MR

The most dangerous consequence of portosystemic shunting is bleeding from esophageal varices (Fig. 105-3). Varices may be identified within the esophageal wall (termed esophageal varices) or surrounding the esophagus (termed paraesophageal varices), although both drain the portal system via the left gastric (cardinal) vein. Additional common sites of variceal formation within the abdomen due to portosystemic shunting include gastric and retroperitoneal varices, spontaneous splenorenal shunts, and recanalized paraumbilical veins. Recanalized paraumbilical veins drain into the epigastric veins along the undersurface of the abdominal wall, often forming a mesh of dilated varices surrounding the umbilicus termed caput medusa (Fig. 105-4). Identification of paraumbilical varices are important in that the draining meshwork of superficial veins along the anterior abdominal wall must be avoided during diagnostic and therapeutic paracenteses that are often performed in patients with chronic liver disease. Although less common, intrahepatic portosystemic (venovenous shunts) may also occur in the setting of chronic liver disease as a result of increased portal resistance. These shunts have been described at the microscopic level⁷ and can also be identified with MR (Fig. 105-5). Other etiologies of intrahepatic portosystemic shunting include congenital malformations and rupture of a portal vein aneurysm into a hepatic vein, whereas post-traumatic shunts are most often associated with surgical interventions such as transhepatic catheter placement.

FIGURE 105-3 Esophageal and paraesophageal varices. Axial 3D GRE images (A, B) demonstrate enlarged venous structures contained within (arrowhead) and also surrounding (arrow) the esophageal wall. Coronal 3D GRE image (C) again demonstrates extensive paraesophageal varices at the gastroesophageal junction, a cause of major morbidity and mortality in the setting of portal hypertension.

FIGURE 105-4 Recanalized paraumbilical vein and caput medusa. Axial 3D GRE (A) and MIP images (B) demonstrate an enlarged, recanalized paraumbilical vein (arrow), which drains to a large meshwork of superficial veins (arrowheads) surrounding the umbilicus (C). Coronal 3D GRE image (D) again demonstrates this site of portosystemic shunting, whereas coronal T2W image (E) provides an alternate “black-blood” method for vascular analysis.

FIGURE 105-5 Veno-venous (intrahepatic) shunt. Anomalous connection (arrows) between the enlarged portal vein (arrowheads) and the IVC is well demonstrated on delayed postcontrast 3D GRE images (A), and a noncontrast TFISP image (B) also clearly demonstrates the shunt (arrow).

In addition to portosystemic shunting, chronic liver injury and fibrosis also causes arterioportal shunting, either secondary to underlying tumor (hepatocellular carcinoma) or cased by the parenchymal changes of fibrosis itself. These arterioportal shunts manifest on MR as small, linear- or wedge-shaped blushes of enhancement on arterial phase imaging, most often located along a capsular surface (Fig. 105-6). These foci of enhancement may be mistaken for a small tumor on CT owing to a relative lack of contrast resolution. However, MRI can more easily differentiate these small arterioportal shunts (APS) from hepatocellular carcinoma (HCC) in the majority of cases because the APS will show a more linear- or wedge-shaped morphology and will not demonstrate the washout and rim enhancement typical of HCC. Arterioportal shunts may also occur in settings other than chronic liver disease, such as trauma, iatrogenic (postbiopsy or surgery), congenital anomalies, or aneurysm rupture.⁸ APS are associated with both benign (hemangiomas) and malignant (HCC) hepatic tumors.⁹ APS also contribute to the flow changes seen in portal hypertension. Studies examining flow characteristics in the portal vein with intermittent occlusion of the hepatic artery have demonstrated that APS are a factor in hepatofugal flow of the portal vein in the setting of chronic liver disease.¹⁰

FIGURE 105-6 Arterioportal shunts. Arterial phase 3D GRE images (A, C) demonstrate non–mass-like, peripheral blushes of arterial enhancement (arrows). These areas become isointense on delayed 3D GRE images (B, D), without washout or rim enhancement that would be expected with hepatocellular carcinoma. These findings are in keeping with small vascular perfusion anomalies.

Medical

Medical treatment consists of managing the patient’s fluid and nutritional status, in addition to treating underlying causes such as hemochromatosis and Wilson’s disease.

