Upper Abdomen:
Liver, Pancreas, Biliary System, and Spleen 9
P. Reimer, B. Tombach
Contents
9.1 General Clinical Indications . . . 272
9.2 Coils . . . 272
9.3 Pulse Sequences . . . 272
9.4 Liver . . . 274
9.4.1 Liver Anatomy . . . 274
9.4.2 Contrast Agents for Liver MRI . . . 274
9.5 Liver Pathology – Diffuse Liver Disease . . . 277
9.5.1 Fatty Liver . . . 277
9.5.2 Cirrhosis . . . 277
9.5.3 Iron Overload . . . 278
9.5.4 Vascular Liver Disease . . . 279
9.5.5 Budd-Chiari Syndrome . . . 281
9.5.6 Infectious Disease . . . 281
9.5.7 Granulomatous and Lymphomatous Disease . . . 285
9.6 Liver Pathology – Focal Liver Disease . . . 285
9.6.1 Cyst . . . 286
9.6.2 Hemangioma . . . 287
9.6.3 Focal Nodular Hyperplasia . . . 290
9.6.4 Adenoma . . . 292
9.6.5 Metastases . . . 293
9.6.6 Hepatocellular Carcinoma (HCC) . . . 298
9.6.7 Cholangiocarcinoma (CCC) . . . 301
9.7 Biliary System . . . 301
9.7.1 Biliary Anatomy . . . 301
9.7.2 Technique . . . 301
9.7.3 Benign Biliary Disease . . . 301
9.7.4 Malignant Biliary Disease . . . 303
9.8 Pancreas . . . 304
9.8.1 Pancreas Anatomy . . . 304
9.8.2 Technique . . . 304
9.8.3 Congenital Anomalies and Diseases . . . 305
9.8.3.1 Pancreas Divisum . . . 305
9.8.3.2 Hemochromatosis . . . 305
9.8.3.3 Cystic Fibrosis . . . 305
9.8.3.4 Lipomatosis . . . 305
9.8.4 Pancreatitis . . . 305
9.8.4.1 Acute Pancreatitis . . . 305
9.8.4.2 Chronic Pancreatitis . . . 307
9.8.5 Tumors . . . 308
9.8.5.1 Cystic Tumors . . . 308
9.8.5.1.1 Dysontogenic Pancreatic Cysts . . . 308
9.8.5.1.2 Pseudocysts . . . 308
9.8.5.1.3 Cystic Neoplasm . . . 308
9.8.5.2 Solid Tumors – Pancreatic Adenocarcinoma . . . 309
9.8.5.3 Islet-Cell Tumors . . . 313
9.8.5.4 Lymphoma . . . 313
9.8.5.5 Metastases . . . 313
9.8.6 Trauma and Surgical Complications . . . 314
9.8.6.1 Trauma . . . 314
9.8.6.2 Pancreatic Resection . . . 314
9.8.6.3 Transplantation . . . 314
9.9 Spleen . . . 314
9.9.1 Spleen Anatomy . . . 314
9.9.2 Technique . . . 315
9.9.3 Diffuse Diseases . . . 316
9.9.4 Infection . . . 316
9.9.5 Benign Lesions . . . 317
9.9.6 Malignant Lesions . . . 317
Further Reading . . . 318
9.1
General Clinical Indications
Magnetic resonance (MR) imaging is a widely used modality for the evaluation of diffuse liver disease and the detection as well as further characterization of focal liver disease. Compared with spiral-computed tomog- raphy (CT), multislice CT, and ultrasound, MRI was considered more of a problem-solving tool for the pan- creas and spleen. However, recent developments have changed this view, with MRI presenting a comprehen- sive but also more complex approach compared with other imaging modalities. In particular, the biliary system requires clinical attention because of its nonin- vasive and unenhanced visualization of the biliary tree and pancreatic ducts compared with invasive endo- scopic retrograde cholangiopancreatography (ERCP).
9.2 Coils
Patients are scanned in the supine position (feet or headfirst) with either the body coil, which is imple- mented in every system inside the magnet bore, or pref- erably a phased-array coil. Phased-array coils combine a number of small coils, typically positioned anterior and posterior to the patient and wrapped together (wrap-around coil), providing a higher signal-to-noise ratio and a better image quality. These coils increase the hardware costs, depending on the vendor and the amount of data acquired, which increases the demand for better data processing and storage capacity. Since the anteroposterior diameter of patients varies consid- erably, scanning technicians need to adjust the signal amplification of the middle third of the body specifical- ly to the individual’s anteroposterior diameter to avoid a layering effect with a higher signal towards the coil and a lower signal towards the middle of the body. The inhomogeneous signal within phased-array coils makes signal measurements for signal quantification more dif- ficult than within the body coil.
9.3
Pulse Sequences
The minimum protocol for the parenchymal organs of the upper abdomen consists of two-dimensional (2D)
or 3D T1-weighted (T1-W) and 2D or 3D T2-W sequences obtained in the axial plane. The section thickness varies from 4 mm to 8 mm for the liver and spleen, 2 mm to 4 mm for the pancreas, and 1 mm to 4 mm for vessels and cholangiopancreatography.
Breathing-related movements are the major source of artifacts of the upper abdomen, and a variety of com- pensatory techniques have been developed, such as res- piratory compensation, cranial, caudal, and anterior saturation pulses, multiple averaging, fat suppression, and navigator echoes. An effective technique is to use breathhold sequences with acquisition times of 25 s or less, combined with cranial and caudal saturation puls- es to further minimize pulsation artifacts. Typically, an expiratory breathhold is performed to ensure reprodu- cible slice positioning. If the patients cannot suspend respiration for around 20 s, a non-breathhold sequence with multiple averaging and saturation pulses is prefer- able. Fat suppression may be applied with both T1-W and T2-W pulse sequences, using the available technol- ogy for fat suppression on each scanner; this provides more advantages for the pancreas and biliary system than for the liver and spleen.
Breathhold spoiled gradient-echo (GRE) sequences, such as fast low-angle shot imaging (FLASH), are pref- erable for T1-W imaging (T1-WI) and are referred to within the text. The echo time (TE) of spoiled GRE sequences should be chosen close to in-phase (1.0 T:
6.9 ms and 1.5 T: 4.6 ms) and out-of-phase (1.0 T:
3.45 ms and 1.5 T: 2.3 ms) to characterize fatty tissue.
TE close to optimal in-phase echo-times may be used, depending on specific pulse-sequence optimization strategies. Current sequences allow for coverage of the entire liver during a single breathhold at the cost of some artifacts, because the increase in the number of sections is typically achieved by applying the spoiler pulses just before acquisition of the data set and not before each phase-encoding step (see also Chapter 1).
