Figure 55-1. U.S. pancreatic cancer new cases, death rate, and 5-year survival. Adapted from EER Cancer Statistics Factsheets: Pancreas Cancer. National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/statfacts/html/pancreas.html. Accessed March 10, 2016.

In addition to well-defined genetic syndromes, a number of common conditions have been thought to be etiologic factors in the development of pancreatic cancer. An apparent association between diabetes and pancreatic cancer has been suggested. Approximately 80% of patients diagnosed with pancreatic cancer have impaired glucose metabolism, impaired glucose tolerance, or diabetes mellitus. It is unclear if alterations in glucose tolerance/metabolism are a causative factor for pancreatic cancer or represent reaction to an enlarging malignancy in the pancreas. Among patients with newly diagnosed diabetes, 0.85% went on to be diagnosed with pancreatic cancer within 3 years.⁴ Type II diabetes of at least 5 years duration has been shown to increase the risk of pancreatic cancer twofold.

The risk of pancreatic cancer has been shown to increase as body mass index increases. Examination of data from the Nurses’ Health Study and the Health Professional’s follow-up study show a 1.72 relative risk (95% CI 1.19–2.48) of pancreatic cancer in patients with a BMI >30 kg/m² as compared to individuals with a BMI <23 kg/m².

Chronic pancreatitis of any cause has been associated with a 25-year cumulative risk for the development of pancreatic cancer of approximately 4%. Other conditions for which a possible association with pancreatic cancer has been demonstrated include thyroid and other benign endocrine tumors, cystic fibrosis, and pernicious anemia.

Most cases of pancreatic cancer have no obvious predisposing factors. However, it is believed that between 5% and 10% of pancreatic cancers arise because of a familial predisposition. Six genetic syndromes have been associated with an increased risk for the development of pancreatic cancer (Table 55-2). These include hereditary nonpolyposis colon cancer, familial breast cancer associated with the BRCA2 mutation, Peutz–Jeghers syndrome (PJS), ataxia–telangiectasia syndrome, familial atypical multiple mole–melanoma syndrome, and hereditary pancreatitis.

MOLECULAR GENETICS

Invasive pancreatic ductal adenocarcinoma (PDAC) are genetically very complex, with wide-spread chromosome abnormalities, numerous losses and gains of large segments of DNA, and on average, more than 60 exomic alterations in each cancer.⁵ PDAC harbors an average of 63 genome alterations, of which the majority are point mutations. Four key genes are frequently altered in PDAC: KRAS, CDKN2A, TP53, and SMAD4 (Table 55-3). The most common gene alteration is in KRAS (Kirsten rat sarcoma viral oncogene homolog), where mutations occur in codons 12, 13, and 61. More than 90% of PDAC contain KRAS mutations. Point mutations of the K-ras oncogene impair the intrinsic guanosine triphosphatase activity of its gene product; the result is a protein that is constitutively active in signal transduction and activates various downstream signaling pathways, including the mitogen-activated protein kinase (MAPK) cascades. Ras proteins are involved in a variety of cellular functions, including proliferation, differentiation, and survival. Cyclin-dependent kinase inhibitor 2A gene (CDKN2A) is also inactivated in up to 90% of PDAC, due to intragenic mutations in association with allelic loss, homozygous deletion, or hypermethylation of the gene promoter. CDKN2A encodes a cyclin-dependent kinase inhibitor that controls G1–S transition in the cell cycle. Inactivation of CDKN2A leads to the loss of an important cell cycle checkpoint and therefore relatively unchecked proliferation. TP53 is one of the most frequently mutated genes in many types of cancer, and is inactivated in about 75% of PDAC, mainly due to point mutations or small deletions. The p53 gene product is a DNA-binding protein that acts as both a cell-cycle checkpoint and an inducer of apoptosis. Inactivation of the p53 gene in pancreatic cancer leads to the loss of two important controls of cell growth: regulation of cellular proliferation and induction of cell death. SMAD4 (DPC4, SMAD family member 4 gene). SMAD4 encodes a transcription factor that mediates signaling of the transforming growth factor-β (TGF-β) superfamily. SMAD4 is a tumor-suppressor gene that has been identified on chromosome 18q. This chromosome has been shown to be missing in nearly 90% of pancreatic cancers. The SMAD4 gene is inactive in almost 50% of pancreatic carcinomas. The mutation appears to be a homozygous deletion in 30% of pancreatic cancers, and a point mutation in another 20% of tumors. SMAD4 mutations are more specific than p53 or p16 mutations for pancreatic cancer.

