Pancreas Flashcards
Regions of pancreas
Head:
-Posterior to transverse mesocolon
-Anterior to: vena cava, right renal artery, both renal veins
Neck:
-Anterior to: portal vein, vertebral body of L1 & L2 *blunt trauma
Body:
-Anterior to aorta at origin of SMA
Tail:
-Near splenic flexture of left colon *avoid injury during left colectomy or splenectomy
Ucinate process wraps around SMA/SMV
-Divide gastrocolic omentum: body & tail of pancreas along floor of lesser sac, posterior to the stomach pancreatic pseudocysts develop here= drainage into stomach
-Base of transverse mesocolon attaches to inferior margin of body & tail of pancreas drain pancreatic cysts through transverse mesocolon
What is the location of the pancreas uncinate process?
Rests on aorta, behind SMA & SMV
Venous supply to pancreas
*Venous return= splenic & SMV (portal system)
-Inferior mesenteric vein joins splenic vein near junction with portal vein
-Superior mesenteric vein: joins splenic vein at inferior border of neck of pancreas
-Usually no anterior venous tributaries= plane developed between neck of pancreas & portal & superior mesenteric veins during pancreatic resection
Arterial supply to pancreas
-Branches from celiac & SMA
-Common hepatic (branch from celiac): gives rise to gastroduodenal artery (supplies stoamch, duodenum, pancreas) & proper hepatic artery
-Gastroduodenal artery: right gastroepiploic artery (great curvature of stomach) & superior pancreaticoduodenal arteries
-Gastroduodenal artery travels posterior to duodenal bulb * posterior ulcer in duodenal bulb can erode into GDA*
-Superior & inferior pancreaticoduodenal arteries join
-Inferior pancreaticoduodenal artery: branch off SMA impossible to resect head of pancreas without devascularizing duodenum unless rim of pancreat containing pancreaticoduodenal arcade is preserved
-Replaced right hepatic artery: arises from SMA and travels upwards toward liver along posterior aspect of head of pancreas
What are the arterial supplies to the head of the pancreas?
-Superior pancreaticoduodenal artery (off GDA)
-Inferior pancreaticoduodenal artery (off SMA)
What arteries supply the body of the pancreas?
Great, inferior, and caudal pancreatic arteries (off splenic artery)
What arteries supply the tail of the pancreas?
Splenic dorsal arteries
Pancreas nerves
-Afferent sensory fibers responsible for intense pain associated with advanced pancreatic cancer as well as acute and chronic pancreatitis
-Somatic fibers travel superiorly to the celiac ganglia = celiac plexus block stop transmission of pain
Pancreas lymphatics
-Celiac & SMA nodes
-Pancreatic lymphatics communicate with lymph nodes in the transverse mesocolon & mesentery of the proximal jejunum
-Tumors in the body & tail of the pancreas often metastasize to nodes & lymph nodes along the splenic vein & in the hilum of the spleen
What do ductal cells in the pancreas secrete?
-Ductal cells secrete bicarbonate and have carbonic anhydrase -High flow leads to high bicarbonate and low chloride.
Secretin released from cells in duodenal mucosa in response to acidic chyme passing through pylorus into duodenum; secretin stimulates bicarbonate secretion
Truncal vagotomy= reduction in bicarbonate secretion
What is the function of acinar cells in the pancreas?
Acinar cells (exocrine) secrete digestive enzymes- amylase, proteases, lipases
Destruction of branching tree from recurrent inflammation/ scarring/ deposition of stones in chronic pancreatitis= destruction of exocrine pancreas= exocrine pancreatic insufficiency
Which pancreatic enzyme is secreted in active form?
Amylase is the only pancreatic enzyme secreted in active form. Hydrolyzes starch and glycogen. Faastests to be cleared in pancreatitis.
