eMedicine Specialties > Radiology > Gastrointestinal

Pancreatitis, Chronic

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute; Aali J Sheen, MD, MBChB, FRCS, Consulting Hepatobiliary Surgeon, HepatoBiliary Unit, Manchester Royal Infirmary

Updated: Mar 12, 2009

Introduction

Background

Chronic pancreatitis is characterized by progressive pancreatic damage that eventually leads to impairment of both exocrine and endocrine functions of the pancreas. The most common cause of chronic pancreatitis in Western societies is alcohol abuse. Understanding of the pathogenesis of chronic pancreatitis has improved primarily because of advances in the understanding of the mechanisms responsible for development of pancreatic fibrosis after repeated acute attacks of pancreatic necroinflammation. The pancreatic stellate cells are considered to be the key cells in fibrogenesis, particularly when they are activated by toxic factors such as alcohol, its metabolites, or oxidant stress or by cytokines released during pancreatic necroinflammation.^1,2

Chronic pancreatitis. Plain abdominal radiograph shows calcification in the pancreas associated with osteomalacia secondary to malabsorption. Note the pseudofracture in the right 11th rib (arrow).

Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows granular calcification in the pancreas, associated with a 4-cm pseudocyst to the right of the head of the pancreas.

For excellent patient education resources, visit eMedicine's Liver, Gallbladder, and Pancreas Center. Also, see eMedicine's patient education article, Pancreatitis.

Pathophysiology

Causes of chronic pancreatitis

The main causes of chronic pancreatitis include the following:

• Alcoholism: Changes appear to develop slowly and may develop after excessive alcohol consumption for 10 years or more. Alcoholism is associated with chronic pancreatitis in 70% of patients.⁴
• Cholelithiasis: Cholelithiasis is a common cause of acute pancreatitis, but it probably is associated with chronic pancreatitis in 20-25% of patients.⁵
• Idiopathic: Etiology is idiopathic in 20% of patients.⁴
• Drug use: Usually, drug-induced pancreatitis is an acute process and does not evolve into a chronic form.
• Hereditary causes: Hereditary pancreatitis is an autosomal dominant disorder. Symptoms usually appear in the patient's first decade of life and eventually lead to both exocrine and endocrine pancreatic dysfunction.
• Autoimmune disease: Autoimmune pancreatitis is a rare condition that is often seen in patients with primary sclerosing cholangitis.
• Congenital causes: A congenital abnormality of fusion, pancreas divisum, can cause chronic pancreatitis
• Cystic fibrosis: This disease is associated with pancreatic atrophy and chronic pancreatitis
• Other conditions: Hyperlipidemia, hyperparathyroidism, and uremia can cause chronic pancreatitis.

Categories of chronic pancreatitis

Chronic pancreatitis can be classified into 3 categories:

• Chronic calcifying pancreatitis
• Chronic obstructive pancreatitis
• Chronic inflammatory pancreatitis

Chronic calcifying pancreatitis

Chronic calcifying pancreatitis is invariably related to alcoholism. The earliest finding is precipitation of proteinaceous material in the pancreatic ducts that forms protein plugs that subsequently calcify. The ducts and lobules are initially involved in a random manner, and they are surrounded by normal parenchymal tissue. However, as the disease progresses, these normal areas become more diffuse. The pancreatic ductal epithelium undergoes atrophy, hyperplasia, and metaplasia at the site of the protein plugs. Many of the small pancreatic ductules dilate, while others are obliterated by fibrosis.

The main pancreatic duct shows a chain-of-lakes appearance due to alternating stenoses and dilatation. In approximately 50% of patients with chronic calcific pancreatitis, the pancreatic parenchyma contains cysts of varying sizes (several millimeters to 5 cm). These cysts are lined by cuboidal epithelium and contain pancreatic enzymes. Peripancreatic fibrosis is usually a late finding that involves the portal and/or splenic veins. Peripancreatic fibrosis causes stenosis or occlusion of retroperitoneal lymph channels. Ascites may complicate chronic calcific pancreatitis as a result of portal hypertension or lymphatic obstruction in 1-2% patients.

Chronic obstructive pancreatitis

In chronic obstructive pancreatitis, the prominent histologic changes are periductal fibrosis and subsequent ductal dilatation. These changes are much more focal than those in the other forms, and in most patients, the changes involve only the portion of the pancreas in which ductal drainage is impaired. Diffuse changes may occur, in which the main pancreatic duct or ampulla is obstructed. Although protein inspissation may occur, histologic changes in the ductal mucosa are less common, and calcification is unusual. Moreover, the pancreatic duct is dilated, and the pancreas is normal in size, atrophic, or focally and/or globally enlarged. A variety of factors are implicated in chronic obstructive pancreatitis; these include ductal obstruction due to ampullary stenosis, inflammatory or neoplastic causes, surgical ductal ligation, and fibrosis due to a pseudocyst as a complication of an episode of acute pancreatitis.

Chronic inflammatory pancreatitis

Chronic inflammatory pancreatitis is rare and can affect elderly persons without a previous history of alcohol excess.

