Pancreatic ductal adenocarcinoma (PDAC) is the most common and most aggressive pancreatic malignancy, accounting for 85-90% of all pancreatic cancers. It originates from ductal epithelial cells and typically occurs between ages 60-80 with a male-to-female ratio of 1.3:1. Smoking, chronic pancreatitis, diabetes, obesity, and family history are the main risk factors. The tumor contains dense desmoplastic stroma, and this fibrotic composition forms the basis of its hypovascular imaging appearance. 60-70% of cases are located in the pancreatic head presenting with obstructive jaundice; body and tail tumors present late with advanced-stage disease. At diagnosis, only 15-20% of cases are surgically resectable. Median survival is 20-24 months for resectable disease and 6-11 months for metastatic disease.
Age Range
60-80
Peak Age
70
Gender
Male predominant
Prevalence
Common
PDAC develops through a stepwise progression from normal ductal epithelium through pancreatic intraepithelial neoplasia stages (PanIN-1→PanIN-2→PanIN-3→invasive carcinoma). KRAS oncogene mutation is found in >90% of cases and represents the early driving genetic event, followed by p16/CDKN2A (95%), TP53 (75%), and SMAD4/DPC4 (55%) inactivations. The most prominent histological feature is dense desmoplastic stromal reaction — up to 80% of tumor volume may consist of fibrotic stroma. This desmoplasia both renders the tumor hypovascular and impedes drug penetration. Hypovascularity manifests on CT as a mass that enhances less than surrounding parenchyma (hypodense) during the pancreatic phase, because tumor vessels are sparse compared to the rich capillary network of normal pancreatic tissue. The tumor has a strong propensity for perineural invasion, lymphatic spread, and vascular encasement. Obstruction of the main pancreatic duct and/or common bile duct leads to upstream ductal dilatation and pancreatic atrophy — the radiological finding known as the 'double duct sign'.
Simultaneous dilatation of the main pancreatic duct and common bile duct with abrupt cutoff at the level of the pancreatic head. This finding is 78-85% specific for pancreatic head malignancy and indicates one of the most common causes of obstructive jaundice. Can also be demonstrated non-invasively with MRCP.
Distinctly hypodense mass relative to pancreatic parenchyma in the pancreatic phase (40-50 seconds after arterial phase, ~65-70 s post-bolus). Normal pancreatic parenchyma enhances intensely during this phase (~100-150 HU), while the tumor remains at low density (~40-80 HU) due to desmoplastic stroma. This phase provides the highest tumor-parenchymal contrast difference and is the most critical CT phase for PDAC detection. In small tumors (<2 cm), the contrast difference may be less conspicuous.
Report Sentence
A distinctly hypodense mass relative to pancreatic parenchyma is identified in the pancreatic phase, consistent with ductal adenocarcinoma.
In pancreatic head tumors, simultaneous dilatation of the main pancreatic duct (>3 mm) and common bile duct (>7 mm) — the 'double duct sign'. Dilated ducts show abrupt cutoff at the level of the pancreatic head. This finding is highly specific for pancreatic head malignancy but can also be seen in ampullary tumors and distal cholangiocarcinoma. Portal venous phase depicts the dilated ducts more clearly as duct wall contrast uptake increases.
Report Sentence
Simultaneous dilatation of the main pancreatic duct and common bile duct at the level of the pancreatic head (double duct sign) is identified, consistent with pancreatic head malignancy.
Tumoral soft tissue encasement around the celiac trunk, superior mesenteric artery (SMA), and/or portal vein/SMV. The degree of vascular invasion determines resectability per NCCN criteria: arterial encasement >180° or aortic contact = borderline resectable/unresectable; venous encasement >180°, thrombosis, or contour deformity = borderline/unresectable. Arterial phase best evaluates the relationship between vascular structures and tumor as arteries show maximal enhancement.
Report Sentence
The tumor demonstrates soft tissue encasement around the SMA/celiac trunk/portal vein, and resectability assessment regarding vascular invasion is recommended.
Distinctly hypointense mass relative to pancreatic parenchyma on T1-weighted fat-suppressed sequences. Normal pancreas shows high signal on T1 due to protein-rich acinar cells; the desmoplastic stroma of PDAC disrupts this high signal. Post-contrast dynamic series demonstrate hypovascular enhancement pattern similar to CT. MRCP sequences can non-invasively demonstrate ductal dilatation and abrupt cutoff.
Report Sentence
A hypointense mass relative to pancreatic parenchyma on T1-weighted fat-suppressed sequences is identified, with ductal cutoff on MRCP, consistent with ductal adenocarcinoma.
Distinctly hyperintense signal on DWI (b=800-1000) with low ADC values (<1.2 × 10⁻³ mm²/s) on ADC maps. Diffusion restriction reflects the dense cellularity and desmoplastic stroma of PDAC. DWI provides added value particularly for detecting small tumors that are isoenhancing on CT. ADC values can also serve as biomarkers for tumor aggressiveness and treatment response monitoring.
Report Sentence
The mass demonstrates marked diffusion restriction on DWI (ADC <1.2 × 10⁻³ mm²/s), reflecting high cellularity and desmoplastic composition.
Hypoechoic, irregularly marginated solid mass relative to pancreatic parenchyma. In pancreatic head tumors, dilatation of the intrapancreatic common bile duct and/or main pancreatic duct accompanies. US sensitivity depends on tumor size — 75-90% for tumors >2 cm, but may fall below 50% for tumors <2 cm. Retroperitoneal gas and obesity limit image quality. US is usually the initial examination showing the level of obstruction in jaundice etiology.