More recently, 3D T1-W spoiled GRE sequences with fat saturation have been developed, allowing the acquisi- tion of even thinner sections of the order of 3–4 mm at the cost of some artifacts (see Chapter 1). T1-W sequences are combined with extracellular gadolinium- chelates (Magnevist®, Dotarem®, Omniscan®, ProHance®, or Gadovist®), paramagnetic hepatobiliary agents (Teslascan® or MultiHance®), and superpara- magnetic iron oxides (Endorem® or Resovist®). In this chapter, the use of clinically approved agents will be referred to (see also Chapter 2).
Table 9.1. Pulse sequence recommendations for the upper abdomen
Pulse WI Plane No. of TR (ms) TE (ms) Time Flip Echo Section Matrix FOV No. Acq.
sequence sections delay angle train thickness of time
(ms) length (mm) acq.
MR imaging:
FLASH T1 Axial 10–20 100–200 4.1 (1.5 T) 60–90º 3–10 128×256 300–450 1 <25 s
breath- hold
In-phase T1 Axial 10–20 100–200 4.6 (1.5 T) 60–90° 3–10 128×256 300–450 1 <25 s
FLASH 6.9 (1 T)
breath- hold
Out-of- T1 Axial 10–20 100–200 2.3 (1.5 T) 60–90° 3–10 128×256 300–450 1 <25 s
phase 3.45 (1 T)
FLASH breath- hold
3D out- T1 Axial 20–40 <10 2–3 (1.5 T) 10–20° 2–6 128×256 300–450 1 <25 s
of-phase FS- breath- hold FLASH
SE/TSE T2 Axial 15–20 >2500 1 : 40–100 <180° <12 3–10 128×256 300–450 2–6 >4 min
non- 2 : 150–200
breath- hold
TSE T2 Axial 5–15 <4000 75–150 <180° >20 5–10 100×256 300–450 1 <20 s breath-
hold
HASTE T2 Axial 15–20 <10 50–100 800–1000 <180° >128 5–10 128×256 300–450 1 <25 s breath-
hold
True- T2 Axial or 10–20 <10 2 –5 (1.5 T) 60– >128 5–30 256×256 300–450 1 <25 s
FISP coronal 90°
breath- hold
MR angiography:
3D CE- T1 Coronal =40 =5 =2 20–50° =2 >128× 300–450 1 <25 s
MRA 256
2D TOF T1 Axial or 1–3 5–10 2–10 20–50° =5 >128× 300–450 1 <5 s
coronal 256
MR cholangiopancreatography
2D T2 Coronal <20 <20 >50 <180° >128 =5 128×256 300–450 1 <30 s
HASTE
3D TSE T2 Axial or 10–20 >3000 >500 <180° >128 1–10 128×256 300–450 1 >5 min (respira- coronal
tory trig- gered)
3D TSE T2 Coronal 1 slab >3000 >500 <180° >128 50–100 128×256 300–450 1 <20 s (thick
slab)
The FOV is individually adjusted to the patient using rectangular FOV, and the section thickness depends on the organ or pathology imaged. WI weighting of images, Matrix phase × frequency matrix, Acq. acquisition(s)
A variety of sequences are available for T2-WI.
Turbo spin-echo imaging (TSE) is widely preferred over SE with different options for breathhold and non- breathhold sequences. However, conventional SE still represents a diagnostic standard for T2-WI of the liver and can be used with a 128×256 matrix, cranial and caudal saturation pulses, two acquisitions, and fat satu- ration. Breathhold TSE sequences use increasing num- bers of echoes per TR (echo train length ‘ETL’) to decrease the acquisition time at the same anatomical resolution or increase the anatomical resolution at the same temporal resolution. However, the use of sequenc- es with increasing ETL with numerous 180° refocussing pulses also decreases the susceptibility weighting, which is an important contributor to lesion contrast within parenchymal organs. Therefore, TSE sequences may provide lower lesion contrast for solid lesions than conventional SE sequences, but this disadvantage may be compensated by an increased image quality. Thus, non-breathhold sequences with a limited number of echoes but stronger susceptibility weighting are still relevant for clinical MR imaging and provide stable image quality. Breathhold, multishot, rapid-acquisition relation enhancement imaging (RARE) sequences have been recently improved by using fast read-outs, half- Fourier acquisitions, and single-shot half-Fourier TSE (HASTE) techniques and are becoming clinically useful.
T2-W sequences with susceptibility weighting are com- bined with superparamagnetic iron oxides and will be referred to in this chapter.
MR angiography of the portal-venous system, sup- plying the visceral arteries and visceral veins, is increas- ingly performed with contrast-enhanced MR angiogra- phy (CE-MRA) techniques that utilize a combination of gadolinium-chelates and breathhold, coronal, 3D, non- spoiled GRE sequences as described in Chapters 1 and 13. Clinically approved low-molecular-weight gadolin- ium-chelates are intravenously injected by means of power injectors following calculation or automatic measurement of the individual bolus transit time. This technique requires fast gradients and is available mainly on high-field systems (81 T). Alternatively, plain breathhold axial or coronal 2D TOF sequences, which may also be combined with superparamagnetic iron oxides, are suited for imaging of the intrahepatic vascu- lature and vasculature of the upper abdomen. Indi- vidual angiographic sections should always be viewed together with postprocessed maximum intensity pro- jection (MIP) angiograms. More recently, balanced
nonspoiled GRE sequences have gained particular im- portance (true-FISP [Siemens] or balanced FFE [Philips]).
Typically acquired as 2D sequences, this technique pro- vides bright vessels almost irrespective of the flow direction and velocity as well as bright fluid-filled structures. Therefore, these sequences are useful in demonstrating the patency of a vessel without the use of contrast agents. This technique also requires fast gra- dients and is available mainly on newer high-field systems (81 T).
MR cholangiopancreatography (MRCP) has been improved with the refinement of TSE/FSE/HASTE pulse sequences. Current approaches differ according to scanner technology and use predominantly either breathhold 2D sequences or non-breathhold and often respiratory-triggered 3D sequences. Intraductal fluid is visualized bright, based on long TE compared with background tissues, which have already lost their sig- nal. Individual sections should always be viewed together with postprocessed MIP cholangiograms and pancreaticograms.
Table 9.1 provides general guidelines for sequence parameters which are discussed further in the text (see also Chapter 1).
9.4 Liver 9.4.1
Liver Anatomy
The liver demonstrates higher SI (SI) on T1-W sequenc- es and lower SI on T2-W sequences than the spleen. SI from normal parenchyma is homogeneous on both sequences (Fig. 9.1).
9.4.2
Contrast Agents for Liver MRI
Nonspecific, low-molecular-weight, extracellular gado- linium-chelates are currently most frequently used for contrast-enhanced liver MR imaging and are useful in characterizing liver disease. These compounds behave pharmacologically similarly to iodinated X-ray contrast agents and can be bolus injected to perform dynamic studies using multisection spoiled GRE techniques with approximately 20–25 sections in a single breathhold.
