Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

Prevalence of pseudoaneurysms in pancreatitis patients is difficult to gauge but probably is around 10%. Many of the smaller ones remain silent unless rupture occurs or they are discovered with an imaging study. Spontaneous arterial hemorrhage associated with a pseudocyst is not uncommon. The involved vessel becomes dilated (pseudoaneurysm formation) and ruptures. Bleeding is into the pseudocyst, intraperitoneal, into the gastrointestinal tract, through the papilla of Vater (hemosuccus pancreaticus), or into any structure surrounding the cyst. Bleeding is generally from one of the peripancreatic arteries (49), although any nearby artery, including the splenic artery and even the middle colic artery, can be involved. Bleeding ranges from slow to massive to the point of exsanguination.

Contrast-enhanced CT should detect high attenuation blood within a pseudoaneurysm. During an acute bleed CT may detect extravasating contrast.

Ultrasonography identifies an aneurysm as a cyst, often with an adjacent crescent rim. Doppler US should detect blood flow and allows differentiation of a pseudoaneurysm from a pseudocyst or other fluid collection.

Angiography allows transcatheter embolization of the feeding vessel. Although embolization arrests most acute bleeding, it may recur and require reembolization. Steel coil embolization is more successful than Gelfoam embolization. Unsuccessful bleeding artery embolization usually necessitates a pancreatectomy (49).

Infection turns a pseudocyst into an abscess. Differentiation of a noninfected from an infected pseudocyst is an art and relies on clinical and imaging findings. Positive Tc-99m- HMPAO leukocyte scintigraphy suggests a pancreatic abscess; on the other hand, a normal scintigram points toward a noninfected pseudocyst.

A pseudocyst may obstruct any adjacent hollow viscus. Thus with bile duct compression patients develop obstructive jaundice. A rare large pseudocyst results in gastric or small bowel obstruction.

Pseudocyst Therapy

Pseudocysts are treated by a number of percutaneous (repeat cyst aspiration, external catheter drainage, transgastric catheter

ADVANCED IMAGING OF THE ABDOMEN

drainage), endoscopic (transgastric catheter, transampillary stenting, insertion of nasocystic drainage catheter), and surgical procedures. Internal drainage to the stomach or bowel has varying degrees of success. The type and degree of aggressive intervention varies depending on the expertise of the physicians involved and the traditions of the institution. Overall, a trend has been away from open surgical drainage to nonsurgical intervention. Simple aspiration has a high recurrence rate and is not often performed. Percutaneous catheter drainage has a recurrence rate similar to surgical internal drainage, but is associated with fewer complications. A percutaneous transgastric approach, with resultant internal drainage into the stomach, is used in a number of institutions with good results and a low recurrence rate. A percutaneous catheter allows serial study of cyst size and any pancreatic duct communication. A double-mushroom stent has been described to provide internal drainage into the stomach (percutaneous cystogastrostomy), thus avoiding an external catheter. Recurrence of a pseudocyst should suggest a persistent or recurrent pancreatic duct obstruction by a stone.

Endoscopic drainage of pancreatic pseudocysts is performed in some centers. Endoscopic US prior to the procedure detects any interposed larger vessels (including varices) and aids in establishing the best site for drainage. A pancreaticoportal fistula is a complication after an endoscopic cystogastrostomy (50).

In general, a high-resolution imaging study aimed at detecting any associated pseudoaneurysm is performed prior to pseudocyst drainage. If a pseudoaneurysm is detected, angiography allows confirmation and embolization.

Intrasplenic pseudocysts have been drained percutaneously. A percutaneous paraspinal, extrapleural CT-guided approach was used to drain a mediastinal pseudocyst (51).

Abscess

Some pancreatic phlegmons evolve into an abscess. A pseudocyst can become infected. The infecting agent usually is bacterial, with only an occasional one being fungal. Klebsiella sp.,

Escherichia coli, and Staphylococcus aureus predominate, and most infections contain only one organism.

PANCREAS

The presence of gas suggests an abscess, but not all abscesses contain gas. Gas is also found secondary to an infection of necrotic pancreatic tissue with gas-forming organisms, so-called gas gangrene. An enteric communication also leads to intrapancreatic gas collections.

Computed tomography and MR show a pancreatic abscess as a thick-walled cavity containing low-attenuation fluid (Fig. 9.12). Adjacent pancreatic parenchyma usually enhances with contrast. Infected necrotic tissue, on the other hand, consists of nonenhancing or poorly enhancing liquefied pancreatic tissue.

