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FUNDAMENTALS OF BODY CT > Pancreas > Flashcards

Pancreas Flashcards

1
Q

Pancreas CT protocol

A
  1. Non-contrast
  2. Arterial phase: 30-35 sec
  3. Venous phase: 60-70 sec
  4. Delayed phsase: 3-5 mins
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2
Q

Pancreas Normal Anatomy

A
  • Location: Anterior pararenal compartment of the retroperitoneal space
  • Divided in 4 parts: Head (including the uncinate process), neck, body and tail
  • The main duct (Wirsung) joins the CBD at the sphincter of Oddi and enter the duodenum.
  • The accesory duct (Santorini) drains via the minor papilla.
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3
Q

Pancreas and pancreatic duct normal maximum width

A

Pancreas: Head: 3,0 cm, Body: 2,5 cm, Tail: 2,0 cm
Pancreatic Duct: Head: 3,5 mm, Body: 2,5 mm, Tail: 1,5 mm

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4
Q

Pancreas Divisum

A
  • The most common anomaly of the pancreatic duct, which is present in 4-10% of the population.
  • Failure of fusion of the dorsal and ventral pancreas during embryologic development
  • Dorsal duct drains into the minor papilla via the duct of Santorini.
  • There might be a “Santorinicele”
  • In most patients this is an incidental finding.
  • There is a constriction at the minor papilla –> predisposes to recurrent pancreatitis 25-38% of the patients.
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5
Q

Fatty Infiltration of the pancreas

A

Commonly associated with aging and obesity without affecting the funcion of the pancreas. However in advanced cystic fibrosis the pancreas is atrophic and diffusely replaced by fat, while exocrine function of the pancreas is severely impaired.

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6
Q

Acute pancreatitis: Definition

A

Inflammation of the pancreas damages acinar tissue and leads to focal disruption of small ducts resulting in leakage of pancreatic juice to surrounding tissues

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7
Q

How is the diagnosis of pancreatitis made?

A

Clinically: Abdominal pain + Elevation of serum amylase and lipase levels

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8
Q

What is the Role of CT in pancreatitis?

A

To document the presence, severity and complications (Prognosis)

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9
Q

Atlanta Classification of Acute Pancreatitis (2012) Subtypes (2)

A
  1. Interstitial edematous pancreatitis
  2. Necrotizing pancreatitis
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10
Q

Interstitial edematous pancreatitis

A
  • 90-95% of acute pancreatitis.
  • Diffuse or localized enlargement of the pancreas due to edema.
  • The entire pancreas enhances homogenously or slightly heterogeneously.
  • Peripancreatic inflammatory changes and Fat stranding
  • Peripancreatic fluid of varying volumes
  • Might generate: Acute peripancreatic fluid collections and pseudocysts
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11
Q

Acute peripancreatic fluid collections Characteristics

A

Associated with interstitial edematous pancreatitis:
- Non-capsulated, non-enhancing, low attenuation, liquefied collections without solid components
- <4 weeks of onset of symptoms
- No necrotic tissue or walls

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12
Q

Pancreatic Pseudocysts Characteristics

A

Associated with interstitial edematous pancreatitis:
- Homogeneous simple fluid collection.
- Visible walls.
- >4 weeks of onset of symptoms.
- Contain only fluid.
- Generally don’t require drainage unless infected (Ex. gas within collection).

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13
Q

Necrotizing pancreatitis characteristics

A
  • 5-10% of acute pancreatitis
  • Best characterized on early arterial phase
  • CT is most sensitive to necrosis >72 hrs following the onset of symptoms
  • Necrosis: Abscense of enhancement of pancreatic parenchyma and/or surrounding tissues
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14
Q

Necrotizing pancreatitis morphologic forms (3)

A
  1. Pancreatis parenchymal necrosis with peripancreatic necrosis.
  2. Pancreatis necrosis alone.
  3. Peripancreatic necrosis alone.
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15
Q

Pancreatis parenchymal necrosis with peripancreatic necrosis - characteristics

A
  • 75% of necrotizing pancreatitis
  • Lack of parenchymal contrast enhancement and heterogeneous non-liquefied areas of non-enhancement in the peripancreatic tissues
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16
Q

