegaly = Felty's syndrome (RA + splenomegaly + neutropenia)
2. SLE (systemic lupus erythematosus)
3. Sarcoidosis
4. Autoimmune haemolytic anaemia

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VI. INFILTRATIVE / MISCELLANEOUS

1. Primary splenic tumors (haemangioma most common benign)
2. Cysts (congenital, hydatid)
3. Polycystic disease

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CAUSES OF MASSIVE SPLENOMEGALY (>20 cm)

• CML (chronic myeloid leukaemia)
• Chronic malaria (hyperreactive malarial splenomegaly)
• Myelofibrosis
• Gaucher disease
• Thalassaemia major
• Visceral Leishmaniasis (kala-azar)

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ROLE OF IMAGING

1. Ultrasound (First-Line Investigation)

• Homogeneous, fine echotexture (similar to kidney)
• Length <12-13 cm; width <7 cm
• Smooth margins with notch superiorly

• Spleen length >12-13 cm (measure on longitudinal axis)
• Displacement of adjacent organs (stomach, splenic flexure, left kidney)
• Splenic infarcts: Peripheral wedge-shaped hypoechoic areas, no Doppler flow (in sickle cell, lymphoma, IE)
• Splenic cysts: Simple (anechoic, thin-walled), hydatid (daughter cysts)
• Splenic abscess: Hypoechoic/complex lesion, gas within (echogenic foci)
• Portal hypertension: Dilated portal vein (>13 mm), splenomegaly, ascites, portosystemic collaterals (colour Doppler shows hepatofugal flow), splenorenal/gastrorenal shunts
• Lymphoma involvement: Focal hypoechoic lesions OR diffuse enlargement with homogeneous texture
• Gaucher disease: Heterogeneous texture; "Gaucher cells" - focal hyperechoic nodules

1. Size measurement (length, width, thickness)
2. Parenchymal echotexture
3. Focal lesions
4. Portal/splenic vein diameter (Doppler)
5. Adjacent structures (liver, lymph nodes, ascites)

2. CT Scan

• Splenomegaly + varices (splenic hilum, perigastric, oesophageal)
• Dilated splenic vein
• Cirrhotic liver (nodular contour, right lobe atrophy, caudate hypertrophy)
• Ascites
• Porto-systemic collaterals (MIP reconstructions)

• Diffuse enlargement, homogeneous OR
• Multiple focal hypodense lesions (non-Hodgkin's)
• Lymphadenopathy (abdominal, mediastinal, axillary)
• PET/CT: FDG-avid lesions confirm activity

• Massive homogeneous splenomegaly (CML)
• Splenic infarcts (wedge-shaped hypodense, peripheral)
• Lymphadenopathy

• Massive splenomegaly
• Extramedullary haematopoiesis: paravertebral soft tissue masses, hepatomegaly
• Transfusion haemosiderosis: liver/spleen/bone marrow hyperdensity (>75 HU)
• Bone changes: "hair on end" skull (X-ray), marrow expansion

• Massive splenomegaly
• Hypodense nodules within spleen (Gaucher cell infiltration)
• "Swiss cheese" pattern
• Bone involvement: Erlenmeyer flask deformity on X-ray (long bones), AVN, bone crises

• Massive splenomegaly
• Extramedullary haematopoiesis (liver, spleen, paravertebral, epidural)
• Bone marrow: sclerotic bones on CT/XR
• CT: marked splenomegaly, hepatomegaly, paravertebral masses

• Moderately enlarged spleen (rarely massive)
• Periportal lymphadenopathy
• Heterogeneous echotexture
• Risk: spontaneous splenic rupture (avoid contact sports for 4-6 weeks)

• Massive splenomegaly
• Hepatomegaly
• Retroperitoneal lymphadenopathy
• Hypersplenism features

3. MRI

• Haemosiderosis: T2 signal loss (very dark spleen on T2) from iron deposition
  • Diffuse/uniform: transfusional haemosiderosis
  • Peripheral/ring: sickle cell splenic siderosis
• Extramedullary haematopoiesis: Paravertebral T1/T2 intermediate signal masses
• Lymphomatous lesions: T2 hyperintense focal lesions, restricted diffusion on DWI
• Splenic haemangioma: Very bright on T2; progressive centripetal fill-in on dynamic MRI

4. Nuclear Medicine

• Reduced uptake in functional hyposplenism (sickle cell, amyloid)
• Increased splenic uptake relative to liver in portal hypertension
• Extramedullary haematopoiesis: activity in liver/spleen/bone marrow

• Identifies functional asplenia vs. splenomegaly

• Metabolically active lymphoma (high SUV)
• Splenic involvement in lymphoma: diffuse FDG uptake vs. focal lesions

5. Plain X-Ray

• Displaced gastric air bubble (medially, to right)
• Elevated left hemidiaphragm
• Splenic mass causing displacement of colon (splenic flexure)
• Calcification within spleen (hydatid, old infarcts, histoplasmosis)

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COMPLICATIONS OF SPLENOMEGALY

1. Hypersplenism: Sequestration → pancytopenia (anaemia, thrombocytopenia, neutropenia)
2. Splenic rupture: Spontaneous (EBV-most common) or traumatic
3. Splenic infarction: Embolic (IE), thrombotic (sickle cell, malignancy)
4. Splenic vein thrombosis: Left-sided portal hypertension, gastric varices
5. Perisplenitis (Friable capsule)

RADIOLOGICAL APPROACH TO SPLENOMEGALY

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COMPLETE EXAM ANSWERS - SUMMARY INDEX

Note for Q32: The question was not visible/blank in the image provided. If you have the question text, send it and I will write the full 30-mark answer immediately.

RADIOLOGY UNIVERSITY THEORY EXAM - FULL ANSWERS (30 Marks Each)

Questions 36-46

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Q36. PNEUMATOSIS INTESTINALIS

Definition

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PATHOPHYSIOLOGY - THEORIES OF GAS FORMATION

1. Mechanical / Mucosal Disruption Theory

• Disruption of mucosal barrier allows intraluminal gas to dissect into bowel wall
• Elevated intraluminal pressure forces gas through mucosal defects
• Most important mechanism in bowel ischemia, obstruction, trauma

2. Bacterial / Fermentation Theory

• Gas-producing bacteria (Clostridium, E. coli) invade bowel wall
• Produce hydrogen, methane, CO2 within wall
• Dominant mechanism in necrotizing enterocolitis (NEC) and infective causes

3. Pulmonary Theory

• Alveolar rupture → mediastinal emphysema → dissects along mesenteric vessels → bowel wall
• Explains PI in COPD, asthma, mechanical ventilation (barotrauma)

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CLASSIFICATION

A. PRIMARY PNEUMATOSIS (Idiopathic - 15%)

• No identifiable underlying cause
• Benign; multiple thin-walled subserosal cysts (pneumatosis cystoides intestinalis)
• Most commonly affects colon (sigmoid, descending)
• Incidental finding; patient asymptomatic
• Cysts contain predominantly N2 (nitrogen) and H2
• Self-limiting; may resolve with oxygen therapy

B. SECONDARY PNEUMATOSIS (85%) - Clinically important

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RADIOLOGICAL INVESTIGATIONS

1. Plain Abdominal X-Ray (AXR)

• First investigation

• Linear intramural gas: Thin lucent line parallel to bowel wall (submucosal gas tracking along bowel)
• Bubbly/frothy pattern: Multiple small bubbles along bowel wall
• Cystic pattern: Round/oval lucencies projecting from bowel wall (cystoides type)
• Curvilinear gas: Gas outlining contour of bowel loop
• Pneumatosis of colon: "Tram-track" or "halo" pattern around colonic wall
• NEC appearance: Intramural gas in small + large bowel; "Bubbly" pattern in neonates

• Portal venous gas (PVG): Branching linear lucencies extending to liver periphery (within 2 cm of liver edge on AXR - differentiates from biliary gas which is central/hilar)
• Pneumoperitoneum: Free gas under diaphragm = perforation (surgical emergency)
• Dilated loops (obstruction/ischemia)

2. CT Scan - MOST SENSITIVE AND DEFINITIVE INVESTIGATION

• Detecting small amounts of intramural gas
• Identifying cause and distribution
• Detecting complications

• Intramural gas: Low-attenuation (air density, -1000 HU) within bowel wall
  • Linear: submucosal layer (more serious)
  • Cystic: subserosal (more benign)
• Location in bowel wall:
  • Subserosal: rounded/oval gas collections outside muscularis propria
  • Submucosal: linear/bubbly gas parallel to muscularis mucosae
• Distribution: Focal (ischemia - concerning), diffuse (benign/pulmonary)

• Bowel wall thickening with intramural gas
• Portal venous gas: Branching hypodense areas within liver parenchyma (extending to peripheral liver)
• Mesenteric venous gas: Gas in mesenteric veins/SMV
• Absent bowel wall enhancement: Non-enhancing bowel wall after IV contrast = ischemia (normal wall: 3-layered enhancement)
• Pneumoperitoneum (free intraperitoneal gas)
• "Paper-thin" bowel wall: Hyperemia then ischemic thinning
• Mesenteric fat stranding
• Ascites (peritoneal irritation)
• Occlusion of SMA/SMV on CT angiography

• Gas (hypodense foci) in peripheral branches of portal vein (extending to within 2 cm of liver capsule)
• Differentiates from biliary gas (pneumobilia):
  • PVG: peripheral distribution, non-branching, not at hilum
  • Biliary gas: central, at hilum, branching pattern
• PVG with PI = 75% mortality in ischaemic bowel (historically); now improved with CT-directed treatment

3. Ultrasound

• "Dirty shadowing" or "comet-tail artefact" from intramural gas
• Portal venous gas: echogenic foci with "comet-tail" shadowing within liver on real-time USG
• Less sensitive than CT; operator-dependent
• Useful at bedside in unstable patients (neonates with NEC)

4. MRI

• Not routinely used for PI
• Gas appears as signal void (hypointense) on all sequences
• Used in chronic/benign cases (cystoides) to characterize cyst contents

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SPECIAL ENTITY: NECROTIZING ENTEROCOLITIS (NEC) - In Neonates

• Bubbly intramural gas (Stage IIA+)
• Portal venous gas (Stage IIB+) = worsening prognosis
• Fixed loop (unchanging bowel loop over serial X-rays = infarction)
• Pneumoperitoneum = perforation (Stage IIIB - surgical emergency)

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CLINICAL SIGNIFICANCE AND MANAGEMENT

• Primary idiopathic, pulmonary-associated, drug-related
• Subserosal cysts, asymptomatic patient, no portal gas, no systemic signs
• Management: Oxygen therapy (high-flow O2 displaces N2 from cysts), antibiotics (metronidazole), treat underlying cause

• Linear submucosal gas + portal venous gas + bowel wall non-enhancement + systemic signs
• Management: Emergency laparotomy, bowel resection, intensive care

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Q37. MECKEL'S DIVERTICULUM

Definition

Rule of 2s (Classic Mnemonic)

• 2% of population
• 2 feet (60 cm) from ileocaecal valve (antimesenteric border)
• 2 inches (5 cm) in length
• 2:1 male to female ratio for symptomatic cases
• 2 types of ectopic mucosa: gastric (most common, 60%) and pancreatic
• Presents in first 2 years of life (in children)

Pathology

• Remnant of proximal vitello-intestinal duct
• Antimesenteric border of ileum, 60 cm from ileocaecal valve
• True diverticulum: mucosa + submucosa + muscularis propria + serosa
• 60% contain ectopic tissue: gastric mucosa most common (causes acid secretion → bleeding/ulceration), pancreatic tissue, colonic, duodenal
• Only symptomatic in 4% of those who have it (lifetime risk)

Clinical Presentations

1. Bleeding (most common in children): Painless rectal bleeding - ectopic gastric mucosa secretes acid → ulceration of adjacent ileal mucosa → bleeding
2. Intestinal obstruction: Volvulus around fibrous band connecting diverticulum to umbilicus; intussusception (MD as lead point); adhesions
3. Meckel's diverticulitis: Mimics acute appendicitis; right lower quadrant pain; may perforate
4. Diverticulitis + perforation: Peritonitis
5. Umbilical fistula/sinus: If vitello-intestinal duct remains patent
6. Rarely: Meckel's hernia (Littre's hernia = herniation of Meckel's diverticulum in inguinal hernia sac)

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RADIOLOGICAL INVESTIGATIONS

1. Plain X-Ray

• Usually normal
• Occasionally: ectopic calcification (enteroliths within diverticulum)
• Obstruction pattern: dilated small bowel loops, air-fluid levels
• Pneumoperitoneum if perforated
• Limited diagnostic value for primary lesion

