MRI Liver — hepatobiliary contrast agent

Contrast

Gadoxetate disodium at a typical weight-based dose of about 0.025 mmol/kg — one quarter of the 0.1 mmol/kg used for a standard macrocyclic extracellular agent. At the marketed 0.25 mmol/mL concentration that is roughly 0.1 mL/kg, so about 7 mL in a 70 kg adult against roughly 14 mL of an extracellular agent. Injected at a deliberately slower rate than an extracellular bolus, commonly around 1-2 mL/s, followed by a 20-30 mL saline chaser.

• The low dose is not a safety compromise, it is what the agent is licensed at — but it is exactly why the arterial phase is harder here. A quarter of the gadolinium in a smaller volume gives a shorter, lower-amplitude bolus, so the arterial window is narrower and an empirical fixed delay is far more likely to miss it than with an extracellular agent. Bolus tracking or a test bolus is strongly preferred.
• The same small volume drives the mitigation strategies: diluting the dose to 1:1 with saline to lengthen the bolus, and slowing the injection rate, both widen the arterial window at some cost in peak enhancement.
• Transient severe motion — an abrupt few-second dyspnoea during the arterial breath-hold — is a recognised gadoxetate-specific phenomenon reported in a few per cent up to around 10-20% of patients in some series. It hits the arterial phase specifically and the narrow bolus leaves no margin to absorb it, which is why this agent loses arterial phases that an extracellular agent would not.
• Typical dynamic timing: late arterial at roughly 20-35 s from injection (bolus-tracked), portal venous at about 60-70 s, transitional/delayed at about 3 minutes.
• The hepatobiliary phase is conventionally acquired around 20 minutes after injection in normal liver function; reported acceptable windows begin at approximately 10-15 minutes.
• In cirrhosis or cholestasis, hepatocyte uptake is slower and the delay may need extending, sometimes considerably.

Acquisition

Breathing

Breath-hold for the dynamic phases. The hepatobiliary acquisition can be respiratory-triggered because there is no timing pressure.

Reconstruction

Subtractions where needed; thin reformats of the hepatobiliary dataset for biliary anatomy.

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.

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.

5. Hepatobiliary phase (hepatocyte-specific gadolinium)Typically ~20 min after gadoxetate injection in a patient with normal hepatic function (adequate images often achievable from ~10–15 min); substantially longer, and sometimes unobtainable, in cirrhosis, cholestasis or hyperbilirubinaemia. Confirm locally.

   A hepatocyte-specific agent is taken up by functioning hepatocytes via organic-anion transporters and excreted into bile, so late imaging shows liver parenchyma at high signal and biliary structures opacified. The transferable principle is that this phase reports FUNCTION rather than vascularity: anything without working hepatocytes and intact biliary drainage — metastasis, most malignancy, cyst, scar — appears as a defect against bright liver, which is why it is the most sensitive phase for small focal lesions. Two corollaries follow directly. Lesions that do contain functioning hepatocytes need not be defects, so the phase characterises as well as detects; and because uptake competes with excretion, a failing or cholestatic liver produces a weak or absent hepatobiliary phase, degrading exactly the population most often being screened.

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