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CT Liver — Four Phase (LI-RADS Compliant)

Liver only for the unenhanced and arterial acquisitions where dose matters; the portal venous acquisition usually extends through the abdomen and pelvis when staging.

Typical, not policy

Timings, volumes and delays here are representative values drawn from published guidance. Scanner generation, injector, cardiac output and local preference all move them. Confirm against your department's own protocol before you rely on a number.

When to use it

  • Surveillance and diagnosis of hepatocellular carcinoma in a patient at risk (cirrhosis, chronic hepatitis B, current or prior HCC).
  • Characterisation of an indeterminate liver lesion found on ultrasound or single-phase CT.
  • Assessment of treatment response after locoregional therapy.
  • Detection of hypervascular metastases (neuroendocrine, renal, melanoma, thyroid) that are invisible in the portal venous phase alone.

Technique

  • The arterial acquisition must be LATE arterial — hepatic arteries fully enhanced with portal vein already opacified but hepatic veins not yet. Early arterial timing is the classic reason a hypervascular lesion is missed.
  • Fixed-delay arterial timing is widely quoted at around 20-35 s after the start of injection, but published technical guidance is explicit that the optimal delay depends on the agent, the concentration, the injection rate and the timing method, and recommends bolus tracking or a timing run rather than one universal number.
  • The portal venous acquisition follows at roughly 60-80 s and the delayed acquisition at around 3-5 minutes.
  • The unenhanced series is used to identify treated lesions, calcification, iron and fat, and is part of the standard multiphase set for treatment response assessment.

Where it goes wrong

  • An early arterial phase — before the portal vein opacifies — is the commonest technical failure and directly causes missed hypervascular lesions.
  • A slow injection rate lowers the arterial peak and flattens the enhancement difference the study depends on.
  • Inconsistent breath-hold between phases makes lesion-by-lesion comparison unreliable, particularly for small lesions near the dome.
  • Positive oral contrast degrades the reformats and adds nothing.
  • A single portal-venous acquisition submitted as "triple phase" cannot support a LI-RADS category.

Contrast

Iodinated, intravenous

An extracellular iodinated agent at high iodine flux — commonly 1.5 mL/kg or so of a high-concentration agent at 4-6 mL/s with a saline chaser. Iodine delivery rate, not total volume, drives arterial-phase lesion conspicuity.

  • No positive oral contrast.

Acquisition

Breathing
Matched end-expiratory or end-inspiratory breath-hold for every phase.
Reconstruction
Thin axial reconstructions for each phase with coronal reformats and matched slice positions for subtraction-style visual comparison.
Preparation
No positive oral contrast — it degrades multiplanar and vascular reformats and adds nothing to lesion characterisation. Power-injectable cannula; the arterial phase depends on a tight bolus.

Phases

Each phase is authored once and shared across every protocol that uses it, so the physiology below is the same wherever you meet it.

  1. Non-contrast (unenhanced)No injection. Acquired before any contrast is given.

    Shows intrinsic tissue attenuation, and nothing else. The transferable principle is that contrast is anti-signal for anything that is already dense: calcification, acute haemorrhage, urinary and biliary calculi, iodine-containing or haemorrhagic fluid, and intrinsic fat all lose conspicuity, or become uninterpretable, once surrounding tissue enhances. It is also the only baseline against which enhancement can be measured, so any protocol that quantifies enhancement or washout (a lesion "enhances by X HU", adrenal absolute washout, renal mass characterisation) is arithmetically impossible without it. Conversely, an unenhanced series adds dose and no information whenever the question is purely about vascularity or perfusion.

  2. Late arterial phase (arterial-dominant)Typically ~30–40 s after the start of injection. Confirm locally.

    Arteries are still dense and solid organs supplied by arteries have begun to enhance, but the portal vein has not yet delivered its load to the liver. The transferable principle is that HYPERVASCULAR lesions peak here and are maximally conspicuous against a still-dark background: this is where arterially hyperenhancing tumours, hypervascular metastases and vascular malformations declare themselves. The window is narrow and cardiac-output dependent — mistiming by ten seconds in either direction converts a diagnostic study into a non-diagnostic one, which is why bolus tracking rather than a fixed delay is preferred whenever the clinical question is hypervascularity.

  3. Portal venous phaseTypically ~60–90 s after the start of injection. Confirm locally.

    The portal vein and hepatic veins are opacified and the liver is at maximum parenchymal enhancement; bowel wall, mesentery, spleen and peritoneum are all well enhanced. The transferable principle is that HYPOVASCULAR lesions are most conspicuous when the BACKGROUND peaks, so this is the single most productive general-purpose abdominal phase and the correct default when the question is "what is wrong in this abdomen?". Its corollary is the classic error: a hypervascular lesion that was obvious 30 s earlier can become isodense and invisible here, so a normal portal venous study never excludes hypervascular disease.

  4. Delayed / equilibrium (washout) phaseQuestion-dependent: ~3–5 min for hepatic equilibrium/washout, ~15 min for adrenal absolute-washout calculations. Confirm locally.

    Intravascular and interstitial compartments have equilibrated and contrast is being cleared, so most normal tissue is falling in attenuation. The transferable principle is that the diagnostic information is now in the RATE OF CHANGE rather than in the absolute density: tissues with rapid capillary exchange and a small interstitium wash out quickly, whereas fibrous, myxoid or otherwise expanded interstitial spaces retain contrast and become relatively dense. That single mechanism underlies delayed enhancement of scar and fibrosis, retained enhancement in cholangiocarcinoma and haemangioma fill-in, and the arithmetic of adrenal washout — all of which require a matched earlier acquisition to be interpretable at all.

Safety checks this protocol carries

Derived from the contrast agent and phases above, not authored here — which is why they cannot drift apart from what the protocol actually does.

  • Prior contrast reaction and elective premedication· nurse pre scan
  • Intravenous access adequate for the planned injection· radiographer at scan
  • Metformin and iodinated contrast· radiographer at scan
  • Child-sized technique and contrast dose· radiographer at scan
  • Pregnancy status before an ionising exposure· radiographer at scan
  • Kidney function and intravenous iodinated contrast· radiographer at scan