(Lipase: most specific enzyme; pancreatic lipase is secreted in active form but needs colipase to increase activity)
Chymotrypsinogen
-Converted to active chymotrypsin by trypsin
-Digests protein
Trypsin
-Trypsinogen converted to active form trypsin by enterokinase on intestinal brush border
-Trypsin activates the other proteolytic enzymes
-Trypsinogen activation within pancreas prevented by inhibitors also secreted by acinar cells
-Failure to express normal trypsinogen inhibitor- PSTI also known as SPINK1- is a cause of familial pancreatitis
-Missense mutation on the cationic trypsinogen isoform (PRSS1) results in premature, intrapancreatic activation of trypsinogen - is a cause of hereditary pancreatitis
Pancreas secretion physiologic control
-Cholecystokinin: pancreatic enzyme secretion
-Secretin: pancreatic fluid and bicarbonate secretion
Pancreatic Islet Peptide Products
Insulin:
-Beta cell (at islet center; 70% of mass)
-Decreases: gluconeogenesis, glycogenolysis, lipolysis, ketogenesis
-Increases: glycogenesis, protein synthesis, glucose uptake in muscle & adipose tissue
-Stimulated by: glucose & fatty acids
-Incretin effect: response to oral glucose > IV glucose; mediated by GIP and GLP-1
Glucagon:
-Alpha cell (in islet periphery; 20% of mass)
-Increases hepatic glycogenolysis & gluconeogenesis
-Stimulated by low glucose
Somatostatin:
-Delta cell
-Inhibits secretion & action of all pancreatic & gut peptides
-Inhibits cell growth
Ghrelin
-Epsilon cell
-Decreases insulin secretion & action
-Appetite stimulating; increased in obesity
Pancreatic polypeptide (PP):
-PP or F cell
-Inhibits pancreatic exocrine secretion & facilitates hepatic action of insulin
-Vagal stimulation of pancreas= most important regulator of PP secretion. Vagotomy completeness: test PP levels
Islet distribution
-Beta and delta evenly distributed throughout pancreas
-Islets in head & uncinate process have higher percentage of PP cells and fewer alpha cells
-Islets in body and tail contain the majority of alpha cells & few PP cells
-Clinically significant: pancreatoduodenectomy removes 95% of PP cells in pancreas; higher incidence of glucose intolerance after Whipple procedure compared to distal pancreatectomy
-Chronic pancreatitis= disproportionately affects pancreatic head; associated with PP deficiency & pancreatic diabetes
-Alpha cells in body & tail= typical location of glucagonomas
What does the ventral pancreatic bud form?
-Uncinate and inferior portion of the head
-Contains the duct of Wirsung (main duct). Connects directly to the common bile duct.
-Most of the pancreas drains through the duct of Wirsung into the common channel formed from the bile duct and pancreatic duct. Empties at ampulla of Vater or major papilla (at 2nd portion of duodenum). Muscle fibers around ampulla form spinchter of Oddi-> contraction/ relaxation by
What does the dorsal pancreatic bud form?
-Body, tail, and superior portion of the head
-Duct of Santorini
-Drains directly into duodenum
Pancreatic divisum
-Ventral & dorsal buds fails to fuse
-Complete/classic: minor papilla drains large duct of Santorini (majority of pancreas is drained through duct of Santorini); major papilla drains small duct of Wursung (inferior portion of pancreatic head and uncinate drains through duct of Wursung).
-Incomplete: small branch of ventral duct (Santorini) communicates to dorsal duct (Wirsung)
-95% asymptomatic
-If minor papilla inadequate= outflow obstruction= pancreatitis
Dx: CT or MRCP
-Gold standard= secretin-enhanced MRCP (secretin improves visualization of pancreatic duct)
Tx:
-Mild sx: low-fat diet, pain control
-Severe/recurrent sx: ERCP with minor papilla sphincterotomy. Avoid stenting- high complication rate. if fails: surgery- duodenotomy & minor papilla sphincteroplasty
What marks the transition from foregut to midgut?
Sphincter of Oddi marks the transition of foregut to midgut, where celiac supply stops and SMA takes over.
What is the most common location for heterotopic pancreas?
-90% in upper GI tract (stomach, duodenum, jejunum)
-Most common location= duodenum
-Most asx; surgical resection if symptoms (abdominal pain & distention)
What is the most common diagnosis for annular pancreas?