Autoimmune pancreatitis

Autoimmune-related chronic pancreatitis is a distinct clinical entity, which may present with signs of acute or chronic pancreatitis, sometimes associated with cholestatic jaundice. On imaging, it may appear as diffuse (duct destructive) or pseudotumoral lesions. These 2 aspects are probably different clinical forms of chronic autoimmune pancreatitis.⁶

Some autoimmune diseases are associated with chronic autoimmune pancreatitis, but not consistently. One such disease involves a bile disorder that is very similar to primary sclerosing cholangitis but is responsive to corticosteroid treatment. Pancreatitis may be associated with Crohn disease and ulcerative colitis and thus provides justification to investigate patients with idiopathic pancreatitis for underlying inflammatory bowel disease. Chronic autoimmune pancreatitis must always be considered in patients with a pancreatic mass that is atypical for carcinoma on imaging or clinical findings. Corticosteroid therapy for 4 weeks in patients with pancreatic adenocarcinoma is probably less harmful than pancreatectomy (or chemotherapy) in patients with chronic autoimmune pancreatitis.

Diagnosis depends on clinical and radiologic findings. The diagnostic value of serologic markers and, especially, autoantibodies must still be clarified.⁶  

Frequency

United States

The incidence of chronic pancreatitis is 4 per 100,000 population in the West.⁴
Alcoholism is responsible for 70% of the cases of pancreatitis in the United States.

International

The exact frequency of chronic pancreatitis is unknown.

Mortality/Morbidity

Morbidity associated with chronic pancreatitis can be related to surgical approaches that are occasionally attempted to control intractable pain (see Intervention).

• Morbidity also results from surgical management of pseudocysts.
• In patients with chronic pancreatitis and in nonaffected family members, the incidence of pancreatic adenocarcinoma is increased.

Race

A form of calcific pancreatitis occurs in children and young adults in southern India and other developing countries; this form is termed nutritional or tropical pancreatitis.

Sex

A slight male preponderance exists.

Age

• Any age group can be affected, but chronic pancreatitis is unusual in children younger than 10 years. Most patients are aged 40-50 years.
• Nutritional or tropical pancreatitis affects children and young adults in southern India and other developing countries.

Anatomy

The gastroduodenal artery may be seen anteriorly at the pancreatic head and neck. The head of the pancreas is the most bulbous part of the gland, which then narrows to the neck. The union of the superior mesenteric and splenic veins, which forms the portal vein posteriorly, marks the anatomic position of the pancreatic neck. The pylorus lies anteriorly. The lesser sac lies anterior to the pancreas, whereas the splenic vein runs along its posterosuperior surface. The tail of the pancreas is related to the spleen, left adrenal gland, and upper pole of the left kidney.

Sonograms of the pancreas typically demonstrate a homogeneous echo pattern, and the pancreas is more echogenic than the liver. The pancreatic head measures 2.5-3.5 cm; the body, 1.75-2.5 cm; and the tail, 1.5-3.5 cm. The size of the pancreas varies considerably; therefore, reliance on size alone can lead to diagnostic errors. Generally, the size of the gland decreases with patient age, while echogenicity increases. The pancreas is more echogenic than the liver in 52% of young adults and equally echogenic in 48%. With the use of modern ultrasonographic machines, the main pancreatic duct can be identified in 85% of patients. On sonograms, the normal duct diameter is 1.3 mm ± 0.3. In patients with gallstones, the average diameter is 1.4 mm.

The typical criteria for pancreatic size on CT scans are the following: the head is 23 mm; neck, 19 mm; body, 20 mm; and tail, 15 mm. By using optimal CT techniques, the pancreatic duct can be identified in just more than 50% of the patients. Normally, the pancreatic diameters demonstrated on CT scans vary from 2-4 mm, but the effect of pixel averaging on normal pancreatic duct measurements is significant and can make such measurements unreliable. Errors of 1 or 2 mm may occur.

In most patients, a normal pancreatic duct is seen on images obtained with T2-weighted short-tau inversion recovery MRI sequences and magnetic resonance cholangiopancreatography (MRCP).

Presentation

Signs and symptoms

The most common presentation of chronic pancreatitis, irrespective of its etiology, is abdominal pain. Pain can be episodic, lasting hours to days, or it can persist for months or even years. The pain is characteristically steady in the epigastrium, and it frequently radiates to the back.

Most patients lose weight during the course of the disease. This weight loss may be related to malabsorption due to pancreatic exocrine deficiency or related to the fear of eating, because food intake exacerbates the pain. On occasion, the disease process can be painless, and patients may present with steatorrhea, weight loss, or diabetes mellitus.

Complications

Chronic pancreatitis is a relapsing condition that presents with abdominal pain. As the disease progresses, the frequency and duration of episodes of abdominal pain increase. Consequently, narcotic addiction is a common problem because of the intractable pain. Weight loss and malabsorption are also common.

Complications of chronic pancreatitis include pseudocyst and fistula formation, pseudoaneurysms of large arteries close to the pancreas, stenosis of the common bile duct, and splenic and/or portal venous obstruction.

Diabetes can develop in 58% of patients with chronic calcific pancreatitis.⁴ Diabetes tends to be brittle in these patients, probably because of the lack of both insulin and glucagon. However, patients with diabetes associated with chronic pancreatitis are less prone to complications such as retinopathy, nephropathy, atherosclerosis, and ketoacidosis than are patients with primary diabetes. On the other hand, neuropathy and myopathy can occur in one third of patients with chronic pancreatitis–associated diabetes. However, the exact etiology of neuropathy and myopathy in these patients is controversial, because these conditions occur with alcohol abuse in the absence of pancreatitis.

Preferred Examination

Plain radiographs show pancreatic calcification in 25-59% of patients. This feature is pathognomonic for chronic pancreatitis. Gastrointestinal (GI) tract barium testing still has a place in the management of chronic pancreatitis. First, some patients with chronic pancreatitis present with atypical abdominal complaints, and initially, barium studies may be ordered. Second, complications from chronic pancreatitis may cause obvious changes in the GI tract.