Ultrasonography shows a pancreatic abscess as a thick-walled hypoechoic cavity. US cannot distinguish whether a focus of necrotic tissue is infected or not. Similarly, US cannot determine whether a pseudocyst is infected or not.

Percutaneous needle aspiration using imaging guidance should detect pancreatic infection. Established abscesses are amenable to percutaneous catheter drainage; necrosis, on the other hand, whether infected or not, generally requires surgical debridement.

Gastrointestinal Tract

Severe ileus is common but generally clears as pancreatitis improves.

Duodenal obstruction is a known complication of pancreatitis, with the diagnosis generally

Figure 9.12. Abscess involving pancreatic tail. Contrastenhanced magnetic resonance imaging (MRI) identifies a peripheral enhancing rim (arrows) containing nonenhancing components. (Source: From Burgener FA, Meyers SP, Tan RK, Zaunbauer W. Differential Diagnosis in Magnetic Resonance Imaging. Stuttgart: Thieme, 2002, with permission.)

suspected clinically. An oral barium study is diagnostic. Obstruction in a setting of acute pancreatitis often clears spontaneously, but fibrosis developing in chronic pancreatitis usually requires surgical correction. No one surgical procedure is applicable in all patients, with the myriad procedures performed reflecting concomitant common bile duct and pancreatic duct obstruction in some of these patients.

Transverse colon involvement in necrotizing pancreatitis is rare but is associated with colon necrosis, perforation, and peritonitis. The sequelae also include colon stenosis.

Biliary

Occasionally severe acute necrotizing pancreatitis results not only in biliary obstruction but also in a bile duct leak or even necrosis of the adjacent common bile duct. Percutaneous biliary drainage provides temporary relief, with definitive surgical correction performed, as necessary, after pancreatitis subsides.

Fasting and postprandial gallbladder volumes are increased above normal, and gallbladder contraction is reduced in patients with chronic pancreatitis, possibly due to decreased cholecystokinin secretion.

Spleen

Splenic complications of pancreatitis are not common but include splenic infarct, subcapsular hematoma, and abscess. The absence of CT contrast enhancement of splenic parenchyma suggests a splenic infarction. A pseudocyst in the tail of the pancreas and splenic vein thrombosis led to splenic rupture (52).

Vascular

Disseminated intravascular coagulopathy is common in acute pancreatitis. Peripancreatic hematomas develop in some patients, including duodenal intramural hematomas.

Splenic vein, portal vein, or superior mesenteric vein thromboses complicate acute and chronic pancreatitis. Often such thrombosis is asymptomatic, and extensive collateral vessels are a first manifestation. Some of these patients develop gastric varices; esophageal varices are not common. Because collateral vessels bypass thrombosed veins and the intrahepatic vascu-

larity is intact, these patients tend not to develop variceal bleeding to the extent seen in patients with hepatic cirrhosis. Acute mesenteric vein thrombosis can lead to small bowel infarction. Some of these thrombi are reversible and follow-up CT identifies resolution after pancreatitis clears.

A thrombus can be detected with most imaging. Computed tomography shows a hypodense splenic vein and a normal portal vein. Gray-scale US reveals an echogenic intraluminal thrombus.

ADVANCED IMAGING OF THE ABDOMEN

Leptospirosis

Leptospirosis rarely presents with pancreatitis. In a rare patient infection with Leptospira icterohaemorrhagiae mimics pancreatitis.

Clonorchis Infestation

Computed tomography identifies small pancreatic cysts in patients with pancreatitis associated with Clonorchis sinensis infestation (56).

Other Complications

An occasional patient develops pleural effusion and even pericardial effusion during acute pancreatitis. Even cardiorespiratory arrest has developed secondary to chylous cardiac tamponade.

At times pancreatitis involves the peripancreatic tissues to the point of obliterating the perivascular fat planes, and imaging suggests an infiltrating carcinoma.

The development of acute renal failure in acute pancreatitis is associated with a high mortality.

Pancreatic ascites is a result of pancreatic duct disruption; it is more common in chronic than acute pancreatitis; at times massive chylous ascites develops months after onset of pancreatitis.