Gadolinium-enhanced images can be interpreted very similarly to contrast-enhanced CT images, because gado- linium shortens the T1-relaxation time, resulting in tis- sue signal enhancement on T1-WI (Fig. 9.1). Contrast timing requires the acquisition of arterial phase (20–30 s following injection) images to detect and char- acterize hypervascular lesions [focal nodular hyperpla- sia (FNH), adenoma, hepatocellular carcinoma (HCC), hypervascular metastases: renal cell cancer, islet-cell tumors, carcinoid, pheochromocytoma, etc.]. In the arte- rial phase, contrast material is present in the visceral
arteries, with strong enhancement of the pancreas and renal cortex without opacification of the hepatic veins.
The normal spleen should show an arciform or serpigi- nous enhancement pattern (see Sect. 9.9). Portal phase images (50–90 s following injection) demonstrate strong parenchymal enhancement to detect hypovascu- lar lesions with best conspicuity during this phase (Fig. 9.2). Equilibrium phase images acquired more than 2 min following injection (up to 10 min) result in a dif- fuse enhancement that can be useful to allow heman- giomas to fill in and inflammatory changes to enhance.
Fig. 9.1A–D. Perfusion defect in the right liver lobe. Plain T1-W spoiled GRE (A), T2-W TSE (TE 138 ms) (B), arterial phase, gado- linium-enhanced, T1-W spoiled GRE (C), and portal venous phase, gadolinium-enhanced, T1-W spoiled GRE (D) show a large mass in the right liver lobe with a perfusion defect. The biopsy- proven intrahepatic cholangiocarcinoma demonstrates low SI on T1-WI (A), slightly high SI on T2-WI (B), and peripheral contrast
enhancement (C,D). The mass compresses the right portal vein, which causes a wedge-shaped portal perfusion defect. The liver parenchyma within the perfusion defect enhances more strongly during the capillary phase due to a relative increase in the arterial supply compared with liver parenchyma that has normal portal perfusion (C). The difference in parenchymal enhancement fades away on portal venous phase images (D)
Liver-specific intracellular contrast agents have been developed to further improve liver imaging, and some of them are already clinically available. The first clini- cally approved paramagnetic hepatobiliary agent Teslascan® (mangofodipir trisodium, formerly known as Mn-DPDP) is partially excreted into the bile follow- ing uptake into hepatocytes and causes an increase of SI on T1-WI. In Europe, Teslascan® is drip-infused, and therefore, dynamic scanning cannot be performed. The compound enhances the liver parenchyma and was advocated to differentiate tumors of hepatocellular origin from nonhepatocellular origin. However, the spe-
cificity for differentiation of hepatocellular tumors is lower than expected. Since tumors of nonhepatocellular origin show nonspecific intratumoral enhancement, a second MR study with a time delay of several hours (typically 1 day) is required to allow for diffusion of the contrast agent out of the intratumoral interstitium.
A perilesional rim may be visible, and small metasta- ses may be detected only on these images. A second compound with comparable enhancement character- istics on T1-WI, MultiHance® (gadobenate dimeglu- mine), is clinically available for liver imaging but has gained more attention for vascular imaging as off- Fig. 9.2A–D. Hepatocellular carcinoma (HCC) in chronic hepatitis
C with liver cirrhosis. Plain T1-W spoiled GRE (A), T2-W HASTE (TE 64 ms) (B), arterial phase, gadolinium-enhanced, T1-W spoiled GRE (C), and portal venous phase, gadolinium-enhanced, T1-W spoiled GRE (D) of a patient with HCC following chronic hepatitis C with liver cirrhosis, portal hypertension, and ascites. A mildly hypointense lesion on T1-W spoiled GRE (A) and mildly hyperintense lesion on T2-W HASTE (B) are depicted in the later- al right liver lobe. The liver demonstrates higher SI than the spleen
on T1-W sequences and lower SI than the spleen on T2-W sequences. Liver cirrhosis with hypertrophy of the left lobe, sple- nomegaly, and ascites is present. Arterial phase images demon- strate the hypervascularity of the lesion already visible on plain images and two additional enhancing smaller lesions anterior to the larger lesion (C) with decreasing contrast on portal venous phase images (D). Imaging findings were confirmed following liver transplantation
label use. The compound can be bolus injected, and imaging studies may be designed as described for non- specific gadolinium compounds combined with delayed scans some hours later for tumor detection because of nonspecific uptake in focal liver lesions (see Chapter 2).
A third compound, Gd-EOB-DTPA, should become available in the near future. This compound is asso- ciated with a strong biliary excretion and can be bolus injected with imaging studies as described for non- specific gadolinium compounds combined with de- layed scans as early as 20 min postinjection (see Chap- ter 2).
Superparamagnetic iron-oxide particles (SPIO) accumulate efficiently within minutes of administration within phagocytic cells in the liver (approximately 80%) and in the spleen (5%–10% of the injected dose).
Malignant tumors are typically devoid of a substantial number of phagocytic cells appearing as hyperintense/
bright lesions in a hypointense/black liver on T2-W sequences. Tumors with a substantial number of phago- cytic cells, such as focal nodular hyperplasia, hepato- cellular adenoma, well-differentiated hepatocellular carcinoma, hypervascular metastases, and/or a signifi- cant blood pool (hemangiomas) may show sufficient uptake of SPIO and, thus, decrease in SI on T2-W sequences. The signal decrease is related to the Kupffer cell activity and tumor vascularity. Clinically approved Endorem® is currently administered by drip infusion in glucose or saline at a dose of 10–15µmol Fe/kg body weight over 30 min with a flow rate of approximately 3 ml/min, since side-effects (facial flush, dyspnea, rash, lumbar pain) occur at higher injection rates. The patient is then brought back into the magnet, typically on the same day, with a large time-window of several hours to acquire postcontrast images. Resovist® is bolus-injectable and has been clinically available for liver MR imaging in Europe since 2001. Patients may either be scanned within one session or up to 1–4 days postcontrast (see also Chapter 2).
Ultrasmall SPIO particles (USPIO; Sinerem®) have a longer blood half-life and accumulate primarily in the liver, spleen, bone marrow, and lymph nodes. Since USPIO have a stronger T1 effect than SPIO and a long- er blood half-life, they can also be used as T1 (brighten- ing) blood-pool agents for MR angiography or liver lesion characterization. Well-perfused lesions increase in SI on T1-W images and decrease in SI on T2-W imag- es. Thus, USPIO yields information regarding the vas- cular nature of liver lesions during accumulation phase
images. This compound is under phase-3 clinical inves- tigation and may become available within the near future (see also Chapter 2).