Ultrasonography is the first modality to be used in patients presenting with upper abdominal pain, although the direct diagnosis of chronic pancreatitis is not always possible. Sonography can help in determining the cause of chronic pancreatitis (eg, alcoholic liver disease, calculus disease) and in assessing the complications of the disease (eg, pseudocysts, ascites, splenic/portal venous obstruction).

Magnetic resonance imaging (MRI), particularly MR cholangiopancreatography (MRCP), is a noninvasive technique. MRI provides excellent images that may show the changes in the diseased pancreas and the complications of chronic pancreatitis. The use of secretin with MRCP can demonstrate pancreatic exocrine reserve, as well as a "santorinocele" (ie, a dilated Santorini duct seen in pancreas divisum).

CT is excellent for imaging of the retroperitoneum, and it is useful in differentiating chronic pancreatitis from pancreatic carcinoma. Cholangiopancreatography is the most sensitive imaging modality; it is used to show the ductal anatomy directly and when intervention (eg, stricture dilatation, stent placement) is being considered. Angiography is reserved for patients with suspected complications resulting from chronic pancreatitis.

Optical coherence tomography

Optical coherence tomography (OCT) allows high-resolution imaging of tissue microstructures by using a probe inserted into the main pancreatic duct (MPD) through an endoscopic retrograde cholangiopancreatography (ERCP) catheter. Perkins conducted a prospective study to assess the capacity of OCT to differentiate between noncancerous and cancerous lesions in patients with MPD segmental strictures investigated by endoscopic ultrasonography (EUS), with fine-needle aspiration cytology if necessary, and ERCP, followed by brush cytology and OCT scanning.⁷ OCT identified 3-layer architecture in all cases with normal MPD or chronic pancreatitis; in all the neoplastic lesions, the 3-layer architecture was totally subverted, with heterogeneous backscattering of the signal. OCT was 100% accurate in detecting cancer tissue, compared with 66.7% for brush cytology. OCT is therefore feasible with ERCP in cases of MPD segmental stricture and superior to brushcytology in distinguishing noncancerous from cancerous lesions.

Limitations of Techniques

On anteroposterior radiographs, the spine may mask small punctate calcifications; therefore, the acquisition of additional oblique or lateral imaging may be indicated.

On sonograms, the pancreas may appear normal even in the presence of advanced disease. In patients who are obese, excessive intraperitoneal gas may obscure the pancreas. Gas overlying the pancreas also can make visualization of the pancreas difficult.

Differential Diagnoses

Pancreas Divisum
Pancreas, adenocarcinoma with extrapancreatic spread
Pancreas, Mucinous Cystic Neoplasm
Pancreas, Serous Cystadenoma
Pancreatitis, Acute

Radiography

Chronic pancreatitis. Plain abdominal radiograph shows coarse calcification in the distribution of the pancreas due to chronic calcific pancreatitis.

Chronic pancreatitis. Plain abdominal radiograph shows calcification in the pancreas associated with osteomalacia secondary to malabsorption. Note the pseudofracture in the right 11th rib (arrow).

Chronic pancreatitis. Upper gastrointestinal tract barium study shows a reverse 3 in the duodenum due to chronic pancreatitis. Pancreatic carcinoma can have a similar appearance.

Chronic pancreatitis. Plain abdominal radiograph (in the same patient as in Images 10-11 in Multimedia) shows a common bile duct stent in situ and fairly extensive pancreatic calcification.

Findings

Plain radiography

Pancreatic calcifications are a common finding in chronic calcific pancreatitis and are considered pathognomonic for alcoholic chronic pancreatitis. Calcification primarily represents intraductal calculi, either in the main pancreatic duct or in the smaller pancreatic ductal radicles. Calcification is punctate or coarse, and it may have a focal, segmental, or diffuse distribution.

Upper GI tract barium series

Even in the age of cross-sectional imaging, upper GI tract barium series may provide information that is critical to the treatment of patients with chronic pancreatitis.

Esophageal involvement rarely occurs in chronic pancreatitis, and obstruction is usually the result of mediastinal extension of a pseudocyst. Pancreatic enlargement or a pseudocyst may compress the stomach. Peripancreatic fibrosis may involve the antrum of the stomach or duodenum, resulting in stenosis. The anatomic proximity of the pancreatic head and stomach antrum is constant, and enlargement of the pancreatic head usually causes effacement of the antrum; this has been termed the pad sign. Chronic pancreatitis may cause gastric nodularity and thickening of the mucosal folds; these findings are most prominent on the posterior aspect.

Gastric varices secondary to splenic venous thrombosis may have similar findings. The C loop of the duodenum may be widened because of mass effect from an enlarged pancreatic head, or it may be present as an inverted 3 sign due to traction on the medial wall of the duodenum. In the duodenum, mucosal changes occur, such as spiculation, flattening, or slight nodularity of the mucosal folds of the medial border of the duodenum or concentric narrowing due to periduodenal fibrosis.

Small-bowel changes infrequently occur in chronic pancreatitis. Displacement and stretching may occur as a result of pseudocysts. Small-bowel changes may occur as a result of exudation of pancreatic enzymes during the early stages of chronic pancreatitis, when the pancreatic secretory function is still intact. The enzymes may affect the mesenteric vessels at their roots, causing small-bowel ischemia, fibrotic stricture, and malabsorption pattern. As a result of the close anatomic relationship between the transverse colon and the pancreas, the pancreatic enzymes have direct access to the colon.