Pancreatis necrosis alone - characteristics

A
  • 5% of necrotizing pancreatitis.
  • Focal or diffuse areas of abscent parenchymal enhancement without associated collections.
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17
Q

Peripancreatic necrosis alone -characteristics

A
  • 20% of necrotizing pancreatitis.
  • Non-enhancement of peripancreatic tissues with normal enhancement of all pancreas parenchyma.
  • Peripancreatic collections contain liquefied and non-liquefied components.
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18
Q

Acute necrotic collections - Characteristics

A
  • Associated with necrotizing pancreatitis.
  • Heterogeneous collections containing necrotic pancreatic parenchyma, hemorrage and nefrotic fat.
  • <4 weeks of onset of symptoms.
  • Collections within or surrounding the pancreas.
  • Might complicate with: Walled off necrosis.
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19
Q

Walled off necrosis - Characteristics

A
  • Acute necrotic collections that develops an enhancing wall.
  • > 4 weeks from onset of symptoms.
  • Heterogeneous and complex in appearance.
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20
Q

Necrotic tissue infection signs and treatment

A
  • CT demonstration of gas within collection.
  • Percutaneous aspiration and drainage are needed as treatment.
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21
Q

Organ failure with acute pancreatitis: Classification

A
  1. Mild: No complications or organ failure.
  2. Moderate: Organ failure <48 hrs.
  3. Severe: Organ failure >48 hrs.
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22
Q

Acute pancreatitis complications (7)

A
  1. Secondary infection
  2. Hemorrage
  3. Pseudoaneurysms
  4. Thrombosis
  5. Disconnection of the pancreatic duct
  6. Pancreatic ascites
  7. Recurrence of pancreatitis
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23
Q

Causes of Acute pancreatitis (12)

A
  1. Gallstone
  2. Alcohol Abuse
  3. Smoking
  4. Metabolic disorders
  5. Trauma
  6. Autoimmune disease
  7. Penetrating ulcer
  8. Malignancy
  9. Drugs
  10. Infection
  11. Structural
  12. Idiopathic
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24
Q

Causes of metabolic acute pancreatitis (6)

A
  1. Diabetes mellitus
  2. Autosomal dominant hereditary pancreatitis
  3. Cystic fibrosis
  4. Hypercalcemia
  5. Hyperlipidemia, hypertriglyceridemia
  6. Malnutrition
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25
Q

Causes of trauma acute pancreatitis (3)

A
  1. Blunt abdominal trauma
  2. Abdominal surgery
  3. CPRE
26
Q

Causes of autoimmune acute panreatitis (2)

A
  1. Autoimmune pancreatitis
  2. Celiac disease
27
Q

Drugs that might cause acute pancreatitis (3)

A
  1. Corticosteroids
  2. Tetracycline
  3. Furosemide
28
Q

Infections that might cause acute pancreatitis (6)

A
  1. Mumps
  2. Hepatitis
  3. HVB
  4. AIDS
  5. Clornochiasis
  6. Ascariasis
29
Q

Structural causes of acute pancreatitis (2)

A
  1. Choledococele
  2. Pancreas divisum
30
Q

Chronic Pancreatitis - Definition

A

Chronic inflammatory disease of the pancreas with progressive pancreatic damage a irreversible fibrosis

31
Q

Chronic pancreatitis - CT Findings

A
  • Parenchyma atrophy - 54%
  • Calcifications 30-50%
  • Stricture and dilation of the pancreatic duct- 68%
  • Dilation of bile ducts
  • Fluid collections - 30%
  • Pseudocysts - 25-40%
  • Pseudomass formation - 30%
  • Alterations of pancreatic mass
32
Q

Main causes of chronic pancreatitis

A
  • Alcoholism (60%).
  • Hereditary autosomic disorder.
  • Autoimmune disease.
  • Tropical pancreatitis.
  • Non-alcoholic duct-destructive pancreatitis.
  • Idiopathic (30%).
33
Q