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

• Low sensitivity (~50%) for demonstrating Meckel's diverticulum
• Findings:
  • Blind-ending pouch/sac projecting from antimesenteric border of terminal ileum
  • Tubular or conical outpouching
  • May contain food residue or calcified enterolith
  • Fold pattern within MD
  • Mucosal pattern within diverticulum (gastric folds if ectopic gastric mucosa present)
• Enteroclysis (intubation technique) superior to SBFT
• Not first-line for acute presentation

3. Tc-99m Pertechnetate Scan (Meckel's Scan) - INVESTIGATION OF CHOICE FOR BLEEDING

• IV injection of Tc-99m pertechnetate
• Images acquired at 5-minute intervals for 60 minutes
• Pentagastrin/H2 blockers/cimetidine can be given beforehand to enhance sensitivity

• Focal area of increased uptake in right lower quadrant (corresponding to location of MD)
• Activity appears simultaneously with gastric uptake
• Activity increases over time (like stomach)
• Activity does NOT shift with voiding (differentiates from bladder)

• Ureteral obstruction (stasis/ureteric activity)
• Small bowel tumors with gastric mucosa (duplication cysts)
• Inflammatory bowel disease
• Appendicitis
• Intussusception

• MD without ectopic gastric mucosa (40%)
• Previous barium (barium attenuates gamma radiation)
• Small amount of gastric mucosa

• Pentagastrin: Increases uptake by gastric mucosa (enhances sensitivity)
• Cimetidine (H2 blocker): Blocks acid secretion but NOT pertechnetate uptake → increases retention in diverticulum (reduces wash-out) → improves sensitivity
• Glucagon: Reduces peristalsis (reduces tracer movement artefact)

4. CT Scan

• Outpouching from antimesenteric border of ileum in right lower abdomen
• Blind-ending tubular/spherical structure adjacent to ileum
• Fluid-filled or air-containing structure
• Wall similar to bowel (muscular, enhancing)
• Meckel's diverticulitis: Wall thickening, surrounding fat stranding, perilesional fluid (mimics appendicitis but appendix separately identified)
• Obstruction: Fibrous band tethering to anterior abdominal wall visible; closed-loop obstruction pattern
• Enterolith within MD: Calcification
• Perforation: Free gas, free fluid, peritoneal contamination

• Blind-ending bowel loop connected to ileum
• Location: right lower quadrant, antimesenteric
• Thickened wall (in diverticulitis)
• No communication with colon

• Better mucosal detail
• Oral contrast distends small bowel
• Superior to conventional CT for small bowel pathology

5. Ultrasound

• Limited role; operator-dependent
• May identify: blind-ending fluid-filled structure in RLQ; adjacent fat stranding; free fluid (perforation)
• Meckel's diverticulitis: Thickened-walled tubular structure, hyperaemia on Doppler, perilesional echogenicity
• Useful in children (less body fat → better visualization)

6. MRI / MR Enterography

• Excellent for soft tissue characterization
• Identifies MD as blind-ending sac from ileum
• No radiation (preferred in children)
• T2: fluid-filled diverticulum (bright); T1 post-contrast: wall enhancement in diverticulitis
• DWI: restricted diffusion if inflammation/necrosis

7. Angiography (Selective Mesenteric)

• For active GI bleeding not identified by Meckel's scan
• Identifies ectopic vessels/blush from MD
• Therapeutic embolization possible

8. Capsule Endoscopy

• Identifies bleeding lesion in small bowel including MD
• Mucosal view
• Cannot distinguish MD from other causes without specific features

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COMPLICATIONS AND THEIR IMAGING

Differentiating MD from Appendicitis on CT

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Q38. ACUTE ABDOMEN IN A 50-YEAR-OLD FEMALE

Definition

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CAUSES IN A 50-YEAR-OLD FEMALE (Differential Diagnosis)

SURGICAL CAUSES

1. Acute appendicitis
2. Peptic ulcer perforation
3. Intestinal obstruction (adhesions, hernia, volvulus)
4. Acute cholecystitis / Biliary colic
5. Acute pancreatitis
6. Mesenteric ischemia
7. Colonic diverticulitis (sigmoid - very common at this age)
8. Colonic perforation
9. Intussusception
10. Volvulus (sigmoid, caecal)
11. Incarcerated hernia

• Acute cholangitis (Charcot's triad)
• Hepatic abscess
• Splenic infarct/rupture

• Ruptured abdominal aortic aneurysm (AAA)
• Mesenteric vascular occlusion (SMA embolism)
• Splenic artery aneurysm rupture

GYNAECOLOGICAL CAUSES (Important in females)

1. Ectopic pregnancy (less likely at 50 but not impossible if premenopausal)
2. Ovarian cyst accident: Torsion, rupture, haemorrhage (most common gynaecological cause at 50)
3. Pelvic inflammatory disease (PID) / Tubo-ovarian abscess
4. Ovarian carcinoma (complication - torsion, ascites)
5. Uterine pathology: Fibroid degeneration, fibroid torsion
6. Endometriosis (chocolate cyst rupture)
7. Perimenopausal causes: Ovarian cysts common

UROLOGICAL CAUSES

1. Ureteric colic (renal stone)
2. Pyelonephritis / Renal abscess
3. Urinary retention

MEDICAL / NON-SURGICAL CAUSES

1. Diabetic ketoacidosis
2. Inferior myocardial infarction (referred pain)
3. Lower lobe pneumonia (referred pain)
4. Acute porphyria
5. Sickle cell crisis
6. Herpes zoster

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RADIOLOGICAL APPROACH AND INVESTIGATIONS

Step 1: Clinical Assessment

• Site of pain, onset, radiation, severity, associated symptoms (vomiting, fever, urinary, gynaecological history)
• Last menstrual period (LMP), menstrual status (peri/post-menopausal)
• Vital signs

Step 2: Initial Investigations

• Erect CXR: Free gas under diaphragm (perforation)
• AXR Supine:
  • Dilated bowel loops (obstruction)
  • Sentinel loop (localised ileus suggesting adjacent inflammation - pancreatitis, appendicitis)
  • "Colon cut-off sign" (pancreatitis)
  • Calcification: renal calculi (ureteric line), gallstones (10% radio-opaque), aortic aneurysm (eggshell calcification), appendicolith (faecolith)
  • Pneumatosis intestinalis (ischemia)
  • Opaque renal calculus in ureter ("stone in line")
• Erect AXR: Air-fluid levels (obstruction/perforation/ileus)

• Safe (no radiation); portable; real-time
• Excellent for:
  • Biliary system (cholecystitis, gallstones, CBD dilatation)
  • Liver (abscess, haematoma)
  • Renal tract (hydronephrosis, stones, abscess)
  • Gynaecological organs (ovarian cyst, TOA, free pelvic fluid, uterus)
  • Aorta (AAA)
  • Free fluid (peritoneal fluid)

• Gallstones (hyperechoic with acoustic shadow)
• Gallbladder wall thickening (>3 mm)
• Pericholecystic fluid
• Positive Murphy's sign (maximal tenderness over gallbladder with probe)
• Gallbladder distension (>4 cm width)
• "Halo" sign (oedematous wall)

• Ovarian cyst: size, morphology (simple/complex), septa, internal echoes, Doppler
• Torsion: absent/reversed Doppler in ovarian vessels; heterogeneous enlarged ovary; "whirlpool sign" of twisted pedicle
• TOA: complex thick-walled adnexal mass; low-level echoes; adjacent inflammation
• Free fluid in POD (pouch of Douglas)
• Uterine fibroid: hypoechoic intramural/pedunculated mass

• Hydronephrosis (pelvicalyceal dilatation) secondary to ureteric stone
• Renal abscess (complex focal lesion)

• Aortic dilatation (>3 cm = AAA)
• Retroperitoneal haematoma (AAA rupture)

• Dilated appendix (>6 mm outer diameter)
• Wall thickening, wall enhancement
• Periappendiceal fat stranding
• Appendicolith (calcified faecolith in 30%)
• Pericaecal free fluid
• Complications: abscess, perforation (free gas/fluid)

• Sigmoid wall thickening (>4 mm)
• Pericolonic fat stranding (hallmark)
• Diverticula visible in/around sigmoid
• Pericolic fat infiltration
• Complications: abscess (fluid collection + rim enhancement), fistula, perforation, obstruction
• Modified Hinchey classification on CT:
  • Stage I: Pericolic abscess
  • Stage II: Pelvic/distant abscess
  • Stage III: Purulent peritonitis
  • Stage IV: Faeculent peritonitis

• Pneumoperitoneum (free gas under diaphragm on erect CXR / CT)
• Free fluid (peritoneal contamination)
• Leakage of contrast if oral contrast given
• Gastric wall thickening at perforation site

• Pancreatic enlargement, loss of lobular margin
• Peripancreatic fat stranding
• Fluid collections (APFC → pseudocyst)
• Non-enhancing pancreatic parenchyma = necrosis
• Balthazar/CTSI scoring

• Enlarged, heterogeneous ovary (>5 cm)
• "Whirlpool sign": twisted vascular pedicle
• Absent Doppler (absent flow = torsion; but present Doppler does NOT exclude torsion)
• Adjacent free fluid
• Associated cyst (>5 cm increases risk)

• Bowel wall thickening with absent enhancement (transmural ischemia)
• Pneumatosis intestinalis
• Portal/mesenteric venous gas
• SMA occlusion (filling defect on CTA)
• Mesenteric fat stranding
• Free fluid (peritoneal exudate)

• Retroperitoneal haematoma
• Hyperdense blood around aorta
• Draped aorta sign
• Active extravasation of contrast (if CTA with contrast)

• For suspected ureteric colic with complications
• Non-contrast CT most sensitive for stones (>95%)
• Ureteric stone: hyperdense calculus in ureteric lumen; hydroureteronephrosis; periureteric stranding

• Gynaecological causes (ovarian torsion, endometrioma, fibroid degeneration)
• Avoids radiation in peri-menopausal women
• Bowel ischemia assessment
• Pregnant patients: MRI preferred over CT

• Hepatobiliary iminodiacetic acid (HIDA) scan: acute cholecystitis when USG equivocal
• Negative HIDA (no gallbladder filling) = acute cholecystitis
• Tc-99m WBC scan: occult infection/abscess

• When imaging inconclusive
• Both diagnostic and therapeutic
• For suspected ovarian pathology, appendicitis, pelvic pain

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SUMMARY TABLE: KEY CONDITIONS IN 50-YEAR-OLD FEMALE

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Q39. HOW WILL YOU INVESTIGATE A 40-YEAR-OLD MALE PATIENT COMPLAINING OF HAEMOPTYSIS IN A FULLY EQUIPPED RADIO-IMAGING CENTRE?