Changes in the colon include thickening of the haustral folds due to mucosal edema and luminal narrowing. These changes are usually confined to the inferior haustral row of the transverse colon and the splenic flexure. Rarely, fistula formation may occur. All 3 of these colon findings are best appreciated on barium enema examination.

Endoscopic retrograde cholangiopancreatography

Earliest changes are observed in side branches of the pancreatic duct, including dilatation without stenosis, dilatation with downstream stenosis, intraluminal mucosal irregularity, and intraluminal filling defects due to protein plugs or calculi. The number of opacified side branches may be reduced in a focal or diffuse manner because of ductal occlusion.

Chronic pancreatitis. Endoscopic retrograde cholangiopancreatogram shows a dilated common bile duct (CBD) associated with a stricture of the lower CBD (not well shown on this image) and a dilated ectatic tortuous pancreatic duct (in the same patient as in Images 11-12). A stent was subsequently placed across the CBD stricture.

The pancreatic duct may show beading or a chain-of-lakes or string-of-pearls appearance because of alternating stenosis and dilatation of the pancreatic duct.

Small (1-2 cm), round or oval, irregular or well-delineated pancreatic parenchymal cavities may be observed.

Occasionally, contrast material may fill large pseudocysts via fistulous communications. Prolonged emptying of contrast material may be observed.

Common bile duct changes are common in chronic pancreatitis. The most common finding is a long, smooth narrowing of the duct, with gradual tapering of the distal segment due to periductal fibrosis.

In 25% patients with chronic pancreatitis, alternating stenosis and dilation may cause the common bile duct to have an hourglass appearance.

Degree of Confidence

The sensitivity of plain abdominal radiography in the detection of pancreatic calcification is approximately 80%, which is higher than that of sonography but lower than that of CT. When seen, pancreatic calcification is pathognomonic for chronic pancreatitis. Barium study findings can be specific for GI tract changes secondary to chronic pancreatitis in the appropriate clinical setting.

ERCP is the most sensitive and specific technique for chronic pancreatitis, although it is invasive and may cause an acute episode of pancreatitis and ascending cholangitis.

False Positives/Negatives

On anteroposterior radiographs, the spine may mask small punctate calcifications; therefore, the acquisition of additional oblique or lateral images may be indicated. Bowel contents may obscure pancreatic calcification, and calcification in the pancreas and pancreatic bed is not specific for chronic pancreatitis. Causes of pancreatic calcification include acute pancreatitis, cavernous lymphangioma, hemangioma, cystic fibrosis, pancreatic hematoma/infarction, cystadenoma and/or cystadenocarcinoma, islet tumors, metastasis, pseudocysts, and kwashiorkor. Calcification in a vascular atheroma, an aortic aneurysm, or branches of the aorta can occasionally be confused with pancreatic calcification on plain abdominal radiographs.

Gastric displacement seen on barium examination is not specific for chronic pancreatitis and may be due to pancreatic carcinoma, a variety of peripancreatic masses (including adrenal gland or renal masses), aortic aneurysms, exophytic gastric or duodenal tumors, lymphoma and other retroperitoneal tumors, mesenteric cysts, splenic masses, or enlargement of the left lobe of the liver. In some patients, nodular mucosal changes on the medial border of the duodenum may be prominent and may mimic pancreatic carcinoma. Thickened gastric mucosal folds are not specific for chronic pancreatitis; similar thickening can occur with pancreatic carcinoma, lymphoma, gastric carcinoma, gastric sarcoidosis, and Ménétrier disease.

Widening of the duodenal loop is reported as a normal variant, but a similar abnormality is reported with aortic aneurysm; choledochal cysts; duodenal hematoma; retroperitoneal lymphadenopathy; retroperitoneal tumors; parasitic disease; and neoplasms of the stomach, colon, and kidney.

Small-bowel changes in chronic pancreatitis may mimic other causes of intestinal ischemia, Crohn disease, and malabsorption. Colonic changes may mimic vascular ischemia, Crohn disease, and primary colonic carcinoma.

Although ERCP findings can be specific in patients with chronic pancreatitis, they may be confused with those of pancreatic carcinoma in 10% of patients. Such confusion may arise with focal forms of chronic pancreatitis, pancreatic carcinoma extending through the entire pancreas, and coexisting chronic pancreatitis and pancreatic carcinoma.

Intraductal papillary mucinous neoplasm (IPMN) may have imaging findings identical to those of chronic pancreatitis, such as main duct and side-chain dilatation. ERCP can be used to differentiate main duct IPMN from chronic pancreatitis, because the former often shows mucin bulging from the ampulla.

Computed Tomography

Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows granular calcification in the pancreas.

Chronic pancreatitis. Enhanced axial CT scan through the pancreas shows a low-attenuating mass at the junction of the head and body of the pancreas due to focal chronic noncalcific pancreatitis.

Chronic pancreatitis. Enhanced axial CT scan through the pancreas (in the same patient as in Image 5) shows a mildly dilated pancreatic duct.

Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows granular calcification in the pancreas, associated with a 4-cm pseudocyst to the right of the head of the pancreas.

Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows a reverse 3 in the Gastrografin-filled duodenum. Note the patchy attenuation in the head of the pancreas. A contrast-enhanced study was not performed because the patient was allergic to intravenous iodinated contrast material.

Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas (in the same patient as in Images 13-14) shows an enlarged pancreas associated with punctate calcification.