Germline mutations in BRCA2 and CDKN2A, and less frequently in BRCA1, PALB2 and ATM have been identified in a small subset of patients with familial pancreatic cancer. The inactivation of BRCA2, which encodes a protein involved in DNA damage repair, is associated with a 3.5- to 10-fold increased risk of pancreatic cancer, as well as increased risk of breast and ovarian cancer. In addition, patients with Lynch syndrome (caused by germline mutation in one of the mismatch repair genes MLH1, MSH2, MSH6, or PMS2) and PJS (caused by germline mutation of the STK11 gene) are at increased risk of pancreatic cancer. Approximately 4% of pancreatic cancers can be characterized by disorders of DNA mismatch–repair genes.⁶

PATHOLOGY

Tumors of the exocrine pancreas can be classified based on their cell of origin (Table 55-4). The most common neoplasms of the exocrine pancreas are ductal adenocarcinomas. Approximately 65% of pancreatic ductal cancers arise in the head, neck, or uncinate process of the pancreas; 15% originate in the body or the tail of the gland; and 20% diffusely involve the whole gland.

Solid Epithelial Tumors

Ductal Adenocarcinomas

Ductal adenocarcinomas account for more than 75% of all nonendocrine pancreatic cancers. Grossly, they are white–yellow, poorly defined, hard masses that often obstruct the distal common bile duct or main pancreatic duct. They are often associated with a desmoplastic reaction that causes fibrosis and chronic pancreatitis. Microscopically, they contain infiltrating glands of varying size and shape surrounded by dense, reactive fibrous tissue (Fig. 55-2). The epithelial cells sometimes form papillae and cribriform structures, and they frequently contain mucin. The nuclei of the cells can show marked pleomorphism, hyperchromasia, loss of polarity, and prominent nucleoli.

Ductal adenocarcinomas tend to infiltrate into vascular, lymphatic, and perineural spaces. At the time of resection, most ductal carcinomas have already metastasized to regional lymph nodes. In addition to the lymph nodes, PDAC frequently metastasize to the liver (80%), peritoneum (60%), lungs and pleurae (50% to 70%), and adrenal glands (25%). They also can directly invade the duodenum, stomach, transverse mesocolon, colon, spleen, and adrenal glands.

1 The histologic examination of a pancreas resected for cancer frequently reveals the presence of precursor lesions in the pancreatic ducts and ductules adjacent to the cancer. This suggests that much like colon cancer, which arises from benign adenomas, pancreatic cancer may also demonstrate progression to malignant from benign precursor lesions. These precursor lesions are referred to as pancreatic intraepithelial neoplasia (PanIN). Briefly, PanIN-1A and PanIN-1B are proliferative lesions without remarkable nuclear abnormality that have a flat and papillary architecture, respectively. PanIN-3 is associated with severe architectural and cytonuclear abnormalities, but invasion through the basement membrane is absent. The older term for PanIN-3 includes carcinoma in situ (CIS). PanIN-2 is an intermediate category between PanIN-1 and PanIN-3 and is associated with a moderate degree of architectural and cytonuclear abnormality.⁷ Several lines of evidence suggest that PanINs are precursors of infiltrating pancreatic cancer: PanINs are often found in association with ductal adenocarcinomas, three-dimensional mapping techniques that demonstrated a stepwise transformation from mild dysplasia to severe dysplasia in pancreatic duct lesions, and PanINs demonstrate some of the same genetic changes seen in infiltrating adenocarcinomas, most notably activating point mutations in codon 12 of K-ras and mutations in the p16 and p53 tumor-suppressor genes.

Adenosquamous Carcinomas

Adenosquamous carcinoma is a rare variant of ductal adenocarcinoma that shows both glandular and squamous differentiation. This variant appears to be more common in patients who have undergone previous chemoradiation therapy. The biologic behavior of adenosquamous carcinoma appears to be similar to that of ductal adenocarcinoma, with similar rates of perineural invasion, lymph node metastases, and dissemination.