Surgical/Interventional

Transjugular intrahepatic portosystemic shunts are often placed to decompress the portal circulation, with less morbidity and mortality than surgically created shunts. The treatment of choice for decompensated cirrhosis is liver transplantation.

KEY POINTS

Causes of portal hypertension include prehepatic, intrinsic, and posthepatic causes.

Vascular changes include dilation of the portal and mesenteric vasculature with development of portosystemic collateral vessels.

MRI can evaluate the underlying hepatic parenchymal abnormalities in addition to vascular changes of portal hypertension.

Clinical Presentation

Clinical presentation may be acute or chronic and involves nonspecific symptoms such as abdominal pain, nausea, vomiting, and anorexia. As such, imaging plays a key role in the diagnosis.

MR

Intraluminal thrombus within the SMV is well demonstrated on MRI with 3D GRE images, providing a noninvasive method for diagnosis (Fig. 105-7). In addition, evaluation of the end-organ effects of mesenteric occlusion is important because the clinical picture varies between acute and chronic presentations, and not all patients require surgery. Bowel pathology can be evaluated concurrently with the vasculature using MRI, with ischemia demonstrating increased signal on fat-saturated T2W images secondary to inflammation and edema caused by venous congestion. The presence of bowel ischemia as identified by MR may prompt more aggressive therapy, with both percutaneous and intraoperative catheter-directed therapy demonstrating good results.¹¹ Thrombosis of the splenic vein is a cause of isolated gastric varices and has been treated with splenectomy in the past, although percutaneous therapy has also been successful.

FIGURE 105-7 Cavernous transformation of the portal vein. Coronal (A) and axial (B) 3D GRE images demonstrate low-signal intensity thrombus (arrow) in the portal vein, with the development of multiple, serpiginous venous collaterals (arrowheads) extending into the liver hilum.

From Clinical Presentation

Due to nonspecific symptomatology, the differential diagnosis is often quite broad on a clinical basis.

From Imaging Findings

Evaluation with postcontrast 3D GRE sequences allows direct identification of intraluminal thrombus within the SMV and portal vein, allowing for a specific diagnosis.

Medical

Medical therapy includes supportive care and identification and treatment of the underlying cause. In addition, patients receive systemic anticoagulation with follow-up imaging. Systemic thrombolytic therapy is not widely employed.

Surgical/Interventional

Surgical clot decompression is performed in cases with an acute, life-threatening presentation, with signs of bowel infarction or peritonitis. This also allows the resection of infarcted segments of bowel. However, percutaneous therapy with catheter-directed thrombolysis has also been performed with good results in patients without symptoms of bowel perforation, either alone or with surgical assistance.

KEY POINTS

Due to nonspecific clinical symptoms, imaging is critical for the diagnosis of portal and mesenteric thrombus.

MRI (including postcontrast 3D GRE images) is well-suited for identification of the intraluminal thrombus and the end-organ effects of mesenteric occlusion.

Portal thrombosis often occurs in the setting of chronic liver disease owing to altered flow dynamics.

Clinical Presentation

Vascular invasion by tumor again produces nonspecific symptoms that are often identical to bland thrombus, again emphasizing the importance of imaging in the diagnosis. Patients will often present with predisposing factors such as cirrhosis, viral infection, or chronic biliary obstruction.

MR

MRI has been shown to be highly sensitive and specific for HCC,¹² a tumor that is strongly associated with chronic liver disease. In the well-defined, focal type of HCC, defined MR features include an arterial enhancing lesion that demonstrates washout with rim enhancement on delayed images. The tumor washes out to become hypointense to adjacent liver parenchyma, a direct result of the differential vascular supply between tumor (fed primarily by hepatic artery) and adjacent liver parenchyma (fed primarily by portal vein). T2 signal, if elevated, supports the diagnosis, although this is not a necessary feature. These imaging features are distinct from intrahepatic cholangiocarcinoma (IHC), the second primary hepatic malignancy that tends to invade hepatic vasculature. MRI is also the imaging modality of choice for the evaluation of IHC. After the administration of gadolinium chelate, the tumor does not avidly enhance on arterial phase images, but demonstrates gradual accumulation of contrast on delayed imaging, likely due to leakage of gadolinium into the interstices of the tumor over time. IHC is usually associated with ill-defined T2 signal, and at least some degree of biliary ductal dilation is usually present. Both of these neoplasms invade intrahepatic portal and hepatic venous branches, a finding especially common in the infiltrative type of HCC. The distinction between tumor thrombus and bland thrombus in the setting of these neoplasms is important, especially in the setting of HCC when liver transplantation is considered. The diagnosis of tumor thrombus can be made with the use of 3D GRE sequences. Bland thrombus has no associated vascularity and will not have any signal on postgadolinium imaging, producing images of a black clot. Tumor thrombus, alternatively, will take up gadolinium on delayed imaging, which can be easily demonstrated with comparison to precontrast images. Any enhancement within a thrombus associated with these tumors is indicative of vascular tumor invasion (Fig. 105-8).

