Pancreatitis

Pancreatic pathology part- 1 {PANCREATITIS}

DR ARIF KHAN S

DEPARTMENT OF RADIODIAGNOSIS

A.J SHETTY MEDICAL COLLEGE

ANATOMY

• Length – 15 cm.• The pancreas is located in the anterior pararenal space of the

retroperitoneum, just anterior to the perirenal (Gerota's) fascia and posterior to the parietal peritoneum.

• Head, uncinate process, neck, body, tail• Gradually tapering “Horse shoe” shape.

• Head – 23 +/- 3 mm• Neck – 19 +/- 2.5 mm• Body – 20 +/- 3 mm• Tail – 15 +/- 2.5 mm

The long axis of the body and tail of the pancreas is in an oblique orientation, extending from the hilum of the spleen to the midline of the body, where the pancreas lies anterior to the portal vein, which is the point of transition from the body to the neck .

• The neck of the pancreas is anterior to the superior mesenteric artery and can vary greatly in thickness

• The head of the pancreas is located in the C loop of the duodenum, bounded superiorly by the bulb, laterally by the second portion of the duodenum, inferiorly by the third portion of the duodenum, and medially by the superior mesenteric vein; it is anterior to the inferior vena cava

• The uncinate process, the inferiormost portion of the head of the pancreas, is triangular or wedge shaped and lies just posterior to the superior mesenteric artery and vein

Shape of pancreas

• common is the gradually tapering pancreas, where the head is larger than either the body or the tail, and the tail is the narrowest

IMAGING OF PANCREAS

• Radiograph – calcifcations

• Usg – screening tool and for followup

• Ct scan – MDCT is GOLD STANDARD For pancreatic lesions.

• MRI and MRCP are complementary to CT .

• imaging modalities are used to detect the cause .

ULTRASONOGRAPHY

• Widely available

• Easily accessible

• Can be repeated as often as necessary

• Cheap

• No ionizing radiation

• Portability

• Other causes of medical and surgical acute abdomen can be identified and excluded

CT SCAN

• Gold standard for all pancreatic pathologies

• Detects complications

• Helps in staging of tumors

• Post processing techniques are of additional help

Pancreatitis

• Acute

• Chronic

Acute pancreatitis

• Defenition: acute inflammatory process that is followed by complete restoration of structural and functional normalcy after the attack subsides. (provided that no part of pancreas undergo necrosis)

• Clinical features : Nausea , epigastric pain, fever, tachy cardia.

• Diagnosis is confirmed by serum Lipase and amylase assessment.

• All Radiological investigations are just supplementary role in diagnosis, moreover in assessment of severity.

• Identification of necrosis in pancreas indicates bad prognosis, severity increases with increase in area of necrosis.

Causes

• Cholelithiasis; Ethanol abuse

• Idiopathic

• Medications : Azathioprine

• Hyperlipidemia

• Tumors

• Trauma

• Pancreas divisum

Classification

• Mild Acute (oedematous interstium )

• Sever Acute (necrotizing)

Intermedeate forms are more common at the diagnosis .

CECT is best modality to differentiate the lesions based on severity and extend of involvement

Mild acute pancreatitis

• Self limiting disease process.

• responds well to early conservative management

• Microscopic acinar cell necrosis is seen .

• Peri pancreatic tissue necrosis is also seen.

• No macroscopic necrosis.

• Failure to improve after 48 hrs of conservative management CT

IMAGING

• USG in mild acute pancreatitis , the pancreas is normal or increased in size .

Free fluid and fat stranding may be visualized.

• CT

Increase in the volume of pancreas

Oedematous changes

Peripancreatic fluid collections

Peripancreatic fat stranding

Post contrast shows uniform enhancement (capillaries)

• A, Axial contrast-enhanced MDCT reveals a diffusely enlarged, enhancing pancreas with an acute inflammatory fluid collection in the peripancreatic region .