9.5
Liver Pathology – Diffuse Liver Disease 9.5.1
Fatty Liver
Fatty liver may cause severe problems with ultrasound (US) and CT by obscuring focal lesions; however, MRI is very effective in fatty liver since fat contributes to the SI, and a signal from fat can be eliminated selectively (fat suppression). The follow-up of patients with chemo- therapy-induced fatty liver suspicious of metastases is therefore best evaluated by MRI. High signal on T1-WI and decreasing signal with fat-suppression techniques prove the presence of fat. Out-of-phase GRE techniques are clinically useful to differentiate focal fatty infiltra- tion and focal sparing in diffuse fatty infiltration from mass lesions. Some lesions have to be considered for differential diagnoses. Well-differentiated HCC is typi- cally better delineated and often encapsulated with spotted areas of fat. Hepatic adenoma can be differen- tiated by strong early enhancement following gadolin- ium injection, by late enhancement following infusion of hepatobiliary agents such as Teslascan®, or by late enhancement on delayed images following infusion or injection of SPIO (Fig. 9.3). Hemorrhage, melanin, pro- tein, and copper may also cause increased signal on T1-WI (see Chapter 3).
9.5.2 Cirrhosis
Liver cirrhosis is characterized by irreversible fibrosis with destruction of the hepatic architecture. Atrophy of the right liver lobe and the medial segment of the left liver lobe with consecutive hypertrophy of the lateral segment of the left lobe and caudate lobe is frequently present. An irregular parenchymal pattern is often also present (Fig. 9.2). Regenerative nodules develop from heterogeneous regeneration and dysplasia. MR imaging is superior to CT and US in depicting regenerative nod- ules, which present with lower SI compared to the cir- rhotic liver on T2-WI. SPIO-enhanced and gadolinium-
enhanced MR imaging can be used to differentiate regenerative nodules with higher SI on T2-WI compared to HCC. Regenerative nodules appear hypointense on early gadolinium-enhanced T1-WI and reveal a sub- stantial uptake of SPIO, resulting in a signal decrease, which is rarely observed in well-differentiated HCC.
Liver cirrhosis is the most common cause of portal hypertension due to a sinusoidal obstruction with sub- sequent complications, such as variceal bleed, ascites, and splenomegaly (Fig. 9.2). The normal hepatopetal flow may reverse in severe cirrhosis and become hepa- tofugal, which can be easily demonstrated by MR flow measurements. Portal varices and shunts (splenorenal, splenocaval, etc.) are demonstrated by true-FISP, PC-
MR, TOF-MR, and gadolinium-enhanced MR angiogra- phy.
9.5.3
Iron Overload
The signal appearance of iron overload is similar to postcontrast SPIO-enhanced images with low SI on T2/T2*-WI. Severe iron overload may also lead to low SI on T1-WI (Fig. 9.4). MR imaging is the most sensitive imaging technique to demonstrate iron overload, with muscle and fat serving as inherent reference tissues.
Hepatic iron overload is caused either by idiopathic Fig. 9.3A–D. Liver adenoma. T2-W TSE images before (A: TE
83 ms and B: TE 165 ms) and 10 min following intravenous injec- tion of 10µmol Fe/kg body weight (Resovist) (C: TE 83 ms and D:
TE 165 ms). The focal lesion in the dorsal part of the right liver lobe decreases slightly in signal at the longer echo-time on pre-
contrast T2-W images (A,B). The lesion significantly decreases in SI on postcontrast T2-W images (C,D). Imaging was performed for tumor staging in a young woman with breast cancer and sub- sequent biopsy to rule out a hypervascular metastasis which revealed a liver adenoma
(primary) hemochromatosis, transfusional iron over- load, hemolytic anemia, or associated with liver cirrho- sis.
Idiopathic hemochromatosis results from increased absorption and accumulation of dietary iron, affecting primarily the liver, pancreas, and heart. Iron accumula- tion can be fatal due to the development of liver cirrho- sis, HCC, diabetes mellitus, and cardiomyopathy. Iron accumulation starts in the liver; it should be diagnosed early, since therapy before accumulation in the pancre- as and heart may result in a normal life expectancy. The spleen is typically spared, and involvement of the pan- creas typically presents when liver cirrhosis has already developed. Patients with liver cirrhosis are at risk of HCC, and nonsiderotic nodules in patients with hemo- chromatosis should be considered as malignant until proven otherwise. Regenerative nodules contain iron and have a lower SI than HCC, which also serves as a test by means of SPIO-enhanced MR imaging to differ- entiate regenerative nodules from HCC in patients with liver cirrhosis but without iron overload. However, hepatocellular iron may also be mildly increased in patients with liver cirrhosis. Dysplastic nodules or ade- nomatous hyperplasia may show variable iron uptake and thus, may also appear as relatively bright lesions within the hypointense liver as a differential diagnosis to HCC.
Transfusional iron overload with iron deposition in the reticuloendothelial system (RES) of the liver, spleen, and bone marrow spares hepatocytes, pancreas, heart,
and other parenchyma. Unless severe iron overload is present at later stages of the disease, involvement of the spleen (transfusional iron overload) versus the pancre- as (idiopathic hemochromatosis) helps to differentiate RES iron from hepatocellular iron overload.
Hemolytic anemias frequently require blood trans- fusions, and, therefore, a coexisting transfusional iron overload may develop. Patients with thalassemia vera without transfusions but with increased absorption of dietary iron may develop erythrogenic hemochromato- sis, primarily affecting the liver. Filtration and tubular absorption of free hemoglobin in sickle cell anemia explain the decreased signal of the renal cortex.
Paroxysmal nocturnal hemoglobinuria often leads to iron overload in the liver and renal cortex.
9.5.4
Vascular Liver Disease
Portal thrombosis may occur in malignant liver tumors (HCC), coagulopathies (cirrhosis), inflammation (pan- creatitis), or extrinsic compression (CCC, metastases, lymphomas, etc.) of portal veins and may lead to a cav- ernous transformation of the portal vein (Fig. 9.5).
Higher signal on T2-WI and enhancement on T1-W gadolinium images typically characterize tumor throm- bus. Bland thrombus (see Chapter 3) shows a lower sig- nal on T2-WI and no gadolinium enhancement. Areas with decreased portal perfusion are usually wedge- Fig. 9.4A,B. Idiopathic hemochromatosis. Plain T1-W spoiled GRE
(TE 5 ms) (A) and T2-W TSE (TE 90 ms) (B) in a 23-year-old patient. The liver demonstrates low SI on T1-W and T2-W
sequences without a signal decrease within the pancreas, heart, or spleen. No signs of liver cirrhosis are present
Fig. 9.5A–F.
shaped and may demonstrate an earlier and stronger enhancement during the capillary phase due to a rela- tive increase in their arterial supply compared with liver regions with normal portal perfusion. The differ- ence in parenchymal enhancement fades away on delayed contrast-enhanced images (Fig. 9.1). Liver infarcts may occur following surgery, chemoemboliza- tion, trauma, and portal thrombosis, resulting in hypo- perfused wedge-shaped defects (Fig. 9.6). Extrahepatic and intrahepatic liver vessels are well demonstrated on gadolinium-enhanced 3D MR angiography (Fig. 9.7).