-Ring of pancreatic tissue surrounds 2nd portion of duodenum from failure of ventral bud rotation
-RF: Down’s syndrome
-Equal frequency in adults and children
-Dx: CT, UGI, MRCP; children most commonly diagnosed on prenatal US
-Most asymptomatic
-Presentation: duodenal obstruction, pancreatitis, bleeding, abdominal pain
Tx if sx: bypass annulus- duodenojejunostomy or gastrojejunostomy; neonates= duodenoduodenostomy;
-Pancreas no resected; if pancreatitis is the problem, ERCP and sphincteroplasty
Pancreatic insufficiency
-Loss of exocrine function
-Fat malabsorption, steatorrhea, malabsorbtion of fat-soluble vitamins
-Chronic pancreatitis (most common; once >90% acinar function lost), cystic fibrosis (2nd most common; CFTR- cystic fibrosis transmemebrane conductance regulator)
-Fecal elastase-1: mosr sensitive & specific indirect test
- <20 g of fecal fat is consistent with an intestinal etiology, whereas >20g of fecal fat is consistent with pancreatic insufficiency (after replacing enzymes)
-Direct secretin simulation test
Secretin stimulation test
-Evaluates pancreatic exocrine function
-Normal: total volume 2 cc/kig/hr, bicarbonate: > 10 mmol/L in 1 hr, enzyme/amylase secretion: 6-18 U/kg
Abnormalities
-Chronic pancreatitis: decreased bicarb
-End-stage pancreatitis: volume, bicarb, and amylase decreased
-Pancreatic cancer: volume decreased
-Malnutrition: amylase decreased
Zollinger-Ellison - Increased volume
Diabetes
-Type 1 DM: pancreas does not produce insulin (loss of beta cells)
-Type 2: body does not respond to insulin (insulin reisistance)
-Type 3C: Pancreatic diabetes mellitus induced by exocrine disease due to chronic pancreatitis or resection
-Impairment of beta cells & alpha cells
-Decreased secretion of insulin, glucagon, & pancreatic polypeptide
-Increased risk of hypoglycemia compared to type 1 DM given that alpha cells also affected
-DKA/hyperglycemia rare
Acute pancreatitis
-Smoking= independent risk factor
-Gallstones most common, alcohol 2nd most common
-Post-ERCP risk increased with sphincter of Oddi dysfunction
-Hyperlipidemia, hypercalcemia (colocalization & activation of trypsin)
-Hereditary: autosomal dominant, mutation in PRSS1= premature activation of trypsinogen to trypsin + abnormalities of ductal secretion
-Pancreatic or periampullary tumor: consider in idiopathic acute pancreatitis, esp if over 50 yo
-Drugs: thiazide diuretics, furosemide, estrogen replacement therapy, steroid therapy in children
Acute pancreatitis diagnosis
-Severe constant epeigastric pain that radiates through to mid back
-N/v, fever
Dx: >=2
-Acute, persistent severe epigastric pain
-Elevation of serum amylase or lipase >=3x normal
-Imaging only when above not met
-Serum amylase increases immediately, peaks within several hours, remains elevated for 3 to 5 days
-No correlation between amylase elevation & severity: severe disease pancreas may not have capacity to release enzyme & hemoconcentration from 3rd space fluid loss
-Cullen’s sign: umbilucus; Grey Turner’s sign: flank discolration from bleeding into retroperitoneum
Acute pancreatitis fluids
-Fluid therapy to restore/ maintain circulating blood volume= most important intervention in early management
-Ballanced crystalloid, aim to restore normal blood volume, blood pressure, and urine output
-LR suprerior to NS in reducing SIRS
Acute pancreatitis nutriton
-Early refeeding (<= 48 hours) if stable & tolerating diet
-If not tolerating diet: give enteral nutrition through jejunal feeding tube
What to avodid in pancreas pain management
Avoid morphine= potential to cause sphincter of Oddi spasm
Ranson’s Criteria
Bedside index for severity in acute pancreatitis
Ranson’s Criteria with 3 or more points indicates severe pancreatitis, leading to ICU admission.
