PAPER III Q 1 (1x30) Role of radio imaging in management of renal transplantation- from normal to complications Q 2 (1x30) Pathophysiology, x rays, ultrasound and CT scan findings in Genito urinary tract TB Q 3 (2x10) 1 radio imaging in ectopic pregnancy 2 radio imaging of necrotising enterocolitis Q 4 (2x10) 1 cystic pancreatic tumours and radio imaging of any one 2 Radio imaging in hepatic cirrhosis ---- Radiology university exam full answer writing.

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PAPER III - RADIOLOGY UNIVERSITY EXAM - FULL ANSWERS

Q1 (30 Marks) - ROLE OF RADIO IMAGING IN MANAGEMENT OF RENAL TRANSPLANTATION: FROM NORMAL TO COMPLICATIONS

Introduction

Renal transplantation is the definitive treatment for end-stage renal disease. Imaging plays an indispensable role at every stage - from pre-transplant donor/recipient evaluation through the immediate postoperative period and long-term follow-up. A logical, modality-by-modality approach to imaging is required.

IMAGING MODALITIES USED

1. Ultrasound (US) - THE PRIMARY MODALITY

Ultrasound with colour and spectral Doppler is the first-line imaging tool for the renal transplant. It is radiation-free, bedside-accessible, and repeatable.

Normal US Appearances:

The transplant is placed in the iliac fossa (right more commonly), making it superficially located and ideal for ultrasound
Normal cortical echotexture: slightly echogenic cortex with well-defined medullary pyramids
Normal corticomedullary differentiation is preserved
Resistive Index (RI): Normal RI is 0.6-0.7 (< 0.8). The RI = (Peak Systolic Velocity - End Diastolic Velocity) / Peak Systolic Velocity
Colour Doppler shows symmetric perfusion throughout the kidney - cortex to medulla
The collecting system should be non-dilated
Ureteric anastomosis (ureteroneocystostomy) should be identified without peristaltic jets

Key serial measurements on US:

Renal length (should be stable; increase = oedema/rejection; decrease = chronic rejection/scarring)
Resistive index at arcuate/interlobar arteries
Perinephric collections - assessed for complexity, size, origin

2. Computed Tomography (CT)

CT is used when US is inconclusive, when bowel gas obscures detail, or when the patient becomes systemically unwell. Dedicated renal CT angiographic or urographic phases with multiplanar reconstruction are used. CT provides excellent visualization of vascular anatomy, urological, and extra-renal complications.

Disadvantages: Ionising radiation + nephrotoxic iodinated contrast - relevant in younger patients and in those with significant graft dysfunction.

3. Magnetic Resonance Imaging (MRI)

MRI is an excellent alternative when repeated radiation or iodinated contrast is undesirable. MR protocols include:

MR angiography (unenhanced or gadolinium-enhanced)
MR urography
MR renography

Caution: Gadolinium-based agents are contraindicated in patients with eGFR < 30 mL/min due to the risk of Nephrogenic Systemic Fibrosis (NSF).

4. Catheter-Based Angiography and Fluoroscopy

Conventional angiography is reserved as a prelude to intervention, or when US/CT/MRI cannot exclude or define an abnormality. Cystography is used to evaluate:

Bladder injury in the immediate post-surgical period
Vesico-ureteric reflux into the transplant (if recurrent pain or infection)

5. Radionuclide Scintigraphy (Isotope Studies)

Tc-99m MAG3 (Mercaptoacetyltriglycine) scintigraphy:

Provides quantitative assessment of graft perfusion and function
Useful for differentiating ATN from acute rejection by time-course analysis
ATN: delayed function but progressive improvement
Rejection: poor or deteriorating function
Many centres now favour renal biopsy over scintigraphy for definitive diagnosis

COMPLICATIONS: IMAGING APPEARANCES

A. EARLY COMPLICATIONS (0-1 week)

1. Acute Tubular Necrosis (ATN)

Commonest cause of early failure following cadaveric transplantation
Related to prolonged cold ischaemic time
US: Can be normal, or may show elevated RI; clinically significant ATN can occur with normal RI
Scintigraphy: Delayed excretion but preserved perfusion; serial studies help differentiate from rejection
Biopsy is the gold standard when ATN vs rejection distinction is required

2. Renal Artery / Vein Thrombosis

Occurs in 1%-5% of renal transplants, usually in the early postoperative period
Arterial thrombosis: US shows complete absence of intra-renal arterial flow; urgent surgical re-exploration is required
Venous thrombosis: US shows absence of renal vein Doppler flow, with reversal of diastolic flow in interlobar arteries (high-resistance pattern), and poor colour flow in the kidney
CT angiography confirms if US is inconclusive

3. Haematoma / Perinephric Collection

Common after transplant or biopsy
US: Hypoechoic/heterogeneous perinephric collection; complexity suggests infection
CT: Demonstrates exact extent of haematoma, active arterial bleeding on arterial phase (active extravasation)
If active arterial bleeding is confirmed on CT, formal angiography with embolisation is indicated

