Complications of Pancreatitis

Pancreatic necrosis and infection were discussed in a previous section. The complications covered here include pancreatic and gastrointestinal fistulas, pseudocysts, and changes involving other structures.
Fistulas Pancreatic duct disruption leads to an undrained collection and pseudocyst formation; in a similar setting a pancreatic fistula forms after necrosectomy and external drainage. In general, the mortality rate is higher with a gastrointestinal fistula as compared to a pancreatic fistula or pseudocyst. A persistent pancreatocutaneous fistula develops in about half of patients after percutaneous drainage of pancreatic fluid collections; whether a fistula develops or not appears related primarily to the severity of pancreatitis rather than to its cause. A pancreaticopleural fistula is rare. An occasional pancreatic duct fistula is visualized by ERCP. Some of these fistulas are also identified by CT and US. Biliary scintigraphy appears worthwhile with a suspected biliary fistula developing in a setting of chronic pancreatitis. Anecdotal reports describe fibrin glue being used to successfully occlude these fistulas.
Pseudocyst Clinical Pancreatic pseudocysts develop in both acute and chronic pancreatitis. It takes 4 to 6 weeks for a pseudocyst to “mature” and form into a welldefined
structure with an identifiable wall. These cysts can be classified as intrapancreatic or extrapancreatic in location; the location is best defined with CT.A mature cyst may or may not communicate with the pancreatic ductal system; such communication is best established with ERCP. Noncommunicating cysts are probably secondary to necrotic liquefaction of pancreatic tissue or prior limited communication with pancreatic ducts. In chronic pancreatitis the cysts generally communicate with ducts and tend to be associated with main pancreatic duct obstruction.
Although the most common site for pseudocysts is around the tail of the pancreas, they have been reported in almost any location in the
abdomen and occasionally even in the chest. Pseudocysts have developed in intrahepatic and intrasplenic locations. They have involved both the right and left liver lobes. A pseudocyst originating from the tail of the pancreas has
extended into the left renal space and has mimicked a renal cyst on CT. Pseudocysts vary considerably in size. Most small pseudocysts resolve spontaneously. The wall of some chronic pseudocysts calcifies. Pseudocyst content amylase and lipase levels do not correlate with exocrine pancreatic function, and cyst enzyme levels vary considerably between consecutive punctures of the same cyst; with noncommunicating cysts the pseudocyst content differs from pancreatic juice.
Diagnosis Computed tomography of an uncomplicated pseudocyst shows fluid of near-water density. Either hemorrhage or infection increases attenuation. Pseudocysts have smooth margins
Radiology images of pseudocyst in pancreatic head,an unusual location (arrow).

An uncomplicated pseudocyst is anechoic, but hemorrhage, debris, or infection produces a heterogeneous complex echo pattern. Blood clots appear as a solid component. An MRCP readily detects these cystic structures. Communication with pancreatic ducts is not as readily apparent as with ERCP. It is worthwhile to emphasize that not all pancreatic cysts are pseudocysts. Cystic pancreatic neoplasms and true cysts are also in the differential diagnosis. About three quarters or more of all pancreatic cysts are pseudocysts secondary to pancreatitis, with the others being primarily neoplastic. Complicating the issue is that some pancreatic neoplasms are associated with pancreatitis. It is essential to differentiate among a pseudocyst, a neoplastic cyst, and other nonneoplastic cysts. A number of reports describe what initially appears to be a pseudocyst, which is treated by a cystenterostomy,with subsequent dire consequences. Even a gastric duplication has been misdiagnosed as a pancreatic pseudocyst. A cystic neoplasm should be considered especially in patients without a history or risk factors for pancreatitis. A reverse misdiagnosis can also occur. Thus imaging in a 37-year-old asymptomatic man being investigated for hypertension detected two small cysts and a larger unilocular cyst containing a mural nodule in the pancreas; ERCP showed communication of the pancreatic duct with a cyst but no ductal changes, suggesting chronic pancreatitis was evident and a tentative diagnosis of a malignant mucinous cystic neoplasms
was made. Intraoperative frozen section of the cyst wall revealed a pseudocyst, with mural nodules representing sludge within the pseudocyst.
A cystic pancreatic neoplasm and a pseudocyst have a similar US appearance. Serial US, especially if obtained early in the formation of a pseudocyst, aids in differentiating between these two. When small, an aneurysm is also in the US differential diagnosis; Doppler US should differentiate these. The relative MR signal intensity on T1- weighted images of pseudocysts, other benign cysts, and cystic neoplasms overlaps. Other rare
cystic nonneoplastic pancreatic lesions include retention cysts and simple cysts.
Pseudocyst Complications A pseudocyst can rupture into any adjacent structure. Spontaneous rupture into surrounding structures results in surrounding inflammation and possible sinus tracts between the pseudocyst and duodenum. Perforation can occurred into the colon.A pseudocyst can erode into the portal vein, with embolization of pseudocyst content into the intrahepatic portal vein branches. Rupture into the peritoneal cavity results in acute peritonitis. Differentiation from infected pancreatic ascites is difficult.
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, 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. 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 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. 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.
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
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. 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.
Radiology images of abscess involving pancreatic tail. Contrastenhanced magnetic resonance imaging (MRI) identifies a peripheral enhancing rim (arrows) containing nonenhancing components.

Gastrointestinal Tract
Severe ileus is common but generally clears as pancreatitis improves. Duodenal obstruction is a known complication of pancreatitis,with the diagnosis generally 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.
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.
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.
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.
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. Most unusual was a patient with acute pancreatitis developing splenic vein thrombosis, splenic infarction, and spinal cord infarction resulting in paraplegia

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