Hepatobiliary & Pancreatic Radiology
Radiology · GIT · lean revision notes
Hepatobiliary & Pancreatic Radiology
A high-yield walk-through of liver, biliary tree and pancreatic imaging for NEET PG — pattern recognition on ultrasound (USG), CT and MRI, with the classic "buzzword" signs examiners love. Master the imaging characteristic → diagnosis links and the named scoring systems.
Imaging modalities — when to use what
Choosing the correct first investigation is itself a favourite single-best-answer.
| Modality | Best for | Limitation |
|---|---|---|
| USG | First-line screening for liver/gallbladder, gallstones, ductal dilatation, ascites, cysts | Operator-dependent, poor for pancreas (bowel gas), poor in obese |
| Triple/Quadruple-phase CT | Characterising focal liver lesions (HCC), pancreatic carcinoma, trauma | Radiation, iodinated contrast (nephrotoxic) |
| MRI / MRCP | Biliary tree mapping, characterising indeterminate lesions, FNH, haemangioma | Cost, availability, claustrophobia |
| ERCP | Therapeutic (stone removal, stenting) + tissue/brush cytology | Invasive — pancreatitis risk |
| HIDA scan | Acute cholecystitis (non-visualised GB), bile leak, biliary atresia | Functional only, no anatomy |
High-yield: USG is the investigation of choice (IOC) for gallstones (>95% sensitivity). MRCP is the non-invasive IOC for biliary tree / CBD stones. Triple-phase CT is the IOC for characterising a liver mass and for HCC.
The liver CT phases — and the windows in which lesions become conspicuous — recur constantly:
- Arterial phase (~20–35 s): HCC enhances brightly (it is hepatic-artery fed).
- Portal venous phase (~60–70 s): metastases best seen (hypodense against bright parenchyma); HCC washes out.
- Delayed/equilibrium phase (3–10 min): cholangiocarcinoma and haemangioma show progressive/delayed fill-in; HCC capsule enhances.
Hepatocellular carcinoma (HCC)
Background
The commonest primary malignant liver tumour. Arises on a background of cirrhosis (alcohol, chronic HBV/HCV, NASH, haemochromatosis, aflatoxin). HBV can cause HCC even without cirrhosis. Spreads characteristically by vascular invasion — portal and hepatic veins.
Imaging hallmarks
The pathognomonic CT/MRI behaviour is arterial hyperenhancement with portal-venous/delayed washout plus a delayed-enhancing capsule ("LI-RADS" major features).
- Mosaic pattern — internal nodules/septa of varying attenuation/signal, reflecting fibrosis, fat, necrosis and haemorrhage.
- Capsule — peripheral rim showing delayed enhancement.
- Tumour thrombus — enhancing soft tissue within the portal vein (distinguishes from bland thrombus).
- Nodule-in-nodule appearance during malignant transformation of a dysplastic nodule.
High-yield: HCC = arterial enhancement + venous washout + capsule + mosaic pattern, on a cirrhotic liver, with portal vein tumour thrombus. Tumour marker = alpha-fetoprotein (AFP); >400 ng/mL is highly suggestive.
Diagnostic flow: Cirrhotic liver + new nodule → triple-phase CT/MRI → arterial enhancement + washout (LI-RADS 5) → diagnosis can be made without biopsy (avoid biopsy to prevent seeding). → AFP supports. → Staging with Barcelona Clinic Liver Cancer (BCLC) system.
| Lesion | Arterial | Portal/Delayed | Clue |
|---|---|---|---|
| HCC | Hyper (bright) | Washout + capsule | Cirrhosis, AFP, vascular invasion |
| Haemangioma | Peripheral nodular discontinuous enhancement | Progressive centripetal fill-in | Follows blood pool; T2 "light-bulb" bright |
| FNH | Homogeneous bright | Iso to liver | Central scar (T2 bright, delayed enhancement) |
| Metastasis | Variable, often rim | Hypodense in portal phase | Multiple, known primary |
| Cholangiocarcinoma | Hypo, peripheral rim | Progressive delayed enhancement | Capsular retraction, biliary dilatation |
High-yield: Hepatic haemangioma = commonest benign liver tumour; peripheral nodular enhancement → centripetal fill-in; "light-bulb sign" (very bright) on T2 MRI. FNH = central stellate scar that enhances on delayed images; contains Kupffer cells → takes up sulphur colloid / hepatobiliary contrast.