Definition

Causes of Haemoptysis

1. Bronchogenic carcinoma (most common cause in 40-year-old male smoker)
2. Pulmonary tuberculosis (globally most common cause)
3. Bronchiectasis
4. Lung abscess / Necrotizing pneumonia
5. Pulmonary embolism / Pulmonary infarction
6. Aspergilloma (mycetoma in pre-existing cavity)
7. Pneumonia (bacterial, viral)
8. Carcinoid tumour (bronchial)
9. Pulmonary AVM (arteriovenous malformation)

1. Mitral stenosis (left heart failure → pulmonary hypertension)
2. Left ventricular failure
3. Pulmonary venous hypertension

1. Trauma (tracheobronchial injury)
2. Foreign body
3. Coagulopathy
4. Goodpasture syndrome
5. Wegener's granulomatosis (GPA)
6. Hereditary haemorrhagic telangiectasia (HHT - Osler-Weber-Rendu)
7. Iatrogenic (post-bronchoscopy, post-biopsy)

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RADIOLOGICAL INVESTIGATION PROTOCOL

Step 1: Chest X-Ray (CXR) - FIRST INVESTIGATION

• Hilar/perihilar mass: Bronchogenic carcinoma (central)
• Peripheral mass: Peripheral carcinoma, abscess, AVM
• Upper lobe infiltrate/cavitation: Tuberculosis, aspergilloma
• Ring shadows + tram-track opacities: Bronchiectasis

• Upper lobe cavitation with air-crescent sign: Aspergilloma (mycetoma - fungal ball in cavity)
• Cavitation with thick wall: Lung abscess, TB, squamous cell carcinoma
• Thin-walled cavity: Cystic bronchiectasis

• Kerley B lines + cardiomegaly: Mitral stenosis/LVF
• Hampton's hump + Fleischner's sign: Pulmonary embolism
• Consolidation: Pneumonia, haemorrhage
• Hilar lymphadenopathy: TB, sarcoid, lymphoma
• Apical pleural thickening: Healed/active TB
• Mediastinal widening: Mediastinal mass, aortic aneurysm
• Normal CXR (in 30-40%): Does NOT exclude significant pathology

Step 2: High-Resolution CT (HRCT) Chest - MOST IMPORTANT INVESTIGATION

• Spiculated/lobulated mass with irregular margins
• Satellite nodules, pleural tethering
• Mediastinal invasion, hilar adenopathy
• Endobronchial lesion: "Tramline" obstruction, post-obstructive collapse/consolidation
• CT staging (TNM): mass size, nodal involvement, distant metastases
• PET-CT: Metabolic staging of lung cancer

• Upper lobe consolidation, cavitation
• "Tree-in-bud" pattern (endobronchial spread)
• Centrilobular nodules
• Apical fibrosis + traction bronchiectasis
• Calcified lymph nodes (Ghon complex)
• Active TB: cavitation, bronchogenic spread, consolidation

• "Tram-track" sign: Parallel dilated bronchial walls (cylindrical)
• "Ring shadow" / "Signet ring" sign: Bronchus diameter > adjacent artery (normally 1:1)
• Varicoid: Beaded dilated bronchi
• Cystic: Clustered cystic spaces ("bunch of grapes")
• Bronchial wall thickening, mucoid impaction ("finger-in-glove")
• Distribution: Lower lobe (post-infective), upper lobe (CF/ABPA), dependent segments

• Thick-walled cavity with air-fluid level
• Irregular inner wall
• Adjacent consolidation, pleural effusion

• "Air crescent sign": Semilunar lucency (air) around a central soft tissue density (mycetoma) within pre-existing cavity
• Mobile (changes with positioning of patient)
• Pleural thickening adjacent to cavity

• Serpiginous mass connected to feeding artery and draining vein
• CECT: enhancing vascular structure
• CTA: feeding pulmonary artery + draining vein

• CT Pulmonary Angiography (CTPA): filling defect in pulmonary arteries (direct sign)
• Peripheral wedge-shaped infarct (Hampton's hump)
• Pleural effusion, atelectasis
• "Mosaic attenuation" pattern (oligaemia)

Step 3: CT Pulmonary Angiography (CTPA) - For Vascular Lesions

• Suspected pulmonary embolism
• Pulmonary AVM
• Massive haemoptysis (to identify bleeding vessel before bronchial artery embolization)
• Pulmonary hypertension

• Bolus-tracking technique; 100-150 mL IV contrast
• Timing: Pulmonary arterial phase (80-90% maximum enhancement)
• Thin-slice (1.25 mm) for maximum detail
• 3D MIP, VR reconstructions

• Hypertrophied bronchial arteries (>2 mm = abnormal; normal <1.5 mm)
• Source of bleeding in 90% of haemoptysis (bronchial arteries)
• Identifies feeding vessels for transcatheter embolization

Step 4: Fibreoptic Bronchoscopy (FOB) - Endoscopic Investigation

• Localizes bleeding to specific bronchopulmonary segment
• Biopsies visible endobronchial lesions
• Therapeutic: endobronchial tamponade, lavage
• Complements imaging with direct visualization
• Rigid bronchoscopy for massive haemoptysis control

Step 5: Bronchial Arteriography / Selective DSA - For Massive Haemoptysis

• Massive haemoptysis not controlled by medical management
• Pre-embolization mapping

• Selective catheterization of bronchial arteries (usually originate from aorta at T4-T6)
• Systematic injection of right + left bronchial arteries
• Look for: hypertrophied vessels, neovascularity, active extravasation, AVM

• Enlarged, tortuous bronchial arteries
• Neovascularity, tumour blush
• Arteriovenous shunting
• Active extravasation (contrast blush from vessel)
• Bronchopulmonary arterial anastomoses

• Gold standard therapeutic procedure for massive haemoptysis
• PVA (polyvinyl alcohol) particles, coils, gelfoam
• Success rate: 73-99% for immediate control
• Complications: spinal cord ischemia (artery of Adamkiewicz - "great anterior radicular artery" shares intercostal/bronchial origin), chest pain, oesophageal ischemia
• Pre-embolization: always look for anterior spinal artery origin from bronchial/intercostal arteries

Step 6: MRI Chest

• For mediastinal involvement by carcinoma (T4 staging)
• Vascular invasion assessment
• Brachial plexus involvement (Pancoast tumor)
• Not primary investigation for haemoptysis
• MRA: AVM characterization without radiation

Step 7: PET/CT (18F-FDG)

• Metabolic staging of bronchogenic carcinoma
• Identifies mediastinal nodes (N2/N3), distant metastases (M1)
• Response assessment after treatment
• Differentiates active disease from scar tissue

Step 8: Radionuclide Imaging

• V/Q scan (Ventilation-Perfusion): For pulmonary embolism (alternative to CTPA, especially in renal failure/contrast allergy/pregnancy)
• Ga-67 / FDG PET: Sarcoidosis, inflammatory lung disease

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ALGORITHM FOR HAEMOPTYSIS INVESTIGATION

40-year-old male with HAEMOPTYSIS
        ↓
1. CXR (PA + lateral)
        ↓
Normal/Non-diagnostic → HRCT Chest (parenchymal evaluation)
        ↓
Mass lesion → CT Chest with contrast + CT staging + PET/CT (bronchogenic Ca)
        ↓
Cavitation/Infiltrate → HRCT + sputum AFB (TB, Aspergilloma)
        ↓
Suspected vascular → CTPA (PE, AVM)
        ↓
Bronchoscopy (localize site, biopsy)
        ↓
Massive haemoptysis → Bronchial arteriography + BAE (therapeutic)

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SUMMARY TABLE

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Q40. ROLE OF MDCT IN ACUTE ABDOMEN

Introduction

Advantages of MDCT in Acute Abdomen

1. Fast acquisition: Entire abdomen and pelvis in <10 seconds (eliminates motion artifact)
2. Isotropic voxels: Equal resolution in all planes; MPR, MIP, VR reconstructions
3. High spatial resolution: 0.5-0.625 mm detector collimation
4. Universal applicability: Evaluates all abdominal organs simultaneously
5. Sensitivity 94-100% for most acute abdominal conditions
6. Alters management in 30-50% of cases
7. Reduces time to diagnosis and unnecessary explorations
8. Available 24/7 in emergency settings

CT Protocol for Acute Abdomen

1. Non-contrast CT (first run): Detect calculi, fresh haemorrhage, pneumatosis, calcification, free gas
2. Arterial phase (25-30 sec): Vascular pathology (mesenteric ischemia, AAA rupture, solid organ trauma, active bleeding)
3. Portal venous phase (70-80 sec): Solid organ parenchyma, bowel wall, lymph nodes, portal system
4. Delayed phase (3-10 min): Urinary tract (stone disease, ureteric phase), leak detection
5. Oral contrast: Water-soluble contrast (Gastrografin) or dilute barium; helps bowel delineation; optional in emergency

• Automatic tube current modulation
• Iterative reconstruction algorithms
• Low-kV protocols (80-100 kV for vascular studies)

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ROLE OF MDCT IN SPECIFIC ACUTE ABDOMINAL CONDITIONS

1. Acute Appendicitis

• Appendiceal diameter >6 mm (normal <6 mm)
• Periappendiceal fat stranding (most sensitive sign)
• Appendiceal wall enhancement
• Appendicolith (calcified faecolith - 30%)
• Pericaecal free fluid
• "Arrowhead sign": Thickened caecal apex pointing to appendix
• Non-filling of appendix with oral contrast

• Abscess: rim-enhancing fluid collection (CT-guided drainage)
• Perforation: free gas, free fluid, fat stranding extending beyond periappendiceal region
• Phlegmon: poorly marginated inflammatory mass (non-surgical - antibiotics)

2. Acute Cholecystitis

• Gallbladder wall thickening >3 mm (with hydropic distension)
• Pericholecystic fat stranding
• Gallstones (hyperdense >70 HU or soft-tissue dense on NECT)
• Gallbladder distension (>5 cm long, >3 cm wide)
• Pericholecystic fluid
• Gallbladder wall oedema (low-density striations in wall)

• Emphysematous cholecystitis: Gas in gallbladder wall/lumen (life-threatening; diabetics)
• Gangrenous cholecystitis: Irregular wall, lack of enhancement, intraluminal membranes
• Perforation: Free pericholecystic fluid, defect in wall, local abscess

3. Acute Diverticulitis

• Sigmoid wall thickening (>4 mm)
• Pericolonic fat stranding (essential feature)
• Diverticula (outpouchings from colonic wall)
• "Dirty fat" sign: streaky pericolonic infiltration
• Arrow-head sign at diverticular neck

• Stage 0: Mild diverticulitis; no CT complications
• Stage Ia: Pericolonic inflammation/phlegmon
• Stage Ib: Pericolonic/mesenteric abscess
• Stage II: Pelvic/distant abscess (CT-guided drainage)
• Stage III: Purulent peritonitis
• Stage IV: Faeculent peritonitis (emergency surgery)

4. Intestinal Obstruction

• Dilated loops proximal to obstruction (>3 cm small bowel; >6 cm colon; >9 cm caecum)
• Transition zone: Point where dilated loops become decompressed (identifies site and level)
• Cause identification:
  • Adhesive band: Abrupt kink at transition zone, no mass
  • Hernia: Bowel entering hernia sac
  • Volvulus: "Whirlpool sign" of mesenteric vessels, "beak sign" at twist
  • Mass/Tumour: Enhancing soft tissue mass causing luminal compromise
  • Intussusception: "Target sign" on cross-section
• Closed-loop obstruction: Two adjacent transition zones; C-shaped or U-shaped dilated loops; dilated loop with mesenteric vessels converging ("radial" pattern)
• Strangulation (bowel ischemia): Pneumatosis, absent wall enhancement, mesenteric venous gas, ascites

5. Mesenteric Ischemia

• SMA/celiac occlusion: Filling defect within SMA lumen (embolism) or non-opacification
• Aortic atherosclerosis: Calcification, irregular lumen
• Venous thrombosis: Hyperdense thrombus in SMV/portal vein without contrast; filling defect with contrast

• Hyperenhancement (early): Reactive ischemia
• Absent enhancement (late/transmural): Infarction
• Wall thickening (early) → Paper-thin wall (late)
• Pneumatosis intestinalis
• Portal/mesenteric venous gas

• Fat stranding (ischemia/inflammation)
• Ascites (peritoneal exudate)
• Pneumoperitoneum (perforation)

6. Ruptured AAA

• Hyperdense blood in retroperitoneum (45-50 HU)
• Retroperitoneal haematoma
• Aortic wall calcification delineating aneurysm

• Active extravasation of contrast (blush outside aortic wall)
• "Draped aorta sign": posterior aortic wall not visible; aorta drapes over vertebral body
• "Crescent sign": Hyperdense crescent within mural thrombus = impending rupture
• Intraperitoneal blood (worst prognosis)

7. Acute Pancreatitis

• Pancreatic enlargement, oedema
• Peripancreatic fat stranding (hallmark)
• Fluid collections (APFC)
• Non-enhancing parenchyma = Necrosis (CTSI scoring)
• Gas in collections = infected necrosis

• Score 0-3: Mild (<10% morbidity)
• Score 4-6: Moderate (35% morbidity)
• Score 7-10: Severe (92% morbidity, 17% mortality)

8. Hollow Viscus Perforation

• Pneumoperitoneum: Free gas under diaphragm (erect); anterior to liver (supine - "football sign" in neonates); falciform ligament sign
• Oral contrast leakage: if oral contrast given
• Peritoneal fluid (early - minimal; later - turbid/infected)
• Site identification:
  • Peptic ulcer: lesser sac gas, perigastric fluid
  • Diverticular: pericolic gas + fat stranding
  • Appendiceal: periappendiceal gas
• Sensitivity of CT for free gas: >95% (vs. CXR 70-80%)

9. Renal/Ureteric Colic

• Sensitivity 96-97%; Specificity 96-100% (superior to IVU)
• Hyperdense calculus (>80 HU) in ureter
• Hydroureteronephrosis
• Periureteric fat stranding ("rim sign")
• Renal enlargement (acute obstruction)
• Secondary signs: perinephric fat stranding, renal enlargement

10. Gynaecological Emergencies

• Ovarian torsion: Enlarged ovary, whirlpool sign (twisted pedicle), absent enhancement, ascites
• Ruptured ectopic: Adnexal mass, haemoperitoneum (hyperdense), collapsed uterine cavity
• TOA: Complex thick-walled pelvic mass, multiple internal septations