Report Sentence
A hypoechoic solid mass in the pancreatic head is identified with accompanying dilatation of intrahepatic bile ducts and main pancreatic duct; further imaging (contrast-enhanced CT) is recommended.
Marked atrophic thinning of pancreatic parenchyma proximal (toward the tail) to the tumor. Chronic ductal obstruction leads to acinar cell loss, fibrosis, and fatty replacement. The atrophic parenchyma shows decreased density (due to fatty infiltration) and volume loss. This finding reflects the chronic obstructive effect of the tumor and helps differentiate from acute pancreatitis.
Report Sentence
Marked atrophic thinning and fatty replacement of pancreatic body and tail parenchyma proximal to the tumor is noted.
Criteria
Tumor localized in pancreatic head or uncinate process (60-70%). Earlier symptomatic type — presents with obstructive jaundice.
Distinct Features
Double duct sign, dilated bile ducts, Courvoisier gallbladder (distended, painless), pancreatic body/tail atrophy. CBD dilatation >10 mm and pancreatic duct dilatation >4 mm are typical.
Criteria
Tumor localized in pancreatic body or tail (30-40%). Late symptomatic — usually advanced stage at diagnosis.
Distinct Features
Biliary obstruction rare, jaundice not expected. Celiac trunk and splenic artery invasion more common. Splenic vein thrombosis and left-sided portal hypertension (sinistral portal HT) may develop. Peripancreatic fat infiltration and adjacent organ invasion common at diagnosis.
Criteria
Histologically contains >80% extracellular mucin pools. Comprises 1-3% of all PDACs. May develop from IPMN background.
Distinct Features
Better prognosis than conventional PDAC (5-year survival 55% vs 15%). May show lower density on CT due to high mucin content. High signal on T2 MRI (mucin). May be better circumscribed.
Criteria
Contains both ductal adenocarcinoma and squamous cell carcinoma components (30%+ squamous). Comprises 1-4% of all pancreatic cancers.
Distinct Features
More aggressive course than conventional PDAC, worse prognosis. Cystic/necrotic components may be more prominent. Heterogeneous hypodense mass on CT, necrotic areas may be more extensive than conventional PDAC.
Distinguishing Feature
In focal pancreatitis, ductal obstruction typically shows smooth tapering or 'duct-penetrating sign', while PDAC shows abrupt duct cutoff. In focal pancreatitis, enhancement increases in the delayed phase (fibrosis), while PDAC remains hypovascular. Focal pancreatitis may also show restriction on DWI but ADC values are generally higher than PDAC.
Distinguishing Feature
Autoimmune pancreatitis characteristically shows diffuse 'sausage-shaped' pancreatic enlargement, peripancreatic capsule-like rim, elevated IgG4, and dramatic response to steroid therapy. PDAC shows focal mass, vascular encasement, and metastases. Homogeneous delayed-phase enhancement in autoimmune pancreatitis distinguishes from persistent hypovascularity of PDAC.
Distinguishing Feature
Pancreatic neuroendocrine tumors show hypervascular enhancement in arterial phase while PDAC is hypovascular — this is the most fundamental distinguishing point. NETs are usually well-defined, round masses; PDAC has irregular, infiltrative margins. Ductal obstruction and upstream atrophy are much rarer in NETs. Functional NETs present with clinical syndromes (insulinoma, gastrinoma).
Distinguishing Feature
Chronic pancreatitis mass is accompanied by irregular ductal dilatation ('chain of lakes'), parenchymal calcifications, and pseudocysts. In PDAC, ductal dilatation is regular and calcification is rare. On MRI, chronic pancreatitis mass shows increasing delayed-phase enhancement; PDAC remains persistently hypovascular. Secretin-stimulated MRCP shows decreased ductal compliance in chronic pancreatitis.
Distinguishing Feature
In pancreatic lymphoma, the mass is usually homogeneous, low-attenuation, and 'surrounds but does not compress' vessels (vessel encasement without stenosis). In PDAC, vascular encasement leads to luminal narrowing. Regional and distant lymphadenopathy is more prominent in lymphoma. Ductal obstruction is less conspicuous in lymphoma compared to PDAC.
Urgency
urgentManagement
surgicalBiopsy
NeededFollow-up
specialist-referralMultidisciplinary tumor board evaluation is mandatory at PDAC diagnosis. Resectability is determined by CT angiography based on degree of vascular invasion (NCCN criteria: resectable / borderline resectable / locally advanced / metastatic). In resectable disease, Whipple procedure (pancreaticoduodenectomy) or distal pancreatectomy is performed; neoadjuvant chemotherapy is increasingly preferred in borderline resectable cases. Histopathological confirmation via EUS-FNA is usually required before neoadjuvant chemotherapy or in unresectable disease. CA 19-9 tumor marker is valuable in monitoring but insufficient alone for diagnosis. In metastatic disease, FOLFIRINOX or gemcitabine+nab-paclitaxel is standard chemotherapy.
Pancreatic ductal adenocarcinoma has an aggressive course with only 15-20% of patients being resectable at diagnosis. Early detection and surgical resection (Whipple procedure) is the most important prognostic factor. Vascular invasion determines resectability: >180° SMA/celiac trunk encasement is considered unresectable.