Scored over 48 hours
BISAP: BUN > 25, impaired mentation, SIRS >= 2, Age > 65, pleural effusion
Chronic pancreatitis causes & symptoms
-Inflammation & fibrosis leading to injury/loss of acinar & islet cells (exocrine and endocrine function decreased)
-Alcohol most common cause (50%)
Sx: chronic pain, weight loss
Chronic pancreatitis diagnos & work up
Dx:
-Triad: pancreatic calcifications, steatorrhea, diabetes (seen in advanced disease)
-Lipase/amylase normal/slightly elevated
-CT: pancreas sunken & calcified with main duct beading & ectatic side branches (“Chain of lakes”)
Work up:
- CT if abnormality: EUS with biopsy to rule out cancer
- If no mass on EUS, ERCP to look for strictures
-ERCP most sensitive test to Dx chronic pancreatitis
Chronic pancreatitis complications
-Pleural effusion or pancreatic ascites: from retroperitoneal fluid leak, may lead to fistula (Tx= thoracentesis/ paracentesis, NPO, octreotide; 50% resolve in 2-3 weeks)
-Bile duct obstruction
-Splenic vein thrombosis
-Pseudoaneurysm
Risk for pancreatic cancer with chronic pancreatitis
Chronic pancreatitis treatment
Initial treatment
-Non-narcotic pain control
-No alcohol or tobacco, small low-fat meals, consider pancreatic enzyme replacement
-Specialized option if medical treatment fails: endoscopic decompression (less effective thanan surgery), celiac nerve block (limited success)
-Frey, Puestow, whipple, beger, distal resection
-If other surgeries fail: total pancreatectomy & islet cell autotransplantation
-Surgical indications for chronic pancreatitis – only consider after all medical and endoscopic therapy have been maximized
Chronic pancreatitis treatment: enlarged ducts
If > 6 mm: Decompression
Inflammatory Mass in Head: Frey Procedure
-Fibrotic Parenchyma & Enlarged Head with Poor Drainage
No Mass & Good Drainage: Puestow Procedure
Chronic pancreatitis treatment: small to normal ducts
-Isolated head: Whipple or Beger procedure
-Isolated tail: distal resection
-Not isolated: total pancreatectomy & islet cell autotransplant
Surgery for chronic pancreatitis:
Dilated pancreatic duct ≥ 6 mm = These patients NEED a procedure to drain the bile duct
* Peustow’s procedure: Roux en y Longitudinal pancreaticojejunostomy for diffusely dilated/strictured main pancreatic duct with no inflammation of pancreatic head
o Requires a minimum of 6 cm length of anastomosis to pancreatic duct
* Frey procedure (Peustow plus coring out head of pancreas), without transection of pancreatic neck): Duodenum preserving longitudinal Roux en y pancreaticojejunostomy with pancreatic head resection
o For isolated pancreatic head involvement and main duct dilation
o More commonly performed because technically easier to perform vs Beger
Non dilated pancreatic duct = These patients NEED resection, not drainage
* Beger procedure (duodenum preserving pancreatic head resection and Roux en y with two pancreaticojejunostomies using the same limb with pancreatic neck transection)
o for isolated pancreatic head involvement without ductal dilation
o Has more extensive vascular dissection of duodenum, can lead to duodenum necrosis
- Whipple - normal ducts, isolated pancreatic head, or salvage after other failed procedures
o Worse quality of life when compared to pancreas preserving surgeries above - Distal pancreatectomy - for normal ducts, but only distal gland affected
- Diabetes long term complication after these surgeries
- Bilateral splanchnicectomy or celiac ganglionectomy 80% pain control
Total pancreatectomy with auto islet transplantation for chronic pancreatitis, indicated for: - Last resort
- Patients with small ducts and diffuse disease
- Minimal change chronic pancreatitis
-Puestow Procedure vs Beger Procedure vs Frey procedure
-Puestow Procedure= Longitudinal pancreaticojejunostomy
-For dilated pancreatic duct (6mm or greater) would go with Peustow, so long as pancreatic head is normal
-Beger Procedure= Resection of pancreatic head up to wall of duodenum with either end to end or side to side pancreaticojejunostomy (Duodenum preserving pancreatic head resection)
-Frey Procedure= Lateral longitudinal pancreaticojejunostomy with an excavation of the pancreatic head (Core out head of pancreas but avoid pancreatic transection required of Beger procedure)