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MDCT in TRAUMA (Acute Abdomen from Trauma)

• Liver: Lacerations (low-density irregular areas), subcapsular haematoma, active bleeding (contrast blush)
• Spleen: Laceration, devascularization, contained vs. free haemoperitoneum
• Kidney: Laceration, contusion, vascular injury (AAST grading I-V)
• Active bleeding: "Blush" of contrast extravasation on arterial phase
• FAST equivalent: Free peritoneal fluid in all spaces (Morrison's pouch, splenorenal, pelvic)

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MDCT vs. Other Modalities

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Q41. ELASTOGRAPHY IN LIVER LESIONS

Introduction

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TYPES OF ELASTOGRAPHY

A. ULTRASOUND-BASED ELASTOGRAPHY

1. Transient Elastography (TE) - FibroScan®

• A mechanical vibrator produces a low-frequency (50 Hz) shear wave that propagates through liver
• Shear wave speed is measured by ultrasound; converted to liver stiffness measurement (LSM) in kilopascals (kPa)
• Measures stiffness of a cylinder of liver parenchyma (~1 cm diameter, 4 cm length)

• M probe: BMI <30; depth 25-65 mm (most patients)
• XL probe: BMI >30; overweight/obese patients
• Normal liver stiffness: 2-6 kPa
• 10 valid measurements; IQR/median ratio <30% for reliability

• Non-invasive, reproducible
• Rapid (<10 min), outpatient-based
• Well-validated for HCV, HBV, NASH, NAFLD, alcoholic liver disease
• Can monitor treatment response

• Blind technique (no B-mode during measurement)
• Unreliable in ascites (shear wave reflected)
• Unreliable with high BMI (XL probe helps partially)
• Elevated in acute hepatitis/inflammation (false elevation unrelated to fibrosis)
• Operator-dependent patient positioning
• Cannot assess focal lesions

2. Real-Time Sonoelastography (Strain Elastography)

• Tissue compression by external probe or cardiac/vascular pulsation (internal)
• Measures relative deformation (strain) between tissue layers
• Soft tissue shows high strain (blue = soft); hard tissue shows low strain (red = hard) - colour mapped

• Freehand compression with transducer over focal lesion
• Colour overlay (red-green-blue) on B-mode image
• Strain ratio: Ratio of stiffness of focal lesion to normal liver parenchyma

• Malignant lesions (HCC, metastases): High stiffness (red colour = hard); strain ratio >3.5 suggests malignancy
• Benign cysts: Anechoic, no strain (pseudo-soft appearance)
• Haemangioma: Variable (soft to intermediate)
• Limitations: Qualitative, operator-dependent; cannot quantify stiffness absolutely

3. ARFI (Acoustic Radiation Force Impulse) Elastography - Point SWE (pSWE)

• Focused ultrasound "push pulse" creates mechanical displacement of tissue
• Shear wave generated propagates laterally from push pulse
• Two tracking beams measure shear wave speed (m/s)
• Converted to stiffness (kPa = ρ × V²)

• ROI placed within ROI on B-mode image (operator chooses site - guided)
• Reports velocity in m/s
• Normal liver: 1.0-1.2 m/s
• Cirrhosis threshold: >1.8-2.0 m/s (kPa equivalent: >14 kPa)

• Integrated with B-mode ultrasound (guided placement)
• Works in ascites
• Can assess individual liver segments
• Can be applied to focal lesions

4. 2D/3D Shear Wave Elastography (SWE) - pSWE vs 2D-SWE

• Multiple focused push pulses generate shear waves
• Wide 2D colour-coded elastogram overlaid on B-mode
• Quantitative stiffness map (kPa or m/s)
• Can measure ROI within specific zones

• ElastPQ (Philips)
• SWE (Supersonic Imagine - Aixplorer®): First commercial 2D-SWE
• VTIQ (Siemens)

• HCC: Mean stiffness significantly higher than surrounding liver (>30-40 kPa)
• Metastases: Very high stiffness (>50 kPa for hard metastases - colon, gastric)
• Haemangioma: Intermediate (10-20 kPa)
• Simple cysts: Very low (soft blue on map)
• Regenerative nodule (in cirrhosis): Lower than HCC

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B. MR ELASTOGRAPHY (MRE) - MOST ACCURATE METHOD

• External passive pneumatic driver (mechanical vibrator) placed on right upper abdomen
• Low-frequency shear waves (60 Hz) propagate through liver
• Specialized phase-contrast MR sequences (gradient echo or spin echo) encode wave propagation
• 4D wave image reconstructed into stiffness map (elastogram) in kPa

• Gradient Recalled Echo (GRE-MRE): Fast, less motion artifact
• Spin Echo EPI (SE-EPI): Better in iron-overloaded liver
• GRE-MRE: Normal liver 1.5-2.5 kPa; cirrhosis >5-6 kPa

• Most accurate: AUC 0.93-0.98 for cirrhosis (superior to US-based)
• Large liver volume sampled (entire liver)
• Unaffected by ascites, obesity, iron overload (with SE-EPI)
• Reproducible, operator-independent
• Can be combined with liver MRI protocol
• Good for focal lesion characterization

• Expensive
• MRI availability/time
• Claustrophobia
• Metal implants (contraindication)
• Requires specialized software/hardware

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CLINICAL APPLICATIONS OF LIVER ELASTOGRAPHY

1. Liver Fibrosis / Cirrhosis Staging

• Primary application: Non-invasive replacement/complement to liver biopsy
• Validated for: HCV, HBV, NAFLD/NASH, alcohol-related liver disease, PBC, PSC
• EASL guidelines 2017: TE recommended for initial fibrosis assessment; liver biopsy reserved for indeterminate cases
• Serial assessment: monitoring antiviral treatment response (LSM decreases with successful viral clearance)
• Post-SVR (sustained virological response): LSM decreases by 30-40%

2. Portal Hypertension Assessment

• Liver stiffness correlates with portal pressure (hepatic venous pressure gradient - HVPG)
• TE >20-25 kPa: high probability of clinically significant portal hypertension (CSPH)
• Spleen stiffness measurement: correlates better with portal hypertension

3. Characterization of Focal Liver Lesions

• Adjunct to CECT/MRI; does NOT replace them
• Differentiates malignant from benign lesions (stiffness threshold varies)
• Can guide biopsy to hardest (most viable tumour) part

4. Differentiation of Diffuse Liver Disease

• Fatty liver (hepatic steatosis): normal stiffness initially; elevated only with fibrosis
• Controlled Attenuation Parameter (CAP) - co-measured with FibroScan:
  • Measures hepatic steatosis (ultrasound attenuation coefficient in dB/m)
  • CAP <238 dB/m = S0 (no steatosis)
  • CAP ≥280 dB/m = S2-S3 (significant steatosis)

5. Monitoring Treatment Response

• Hepatitis B/C antiviral treatment
• Post-TIPS (reduction in portal pressure)
• Weight loss in NAFLD (LSM and CAP reduction)

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LIMITATIONS AND CONFOUNDERS OF LIVER ELASTOGRAPHY

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Q42. DESCRIBE THE SEGMENTAL ANATOMY OF LIVER BY CT SCAN. EXPLAIN THE DIFFERENT ENHANCEMENT PHASES OF LIVER ON CECT AND ENUMERATE THE CAUSES OF FOCAL LIVER LESIONS

PART A: SEGMENTAL ANATOMY OF LIVER ON CT (Couinaud Segmentation)

Couinaud Liver Segments - Standard System

• Horizontal division: Portal plane (plane of right and left portal vein branches)
• Vertical division: Three hepatic veins (right, middle, left) divide liver into 4 sections
• Segment I (Caudate lobe): Separate entity with autonomous portal and venous drainage directly to IVC

Hepatic Landmarks on CT for Segment Identification

• Right hepatic vein (RHV): Separates right anterior section (V, VIII) from right posterior section (VI, VII)
• Middle hepatic vein (MHV): Separates right lobe from left lobe (principal plane / Cantlie's line)
• Left hepatic vein (LHV): Separates left medial section (IV) from left lateral section (II, III)

• Main portal vein → Right + Left portal branches (at hepatic hilum)
• Right portal vein → Right anterior branch (segments V, VIII) + Right posterior branch (segments VI, VII)
• Left portal vein → Segments II, III, IV, I

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Individual Segments - CT Location

• Bounded: IVC (posteriorly), ligamentum venosum (left), portal vein (anterior)
• Separate venous drainage: direct to IVC (spared in Budd-Chiari syndrome)
• Hypertrophy in Budd-Chiari: caudate > 65% of right lobe width

1. Find IVC entering right atrium → Level of hepatic veins
2. Identify three hepatic veins draining into IVC (fan-shaped appearance)
3. Trace right, middle, left hepatic veins to divide sectors
4. Find portal bifurcation → divides each sector into upper/lower segments
5. Gallbladder fossa (right of falciform) = boundary between segments IVb (left) and V (right)
6. Falciform ligament = boundary between segments II/III (lateral left) and IVa/IVb (medial left)
7. Ligamentum venosum (fissure) = boundary between caudate (I) and segment II/III

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CT Imaging Planes for Segment Identification

• Most commonly used; systematic level-by-level analysis
• Cranial slices: Segments I, II, IV, VII, VIII visible
• Mid-level: Segments I, III, IVb, V, VI visible
• Caudal: Segments III, IVb, V, VI visible

• Best for superior-inferior extent of segments
• Shows right lobe anterior/posterior relationships

• Falciform ligament visible
• Left lobe anatomy

• Surgical planning
• Virtual hepatectomy (residual liver volume calculation)

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PART B: ENHANCEMENT PHASES OF LIVER ON CECT

Standard Multiphasic CT Protocol

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Detailed Explanation of Each Phase

1. Non-Contrast Phase (NECT)

• Liver parenchyma: 50-65 HU (homogeneous)
• Baseline: Identifies calcification, haemorrhage (hyperdense), fat (hypodense <20 HU)
• Applications:
  • Liver calcification (healed granulomas, haemangioma)
  • Acute hepatic haemorrhage: >50 HU
  • Hepatic steatosis: <40 HU (vs. spleen density)
  • Hyperechoic lesions (hyperdense haemangiomas with thrombosis)
  • Unenhanced characterization of cysts (simple cyst: 0-20 HU)

2. Early Arterial Phase (15-20 sec after contrast injection)

• Aorta enhances maximally
• Hepatic arteries and their branches visible
• Liver parenchyma: minimal enhancement (portal vein not yet opacified)
• Used primarily for: aortic studies, celiac/SMA angiography planning
• NOT ideal for hepatic lesion detection

3. Late Arterial Phase (Hepatic Arterial Phase - 35-45 sec)

• Hepatic arteries: Peak enhancement
• Portal vein: Beginning to opacify (but not maximum)
• Liver parenchyma: 80-100 HU (early enhancement mainly from hepatic artery)
• Hepatic veins: Not yet opacified
• Application:
  • Detection of HYPERVASCULAR lesions (HCC, haemangioma, FNH, hepatic adenoma, hypervascular metastases - NET, RCC, melanoma, breast, thyroid, choriocarcinoma)
  • HCC: arterial hyperenhancement (bright) = hallmark
  • FNH: central scar enhancement + spoke-wheel arterial pattern
  • Haemangioma: peripheral nodular enhancement (arterial phase)

4. Portal Venous Phase (60-80 sec) - MOST IMPORTANT PHASE FOR LIVER

• Portal vein: Maximum opacification (best visualization of portal anatomy)
• Liver parenchyma: MAXIMUM ENHANCEMENT (120-140 HU) - 75% from portal blood
• Hepatic veins: Begin to opacify
• Best phase for: Liver parenchymal pathology, portal vein thrombosis, bowel, lymph nodes, solid organs

• Hypovascular lesions appear as hypodense defects: most metastases (colorectal, GIT), cholangiocarcinoma
• Portal vein thrombosis: filling defect in portal vein
• HCC washout: HCC appears isodense or hypodense (washout) in portal phase after arterial hyperenhancement
• Normal liver parenchyma enhancement is maximum here → lesion-to-liver contrast highest

5. Equilibrium Phase (3-5 minutes)

• Contrast distributes into extracellular spaces (equilibrium between vascular and interstitial)
• Liver parenchyma: 80-100 HU (declining from peak)
• Application:
  • "Washout" of HCC: HCC remains hypodense compared to surrounding liver (portal venous contrast retained in normal liver, washed out from HCC) → LI-RADS washout criterion
  • Peripheral washout appearance + "capsule" enhancement of HCC
  • Cholangiocarcinoma: Progressive retention of contrast (fibrous stroma) = centripetal fill-in
  • Haemangioma fill-in: Becomes isodense or hyperdense (complete fill-in)