Acinar Cell Carcinomas

Acinar cell carcinomas account for only 1% of pancreatic exocrine tumors. Acinar tumors are typically smooth, fleshy, lobulated, hemorrhagic, or necrotic. Histologically, they form acini, and the cells display an eosinophilic, granular cytoplasm. Immunohistochemical staining demonstrates expression of trypsin, lipase, chymotrypsin, or amylase. These tumors are more common in males with a male-to-female predominance of approximately 3:1. The age of diagnosis is usually in the fifth to seventh decades. These tumors tend to be larger than ductal adenocarcinomas, often being larger than 10 cm. Although data are limited, it appears that patients with acinar cell carcinoma have a slightly better prognosis than patients with ductal carcinoma.⁸ Therefore, surgical resection is the treatment of choice.

Giant Cell Carcinomas

Giant cell carcinomas account for less than 1% of nonendocrine pancreatic cancers. They tend to be large, with average diameters greater than 15 cm. Microscopically, they contain large, uninucleated or multinucleated tumor cells, many of which are pleomorphic. The nuclei contain prominent nucleoli and numerous mitotic figures. Giant cell carcinomas are associated with a poorer prognosis than ductal adenocarcinomas. There is a variant of giant cell carcinoma termed giant cell carcinoma with osteoclast-like giant cells. These lesions tend to be well circumscribed with nonpleomorphic giant cells and are less aggressive than standard giant cell carcinomas.

Pancreatoblastoma

Pancreatoblastomas occur primarily in children ages 1 to 15 years. Pancreatoblastomas contain both epithelial and mesenchymal elements. The epithelial component appears to arise from acinar cells. The tumors are typically larger than 10 cm and often contain areas of degeneration and hemorrhage. The prognosis appears to be more favorable than that for typical ductal adenocarcinoma if the tumor can be resected.

Cystic Epithelial Tumors

Cystic neoplasms also arise from the exocrine pancreas. Cystic neoplasms are less common than ductal adenocarcinomas, tend to occur in women, and are evenly distributed throughout the gland. Many pancreatic and peripancreatic cysts are actually benign inflammatory pseudocysts. It is important to identify cystic neoplasms because their management is very different from that of nonneoplastic cysts. With advancements in imaging technology, cystic lesions of the pancreas are being detected with increased frequency. With routine application of cross-sectional imaging to early diagnostic processes in medicine, pancreatic cysts are often detected incidentally.⁹ Although many of these lesions are small and asymptomatic, they can have malignant potential. Therefore, the management of these patients is complex, and knowledge of pancreatic cyst natural history and predictors of neoplasia are important.

Serous Cystic Neoplasms

Serous cysts are epithelial neoplasms composed of uniform cuboidal glycogen-rich cells that usually form numerous small cysts containing serous fluid. Serous cystadenomas or microcystic adenomas are more common in women than in men (3:1 preponderance). These tumors can vary from a few centimeters to more than 10 cm in size. Twenty-five percent to 30% of patients are asymptomatic; however, most patients present with symptoms such as abdominal or epigastric pain, dyspepsia, nausea, or vomiting. Serous cystadenomas can be located anywhere in the pancreas – head, body, or tail – and usually do not communicate with the pancreatic ducts. Plain computed tomography (CT) shows a honeycomb pattern of microlacunae, with thin septa separating different segments. Serous cystic neoplasms can have a sunburst pattern of central calcification, which is seen in 10% to 30% of cases. Grossly, they appear as spongy, well-circumscribed, multiloculated cysts. Microscopically, they consist of a layer of simple cuboidal cells separated by dense fibrous bands. Most serous cystic neoplasms are benign, although malignant behavior has been reported rarely (<1% with metastases to the liver or peripancreatic lymph nodes). Symptomatic cysts or cysts that cannot be differentiated from other potentially malignant cysts should undergo surgical excision.

Mucinous Cystic Neoplasms

Mucinous cystic neoplasms (MCNs) are neoplasms composed of mucin-producing epithelial cells associated with an ovarian-type of stroma. These cysts usually do not communicate with the larger pancreatic ducts. MCNs are relatively uncommon but account for almost 30% of all cystic neoplasms. The mean age at diagnosis is between 40 and 50 years. MCNs are more common in women with a female-to-male ratio of 9:1. Most patients with MCNs present with vague abdominal symptoms that include epigastric pain or a sense of abdominal fullness. The majority (70% to 90%) of MCNs arises in the body or tail of the pancreas, and only a minority (10% to 30%) involves the head of the gland. Microscopically, the cysts are lined by tall columnar mucin-producing epithelium. These columnar cells have basal nuclei and abundant intracytoplasmic apical mucin and can form flat sheets or papillae. The walls of the cysts contain a very distinctive “ovarian-type” stroma. This stroma is composed of densely packed spindle cells with sparse cytoplasm and uniform elongated nuclei. All MCNs are considered to be premalignant lesions and should be completely resected to prevent progression to malignancy.