B. INTERMEDIATE/LATE COMPLICATIONS

4. Acute Rejection

Peaks at 1-3 weeks post-transplant
US findings (non-specific, may be normal):
- Oedematous graft with swelling of medullary pyramids
- Reduced cortical echotexture
- Loss of corticomedullary differentiation
- In severe cases: absent diastolic flow or flow reversal (RI approaching or exceeding 1.0)
- Doppler findings are not specific - overlap with ATN, renal vein thrombosis, drug toxicity
Biopsy remains the gold standard for diagnosis; empirical immunosuppression may be started with supporting clinical and sonographic findings

5. Renal Artery Stenosis (RAS)

Usually a late complication; stenosis typically at the anastomosis
Clinical: severe hypertension or renal dysfunction
US Doppler criteria: Renal artery velocity > 200 cm/s; gradient of 2:1 between stenotic and pre-stenotic segment; spectral broadening
Secondary finding: tardus parvus waveform downstream to stenosis (delayed, low-amplitude systolic upstroke)
CT/MR angiography confirms and plans intervention
Treatment: angioplasty + stenting (DSA guided)

6. Arteriovenous Malformations (AVM) and Pseudoaneurysms

Usually result of prior biopsy or nephrostomy
US: AVM shows area of mixed turbulent colour flow within renal parenchyma; characteristic high velocity, low-resistance Doppler waveform ("to-and-fro" for pseudoaneurysm)
Conventional angiography for definitive diagnosis and treatment (coil embolisation)

7. Chronic Rejection

Associated with intra-renal arterial segmental narrowing
US shows progressively rising RI, reduced renal cortical flow
CT/MR: Cortical thinning, reduced contrast enhancement, progressive renal atrophy

C. UROLOGICAL COMPLICATIONS

8. Hydronephrosis / Ureteric Obstruction

Causes: ureteric stricture, blood clot, lymphocoele extrinsic compression, technical stenosis at anastomosis
US: Dilatation of the collecting system - pelvicalyceal dilatation; jetting at VUJ may be absent
MRI: Balanced SSFP sequences show hydronephrosis clearly
Nephrostomy (US-guided) is used for urgent decompression
Antegrade pyelography delineates the site and level of obstruction

9. Urinoma

Collection of extravasated urine, usually near the ureter or bladder
US: Simple anechoic fluid collection near the collecting system
MAG3 scintigraphy: Shows radiotracer leak outside the collecting system
CT urography: Demonstrates urine leak site

10. Lymphocoele

Collection of lymph fluid in the perinephric space
US: Simple or septated anechoic perinephric collection; can compress ureter causing hydronephrosis
CT: Well-defined low-density fluid collection; no internal enhancement

D. TRANSPLANT BIOPSY COMPLICATIONS

US-guided biopsy is performed from the lower pole, taking cores from the cortex only
Post-biopsy complications include bleeding into the calyceal system, perinephric haematoma, or retroperitoneal haemorrhage
If significant bleeding occurs: Dynamic CT of the transplant is recommended to assess for active retroperitoneal haemorrhage (active extravasation on arterial phase)
Formal angiography with embolisation is advised for active arterial bleeding

E. NEOPLASTIC COMPLICATIONS

Transplant recipients on immunosuppression have increased risk of malignancy
US/CT: Focal hypovascular or hypervascular mass in the transplant parenchyma
Example: Papillary renal cell carcinoma - poorly enhancing focal mass; treated with radiofrequency ablation
Transitional cell carcinoma of ureter: CT shows obstructing soft-tissue mass causing hydronephrosis

F. ISOTOPE SCINTIGRAPHY - SPECIFIC PATTERNS

Diagnosis	Perfusion Phase	Function Phase
Normal	Good uptake	Prompt excretion
ATN	Reduced/delayed	Progressively improving
Rejection	Poor	Deteriorating over time
Obstruction	Variable	Accumulation, delayed drainage
Urinoma	Normal	Leak of tracer outside kidney

Summary: US (with Doppler) is the workhorse of transplant imaging. CT answers complex vascular and urological questions. MRI is preferred for repeated follow-up imaging when contrast/radiation must be minimised. Scintigraphy is valuable for functional assessment. Biopsy, guided by imaging, remains the gold standard for histological diagnosis of rejection.

Q2 (30 Marks) - PATHOPHYSIOLOGY, X-RAYS, ULTRASOUND AND CT SCAN FINDINGS IN GENITOURINARY TRACT TUBERCULOSIS

Introduction

Genitourinary tuberculosis (GU-TB) is the second most common form of extrapulmonary tuberculosis after lymphadenopathy, accounting for 1.1%-1.5% of all TB cases and 5%-6% of extrapulmonary TB. It is caused by Mycobacterium tuberculosis. Men are affected twice as often as women. The latent period from primary pulmonary infection to clinical GU-TB averages 22 years (range 1-46 years), reflecting haematogenous seeding during primary infection.