6. Hepatobiliary Phase (Gadoxetate/Primovist - MRI ONLY, 20 minutes)

• Gadoxetate disodium (Gd-EOB-DTPA / Primovist) taken up by hepatocytes via OATP1B1/B3 transporters
• Excreted into bile (50% in normal liver)
• Application (MRI):
  • FNH: Hyperintense (retains contrast; has functioning hepatocytes + biliary canaliculi)
  • HCC: Hypointense (loss of hepatocyte function and OATP transporter)
  • Hepatic adenoma: Usually hypointense; some show uptake (β-catenin type)
  • Liver metastases: Hypointense (no hepatocytes)
  • Distinguishes FNH from adenoma (key clinical use)
  • Bile leak detection
  • Biliary anatomy mapping

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LI-RADS Classification (for HCC on CT/MRI in at-risk patients)

• ≥10 mm with: Arterial phase hyperenhancement (APHE) + Washout OR APHE + Enhancing capsule OR APHE + Threshold growth (≥50% in 6 months)

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PART C: CAUSES OF FOCAL LIVER LESIONS

BENIGN FOCAL LIVER LESIONS

• Most common benign lesion (5-10% prevalence)
• Congenital; lined by biliary epithelium
• CT: well-defined, thin-walled, homogeneous, 0-20 HU, no enhancement
• USG: Anechoic, thin wall, posterior acoustic enhancement

• Most common benign hepatic tumor (0.4-20% prevalence)
• Dilated vascular channels filled with blood
• CT: NECT - hypodense; CECT - ARTERIAL: peripheral nodular enhancement; PORTAL: progressive centripetal fill-in; DELAYED: complete iso/hyperdense fill-in
• "Flash fill" in small haemangiomas (<2 cm)
• MRI: T2 very bright ("light bulb sign")
• Tagged RBC scan: delayed fill-in (pathognomonic)

• 2nd most common benign hepatic tumor
• Hepatocytic hyperplasia around aberrant artery
• Predominantly in young women
• CT: Arterial - hyperenhancement (spoke-wheel arteries); Portal - iso/hyperdense; Delayed - central scar enhances
• MRI with Primovist: hyperintense in hepatobiliary phase (key differentiator from adenoma)
• Central scar: T2 bright; delayed CT enhancement

• Young women on oral contraceptives
• Risk of bleeding, rupture, malignant transformation
• CT: variable enhancement; may have intratumoral fat or haemorrhage
• MRI: chemical shift imaging (signal drop on out-of-phase if fat)
• Hepatobiliary phase: hypointense (no OATP transport)

• Tiny (<5 mm) multiple white nodules
• CT: multiple tiny hypodense foci
• MRI: T2 very bright (bile content)

• Echinococcus granulosus
• CT: Hypodense cyst; daughter cysts (lower density); "rim calcification"; "water lily sign" (detached endocyst); "double line sign"
• MRI: T2 bright outer cyst, hypointense pericyst wall

• Pyogenic: rim-enhancing multilocular/unilocular fluid collection; gas within (Clostridium); "double target sign" (central fluid + inner rim of oedema + outer hypervascular zone)
• Amoebic: usually right lobe; well-defined; "comet sign" (pointing to right hepatic vein)
• MRI DWI: restricted diffusion (bright DWI, low ADC)

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MALIGNANT FOCAL LIVER LESIONS

• Most common primary liver malignancy; associated with cirrhosis, HBV, HCV
• CT: Arterial hyperenhancement + Portal washout + Capsule enhancement (LR-5)
• AFP elevated (>400 ng/mL highly specific)
• Variants: Mosaic architecture, fat-containing, diffuse infiltrative, fibrolamellar (young, non-cirrhotic, central scar)

• Intrahepatic (mass-forming), perihilar (Klatskin), distal
• CT: Progressive centripetal enhancement (fibrous stroma retains contrast); capsular retraction
• MRCP: biliary obstruction level, ductal involvement
• CA 19-9 elevated

• Most common malignant hepatic lesion overall
• CT: Usually hypovascular (best seen portal phase): colorectal, GI, pancreatic, lung, breast
• Hypervascular (best seen arterial phase): NET, RCC, melanoma, breast, thyroid, choriocarcinoma, sarcoma
• MRI DWI: restricted diffusion; T2 bright; no hepatobiliary phase uptake (always hypointense in hepatobiliary phase)

• Usually secondary (NHL)
• CT: Hypodense, homogeneous, no necrosis; minimal enhancement; periportal extension
• Primary hepatic lymphoma: rare; large, heterogeneous

• Rare malignant vascular tumor; associated with vinyl chloride, Thorotrast, arsenic
• CT: Hypervascular, large, necrotic, haemorrhagic; multifocal

• Low-grade vascular malignancy
• CT: Peripheral, multiple, lobulated; "halo" sign; coalescing lesions; capsular retraction; calcification

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SUMMARY TABLE: CT ENHANCEMENT CHARACTERISTICS

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Q43. CROHN'S DISEASE

Definition

Epidemiology

• Peak age: 15-35 years (bimodal: 2nd peak at 55-60)
• Equal sex distribution (slight male predominance)
• More common in Western countries, Ashkenazi Jews
• Associated with smoking (unlike UC - protective in UC)

Pathology

• Transmural inflammation (full thickness - all layers of bowel wall): key distinguishing feature from UC (mucosal only)
• Non-caseating granulomas (50-60%) - pathognomonic on biopsy
• Skip lesions (discontinuous involvement)
• Cobblestone mucosa (longitudinal + transverse ulcers)
• Fissuring (knife-like deep ulcers)
• Creeping fat (mesenteric fat wrapping around bowel)
• Stricture formation (fibromuscular proliferation)
• Fistula formation

Distribution

• Terminal ileum only: 40%
• Ileocolic: 30%
• Small bowel only (non-ileal): 15-20%
• Colonic only: 15-20%
• Perianal: 30-40%
• Upper GI (stomach, duodenum, oesophagus): 5-10%

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RADIOLOGICAL INVESTIGATIONS

1. Plain X-Ray

• Limited; used for complications
• Dilated loops of bowel (obstruction/toxic dilatation)
• "Thumbprinting" of colonic wall (transmural oedema)
• No gas in right iliac fossa (terminal ileum disease)
• Sacroiliitis (extraintestinal manifestation)

2. Barium Studies (SBFT / Enteroclysis / Barium Enema)

• Aphthous ulcers: tiny ulcers 1-2 mm (earliest mucosal change); tiny barium collection surrounded by radiolucent halo
• Mucosal fold thickening and nodularity

• "String sign of Kantor": Long segment of narrowed, contracted ileum (due to spasm or fibrosis)
• "Cobblestone" appearance: Network of deep longitudinal and transverse ulcers with islands of oedematous mucosa
• "Rose thorn" / "Bear claw" ulcers: Deep penetrating transverse fissure ulcers
• Skip lesions: Alternating normal + diseased segments
• Pre-stenotic dilatation (dilation proximal to stricture)
• Separation of bowel loops: thickened mesentery/creeping fat
• "Sinus tracts" (early fistulae)

• Stierlin's sign: Rapid emptying of barium from diseased segment (spasm)
• "Pipe stem" ileum: Rigid, narrowed terminal ileum
• "Pseudo-Diverticulum": Sacculations on anti-mesenteric border (asymmetric fibrosis)
• "Delta sign": Separation of ileal loops by thickened mesentery

• Skip lesions in colon
• Cobblestone pattern
• Rectal sparing (unlike UC - UC always involves rectum)
• Asymmetric involvement
• Strictures (asymmetric, irregular)
• Deep ulcers + Rose thorn pattern
• "Collar button" ulcers: Less common than UC; when present in CD, deeper than UC

3. CT Enterography (CTE) / CT Enteroclysis - INVESTIGATION OF CHOICE

• Neutral oral contrast: methylcellulose or VoLumen (mannitol/sorbitol) - distends bowel without opacifying (allows wall assessment)
• IV contrast: portal venous phase primarily; arterial phase for vascularity
• Multi-planar reconstruction (coronal + sagittal)

• Bowel wall thickening (most consistent feature): >3 mm (normal <2 mm); in active CD typically 7-15 mm
• Mural stratification / "Target sign": Mucosa (inner enhancing) + submucosa (low attenuation - oedema) + muscularis/serosa (outer enhancing)
• Hyperenhancement of mucosa (active inflammation)
• Deep mural ulcers (transmural fissures)

• "Creeping fat": Fibrofatty proliferation of mesenteric fat wrapping around bowel wall ("fat halo") - pathognomonic of CD
• Mesenteric fat stranding (active disease)
• "Comb sign": Engorged vasa recta (straight mesenteric vessels) arranged like teeth of a comb = hypervascularization of mesentery (active disease)
• Mesenteric lymphadenopathy (reactive)

• Fistulae: Enhancing tubular tracts between loops of bowel (entero-enteral), bowel and bladder (entero-vesical - pneumaturia, UTI), bowel and skin (entero-cutaneous), bowel and vagina
• Abscesses: Rim-enhancing fluid collection (CT-guided drainage if accessible)
• Stricture: Short segment narrowing with pre-stenotic dilatation; bowel thickening ± fibrosis (low-density wall = fibrosis)
• Bowel obstruction: Dilated upstream bowel
• Perforation: Free gas, peritoneal signs

• Bowel wall thickness, contrast enhancement, mesenteric change, lymphadenopathy
• Guides medical vs. surgical management

4. MR Enterography (MRE) - PREFERRED MODALITY (Especially Young Patients)

• No ionizing radiation (critical in young patients with lifelong monitoring)
• Better soft tissue contrast than CT
• Multiplanar capability
• Assessment of fistulae and perianal disease
• Can assess disease activity (Magnetic Resonance Index of Activity - MaRIA score)

• T2 (True FISP/HASTE): Bowel wall oedema (bright) = active inflammation; dark wall = fibrotic
• T1 post-Gd (VIBE): Mucosal hyperenhancement = active disease
• DWI: Restricted diffusion in active inflammation (bright DWI, low ADC)
• T2 fat-suppression: Free fluid, mesenteric oedema

• Wall thickening + T2 hyperintense wall (oedema) = ACTIVE disease
• Mucosal hyperenhancement on T1 post-Gd
• DWI restriction
• Mesenteric oedema, enlarged lymph nodes

• Wall thickening + T2 hypointense (fibrous tissue = low signal) = FIBROTIC
• Less enhancement
• Pre-stenotic dilatation
• Key clinical question: Active (inflammatory - treat medically) vs. Fibrotic (fixed - surgical)
• MRE can differentiate active inflammation from fibrosis

• T2 hyperintense tracts between bowel/structures
• Enhancement of tract wall on post-Gd images
• Complex fistulae in perianal CD: MRI is gold standard

• MRI of pelvis: best modality for perianal fistulae mapping
• Parks' classification of fistula on MRI:
  • Intersphincteric (most common)
  • Trans-sphincteric
  • Suprasphincteric
  • Extrasphincteric
• Horseshoe fistulae, perianal abscess
• T2 hyperintense fistula tracts
• "Seton" in place

11 = severe active disease; threshold for initiating biologics

5. Ultrasound (Bowel USG / Intestinal USG)

• Bowel wall thickening (>3 mm in small bowel, >4 mm colon): "Stratified" or "target" appearance
• Increased vascularity on Doppler (Resistive Index measurements)
• Mesenteric fat echogenicity (creeping fat = hyperechoic, non-compressible)
• Lymphadenopathy
• Free fluid (active disease)
• Fistulae (tubular hypoechoic tracks)
• "SICUS" (Small Intestine Contrast Ultrasonography): Oral water-soluble contrast + real-time USG; excellent sensitivity for CD in thin patients

6. Capsule Endoscopy

• Detects early mucosal lesions (aphthous ulcers) not visible on CT/MRE
• Sensitivity >90% for small bowel CD
• Contraindicated in strictures (capsule retention risk - must exclude stricture by patency capsule or CTE first)
• Golden standard for small bowel mucosal assessment when other tests equivocal

7. Nuclear Medicine

• Tc-99m labelled WBC scan (Leukoscan): Identifies active inflammation; sites of disease
• Tc-99m HMPAO white cell scan: Active inflammatory segments
• FDG PET: Detects active inflammatory bowel segments (not standard care)

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COMPLICATIONS OF CROHN'S DISEASE (Radiological Assessment)