FIGURE 105-8 Hepatocellular carcinoma with vascular invasion. An ill-defined hepatic tumor is demonstrated on axial postcontrast 3D GRE (A), with coronal 3D GRE images showing thrombus (arrows) extending into the hepatic veins and IVC (B). This clot shows enhancement after Gd administration in keeping with tumor thrombus. Vascular involvement is also well demonstrated on coronal T2W image (C), with loss of normal signal void secondary to tumor thrombus extending into the right atrium.

Medical

For unresectable disease, chemotherapy is the mainstay of medical treatment, in addition to supportive care.

Surgical/Interventional

HCC meeting the Milan criteria is treated with liver transplantation, whereas unresectable disease is often managed in a palliative manner by percutaneous chemo-embolization. The treatment of choice for cholangiocarcinoma is resection, although extensive portal and mesenteric tumor invasion will likely exclude surgery.

KEY POINTS

Tumor thrombus demonstrates enhancement on postcontrast 3D GRE images, as opposed to bland thrombus which appears black.

Hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (IHC) are the two primary liver neoplasms associated with portal vein invasion.

HCC and IHC have very different imaging and perfusion characteristics on MRI, allowing clear differentiation between the tumor types in the majority of cases.

Clinical Presentation

Liver transplantation is the treatment of choice for patients with end-stage liver disease, and is also intended as a curative procedure for patients with HCC meeting specific imaging criteria.¹³ Patency of the portal and mesenteric vasculature is critical in the pretransplant cirrhotic patient because portal thrombosis will hasten liver failure. In addition, extension of thrombus into the SMV directly affects the technical feasibility of liver transplantation. If the patent portion of the SMV is large enough, the surgeon may attempt an interposition graft from the SMV to the transplanted liver. If, however, the patent SMV tributaries are small or replaced by varices, liver transplantation is not technically feasible. MRI is an excellent technique to evaluate mesenteric thrombosis and the technical feasibility of transplantation, providing accurate evaluation of vessel size and varices.

MR

MR has been shown to be equivalent to CTA in the preoperative evaluation of hepatic vascular anatomy,¹⁴ but with the added benefits of improved parenchymal soft tissue evaluation compared to CT and also the lack of ionizing radiation, an especially important issue in the pediatric population. Of note, liver transplantation is usually performed with intent to cure and not as a palliative procedure. In this setting, cumulative radiation dose is a consideration, especially in patients with chronic liver disease who undergo surveillance imaging. MRI provides a superior imaging modality for evaluation of parenchymal and vascular changes associated with liver disease without contributing to cumulative radiation doses in a patient set to undergo curative surgery.

MRI performs quite well in the vascular assessment of the postoperative transplanted liver. In the immediate postoperative setting, complex and hemorrhagic blood products are often identified in and around the surgical bed. The most serious immediate postoperative complication is hepatic artery thrombosis, which occurs at variable rates from 3% to 9% and is more common with LDLT in centers with less experience.¹⁵ MRI not only directly detects hepatic artery thrombosis (HAT), but also the resultant changes in the hepatic parenchyma related to arterial devascularization. The consequences of acute hepatic artery thrombosis are severe and often require retransplantation to avoid graft loss. More commonly, HAT results in defined biliary complications because the sole vascular supply of the biliary system is via the hepatic artery in graft livers. These biliary complications include ductal dilation, biloma formation, and sepsis secondary to a resultant cholangitis (Fig. 105-9). MRI can also demonstrate the acute hepatic inflammation that is associated with bile stasis and infection¹⁶ better than any other imaging modality. Thromboses of the IVC, hepatic and portal veins are less common complications, but also are well assessed with 3D GRE imaging. Another rare vascular complication is the splenohepatic arterial steal syndrome. This is characterized by arterial malperfusion and ischemic damage of the hepatic graft caused by diversion of blood flow to a markedly enlarged spleen. Splenohepatic arterial steal syndrome may ultimately result in graft loss if it is recognized too late. A post-transplantation splenectomy represents a successful therapeutic approach for this condition. Even in the absence of pathology, a transplanted liver may be identified with MR by reproducible mild narrowing at the IVC and portal vein anastomosis with mild susceptibility artifact at the IVC anastomosis (Fig. 105-10).