PATHOPHYSIOLOGY

Mechanism of Infection

Primary pulmonary TB occurs via inhalation of M. tuberculosis
During the bacteraemic phase of primary infection, haematogenous dissemination seeds the renal cortex bilaterally
The renal cortex is highly susceptible due to its high oxygen tension and rich blood supply
Organisms remain dormant for years to decades in cortical granulomas
Reactivation is triggered by immunosuppression, malnutrition, or advancing age
Reactivation occurs in one kidney only in 75% of cases (characteristically unilateral disease)

Anatomical Spread

Kidney: Most commonly affected (60%-100% of cases). Reactivation leads to caseous necrosis of the renal papillae (papillary necrosis), which extends into the collecting system
Ureter: Contiguous spread of bacilluria from the kidney; affects 19%-41% of cases; causes multiple strictures
Bladder: Ascending infection from ureters; 15%-20% of cases. Begins at the ureteric orifices and trigone
Prostate/Epididymis: Haematogenous dissemination (not contiguous spread); 20%-50% of men
In women: fallopian tube and endometrial involvement leads to infertility

Pathological Progression in the Kidney

Cortical granuloma formation (haematogenous seeding)
Caseous necrosis of papillae - earliest detectable lesion
Papillary necrosis and calyceal erosion (characteristic early radiological finding)
Cavitation of renal parenchyma - necrotic areas liquefy and drain into collecting system
Calyceal clubbing and infundibular stenosis - fibrosis causes narrowing of infundibula
Hydronephrosis / hydrocalyx - obstructed segments
Putty kidney / Autonephrectomy - entire kidney undergoes dystrophic calcification; end-stage GU-TB (seen in 23%-33%)

Bladder Pathology

Initial: oedematous, hyperaemic mucosa with visible yellow tubercles (red halo)
Progressive: fibrosis and contraction = "thimble bladder" (very small contracted bladder)
Late: calcification, fistula formation (vesicovaginal, enterovesical)

CLINICAL FEATURES (Brief)

Insidious onset: fever, weight loss, night sweats (systemic)
Urinary: frequency, dysuria, haematuria, flank pain
Classic finding: sterile pyuria (pyuria on urine microscopy with negative routine culture)
50% of patients have no localizing GU symptoms
Chest X-ray is abnormal in 67%-75% (usually inactive pulmonary disease)

IMAGING FINDINGS

A. PLAIN X-RAY (KUB - Kidney, Ureter, Bladder)

Plain X-ray is the simplest initial imaging tool for suspected GU-TB.

Renal Calcifications (most important X-ray finding):

Amorphous/granular calcification - within a cavitating lesion; irregular flecks
Lobar/segmental calcification - involving a segment of the kidney
"Putty kidney" (autonephrectomy) - diffuse dystrophic calcification of the entire non-functioning kidney; characteristic "eggshell" or irregular dense calcification outlining the kidney
Calcification is present in 50% of cases on CT; plain X-ray detects the grosser calcifications
Unilateral nature is characteristic

Ureteral Calcification:

Linear calcification along the course of the ureter ("pipe-stem ureter") - very specific for TB

Bladder:

Thimble bladder may be identified as a small contracted bladder outline
Bladder wall calcification (fine curvilinear)

Chest X-Ray:

Should always be obtained
Active or inactive pulmonary TB (Ghon complex, fibronodular apical disease, cavitation)
Abnormal in 67%-75% of cases

B. ULTRASOUND

Ultrasound is widely used but may underdiagnose early disease. It is best for:

Assessing renal size, parenchymal echogenicity, hydronephrosis
Detecting calcifications (with acoustic shadowing)
Evaluating the bladder wall

Renal US Findings:

Early disease: Normal or slightly increased cortical echogenicity; small hypoechoic foci within the parenchyma (granulomas/microabscesses)
Cavitary lesions: Focal areas of cavitation - hypo- to anechoic parenchymal lesions, may communicate with the collecting system
Calyceal dilatation / hydronephrosis: When infundibular stenosis develops; may be focal (affecting one calyx = hydrocalyx)
Renal calcifications: Highly echogenic foci with posterior acoustic shadowing; distributed throughout the parenchyma
End-stage (autonephrectomy): Complete replacement of renal architecture by a calcified mass; strong posterior shadowing obscuring the organ
Renal atrophy: Markedly small kidney with increased echogenicity and loss of corticomedullary differentiation

Ureteric US Findings:

Ureteric wall thickening (echogenic, thickened walls)
Proximal hydroureter due to strictures
Multiple strictures create a "beaded" appearance

Bladder US Findings:

Bladder wall thickening (diffuse or focal) - earliest finding
Reduced bladder capacity in contracted "thimble bladder"
Bladder wall echogenic calcifications
Post-void residual volume may be increased
Vesico-ureteric reflux may be detected on cystography

C. CT UROGRAM (Gold Standard)

CT urography with multiplanar reformations is now the preferred imaging modality for GU-TB, replacing the traditional IVP (intravenous pyelography).

