MRI Abdomen and Liver

MRI of the abdomen and liver is a multiparametric study of the liver, biliary tree, pancreas, spleen, kidneys, adrenals and retroperitoneum. It is the best non-invasive test for characterising focal liver lesions and for assessing diffuse liver disease.

The study uses a 1.5 or 3 tesla scanner with a phased array body coil. Slices are 4 to 6 mm thick. Most sequences are acquired in a breath hold of 15 to 20 seconds, and the whole study takes 30 to 45 minutes.

Core sequences are T1-weighted in phase and opposed phase (chemical shift imaging for fat and iron), T2-weighted with fat suppression, diffusion weighted imaging, and dynamic contrast enhanced T1 with fat suppression (arterial, portal venous, equilibrium and delayed phases). Hepatobiliary phase imaging uses gadoxetate (20 to 40 minutes after injection), and quantitative sequences measure liver fat, iron and stiffness.

Focal liver lesions are found in 20 to 30% of adults, and most are benign. MRI has a sensitivity of over 90% and a specificity of 90 to 95% for characterising lesions as benign or malignant. It detects liver metastases smaller than 1 cm better than CT, and diagnoses hepatocellular carcinoma in cirrhosis with a sensitivity of 80 to 90% through typical enhancement.

Chronic liver disease affects hundreds of millions of people (fatty liver in about 25% of adults, viral hepatitis, alcohol). MRI proton density fat fraction quantifies steatosis accurately, and iron overload is measured by T2* or R2 relaxometry.

Indications.

• Characterisation of indeterminate liver lesions found on ultrasound or CT.
• Surveillance and diagnosis of hepatocellular carcinoma in cirrhosis, and staging.
• Liver metastases detection before resection or ablation (colorectal cancer, neuroendocrine tumours).
• Cholangiocarcinoma and gallbladder cancer staging.
• Pancreatic lesions: solid masses, cystic neoplasms, neuroendocrine tumours, pancreatitis.
• Quantification of liver fat, iron and fibrosis (elastography).
• Budd-Chiari syndrome, portal vein thrombosis and vascular disease.
• Renal and adrenal masses that are indeterminate on CT or ultrasound (adrenal adenoma versus metastasis, phaeochromocytoma).
• Spleen lesions and lymph nodes.
• Abdominal wall and retroperitoneal masses.
• Inflammatory bowel disease, and appendicitis in pregnancy.
• Pre-operative planning for liver resection, live donor transplantation and ablation.
• Post-treatment response (ablation, embolisation, chemotherapy).
• Patients with contraindication to iodinated contrast or radiation.

Not for routine investigation of non-specific abdominal pain, or for patients who cannot hold their breath or lie still.

Contraindications and precautions.

• The usual MRI safety screening (pacemakers, clips, implants, metal fragments). Surgical clips in the abdomen cause local artefact.
• Gadolinium: avoid in severe renal impairment with linear agents. Macrocyclic agents are used at the lowest dose. Gadoxetate is also excreted via the bile and gives lower dynamic enhancement.
• Pregnancy: non-contrast MRI if needed.
• Claustrophobia, large body size exceeding the bore, and inability to hold the breath.
• Fasting for 4 to 6 hours reduces bowel motion and gallbladder contraction. Hyoscine or glucagon may be given.
• Oral contrast (negative agents or water) is optional for pancreatic and bowel studies.

Preparation and technique.

The patient fasts for 4 to 6 hours. A cannula is placed in the antecubital vein. The patient lies supine with the coil over the abdomen and learns the breath hold instructions.

T2 images are taken in axial and coronal planes, with fat suppression and respiratory triggering for free breathing sequences. Chemical shift (in- and opposed phase) images detect fat and iron. Diffusion weighted images are taken with b values of 50 and 800 or higher.

Dynamic contrast imaging uses a 3D gradient echo sequence with bolus timing, and arterial, portal venous and delayed phases. For gadoxetate, the transitional phase at 3 minutes and the hepatobiliary phase at 20 minutes are added.

MR elastography uses a passive driver on the chest wall to measure liver stiffness. Proton density fat fraction and T2* maps are acquired in a single breath hold each.

Normal appearances.