FIGURE 105-9 Hepatic artery thrombosis (HAT) and resultant parenchymal abscess postorthotopic liver transplantation. Coronal (A) fat suppressed T2W HASTE images show a large, complex intrahepatic fluid collection. The etiology of this abscess is demonstrated on postgadolinium 3D GRE arterial phase MIP images (B), showing occlusion of the hepatic artery (arrow). A second case of HAT with resultant intrahepatic biliary ductal dilation (C, arrowheads) and biloma formation (D, arrow) is clearly demonstrated on axial 3D GRE image. Hepatic artery thrombosis (arrow) is confirmed on CE 3D GRE MIP image (E).

FIGURE 105-10 Normal post liver transplant MR. Susceptibility artifact is seen at the IVC anastomosis on 2D T1 FLASH (A, arrow) image due to prior transplant, resulting in mild, expected narrowing of the IVC at this site on postcontrast 3D GRE (B, arrowhead) image. Coronal 3D GRE (C) of a normal post-transplant liver also shows mild narrowing at the portal vein anastomosis (arrowhead), and the transplant hepatic parenchyma demonstrates normal perfusion. Residual changes of portal hypertension, including an enlarged spleen, persist.

KEY POINTS

Liver transplantation is the treatment of choice for patients with end-stage liver disease and HCC meeting specific criteria.

Thrombosis of the portal vein and SMV will directly affect the feasibility of transplantation, and preoperative imaging is critical.

Hepatic artery thrombosis is an important post-transplant complication that results in biliary necrosis.

Clinical Presentation

Budd-Chiari may manifest acutely with fulminant hepatic failure, encephalopathy, and ascites, with biopsy demonstrating rapid hepatocellular necrosis. However, in the majority of cases, the presentation is subacute or chronic in nature because some hepatic venous outflow may be preserved by draining through a variety of accessory hepatic veins. These patients present with more advanced changes of cirrhosis and chronic liver disease, with a more gradual onset of symptomatology from portal hypertension.

MR

The diagnosis of Budd Chiari depends on evaluation of the hepatic venous outflow system in addition to the associated parenchymal changes, and MR is the modality best suited for evaluation of both areas. Evaluation of the venous system is performed with postcontrast 3D GRE sequences in axial and coronal planes. Venous patency can also be assessed on additional imaging sequences, such as evaluating vascular signal on TFISP imaging and “black blood” flow void on T2W images. The ability to assess vessel patency on additional imaging sequences provides an inherent level of redundancy within the image acquisition that contributes to the high sensitivity and specificity of MR compared to CT. Parenchymal changes in Budd-Chiari are also well evaluated with MR. The most consistent feature is marked hypertrophy of the caudate lobe (sometimes quite massive) due to its separate drainage into the IVC, thus sparing the caudate from the effects of venous outflow obstruction (Fig. 105-11). In the acute setting, the liver is usually enlarged secondary to edema, whereas in the chronic setting there is atrophy of the peripheral aspects of the liver and sparing of the caudate. Postcontrast 3D GRE images demonstrate decreased perfusion of the peripheral aspects of the liver secondary to altered flow dynamics induced by liver injury. An additional parenchymal finding is the presence of focal nodules in the liver parenchyma. These nodules are termed “large regenerative nodules” or “multiacinar regenerative nodules”¹⁸ and correlate to nontumorous liver parenchyma surrounded by variable amounts of fibrous stroma.¹⁸ These nodules characteristically show no distinctive enhancement features compared with adjacent liver parenchyma or arterial phase images.

FIGURE 105-11 Hepatic changes of Budd Chiari. Axial fat-saturated T2 HASTE images (A, B) demonstrate massive enlargement of the caudate lobe (A, arrows). Patchy increased T2 signal is present along the periphery of the liver (B, arrowheads) due to hepatic congestion and edema, with relative sparing of the more central portions of the liver. Saturation-recovery postcontrast Turbo FLASH (C) demonstrates no enhancement of the occluded hepatic veins and intrahepatic IVC.