CT Findings - Kidney:

Stage	CT Finding
Early	Hypoattenuating cortical granulomas/microabscesses; subtle papillary irregularities
Papillary necrosis	Erosions and "moth-eaten" appearance of renal calyces; papillary sloughing
Cavitation	Irregular thick-walled parenchymal cavities communicating with the collecting system; low-density central necrosis
Hydrocalyx	Dilated calyx due to infundibular stenosis; "phantom calyx" - calyx fills on retrograde but not on IVP
Calcification	Irregular flecks or amorphous calcification within cavities; dystrophic calcification in healed lesions
Autonephrectomy	Complete calcification of a non-functioning shrunken kidney ("putty kidney")
Cortical loss	Loss of functioning parenchyma; cortical thinning with non-enhancement

CT Findings - Ureter:

Ureteric wall thickening (circumferential mural thickening with enhancement)
Multiple strictures: "beaded ureter" - short segment strictures alternating with normal calibre
Hydroureter proximal to strictures
Strictures most common at the ureteropelvic junction (UPJ) and vesicoureteric junction (VUJ)
"Pipestem ureter" - diffuse calcification of ureteric wall (late finding)

CT Findings - Bladder:

Wall thickening (focal or diffuse)
Reduced bladder capacity
Bladder calcifications
"Thimble bladder" - severely contracted, small-capacity bladder
Fistulous tracks (late disease)

CT Findings - Epididymis/Prostate:

Enlarged, heterogeneous epididymis with low-attenuation necrotic areas
Prostate: heterogeneous with calcifications; can mimic prostate carcinoma
"Beaded" vas deferens on CT (thickened with calcifications)

Additional CT Features:

Retroperitoneal lymphadenopathy (may have central necrosis)
Contralateral kidney compensation (hypertrophy) when one kidney is destroyed
CT allows detection of silent contralateral upper tract disease

Diagnostic Summary:

Modality	Key Finding
Plain X-ray	Putty kidney; calyceal calcification; abnormal CXR
IVP (historical)	Calyceal irregularity; phantom calyx; grossly dilated collecting system
Ultrasound	Hydronephrosis; renal calcifications; bladder wall thickening; cavitary lesions
CT Urogram (gold standard)	Papillary necrosis; infundibular stenosis; ureteric strictures; renal cavity; calcification; thimble bladder

Q3 (20 Marks)

PART 1 - RADIO IMAGING IN ECTOPIC PREGNANCY (10 Marks)

Introduction

Ectopic pregnancy (EP) is defined as the implantation of a fertilised ovum outside the endometrial cavity. It occurs in approximately 2% of the general population and 2.1%-8.6% in the IVF population (up to 11% with underlying fallopian tube abnormality). It is a gynaecological emergency that can lead to haemoperitoneum and death from rupture.

Sites of Implantation

Fallopian tube (82%) - most common; the ampullary region is the most common specific site
Ovary: 5%
Interstitium (cornual): 2-4% - highest risk of catastrophic haemorrhage (presents later than tubal EP)
Caesarean scar: 1%
Cervix: rare
Intra-abdominal (heterotopic/primary): 1.4%
Bilateral ectopic pregnancies: very rare (1:750-1580)

ULTRASOUND - PRIMARY AND MOST IMPORTANT MODALITY

Transvaginal ultrasound (TVS) is the gold standard imaging investigation, supplemented by transabdominal ultrasound.

Ultrasound Features:

1. Absence of Intrauterine Gestational Sac (IUG)

No IUG when serum β-hCG ≥ 2000 mIU/mL is the discriminatory level
Below this level, a normal early IUG may not yet be visible

2. Extrauterine Mass

An adnexal mass separate from the ovary is the most sensitive (84%) and specific (98%) sign of EP
May appear as:
- Heterogeneous adnexal mass (most common)
- Tubal ring sign: hyperechoic ring of increased vascularity surrounding a small gestational sac
- Embryo with/without cardiac activity (highly diagnostic when seen)
- Note: no extrauterine mass is visible in 35% of cases

3. "Ring of Fire" Sign

On colour Doppler: intense circumferential vascularity around the ectopic sac
Highly specific (99.5%-100%) but low sensitivity (20%-65%)

4. "Tubal Ring" Sign

A hyperechoic ring in the adnexa separate from the ovary
Represents the trophoblastic reaction around the ectopic implantation

5. Haemoperitoneum

Echogenic free fluid in the pouch of Douglas or throughout the peritoneal cavity
Echogenicity (vs. simple fluid) indicates bleeding = 96% specificity for EP
Echogenic fluid + adnexal mass = strongly indicative of ruptured EP

6. Endometrial Changes

Decidual reaction: thickened, echogenic endometrium without a true gestational sac
"Pseudogestational sac" - central uterine fluid collection (accumulated blood/secretions) that can mimic an intrauterine sac; it is intracavitary, centrally located, has no double decidual sign
True IUG has: double decidual sign (two echogenic rings), eccentric implantation, yolk sac, embryo

Site-Specific US Findings:

