Pancreatic ductal adenocarcinoma
Pancreatic ductal adenocarcinoma makes up the vast majority (~90%) of all pancreatic neoplasms and remains a disease with a very poor prognosis and high morbidity.
On imaging, it usually presents as a hypodense mass on CT that is poorly marginated, which may encase vessels and the common bile duct.
Pancreatic cancer accounts for 22% of all deaths due to gastrointestinal malignancy, and 5% of all cancer deaths 1. In general, it is a malignancy of the elderly with over 80% of cases occurring after the age of 60 1.
Risk factors include:
- cigarette smoking: the strongest environmental risk factor
- a diet rich in animal fats and protein
- family history: three or more first-order relatives with pancreatic cancer results in ~20x risk 8
- hereditary syndromes 6
Perhaps surprisingly there is only a weak if at all present association with heavy alcohol consumption 1.
- pain (most common)
- Courvoisier gallbladder: painless jaundice and enlarged gallbladder
- Trousseau syndrome: migratory thrombophlebitis
- new-onset diabetes mellitus
lipase hypersecretion syndrome (10-15%) 9
- polyarthralgia and subcutaneous fat necrosis +/- lytic bone lesions
- elevated serum lipase and eosinophilia
Three precursor lesions for pancreatic adenocarcinoma have been identified 8:
- pancreatic intraepithelial neoplasia (PanIN)
- intraductal papillary mucinous neoplasm (IPMN)
- mucinous cystic neoplasm
Cancerous cells arise from the pancreatic ductal epithelium. As the majority of tumors (90%) 1 are not resectable, diagnosis is usually achieved with imaging (typically CT scan) although laparoscopy is often required to confirm resectability 1,2. The key to accurate staging is the assessment of the SMA and celiac axis, which if involved exclude the patient from any attempted resection 1,2.
- adenocarcinoma: majority
- acinar cell carcinoma of the pancreas
- adenosquamous carcinoma of the pancreas
- undifferentiated with osteoclasts giant cells
Location and classification
- head and uncinate process: two-thirds of cases
- body and tail: one-third of cases 1
Please see pancreatic ductal adenocarcinoma staging.
Barium meal/small bowel follow-through
If large enough may demonstrate a reverse impression on the duodenum: Frostburg inverted 3 sign or a wide duodenal sweep.
Findings are non-specific and include:
- hypoechoic mass
- double duct sign may be seen
CT is the workhorse of pancreatic imaging. Typically ductal adenocarcinomas appear as poorly defined masses with extensive surrounding desmoplastic reaction. They enhance poorly compared to adjacent normal pancreatic tissue and thus appear hypodense on arterial phase scans in 75-90% of cases, but may become isodense on delayed scans 1 (thus the need for multiple phase scanning when pancreatic cancer is the clinical question). Double duct sign may be seen.
CT correlates well with surgical findings in predicting unresectability (positive predictive value of 89-100% 3). The most important feature to assess locally is the relationship of the tumor to surrounding vessels (SMA and celiac axis). If the tumor surrounds a vessel by more than 180 degrees, then it is deemed T4 disease and is unresectable 3.
Signal characteristics include:
- T1: hypointense cf. normal pancreas 5
- T1 FS: hypointense cf. normal pancreas 5
- T1 + C (Gd): slower enhancement than the normal pancreas, therefore dynamic injection with fat saturation with arterial phase imaging is ideal
- T2/FLAIR: variable (therefore not very useful), depending on the amount of reactive desmoplastic reaction 1,5
- MRCP: double duct sign may be seen
Treatment and prognosis
Most tumors are not resectable at diagnosis.
Even when resection is possible, the majority of patients succumb to recurrence, with only a doubling of survival in operated patients 1, from 5% to 10% at 5 years 4. At 12 months following the diagnosis, almost a quarter of the patients will have died 4.
General imaging differential considerations include:
- acute pancreatitis
- chronic pancreatitis
- other pancreatic neoplasms
fatty infiltration of the pancreatic head
- usually involving the anterior portion
- no secondary signs (e.g. pancreatic duct or common bile duct dilatation)
- high signal on T1 and signal drop on chemical shift sequences
- periampullary tumors
- pancreatic metastases
- 1. Evans DB, Pisters PW, Abbruzzese JL. Pancreatic cancer. Springer Verlag. (2002) ISBN:0387951857. Read it at Google Books - Find it at Amazon
- 2. Greene FL, Cancer AJ, Society AC. AJCC cancer staging handbook, from the AJCC cancer staging manual. Springer Verlag. (2002) ISBN:0387952705. Read it at Google Books - Find it at Amazon
- 3. Lu DS, Reber HA, Krasny RM et-al. Local staging of pancreatic cancer: criteria for unresectability of major vessels as revealed by pancreatic-phase, thin-section helical CT. AJR Am J Roentgenol. 1997;168 (6): 1439-43. AJR Am J Roentgenol (abstract) - Pubmed citation
- 4. DeVita VT, Lawrence TS, Rosenberg SA et-al. DeVita, Hellman, and Rosenberg's cancer, principles & practice of oncology. Lippincott Williams & Wilkins. (2008) ISBN:0781772079. Read it at Google Books - Find it at Amazon
- 5. Mergo PJ, Helmberger TK, Buetow PC et-al. Pancreatic neoplasms: MR imaging and pathologic correlation. Radiographics. 17 (2): 281-301. Radiographics (abstract) - Pubmed citation
- 6. Schenk M, Schwartz AG, O'neal E et-al. Familial risk of pancreatic cancer. J. Natl. Cancer Inst. 2001;93 (8): 640-4. J. Natl. Cancer Inst. (link) - Pubmed citation
- 7. Morgan DE, Waggoner CN, Canon CL et-al. Resectability of pancreatic adenocarcinoma in patients with locally advanced disease downstaged by preoperative therapy: a challenge for MDCT. AJR Am J Roentgenol. 2010;194 (3): 615-22. doi:10.2214/AJR.08.1022 - Pubmed citation
- 8. Polvani S, Tarocchi M, Tempesti S et-al. Nuclear receptors and pathogenesis of pancreatic cancer. World J. Gastroenterol. 2014;20 (34): 12062-81. doi:10.3748/wjg.v20.i34.12062 - Free text at pubmed - Pubmed citation
- 9. Riediger C, Mayr M, Berger H et-al. Transarterial chemoembolization of liver metastases as symptomatic therapy of lipase hypersecretion syndrome. J. Clin. Oncol. 2012;30 (23): e209-12. doi:10.1200/JCO.2011.40.7627 - Pubmed citation
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