From Clinical Presentation

Other etiologies for acute, fulminant hepatic failure and chronic liver disease are clinical considerations, but can often be excluded with imaging.

From Imaging Findings

The diagnosis of Budd-Chiari should be differentiated from a distinct entity termed hepatic veno-occlusive disease. Seen most often in the post–stem-cell transplant setting, this is an inflammatory process that results in the destruction of the vascular endothelium of the hepatic venules.

Medical

Supportive care and aggressive treatment of any underlying causes are the mainstay of medical management. Anticoagulation with heparin followed by warfarin is also employed

Surgical/Interventional

Because a large majority of these patients present with advanced-stage liver disease and portal hypertension, liver transplantation is usually the only effective treatment, although placement of a TIPS may allow for a bridge to transplantation. Some centers have performed TIPS and catheter-directed thrombolysis in specific clinical scenarios.

KEY POINTS

Hepatic venous outflow obstruction results in sinusoidal congestions and liver injury.

Vascular patency and underlying parenchymal changes are best evaluated with MRI, including changes of portal hypertension.

Liver transplantation is the treatment of choice.

Clinical Presentation

Patients may present with vague clinical symptomatology, but acute rupture leads to hemodynamic instability and substantial perioperative morbidity and mortality, underscoring the importance of therapy at the time of diagnosis, even if the patient is asymptomatic.¹⁹

MR

MRI is highly sensitive for the detection of splanchnic artery aneurysms, which may be detected on CE 3D MRA or 3D GRE imaging. 3D GRE images better depict the aneurysm wall and associated thrombus, and are more helpful for distinguishing true from false aneurysms. Important preoperative information that is depicted with MR includes the type and location of the aneurysm, diameter and extent along the vessel, involvement of branch vessels, presence of mural thrombus, and whether the aneurysm has already ruptured.²¹ Morphologic imaging, including T2W images and TFISP, are also important for aneurysm assessment. Hepatic and gastroduodenal aneurysms may manifest with obstructive jaundice secondary to compression of the biliary tree, which is demonstrated well with T2W images (Fig. 105-13). Mycotic aneurysms show perianeurysmal inflammation, which is depicted as surrounding high signal on fat-suppressed T2W images.

FIGURE 105-13 Gastroduodenal pseudoaneurysm. Coronal single-shot T2 HASTE (A) demonstrates a complex rounded mass (arrow) with hypointense signal at the periphery due to blood products. T2W images also show compression of the common bile duct by the mass (arrowhead), causing intra and extrahepatic biliary ductal dilation. Coronal CE 3D MRA MIP image (B) shows the irregular, bilobed pseudoaneurysm arising from the gastroduodenal artery, with shunting of blood from a branch of the superior mesenteric artery (arrow). The MRA source image (C) better demonstrates the peripheral, thrombosed portions of the aneurysm. 3D GRE images (D) not only demonstrate the patent lumen (arrow), but also best demonstrate the wall and extensive mural thrombus.

Differential Diagnosis from Clinical Presentation

Other etiologies of gastrointestinal bleeding, such as angiodysplasia, diverticulitis, or carcinoma may be considered clinically.

Medical

Medical therapy includes supportive management and blood transfusions in the case of active hemorrhage.

Surgical/Interventional

Because the natural course of splanchnic artery aneurysms (especially pseudoaneurysms) may lead to rupture, MRI is critical in providing the correct diagnosis to prompt therapy and treatment planning. Although therapy is clearly mandated in patients with asymptomatic aneurysms or contained rupture (pseudoaneurysms), the following asymptomatic lesions also warrant intervention: (1) splenic artery aneurysms in patients with the potential to become pregnant or requiring liver transplantation; (2) common or proper hepatic artery aneurysms in patients with polyarteritis nodosa or fibromuscular dysplasia; and (3) splenic or hepatic artery aneurysms greater than 2.0 cm in diameter.²² Percutaneous treatment with aneurysm coiling has demonstrated excellent results compared to surgery and should be the first line of therapy.

KEY POINTS

Splanchnic artery aneurysms are divided into true (congenital) or pseudoaneurysms (secondary to vessel wall disruption).