Distinguishing Crohn's vs. Ulcerative Colitis on Imaging

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RADIOLOGY UNIVERSITY THEORY EXAM - FULL ANSWERS (30 Marks Each)

Questions 44, 45, and 46

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Q44. EXPLAINING EACH PHASE (CECT Liver Enhancement Phases - Full Detailed Answer)

Introduction

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PHASE 1: NON-CONTRAST (UNENHANCED) PHASE

• Attenuation: 50-65 HU (homogeneous)
• Normal liver is slightly denser than spleen (spleen: 40-55 HU)
• Normal liver is significantly denser than fat (-100 HU)

Hepatic Steatosis (Fatty Liver)

• Normal liver-spleen attenuation difference: liver > spleen by 5-10 HU
• Steatosis: Liver attenuation < spleen by >10 HU; OR absolute liver HU < 40 HU
• Grading of Fatty Liver (CT):
  • Mild: Liver-spleen difference 1-10 HU (liver slightly less dense)
  • Moderate: Liver-spleen difference 10-20 HU
  • Severe: >20 HU difference or liver < 30 HU
• Focal fat sparing: Area of normal liver parenchyma within fatty liver (common near gallbladder fossa, porta hepatis) - appears relatively hyperattenuating; no mass effect; vessels traverse without displacement

Haemorrhage / Fresh Blood

• Acute haematoma: 45-80 HU (hyperdense)
• Subcapsular haematoma: hyperdense crescent beneath liver capsule
• Used to detect spontaneous hepatic haemorrhage (HCC rupture, adenoma rupture)

Calcification

• Old haemangioma calcification: peripheral
• Granulomata calcification (TB, histoplasmosis): punctate
• Cholangiocarcinoma: irregular
• Echinococcal cyst: rim/peripheral
• Parasitic calcification

Hyperdense Lesions (NECT)

• Melanoma metastases: hyperdense (melanin content)
• Haemorrhagic metastases (choriocarcinoma, renal cell carcinoma)
• Mucinous metastases: may calcify

Simple Cyst Characterization

• Water density (0-20 HU): confirms simple cyst
• Any enhancement excludes simple cyst

Iron Overload / Haemosiderosis

• Increased attenuation of liver parenchyma (>75 HU) from iron deposition
• Liver > spleen attenuation (primary haemochromatosis)
• Liver = spleen attenuation, both elevated (secondary haemosiderosis)

Biliary Gas vs. Portal Venous Gas

• Biliary gas (pneumobilia): central branching (hilar) distribution
• Portal venous gas: peripheral distribution (within 2 cm of liver capsule)

Portal Vein Thrombus

• Acute thrombus: hyperdense filling defect in portal vein on NECT (before contrast)

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PHASE 2: EARLY ARTERIAL PHASE

• Aorta: maximum enhancement (300-400 HU)
• Hepatic arteries: well opacified
• Portal vein: NOT yet opacified (portal enhancement begins ~30 sec)
• Hepatic veins: NOT opacified
• Liver parenchyma: minimal enhancement (only from hepatic artery = 25% supply)
• Splenic enhancement: "Arcades" pattern - heterogeneous stripes (splenic cords)

• CTA of coeliac axis and SMA: Preoperative vascular mapping for hepatic surgery (living donor transplant planning, surgical planning)
• Assessment of hepatic artery variants:
  • Replaced right hepatic artery (from SMA) - in 15-20% of population
  • Accessory left hepatic artery (from left gastric artery)
• Aortic aneurysm assessment
• Hypervascular lesion "blush" - some lesions (haemangiomas, HCC) begin to enhance
• NOT optimal for hepatic parenchymal assessment (liver still relatively unenhanced → lesion-to-background contrast poor)

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PHASE 3: LATE ARTERIAL PHASE (HEPATIC ARTERIAL PHASE - HAP)

• Hepatic arteries: peak enhancement
• Portal vein: beginning to opacify (50-60% of eventual maximum)
• Liver parenchyma: 80-100 HU (partial enhancement)
• Hepatic veins: not yet opacified (critical - if veins opacify, scan is too late = portal phase)

Hepatocellular Carcinoma (HCC)

• Arterial Phase Hyperenhancement (APHE): HCC enhances brightly (hyperdense relative to liver) due to arterial neoangiogenesis
• Nodule-in-nodule pattern visible
• Arterial enhancement of tumour thrombus
• APHE is the cardinal feature of HCC (LI-RADS major criterion)
• Small HCC: may show diffuse APHE; large HCC: heterogeneous (necrosis + APHE areas)

Hypervascular Metastases

• Ring enhancement or diffuse enhancement in arterial phase
• Appear as bright foci against partially enhanced liver

Haemangioma (Cavernous)

• Peripheral nodular/globular enhancement in arterial phase
• Enhancement density similar to aorta/hepatic artery (blood pool enhancement)
• Small haemangiomas (<2 cm): "Flash fill" complete enhancement in arterial phase
• Large haemangiomas: peripheral nodular pattern; central scar does not enhance arterially

Focal Nodular Hyperplasia (FNH)

• Intense homogeneous arterial enhancement (bright, uniformly)
• Spoke-wheel arterial pattern: Central feeding artery with radiating branches visible
• Central scar: NOT enhanced in arterial phase (enhances in delayed phase)
• This arterial enhancement is very characteristic of FNH

Hepatic Adenoma

• Variable arterial enhancement
• May contain fat (signal drop on MR chemical shift - important MRI differentiator)
• Spontaneous haemorrhage: heterogeneous

Cholangiocarcinoma

• Rim/peripheral arterial enhancement
• Progressive enhancement on subsequent phases (hallmark)

Pyogenic Liver Abscess

• Rim enhancement (wall) in arterial phase
• Central non-enhancing liquefied pus

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PHASE 4: PORTAL VENOUS PHASE (PVP) - MOST IMPORTANT PHASE

• Portal vein: MAXIMUM OPACIFICATION (best phase for portal anatomy)
• Liver parenchyma: MAXIMUM ENHANCEMENT (~130-150 HU) - 75% portal supply dominates
• Hepatic veins: Well opacified
• Superior mesenteric vein, splenic vein: fully opacified

Detection of Hypovascular Liver Metastases (Most Common Use)

• Primary cancers with hypovascular liver metastases: colorectal carcinoma (most common), pancreatic carcinoma, gastric carcinoma, cholangiocarcinoma, lung carcinoma, mucinous carcinomas
• Appear as hypodense focal defects against brighter liver parenchyma
• "Target sign": central necrosis + peripheral enhancing rim + outer hypoechoic halo
• Perilesional enhancement: "Halo" of reactive hepatic parenchymal hyperemia around metastasis
• Best phase for detecting and counting metastases

HCC Washout (Critical for LI-RADS Diagnosis)

• HCC: After arterial hyperenhancement, becomes isodense or hypodense in portal phase ("washout appearance")
• Washout = portal venous phase or delayed phase hypointensity relative to liver
• Washout + APHE = LI-RADS major criteria for HCC diagnosis
• Washout reflects reversal of HCC's relative arterial dominance; HCC lacks portal venous supply

Portal Vein Assessment

• Portal vein thrombosis: filling defect in main portal vein, right or left branch
• Tumour thrombus (HCC thrombus): enhancing filling defect (cavernous transformation of portal vein in chronic thrombosis)
• Portal hypertension: dilated portal vein (>13 mm), portosystemic collaterals (perisplenic, gastrorenal, esophageal varices)
• Cavernous transformation: multiple serpentine collateral channels replacing thrombosed portal vein

Hepatic Vein Assessment

• Budd-Chiari syndrome: non-filling of hepatic veins; caudate lobe sparing (direct IVC drainage); ascites; hepatomegaly
• Hepatic vein thrombosis
• Web/stenosis at hepatic vein-IVC junction

Solid Organ Parenchyma (Non-Hepatic)

• Best phase for renal parenchyma, splenic parenchyma, pancreatic parenchyma
• Bowel wall normal enhancement (3-layer stratification)
• Normal lymph node size assessment

Cholangiocarcinoma

• Peripheral (rim) or heterogeneous enhancement; less than arterial phase liver
• Biliary dilatation proximal to mass
• Ductal wall thickening and enhancement

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PHASE 5: EQUILIBRIUM PHASE (LATE VENOUS PHASE)

• Contrast has redistributed from vascular space into extracellular fluid space (interstitium)
• Liver attenuation: decreasing (~90-110 HU)
• Blood vessels: less distinct; venous system partially opacified
• Contrast in extracellular space proportional to lesion water content and fibrous stroma

HCC Washout + Capsule Enhancement (LI-RADS)

• Washout: HCC remains hypodense on this phase relative to liver (strongly confirmed)
• Enhancing capsule: Peripheral rim of enhancement around HCC (fibrous pseudocapsule)
• APHE + Washout + Capsule = definite HCC (LR-5)

Haemangioma: Complete Fill-in

• Small haemangiomas: completely iso- or hyperattenuating (complete fill-in of vascular channels)
• Classic diagnostic sign: peripherally nodular arterial → progressive → complete fill-in on delayed
• Large haemangiomas: may not completely fill
• "Puddling" of contrast: Contrast pools in dilated vascular spaces; lesion becomes bright

Cholangiocarcinoma: Progressive Retention (Key Feature)

• Unlike HCC (washes out), cholangiocarcinoma shows progressive RETENTION of contrast
• Fibrous desmoplastic stroma retains contrast in equilibrium/delayed phase
• Central scar on CT: enhances progressively
• "Centripetal fill-in": Enhancement progresses from periphery inward over time

Fibrosis Detection

• Perilesional fibrosis, capsular retraction (cholangiocarcinoma, metastases with desmoplastic reaction)
• Liver capsular retraction toward lesion

Liver Cysts vs. Necrotic Metastases

• Simple cysts: ZERO enhancement in all phases (0-20 HU, no change)
• Necrotic metastases: rim enhancement persists; central non-enhancement
• Biloma: water density, no enhancement

Urinary System (Delayed/Excretory Phase)

• If delayed phase extended to 7-10 minutes: ureters and bladder fully opacified
• Useful for CT urography: renal papillae, ureters, TCC detection

Abscess

• "Double target sign": Inner ring (enhancing abscess wall) + outer ring (reactive hepatic parenchyma enhancement) surrounding central hypodense pus

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PHASE 6: HEPATOBILIARY PHASE (HBP) - MRI SPECIFIC

1. FNH vs. Adenoma differentiation: FNH = hyperintense (functioning hepatocytes); adenoma = hypointense
2. HCC detection in cirrhosis: All non-hepatocytic lesions are hypointense against bright liver background → highly sensitive for small HCC
3. Bile duct anatomy: Biliary excretion makes bile ducts visible (similar to MRCP)
4. Bile leak detection: Extravasation of contrast outside biliary tree
5. Assessment of biliary patency: Pre/post-operative biliary surgery

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SUMMARY COMPARISON TABLE: CECT PHASES

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CONTRAST INJECTION TECHNIQUE

• Allergy to iodinated contrast (prior contrast reaction - premedicate or use CO2)
• Renal impairment: eGFR <30 mL/min/1.73m² - risk of contrast-induced nephropathy (CIN)
• Metformin (hold 48 hours post-contrast if eGFR <60)
• Thyroid disease requiring radioiodine therapy (iodine load)
• Phaeochromocytoma: premedicate with alpha-blockade

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Q45. MENTION THE CAUSES OF ACUTE ABDOMEN IN ADULT. DESCRIBE ANY FIVE COMMON CONDITIONS WITH THEIR RADIOLOGICAL FINDINGS

PART A: CAUSES OF ACUTE ABDOMEN IN ADULTS

I. GASTROINTESTINAL

1. Acute appendicitis (most common surgical cause)
2. Acute cholecystitis / Biliary colic
3. Acute pancreatitis
4. Acute diverticulitis (most common at sigmoid colon)
5. Meckel's diverticulitis
6. Mesenteric lymphadenitis
7. Inflammatory bowel disease (Crohn's / UC) flare

II. VASCULAR

1. Ruptured abdominal aortic aneurysm (AAA)
2. Aortic dissection (extending to abdomen)
3. Ruptured splenic artery aneurysm
4. Mesenteric artery aneurysm rupture
5. Splenic infarction

III. UROLOGICAL

1. Ureteric colic (renal calculus)
2. Pyelonephritis / Renal abscess
3. Pyonephrosis
4. Renal infarction
5. Urinary retention (acute)

IV. GYNAECOLOGICAL (Females)

1. Ectopic pregnancy (ruptured)
2. Ovarian torsion
3. Ruptured ovarian cyst (functional / haemorrhagic)
4. Pelvic inflammatory disease (PID) / Tubo-ovarian abscess
5. Fibroid degeneration / torsion
6. Endometrioma rupture