Autoimmune chronic pancreatitis - Main characteristics

A
  • Periductal lymphoplasmacytic inflammation.
  • Men 60-70 years old.
  • Clinically: abdominal pain, anorexia, weight loss and obstructive jaundice.
  • Lab: Elevation of IgG4.
  • DD: Neoplasic disease.
  • Associated with: Panniculitis, CBP, ulcerative colitis, fibrosing mediastinitis and retroperitoneal fibrosis.
  • PET CT: Multifocal pancreatic and peripancreatic uptake (not present in CA).
  • Enlarged lymph nodes (21%).
  • Associated renal lessions: Wedge-shaped hypodense lesions, renal nodules, mass-like lesions.
  • Treatment: Resolves with corticosteroids.
34
Q

Autoimmune chronic pancreatitis - Main distribution (3)

A
  1. Diffuse.
  2. Focal.
  3. Multifocal.
35
Q

Diffuse Autoimmune chronic pancreatitis pattern

A
  • Characteristic smooth hypoatenuating hypoenhancing capsule-like rim = “sausage pancreas”.
  • Weak and delayed enhancement of the parenchyma (fibrosis + inflammation).
  • Pancreatic duct difusely and irregularly narrowed.
36
Q

Focal Autoimmune chronic pancreatitis pattern

A
  • Might mimic neoplasia.
  • Commonly affects the head or uncinate process.
  • Slow progressive enhancement (adenocarcinoma is persistant low attenuation without notable enhacement).
37
Q

Groove pancreatitis

A
  • Men 30-50 years old + alcohol.
  • The wall of the duodenum is thickened, fibrotic and with cystic lesions.
  • Duodenal obstruction: abdominal pain, nausea, vomiting, weight loss.
  • CT: Focal low-attenuation inflammation of the pancreatic head with inflammatory thickening and small cysts in the wall of the duodenum and CHD smoothly narrowed.
  • DD: Pancreatic carcinoma, how to differenciate?
    –> No Vascular invasion.
    –> Smooth tapering of the CBD // CA causes abrupt scricture.
38
Q

Solid lesions of the pancreas: Differential diagnosis (Neoplastic solid tumors) (7)

A

1- Ductal adenocarcinoma
2- Pancreatic neuroendocrine tumor
3- Pancreatic lymphoma
4- Metastases
5- Solid pseudopapillary tumor
6- Acinar cell carcinoma
7- Mesenchymal tumors (sarcoma, fibrous histiocytoma, etc.)

39
Q

Solid lesions of the pancreas: Differential diagnosis (Non-neoplastic solid lesions) (7)

A

1- Focal chronic pancreatitis
2- Autoimmune pancreatitis
3- Groove pancreatitis
4- Focal sparing of diffuse pancreatic fatty infiltration
5- Intrapancreatic accesory spleen
6- Developmental pancreas lobulation
7- Sarcoidosis of the spleen

40
Q

Adenocarcinoma of the pancreas - Generalities

A
  • Agressive, fatal tumor, 5 year survival rate of 5%
  • Age 60-80 years old
  • 90% of pancreatic malignancies
  • 10-15% potentially resectable, of those only 70-85% undergoes resection
  • CT angiography is very helpful to determine vascular involvement by the tumor
41
Q

Adenocarcinoma of the pancreas - CT findings (6)

A
  1. Hypodense mass (96%).
  2. Enhanced minimally compared to normal pancreatic parenchyma.
  3. Very similar to focal pancreatitis so biopsy is needed to confirm the diagnosis.
  4. Calcifications are rare.
  5. Location: Head 60%, body 15%, tail 5%, diffuse 20%.
  6. The pancreatic duct and/or CBD is commonly dilated proximal to the tumor.
42
Q

Adenocarcinoma of the pancreas - Signs of potential resectability (5)

A
  1. Isolated mass.
  2. Combined bile duct-pancreatic duct dilatation with-out an identifiable pancreatic mass.
  3. Clear fat planes around the celiac axis, SMA and hepatic artery showing no signs of tumor involvement
  4. Tumor abutment of the SMA <180° is borderline resectable.
  5. Abscence of distortion of SMV and portal veins (if invaded no narrowing of the lumen)
43
Q