Findings

CT features of chronic pancreatitis include those discussed in Anatomy. Other changes that can be visualized on CT scans are dilatation of the main pancreatic duct; calcifications; changes in size, shape, and contour; pseudocysts; and bile duct changes.^8,9

Main pancreatic duct dilatation can be demonstrated, with the width of the main pancreatic duct exceeding 5 mm in the head and 2 mm in the body and tail. CT is the most sensitive and specific modality for depicting pancreatic calcifications, which may be tiny and punctate or larger and coarse. Focal enlargement or atrophy of the pancreas is readily demonstrated on CT scans. Focal enlargement associated with calcification or ductal dilatation in a mass is suggestive of chronic pancreatitis.

Obliteration of the peripancreatic fat, which results in poor definition and an ill-defined pancreatic contour, is usually seen in acute exacerbations of chronic pancreatitis. Obliteration of the fat sleeve around the superior mesenteric artery has been described in both chronic pancreatitis and pancreatic carcinoma.

Obstruction of the common bile duct may be visualized as a gradual tapering of the ductal lumen. By contrast, a pancreatic carcinoma usually results in an abrupt transition of the common bile duct. Vascular complications of chronic pancreatitis are best depicted by contrast-enhanced CT scans. In images of pseudoaneurysms, high-attenuation masses are seen during the arterial phase. Portal and/or splenic vein thrombosis and associated collateral venous channels are better delineated during the portal venous phase of contrast enhancement.

Degree of Confidence

Currently, CT is regarded as the imaging modality of choice for the initial evaluation of suggested chronic pancreatitis. The diagnostic features of pancreatic enlargement, pancreatic calcifications, pancreatic ductal dilatation, thickening of the peripancreatic fascia, and bile duct involvement are depicted well on CT scans.

CT is more sensitive than plain radiography and ultrasonography in the depiction of pancreatic calcification. Moreover, CT depicts calcification in the pancreas, and confusion with nonpancreatic calcification is less likely. The accuracy of CT is 59-95%; the wide variation is due to the wide discrepancy in the criteria used for diagnosis and in the quality of CT scanners. CT helps in the diagnosis of atrophy of the pancreas, providing better results than ultrasonography.

Pancreatic pseudocysts and complications associated with pseudocysts, including various organ involvements, infection, hemorrhage with pseudoaneurysm formation, rupture with fistula formation, and gastrointestinal or biliary obstruction, are well depicted on CT. Detection of these complications are important, as they may necessitate prompt intervention or surgery.^8,10

False Positives/Negatives

Chronic pancreatitis and pancreatic carcinoma share many CT features, and occasionally, differentiation may be impossible. Obliteration of the fat sleeve around the superior mesenteric artery has been described in both chronic pancreatitis and pancreatic carcinoma.

Pseudotumoral enlargement around focal pancreatitis with extensive fibrous tissue proliferation usually fails to enhance after the administration of contrast material. This characteristic makes the differential diagnosis of pancreatic carcinoma difficult.

Magnetic Resonance Imaging

Chronic pancreatitis. Transaxial T2-weighted MRI scan through the tail of the pancreas shows a dilated tortuous pancreatic duct (arrow).

Chronic pancreatitis. Magnetic resonance cholangiopancreatogram (in the same patient as in Images 10 and 12) obtained 24 hours after the placement of a common bile duct stent shows good biliary drainage through the stent. Note the dilated tortuous pancreatic stricture and a downstream stricture in the head of the pancreas (left).

Findings

In most patients, a normal pancreatic duct is seen on images obtained with T2-weighted short-tau inversion recovery MRI sequences and MRCP. MRCP may depict the characteristic beaded appearance of the pancreatic duct in chronic pancreatitis. Pancreatic duct calculi are depicted as round filling defects. In chronic pancreatitis, fat-suppressed T1-weighted images usually show a loss of signal intensity. This loss is explained by the fact that pancreatic fibrosis decreases the proteinaceous fluid content of the pancreas, resulting in loss of pancreatic signal intensity. Fibrosis is associated with decreased vascularity, which causes decreased pancreatic gadolinium enhancement.

Small punctate pancreatic calcification is difficult to detect by using MRI, but larger calcifications may be seen as foci of a signal void. As a result of its ability to depict fluid, T2-weighted MRI may demonstrate pancreatic and common bile duct irregularities and pseudocysts associated with chronic pancreatitis.

Parenchymal gadolinium enhancement is a useful technique in evaluating focal areas of inflammation. Compared with normal pancreatic segments, inflamed areas have decreased enhancement in the arterial phase and increased enhancement in the equilibrium phase.

Currently, the diagnosis of early chronic pancreatitis is difficult. With future improvement in spatial resolution and with the use of secretin-enhanced pancreatography, the detection of subtle changes of the side branches may allow the earlier noninvasive diagnosis of chronic pancreatitis. Secretin-enhanced pancreatography also has the potential to depict the anatomic relationships of pancreatic ducts and pseudocysts and to aid in the evaluation of pancreatic exocrine function.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans.

NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

Because of the introduction of faster imaging sequences and phased-array coils, the accuracy of MRCP has improved considerably, although some concern remains regarding the resolution of smaller pancreatic ducts.

Secretin-enhanced MRCP improves the detection of diseased pancreatic ducts when no abnormality can be shown in physiologic conditions. It also provides additional functional information regarding pancreatic exocrine function. As experience grows, MRI imaging, particularly MRCP, may be increasingly used in assessing and screening for chronic pancreatitis.

False Positives/Negatives

Standard good-quality protocols are important with MRCP; otherwise, poor examination technique may create false lesions, which may increase the frequency of unnecessary ERCP examinations.

Ultrasonography

Chronic pancreatitis. Transverse sonogram shows an echogenic, enlarged pancreas with multiple small hyperechoic nonshadowing foci in the pancreas (in the same patient as in Images 14-15 in Multimedia).