MRA best evaluates the patent aneurysm lumen, whereas postcontrast 3D GRE images provide information about the vessel wall and mural thrombus.

Prompt therapy (either percutaneous or surgical) is necessary for pseudoaneurysms and certain true aneurysms.

Clinical Presentation

Patients with pancreatic adenocarcinoma present with vague clinical symptoms that are often silent early in its course, leading to an advanced stage at final diagnosis. Symptoms arise due to mass effect from the tumor on the biliary system, causing obstructive jaundice (often painless). Acute pancreatitis, on the other hand, manifests with abdominal pain and anorexia, and there is often a history of alcohol abuse or gallstones.

Imaging Indications and Algorithm

MRI of the pancreas continues to evolve with improvement in rapid-acquisition breath-hold or breathing-independent imaging techniques. MR should be considered essential in the imaging evaluation of pancreatic disease, and particularly for optimal presurgical identification, characterization, and staging of pancreatic masses. High resolution CE 3D MRA can easily define arterial vascular anatomy for presurgical planning, and MR assessment of vascular infiltration by tumor reaches a sensitivity and specificity of 83% and 96%, respectively, comparable to CT and endoscopic sonography evaluation.²³ MR also offers concurrent, superior, soft tissue imaging that defines tumor size, invasion into adjacent soft tissue structures, pancreatic and biliary ductal obstruction, and also venous invasion by tumor.

MR

The most common presentation is that of biliary ductal obstruction from tumor in the pancreatic head, at which point assessment of the adjacent portal vein, SMV and SMA are critical if surgical resection is attempted. Evaluation depends on a combination of the coronal MRA source data and 3D GRE images. Vascular tumor infiltration is assumed on the basis of either vessel caliber reduction, vessel encasement (90% circumferential involvement) or vessel occlusion.²⁴ Extensive vascular collaterals may also be demonstrated. Pancreatic adenocarcinoma may also arise within the tail, typically presenting as a larger mass with local infiltration (Fig. 105-14) that commonly encases or occludes the splenic vein, and may invade the splenic hilum, leading to extensive infarction of the spleen.

FIGURE 105-14 Pancreatic adenocarcinoma. Axial TFISP (A) demonstrates a focal mass (arrow) in the pancreatic tail, whereas arterial phase 3D GRE (B) images show the tumor (arrow) has poor vascular perfusion, a finding consistent with poorly differentiated adenocarcinoma. Tumor obliterates the adjacent splenic vein (arrowheads). Splenic vein invasion is also well depicted on coronal 3D GRE (C) and axial 3D GRE MIP image (D, arrow).

Although pancreatic adenocarcinoma is an infiltrative tumor that invades adjacent vasculature, there are several additional pancreatic neoplasms that may compress the splanchnic vasculature owing to overall size and morphology. These include cystic neoplasms of the pancreas, either serous cystadenomas, or mucinous cystadenomas/cystadenocarcinomas. If occurring in the pancreatic head, they more commonly cause compression of the biliary tree, but occasionally these lesions can also compress local vessels, especially the portal confluence. Differentiation of tumor type, in addition to assessment of vascular involvement, is best performed with MR.

Inflammatory processes of the pancreas also commonly involve the adjacent vasculature. This is seen in the setting of acute pancreatitis, which is a well-known cause of splenic vein thrombosis (Fig. 105-15), and has also been reported in at least 20% of patients with chronic pancreatitis. Occlusion of the splenic vein is often seen in association with collateralized venous flow into extensive peripancreatic and perisplenic varices. Splenic vein thrombosis is also a well-known cause of isolated gastric varices, and less commonly a cause of esophageal or colonic varices. Postcontrast 3D GRE imaging is the best sequence for depiction of splenic vein thrombosis and associated collateral flow from varices. The splenic artery may also be secondarily involved in cases of severe pancreatitis, with the formation of aneurysms and pseudoaneurysms secondary to vascular endothelial breakdown from the adjacent inflammatory process. Pseudocysts may erode into the adjacent splenic artery or vein, causing life-threatening episodes of hemorrhage.

FIGURE 105-15 Acute pancreatitis. Peripancreatic edema is present on axial fat-suppressed T2W HASTE (A), whereas precontrast 3D GRE (B) image shows loss of the normal increased pancreatic T1 signal. Postgadolinium 3D GRE (C) shows a narrowed portal vein confluence (arrowhead) and thrombosis of the splenic vein (arrow).