Adenocarcinoma of the pancreas - Signs of unresectability (7)

A
  1. Involvement of major arteries, long segments or occlusion of major veins.
  2. Encasement or invasion of the aorta or inferior vena cava.
  3. Encasement >180° of the SMA or abutment of the celiac axis.
  4. Long-segment occlusion of the SMV or portal vein.
  5. Extension of tumor beyond the margins of the pancreas or adjacent organs (spleen, stomach, duodenum).
  6. Metastases.
  7. Ascites is presumptive evidence of peritoneal carcinomatosis (confirmed by paracentesis).
44
Q

Neuroendocrine tumors (NET) - Main characteristics

A
  • 10% of pancreatic neoplasms
  • May be functional and produce hormones (20-40%)
  • 25% are associated with multiple endocrine neoplasia type 1, neurofibromatosis type 1, VHL or tuberous sclerosis
  • Non-functioning NET (60-80%): clinically silent until symptoms of a large mass
  • Malignancy: Insulinoma 10%, gastrinoma 60%, glucagonoma 70%, vipoma 75%, NF-NET 90%
45
Q

Neuroendocrine tumors (NET) - CT findings

A

Small tumors (1-2 cm):
- Homogeneous and isodense
- Enhances brightly and uniformly during arterial phase
Large tumors (4-20 cm) (Usually NF-NET)
- Heterogeneous with calcifications
- Cystic degeneration, necrosis
- Vascular invasion
- Invasion of nearby structures
- Metastases (20-40%): lymphnodes, liver and distant organs (lungs, bones, peritoneal cavity, brain and breast)

46
Q

Pancreatic lymphoma

A
  • Most commonly by direct extension from peripancreatic lymphadenopathy.
  • Most lymphomas are non-hodkin B-cell lymphomas with pancreatic involvement (30% of patients).
  • Primary pancreatic lymphoma is rare.
  • CT findings: Focal tumor, well circumscribed, homogeneous hypoattenuation (less than muscle), hypovascular (weakly but uniformly).
  • Diffuse: Mimics pancreatitis but without clinical evidence of pancreatitis.
  • Bulky mass with no or minimal dilatation of the pancreatic duct.
  • Lymphadenopathy below the level of the renal veins might be seen (no with adenocarcinoma).
  • Vascular invasion, tumor necrosis and calcifications are rare.
47
Q

Metastases to the pancreas

A
  • Rare 3-12% of advanced malignancies.
  • Most common: Melanoma, kidney, lung or breast.
  • 2-4% of pancreatic masses.
  • CT findings: round or ovoid, smooth discrete margins, heterogeneous contrast enhancement, might be hypervascular, commonly solitary or diffuse.
48
Q

Cystic pancreatic lesions (4)

A
  1. Pseudocysts
  2. Serous cystadenoma
  3. Mucinous cystic neoplasms
  4. True epithelial cysts
49
Q

Pancreatic pseudocysts

A
  • By far the most common cystic lesion in and around the pancreas.
  • Collections of pancreatic fluid + fibrous wall.
  • Fluid aspirated from it has high level of amilase.
  • No solid tissue or enhancing components.
  • Calcifications are ocasionally present.
  • Most are unilocular.
  • Signs of pancreatitis are usually present.
50
Q

Pancreatic serous cystoadenoma

A
  • Asymptomatic, bening cystic lesions, with no malignant potential.
  • Common in patients with VHL.
  • Females, >60 years old.
  • CT morphologic appearances (4)
    1. Unilocular
    2. Polycystic (bunch of grapes) (70%)
    3. Honeycomb (20%)
    4. Macrocystic (oligocystic) (10%)
    DD:
  • Oligocystic closely mimics that of mucinous cystadenoma.
  • Unilocular can be very similar to mucinous cystic neoplasms.
51
Q

Pancreatic serous cystoadenomas vs mucinous cystic neoplasms (5)

A

Favors serous cystoadenomas:
- Lobulated contour.
- Abscense of wall enhancement.
- Pancreatic head location.
- No communication with the pancreatic duct.
- Central stellate scar often with calcifications (important MCN give peripheral calcifications).