The liver has uniform signal: slightly brighter than muscle on T1 and darker than the spleen on T2. In- and opposed phase images show no signal drop (no fat). Normal liver fat fraction is under 5%.

Hepatic and portal veins are bright after contrast. The liver contour is smooth, and the volume of the lobes is balanced. The bile ducts are thin (the common duct is under 6 to 7 mm).

The spleen is homogeneous. The pancreas is bright on fat suppressed T1 and enhances uniformly, with a main duct under 3 mm. The kidneys show corticomedullary differentiation. The adrenals are thin limbs.

After gadoxetate, the liver enhances uniformly in the hepatobiliary phase, and the biliary tree fills with contrast. Lymph nodes are under 10 mm in short axis (up to 15 mm in the porta hepatis).

Interpretation.

• Simple cyst: very bright on T2, no enhancement. Hydatid cyst: daughter cysts and a dark rim.
• Haemangioma: very bright on T2 ("light bulb"), peripheral nodular enhancement with centripetal fill in. Giant haemangioma may have a central scar.
• Focal nodular hyperplasia: isointense or mildly different from liver, a central scar bright on T2, arterial hyperenhancement that fades to isointensity, and uptake of gadoxetate in the hepatobiliary phase (isointense or hyperintense).
• Hepatocellular adenoma: arterial enhancement, fat (signal drop on opposed phase), haemorrhage, and hypointensity in the hepatobiliary phase. Subtypes differ in fat content and bleeding risk.
• Hepatocellular carcinoma: arterial phase hyperenhancement without rim, then washout in the portal or delayed phase, a capsule, restricted diffusion, and hypointensity in the hepatobiliary phase. Threshold growth and tumour in vein are signs of malignancy. Size over 2 cm with these features is diagnostic in cirrhosis.
• Dysplastic and regenerative nodules: low T2 signal, hyperintense on T1 (iron free), and no arterial enhancement. High grade dysplastic nodules overlap with early cancer.
• Metastases: moderately bright on T2, restricted diffusion, rim enhancement or hypoenhancement, and hypointensity in the hepatobiliary phase. Hypervascular metastases (neuroendocrine, renal, thyroid, melanoma) enhance in the arterial phase. Lesions under 1 cm are detected best with diffusion and hepatobiliary imaging.
• Cholangiocarcinoma: infiltrating mass with delayed progressive enhancement, capsular retraction, dilated ducts beyond the tumour, and hilar tumours (periductal thickening). Gallbladder cancer: wall thickening or mass invading the liver.
• Abscess: rim enhancement, central restricted diffusion, a double target sign, and adjacent perfusion change. Pyogenic and amoebic abscesses are similar, so serology and clinical features help.
• Fatty liver: signal drop on opposed phase and fat fraction over 5%. Focal fat and focal sparing have geographic shapes (around the gallbladder fossa and portal bifurcation) without mass effect.
• Iron overload: low signal in the liver on T2 and in phase T1 (haemochromatosis and transfusional siderosis), with shortened T2* and increased R2. Spleen and pancreas signal indicate the pattern (haemochromatosis spares the spleen, transfusional iron involves it).
• Cirrhosis: nodular contour, enlarged caudate lobe and left lateral segment, small right lobe, ascites, splenomegaly, varices and portosystemic shunts, and increased stiffness on elastography (over 5 kPa suggests advanced fibrosis, depending on the method). Siderotic nodules appear dark.
• Vascular: portal vein thrombosis (filling defect, cavernous transformation), Budd-Chiari syndrome (hepatic vein occlusion, caudate hypertrophy, patchy enhancement), and arteriovenous malformations.
• Pancreas: adenocarcinoma (hypoenhancing mass with upstream ductal dilatation and vascular encasement), neuroendocrine tumour (arterial hyperenhancement, bright on T2), serous cystadenoma (microcystic with a central scar), mucinous cystic neoplasm, intraductal papillary mucinous neoplasm (communication with the duct, mural nodules suggest malignancy), pancreatitis (oedema, necrosis, collections), and autoimmune pancreatitis (sausage shaped gland with a capsule like rim).
• Biliary: stones (signal void), strictures, primary sclerosing cholangitis (beaded ducts), and congenital anomalies.
• Kidney: simple and complex cysts, renal cell carcinoma (enhancing, restricted diffusion), angiomyolipoma (fat on T1 and opposed phase), and renal vein thrombosis.
• Adrenal: adenoma (signal drop on opposed phase), phaeochromocytoma ("light bulb" T2 signal), metastasis and myelolipoma.
• Spleen: cysts, haemangioma, lymphoma, and infarct.
• Lymph nodes and retroperitoneum: lymphoma and metastases (round, restricted diffusion), fibrosis (low T2 signal), and masses.
• Post-ablation and post-embolisation: non-enhancing zone with a thin enhancing rim early on, and nodular enhancement at the margin suggests residual tumour.