-If pancreatic head dominant disease with or without duct dilation= Frey procedure
-If distal pancreatic duct stricture with side branch changes and normal pancreatic head= distal pancreatectomy
-Minimal change pancreatitis- resection/ drainage will not help- denervation operation (bilateral thoracoscopic splanchnicectomy)
CBD stricture 2/2 to chronic pancreatitis:
CBD stricture 2/2 to chronic pancreatitis: Dx with MRCP. Do ERCP with brush biopsy if cannot rule out CA on MRCP. Tx: Choledocho-jejunostomy, NOT ERCP with stent
Alcohol & pancreatitis
-Induces sphincter of Oddi spasm, increases secretion & permeabilit, decreases blood flow
-Stellate cells: activated to myofibroblast phenotype= proinflammatory mediators & cytokines
-Ethanol induces ductal permeability= prematurely activated enzymes to cause damage to pancreatic parenchyma
-Forms protein plugs
-Timing: males 18 years of drinking, females 11 years of drinking
Hereditary & tropical pancreatitis
Hereditary pancreatitis:
-Autosomal Dominant
-PRSS1 Mutation – Cationic Trypsinogen Gene
Tropical pancreatitis:
-Autosomal Recessive
-SPINK1 Mutation – Serine Protease Inhibitor Kazal Type 1
-Associated with Eating Cassava Root
Both:
-Recurrent Acute Pancreatitis in Pediatrics & Chronic Pancreatitis in Adults
-High Risk for Pancreatic CA
-Treatment same as chronic pancreatitis
Autoimmune pancreatitis
-Type 1: IgG4-related; extrapancreatic complications: biliary stricture, retroperitoneal fibrosis, interstitial nephritis
-Type 2: not IgG4-related; limited to pancreas
-CT: Diffuse hypoechoic enlargement & main duct narrowing
-Biopsy: Plasma & lymphocytic infiltrate
-Tx: Steroids
Infected pancreatic necrosis, walled off collections or infected Pseudocyst
Infected pancreatic necrosis, walled off collections or infected Pseudocyst with no main duct disruptions
- Optimal timing for pancreatic intervention is >4 weeks after onset of pancreatitis
- Try to delay any intervention if possible unless you have positive gram stain on FNA or patient is getting unstable
- 1st step after failed medical management/more septic is: ALMOST ALWAYS START WITH drainage: CT guided retroperitoneal drain placement. Then wait 72 hours and can place more drains if more sick or collections are larger
- This can be followed by video assisted retroperitoneal debridement or endoscopic debridement (step up approach)
- Alternate first line therapy: endoscopic transmural drainage (needs to be 2 cm from stomach/duodenum)
- Otherwise percutaneous drains have fallen out of favor and endoscopic drainage is first choice and now preferred over drains
- Open debridement of the pancreas (last line) is only indicated for infected necrosis or abscess of pancreas, for which endoscopic measures have failed
RF for necrotizing pancreatitis: obesity
In necrotizing pancreatitis – enteral feeds decreased the rate of conversion to infected necrotizing pancreatitis
If you have a pancreatic pseudocyst and completely disrupted pancreatic duct only real solution is surgery with lateral pancreaticojejunostomy
Prophylactic antibiotics should not be started if no signs of infection. If empiric antibiotics initiate: carapenem; or cefepime + metronidazole
Pancreatic pseudocyst
Pancreatic pseudocyst FNA No glycogen, no mucin, high amylase (>5000)
- EUS with FNA is only done if diagnosis of pseudocyst is not clear
- Patients who are symptomatic, have rapidly enlarging pseudocysts, or who have infected pseudocysts that do not improve with medical management endoscopic drainage through stomach or duodenum (NEED TO BE AT LEAST 2 CM AWAY or less)
- Open cyst gastrostomy – anterior gastrostomy drain pseudocyst from posterior wall of stomach using linear stapler close anterior wall
- Cystduodenostomy if near pancreatic head/duodenum
- Roux en y cystojejunostomy – if away from stomach and duodenum
- The only indication to place a percutaneous drain in a pseudocyst, is in an infected pseudocyst in a pt who cannot tolerated endoscopic or surgical intervention
Pseudocyst
-MC w chronic pancreatitis, than acute pancreatitis
-Resolve spontaneously; manage expectantly for at least 6 weeks (ideally 3mo). Also allows wall to mature. Consider intervention if >6cm or symptomatic.
