PANCREATITIS

Cause: A.IDIOPATHIC (20%)B.ALCOHOLISM: acute pancreatitis (15%); chronic

pancreatitis (70%)C.CHOLELITHIASIS: acute pancreatitis (75%); chronic pancreatitis
(20%)D.METABOLIC DISORDERS1.Hypercalcemia in hyperparathyroidism (10%),
multiple myeloma, amyloidosis, sarcoidosis2.Hereditary pancreatitis: autosomal
dominant, only Caucasians affected, most common cause of large spherical
pancreatic calcifications in childhood, recurrent episodes of pancreatitis,
development into pancreatic carcinoma in 20-40%; pronounced dilatation of
pancreatic duct; pseudocyst formation (50%); associated with type I
hypercholesterolemia3.Hyperlipidemia Types I and V4.Kwashiorkor = Tropical
pancreatitisE.INFECTION / INFESTATION1.Viral infection (mumps, hepatitis,
mononucleosis)2.Parasites (ascariasis, clonorchis)F.TRAUMA1.Penetrating
ulcer2.Blunt / penetrating trauma3.Surgery (in 0.8% of Billroth-II resections, 0.8% of
splenectomies, 0.7% of choledochal surgery, 0.4% of aortic graft
surgery)G.STRUCTURAL ABNORMALITIES1.Pancreas
divisum2.CholedochoceleH.DRUGSAzathioprine, thiazide, furosemide, ethacrynic
acid, sulfonamides, tetracycline, phenformin, steroids (eg, renal transplant),
asparaginase, procainamide I.MALIGNANCYPancreatic carcinoma (in 1%),
metastases, lymphoma Theories of pathogenesis: Reflux of bile / pancreatic
enzymes / duodenal succus (a)terminal duct segment shared by common bile duct
+ pancreatic duct(b)obstruction at papilla of Vater from inflammatory stenosis,
edema / spasm of sphincter of Oddi, tumor, periduodenal
diverticulum(c)incompetent sphincter of Oddi
Acute Pancreatitis =inflammatory disease of pancreas producing temporary
changes with restoration of normal anatomy + function following resolutionPath:
1.EDEMATOUS PANCREATITIS:edema, congestion, leukocytic infiltrates; mortality
rate of 4% 2.NECROTIZING PANCREATITIS:proteolytic destruction of pancreatic
parenchyma; mortality rate of 80-90% (a)HEMORRHAGIC PANCREATITIS:+ fat
necrosis and hemorrhage (b)SUPPURATIVE PANCREATITIS:+ bacterial infection A.
Diffuse pancreatitis (52%) B. Focal pancreatitis (48%): location of head:tail = 3:2
Clinical stages: I=EDEMATOUS PANCREATITIS (75%)
rapid improvement following conservative therapy
gradual decrease of elevated enzymesMortality:1-5%II=PARTIALLY NECROTIZING
PANCREATITIS
delayed / no response to conservative therapy
delayed / no normalization of enzymes
leukocytosis of <16,000
hyperglycemia of <200 mg/100 mL

hypocalcemia of >4 mval/L

base deficit of <4 mval/LMortality:30-75%III=TOTALLY NECROTIZING PANCREATITIS
deterioration under conservative therapy
leukocytosis of >16,000
hyperglycemia of >200 mg/100 mL
hypocalcemia of <4 mval/L
base deficit of >4 mval/LMortality:100% (40% by 2nd day, 75% by 5th day, 100% by
10th day)
acute abdominal pain (peaking after a few hours, resolving in 2-3 days), nausea,
vomiting
raised pancreatic amylase + lipase in blood + urine
increased amylase-creatinine clearance ratio
signs of hemorrhagic pancreatitis:
Cullen sign = periumbilical ecchymosis
Grey-Turner sign = flank ecchymosis
Fox sign = infrainguinal ecchymosis
NO findings on US / CT in 29%Abdominal film:
"colon cutoff" sign = dilated transverse colon with abrupt change to a gasless
descending colon (inflammation via phrenicocolic ligament causes spasm +
obstruction at the splenic flexure impinging on a paralytic colon)
"sentinel loop" (10-55%) = localized segment of gas-containing bowel in duodenum
(in 20-45%) / terminal ileum / cecum
"renal halo" sign = water-density of inflammation in anterior pararenal space
contrasts with perirenal fat; more common on left side
mottled appearance of peripancreatic area (secondary to fat necrosis in pancreatic
bed, mesentery, omentum)
intrapancreatic gas bubbles (from acute gangrene / suppurative pancreatitis)
"gasless abdomen" = fluid-filled bowel associated with vomiting
ascitesCXR (findings in 14-71%):

