You are in: eMedicine Specialties > Radiology > GASTROINTESTINAL Pancreatitis, ChronicArticle Last Updated: Jun 14, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Ali Nawaz Khan, MBBS, LRCP, FRCS, FRCP, FRCR, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia Ali Nawaz Khan is a member of the following medical societies: American Institute of Ultrasound in Medicine, Radiological Society of North America, Royal College of Physicians, Royal College of Physicians and Surgeons of the USA, Royal College of Radiologists, and Royal College of Surgeons of England Coauthor(s): Sumaira Macdonald, MBChB, MRCP, FRCR, PhD, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute; Aali J Sheen, MBChB, FRCS, Specialist Registrar, Department of HPB Surgery, Manchester Royal Infirmary Oxford Road Manchester UK Editors: Glenn Krinsky, MD, Chief of Abdominal Imaging Section, Associate Professor, Department of Radiology, New York University School of Medicine; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; 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; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; John Karani, MBBS, FRCR, Consulting Staff, Department of Radiology, King's College Hospital, London Author and Editor Disclosure Synonyms and related 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. INTRODUCTIONSection 2 of 12
  BackgroundChronic 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. For excellent patient education resources, visit eMedicine's Liver, Gallbladder, and Pancreas Center. Also, see eMedicine's patient education article, Pancreatitis. PathophysiologyCauses of chronic pancreatitisThe main causes of chronic pancreatitis include the following:
Categories of chronic pancreatitisChronic pancreatitis can be classified into 3 categories: (1) chronic calcifying pancreatitis, (2) chronic obstructive pancreatitis, and (3) chronic inflammatory pancreatitis. Chronic calcifying pancreatitis 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 Chronic inflammatory pancreatitis Autoimmune pancreatitisAutoimmune-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.4 FrequencyUnited StatesThe incidence of chronic pancreatitis is 4 per 100,000 population in the West.2 InternationalThe exact frequency of chronic pancreatitis is unknown. Mortality/MorbidityMorbidity associated with chronic pancreatitis can be related to surgical approaches that are occasionally attempted to control intractable pain (see Intervention).
RaceA 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. SexA slight male preponderance exists. Age
AnatomyAn understanding of pancreatic anatomy is important in delineating the cross-sectional anatomy of the pancreas and the causation of pain in pancreatic disease. The pancreas varies in shape and lies in the anterior pararenal space. The head of the pancreas lies within the curve of the duodenal loop, and the inferior vena cava and right renal vessels lie posteriorly. The common bile duct receives the main pancreatic duct as it passes through the pancreatic head and then drains into the duodenum at the ampulla. 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). Clinical DetailsSigns 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.2 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 ExaminationPlain 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.5 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 TechniquesOn 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. DIFFERENTIALSSection 3 of 12
Pancreas Divisum Pancreas, adenocarcinoma with extrapancreatic spread Pancreas, Mucinous Cystic Neoplasm Pancreas, Serous Cystadenoma Pancreatitis, Acute RADIOGRAPHSection 4 of 12
FindingsPlain 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. In late stages of the disease, changes in the main pancreatic duct are prominent and are similar to those in the side branches, such as ductal dilatation with or without stenosis, short segmental narrowing or long strictures, and intraluminal filling defects due to protein plugs or calculi. 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 ConfidenceThe 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/NegativesOn 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. CT SCANSection 5 of 12
FindingsCT 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. 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 ConfidenceCurrently, 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. False Positives/NegativesChronic 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. MRISection 6 of 12
FindingsIn 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 recently 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. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. 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 troublemoving 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 ConfidenceBecause 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/NegativesStandard good-quality protocols are important with MRCP; otherwise, poor examination technique may create false lesions, which may increase the frequency of unnecessary ERCP examinations. ULTRASOUNDSection 7 of 12
FindingsUltrasonography 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. 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 ConfidenceAlthough 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/NegativesSonograms 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 MEDICINESection 8 of 12
FindingsFDG-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.6 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.7 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.8, 9 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 ConfidenceIn the studies note above,6, 7 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/NegativesAutoimmune-related pancreatitis may be a source of a positive FDG-PET.8 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. ANGIOGRAPHYSection 9 of 12
FindingsAngiographic 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 ConfidencePancreatic 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/NegativesThe 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:
INTERVENTIONSection 10 of 12
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. Medical/Legal Pitfalls
MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
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