Chronic pancreatitis. Longitudinal sonogram through the head of the pancreas (in the same patient as in Images 13 and 15 in Multimedia) shows an echogenic pancreas with multiple, small, hyperechoic, nonshadowing foci.

Chronic pancreatitis. A 52-year-old woman known to have chronic pancreatitis (same patient as in Images 17-19 in Multimedia) presented with moderate left upper quadrant pain. Transverse sonogram through the pancreas shows a 4.37-cm pseudocyst in the tail of the pancreas (arrow).

Chronic pancreatitis. Longitudinal sonogram (in the same patient as in Images 16, 18, and 19 in Multimedia) shows a pseudocyst at the splenic hilum. Doppler sonogram (not shown) showed no signal in the splenic vein.

Findings

Ultrasonography may be useful in depicting the anatomy of pancreas (see Anatomy). Primary findings on abdominal sonography include changes in the size, shape contour, and echotexture of the pancreas. Irregular pancreatic contour is seen in 45-60% of patients, focal enlargement is detected in 12-32%, and diffuse enlargement occurs in 27-45%. Peripancreatic fascial thickening and blurring of the pancreatic margins are seen in approximately 15% of patients.^11,12,13

In early disease, the pancreas may be enlarged and hypoechoic, with ductal dilatation. Later, the pancreas becomes heterogeneous, with areas of increased echogenicity and focal or diffuse enlargement. Pseudocysts may occur, and focal hypoechoic inflammatory masses may mimic pancreatic neoplasia. Calculi and calcification in the gland result in densely echogenic foci, which may show shadow. The pancreatic and common bile ducts may be dilated.

In late stages of the disease, the pancreas becomes atrophic and fibrotic, and it shrinks. These changes result in a small, echogenic pancreas with a heterogeneous echotexture. The pancreatic duct remains dilated and has a beaded appearance because of multiple stenoses. When seen, biliary dilation is mild.

Other complications, such as arterial pseudoaneurysms, left-sided portal hypertension (ie, splenic venous thrombosis), and pleural effusions are readily detected by using sonography.

Endoscopic ultrasonography (EUS) is more sensitive at showing the changes mentioned above, and the changes can be seen at an earlier stage of disease. The most characteristic EUS findings in chronic pancreatitis are parenchymal changes presenting as oval hypoechoic areas that are smaller than 1 mm and separated by hyperechoic fibrous septa.

Degree of Confidence

Although ultrasonography cannot always help in the diagnosis of chronic pancreatitis, it is a highly accurate noninvasive technique for detecting the complications of chronic pancreatitis. Ultrasonography also can help in detecting other causes of epigastric pain.

False Positives/Negatives

Sonograms may demonstrate a normal pancreas in the presence of established chronic pancreatitis. The pancreas is not always seen; it may be obscured by gas or fat. Differentiation between chronic pancreatitis and pancreatic carcinoma may be difficult and sometimes impossible.

Nuclear Imaging

Findings

FDG-PET in the Detection of Pancreatic Carcinoma in Chronic Pancreatitis

Patients with chronic pancreatitis are at risk of developing pancreatic cancer. FDG-PET has been established as a tool for the diagnosis of pancreatic carcinoma. Early detection is mandatory, as cure can only be achieved in nonadvanced disease; however, this is very difficult with conventional radiologic techniques. Van Kouwen et al investigated whether FDG-PET can detect pancreatic cancer in the setting of chronic pancreatitis.¹⁴   Their results revealed that in 67 of the 77 patients with chronic pancreatitis (87%), pancreatic FDG accumulation was absent. Of the 6 patients with pancreatic cancer complicating chronic pancreatitis, focal uptake was seen in 5 patients and minor uptake in 1 patient. FDG-PET was positive in almost all pancreatic cancer patients (used as controls). FDG-PET was negative in the large majority (87%) of  patients, which suggests that a positive PET scan in chronic pancreatitis patients must lead to efforts toexclude a malignancy. These data suggest that FDG-PET has a potential role as a diagnostic tool for detecting pancreatic cancer in long-standing chronic pancreatitis. Rasmussen and associates, however, could not confirm or exclude malignancy in 25 indeterminate pancreatic head masses using FDG-PET imaging. 11C-acetate-PET provided no additional diagnostic benefits.¹⁵

FDG-PET of autoimmune- related pancreatitis: preliminary results

Nakamoto Y et al described FDG-PET findings in 6 patients with autoimmune-related pancreatitis (AIP), which is considered a reversible form of chronic pancreatitis.^16,17 PET demonstrated intense uptake in the whole pancreas, which appeared swollen on CT, and the accumulation increased with time in 3 patients. In 1 patient, intense focal uptake in the pancreatic head was observed, and the accumulation decreased over time. In the remaining patient, no abnormal accumulation in the pancreas was observed. In 3 patients, follow-up PET scanning was performed after steroid therapy, and intense FDG uptake was no longer observed. The author’s preliminary data show that AIP can cause intense FDG uptake in the pancreas. This fact, along with the benign status of the condition, should be kept in mind when making a diagnosis with FDG-PET in patients with pancreatic disorders.

Degree of Confidence

In the studies note above,^14,15 FDG-PET was positive in almost all pancreatic cancer patients (used as controls) and cancer complicating chronic pancreatitis. FDG-PET was negative in the large majority (87%) of chronic pancreatitis patients, which suggests that a positive PET scan in chronic pancreatitis patients must lead to efforts to exclude a malignancy.