V. MEDICAL (NON-SURGICAL)

1. Inferior myocardial infarction (referred pain)
2. Lower lobe pneumonia / pleuritis
3. Diabetic ketoacidosis (DKA)
4. Acute porphyria
5. Sickle cell crisis
6. Herpes zoster (thoracic - radicular pain)
7. Addisonian crisis
8. Henoch-Schonlein purpura (HSP)
9. Familial Mediterranean Fever (FMF)

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PART B: FIVE COMMON CONDITIONS WITH RADIOLOGICAL FINDINGS

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CONDITION 1: ACUTE APPENDICITIS

Plain X-Ray (AXR)

• Usually normal (60-70%)
• Appendicolith (faecolith): Calcified density in right iliac fossa (25-30%)
• Sentinel loop: Localised ileus of terminal ileum (localised dilated loop in RIF)
• Psoas shadow obliteration (periappendiceal inflammation)
• Scoliosis with concavity to right (pain posture)
• Soft tissue density mass (periappendiceal abscess)

Ultrasound (First-Line in Children, Thin Patients, Pregnant Women)

• Non-compressible tubular structure (worm-like) in RIF
• Diameter >6 mm (outer wall to outer wall) - normal appendix <6 mm
• Wall thickness >3 mm
• Hyperechoic mesoappendix (periappendiceal fat infiltration)
• Target sign on transverse section: concentric rings (inner hyperechoic mucosa + hypoechoic muscle layer)
• Appendicolith: hyperechoic focus with posterior acoustic shadow within appendix
• Absence of compressibility and peristalsis
• Increased vascularity on colour Doppler (inflamed wall hyperaemic)
• Free fluid in RIF (periappendiceal exudate)
• Abscess: complex fluid collection with thick wall (complication)

CT Scan (Investigation of Choice in Adults - Sensitivity 91-98%)

• Appendiceal diameter >6 mm (measured outer wall to outer wall)
• Appendiceal wall thickening (>2 mm) with wall enhancement
• Periappendiceal fat stranding: "Dirty fat" appearance around appendix (most sensitive sign)
• Appendicolith (hyperdense, 30-40%): within or at tip
• "Arrowhead sign": Thickened oedematous caecal wall with arrow pointing to appendiceal orifice
• Pericaecal free fluid (small amount)
• Non-filling of appendix with oral contrast
• Adjacent bowel wall thickening (regional inflammation)

• Perforation: Free gas (localized to RIF or free intraperitoneal); free fluid extending beyond periappendiceal region
• Abscess: Rim-enhancing fluid collection in RIF or pelvis; may contain gas
• Phlegmon: Ill-defined soft tissue mass without liquid centre; inflammatory mass (conservative management - IV antibiotics)
• Extraluminal appendicolith: faecolith outside appendix lumen (invariably = perforation)

• Score ≤3: Low risk - discharge
• Score 4-6: Intermediate - CT recommended
• Score ≥7: High risk - direct to theatre (CT if clinical doubt)

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CONDITION 2: ACUTE PEPTIC ULCER PERFORATION

Erect Chest X-Ray (CXR) - FIRST INVESTIGATION

• Pneumoperitoneum: Free gas under right hemidiaphragm (right subphrenic space)
  • Classical "crescent of gas" under right diaphragm
  • Bilateral subphrenic gas in large perforations
  • Sensitivity: 70-80% (not all perforations show free gas on CXR)
  • Gas must be present >1 mL to be detectable
• "Rigler's sign" (Double bowel wall sign): Both inner AND outer surfaces of bowel wall visible (gas on both sides) - seen on supine AXR with large pneumoperitoneum
• "Football sign": Large oval gas shadow outlining entire peritoneal cavity (more common in neonates/infants)
• "Ligamentum teres sign": Gas outlines falciform ligament as vertical linear opacity in right upper quadrant

CT Scan - MOST SENSITIVE (99%) - Investigation of Choice

• Free intraperitoneal gas: Air density collections in:
  • Right subphrenic space (most common)
  • Under anterior abdominal wall (on supine CT - anterior to liver)
  • Hepatogastric ligament
  • Perihepatic spaces
  • Pouch of Douglas (late, gravity-dependent)
• Site localisation:
  • Perigastric free gas + defect in gastric wall = gastric perforation
  • Periduodenal gas (right of duodenum) = duodenal perforation
  • Gas in lesser sac (between stomach and pancreas)
• Peritoneal fluid: Free fluid (initially sterile chemical peritonitis; later turbid)
• Fat stranding: Around site of perforation (omentum, mesentery)
• Gastric/Duodenal Wall Thickening: At perforation site
• Omental fat thickening: "Omental cake" pattern in late peritonitis
• Water-soluble oral contrast: Extravasation of contrast at perforation site (direct sign - if patient given oral contrast)

• Detects tiny pneumoperitoneum invisible on CXR (as little as 1 mL)
• Identifies site and cause of perforation
• Excludes alternative diagnoses
• Guides surgical approach

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CONDITION 3: ACUTE PANCREATITIS

Ultrasound (First-Line - Primarily for Aetiology)

• Gallstones: Hyperechoic foci with posterior acoustic shadow in gallbladder (identifies gallstone aetiology)
• CBD dilatation >8 mm (implies biliary obstruction - stone in CBD)
• Pancreatic changes (often limited by overlying bowel gas):
  • Pancreatic enlargement
  • Decreased (hypoechoic) echogenicity
  • Loss of lobular borders
  • Peripancreatic fluid
• Ascites
• Limitations: Bowel gas overlies pancreas in 25-40%; CT preferred for severity assessment

CT Scan (Investigation of Choice for Severity - Best at 48-72 Hours)

• Pancreatic enlargement (focal or diffuse)
• Heterogeneous density (areas of oedema, necrosis)
• Loss of lobular margin ("feathery" margins lost)
• Peripancreatic fat stranding (hallmark) - "dirty fat" in peripancreatic space
• Peripancreatic fluid collections (APFC - Acute Peripancreatic Fluid Collections)
• Thickening of Gerota's fascia
• "Halo" sign (fluid around pancreas)
• Retroperitoneal extension of fluid (along fascial planes)

• Non-enhancing pancreatic parenchyma after IV contrast (necrosis = no blood supply = no enhancement)
• Contrast-enhanced CT (CECT) at 48-72 hours: Normal pancreas enhances to >100 HU; necrotic areas remain <50 HU
• Extent of necrosis determines severity

• Pseudocyst (>4 weeks): Well-defined wall, homogeneous water density, no solid component
• Walled-off necrosis (WON): Heterogeneous content (liquid + solid necrotic debris) with defined wall
• Infected necrosis: Gas bubbles within necrotic collection (pathognomonic of infection)
• Pseudoaneurysm: Round enhancing vascular structure adjacent to pancreas (splenic artery most common)
• Splenic/portal vein thrombosis: Filling defect in splenic vein/portal vein
• Pleural effusion (left-sided, most common extraperitoneal complication)
• Colon necrosis: Most common bowel complication (splenic flexure)

• 0-3: Low severity; <3% mortality
• 4-6: Moderate severity; 6% mortality, 35% morbidity
• 7-10: Severe; 17% mortality, 92% morbidity

MRI / MRCP (Ductal Assessment)

• Better than CT for characterizing fluid collections (solid vs. liquid content)
• MRCP: Main pancreatic duct disruption, biliary pathology, CBD stone
• No radiation (preferred in young patients for follow-up)
• T2: Bright peripancreatic fluid; necrotic areas remain hypointense
• T1 fat-suppressed: Necrosis = loss of normal T1 bright pancreatic signal

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CONDITION 4: SIGMOID VOLVULUS

Plain X-Ray (AXR) - Often DIAGNOSTIC

• "Omega sign" / "Coffee bean sign": Massively distended sigmoid loop folded on itself, resembling coffee bean (two limbs of sigmoid separated by dense white line = "fusion line" of apposed walls)
• Ahaustral dilated large bowel loop (haustrations lost due to distension)
• Loop extends from pelvis to right upper quadrant (or left upper quadrant)
• "Northern exposure" sign: The apex of the distended sigmoid reaches above T10
• Loss of haustra in distended loop (vs. small bowel which has valvulae conniventes)
• Distal colon: collapsed (decompressed)
• "Inverted U" or "Bent inner tube": Appearance of closed sigmoid loop

• Two large air-fluid levels within the distended loop

Contrast Enema (Water-Soluble) - Diagnostic and Therapeutic

• "Bird beak sign" / "Ace of spades" sign: Smooth, gradual tapering of the contrast column at the site of volvulus (at the rectosigmoid junction)
• Contrast arrested at site of twist (rectosigmoid)
• "Whirl pattern": Twisted mucosal folds at point of torsion
• Contrast does NOT enter the distended loop (obstructed beyond twist)
• Can be both diagnostic AND therapeutic (hydrostatic reduction possible)

CT Scan - Investigation of Choice for Atypical Cases or Complications

• "Whirlpool sign": Twisted mesenteric vessels and bowel wrapping around a central axis (pathognomonic of volvulus)
• "Beak sign": Gradual tapering of the bowel to a point at the site of torsion
• "Bird beak": Smooth tapering of both limbs at the volvulus site
• Massively distended sigmoid loop (>6 cm; often >10-15 cm)
• Two limbs of the sigmoid converge to a point in the pelvis
• "Split left diaphragm sign": Gas on both sides of left hemidiaphragm when sigmoid extends into left chest
• Signs of ischaemia (strangulation):
  • Loss of bowel wall enhancement
  • Pneumatosis intestinalis (intramural gas)
  • Mesenteric fat stranding
  • Ascites
  • Portal venous gas (late, severe)

• AXR: Diagnostic in 70-80% (classic coffee bean sign)
• CT: More sensitive for atypical cases; identifies ischemia; distinguishes sigmoid from caecal volvulus

Management

• Flexible sigmoidoscopy / rigid proctoscopy: Endoscopic detorsion (first-line if no ischaemia)
• Emergency surgery: If ischaemia/perforation (sigmoid colectomy + Hartmann's procedure)
• Elective surgery after detorsion: To prevent recurrence (high recurrence rate ~50%)

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CONDITION 5: ACUTE MESENTERIC ISCHAEMIA

1. SMA embolism (50%): Cardiac emboli from AF, MI, valve disease; lodges at SMA just distal to middle colic artery origin
2. SMA thrombosis (15-25%): Atherosclerotic disease of SMA origin; acute-on-chronic
3. Non-occlusive mesenteric ischaemia (NOMI) (20-25%): Low flow states - shock, sepsis, heart failure, vasoconstrictors (vasopressors, digoxin, cocaine)
4. Mesenteric venous thrombosis (MVT) (5-10%): Hypercoagulable states, portal hypertension, pancreatitis, IBD

Plain X-Ray (AXR)

• Often NORMAL in early stages (significant disease can have normal AXR)
• Late/advanced findings:
  • "Thumb printing": Rounded soft tissue indentations into bowel lumen from submucosal haemorrhage/oedema
  • Dilated loops of small bowel (ileus pattern)
  • Pneumatosis intestinalis: intramural gas (linear/bubbly)
  • Portal venous gas: Branching linear lucencies in liver periphery (very late, grave sign)
  • Pneumoperitoneum: Perforation
  • Gasless abdomen (all loops fluid-filled in early ischaemia)

CT Angiography (CTA) - INVESTIGATION OF CHOICE (Sensitivity 93%; Specificity 100%)

• Filling defect (hypodense) within SMA lumen (usually distal to middle colic artery origin - "saddle embolus")
• Abrupt cut-off of SMA branch
• Calibre change: SMA normal calibre proximally; abrupt non-filling distally
• SMA: sharply defined intraluminal filling defect

• Filling defect at or near SMA origin (ostium/proximal SMA)
• Background atherosclerosis: calcified plaques throughout aorta and mesenteric vessels
• Gradual occlusion from calcified plaque
• Collateral vessels (arc of Riolan, marginal artery of Drummond) visible if chronic

• No occlusion of main SMA
• Diffuse, segmental SMA branch narrowing ("beading") with poor filling
• Low flow state: Small calibre mesenteric arteries
• Bowel findings predominate

• Filling defect within SMV (portal/mesenteric venous phase)
• SMV wall oedema (inflammatory rim enhancement around clot)
• "Target sign" of SMV: Central hypodense thrombus + peripheral enhancing wall
• Extension to portal vein (portal thrombosis)
• Ascites (more commonly than arterial ischaemia)
• Bowel wall oedema/thickening (venous congestion)