Invasive mucinous cystadenocarcinomas are MCNs associated with an invasive carcinoma, whereas noninvasive mucinous neoplasms can be categorized into MCNs with low-grade dysplasia (adenoma), MCNs with moderate dysplasia (borderline) neoplasms, and MCNs with high-grade dysplasia (carcinoma in situ) based on the degree of architectural and cytologic atypia of the epithelial cells. In surgical series between 15% and 30% of all MCNs are associated with invasive carcinoma. Patients with mucinous cystadenocarcinomas tend to be 5 to 10 years older than patients with benign MCNs. The extent of invasive and in situ carcinomas in MCNs can be very focal. Therefore, a benign diagnosis cannot be established on biopsy alone and the lesions should be completely resected. The prognosis for patients with resected benign or borderline tumors is excellent. Patients with mucinous cystadenocarcinoma tend to do better than patients with ductal adenocarcinoma, with a 5-year survival of approximately 50%.

Intraductal Papillary-Mucinous Neoplasms

Intraductal papillary-mucinous neoplasms (IPMNs) are intraductal mucin-producing neoplasms with tall, columnar, mucin-containing epithelium with or without papillary projections. These neoplasms extensively involve the main pancreatic ducts and/or major side branches. In addition, IPMNs lack the ovarian stroma characteristic of MCNs. Similar to the well-defined adenoma–carcinoma sequence in PDAC (PanIN to invasive ductal carcinoma), IPMNs seem to follow a similar pattern progressing from IPMN with low-grade dysplasia to invasive carcinoma. Microscopically, they consist of papillary projections lined by columnar mucin-secreting cells. They show varying degrees of cellular atypia. The noninvasive IPMNs are graded on the basis of greatest degree of dysplasia and classified into low-grade, moderate-grade, and high-grade dysplasia or carcinoma in situ. Invasive IPMNs are either colloid or tubular, with the latter having a worse prognosis. The mean age of patients with invasive carcinoma is approximately 5 years older than patients with noninvasive IPMNs suggesting an approximately 5-year lag period for progression to malignancy. Further histologic subtyping of epithelial differentiation is based on the cell lineage, the morphology of the papillae, and the immunophenotype, and includes classification into intestinal, gastric, pancreaticobiliary, and oncocytic subtypes.

IPMNs are subclassified as main- and branch-duct types and as a mixed type that contains elements of both. Main-duct IPMN is characterized by involvement of the duct of Wirsung, which is dilated to more than 1 cm in diameter. Branch-duct IPMN originates in the side branches of the pancreatic ductal system and appears as a multilobular cystic lesion communicating with a nondilated main pancreatic duct. Typically, branch-duct IPMN occurs in the uncinate process–head of the gland, but it can also be seen in the neck and distal pancreas. If the main duct is dilated with synchronous involvement of the branch ducts, it is described as a mixed IPMN.

IPMNs are usually found in individuals in their 60s to 80s. Some patients may experience symptoms that include: abdominal pain, steatorrhea, weight loss, jaundice, diabetes, and chronic pancreatitis. A substantial number of these lesions are also detected as incidental findings on cross-sectional imaging studies performed for other indications. IPMNs appear to be more common in the head, neck, and uncinate process of the pancreas but can be found diffusely throughout the whole gland. CT scans will typically reveal a cystic mass in the head of the pancreas that appears to communicate with the pancreatic ductal system. On endoscopy, mucin can be seen oozing from the ampulla of Vater. Endoscopic retrograde cholangiopancreatography (ERCP) can be used to confirm that the cysts communicate with the pancreatic ducts.

MCNs are the main entity to consider in the differential diagnosis of IPMNs (Table 55-5). Two morphologic features distinguish IPMNs from MCNs: IPMNs communicate with ducts, mucinous cysts do not; IPMNs also lack an ovarian stroma that is present in mucinous cysts. In addition, mucinous cysts are usually seen in the tail of the pancreas and occur in middle-aged women, whereas IPMNs are found in the head of the pancreas and occur in older individuals of either sex.