-Need ERCP or MRCP prior to intervention
-Approaches: transpapillary endoscopic stenting, endoscopic transluminal drainage, open cystgastrostomy, laparoscopic cystgastrostomy
If you see “septations” in pancreatic cyst, this is a solid component concerning for malignancy NOT pseudocyst
Atlanta classification
Acute necrotic collection - < 4 weeks, heterogenous, no defined wall
Walled off necrosis – takes 4 weeks to mature, has capsule, all have necrotic debris in collection = heterogenous, can be intra or extrapancreatic
Acute pancreatic fluid collection: <= 4 weeks, homogenous , no defined wall
Pseudocyst – takes 4 weeks to mature. Fluid collection is homogenous, no internal septa, usually extra pancreatic
-Antibiotics for necrotizing pancreatitis w signs of infection
-Clinical signs: fever, elevated WBC
-CT guided FNA with organisms
-Imipenem is antibiotic of choice
Pancreatitis risk of mortality
-Mild (no local/systemic complications): less than 1%
-Moderate (transient organ failure < 48 hr): 10%
-Severe (persistent organ failure): 20-40%
-Critical: > 50%
Elevated BUN/ creatinine &/or persistent SIRS after adequate fluid retention
Most common causes of death:
-Early (< 2 weeks): SIRS & organ failure
-Later (> 2 weeks): sepsis
Gallstone pancreatitis
-25-30% risk of recurrence within 6-18 weeks
-All should undergo elective cholecystectomy during same admission
-Mild-moderate pancreatitis: early (< 48 hours)
-Severe: wait until reolsved
-cholangitis or signs of clear obstruction: ERCP & spincterotomy
What is the characteristic finding in serous cystic neoplasms?
Serous Cystic Neoplasm (Serous Cystadenomas)
Benign
MC in pancreatic tail
MC women
No connection with pancreatic duct
Usually have numerous loculations
High in glycogen, low CEA
Present with abdominal pain, N/V, dyspepsia
CT: Shows:
- Classically will show a central scar (central calcification)
- Honeycomb pattern
Tx: Nothing, unless symptomatic or > 4 cm resect
What is the main characteristic of mucinous cystic neoplasms?
Mucinous Cystic Neoplasms
90% arise in body or tail
Female to male 9:1
Usually have single loculation
Premalignant lesions
Classically CT will show “peripheral egg-shell” = calcifications in the wall = diagnostic!!
Cyst FNA low amylase, high CEA, KRAS positive, + mucin
Walls of the cyst contain “ovarian-type stroma” on path
THESE DO NOT COMMUINCATE WITH MAIN PANCREATIC DUCT contrast to IPMN
ALL OF THESE Should be completely resected due to risk of CA
If found in distal pancreas MC operation is laparoscopic spleen preserving distal pancreatectomy
Intraductal papillary-mucinous neoplasm (IPMN)?