Intrahepatic vessels are also visualized on iron-oxide- enhanced 2D TOF images, contrasting the portal venous system in the dark liver parenchyma (Fig.
9.8).
9.5.5
Budd-Chiari Syndrome
Venous outflow in Budd-Chiari syndrome is often not completely eliminated due to accessory hepatic veins, segmental obstruction, or small veins (Fig. 9.9).
Shunting into the portal vein may cause reversed portal flow in patients with portal hypertension. Typically, the caudate lobe and central parts are spared, and the right lobe is atrophic. Portosystemic shunts, intrahepatic col- laterals, and capsular collaterals are often present.
Gadolinium enhancement varies from acute disease
with more decreased enhancement to chronic disease with increased enhancement relative to normal or hypertrophied segments. Central parts may therefore appear as low SI mass-like lesions. Nodular regenerative hyperplasia may develop in chronic disease, demon- strating a similar signal pattern to adenomatous hyper- plastic nodules with high SI on T1-WI, intermediate to low SI on T2-WI, and early enhancement on gadolin- ium-enhanced images. The differential diagnosis of HCC within individual patients may become quite diffi- cult. Hepatobiliary agents cause an increased signal enhancement and SPIO a decreased signal enhance- ment.
9.5.6
Infectious Disease
Pyogenic abscesses typically show low SI on T1-WI, moderate to high SI on T2-WI (hyperintense necrotic center), and a thick rim of perilesional enhancement on gadolinium-enhanced T1-WI with an indistinct or irregular outer margin. Amebic abscesses basically reveal a similar pattern, although they are more encap- sulated with enhancement of the capsule (Fig. 9.8).
Echinococcal disease presents as an encapsulated multicystic lesion with potential satellite cysts (<20% of patients). The signal behavior can be complex, with mixed signal (debris, protein) on T1-WI and T2-WI and Fig. 9.5A–H. Cavernous portal vein trans-
formation in a child. Portal venous phase, gadolinium-enhanced, T1-W spoiled GRE (A), T2-W HASTE (TE 90 ms) (B), coronal true-FISP (C,D), single sections from con- trast-enhanced, time-resolved MRA dur- ing the portal phase (E,F), and MIPs of the arterial phase (G) and portal venous phase (H). The portal vein is absent, and large collateral vessels are visible within the hepatoduodenal ligament. The spleen is markedly enlarged, with small siderotic nodules within the parenchyma, and ascites is present. Displayed arteries are completely normal. The most likely reason is an umbilical vein catheter during the first weeks of life
calcifications, which are often present within the cyst wall. MR imaging cannot reliably distinguish the fibrous tissue of the capsule from calcifications. The fibrous capsule and the internal septations are well shown on gadolinium-enhanced MR imaging.
Fungal infections, typically Candida albicans, present as microabscesses with small lesions in size (<2 cm) and low signal on T1-WI and T2-WI. C. albi- cans predominantly involves the liver and spleen (hepatosplenic candidiasis) and occasionally the kid- ney. FS T2-WI and gadolinium-enhanced, dynamic T1-WI is most useful in depicting the lesions. Acute
lesions may show an almost cystic signal pattern (low SI on T1-WI and high SI on T2-WI) without peripheral enhancement. Granulomatous reactions as a treatment response demonstrate central high SI on plain T1-WI and T2-WI and gadolinium-enhancement on T1-WI with a dark peripheral ring. Chronic lesions with scar- ring show low SI on T1-WI and are typically invisible on T2-WI. Irregular lesions without gadolinium enhance- ment are best visualized on early gadolinium-enhanced T1-WI. Liver-specific agents do not provide additional clinically relevant information.
Fig. 9.6A–D. Liver infarct following chemoembolization. Plain T1- W spoiled GRE (A), T2-W HASTE (TE 90 ms) (B), arterial phase, gadolinium-enhanced, T1-W spoiled GRE (C), and portal venous phase, gadolinium-enhanced, T1-W spoiled GRE (D). The liver
demonstrates a wedge-shaped perfusion in segment 5/6 with no enhancement following gadolinium injection and high signal on T2-W HASTE due to liquefactive necrosis
Fig. 9.7A–F. Klatskin tumor. Arterial phase, gadolinium-enhanced, T1-W spoiled GRE (A) and gadolinium-enhanced, FS T1-W spoiled GRE at the level of the tumor (B) reveal dilated intrahepat- ic biliary ducts (dark) and a relatively hypointense infiltrative mass lesion in the hilus surrounding the portal vein (bright). The second gadolinium-enhanced, FS T1-W spoiled GRE section (C) at the level of the papilla of Vater shows contrast enhancement of the tissue adjacent to the papilla due to inflammatory changes follow- ing ERCP. The two HASTE (TE 90 ms) images at the level of the
tumor (D) and the gallbladder (E) portray the dilated intrahepat- ic ducts as bright and the portal vein as dark. The gallbladder shows a fluid-fluid level due to sludge (lower SI) below the bile (higher SI). Bright ascites is also present. CE-MRA displaying the portal venous phase (F) was obtained with 0.2 mmol gadolin- ium/kg body weight. The distal part of the main portal vein shows direct tumor infiltration with significant narrowing of the lumen.
Explorative laparotomy confirmed tumor infiltration into the main portal vein with peritoneal carcinomatosis
Fig. 9.8A–D. Amebic liver abscess. Axial and coronal 2D-TOF images before (A,B) and 10 min following i.v. injection (Resovist) of 10µmol Fe/kg body weight (C,D) of a patient with an amebic liver abscess in the right liver lobe. A thick wall and a necrotic cen-
ter characterize the abscess. Liver-vessel contrast is increased on SPIO-enhanced images due to a decrease in liver SI with improved visualization of the portal venous vessels
9.5.7
Granulomatous and Lymphomatous Disease
Sarcoidosis typically presents as multifocal small lesions (1 cm) in the liver and spleen. Granulomas are hypointense on T1-WI and T2-WI and show delayed gadolinium enhancement. Focal lymphomatous disease demonstrates low signal on T1-WI and a slightly high signal on T2-WI. Gadolinium-enhanced T1-WI shows no significant increase in lesion SI, but occasionally perilesional enhancement. Liver-specific agents offer a better delineation of lesions on accumulation phase images.