In addition to the identification of vascular involvement, MR is also able to delineate parenchymal changes of acute and chronic pancreatitis. Acute pancreatitis demonstrates edema and inflammation in and around the pancreas and retroperitoneum, manifested as increased signal on fat-saturated T2W images. Chronic pancreatitis, in contrast, shows loss of normal T1 signal within the pancreatic parenchyma, and persistent enhancement on delayed imaging secondary to fibrosis. Additional morphologic images are helpful for diagnosing the etiology of the pancreatitis, such as from stone disease or tumor. Evaluation of the parenchymal and vascular changes of acute and chronic pancreatitis in the same imaging examination provides a comprehensive evaluation that is important for diagnosis and clinical management.

From Clinical Presentation

Clinical symptoms are usually nonspecific, although painless jaundice is concerning for pancreatic adenocarcinoma.

From Imaging Findings

Focal pancreatitis at times may mimic an aggressive neoplasm, but evaluation of dynamic, contrast-enhanced MRI, in combination with fat-saturated T2W images, can make the correct diagnosis in the vast majority of cases.

Medical

Pancreatitis is treated with supportive care, especially fluid replacement. Chronic pancreatitis may require enzyme replacement.

Surgical/Interventional

The treatment of choice for pancreatic adenocarcinoma is a Whipple procedure, and preoperative MRI is important to establish resectability. Repetitive, chronic pancreatitis may require surgical drainage such as a Frey procedure to provide symptom relief.

KEY POINTS

The close relationship of the pancreas to the SMA, SMV, splenic and portal vein causes vascular compromise in a variety of pancreatic pathologies.

Vascular involvement is best demonstrated with a combination of MRA and 3D GRE images.

MRI also provides excellent soft tissue imaging which allows evaluation of the underlying neoplastic or inflammatory etiology.

Clinical Presentation

Splenic infarction is a relatively common occurrence, and at times, the acute event causes symptoms referable to the left upper quadrant. However, it is more frequently asymptomatic, with residual features seen only on future imaging studies.

MR

On MRI, splenic infarcts are seen as peripheral wedge-shaped or linear defects that exhibit decreased signal intensity on both T1W and T2W images. These areas show no internal perfusion after the administration of Gd, most clearly defined on delayed postcontrast images (Fig. 105-16). Complications of splenic infarctions include abscess, splenic pseudocyst formation, splenic rupture and hemorrhage—all features that are easily depicted with MRI. Rarely, the entire spleen may be infarcted, demonstrating diffuse low-signal intensity on T1W images, inhomogeneous high-signal intensity on T2W, and an enhancing capsule on postgadolinium images.

FIGURE 105-16 Splenic infarcts. Axial (A) and coronal (B) T2 HASTE images show a massively enlarged spleen with multiple peripheral, wedge-shaped areas of hypointense signal. These areas show no perfusion on axial (C) and coronal (D) postcontrast 3D GRE images. Also note the splenorenal shunt (C, arrowhead), another indication of portal hypertension in this cirrhotic patient.

Medical

Often supportive care is all that is necessary.

Surgical/Interventional

Surgical therapy may be considered in the case of a complete splenic infarction that has been secondarily infected, requiring resection or drainage.

KEY POINTS

Splenic artery branches are noncommunicating end arteries, with occlusion leading to segmental infarction.

Infarctions occur most often in the setting of splenomegaly and sickle cell disease.

MRI demonstrates a wedge-shaped perfusion defect that is highly specific for infarction. Complications of splenic infarction are also well evaluated with MRI.

Clinical Presentation

The skin, joints, gastrointestinal tract, kidneys, and nervous system are often simultaneously affected. PAN does not characteristically affect single vessels, although there have been reports of single intra-abdominal vessel involvement involving the hepatic and splenic arteries.

MR

The most characteristic finding on MRA is multiple small, peripheral aneurysms, tending to occur at branch points of the affected arteries due to necrosis of the internal elastic lamina of the small- and medium-sized arteries. Other less specific findings include arterial stenosis, thrombosis, and occlusion.