pleural effusion (in 5%), usually left-sided, with elevated amylase levels (in 85%)
left-sided diaphragmatic elevation
left-sided subsegmental atelectasis (20%)
parenchymal infiltrates, pulmonary infarction
pulmonary edema, ARDS
pleural empyema, pericardial effusion
mediastinal abscess, mediastinal pseudocyst
pancreatico-bronchial / -pleural / -pulmonary fistulaUGI:
esophagogastric varices (from splenic vein obstruction)
enlarged tortuous edematous rugal folds along antrum + greater curvature (20%)
widening of retrogastric space (from pancreatic enlargement / inflammation in
lesser sac)
diminished duodenal peristalsis + edematous folds
widening of duodenal sweep + downward displacement of ligament of Treitz
Poppel sign = edematous swelling of papilla
Frostberg inverted-3 sign = segmental narrowing with fold thickening of duodenum
jejunal + ileal fold thickening (proteolytic spread along mesentery)BE:
narrowing, nodularity, fold distortion along inferior haustral row of transverse colon
descending colonCholangiography:
long gently tapered narrowing of CBD
prestenotic biliary dilatation
smooth / irregular mucosal surfaceBone films (findings in 6%): secondary to
metastatic intramedullary lipolysis + fat necrosis
punched out / permeative destruction of cancellous bone + endosteal erosion
aseptic necrosis of femoral / humeral heads
metaphyseal infarcts, predominantly in distal femur + proximal tibiaUS (pancreatic
visualization in 62-78%):
hypoechoic diffuse / focal enlargement of pancreas

dilatation of pancreatic duct (if head focally involved)

perivascular cloaking = spread of inflammatory exudate along perivascular spaces
extrapancreatic hypoechoic mass with good acoustic transmission (= phlegmonous
pancreatitis)
fluid collection: lesser sac (60%), L > R anterior pararenal space (54%), posterior
pararenal space (18%), around left lobe of liver (16%), in spleen (9%), mediastinum
(3%), iliac fossa, along transverse mesocolon / mesenteric leaves of small
intestineFate of fluid collection:(a)complete resolution(b)pseudocyst
formation(c)bacterial infection = abscess
pseudocyst formation (52%): extension into lesser sac, transverse mesocolon,
around kidney, mediastinum, lower quadrants of abdomenCT (pancreatic
visualization in 98%):
no detectable change in size / appearance (29%)
hypodense (5-20 HU) mass in phlegmonous pancreatitis; may persist long after
complete recovery
hyperdense areas (50-70 HU) in hemorrhagic pancreatitis for 24-48 hours
enlargement with convex margins + indistinctness of gland with parenchymal
inhomogeneity
thickening of anterior pararenal fascia
non-contrast-enhancing parenchyma during bolus injection (= pancreatic
necrosis)Angiography:
may be normal
hypovascular areas (15-56%)
hypervascularity + increased parenchymal stain (12- 45%)
venous compression secondary to edema
formation of pseudoaneurysms (in 10% with chronic pancreatitis): splenic artery
(50%), pancreatic arcades, gastroduodenal artery Cx: 1.Phlegmon (18%) = solid
mass characterized by edema, infiltration of inflammatory cells + necrosis:
extension into lesser sac, anterior pararenal space, transverse mesocolon, small
bowel mesentery, retroperitoneum, pelvis2.Pseudocyst formation
(10%)3.Hemorrhage (3%)4.Abscess (2-10%): 2-4 weeks after severe acute
pancreatitis; most commonly due to E. coli