False Positives/Negatives

Autoimmune-related pancreatitis may be a source of a positive FDG-PET.¹⁶ This fact, along with the benign status of the condition, should be kept in mind when making a diagnosis with FDG-PET in patients with pancreatic disorders.

Angiography

Chronic pancreatitis. Manually subtracted celiac-axis angiogram (in the same patient as in Images 16, 17, and 19 in Multimedia) shows stretching of the pancreaticoduodenal artery with arterial tortuosity and a capillary blush in the region of the splenic hilum. These findings are superimposed on the left kidney and suggest an inflammatory mass.

Chronic pancreatitis. Manually subtracted venous-phase celiac-axis angiogram (in the same patient as in Images 16-18 in Multimedia) shows an occluded splenic vein and a large peripancreatic collateral vein that drains into the portal vein.

Findings

Angiographic findings in pancreatitis are related to the duration and severity of disease. Vascular abnormalities are usually minimal in patients who have had the disease for less than 2 years. The tortuosity of the pancreatic vessels is increased and associated with angulation of the pancreatic arcades.

In long-standing disease, the major intrapancreatic arteries and their branches have a beaded appearance in which short dilated segments alternate with narrow segments. Long-standing chronic pancreatitis associated with patch fibrosis results in the prolonged accumulation of contrast material. With diffuse fibrosis, both the number of intrahepatic arteries and the contrast agent accumulation are decreased.

The major vessels around the pancreas may be involved. The splenic artery is particularly susceptible to pancreatitis, and a sleevelike narrowing of the artery may occur. The splenic and superior mesenteric veins may be narrowed or may have luminal irregularities. Venous compression and/or occlusion, particularly in the splenic vein, occurs in 20-50% of patients with chronic pancreatitis. Portoportal shunting and gastric varices without esophageal varices may be seen as a result of splenic vein occlusion.

Degree of Confidence

Pancreatic angiography is usually reserved for patients in whom vascular complications from chronic pancreatitis are suspected. Angiography aids in the diagnosis of pseudoaneurysms, which may be treated by means of transcatheter embolization. By using certain criteria, differentiation between chronic pancreatitis and pancreatic carcinoma is possible in some patients on the basis of angiography (see False Positives/Negatives below).

False Positives/Negatives

The sleevelike narrowing of the splenic artery that occurs in pancreatitis may appear similar to atherosclerosis. However, the splenic artery is straight and narrow in pancreatitis, whereas, in atherosclerosis, it tends to be generally tortuous and irregularly narrowed. Encasement by a carcinoma may cause a similar sleevelike narrowing, but the involved segment is usually short.

Occasionally, differentiation between chronic pancreatitis and pancreatic carcinoma can be difficult with angiography; unfortunately, this also is the case with nearly all available imaging modalities.

The major differentiating features include the following:

• The course of the pancreatic arteries remains relatively unchanged in chronic pancreatitis. In contrast, a pancreatic carcinoma invariably changes the course of the arteries, which is characterized by abrupt angulation and distortion. However, similar changes may occur in chronic pancreatitis when pancreatic fibrosis ensues.
• Changes in arterial luminal caliber in chronic pancreatitis remain relatively smooth. In contrast, a carcinoma results in irregular and jagged-appearing changes in the caliber of the lumen.
• Characteristic arterial changes in chronic pancreatitis tend to be associated with an increase in the number of arteries, whereas, in carcinoma, the overall vascularity is decreased.
• Vascular changes in chronic pancreatitis are more diffuse, and carcinomas usually cause focal changes.

Intervention

Image-guided pancreatic biopsy may be performed. Usually, a cytologist is present at the biopsy, because immediate tissue analysis reduces the need for multiple biopsies. Fine-needle biopsy is usually performed because of the risk of acute pancreatitis with the use of larger needles.

Patients with acute biliary obstruction in the context of active pancreatitis, with or without pseudocyst in the head of the pancreas, can be treated by using temporary biliary stents. The value of dilatation and stent placement in the pancreatic duct has not yet been established. Currently, patients with recurrent acute episodes of pancreatitis may be treated with dilation of pancreatic duct strictures or the placement of temporary pancreatic duct stents. Further studies are necessary to establish the long-term benefits.

Surgical approaches are occasionally attempted to control intractable pain. These procedures include celiac ganglionectomies, splanchnicectomies, and various resections of the pancreas. Surgical series report a 70-90% success rate in alleviating pain. The surgical repair of leaks demonstrated on ERCP may be required.

Medical treatment consists of large-volume paracentesis and total parenteral nutrition. The treatment of pancreatic ascites may be difficult.

Medicolegal Pitfalls

• The use of large biopsy needles should be avoided because of the risk of acute pancreatitis.
• The close relationship of the aorta, inferior vena cava, and mesenteric vessels to the pancreas makes the risk of hemorrhage from a pancreatic biopsy significant.
• Established biliary strictures in end-stage chronic calcific pancreatitis usually do not respond to endoscopically placed stents. In such cases, surgery should be performed whenever possible.
• Chronic pancreatitis should be considered in the differential diagnosis of focal pancreatic masses, even in the absence of supporting clinical evidence.¹⁸

Multimedia

Media file 1: Chronic pancreatitis. Plain abdominal radiograph shows coarse calcification in the distribution of the pancreas due to chronic calcific pancreatitis.

Media file 2: Chronic pancreatitis. Plain abdominal radiograph shows calcification in the pancreas associated with osteomalacia secondary to malabsorption. Note the pseudofracture in the right 11th rib (arrow).