9.6
Liver Pathology – Focal Liver Disease
Plain and contrast-enhanced MR imaging is useful for the detection and characterization of focal liver lesions.
Hepatic MR imaging is best performed with breath- hold T1-W GRE techniques, breathhold T2-W TSE or HASTE techniques, or non-breathhold T2-W TSE or SE techniques.
Metastases are the most common liver tumors in Western countries and HCC in Africa and Asia.
Contrast-enhanced MR imaging exceeds the diagnostic ability of contrast-enhanced spiral CT and portal- enhanced spiral CT to detect and subsequently charac- terize malignant focal liver lesions. Lesion characteriza- tion is of particular importance in patients with pri- mary malignancies, because even in this selected popu-
lation up to 50% of small lesions (<10–15 mm) may be benign. Imaging protocols include transverse plain and contrast-enhanced T1-W and/or T2-W pulse sequenc- es, depending on the contrast agents administered. The acquisition of an additional T1-W or T2-W sagittal or coronal plane may be useful to depict lesions on the upper surface of the liver.
Contrast enhancement with extracellular low-molec- ular gadolinium-chelates requires rapid T1-W spoiled GRE imaging before, during the arterial phase (hyper- vascular lesions), during the portal-venous phase (hypovascular lesions), and plain T2-W images with moderate (detection) and long (characterization) TE.
Fat saturation of T2-W TSE sequences may be advanta- geous to facilitate the detection of superficial lesions.
Delayed T1-WI are recommended to observe slow fill- in patterns.
Contrast enhancement with hepatobiliary agents is best performed with T1-WI before and at different time points following rapid contrast injection (MultiHance®
and Gd-EOB-DTPA) or infusion (Teslascan®). T2-WI with moderate (detection) and long (characterization) TE is typically performed before contrast administra- tion. Dynamic T1-WI is helpful to study the perfusion phase of lesions comparable to extracellular low-molec- ular gadolinium-chelates, and delayed imaging (>2 h for Teslascan® and MultiHance® and >20 min for Gd- EOB-DTPA) has to be performed because of nonspecif- ic enhancement of lesions during the perfusion phase.
Following an initial wash-out, malignant nonhepatocel- lular lesions exhibit a constant signal on T1-W delayed images. However, the presence of hepatocytes in the Fig. 9.9A,B. Budd-Chiari. Portal venous phase, gadolinium-enhanced, T1-W spoiled GRE (A) and T2-W HASTE (B) The liver demon- strates inhomogeneous SI on T1-WI and T2-WI with multiple peripheral infarcts and absent hepatic veins
early stages of HCC may cause enhancement compar- able with liver tissue (see adenoma and FNH).
It is recommended to acquire T1-WI in a second plane as part of the protocol for delayed scanning to look for small lesions close to the liver capsule beneath the diaphragm.
Contrast enhancement with iron oxides is best per- formed with T1-WI and T2-WI before and after 15–30 min following rapid contrast injection (Reso- vist®) or infusion (Endorem® and Sinerem®). Dynamic imaging is helpful to study the perfusion phase of lesions comparable with extracellular low-molecular gadolinium-chelates. Delayed imaging has to be per- formed to utilize the best lesion-liver contrast for the detection of lesions and provides features for lesion characterization. Malignant lesions without phagocytic
cells exhibit constant signal on T2-W accumulation phase images with all three available or tested iron oxides. However, the presence of phagocytic cells in the early stages of HCC may cause enhancement compar- able to adenomatous hyperplasia.
9.6.1 Cysts
Liver cysts appear as well-defined and frequently multi- ple focal lesions with a typical signal pattern demon- strating low signal intensity on T1-WI, homogeneous high SI on T2-WI, and no contrast enhancement with either extracellular or liver-specific contrast agents (Fig. 9.10). MR imaging is superior to CT and US in
Fig. 9.10A–D. Liver cyst and liver metastases. Adjacent sections of T2-W HASTE (TE 90 ms) (A,B) and portal venous phase, gadolin- ium-enhanced, T1-W spoiled GRE (C,D) of a patient with colon carcinoma prior to liver surgery. A cyst with high SI on T2-WI (B) and absent gadolinium enhancement on portal venous phase, gad-
olinium-enhanced, T1-W spoiled GRE (D) is located in the right liver lobe. At least three ring-enhancing lesions are visible on por- tal venous phase, gadolinium-enhanced, T1-W spoiled GRE (C) in the left liver lobe, which appear only slightly hyperintense on T2- WI (A). Findings were confirmed at surgery
depicting and characterizing small cysts. Rarely, cysts may appear with higher signal on T1-WI due to a hemorrhagic or proteinaceous content.
9.6.2 Hemangioma
Hemangioma is the most common benign focal liver lesion and is typically detected incidentally. Cavernous liver hemangiomas are by far more common than cap- illary hemangiomas. The major clinical implication is the misclassification on CT, ultrasound, or scintigraphy,
complicating patient management. MRI is the best modality to detect and characterize liver hemangioma and should be recommended widely for this clinical question. Hemangiomas appear as well defined and lobulated focal lesions. The signal pattern on unen- hanced MR imaging is very similar to cysts with low signal intensity on T1-WI and high SI on T2-WI due to long T1- and T2-relaxation times (>120 ms), which are however shorter than for cysts. Dynamic and serial gad- olinium-enhanced T1-WI are effective in distinguish- ing hemangiomas from malignant lesions, because hemangiomas typically enhance in a peripheral nodu- lar fashion with subsequent complete or almost com-
Fig. 9.11A–H. Liver hemangiomas. T2-W HASTE (TE 90 ms) (A,B), plain T1-W spoiled GRE (C,D), arterial phase, gadolinium- enhanced, T1-W spoiled GRE (E,F), and portal venous phase T1- W spoiled GRE (G,H). The liver demonstrates a larger hemangio- ma within the right liver lobe and a smaller subcapsular heman- gioma showing high SI on T2-WI and low signal on T1-WI. The larger hemangioma demonstrates a type-3 enhancement pattern
with peripheral nodular gadolinium enhancement, followed by a centripetal progression on delayed gadolinium-enhanced T1-WI without complete uniform signal enhancement. The smaller hemangioma reveals a type-1 enhancement pattern with early uniform high signal enhancement and homogeneous SI on delayed T1-WI
plete fill-in of the entire lesion over 5–10 min (Fig. 9.11). Three types of enhancement patterns for dynamic T1-WI have been described:
쐌 Type 1 Uniform high signal enhancement during the early phase, without wash-out (metasta- 쐌 Type 2 Peripheral nodular signal enhancement dur-ses) ing the early phase, followed by a centripetal progression to uniform high signal enhance- 쐌 Type 3 Peripheral nodular signal enhancement dur-ment ing the early phase, followed by a centripetal progression with a persistent central scar Type-1 enhancement is present in small hemangiomas (15 mm), type-3 enhancement typically in large heman-
giomas (>5 cm) or giant hemangiomas (Fig. 9.12), and type-2 enhancement in hemangiomas of each size. The dynamic pattern of enhancement provides additional criteria to establish the diagnosis of a hemangioma.