Hydatid cyst (Echinococcal disease)
Caused by Echinococcus granulosus (dog tapeworm); liver is the commonest site (right lobe). A classic image-based question.
Imaging signs
- Daughter cysts within a mother cyst — the "cyst-within-a-cyst" appearance; gives a rosette / honeycomb / wheel-spoke pattern.
- Water-lily sign (sign of Camalotte) — undulating, detached endocyst membrane floating within the cyst fluid (seen when the membrane delaminates).
- Eggshell / curvilinear mural calcification — indicates an old, often dead cyst.
- "Snowstorm" / hydatid sand on USG — shifting echogenic debris of scolices.
- Serpent / whirl sign — collapsed membranes.
High-yield: Hydatid cyst buzzwords — daughter cysts, water-lily sign (detached membrane), eggshell calcification, snowstorm/hydatid sand. Gharbi/WHO classification stages activity (CE1–CE5). Serology: Casoni test (historical), indirect haemagglutination / ELISA. Eosinophilia present.
Management: Albendazole cover + PAIR (Puncture, Aspiration, Injection of scolicidal, Re-aspiration) for selected cysts, or surgery. Avoid free spillage → anaphylaxis and dissemination.
Liver abscess
Pyogenic vs Amoebic
| Feature | Amoebic | Pyogenic |
|---|---|---|
| Organism | Entamoeba histolytica | E. coli, Klebsiella, anaerobes; polymicrobial |
| Number/site | Usually single, right lobe, posterosuperior | Often multiple |
| Aspirate | "Anchovy sauce" (reddish-brown) sterile pus | Frank pus, organisms cultured |
| Wall | Thin, less defined | Thick, well-defined enhancing rim |
| Serology | Amoebic serology positive | Blood culture / biliary source |
On USG: a hypoechoic to complex collection with low-level internal echoes, near the diaphragm. CT shows a hypodense lesion with peripheral rim enhancement and surrounding oedema; the "double target / cluster sign" (coalescing micro-abscesses) suggests pyogenic abscess.
High-yield: Amoebic liver abscess = single, right lobe, anchovy-sauce pus; drug of choice metronidazole followed by a luminal amoebicide (diloxanide furoate / paromomycin). Aspiration if >5–6 cm, left lobe, or no response in 48–72 h.
Focal fatty change & focal fatty sparing
A frequent mimic that causes diagnostic confusion.
- Focal fatty infiltration: geographic, non-spherical low attenuation; typically adjacent to the falciform ligament / porta hepatis; no mass effect — vessels course normally through it (no displacement).
- Focal fatty sparing: an island of normal liver appearing as a "lesion" in an otherwise fatty (bright on USG) liver, classically anterior to the portal vein / adjacent to the gallbladder fossa.
High-yield: Key discriminator of focal fat from a tumour — NO mass effect, vessels pass through undisturbed, characteristic location, and signal loss on out-of-phase (chemical-shift) MRI. On USG, fatty liver is bright/echogenic ("bright liver").
Hint: On dual-echo MRI, fat-containing tissue drops signal on opposed-phase images compared to in-phase — diagnostic of microscopic fat.
Pancreatic ductal adenocarcinoma (PDAC)
Background
Most pancreatic cancers; ~60–70% in the head. Highly lethal; risk factors — smoking, chronic pancreatitis, hereditary syndromes. Tumour marker CA 19-9.
Imaging
- A hypoenhancing (hypovascular) mass — appears hypodense relative to enhancing pancreas on the pancreatic parenchymal phase of CT.