Media file 3: Chronic pancreatitis. Upper gastrointestinal tract barium study shows a reverse 3 in the duodenum due to chronic pancreatitis. Pancreatic carcinoma can have a similar appearance.

Media file 4: Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows granular calcification in the pancreas.

Media file 5: Chronic pancreatitis. Enhanced axial CT scan through the pancreas shows a low-attenuating mass at the junction of the head and body of the pancreas due to focal chronic noncalcific pancreatitis.

Media file 6: Chronic pancreatitis. Enhanced axial CT scan through the pancreas (in the same patient as in Image 5) shows a mildly dilated pancreatic duct.

Media file 7: Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows granular calcification in the pancreas, associated with a 4-cm pseudocyst to the right of the head of the pancreas.

Media file 8: Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas shows a reverse 3 in the Gastrografin-filled duodenum. Note the patchy attenuation in the head of the pancreas. A contrast-enhanced study was not performed because the patient was allergic to intravenous iodinated contrast material.

Media file 9: Chronic pancreatitis. Transaxial T2-weighted MRI scan through the tail of the pancreas shows a dilated tortuous pancreatic duct (arrow).

Media file 10: Chronic pancreatitis. Endoscopic retrograde cholangiopancreatogram shows a dilated common bile duct (CBD) associated with a stricture of the lower CBD (not well shown on this image) and a dilated ectatic tortuous pancreatic duct (in the same patient as in Images 11-12). A stent was subsequently placed across the CBD stricture.

Media file 11: Chronic pancreatitis. Magnetic resonance cholangiopancreatogram (in the same patient as in Images 10 and 12) obtained 24 hours after the placement of a common bile duct stent shows good biliary drainage through the stent. Note the dilated tortuous pancreatic stricture and a downstream stricture in the head of the pancreas (left).

Media file 12: Chronic pancreatitis. Plain abdominal radiograph (in the same patient as in Images 10-11 in Multimedia) shows a common bile duct stent in situ and fairly extensive pancreatic calcification.

Media file 13: Chronic pancreatitis. Transverse sonogram shows an echogenic, enlarged pancreas with multiple small hyperechoic nonshadowing foci in the pancreas (in the same patient as in Images 14-15 in Multimedia).

Media file 14: Chronic pancreatitis. Longitudinal sonogram through the head of the pancreas (in the same patient as in Images 13 and 15 in Multimedia) shows an echogenic pancreas with multiple, small, hyperechoic, nonshadowing foci.

Media file 15: Chronic pancreatitis. Nonenhanced axial CT scan through the pancreas (in the same patient as in Images 13-14) shows an enlarged pancreas associated with punctate calcification.

Media file 16: Chronic pancreatitis. A 52-year-old woman known to have chronic pancreatitis (same patient as in Images 17-19 in Multimedia) presented with moderate left upper quadrant pain. Transverse sonogram through the pancreas shows a 4.37-cm pseudocyst in the tail of the pancreas (arrow).

Media file 17: Chronic pancreatitis. Longitudinal sonogram (in the same patient as in Images 16, 18, and 19 in Multimedia) shows a pseudocyst at the splenic hilum. Doppler sonogram (not shown) showed no signal in the splenic vein.

Media file 18: Chronic pancreatitis. Manually subtracted celiac-axis angiogram (in the same patient as in Images 16, 17, and 19 in Multimedia) shows stretching of the pancreaticoduodenal artery with arterial tortuosity and a capillary blush in the region of the splenic hilum. These findings are superimposed on the left kidney and suggest an inflammatory mass.

Media file 19: Chronic pancreatitis. Manually subtracted venous-phase celiac-axis angiogram (in the same patient as in Images 16-18 in Multimedia) shows an occluded splenic vein and a large peripancreatic collateral vein that drains into the portal vein.

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Keywords

chronic pancreatitis, pancreatitis, pancreas, chronic calcifying pancreatitis, chronic obstructive pancreatitis, chronic inflammatory pancreatitis, pancreatic dysfunction, alcoholic pancreatitis, calcific pancreatitis, obstructive pancreatitis, inflammatory pancreatitis, pancreatic pseudotumor, autoimmune pancreatitis.

Contributor Information and Disclosures

Author

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP is a member of the following medical societies: American Institute of Ultrasound in Medicine, Royal College of Physicians, Royal College of Physicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons of England
Disclosure: Nothing to disclose.

Coauthor(s)

Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR is a member of the following medical societies: British Medical Association, Royal College of Physicians, and Royal College of Radiologists
Disclosure: Nothing to disclose.

Aali J Sheen, MD, MBChB, FRCS, Consulting Hepatobiliary Surgeon, HepatoBiliary Unit, Manchester Royal Infirmary
Aali J Sheen, MD, MBChB, FRCS is a member of the following medical societies: British Medical Association, International Hepato-Pancreato-Biliary Association, and Royal College of Surgeons of England
Disclosure: Nothing to disclose.

Medical Editor

Glenn Krinsky, MD, Chief of Abdominal Imaging Section, Associate Professor, Department of Radiology, New York University School of Medicine
Glenn Krinsky, MD is a member of the following medical societies: Alpha Omega Alpha and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Udo P Schmiedl, MD, PhD, Clinical Professor, Department of Radiology, University of Washington; Consulting Staff, Swedish Medical Center, University of Washington Medical Center, Seattle Radiologists
Udo P Schmiedl, MD, PhD is a member of the following medical societies: American College of Radiology and Radiological Society of North America
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

John Karani, MBBS, FRCR, Consulting Staff, Department of Radiology, King's College Hospital, London
Disclosure: Nothing to disclose.

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