Nodular enhancement is demonstrated immediately following gadolinium enhancement, which is also fre- quently eccentric. Enhancement fades away over time without a peripheral or heterogeneous wash-out (see metastases). Some hemangiomas may also enhance fairly rapidly, within less than 2 min (Fig. 9.11).
Hypervascular malignant liver lesions (HCC, leiomyo- sarcoma, angiosarcoma, islet-cell tumors) may be indis- tinguishable from small hemangiomas, and considera- tion of the clinical history is a subjective criteria that may have to be applied. The absence of a central scar in an otherwise mass lesion appearing like a giant heman- Fig. 9.11E–H
Fig. 9.12A–F. Giant liver hemangioma. T2-W HASTE (TE 90 ms) (A,B), arterial phase, gadolinium-enhanced, T1-W spoiled GRE (C,D), and delayed (5 min) gadolinium-enhanced T1-W spoiled GRE (E,F). The liver demonstrates a giant hemangioma in the right liver lobe with a central scar showing high SI on T2-WI and absent gadolinium enhancement (type 3). The giant hemangioma
demonstrates peripheral nodular gadolinium enhancement (C,D), followed by a centripetal progression on delayed gadolinium- enhanced T1-W images (E,F). The smaller hemangioma in the left lobe reveals a type-1 enhancement pattern with early uniform high signal enhancement (D) and homogeneous filling on delayed T1-WI (F)
gioma should raise concern, and a biopsy may be required (Fig. 9.12). Large hemangiomas may rarely hemorrhage or compress the adjacent portal vein, resulting in transient increased enhancement on imme- diate post-gadolinium images secondary to an autoreg- ulatory increased hepatic arterial blood supply.
Hepatobiliary contrast agents demonstrate similar patterns of signal enhancement following bolus injec- tion, as is feasible with MultiHance or Gd-EOB-DTPA.
Iron oxides show a decrease in SI on heavily T2-WI (Fig. 9.34), and dynamic imaging with Resovist again shows similar signal patterns as described for T1-W gadolinium-enhanced images (signal increase) and a reversed pattern (signal decrease) on T2 or T2*-WI.
The blood-pool agent Sinerem also results in a signal
increase on T1-WI and a signal decrease on early T2- WI.
9.6.3
Focal Nodular Hyperplasia
Focal nodular hyperplasia (FNH) is more frequently diagnosed in women (80%–90%) than in men (10%–20%). The tumor contains hepatocytes, bile-duct elements, Kupffer cells, fibrous stroma, and frequently possesses a central scar. Hemorrhage is very rare, and the lesion has no malignant potential. The typical signal pattern on plain MR imaging is either slightly lower SI on T1-WI and a slightly higher SI or isointensity on T2-
Fig. 9.13A–D. Focal nodular hyperplasia with central scar. Plain T1-W spoiled GRE (A), T2-W TSE (TE 165 ms) (B), arterial phase, gadolinium-enhanced, T1-W spoiled GRE (C), and portal venous phase, gadolinium-enhanced, T1-W spoiled GRE (D). The liver demonstrates an isointense lesion in the left liver lobe compared with liver on T1-W spoiled GRE and hypointense compared with
liver on T2-W TSE. A central scar is visible (hypointense on T1-W spoiled GRE and hyperintense on T2-W TSE). The lesion strongly enhances on arterial phase, gadolinium-enhanced, T1-W spoiled GRE with persistent enhancement on portal venous phase, gado- linium-enhanced, T1-W spoiled GRE
WI than normal liver parenchyma (Fig. 9.13). The cen- tral scar is a relatively characteristic feature with high SI on T2-WI, but is only present in one-third of patients (Fig. 9.14).
Gadolinium-enhanced MR imaging is useful for the detection and characterization of FNH with a strong uniform blush on arterial phase, gadolinium-enhanced, T1-W spoiled GRE images, also with rapid fading of enhancement within less than 60 s (Figs. 9.13 and 9.14).
A low SI central scar may enhance over time.
Hepatobiliary agents enhance FNH, similar to adeno- mas, reflecting the presence of well-differentiated hep-
atocytes with well-differentiated HCC or early dediffe- rentiation as a differential diagnosis (Fig. 9.15).
All iron oxides are effective for the characterization of FNH on T2-W accumulation-phase images because of phagocytic cells within the tumor, resulting in a sig- nal decrease. Therefore, lesions are less visible on SPIO- enhanced accumulation phase images than on plain images. Additional information for lesion characteriza- tion may be obtained by dynamic imaging with bolus injectable Resovist mimicking dynamic gadolinium- enhanced MR on T1-WI.
Fig. 9.14A–D. Focal nodular hyperplasia. Plain T1-W spoiled GRE (A), T2-W TSE (TE 165 ms) (B), arterial-phase gadolinium- enhanced T1-W spoiled GRE (C), and portal venous-phase gado- linium-enhanced T1-W spoiled GRE (D). The liver demonstrates two lesions in the left liver lobe (ventral) and right liver lobe (dor- sal), which are isointense compared with liver on T1-W spoiled
GRE and hypointense compared with on T2-W TSE. Only the larg- er lesions demonstrate a central hyper-intense scar on T2-W TSE.
Both lesions strongly enhance on arterial-phase gadolinium- enhanced T1-W spoiled GRE with isointensity on portal venous phase gadolinium-enhanced T1-W spoiled GRE
9.6.4 Adenoma
Liver adenomas have a strong association with oral contraception, and more than 90% are found in young women. Necrosis and hemorrhage, which may be life threatening, are common causes of pain. Adenomas may contain fat, intracellular glycogen, may present with a thin pseudocapsule, and show a loose architec- ture. They are primarily derived from hepatocytes. This explains why adenomas vary in signal from hypoin- tense to hyperintense (fat content) on T1-WI and are typically slightly hyperintense on T2-WI. Some adeno- mas are almost isointense to normal liver. Fat-contain- ing adenomas demonstrate a signal decrease on out-of- phase images, and hemorrhage causes mixed signal patterns. Gadolinium-enhanced MR imaging shows a
strong transient blush on arterial phase, gadolinium- enhanced, T1-W spoiled GRE images, also with rapid vanishing of enhancement within less than 60 s.
Hepatobiliary agents enhance adenomas, similar to FNH, reflecting the presence of well-differentiated hep- atocytes within the tumors, again with well-differen- tiated HCC or early dedifferentiation as a differential diagnosis.