• B, and C Follow-up MDCT

Severe acute necrotizing.

• 20-30% of mild acute in 48 hrs.

• Very rapidly progress clinically into multi organ failure.

(apache or ransons criteria scoring for severity assessment)

• Necrosis – patchy or diffuse

• Usg also show oedematous gland with peri pancreatic collection.

• CT done after 3 days is ideal .

CT

• Increase in the volume of pancreas

• Oedematous changes

• Peripancreatic fluid collections

• Peripancreatic fat stranding

• Haemorrhagic areas

• Pancreatic necrosis

• Superinfection

• Vascular complications

CT severity index

Extrapancreatic complications (one or more of

pleural effusion, ascites, vascular complications,

parenchymal complications, or gastrointestinal

tract involvement) - SCORE 2

• Mild 0-2 (no mortality)

• Moderate 4-6

• Severe 8-10

Uses

Improve prognostic prediction.

CT score index of

<2 no mortality or morbidity, 2 has 4% morbidity and no mortality.

7-10 has 17% mortality and 92% morbidity or complication rate.

Acute Fluid Collections.

• Acute collections of enzyme-rich pancreatic juice occur in about 40% of patients

• These fluid collections may be around the gland or intra-pancreatic.

• They lack a capsule and are confined only by the anatomic space within which they arise, most commonly the anterior para-renal space or lesser sac.

• They can dissect into other locations, including the mediastinum and the posterior pararenal space, and can involve solid organs (liver, spleen, kidneys) or the wall of an adjacent bowel loop.

• Acute fluid collections appear hypodense on CT; they are poorly defined with no recognizable capsule or wall..

• These collections resolve spontaneously in about 50% of cases

• Those that do not resolve may evolve into pseudocysts , or they may be associated with a variety of complications, including pain, secondary infection, and hemorrhage.

• Fluid collections, whether encapsulated or not, are amenable to percutaneous catheter drainage if they do not resolve spontaneously or if they become infected

Pseudocyst.

• Pseudocysts are encapsulated, unilocular collections of pancreatic fluid and necrotic and proteinaceous material.

• They may evolve from acute fluid collections by the development of a non-epithelialized wall or capsule, or they may occur in patients with chronic pancreatitis sometime during the course of their disease.

• It takes about 4 weeks or longer for a pseudocyst to evolve from acute pancreatic fluid collections.

• Pseudocysts most often are peripancreatic but can be found throughout the abdomen, as well as within the mediastinum and pelvis.

• Large pseudocysts can cause pain secondary to the inflammatory process, displacement of adjacent structures, or pressure within the pseudocyst

• About half of all pseudocysts that arise in patients with acute pancreatitis resolve spontaneously by means of resorption of fluid or drainage in a bowel loop.

• The remaining half may stabilize, partially resolve, or enlarge and cause complications, necessitating intervention

• It is important to use positive oral contrast when evaluating pseudocyststo avoid mistaking them for the fluid-filled stomach or duodenum.

• On CT, a pseudocyst appears as a round or oval fluid collection with a thin or a thick wall that shows contrast enhancement.

• MRI reveals a well-defined, unilocular lesion that is hypointense on T1-weighted images and hyperintense on T2-weighted images

• Gas bubbles within the pseudocyst may be due to infection, fistula formation, or internal cystotomy, and percutaneous fine-needle aspiration proper clinical details are esentially required for a specific diagnosis.

• Venous stenosis or occlusion with the formation of varices and arterial pseudo-aneurysm may be seen.

• Acute hemorrhage due to enzymatic digestion of vessels or pseudocyst rupture is seen as high-attenuation material within the cyst .

• Occasionally a pseudoaneurysm may be confused with a pseudocyst.

• A dynamic CT scan with intravenous contrast identify a clot within the aneurysm is essential.

• Other complications, such as biliary and gastrointestinal tract obstruction, invasion into the spleen or liver, rupture into the peritoneum, and perforation into the gastrointestinal tract, can also be identified .