As noted, IPMNs represent a continuum of disease from benign to malignant. In a large series of resected IPMNs from the Johns Hopkins Hospital,¹⁰ the prognosis for the benign forms of the disease appears to be significantly better than for invasive IPMNs with 1-, 2-, and 5-year actuarial survivals of 97%, 94%, and 77%, respectively. Although invasive IPMNs are associated with disease progression and death, the prognosis remains markedly better than for invasive ductal carcinoma of the pancreas with survivals of 72%, 58%, and 43% at 1, 2, and 5 years, respectively. It is unclear if this fact is due to earlier presentation or differences in tumor biology.

2 International consensus guidelines for the management of IPMNs have been developed.¹¹ CT or MRI with MRCP is recommended for imaging IPMNs. IPMNs are classified as having either “high-risk stigmata” or “worrisome features.” High-risk stigmata include obstructive jaundice in the setting of a cyst in the head of the pancreas, a main duct >10 mm, or a cyst with a solid enhancing component in the wall. Worrisome features include cyst >3 cm, thickened enhanced cyst walls, nonenhanced mural nodules, main duct size between 5 and 9 mm, abrupt change in the MPD caliber with distal pancreatic atrophy, and lymphadenopathy. All cysts with “worrisome features” and cysts of >3 cm without “worrisome features” should undergo endoscopic ultrasonography (EUS), and all cysts with “high-risk stigmata” should be resected. If no “worrisome features” are present, no further initial work-up is recommended, although surveillance is still required (Algorithm 55-1).

The goal of surgical therapy for IPMNs should be a complete surgical resection yielding negative margins for all invasive and noninvasive disease. Unlike those patients with completely resected noninvasive MCNs (who are routinely cured), patients with completely resected noninvasive IPMNs should undergo careful follow-up and surveillance for the development of recurrent disease. Furthermore, patients with resected invasive IPMNs should also undergo careful follow-up and surveillance as they, too, remain at risk for the development of recurrent disease.

Solid-Pseudopapillary Tumor

Solid-pseudopapillary tumors (SPTs), also termed solid and cystic tumors, papillary cystic tumors, Hamoudi tumors, and Frantz tumor occur primarily in women in their third to fourth decades of life. Grossly, the masses range from 5 to 15 cm in diameter. Radiologically, they present as a well-demarcated heterogeneous mass with solid and cystic components, with a peripheral capsule which rarely shows calcification. EUS-guided fine needle aspiration (FNA) or core biopsy is often diagnostic, showing uniform cells forming microadenoid structures, branching, and papillary clusters with delicate fibrovascular cores. Most SPTs exhibit a benign behavior, and even the less than 20% that have vascular or perineural invasion, lymph node involvement or liver metastases can have a very indolent course. The overall 5-year survival is close to 97% in patients undergoing surgical resection.

CLINICOPATHOLOGIC STAGING

Accurate pathologic staging of pancreatic cancer is important for providing prognostic information to patients and for comparing the results of various therapeutic trials. The American Joint Committee on Cancer (AJCC) staging for pancreatic cancer is shown in Table 55-6. This system, based on the TNM classification, takes into account the extent of the primary tumor (T), the presence or absence of regional lymph node involvement (N), and the presence or absence of distant metastatic disease (M).

DIAGNOSIS

Clinical Presentation

Many of the difficulties associated with the management of pancreatic cancer result from our inability to make the diagnosis at an early stage. The early symptoms of pancreatic cancer include anorexia, weight loss, abdominal discomfort, and nausea. Unfortunately, the nonspecific nature of these symptoms often leads to a delay in the diagnosis. Specific symptoms usually develop only after invasion or obstruction of nearby structures has occurred. Most pancreatic cancers arise in the head of the pancreas, and obstruction of the intrapancreatic portion of the common bile duct leads to progressive jaundice, acholic stools, darkening of the urine, and pruritus. Pain is a common symptom of pancreatic cancer. The pain usually starts as vague upper abdominal or back pain that is often ignored by the patient or attributed to some other cause. It is usually worse in the supine position and is often relieved by leaning forward. Pain may be caused by invasion of the tumor into the splanchnic plexus and retroperitoneum, and by obstruction of the pancreatic duct. Other digestive symptoms are also common in pancreatic cancer (Table 55-7).

