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Emergency & Trauma

Hyperdense MCA sign (acute stroke)

Increased attenuation of the M1 (or M2) middle cerebral artery on non-contrast CT representing acute intraluminal thrombus; one of the earliest CT signs of ischemic stroke, visible within ~90 minutes of onset.

Entity: Acute middle cerebral artery occlusion

Imaging: Focal hyperdensity of the MCA on NCCT; objective criteria include absolute attenuation >43 HU and an MCA density ratio >1.2 versus the contralateral vessel. Specificity is high but sensitivity is moderate. Beware the pitfall of bilateral dense MCAs from high hematocrit/atherosclerotic calcification (pseudo-hyperdense), which is not stroke.

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How to call an indolent enchondroma versus a chondrosarcoma that needs surgery.

  • Deep endosteal scalloping >2/3 of cortical thickness is the most useful discriminator and strongly favors chondrosarcoma; shallow, smooth scalloping favors enchondroma.
  • Cortical breach/destruction with an associated soft-tissue mass strongly favors chondrosarcoma; an intact cortex without a soft-tissue mass favors enchondroma.
  • Larger size (commonly >5-6 cm) favors chondrosarcoma; most long-bone enchondromas are smaller and frequently <2 cm.
  • Deep, unexplained pain attributable to the lesion favors chondrosarcoma; enchondromas are usually incidental and painless.
  • Periosteal reaction, medullary expansion, and progressive growth on serial imaging favor an aggressive lesion. Dynamic contrast-enhanced MRI does NOT reliably separate the two.
CURRENTWhite RD et al. · RadioGraphics 2015;35(3):879-898

BOTTOM LINE: Before any upper-abdominal embolization or surgical planning, map the celiac branching pattern and variant hepatic supply, and recognize median arcuate ligament compression by its focal, hooked, expiration-worsened narrowing of the PROXIMAL celiac — which separates extrinsic compression from fixed ostial atherosclerosis.

Key points

  • Classic celiac trunk = hepatosplenogastric trifurcation (common hepatic, splenic, left gastric); this is the most common configuration, but a sizeable minority have variant hepatic supply.
  • Map replaced/accessory hepatic arteries before TACE, GI-bleed embolization, Whipple, or transplant: a replaced right hepatic typically arises from the SMA and a replaced left hepatic from the left gastric artery.
  • Median arcuate ligament compression causes focal narrowing of the PROXIMAL celiac with a hooked/J-shaped contour that worsens in expiration and improves in inspiration, distinguishing extrinsic compression from fixed, often calcified ostial atherosclerosis.
  • Chronic mesenteric ischemia usually requires significant disease in at least two of the three mesenteric arteries because of the rich pancreaticoduodenal and arc-of-Buhler collateral network between the celiac axis and SMA.
  • Other celiac pathology to recognize: isolated celiac dissection, aneurysm/pseudoaneurysm, and a celiacomesenteric trunk, each of which alters endovascular and surgical strategy.

At the workstation

Before any upper-GI or hepatic embolization, dictate the celiac branching pattern and any replaced/accessory hepatic arteries or celiacomesenteric trunk; when you see proximal celiac narrowing, use the contour and respiratory phase to call median arcuate ligament compression versus atherosclerotic stenosis, since this changes catheter strategy and whether surgery is needed.

Board pearl: A focal superior indentation of the proximal celiac artery with a hooked contour that worsens on expiration indicates median arcuate ligament compression, not atherosclerosis (which is ostial, fixed, and often calcified); stenting without ligament release tends to fail.

Findings & methods

Imaging role: CT and MR angiography with multiplanar/3D reconstructions and catheter angiography define the celiac origin, branching pattern, and variant hepatic supply; expiratory-phase imaging is key when median arcuate ligament compression is suspected.

Key variants: The classic hepatosplenogastric trifurcation is most common, but replaced/accessory right hepatic (typically from the SMA) and left hepatic (from the left gastric) arteries are frequent, and a celiacomesenteric trunk is a high-stakes variant before embolization or surgery.

Pathology & management: The celiac axis is affected by atherosclerotic stenosis/occlusion, extrinsic median arcuate ligament compression, dissection, aneurysm/pseudoaneurysm, and vasculitis; MAL compression often needs surgical ligament release rather than stenting alone.

Limitations & caveats
  • Pictorial/educational review, not a diagnostic-accuracy trial.
  • Median arcuate ligament indentation is frequently seen in asymptomatic people, so imaging must be correlated with clinical symptoms before treatment.
Read the deep dive

The celiac axis is the first major ventral branch of the abdominal aorta and classically trifurcates into the common hepatic, splenic, and left gastric arteries (the hepatosplenogastric pattern). Variant anatomy is frequent and clinically decisive: a replaced or accessory right hepatic artery usually arises from the SMA and courses posterolateral to the portal vein, while a replaced or accessory left hepatic artery arises from the left gastric artery. A celiacomesenteric trunk, in which the celiac axis and SMA share a common origin, is higher-risk because disease or catheter manipulation at that shared origin jeopardizes both mesenteric territories. Mapping these variants before chemoembolization, GI-bleed embolization, pancreaticoduodenectomy, or transplantation prevents non-target embolization and ischemic complications. Pathologically, the celiac axis is narrowed by intrinsic atherosclerosis or extrinsic compression by the median arcuate ligament. The ligament produces a characteristic focal indentation of the superior aspect of the proximal celiac artery with a hooked, J-shaped contour, post-stenotic dilation, and dynamic worsening on expiration with improvement on inspiration — separating it from the fixed, ostial, frequently calcified narrowing of atherosclerosis. Because of the rich pancreaticoduodenal and arc-of-Buhler collaterals between the celiac and SMA circulations, symptomatic chronic mesenteric ischemia generally requires high-grade disease in at least two of the three mesenteric arteries.