Type	US Feature
Ampullary tubal EP	Adnexal mass + tubal ring sign separate from ovary
Interstitial EP	Eccentrically positioned sac within endometrium; ≤5 mm surrounding myometrium; "interstitial line sign"
Cervical EP	"Figure of 8" appearance to uterus (uterus + cervix both containing fluid)
Caesarean scar EP	Sac implanted in anterior lower uterine segment scar; thinning of overlying myometrium

CT SCAN

CT is not routinely used to diagnose EP in the acute setting (concerns about radiation, particularly to gonads). However, CT may detect:

Haemoperitoneum - complex free fluid in the peritoneal cavity
Adnexal mass (heterogeneous)
Intact or ruptured tube
CT is valuable when the clinical presentation is atypical or diagnosis is uncertain (e.g., abdominal EP)

MRI

MRI is rarely used for acute EP but has a role when:

Diagnostic uncertainty exists
Delayed EP presentation with normal or low β-hCG
Differentiating a resolving EP from other pelvic masses
Interstitial, cervical, or caesarean scar EP (complex anatomy)
MRI can precisely define the relationship of the EP to surrounding structures without radiation

MANAGEMENT ROLE OF IMAGING

Imaging Finding	Management Implication
IUG confirmed on TVS	Excludes EP (except in IVF - heterotopic possible)
Empty uterus + β-hCG ≥ 2000	Strongly suspicious for EP; serial β-hCG + repeat TVS
Adnexal ring + no IUG	Medical management (methotrexate) if criteria met
Haemoperitoneum + adnexal mass	Emergency surgical management (laparoscopy/laparotomy)
Interstitial EP	Specialised surgical approach (cornual resection); higher risk

PART 2 - RADIO IMAGING OF NECROTISING ENTEROCOLITIS (10 Marks)

Introduction

Necrotising enterocolitis (NEC) is the most common and devastating gastrointestinal emergency in neonates, predominantly affecting premature infants (< 32 weeks gestation) and low birth weight (< 1500 g) neonates. The ileocaecal region is most commonly affected. Mortality remains 15%-30%.

PATHOPHYSIOLOGY (Brief)

The aetiology is multifactorial. The key mechanism involves:

Bowel mucosal immaturity in preterm neonates (incomplete tight junctions, reduced mucus layer, immature immune defence)
Gut colonisation by pathogenic bacteria (altered microbiome)
TLR4 activation (Toll-Like Receptor 4) within gut mucosa in response to pathogenic bacteria - increases mucosal ischaemia
Ischaemia-reperfusion injury triggers cascade of inflammation, coagulation, and necrosis
Inflammatory mediators (TNF-α, IL-1β, platelet-activating factor) damage the bowel wall
Progression: mucosal inflammation → transmural necrosis → perforation → peritonitis

Risk factors: Prematurity, very low birth weight, hypoxia/ischaemia (birth asphyxia, congenital heart disease), formula feeding (breastmilk is protective), early-onset sepsis, polycythaemia

BELL'S STAGING (for clinical context in exam)

Stage	Features
I (Suspected)	Non-specific: abdominal distension, feeding intolerance, bloody stool
II (Confirmed)	Radiological NEC: pneumatosis intestinalis, portal venous gas
III (Advanced)	Perforation: pneumoperitoneum, cardiovascular deterioration

PLAIN ABDOMINAL X-RAY (FIRST-LINE INVESTIGATION)

Plain AP abdominal X-ray (supine) is the cornerstone of NEC diagnosis and monitoring. Serial films (every 6-8 hours in acute phase) are obtained.

X-ray Findings (in progressive order):

1. Dilated Bowel Loops (Earliest Sign)

Non-specific but may be the first abnormality
Multiple distended loops of bowel; may be asymmetric
Fixed, non-changing dilated loops ("frozen bowel") suggest full-thickness necrosis

2. Pneumatosis Intestinalis (PATHOGNOMONIC)

Gas within the bowel wall - most specific radiological sign of NEC
Appears as: linear/curvilinear gas streaks (subserosal) or bubbly/mottled lucencies (intramural) outlining the bowel wall
Both patterns may coexist
Predominantly affects the right lower quadrant and ascending colon (ileocaecal region)
Must be distinguished from intraluminal faecal gas and stool

3. Portal Venous Gas (Ominous Sign)

Gas in the portal venous system, tracking to the periphery of the liver
Appears as branching lucencies extending to the periphery of the liver shadow ("tree-branching" pattern)
Indicates severe transmural necrosis with gas entering the mesenteric veins
Associated with high mortality (40%-60%)

4. Pneumoperitoneum (Indicates Perforation)

Free intraperitoneal air = bowel perforation = surgical emergency
On supine AP film: look for:
- Rigler's sign: both sides of the bowel wall visible (gas on both sides = free air outside)
- Football sign: large central lucency over the abdomen (massive pneumoperitoneum)
- Falciform ligament sign: gas outlining the falciform ligament
Cross-table lateral view: Free air collects anteriorly above the liver; most sensitive for small amounts of pneumoperitoneum (better than supine AP for small perforations)
Left lateral decubitus view: Free air collects over the liver (right side up); alternative technique

5. Absent Bowel Gas Pattern

"Gasless abdomen" or markedly reduced bowel gas = fluid-filled abdomen (ascites, peritonitis)
Can indicate peritonitis with surgical NEC

6. Asymmetric Bowel Loop Distribution

Persistent, unchanging dilated loops suggest ischaemia/necrosis

ULTRASOUND

Ultrasound is increasingly recognised as a superior adjunct to plain radiography and can detect NEC earlier than plain X-ray. It is dynamic and allows real-time assessment.