• Fat stranding (inflammatory/ischaemic response)
• Haziness and increased attenuation of mesenteric fat

• Moderate amount of mesenteric/peritoneal fluid
• Haemoperitoneum if infarction/perforation

• Perforation: Free gas + peritoneal fluid
• Peritonitis: Thickened peritoneum

MR Angiography

• Alternative to CTA (no iodinated contrast; good for renal failure patients)
• Gadolinium-enhanced MRA of mesenteric vessels
• DWI: Restricted diffusion in ischaemic bowel wall

DSA (Digital Subtraction Angiography) - Therapeutic

• Gold standard for direct vessel visualisation
• Therapeutic: Intra-arterial papaverine (vasodilator for NOMI); thrombolysis (SMA thrombus); thrombectomy/angioplasty
• Increasingly replaced by CT for diagnosis; reserved for intervention

Management Principles

• Early CT angiography → diagnosis
• SMA embolism: Embolectomy / thrombolysis / angioplasty
• SMA thrombosis: Surgical bypass or endovascular
• NOMI: Treat underlying cause; intra-arterial papaverine
• MVT: Anticoagulation (heparin → warfarin)
• Bowel infarction: Emergency laparotomy + bowel resection

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Q46. LIVER MRI SEQUENCES

Introduction

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STANDARD LIVER MRI PROTOCOL

Pre-contrast Sequences

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SEQUENCE 1: T1-WEIGHTED GRADIENT ECHO (T1 GRE) - IN-PHASE AND OUT-OF-PHASE (DUAL ECHO / CHEMICAL SHIFT IMAGING)

• Fat protons precess at slightly different frequency than water protons (3.5 ppm difference = 220 Hz at 1.5T)
• In-Phase (IP): TE chosen so fat and water signal ADD together (TE = 4.6 ms at 1.5T; TE = 2.3 ms at 3T)
• Out-of-Phase (OOP): TE chosen so fat and water signal CANCEL each other (TE = 2.3 ms at 1.5T; TE = 1.15 ms at 3T)
• Voxels containing BOTH fat and water → signal DROPS on OOP image (fat-water cancellation)

Hepatic Steatosis Detection

• Diffuse fatty liver: Liver parenchyma signal drops on OOP compared to IP (globally darker)
• Quantification: Signal intensity index = (IP - OOP) / (2 × IP) × 100 = Fat fraction (%)
• Fat fraction >5% = steatosis

Focal Fat-Containing Lesions

• Hepatocellular carcinoma (HCC): Contains intracellular lipid → signal drop on OOP (fat deposition common in well-differentiated HCC)
• Hepatic adenoma: Fat-rich subtypes (HNF1α mutation) → signal drop on OOP
• Focal fat deposition/sparing: Area of liver with abnormal fat content; signal change matches surrounding liver pattern; NO mass effect; vessels traverse normally

Iron Detection (Haemosiderosis / Haemochromatosis)

• Iron is paramagnetic → causes T2* signal loss
• On GRE sequences: Iron-loaded liver appears very dark (signal void)
• Comparison of IP and OOP: In haemochromatosis, BOTH sequences lose signal (unlike steatosis where only OOP drops)
• Signal loss worsens with increasing TE (T2* decay)
• MRI is more sensitive than CT for iron quantification

• Intermediate signal (brighter than spleen, similar to muscle)
• Hepatic veins: signal void (flow void)

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SEQUENCE 2: T2-WEIGHTED SEQUENCES

A. T2 Half-Fourier Single-Shot Turbo Spin Echo (HASTE / SSFSE)

• Very fast (single-shot; entire image in one breath-hold)
• Motionless image due to speed
• Good for:
  • Biliary anatomy
  • Simple cysts (very bright T2)
  • Ascites
  • Cystic vs. solid lesion differentiation
  • MRCP (heavily T2-weighted HASTE)
  • Screening sequence

B. T2 Turbo Spin Echo (TSE) / Fast Spin Echo (FSE) - with Fat Suppression

• Suppresses fat signal → fluid/oedema stand out more prominently
• Best sequence for: Focal lesion detection and characterization
• Allows differentiation of:
  • Haemangioma: remains very bright (T2 bright = fluid-like blood pool)
  • HCC: intermediate/mildly bright T2 (cellular tumour with less free water)
  • Metastases: moderately bright T2 (variable)
  • Cholangiocarcinoma: moderately bright T2 + surrounding oedema
  • FNH: Central scar is very T2 bright (stellate scar with myxoid stroma)
  • Simple cyst: very bright T2 (water = highest T2 signal)

• T2 signal > free water (CSF-like brightness): Simple cyst, biloma
• T2 signal similar to CSF: Haemangioma ("light bulb sign")
• T2 moderately bright: HCC, metastases, FNH, adenoma
• T2 hypointense: Fibrous lesion (cholangiocarcinoma stroma), calcified lesion, iron-laden

• Haemangioma: T2 very bright (signal intensity ratio to spleen/CSF used for diagnosis)
• HCC: Moderately T2 bright; septal enhancement pattern; mosaic architecture
• Metastases: T2 bright ("bull's eye" with central necrosis)
• FNH: T2 iso/slightly hyperintense; central scar T2 BRIGHT (pathognomonic)

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SEQUENCE 3: DIFFUSION-WEIGHTED IMAGING (DWI)

• Measures Brownian motion of water molecules (random molecular diffusion)
• In tissue with HIGH CELLULARITY (malignancy) or VISCOUS FLUID (abscess, necrosis): water molecules are RESTRICTED in their diffusion
• Restricted diffusion: Appears BRIGHT on high b-value DWI; DARK on ADC map
• Free diffusion (simple cyst, oedema): Bright on low b-value; dark on high b-value; BRIGHT on ADC map

• b=0: T2-weighted (no diffusion weighting)
• b=50-100: Vascular suppression
• b=500-800: Optimal lesion detection
• b=1000+: Highly restricted lesions (abscess, high-grade malignancy)

• Quantitative map derived from multiple b-values
• Low ADC = restricted diffusion = high cellularity/viscosity (malignant, abscess)
• High ADC = free diffusion (cysts, oedema, necrosis)

Focal Lesion Detection

• DWI is highly sensitive for lesion detection (especially for small lesions ≤1 cm)
• Malignant lesions: Bright on DWI (high b-value), dark on ADC
• Benign cysts: Bright on low b-value (T2 shine-through), dark on high b-value, BRIGHT ADC
• Haemangioma: Intermediate DWI signal; ADC relatively high (blood pool)

HCC

• ADC typically lower than benign lesions
• Well-differentiated HCC: ADC may overlap with benign lesions
• Poorly differentiated HCC: Low ADC (restricted)
• DWI identifies viable tumour within treated HCC (residual viable tumour = restricted diffusion)

Liver Metastases

• Typically restricted diffusion (bright DWI, low ADC)
• DWI superior to T2 for detecting small metastases
• Sensitivity for colorectal metastases: 87-97%

Liver Abscess

• Central abscess cavity: RESTRICTED diffusion (bright DWI, dark ADC) due to viscous pus
• Differentiates from necrotic tumour (necrotic tumour: central FREE diffusion = bright ADC)

Cholangiocarcinoma

• Restricted diffusion within tumour
• Periductal oedema: high ADC (free water)

Assessment of Treatment Response

• Viable tumour = restricted diffusion post-TACE/ablation
• Successfully treated tumour = reduced restriction (high ADC)

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SEQUENCE 4: DYNAMIC CONTRAST-ENHANCED (DCE) SEQUENCES

T1 GRE (VIBE/LAVA/THRIVE) - Volumetric Interpolated Breath-hold Examination

• 3D T1 GRE with fat suppression
• Very fast (~15-20 sec scan); isotropic voxels; whole liver in one breath-hold
• Acquired at multiple time points after IV gadolinium: arterial, portal venous, equilibrium (±hepatobiliary) phases

• Pre-contrast: Liver = intermediate T1; blood vessels = dark (flow void)
• Arterial phase: Hepatic arteries brighten; liver parenchyma partially enhances
• Portal venous phase: Portal vein bright; liver parenchyma maximally enhanced
• Equilibrium phase: Contrast in extracellular space; liver enhancement declining

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SEQUENCE 5: HEPATOBILIARY PHASE (HBP) - GADOXETATE (Primovist / Eovist)

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SEQUENCE 6: MR CHOLANGIOPANCREATOGRAPHY (MRCP)

• Heavily T2-weighted (very long TR, very long TE - TE >700 ms)
• Thick slab or thin multi-slice 3D acquisition
• Fat suppression (SPAIR/SPIR)
• Fluid appears bright; solid tissue dark → bile ducts/pancreatic duct appear as bright tubular structures

• Visualisation of biliary tree without invasive endoscopy
• Choledocholithiasis (CBD stones appear as filling defect = dark within bright bile)
• Biliary stricture (primary sclerosing cholangitis, cholangiocarcinoma)
• Pancreatic duct assessment (chronic pancreatitis, pancreatic ductal adenocarcinoma, IPMN)
• Post-operative bile duct complications
• Congenital biliary anomalies (biliary atresia, Caroli disease, choledochal cysts)

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SEQUENCE 7: MR ANGIOGRAPHY (MRA) - TIME OF FLIGHT AND CONTRAST-ENHANCED

• No contrast; blood appears bright (flow-related enhancement)
• Useful for portal vein and hepatic vein patency assessment
• Flow in vessels: bright; stationary tissue: suppressed

• 3D T1 GRE acquired in arterial and portal venous phases
• Hepatic artery anatomy mapping (pre-transplant/surgery)
• Identifies vascular variants (replaced hepatic arteries, portal vein anomalies)
• Portal vein thrombosis
• Budd-Chiari syndrome (hepatic vein patency)
• Hepatic arteriovenous shunts

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SEQUENCE 8: MR ELASTOGRAPHY (MRE) - Detailed

• External passive pneumatic driver (mechanical vibrator plate) applied to right upper abdomen (over liver)
• Frequency: 60 Hz shear waves propagate through liver
• Phase-contrast MR sequence (gradient echo or spin echo) detects wave propagation
• Data processed by wave inversion algorithm → stiffness map (elastogram) in kPa

1. Wave image: Shows propagation of shear waves (visual)
2. Elastogram (stiffness map): Colour-coded map; soft tissue = blue (low kPa); stiff tissue = red (high kPa)
3. Quantitative measurement: Average stiffness in ROI (kPa)

• F1 ≥2.5 kPa; F2 ≥2.88 kPa; F3 ≥3.54 kPa; F4 (cirrhosis) ≥4.67 kPa
• AUC for cirrhosis: 0.97 (best of all elastography methods)

• Samples entire liver (not just small ROI)
• Unaffected by obesity, ascites, operator skill
• Highly reproducible
• Can be integrated with standard liver MRI protocol (add-on ~5 minutes)

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ADDITIONAL SPECIALIZED SEQUENCES

T2* (GRE-T2-star) / Multi-Echo GRE

• Normal liver R2*: <40 Hz (T2* >25 ms)
• Mild iron overload: R2* 40-100 Hz
• Severe iron overload: R2* >100 Hz
• LIC (Liver Iron Concentration): Calculated from R2* using calibration formula
• Replace liver biopsy for iron quantification in haemochromatosis/thalassaemia

Proton Density Fat Fraction (PDFF) - mDIXON / IDEAL

• Corrects for T1 bias and T2* effects
• More accurate fat quantification
• Validated against biopsy (gold standard for hepatic steatosis)
• PDFF <5%: No steatosis; 5-17%: Mild; 17-22%: Moderate; >22%: Severe

Perfusion MRI (DCE-MRI - Quantitative)

• Tracks contrast kinetics through liver
• Derives hepatic arterial fraction (HAF), portal venous fraction, transit time
• Research application: Portal hypertension quantification, treatment response
• Hepatic arterial perfusion increases in cirrhosis/portal hypertension
• Not standard clinical practice yet

Susceptibility-Weighted Imaging (SWI)

• Sensitive to blood products, iron, calcium
• Detects haemorrhage within liver lesions
• Identifies "blood-sensitive" signal in HCC (haemosiderin deposits)
• Cavernous haemangioma with thrombosis: dark signal (haemosiderin)

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PRACTICAL LIVER MRI PROTOCOL (Summary)

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ARTEFACTS IN LIVER MRI

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COMPLETE EXAM ANSWERS - QUESTIONS 36-46 SUMMARY INDEX

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COMPLETE ANSWERS - LOCATION GUIDE

From Response 2 (Questions 36-43):

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From Response 3 (Questions 44-46):

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