On axial images at the midbrain/pontomesencephalic junction, elongated, thickened, horizontally oriented superior cerebellar peduncles plus a deep interpeduncular fossa create the silhouette of a molar tooth. Caused by failure of superior cerebellar peduncle decussation.

Entity: Joubert syndrome and related disorders (a ciliopathy)

Imaging: Axial T2/CT at the level of the upper pons-midbrain junction. Associated findings: cerebellar vermian hypoplasia/aplasia with a midline cleft, and a 'bat-wing' or 'umbrella' shaped fourth ventricle. Joubert syndrome is autosomal recessive and presents with hypotonia, ataxia, oculomotor apraxia, and episodic hyperpnea.

Cystic dilatation of the appendiceal lumen by mucin. 'Mucocele' is a descriptive imaging term, not a pathologic diagnosis — underlying causes range from benign retention/hyperplasia to low-grade appendiceal mucinous neoplasm (LAMN) to mucinous adenocarcinoma. Rupture can seed the peritoneum and cause pseudomyxoma peritonei.

Read the deep dive

An appendiceal mucocele is a cystic, mucin-filled dilatation of the appendix and is best understood as a radiologic description rather than a single pathologic entity, spanning benign retention/hyperplasia, LAMN, HAMN, and mucinous adenocarcinoma. On CT, look for a markedly distended, well-encapsulated, low-attenuation (mucin) appendix; a luminal diameter at or above ~15 mm favors a mucocele over simple appendicitis, and curvilinear mural calcification is a helpful discriminator. The critical teaching point is to avoid percutaneous biopsy and aim for intact en-bloc resection, because rupture can disseminate mucin and produce pseudomyxoma peritonei.

Lobar distribution narrows the bronchiectasis differential fast: read the predominant zone first, then look for the discriminating ancillary sign (mucoid impaction, tree-in-bud, traction within fibrosis, situs inversus).

  • Upper-lobe predominant: cystic fibrosis (most classic), allergic bronchopulmonary aspergillosis (central bronchiectasis + mucoid impaction), prior TB (traction + cicatricial).
  • Lower-lobe predominant: most post-infectious/idiopathic bronchiectasis, primary ciliary dyskinesia (Kartagener with situs inversus), chronic aspiration.
  • Central/perihilar: ABPA and Williams-Campbell syndrome (cartilage deficiency).
  • Traction bronchiectasis within fibrosis: UIP/IPF, NSIP, sarcoidosis, chronic hypersensitivity pneumonitis, radiation fibrosis.
  • Right-middle-lobe/lingula predominant: nontuberculous mycobacterial (MAC) infection (Lady Windermere syndrome) with tree-in-bud nodules.

Mnemonic: CF and ABPA go UP (upper-lobe predominant); TB scarring is upper too. Most else — post-infectious, PCD/Kartagener, aspiration — favors the LOWER lobes. MAC/Lady Windermere picks the RML and lingula.

Where the cord ends, where the cauda equina begins, and the signs of tethering.

  • In the average adult the spinal cord tapers into the conus medullaris ending opposite the L1-L2 disc space (commonly the middle third of L1); normal range spans roughly T12/L1 to the L2-L3 level. A conus terminating below L2-L3 should raise concern for tethered cord.
  • Below the conus, the lumbosacral nerve roots form the cauda equina within the thecal sac.
  • The filum terminale internum is a pial extension (~20 cm) anchoring the conus; at about the S2 level it becomes ensheathed by dura and attaches to the coccyx. A filum >2 mm thick or a fatty filum suggests tethering.

The sequences to run and why you cannot stop at the lumbar spine.

  • Sagittal T1, sagittal T2, and sagittal STIR (or fat-saturated T2) covering the region of concern, with axial T2 (and axial T1 where needed) through the compressive level.
  • Cover the WHOLE spine (or at minimum keep a low threshold to image cervical/thoracic levels) because a higher compressive lesion can mimic cauda equina symptoms; the lumbar-only study can miss the true cause.
  • Add post-contrast T1 with fat saturation if infection (epidural abscess, discitis), tumor/metastatic compression, or leptomeningeal disease is suspected.
  • UK RCR/GIRFT-aligned standard: emergency MRI within 4 hours of request and a radiologist report within 1 hour of acquisition for suspected CES.

On CT, multiple small hepatic abscesses appear to aggregate and coalesce into a larger cavity. What is this sign and which infection does it favor?

Define deterministic (tissue reaction) vs stochastic radiation effects.

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