• Pseudocysts smaller than 5 cm in diameter are likely to resolve spontaneously and should be monitored

• Those larger than 5 cm, increasing in size, causing severe pain, or resulting in gastrointestinal or biliary tract obstruction should be considered for drainage

A, Axial contrast-enhanced MDCT reveals a well-defined, walled-off pseudocyst in the region of the pancreatic body. The pseudocyst is hypodense, with central hyperdensematerial representing hemorrhage with organization

B, T1-weighted fat-suppressed contrast-enhanced MR image in another patient reveals a hypointense pseudocyst(arrows), with central focal hyperintensity representing organized hemorrhage

• Fistula formation with the stomach or duodenum results in mechanical drainage, making surgery unnecessary.

• Fistula formation with colon, however, can result in bacterial colonization and infection and thus requires immediate debridement and bowel diversion

Pancreatic Abscess.

• Pancreatic abscesses are circumscribed intra-abdominal collections of pus located near the pancreas.

• They usually develop 4 weeks or more after the onset of acute pancreatitis and.

• The source of infection can be hematogenous or lymphatic, due to gastrointestinal fistula or perforation, or iatrogenic

• The CT diagnosis of pancreatic abscess is based on the presence of a focal, low-attenuation collection with a relatively thick wall that often contains gas bubbles

• Gas bubbles are not specific for infection, and gas may not always be present. Hence, the final diagnosis depends on correlation with the clinical condition of the patient and confirmation with percutaneous fine-needle aspiration

Infected Necrosis

• Necrotic pancreatic tissue infected.

• Recognized on CT scans as bubbles of gas or air pockets within areas of pancreatic or peripancreatic necrosis (emphysematous pancreatitis)

• CT is sensitive for detecting even the smallest amount of gas. However, when the pancreatic or peripancreatic necrotic tissue does not contain gas, the infection cannot be diagnosed on CT unless percutaneous aspiration is performed.

• It is important to distinguish abscess from infected necrosis, because the mortality rate for the latter is nearly double that of the former, and the specific therapy for each condition is different.

• On CT, an abscess is diagnosed when a normally enhancing pancreas is seen with an adjacent fluid collection composed of liquid pus (determined by needle aspiration).

• Infected necrosis is diagnosed when a zone of nonenhancingheterogeneous pancreas is seen and liquefied infected tissue is detected at needle aspiration.

• Abscesses can be treated effectively with percutaneous catheter drainage, whereas infected necrosis requires surgical necrosectomy and debridement.

• Percutaneous drainage if totally liquefied.

Haemorrhage.

• Hemorrhage in acute pancreatitis usually occurs as a late consequence due to either diffuse leakage from the inflamed granulation tissue or vascular injuries produced by the activated and extravasated pancreatic enzymes

• The splenic artery and its branches or the pancreatico-duodenal arcade arteries are commonly affected.

• Bleeding is commonly preceded by the development of an arterial pseudoaneurysm that ruptures, leading to sudden, massive hemorrhage.

• CT usually shows high-attenuation fluid (blood) within the peritoneal cavity or retroperitoneum or within a preexisting fluid collection or pseudocyst.

• Emergency angiography with selective embolization of the bleeding vessel is the treatment of choice

Chronic Pancreatitis

• Chronic pancreatitis is a progressive fibro-inflammatory disorder characterized by intermittent or continuous abdominal or back pain (or both) due to the persistence of structural damage after the primary cause has been eliminated

• This damage results in loss of pancreatic parenchyma, functional insufficiency (endocrine and exocrine), and complications such as biliary stricture, pseudo cyst, and pseudo aneurysm.