Intraosseous fat necrosis is a rare complication of pancreatitis (53). Most unusual was a patient with acute pancreatitis developing splenic vein thrombosis, splenic infarction, and spinal cord infarction resulting in paraplegia (54).

Dengue Hemorrhagic Fever

Epigastric pain is common in dengue hemorrhagic fever. The diagnosis is established by serologic examination and viral isolation.

Ultrasonography in children with dengue detected an enlarged pancreas in 29%, with the prevalence increasing in those with severe disease (55); relative to the liver, the pancreas was isoechoic in 69%, with the rest being either hyperor hypoechoic. Elevated serum amylase and lipase levels were common in those with severe disease and an enlarged pancreas.

Lipomatosis

Increased pancreatic fat (called lipomatous pseudohypertrophy by some authors) develops in obesity, chronic pancreatitis, diabetes mellitus, cystic fibrosis and other hereditary dysfunctions, long-term steroid therapy, and some viral infections. Occasionally fatty replacement is associated with a pancreatic mesenchymal neoplasm. In a rare patient lipomatosis is idiopathic. The pancreas becomes enlarged secondary to diffuse fatty infiltration. The exocrine glandular tissue is atrophic, but the islets of Langerhans tend to be preserved.

Lipomatosis is readily detected with imaging (Fig. 9.13).

Similar to the liver, focal fatty masses also develop in the pancreas. These lesions generally

Figure 9.13. Fat infiltration of pancreas associated with obesity, detected on contrast-enhanced CT. Similar changes are found in cystic fibrosis patients. (Courtesy of Douglas Katz, M.D.,Winthrop University, Mineolar, New York.)

PANCREAS

are well defined; CT shows these tumors to have the same density as peripancreatic fat. With US, they range from hypoechoic to hyperechoic.

Iron Deposition

In patients with hemochromatosis, iron is deposited not only in the liver but also in pancreatic parenchyma, and these patients develop diabetes mellitus and exocrine abnormalities. With sufficient iron deposition, MRI reveals a hypointense pancreas on T2-weighted images.

Compared to the liver, the pancreas contains limited reticuloendothelial tissue. In distinction to the liver and spleen, after blood transfusions MR reveals little pancreatic change, except that after repeated transfusions and reticuloendothelial saturation iron is deposited in pancreatic parenchymal cells, and these patients develop both endocrine and exocrine abnormalities.

Among 20 patients with transfusiondependent b-thalassemia major, pancreas-to-fat signal intensity ratio was decreased in 85% and increased in 15% on SE T1and fast spin echo (FSE) T2-weighted images (compared with controls) (57); a significant correlation existed between increased pancreas-to-fat signal intensity ratios and decreased serum trypsin levels and a decreased pancreas-to-fat signal intensity ratio and increased serum ferritin levels.

Amyloidosis

Primary amyloidosis of the pancreas is rare. More common is pancreatic involvement in a setting of systemic amyloidosis.

Sarcoidosis

Even with systemic sarcoidosis, pancreatic involvement is rare. In fact, most patients with pancreatic sarcoidosis have no antecedent history of sarcoidosis. The clinical presentation can mimic pancreatitis or a pancreatic malignancy, and can include jaundice. Idiopathic chronic pancreatitis can manifest at the same time as generalized sarcoidosis.

The diagnosis can be suspected if biopsies reveal noncaseating epithelioid granulomas, keeping in mind that granulomas are found as

a reaction to fungi, tuberculosis, some cancers, and foreign substances. Sarcoid infiltration leads to extrinsic narrowing of the distal common bile duct or pancreatic duct.

Tumors

Differential Diagnosis of Focal

Tumors

Benign focal pancreatic tumors can be divided into nonneoplastic and neoplastic (Table 9.3). Considerable overlap exists in the imaging differential diagnosis of these tumors, especially for the cystic varieties, and preoperative differentiation between a pancreatic malignancy and a benign condition continues to pose a dilemma. Most pancreatic surgeons have encountered the patient with a pancreatic tumor who undergoes a laparotomy or even resection for a suspected malignancy only to discover that the condition is benign.

Most pancreatic fibrosis involves the entire pancreas; when focal, neither CT nor US nor MR readily differentiates focal chronic pancreatitis from a malignancy (58).

Nonneoplastic

Lymphoepithelial Cyst

Pancreatic lymphoepithelial cysts are rare. These cysts are lined by squamous epithelium

Table 9.3. Benign focal tumors of the pancreas