Pancreatic ductal adenocarcinoma
Pancreatic ductal adenocarcinoma makes up the vast majority (~90%) of all pancreatic neoplasms and remains a disease with 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 biliary 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
- 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’s gallbladder: painless jaundice and enlarged gallbladder
- Trousseau’s 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 tumours (90%) 1 are not resectable, this is mostly 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 coeliac axis, which if involved exclude the patient from any attempted resection 1-2.
- adenocarcinoma: majority
- acinar cell carcinoma of pancreas
- adenosquamous carcinoma of 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 work-horse 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 tumour to surrounding vessels (SMA and coeliac axis). If the tumour surrounds a vessel by more than 180 degrees, then it is deemed T4 disease and is unresectable 3.
Signal characteristics include:
- T1: hypointense c.f. normal pancreas 5
- T1 FS: hypointense c.f. normal pancreas 5
- T1 + C (Gd): slower enhancement than normal pancreas, therefore dynamic injection with arterial phase imaging with fat saturation 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 tumours are not resectable at diagnosis.
Surgery for stage I and II (see staging of pancreatic cancer) does offer the chance of cure, with however high morbidity (20-30%) and mortality (5%) 3. Resection is performed with a Whipple operation.
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. Almost a quarter of patients are dead 12 months following diagnosis 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 dilation, CBD dilation)
- high signal on T1 and signal drop on IP-OOP sequences
- periampullary tumours
- pancreatic metastases
- cystic neoplasm (cystic pancreatic mass differential diagnosis)
- solid neoplasm
- nonepithelial pancreatic neoplasms
pancreatitis (mnemonic for the causes)
- gallstone pancreatitis
- interstitial oedematous pancreatitis
- necrotising pancreatitis
- haemorrhagic pancreatitis
- revised Atlanta classification of acute pancreatitis
- chronic pancreatitis
- Ascaris-induced pancreatitis
- tropical pancreatitis
- autoimmune pancreatitis
- emphysematous pancreatitis
- hereditary pancreatitis
- pancreatitis associated with cystic fibrosis
- segmental pancreatitis
- acute pancreatitis
- pancreatic atrophy
- pancreatic lipomatosis
- pancreatic trauma
- 1. Evans DB, Pisters PW, Abbruzzese JL. Pancreatic cancer. Springer Verlag. (2002) ISBN:0387951857. Read it at Google Books - Find it at Amazon
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- 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