• Three types

1. Calcifying chronic pancreatitis alcohol and tobacco

2. Obstructive chronic pancreatitis obstruction

3. Autoimmune pancreatitis. lymphoplasmacytic inflammatory process.

Typically, chronic pancreatitis develops in patients with recurrent bouts of acute pancreatitis (e.g., alcoholic and hereditary forms of calcifying pancreatitis);

CT features • Irregular ductal dilation and strictures, parenchymal atrophy, and pancreatic

calcifications are typical CT manifestations of chronic pancreatitis.

• Pancreatic ductal dilation, though a frequent manifestation of chronic pancreatitis, is not specific;

• it can also be seen with pancreatic and ampullary carcinomas.

• Atrophic changes can be missed due to the inflammatory infiltrates in CT

• Pancreatic calculi or calcifications are the most specific CT manifestations of chronic pancreatitis and are not found in association with neoplastic obstruction.

• Biliary ductal dilation at the level of the pancreatic head is a nonspecific finding

• in chronic pancreatitis, common bile duct stenosis tends to be longer and more gradually tapered than in malignant obstructions

• When present, mature pseudocysts with well-defined enhancing walls can be well appreciated on CT.

• The extensive lobular and periductal inflammation and fibrosis may result in the formation of benign inflammatory pancreatic masses.

• Bland pancreatic fibrosis without inflammation or parenchymal destruction can occur with aging, alcoholism, and smoking. It is clinically silent and should be distinguished from chronic pancreatitis

Autoimmune Pancreatitis

• Autoimmune pancreatitis (AIP), first described by Sarles and colleagues in 1961 as “primary inflammatory sclerosis” of the pancreas

• variant of chronic pancreatitis that involves an autoimmune process

• There is an association between AIP and other autoimmune disorders such as Sjogren's syndrome, primary sclerosing cholangitis, primary biliary cirrhosis, ulcerative colitis, and SLE.

• The clinical presentation of AIP is varied and ranges from mild, nonspecific complaints such as upper abdominal pain and fatigability to obstructive jaundice and severe pain mimicking pancreatic malignancy.

• AIP should be distinguished from chronic alcoholic pancreatitis and other types of pancreatitis because 1.steroid therapy for the former type is effective

• 2. morphologic changes are reversible, and

• 3. pancreatic function can return to normal levels without surgical intervention if therapy is instituted at an early stage of the disease.

• The classic CT appearance of the pancreas in AIP is diffuse sausage-shaped enlargement of the pancreas with homogeneous attenuation, moderate enhancement, and a peripheral rim of a hypoattenuation referred as a “halo”.

• Loss of lobularity is common; peripancreatic fat stranding is usually minimal.

• As the disease progresses, involution or retraction of the pancreatic tail is evident.

• Extrapancreatic manifestations include focal lesions in the lungs, kidneys, liver, or soft tissue around the aorta, described as inflammatory pseudotumors.

Diagnostic criteria for AIP

Hereditary Pancreatitis• Hereditary pancreatitis is an autosomal dominant relapsing pancreatitis

with an estimated 80% penetrance.

• It generally manifests during childhood, with a peak incidence at age 5 years.

• However, a second peak at age 17 years may be attributable to the introduction of alcohol in the diet. In addition, factors such as hyperlipidemia and hypercalcemia may play a role.

• Parenchymal and intraductal calcifications occur in approximately 50% of patients.

• Intraductal calculi occur early in the course of the disease; they tend to be large and rounded and are arranged in a linear pattern in the dilated main pancreatic duct.

• Pancreatectomy is TOC

MRI in Pancreatitis• useful in patients who cannot receive iodinated contrast material owing to allergic

reactions or renal insufficiency or

• when equivocal CT abnormalities must be better characterized.

• In acute pancreatitis, fat-suppressed T2-weighted images are helpful for defining subtle diffuse or focal parenchymal abnormalities.

• T2-weighted images can accurately depict fluid collections, pseudocysts, and areas of hemorrhage.

• MRI can assess the internal consistency and drainability of fluid collections, thus influencing the choice of treatment.