Iron oxides again show a similar pattern as described for FNH and observed for regenerating nod- ules and adenomatous hyperplasia with a signal decrease on T2-W accumulation phase images (Fig. 9.3). Additional information for lesion character- ization may be obtained by dynamic imaging with bolus injectable Resovist mimicking dynamic gadolin- ium-enhanced MR on T1-WI.
Fig. 9.15A–C. Focal nodular hyperplasia with Teslascan. T2-W TSE (A), plain T1-W spoiled GRE (B), and delayed manganese- enhanced T1-W spoiled GRE (C). The lesions demonstrate a typi- cal signal pattern on unenhanced images (A,B) and persistent enhancement on delayed T1-WI due to hepatocellular uptake of manganese. (Courtesy of W. Schima, Vienna, Austria)
9.6.5 Metastases
Metastases are typically hypointense on T1-WI and moderately hyperintense on T2-WI. The lesion border may be either irregular or sharp, and the lesion shape can be irregular, oval, or round. Hemorrhage may result in hyperintense lesions on T1-WI and hypointense lesions on T2-WI. Coagulative necrosis (colorectal metastases) results in a hypointense lesion center and hyperintense periphery (viable tumor) on T2-WI.
Mucin-producing tumors demonstrate high SI on T2.
Hypovascular metastases (Fig. 9.10) represent the vast majority (colorectal) of metastases, and the perfu-
sion pattern is based on a diminished blood supply.
Thus, similar to CT, lesions are typically best detected on the portal-venous gadolinium-enhanced T1-WI (Fig. 9.16). Plain images typically show low SI on T1-WI and slightly higher SI or almost isointensity on T2-WI.
Metastases with large amounts of liquefactive necrosis may appear as cystic lesions with a signal void on immediate gadolinium-enhanced T1-WI. A peripheral enhancement is common on portal venous phase and delayed T1-WI. Typically, peripheral ring enhancement begins on immediate contrast-enhanced images with potential enhancement towards the center of the lesion and peripheral wash-out on delayed T1-WI (Fig. 9.16).
It has been demonstrated that the perilesional enhance-
Fig. 9.16A–H. Hypovascular metastases. Two sections of each T2- W HASTE (TE 64 ms) (A,B), plain T1-W spoiled GRE (C,D), arte- rial phase, gadolinium-enhanced, T1-W spoiled GRE (E,F), and portal venous phase, gadolinium-enhanced, T1-W spoiled GRE (G,H) of a patient with a colorectal carcinoma and a probable lesion diagnosed within the right liver lobe at ultrasound. The sec-
tions demonstrate multiple metastases with a necrosis visible on T2-WI. Contrast enhancement clearly improves lesion conspicu- ity, and more lesions are detected than on T2-WI. Most metastases show peripheral ring enhancement with a wash-out on portal venous phase images, suggestive of malignancy. Some metastases demonstrate wedge-shaped perfusion phenomena
ment of metastases on early gadolinium-enhanced MR images correlates with histopathologic hepatic paren- chymal changes, which include peritumoral desmoplas- tic reaction, inflammatory cell infiltration, and vascular proliferation. Large colorectal metastases (Fig. 9.19) may show an additional inhomogeneous ‘cauliflower enhancement’. These enhancement features are also observed with dynamically scanned, liver-specific con- trast agents.
A variety of primary malignancies frequently cause hypervascular metastases (pheochromocytoma, renal cell, islet cell, carcinoid, leiomyosarcoma, thyroid, or melanoma). Hypervascular metastases (Fig. 9.17) may appear with high signal on T2-WI, comparable to hemangiomas, and show an intense peripheral ring enhancement with a potentially progressing centripetal enhancement. Small hypervascular metastases vary in contrast enhancement with immediate and often com-
plete lesion enhancement. The different melanin con- tent of melanoma metastases causes different hyperin- tense/hypointense patterns on T1-WI and T2-WI, because the paramagnetic property of melanin presents hyperintense on T1-WI (Fig. 9.18). Dynamic gadolin- ium-enhanced MR imaging is particularly useful for the detection and characterization of hypervascular liver lesions with immediate ring type, uniform, or irregular enhancement and subsequent wash-out effects. The absence of nodular enhancement within the enhancing ring type periphery, the uniform thickness of the enhancing ring, and the peripheral wash-out help to differentiate malignant lesions from hemangiomas, which also show enhancement over a longer period of time.
One of the major advantages of liver-specific contrast agents is the improved detection of hypovascular liver metastases as compared with gadolinium-enhanced Fig. 9.16E–H.
Fig. 9.17A–H. Hypervascular islet-cell tumor metastases and pan- creatic tumor. Two sections of each plain T1-W spoiled GRE (A,B), T2-W HASTE (TE 64 ms) (C,D), arterial phase, gadolinium- enhanced, T1-W spoiled GRE (E,F), and portal venous phase, gad- olinium-enhanced, T1-W spoiled GRE (G,H) of a patient with an islet-cell tumor of the pancreas and multiple hypervascular liver metastases. The sections in the left column demonstrate a large
hypervascular metastasis in the lateral segment of the left liver lobe with a necrotic area. A small metastasis is visible in the later- odorsal right liver lobe. Both lesions show a strong arterial phase gadolinium enhancement and high SI on T2-W images. The pan- creatic tumor is shown in the right column with central high SI on T2-WI (D) and good conspicuity on gadolinium-enhanced imag- es (F,H)
Fig. 9.17G, H.
Fig. 9.18A,B. Melanoma metastasis. T1-W spoiled GRE (A) and T2-W HASTE (TE 90 ms) (B) images reveal a small hyperintense lesion in segment 5 of the right liver lobe in a patient with malignant melanoma
Fig. 9.19A–B.
Fig. 9.19A–H. Liver metastases with SPIO. Plain T1-W spoiled GRE (A), plain T2-W HASTE (TE 90 ms) (B), plain PDW spoiled GRE before (C) and 10 min following (D) i.v. injection of 1.4 ml Resovist, and dynamic T1-weighted spoiled GRE images at multi- ple time points following injection (E 30 s, F 70 s, G 2 min, and H 5 min) in a patient with colorectal cancer and a large liver metas- tasis within the right liver lobe as diagnosed by ultrasound.
Tumor-liver contrast and lesion conspicuity significantly increase
on Resovist-enhanced PDW-GRE (D), and an additional lesion is now clearly visible near the confluence of the hepatic veins into the inferior vena cava. Dynamic T1-WI show increased and persis- tent signal enhancement within vessel demarcating lesions as known from contrast-enhanced CT or gadolinium-enhanced MRI. Lesion contrast decreases over time with decreasing liver sig- nal (G,H)