Intraductal papillary-mucinous neoplasm IPMN
-MRI is the preferred imaging
-Cyst FNA: High amylase, high CEA (> 200), KRAS positive, + Mucin
-On endoscopy the mucin will protrude through the ampulla and show a classic fish mouth appearance
-If main duct involved: chronic obstructive pancreatitis, pancreatic insufficiency (steatorrhea, diabetes, weight loss)
Main duct IPMN – 60% risk of malignancy
-Resection
Mixed type - very high risk of CA
-Resection
Branch duct IPMN – 25% malignancy
-Further imaging/EUS FNA vs straight to resection
-“High risk features” = straight to RESECTION: obstructive jaundice, enhancing solid component, main pancreatic duct > 1.0 cm
-“Worrisome features” (seen on MRI) = EUS WITH FNA; IPMN > 3 cm in size, thickened or enhancing cyst wall, non-enhancing mural nodule, main pancreatic duct dilation 0.5 cm – 0.9 cm, abrupt caliber change in the main pancreatic duct, symptoms (abdominal pain, pancreatitis)
-If any of these are found on EUS with FNA = RESECTION; mural nodules, thickened walls,+ Mucin, high CEA or + for KRAS
If the branch duct IPMN does not meet any of the above criteria Follow up MRI/CT in 1 year
Pancreatic fistula
Post-operative pancreatic fistula definition (all require amylase > 3 times upper limit of normal from drain)
- Biochemical leak – elevated amylase with no clinical implications no change in vitals, no sepsis, no percutaneous/endoscopic drainage performed, < 3 weeks persistent drainage, no angiography performed for bleeding
- Grade B fistula – elevated amylase + any one of the above clinical implications
- Grade C fistula – elevated amylase + organ failure or reoperation or death
Management:
Any patient with abdominal fluid collection concerning for pancreatic leak and has symptoms requires a PC drain to be placed
1st start with if high output >400 cc then NPO and TPN. If low < 200 then okay to eat.
Octreotide (lowers pancreatic fistula output)
If it doesn’t resolve after 6-8 weeks ERCP, sphincterotomy and stent placement
Need to wait at least 2-3 months before thinking of operating
What is the treatment for pancreatic ascites and pleural effusion?
Caused by retroperitoneal leakage of pancreatic duct disruption or ruptured pseudocyst
Can occur after trauma
This is not a pancreatic pleural fistula
Majority close on their own
Dx: aspiration high amylase and protein > 25
Tx: thoracentesis/paracentesis Then treat like fistula NPO, TPN, octreotide. ERCP with stent placement if that fails
Periampullary mass – 4 types of CA
Pancreatic ductal adenocarcinoma - #1 MC periampullary tumor
- 5YS 7%
Distal cholangiocarcinoma – 2nd MC periampullary tumor (10%)
- Cystic duct to ampulla, basically all of CBD
- 5YS 35%
Ampullary adenocarcinoma – 3rd MC periampullary tumor (8%)
- Ampulla of Vater
- 5YS 65%
Duodenal adenocarcinoma – 4th MC periampullary tumor 4%
- 5YS 50%
Tx: For resection, generally use pancreatic CA guidelines for contraindication etc
Pancreatic ductal adenocarcinoma, pancreatic cancer
Lymphatic spread 1st
RF: # smoking, AGE (older), obesity, diabetes, family history of pancreatic CA, chronic pancreatitis, FAP, BRCA2, Peutz- Jegers,
Prognosis based on vascular and nodal invasion, and ability of R0 resection
KRAS2 – involved in 95% of pancreatic cancer. MC gene mutation.
BRCA2: associated with increased risk of pancreatic CA
CA 19-9: correlates with tumor burden. Higher level, higher tumor stage. If > 1000 then 95% chance it is unresectable.
- Used as marker to monitor response to therapy
Diagnosis:
- CT has 85% sensitivity to diagnose (best initial test),
- ERCP has 90% sensitivity (however should not be used routinely. Only for high suspicion and no mass on CT)
- PET is not recommended for staging
Chemo –
- Gemcitabine + Capecitabine 1st line
- FOLFIRINOX (5-fluorouracil, leucovorin, irinotecan, and oxaliplatin) ONLY for highly functional patients. Actually has better survival when compared to gemcitabine
Adjuvant Chemotherapy: for ALL
If after obtained CT, vascular involvement is still not clear Next step is EUS to check for resectability
Preoperative ERCP and stent placement for a patient with obstructive jaundice before a whipple increases risk of wound infection and pancreatic fistula. Should only be used in cholangitis or severe pruritus. Also dilated duct helps intra-op
If the patient presents with resectable tumor and has obstructive jaundice next step is whipple not stent placement
Palliative treatment of pancreatic CA
- Metal stents for biliary obstruction = longer patency rates.