• Gadolinium-enhanced T1-weighted GRE MRI can depict pancreatic necrosis as areas of non enhanced parenchyma

• MRCP has the advantage of demonstrating possible choledocholithiasis, the presence or absence of ductal disruption or leakage, and the size, location, and possible communication of a pseudocyst with the pancreatic duct, thus making it useful for therapeutic planning.

• In early stages of chronic pancreatitis, increased signal intensity on T2-weighted MR images is due to fatty and fibrous replacement, inflammatory cell infiltration of the pancreatic parenchyma, and impaired pancreatic juice outflow.

• Pre- and postgadolinium fat-suppressed T1-weighted images in chronic pancreatitis reveal decreased enhancement in the arterial phase and increased enhancement in the early venous phase.

A, Axial contrast-enhanced MDCT reveals a well-defined, walled-off pseudocyst in the region of the pancreatic body. The pseudocyst is hypodense, with central hyperdensematerial representing hemorrhage with organization

B, T1-weighted fat-suppressed contrast-enhanced MR image in another patient reveals a hypointense pseudocyst(arrows), with central focal hyperintensity representing organized hemorrhage

• MRCP offers several advantages over ERCP in the evaluation of chronic pancreatitis;

• it is noninvasive,

• avoids the need for contrast media and irradiation,

provides projection images in several planes, and

can be used to assess exocrine pancreatic function

Without the associated disadvantages of ERCP, such as the risk of complications and technical difficulties in postoperative patients

• MRCP well demonstrates dilation, stricture, and irregularity of the main pancreatic duct, as well as filling defects due to pancreatic stones and protein plugs;

• it visualizes the pancreatic ducts distal to sites of complete obstruction and pseudocysts, especially noncommunicating ones.

• Stones smaller than 2 mm and those lying within normal-caliber or minimally dilated side branches of the main pancreatic duct may be difficult to identify.

Groove Pancreatitis

• This is a segmental form of pancreatitis with inflammation in the groove between the duodenum and the head of the pancreas

• the rest of the pancreas enhances normally, and there is normal ductal morphology

• Chronic inflammation and fibrosis may cause duodenal, common bile duct, and distal pancreatic duct stenosis

• Sheet like lesion in pancreatico duodenal groove.

• Shows delayed enhancement.

• Cyst formation in the duodenal wall or pancreaticoduodenal groove has also been described

• Tissue diagnosis to differentiate malignancy

Pancreatic Tuberculosis

• Uncommon especially solitary involvement

• The most common sites of involvement in the abdomen are the mesentery, small bowel, peritoneum, liver, and spleen.

• The diagnosis usually is not suspected before laparotomy

• Focal involvement of the pancreas most frequently occurs in the pancreatic head, followed by the body and tail

• Diffuse pancreatic involvement is rare

• CT reveals a focal hypodense lesion, often displaying internal densities

• Contrast-enhanced CT the well-defined mass may show irregular margins with peripheral enhancement.

• Multi-loculated Appearance if central enhancing areas are present.

• Rarely, diffuse enlargement of the pancreas along with hypodense areas may be seen

• All these findings are non-specific.

• A normal pancreatogram on ERCP, despite a tuberculous mass in the pancreatic head, has been reported to be typical in tuberculouspancreatic involvement.

spotters

• aortoiliac occlusive disease, also known as Leriche's syndrome and Leriche syndrome, is atherosclerotic occlusive disease involving the bifurcation of the abdominal aorta as it transitions into the common iliac arteries

T2 shine-through

• T2 shine-through refers to high signal on DWI images that is not due to restricted diffusion, but rather to high T2 signal which 'shines through' to the DWI image.

• T2 shine through occurs because of long T2 decay time in some normal tissue.

• To confirm true restricted diffusion one should always compare the DWI image to the ADC.

• In cases of true restricted diffusion, the region of increased DWI signal will demonstrate low signal on ADC.