US Findings:

1. Pneumatosis Intestinalis on US

Hyperechoic foci within the bowel wall with or without "dirty shadowing" (ring-down artifact)
More sensitive than X-ray for early/subtle pneumatosis

2. Portal Venous Gas on US

Hyperechoic mobile foci within portal vein and its intrahepatic branches
Highly echogenic dots/streaks moving within the portal venous system
More sensitive than plain X-ray for portal venous gas

3. Free Intraperitoneal Air

Bright echogenic reflectors usually seen anterior to the liver
Associated "dirty" posterior reverberation artifact

4. Echogenic / Complex Ascites

Echogenic peritoneal fluid = haemoperitoneum or infected fluid
Highly predictive of surgical NEC (need for laparotomy)
Simple ascites may be seen early; progressive echogenicity indicates worsening

5. Bowel Wall Thickening and Thinning

Normal neonatal bowel wall: approximately 1-2 mm
Thickening: > 2.6 mm (oedema, inflammation) = early NEC
Thinning: < 1 mm = transmural necrosis, imminent perforation

6. Bowel Wall Perfusion (Colour Doppler)

Increased wall perfusion = active inflammation (early NEC)
Absent wall perfusion = bowel wall ischaemia/necrosis = surgical emergency

7. Absent Peristalsis

Dynamic assessment of peristaltic activity
Absent or markedly reduced peristalsis = bowel ischaemia

8. Focal Fluid Collections / Abscess

Localised complex fluid collection = walled-off perforation or abscess

Prognostic Value of Ultrasound: Free air, absent peristalsis, echogenic ascites, absent bowel wall perfusion, and focal fluid collections on US have all been shown to predict the need for surgery and adverse outcomes including death.

MANAGEMENT ROLE OF IMAGING

Imaging Finding	Interpretation	Management
Dilated loops only	Stage I suspected NEC	Conservative (NBM, antibiotics)
Pneumatosis intestinalis	Stage II confirmed NEC	Continued conservative; serial X-rays
Portal venous gas	Advanced/severe NEC	Strong indicator for surgery
Pneumoperitoneum	Perforation = Stage III	Emergency surgery (laparotomy)
Echogenic ascites on US	Peritonitis	Surgery
Absent bowel perfusion on US	Transmural necrosis	Surgery

Q4 (20 Marks)

PART 1 - CYSTIC PANCREATIC TUMOURS AND RADIO IMAGING OF ONE (10 Marks)

Classification of Cystic Pancreatic Neoplasms

Cystic lesions of the pancreas may be neoplastic or non-neoplastic (pseudocysts). The key neoplastic entities are:

Type	Malignant Potential	Demographics	Key Feature
Serous Cystadenoma (SCA)	Very low (benign)	Older women (mean 60s)	Microcystic; honeycomb; central scar
Mucinous Cystic Neoplasm (MCN)	Moderate-High	Middle-aged women (40-50s)	Macrocystic; ovarian-type stroma; body/tail
Intraductal Papillary Mucinous Neoplasm (IPMN)	Variable (BD-IPMN low, MD-IPMN high)	Older adults; slight male predominance	Communicates with pancreatic duct
Solid Pseudopapillary Neoplasm (SPN)	Low (borderline)	Young women (mean 28)	Mixed solid/cystic; well-circumscribed
Cystic Pancreatic Neuroendocrine Tumour	Variable	Any age	Cystic NET; may have solid component

Brief Description of Each

1. Serous Cystadenoma (SCA)

Composed of innumerable small cysts (< 2 cm each) lined by glycogen-rich cuboidal epithelium
Benign; no malignant potential (serous cystadenocarcinoma is exceedingly rare)
No mucin production
Central stellate scar is characteristic

2. Mucinous Cystic Neoplasm (MCN)

Large, unilocular or oligolocular cysts lined by mucinous (tall columnar) epithelium
Has distinctive ovarian-type stroma (pathognomonic on histology)
Always in body and tail of pancreas
Does NOT communicate with the main pancreatic duct
Malignant transformation rate: 10%-15% (higher with mural nodules, solid components)
Resection is recommended in all surgically fit patients

3. Intraductal Papillary Mucinous Neoplasm (IPMN)

Arises from the epithelium of the pancreatic ductal system
Produces mucin, leading to ductal dilatation
Three types:
- Main duct IPMN (MD-IPMN): Dilatation of the main pancreatic duct > 5 mm; high malignancy risk (40%-60%); always resect if fit
- Branch duct IPMN (BD-IPMN): Grape-like cluster of cysts in communication with side branches; lower malignancy risk
- Mixed type: both components

4. Solid Pseudopapillary Neoplasm (SPN)

Rare, typically occurs in young women (mean age 28 years)
Mixed solid and cystic due to haemorrhagic necrosis (not true cysts)
Low-grade malignancy; most cured by resection

RADIO IMAGING OF IPMN (Intraductal Papillary Mucinous Neoplasm)

IPMN is chosen as the one to describe in detail given its clinical importance and rich imaging features.