Critical values and findings needing immediate action.

• Hepatocellular carcinoma or other malignant liver lesion: multidisciplinary review for resection, ablation, transplantation or systemic treatment.
• Liver abscess: antibiotics and drainage.
• Biliary obstruction with cholangitis: urgent decompression (endoscopic or percutaneous drainage).
• Acute necrotising pancreatitis with infected collections: specialist care.
• Budd-Chiari syndrome or acute portal vein thrombosis: anticoagulation and hepatology review.
• Ruptured or bleeding adenoma or tumour: resuscitation and embolisation.
• Phaeochromocytoma suspected: alpha blockade before any procedure.
• Suspected pancreatic cancer: urgent staging and referral to a hepatobiliary unit.

Limitations and artefacts.

• Breathing and bowel motion degrade image quality, and patients who cannot hold their breath need free breathing or radial sequences. Ascites worsens motion artefact.
• Gadoxetate has transient severe motion artefact in the arterial phase in some patients and weaker portal enhancement. Washout assessment is limited in the hepatobiliary phase, so the transitional phase must not be mistaken for washout.
• Iron overload and metal clips (cholecystectomy, stents) cause signal loss. Susceptibility effects are strong at 3 tesla.
• Washout and capsule appearances are not specific for hepatocellular carcinoma outside cirrhosis. Cholangiocarcinoma, metastases and other tumours can mimic it.
• Small lesions under 1 cm remain indeterminate, and follow up or biopsy is needed.
• Fat suppression failure at the edges of the field produces false bright areas.
• Pancreatic cyst malignancy risk cannot be settled by MRI alone, and endoscopic ultrasound sampling may be needed.
• Quantitative values vary with scanner, field strength and technique, so the same method must be used for follow up.
• Gadolinium retention and nephrogenic systemic fibrosis are concerns. Access, cost and time limit availability.

Special groups.

• Patients with cirrhosis: regular surveillance imaging for hepatocellular carcinoma, with MRI as a problem solving test.
• Patients with chronic viral hepatitis B: tumours can arise without cirrhosis.
• Patients with cancer: MRI for liver metastases before surgery, with hepatobiliary agents.
• Children: liver tumours (hepatoblastoma), biliary atresia and choledochal cysts. Sedation may be needed.
• Pregnant patients: non-contrast MRI.
• Patients with iron overload (thalassaemia): serial T2* of the liver and heart.
• Patients with renal impairment: non-contrast diffusion and T2 sequences, or macrocyclic agents.
• Regions: hepatitis B and C related cirrhosis and hepatocellular carcinoma, liver abscesses (amoebic, pyogenic), hydatid disease, schistosomal periportal fibrosis, and iron overload are common. MRI is rarely available, so ultrasound with alpha fetoprotein is the main tool, and MRI is reserved for tertiary centres.

Follow up tests.

• Ultrasound with Doppler and contrast enhanced ultrasound.
• Multiphase CT for staging.
• Alpha fetoprotein, des-gamma-carboxy prothrombin, CA 19-9, CEA, chromogranin A.
• Liver function tests, viral hepatitis serology, autoimmune markers, ferritin and transferrin saturation, iron studies, and genetic testing for haemochromatosis.
• Transient elastography, and liver biopsy.
• Image directed biopsy of indeterminate lesions.
• Endoscopic ultrasound, MR cholangiopancreatography, and endoscopic retrograde cholangiopancreatography for biliary disease.
• Serology for amoebiasis and hydatid disease.
• Referral to hepatology, hepatobiliary surgery, oncology or transplant services.