- Double-duct sign — simultaneous dilatation of the common bile duct (CBD) and pancreatic duct (of Wirsung) due to a head mass obstructing both. Highly suggestive of periampullary/pancreatic head malignancy.
- Distal pancreatic atrophy + upstream main pancreatic duct dilatation.
- Vascular encasement of coeliac axis / SMA (>180° = unresectable) and SMV/portal vein — determines resectability.
High-yield: Double-duct sign = dilated CBD and pancreatic duct → think carcinoma head of pancreas / periampullary carcinoma (also chronic pancreatitis). Pancreatic CA on CT is a hypovascular/hypoenhancing mass — opposite of HCC. IOC for staging/resectability = multiphase pancreatic-protocol CT; EUS-FNA for tissue.
Resectability flow: Suspected PDAC → pancreatic-protocol CT → assess arterial (coeliac, SMA, hepatic) and venous (SMV/portal) contact + metastases → resectable / borderline / locally advanced / metastatic → resectable head tumour → Whipple (pancreaticoduodenectomy).
High-yield: Painless obstructive jaundice + palpable, non-tender, distended gallbladder = Courvoisier's sign / law → suspect periampullary or pancreatic head malignancy (not a stone, which causes a fibrotic non-distensible GB).
Acute pancreatitis & CT Severity Index
Imaging
USG is limited (gas); contrast-enhanced CT (CECT) at 72 hours to 5–7 days best assesses necrosis (too early underestimates it). Findings: pancreatic enlargement, peripancreatic fat stranding, fluid collections, non-enhancing (necrotic) parenchyma.
CT Severity Index (CTSI) — Balthazar score
Two components are added (max 10):
Balthazar grade (peripancreatic inflammation):
| Grade | Finding | Points |
|---|---|---|
| A | Normal pancreas | 0 |
| B | Focal/diffuse enlargement | 1 |
| C | Pancreatic + peripancreatic inflammation | 2 |
| D | Single fluid collection | 3 |
| E | ≥2 collections and/or gas | 4 |
Necrosis: none = 0; ≤30% = 2; 30–50% = 4; >50% = 6.
High-yield: CTSI = Balthazar grade points + necrosis points (max 10). 0–3 mild, 4–6 moderate, 7–10 severe. Best timing of CECT for necrosis = after 72 h. The Revised Atlanta Classification (2012) defines collections: early (<4 wk) = **acute peri-pancreatic fluid collection** (interstitial) / **acute necrotic collection** (necrotising); late (>4 wk) = pseudocyst (interstitial) / walled-off necrosis (WON) (necrotising).
Complications to recognise on imaging: pseudocyst (mature wall, no epithelium), walled-off necrosis, pseudoaneurysm (classically splenic artery), splenic/portal vein thrombosis, infected necrosis (gas within collection).
Biliary calculi & obstruction
- Gallstones on USG: echogenic focus with posterior acoustic shadowing, mobile with position.
- Acute cholecystitis: distended GB, wall thickening >3 mm, pericholecystic fluid, sonographic Murphy's sign (max tenderness over GB under probe). IOC for confirmation when USG equivocal = HIDA scan (non-visualisation of GB at 1 h = obstructed cystic duct).
- WES (wall-echo-shadow) triad / "double-arc" sign — contracted GB packed with stones.
- CBD stones (choledocholithiasis): CBD dilatation (normal up to ~6 mm, +1 mm/decade after 60; up to ~10 mm post-cholecystectomy). MRCP is non-invasive IOC; ERCP is therapeutic.
- Mirizzi syndrome: stone impacted in cystic duct/Hartmann's pouch → extrinsic compression of the common hepatic duct → obstructive jaundice.
High-yield: Gallstone = echogenic + posterior acoustic shadow + mobile. Acute cholecystitis = GB wall >3 mm + sonographic Murphy's sign + pericholecystic fluid, confirmed by non-visualising HIDA. Porcelain gallbladder (mural calcification) → increased gallbladder carcinoma risk → cholecystectomy.