Ultrasound:

Branch duct IPMN: cluster of cysts ("bunch of grapes") in the pancreatic parenchyma, particularly the uncinate process
Communication with the main duct may be seen on US (mucin plugs appearing as mobile echogenic foci)
Main duct IPMN: dilated main pancreatic duct (> 5 mm) with no obstructing mass
Cystic lesions may show mural nodules (echogenic projections)

CT Scan (with IV contrast):

Branch duct IPMN:
- Uni- or multilocular cystic mass, typically in the pancreatic head/uncinate
- Communication with the main pancreatic duct (key finding) - shown on CT as a channel connecting the cyst to the duct
- Non-enhancing cyst walls (unless malignant transformation); mural nodules enhance
- Cyst size: typically < 3 cm in benign lesions
Main duct IPMN:
- Diffuse or segmental dilatation of the main pancreatic duct (> 5 mm, often > 10 mm in high-grade)
- No obstructing calculus or mass to explain dilatation
- Mucin plugs within the dilated duct
- Solid components within the duct = malignant transformation

High-Risk CT Features (Require Resection):

High-risk stigmata: Enhancing solid component; main pancreatic duct ≥ 10 mm
Worrisome features: Cyst ≥ 3 cm; thickened enhancing cyst walls; non-enhancing mural nodules; MPD 5-9 mm; abrupt change in MPD calibre with distal pancreatic atrophy; lymphadenopathy

MRI/MRCP (Best Modality for IPMN):

MRCP provides exquisite detail of the ductal system without radiation or contrast
Demonstrates communication between the cyst and the main pancreatic duct - pathognomonic of IPMN (distinguishes from MCN which does NOT communicate)
Shows duct dilatation, mural nodules, mucin plugs
T2-weighted: cysts are bright (fluid signal); mural nodules are intermediate signal
T1: mucin can appear hyperintense on T1 due to proteinaceous content

EUS (Endoscopic Ultrasound):

Superior resolution for mural nodules (distinguishes enhancing nodule from mucin clot)
FNA allows cyst fluid analysis: CEA > 192 ng/mL = mucinous cyst; amylase = communication with duct (IPMN/pseudocyst)
Definitive diagnosis of malignant transformation

Surveillance Protocol:

BD-IPMN < 3 cm without worrisome features: MRI surveillance
Interval based on cyst size (6 months to 2 years)
Surgical resection for MD-IPMN, and BD-IPMN with worrisome features or high-risk stigmata

PART 2 - RADIO IMAGING IN HEPATIC CIRRHOSIS (10 Marks)

Introduction

Hepatic cirrhosis is the final common pathway of chronic liver injury, characterised by:

Diffuse hepatic fibrosis
Destruction of normal hepatic lobular architecture
Formation of regenerative nodules

Common causes: viral hepatitis B/C, alcoholic liver disease, NAFLD, biliary cirrhosis, Wilson's disease, haemochromatosis.

ULTRASOUND (First-Line Investigation)

Ultrasound is the initial screening modality. It is cheap, accessible, radiation-free, and highly informative.

A. Liver Morphology:

Surface: Nodular/irregular liver surface - the hallmark finding of cirrhosis; fine nodularity corresponds to the regenerative nodular architecture
Echogenicity: Increased heterogeneous echogenicity of the parenchyma (coarse, heterogeneous echotexture from fibrosis and nodules); "unsmooth liver capsule" with heterogeneously distributed echoes
Volume changes:
- Caudate lobe enlargement (caudate lobe to right lobe ratio > 0.65 is specific for cirrhosis)
- Right lobe atrophy
- Left lobe enlargement (variable)
- Overall liver volume may be reduced in advanced cirrhosis

B. Portal Hypertension Signs on US:

Portal vein diameter > 13 mm (portal hypertension)
Reduced portal venous velocity (normal > 15 cm/s; reduced in portal hypertension)
Reversal of portal venous flow (hepatofugal flow) - portosystemic shunting
Splenomegaly: Longitudinal splenic dimension > 13 cm; a classic sign
Ascites: Free fluid in Morrison's pouch, left subphrenic space, pelvis; may be massive

C. Collateral Vessels (Colour Doppler):

Splenorenal shunt (most common, 21%)
Patent paraumbilical vein/ligament teres - enlarged, recanalized umbilical vein (14%); "Cruveilhier-Baumgarten" murmur clinically
Gastrooesophageal varices (not well seen on US but suggested by periportal varices)
Retroperitoneal collaterals

D. Complications on US:

Hepatocellular carcinoma (HCC): Most important complication; 6-monthly surveillance US is standard practice
- Early HCC: small hypoechoic or mixed echogenicity nodule
- Arterial phase enhancement ("fast-in fast-out") on contrast-enhanced US (CEUS)
Gamna-Gandy bodies: Small echogenic foci within the spleen (haemosiderin deposits from old haemorrhage in hypertensive spleen)

CT SCAN

CT (preferably multiphasic - unenhanced, arterial, portal venous, delayed phases) provides comprehensive morphological and vascular information.