may contain gas within pancreatic bedDDx:air secondary to intestinal

fistula5.Pancreatic ascites6.Biliary duct obstruction7.Thrombosis of splenic vein /
SMV8.Pseudoaneurysm(a)rupture into preexisting pseudocyst(b)digestion of arterial
wall by enzymesIncidence:in up to 10% of severe pancreatitisLocation:splenic artery
(most common), gastroduodenal, pancreatico-duodenal, hepatic
arteryMortality:37% for rupture, 16-50% for surgeryTherapy: 1.Conservative (NPO,
gastric tube, atropine, analgesics, sedation, prophylactic antibiotics) for stage
I2.Early surgery in stages II and III

Chronic Pancreatitis =continuing inflammatory disease of pancreas characterized by

irreversible damage to anatomy + functionA.CHRONIC CALCIFYING PANCREATITIS:
protein plugs / calculi within ductal systemB.CHRONIC OBSTRUCTIVE PANCREATITIS:
secondary to slow growing tumor / surgical duct ligation / ampullary stenosis
dilatation of pancreatic duct
normal sized / focally or diffusely enlarged / small atrophic gland
calcifications uncommon
acute exacerbation of epigastric pain (93%):decreasing with time due to progressive
destruction of gland, usually painless after 7 years
jaundice (42%) from common bile duct obstruction
steatorrhea (80%)
diabetes mellitus (58%)
secretin test with decreased amylase + bicarbonate in duodenal fluid Plain film:
numerous irregular calcifications (in 20-50% of alcoholic pancreatitis)
PATHOGNOMONICUGI:
displacement of stomach / duodenum by pseudocyst
shrinkage / fold induration of stomach (DDx: linitis plastica)
stricture of duodenumCholangiopancreatography (most sensitive imaging modality):
slight ductal ectasia / clubbing of side branches (minimal disease)
"nipping" = narrowing of the origins of side branches

dilatation >2 mm, tortuosity, wall rigidity, main ductal stenosis (moderate disease)
"beading, chain of lakes, string of pearls"=dilatation, stenosis, obstruction of main
pancreatic duct + side branches (severe disease)
intraductal protein plugs / calculi
prolonged emptying of contrast material
may have stenosis / obstruction + prestenotic dilatation of CBDUS / CT:
irregular (73%) / smooth (15%) / beaded (12%) pancreatic ductal dilatation (in 4168%)
small atrophic gland (in 10-54%)
pancreatic mostly intraductal calcifications (4-68%)
inhomogeneous gland with increased echogenicity (62%)
irregular pancreatic contour (45-60%)
focal (12-32%) / diffuse (27-45%) pancreatic enlargement
mostly mild biliary ductal dilatation (29%)
intra- / peripancreatic pseudocysts (20-34%)
segmental portal hypertension (= splenic vein thrombosis + splenomegaly) in 11%
arterial pseudoaneurysm formation
peripancreatic fascial thickening + blurring of organ margins (16%)
ascites / pleural effusion (9%)MR:
loss of signal intensity on fat-suppressed T1WI (from loss of aqueous protein in
pancreatic acini secondary to fibrosis)
diminished contrast enhancement (from loss of normal capillary network replaced
by fibrous tissue)Angiography:
increased tortuosity + angulation of pancreatic arcades + intrahepatic arteries
(88%)
luminal irregularities / focal fibrotic arterial stenoses (25-75%) / smooth beaded
appearance
irregular parenchymal stain
venous compression / occlusion (20-50%)

portoportal shunting + gastric varices without esophageal varicesCx:pancreatic

carcinoma (2-4%), jaundice, pseudocyst formation, pancreatic ascites, thrombosis of
splenic / mesenteric / portal veinRx:surgery for infected pseudocyst, GI-bleeding
from portal hypertension, common bile duct obstruction, gastrointestinal obstruction