MRI Liver — multiphase with extracellular gadolinium
Whole liver on every phase; the portal venous phase is usually extended to include the spleen, upper abdomen and any relevant nodal stations.
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
- Characterisation of an indeterminate focal liver lesion found on ultrasound or CT.
- Hepatocellular carcinoma surveillance and diagnosis in a patient at risk, reported to a structured system.
- Assessment of hypervascular lesions such as focal nodular hyperplasia, adenoma and haemangioma.
- Staging of colorectal or other liver metastases where the number and segmental distribution change surgical planning.
- Follow-up after locoregional therapy or resection.
Technique
- Unenhanced work-up: T2 with and without fat suppression, dual-echo in- and opposed-phase T1 for fat and iron, and diffusion with a low and a high b value plus ADC.
- Fat-suppressed 3D T1 gradient-echo acquired unenhanced then in late arterial, portal venous and delayed phases, all with identical geometry.
- Late arterial phase acquisition should place the centre of k-space at peak arterial enhancement; bolus tracking or a test bolus is more reliable than a fixed delay.
- The delayed (equilibrium) phase is what demonstrates washout and capsule appearance in structured hepatocellular carcinoma reporting.
Where it goes wrong
- Mistimed arterial phase — the single commonest technical failure in liver MRI, and the one that costs the diagnosis.
- Breath-hold inconsistency between phases, so lesions cannot be matched or subtracted.
- Omitting the unenhanced T1 in the same geometry, making subtraction impossible in a T1-bright lesion.
- Diffusion acquired with only a high b value and no low b value, so ADC cannot be computed.
- Truncated superior or inferior liver coverage at the dome and the inferior tip on breath-hold acquisitions.
Contrast
Extracellular macrocyclic gadolinium agent at a typical single dose of about 0.1 mmol/kg by power injector at roughly 2 mL/s with a saline chaser; arterial timing by bolus tracking, a test bolus or a fixed empirical delay.
- The late arterial phase is the one that matters for hypervascular lesions — capture it too early and the lesion has not enhanced, too late and it has washed in with the parenchyma.
Acquisition
- Breathing
- End-expiratory breath-holds of roughly 15-20 seconds for the dynamic acquisitions. Free-breathing radial or motion-robust alternatives exist for uncooperative patients.
- Reconstruction
- Subtraction of the unenhanced from the arterial phase where a lesion is intrinsically T1 bright.
- Preparation
- Fasting for approximately 4 hours reduces bowel motion and gallbladder contraction; confirm the local interval. State whether the patient is in a hepatocellular carcinoma surveillance programme and whether prior CT or MRI exists — it drives agent choice. Breath-hold capacity determines whether dynamic imaging is feasible; flag patients who cannot hold for roughly 15-20 seconds.
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.
- 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
- Kidney function and gadolinium-based contrast· radiographer at scan
- Intravenous access adequate for the planned injection· radiographer at scan
- Metformin and iodinated contrast· radiographer at scan
- MR safety screening for implants and foreign bodies· radiographer at scan
- Kidney function and intravenous iodinated contrast· radiographer at scan