52
Q

Mucinous Cystic neoplasms (general)

A
  • Mucinous cystic neoplasms (MCNs) and intraductal papillary mucinous neoplasms (IPMNs)
  • Mucin producing epithelial tumor cells
  • Pathologic progression: low-grade dysplasia (adenoma) to high-grade dysplasia (carcinoma in situ) to invasive carcinoma
  • Fukoka guidelines 2012 (Tanaka Criteria)
  • Worrisome features and High-risk stigmata
  • Recommends resection without further testing for cystic lesions with high risk stigmata
  • Recommends endoscopic US for cystic lesions with worrysome features and >3 cm without them
53
Q

Fukoka guidelines (Tanaka criteria) - High Risk stigmata

A
  • Common bile duct obstruction with jaundice
  • Cystic tumor in the pancreatic head
  • Enhacement of solid components
  • Main pancreatic duct >10 mm
54
Q

Fukoka guidelines (Tanaka criteria) - Worrisome features

A
  • Cysts >3 cm
  • Enhancing thickened cyst walls
  • Main pancreatic duct 5-9 mm
  • Mural nodules without enhancement
  • Abrupt narrowing of the main pancreatic duct with proximal atrophy of pancreatic parenchyma
  • Regional lymphadenopathy
55
Q

Mucinous cystic neoplasms (MCNs)

A
  • Rary primary tumour of the pancreas
  • Middle age women (95%)
  • All are potential cystoadenocarcinomas
  • Low grade MCS: Excellent prognosis with surgery
  • High grade MCS: poor prognosis
  • Histologic identification of ovarinan stroma confirms the diagnosis
56
Q

Mucinous cystic neoplasms (MCNs) - CT findings

A
  • Multiloculated cysts with thin (<2 mm) septa (visible mostly with enhancement)
  • <6 cysts >6 cm
  • Attenuation of fluid tends to be heterogeneous and varies with content
  • Calcifications are seen in the capsule or septa in 10%
  • Peripheral calcifications are characteristic of MCN
  • Lesions 6-10 cm (large up to 32 cm)
  • Most common location: Distal body or tail
  • Do not communicate with ductal system
57
Q

Intraductal papillary mucinous neoplasms (IPMNs)

A
  • They secrete mucin into the pancreatic ducts, producing progressive dilation
  • Main-duct and branch-duct types
  • IPMN vs MCN: abscence of ovarian stroma
  • Intraductal papillaty solid masses in dilated pancreatic ducts are strong evidence of malignancy
  • Dilation of main pancreatic duct >15 mm is also predictive of malignancy
  • Cholangiopancreatic RM and CPRE show the connection of the cyst with the pancreatic duct
58
Q

Intraductal papillary mucinous neoplasms (IPMNs) - Main-duct characteristics

A
  • Main-duct have worse prognosis (60-92% have cancer)
  • Produce diffuse or segmental enlargement of the main pancreatic duct associated with atrophy of the pancreatic parenchyma
  • Calcifications within the dilated duct
59
Q

Intraductal papillary mucinous neoplasms (IPMNs) - Branch-duct characteristics

A
  • Branch-ducts have better prognosis (15-20% have cancer)
  • Bunch-of-grapes appearance that buldges the contour of the pancreas
  • Most common in the uncinate process
60
Q

True epithelial cysts of the pancreas

A
  • Infrequent
  • Usually solitaire
  • Seen in VHL disease (50% of patients) and autosomal dominant polycystic disease (5% of patients), rarely in cystic fibrosis
  • CT appearance:
    1. Well defined, fluid filled masses
    2. Internal septa and contrast enhancement are not present
61
Q

Von Hippel-Lindau disease Pancreas findings (3)

A

The cystic lesions in the pancreas are benign:
1. True epithelial cysts (50%)
2. Serous cystadenomas (12%)
3. Neuroendocrine tumor (7-12%)

A small number of NET might be malignant.

FUNDAMENTALS OF BODY CT (8 decks)

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