MR

Hepatic involvement occurs in 8% to 31% of cases, and MR images can identify hepatic AVMs and associated features, such as a prominent feeding hepatic artery, dilated portal and/or hepatic veins, and collateral supply involving the gastric, pancreaticoduodenal, splenic, mesenteric and renal vasculature. MR imaging is also used in the staging and follow-up of these abnormalities in patients with HHT.²⁷

AVMs can also uncommonly occur in the spleen. Reports of splenic AVMs have described patients presenting with massive diarrhea, ascites, abdominal pain, and signs of portal hypertension. MRI can demonstrate these lesions as multiple, serpiginous flow voids on T2W images and extensive, serpentine enhancement on 3D GRE images. Dilated feeding vessels in association with AVMs are also common, and are easily depicted on MR.²⁰

Imaging Indications and Algorithm

The role of MRI in patients with acute traumatic injury to the abdomen is less well defined, and CT remains the primary imaging modality in this scenario, primarily due to speed and ease of accessibility. However, MR may be useful in selected cases of traumatic injury. Settings that may benefit from an increased use of MR imaging include the pediatric population, in which trauma patients are often subject to pan-body CT in addition to multiple follow-up examinations. There is an increased lifetime radiation risk in children relative to adults, and the use of CT in the trauma setting may be overused, especially in the pediatric population.²⁸ Other clinical settings include that of underlying allergy to iodinated contrast, or in the setting of chronic renal disease. The risk of contrast-induced nephropathy (CIN) is an important consideration in patients with chronic renal disease. CIN occurs at a rate of approximately 3% in the general population, but increases to 12% to 33% with underlying diabetes and chronic renal disease. In addition, CIN nephropathy has been shown to correlate with increased morbidity and mortality, even if renal dysfunction is transient.²⁹ Consideration of MRI in selected cases such as these would limit patient morbidity induced by imaging and is also useful as a problem-solving modality.

MR

The spleen is the most commonly ruptured organ in blunt trauma, accounting for approximately 40% of abdominal organ injuries. The spleen is particularly susceptible to injury due to its complex ligamentous attachments and spongy parenchymal consistency. MR signal characteristics of splenic subcapsular or intraparenchymal hematomas include intrinsically increased T1 signal with decreased T2 signal secondary to the degradation products of hemoglobin. Splenic contusion and infarction are depicted as focal areas of hypoperfusion, with a lack of enhancement on postgadolinium GRE images.

MRI combined with MRA can also readily identify vascular complications of the abdominal vessels as a complication of different surgeries and procedures (Fig. 105-17). Bile duct injury in the setting of laparoscopic cholecystectomy is a well-known complication. Because biliary injuries sustained during laparoscopic cholecystectomy are known to occur more proximally compared to open cholecystectomy, a higher incidence of concomitant hepatic arterial injury has been described.³⁰ This complication is potentially lethal and often requires partial hepatectomy or liver transplantation. MRA and magnetic resonance cholangiography (MRCP) can be performed emergently in patients with a suspicion of biliary and vascular injury, allowing the simultaneous evaluation of both the biliary tree and the hepatic vascular supply in these patients.

FIGURE 105-17 Gastroduodenal (GDA) pseudoaneurysm, postresection of a pancreatic tail neuroendocrine tumor. Coronal T2W HASTE (A) shows a massive subcapsular liver hematoma with heterogeneous signal intensity. Postcontrast 3D CE MRA coronal (B) image demonstrates the patent lumen of a lobulated GDA pseudoaneurysm. The extent of the pseudoaneurysm is well depicted on postcontrast 3D GRE (C, arrow) image, with the surrounding hematoma that communicates with subcapsular hepatic space.

Medical

Supportive therapy with fluid resuscitation is important. Often, visceral organ injury may be managed with purely supportive care if the patient is hemodynamically stable.

Surgical/Interventional

Hemodynamic compromise will often prompt surgery, with the aim to control active bleeding and repair injuries from penetrating trauma. However, percutaneous therapy, including vessel coiling and embolization, has emerged as the first-line treatment of choice in trauma patients with active bleeding from blunt trauma.

KEY POINTS

CT remains the first-line modality of choice in trauma patients, although MRI should be considered in select patient populations (such as children), chronic renal disease, and pregnancy.

The spleen is the most commonly injured intra-abdominal organ in blunt trauma, with blood products demonstrating characteristic signal intensities on MRI.

Iatrogenic vascular injury, along with associated parenchymal sequelae, are best imaged with MRI.