CT Liver — Triphasic (Unenhanced, Late Arterial, Portal Venous)

Liver for the unenhanced and arterial acquisitions; abdomen and pelvis for the portal venous acquisition 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

Detection of hypervascular metastases where a delayed washout assessment is not required.
Characterisation of a suspected haemangioma, focal nodular hyperplasia or adenoma, where the arterial pattern carries most of the information.
Pre-operative hepatic arterial and portal venous mapping before resection or transplant work-up.
A dose-conscious alternative to the four-phase protocol when the question is not hepatocellular carcinoma.

Technique

Same arterial timing discipline as the four-phase protocol: late arterial, not early.
PHASE 1 — unenhanced, acquired before the injection starts.
PHASE 2 — LATE ARTERIAL, and this one is timed from a bolus trigger rather than from a fixed clock. Monitoring region of interest in the abdominal aorta at about the level of the coeliac axis, trigger at roughly 100 HU above baseline, then a post-trigger diagnostic delay of about 15-20 s. That comparatively long delay is the whole point: it carries the acquisition past the pure angiographic phase into the window where the portal vein is opacified and the hepatic veins are not, which is what "late arterial" means and what a hypervascular lesion is seen in.
A fixed delay for the arterial phase — commonly quoted at around 20-35 s from the start of injection — is the fallback where tracking is unavailable, and it is a fallback rather than an equal option. The correct number moves with the agent concentration, the injection rate, the injection duration and the patient cardiac output, and LI-RADS technical guidance recommends bolus tracking or a timing bolus in preference to any single universal delay.
PHASE 3 — portal venous, at roughly 60-80 s from the start of injection (many protocols use 65-70 s). This one is conventionally a fixed delay, because the portal venous window is many seconds wide where the late arterial window is only a few.
The delayed phase is dropped deliberately, so this protocol should not be used to assess washout in a nodule under hepatocellular carcinoma surveillance.
Scanner generation matters more for the arterial phase than for any other part of this protocol: a fast acquisition can traverse the liver inside the late arterial window, while a slower one may start in it and finish out of it. This is a typical set of values and confirm-locally applies to every number in it.

Where it goes wrong

Using this protocol for a LI-RADS question removes the delayed phase on which washout and capsule appearance depend.
Peripheral nodular enhancement of a haemangioma may not have progressed enough by the portal venous phase alone to be confidently characterised — a delayed acquisition is sometimes needed after all.

Clinical questions that reach this study

Suspected hepatocellular carcinoma in cirrhosis Characterisation of an incidental liver lesion (non-cirrhotic liver)Staging or completion CT in a known solid tumour Liver assessment in a hypervascular primary

Contrast

Iodinated, intravenous

Weight-based dosing is the modern standard here and should be stated as such: roughly 1.5 mL/kg of a high-concentration extracellular agent (350-370 mgI/mL), which is about 100-135 mL in a 70-90 kg adult, at 4-6 mL/s with a 30-40 mL saline chaser. A rate at the top of that range is what a large patient needs, not a courtesy.

Iodine delivery rate — of the order of 1.5-2.0 gI/s — rather than total volume is what drives arterial-phase lesion conspicuity, which is precisely why a fixed 100 mL for every patient is the wrong model. A fixed volume under-doses the large patient in the phase that carries the diagnosis.
An equivalent iodine load can be delivered as a larger volume of a lower-concentration agent at a proportionally higher rate; centres differ on which lever they pull, and the two are not interchangeable at a fixed injection duration.
No positive oral contrast.

Acquisition

Breathing: Matched breath-hold for every phase.
Reconstruction: Thin axial reconstructions per phase with coronal reformats.
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.

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.
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.
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.

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