Level of obstruction logic: Dilated intrahepatic ducts only → high (hilar/Klatskin). Dilated intra- + extrahepatic ducts with normal-calibre pancreatic duct → CBD stone/distal CBD. Both ducts dilated (double-duct) → ampullary/pancreatic head lesion.
Key differentials & quick discriminators
- Cystic liver lesion: simple cyst (anechoic, no septa) vs hydatid (daughter cysts/membrane) vs abscess (debris, rim enhancement, clinical sepsis) vs biliary cystadenoma (septations, mural nodules).
- Arterially enhancing nodule in cirrhosis: HCC vs regenerative/dysplastic nodule (no washout) vs transient hepatic attenuation difference.
- Hypodense pancreatic mass: PDAC (ill-defined, vascular encasement) vs focal chronic pancreatitis (calcifications, ductal beading) vs neuroendocrine tumour (hyper-enhancing, opposite pattern) vs autoimmune pancreatitis ("sausage pancreas", capsule-like rim).
Mnemonic for hypervascular (arterial-enhancing) liver metastases — "CHARMS": Carcinoid/Choriocarcinoma, Hepatoma (HCC), Adenoma, Renal cell, Melanoma/Thyroid (Medullary), Sarcoma/islet cell. (Most other mets, e.g. colon, are hypovascular.)
Recently asked / exam angle
- Image-based: Identify hydatid (daughter cysts / water-lily), HCC (arterial enhancement + washout), gallstone with acoustic shadow — these appear directly as labelled USG/CT images.
- Double-duct sign → carcinoma head of pancreas / periampullary carcinoma (single most repeated pancreatic radiology fact).
- CT Severity Index = Balthazar + necrosis; severe = 7–10; best CECT timing >72 h.
- IOC questions: gallstone → USG; biliary tree/CBD stone → MRCP; HCC characterisation → triple-phase CT; acute cholecystitis when USG equivocal → HIDA.
- Haemangioma peripheral nodular discontinuous enhancement with centripetal fill-in & T2 light-bulb sign; FNH central scar.
- Courvoisier's law with painless obstructive jaundice.
- Revised Atlanta 2012 terminology: pseudocyst vs walled-off necrosis (4-week cut-off).
- Porcelain gallbladder and gallbladder carcinoma association.
Rapid revision
- USG = IOC for gallstones; MRCP = non-invasive IOC for biliary tree/CBD; triple-phase CT = IOC for HCC/liver mass.
- HCC: arterial hyperenhancement → portal-venous washout + delayed-enhancing capsule + mosaic pattern; portal vein tumour thrombus; marker AFP.
- Haemangioma: peripheral nodular discontinuous enhancement, centripetal fill-in, T2 light-bulb sign — commonest benign liver tumour.
- FNH: central stellate scar, delayed scar enhancement, contains Kupffer cells.
- Hydatid: daughter cysts, water-lily (detached membrane), eggshell calcification, snowstorm/hydatid sand; treat with albendazole + PAIR/surgery.
- Amoebic abscess: single, right lobe, anchovy-sauce pus; DOC metronidazole + luminal amoebicide.
- Focal fatty change: no mass effect, vessels traverse, signal drop on opposed-phase MRI.
- Double-duct sign (dilated CBD + pancreatic duct) → carcinoma head of pancreas / periampullary.
- PDAC is hypovascular/hypoenhancing; resectability by SMA/coeliac >180° encasement; surgery = Whipple; marker CA 19-9.
- CTSI = Balthazar grade + necrosis (max 10); 7–10 = severe; image necrosis after 72 h; Revised Atlanta 2012 classification.
- Gallstone USG: echogenic + posterior acoustic shadow + mobile; acute cholecystitis = wall >3 mm + sonographic Murphy + non-visualising HIDA.
- Courvoisier's law: painless jaundice + palpable non-tender GB = periampullary/pancreatic head malignancy; porcelain gallbladder → carcinoma risk.