A. Liver Morphology:

Nodular surface: Well demonstrated on CT; surface irregularity due to regenerative nodules
Heterogeneous parenchyma: Irregular attenuation due to fibrosis, fatty change, and nodules
Caudate lobe hypertrophy relative to right lobe (caudate to right lobe ratio > 0.65)
Segmental atrophy/hypertrophy: Atrophy of segments VI/VII (right posterior lobe); hypertrophy of segment IV and caudate

B. Vascular Changes:

Portal vein dilatation (> 13 mm) with reduced flow on Doppler correlation
Hepatic artery enlargement and tortuosity (compensatory arterialisation as portal flow decreases)
Portosystemic shunts: Oesophageal/gastric varices (perioesopha geal enhancing vessels on CT), splenorenal shunts, paraumbilical vein, retroperitoneal shunts
Reversed portal flow / cavernous transformation (after portal vein thrombosis)
Portal vein thrombosis: low-attenuation filling defect within portal vein

C. Features of Portal Hypertension:

Splenomegaly (> 12 cm longitudinal)
Ascites (low-density fluid in peritoneal cavity)
Oesophageal and gastric varices (serpiginous enhancing structures adjacent to oesophagus and along lesser and greater curvature of the stomach)
Retroperitoneal and mesenteric varices

D. Regenerative and Dysplastic Nodules:

Regenerative nodules: Tiny (< 1 cm), may be slightly hyperdense on unenhanced CT (siderotic); isoattenuating on contrast-enhanced CT
Dysplastic nodules (low grade): Slightly hyperattenuating on portal venous phase; no arterial enhancement
Dysplastic nodules (high grade): Begin to show mild arterial enhancement; difficult to distinguish from small HCC
Key distinction from HCC: regenerative/dysplastic nodules lack the "arterial wash-in and portal venous wash-out" pattern of HCC

E. HCC on CT (LI-RADS Criteria):

LI-RADS 5 (definitely HCC): Major features:
- Arterial phase hyperenhancement (APHE)
- Washout appearance on portal/delayed phase
- Enhancing capsule
- Threshold growth (> 50% diameter increase in < 6 months)
Satellite nodules, vascular invasion (portal vein tumour thrombus - PVTT), lymphadenopathy, distant metastases in advanced disease

MRI

MRI is the most sensitive modality for detecting and characterising liver nodules in cirrhosis, particularly using hepatocyte-specific contrast agents (Gadoxetic acid - Primovist).

MRI Findings:

Liver surface irregularity and heterogeneity better appreciated on T2-weighted imaging
Fibrosis: high signal on T2 (linear areas of T2 hyperintensity)
Siderotic nodules (siderotic regenerative nodules): Low signal on T2*/GRE sequences due to iron content - specific for cirrhosis
Dysplastic nodules: Low T2 signal (iron-containing); intermediate T1 signal
HCC: typically T2 hyperintense, T1 variable; arterial enhancement with portal washout; restricted diffusion on DWI

NUCLEAR MEDICINE

Tc-99m Sulfur Colloid Scan:

Reticuloendothelial cells (Kupffer cells) in the liver and spleen take up the tracer
In cirrhosis: "Colloid shift" - reduced hepatic uptake with markedly increased splenic and bone marrow uptake
Confirms functional hepatic impairment and portal hypertension

ELASTOGRAPHY (Emerging Technique)

Transient elastography (FibroScan) / MR elastography: Measures hepatic stiffness as a surrogate for fibrosis
Non-invasive staging of fibrosis; stiffness > 14-17 kPa suggests cirrhosis
Increasingly used to avoid liver biopsy in straightforward cases

Summary Table - Cirrhosis Imaging

Feature	US	CT	MRI
Nodular surface	++	+++	+++
Caudate hypertrophy	++	+++	+++
Portal vein dilation	+++	+++	+++
Varices	+	+++	+++
Ascites	+++	+++	++
Splenomegaly	+++	+++	++
Regenerative nodules	+	++	+++
HCC detection	+ (with CEUS)	++	+++
Fibrosis	-	-	+++ (elastography)

Sources: Grainger & Allison's Diagnostic Radiology; Brenner & Rector's The Kidney; Campbell-Walsh-Wein Urology; Bailey & Love's Surgery; Schwartz's Principles of Surgery; AJR Radiology (CT and MRI of Cirrhosis); Medscape Cirrhosis Imaging.

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