Occasionally, pancreatic cancer may be discovered in an unusual manner. The onset of diabetes may be the first clinical feature in 10% to 15% of patients. An episode of acute pancreatitis may also be the initial presentation of pancreatic cancer if the tumor partially obstructs the pancreatic duct. It is important to consider a pancreatic cancer in patients presenting with acute pancreatitis, especially those without an obvious cause for their pancreatitis (alcohol or gallstones).

The most common physical finding at the initial presentation is jaundice (Table 55-8). Hepatomegaly and a palpable gallbladder may be present in some patients. In cases of advanced disease, cachexia, muscle wasting, or a nodular liver, consistent with metastatic disease, may be evident. Other physical findings in patients with disseminated cancer include left supraclavicular adenopathy (Virchow node), periumbilical adenopathy (Sister Mary Joseph node), and pelvic drop metastases (Blumer shelf). Ascites can be present in 15% of patients.

Laboratory Studies

In patients with cancer of the head of the pancreas, laboratory studies usually reveal a significant increase in serum total bilirubin, alkaline phosphatase, and γ-glutamyl transferase indicating bile duct obstruction. The transaminases can also be elevated but usually not to the same extent as the alkaline phosphatase. In patients with localized cancer of the body and tail of the pancreas, laboratory values are frequently normal early in the course. Patients with pancreatic cancer may also demonstrate a normochromic anemia and hypoalbuminemia secondary to the nutritional consequences of the disease. In patients with jaundice, the prothrombin time can be abnormally prolonged. This usually is an indication of biliary obstruction, which prevents bile from entering the gastrointestinal tract and leads to malabsorption of fat-soluble vitamins and decreased hepatic production of vitamin K–dependent clotting factors. The prothrombin time can usually be normalized by the administration of parenteral vitamin K. Serum amylase and lipase levels are usually normal in patients with pancreatic cancer.

A wide variety of serum tumor markers have been proposed for use in the diagnosis and follow-up of patients with pancreatic cancer. The most extensively studied of these is CA 19–9, a Lewis blood group-related mucin glycoprotein. Approximately 5% of the population lacks the Lewis gene and therefore cannot produce CA 19–9. When a normal upper limit of 37 U/mL is used, the accuracy of the CA 19–9 level in identifying patients with pancreatic adenocarcinoma is only about 80%. When a higher cutoff value of more than 90 U/mL is used, the accuracy improves to 85%, and increasing the cutoff value to 200 U/mL increases the accuracy to 95%.¹² The combined use of CA 19–9 and ultrasonography, CT, or ERCP can improve the accuracy of the individual tests, so that the combined accuracy approaches 100% for the diagnosis of pancreatic cancer. Levels of CA 19–9 have also been correlated with prognosis and tumor recurrence. In general, higher CA 19–9 values before surgery indicate an increased size of the primary tumor and increased rate of unresectability. In addition, the CA 19–9 level has been used to monitor the results of neoadjuvant and adjuvant chemoradiation therapy in patients. Increasing CA 19–9 levels usually indicate recurrence or progression of disease, whereas stable or declining levels indicate a stable tumor burden, absence of recurrence on imaging studies, and an improved prognosis.

Radiologic Investigations

Radiologic imaging plays a crucial role in the diagnosis, staging, and follow-up of patients with pancreatic cancer. In addition to identifying the primary tumor, the goals of imaging include the assessment of local and regional invasion, evaluation of lymph nodes and vascular structures, identification of distant metastatic disease, and the determination of tumor resectability. Ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI) are all useful noninvasive tests in the patient suspected of having a pancreatic cancer.

Transabdominal ultrasonography (US) will reveal a pancreatic mass in 60% to 70% of patients with cancer. Pancreatic cancer typically appears as a hypoechoic mass on US. Ultrasonography may also demonstrate dilated intrahepatic and extrahepatic bile ducts, liver metastases, pancreatic masses, ascites, and enlarged peripancreatic lymph nodes. Because helical CT is just as sensitive as ultrasonography and provides more complete information about surrounding structures and the local and distant extent of the disease, transabdominal ultrasonography has been largely replaced by CT.

Stay updated, free articles. Join our Telegram channel

Join