- Plastic stents for biliary obstruction need to be exchanged q2-3 months, increased occlusion rates
- For GOO or duodenal obstruction – duodenal stent just as good as gastrojejunostomy. Endoscopic stents better if < 6 months life expectancy. > 6 months = gastroJ
Pancreatic neuroendocrine tumors
2nd MC pancreatic tumor
20% associated with familial syndromes. Mostly sporadic
Most are non-functional
Biochemical workup must be done when found.
Workup:
- Obtain Chromogranin A level: elevated in 60% of functional and nonfunctional and Pancreatic polypeptide
- All need CT/MRI + a somatostatin localization study
- (CT can miss small tumors, especially duodenal gastrinoma)
- If above can’t find it, and especially for DUODENAL gastrinoma EUS
- Can’t use somatostatin study for insulinoma
- Best imaging to localize: 68Ga somatostatin receptor positron emission tomography PET/PET-CT (DODATATE scan)
- However most hospitals don’t have it so use octreotide scan
- All need EUS with FNA: Gives you information about whether its malignant AND if lymph nodes are involved
Non-functional pancreatic neuroendocrine tumors
70% of PNET are non-functional
90% of non-functional tumors are malignant, and they are very aggressive. Most cases have metastatic disease when found
More indolent compared to adenocarcinoma
Tx:
- If < 2 cm, low grade, asymptomatic you can observe vs enucleation
- If > 2 cm, invasive, OR NODE POSITIVE whipple or distal pancreatectomy with splenectomy. All need lymphadenectomy.
- Tumors that are small, not near pancreatic duct, and benign Can enucleate
- OK to resect liver metastatic disease for cure
Functional pancreatic neuroendocrine tumors
Functional pancreatic neuroendocrine tumors
30%
These are usually multifocal especially in MEN1
Octreotide for symptom palliation effective for all except somatostatinoma
MC in pancreatic head - gastrinoma and somatostatinoma
Non-functional > 2 cm, somatostatinoma, gastrinoma, VIPoma all need formal resection with lymphadenectomy +/- splenectomy
Insulinoma
Insulinoma – 90% benign. 99% found in pancreas. Evenly distributed in pancreas. MC to be solitary.
MC NET in pancreas
Sx: “Whipple Triad”= fasting hypoglycemia, neuroglycopenic sx (confusion, combativeness, seizures, visual changes, loss of consciousness), relief with glucose administration
Dx:
- Insulin to glucose ration > 0.3 after fasting
- High C peptide and insulin
- Fasting hypoglycemia <50 and fasting insulin > 24
- These are diagnostic
- Insulin to C-peptide ratio should be < 1.0 if it is more, than this is factitious
CT is the initial localization study
If above doesn’t localize then MRI with DOTATE or endoscopic US
Octreotide scan does not work here for localization
Selective pancreatic arterial calcium stimulation with hepatic venous insulin sampling BEST TEST to localize if can’t see on CT
- VERY INVASIVE, most likely you won’t use this
Treatment:
- <2 cm enucleate. > 2 cm formal resection (whipple or distal pancreatectomy)
Diazoxide – used preop to control hypoglycemia symptoms
Octreotide – also used preop to control symtpoms
Chemo: 5FU and streptazosin and debulking for recurrence or mets.
Gastrinoma
70% found in the duodenum, 25% in pancreas
60% most are malignant and most commonly found in head of pancreas
Most are multifocal
75% sporadic 25% MENI
-Triad= abdominal pain, diarrhea, weight loss in the presence of PUD
Gastrinoma triangle (Passaro Triangle) – junction between cystic duct and CBD, Junction of neck and body of pancreas , 2nd and 3rd portion of duo
Will see prominent gastric folds
MC mets to liver (Strongest prognostic indicator)
Ulcers (MC proximal duodenum, can be found distally though) and DIARRHEA (even with fasting)
MC found in duodenum, MC 1st portion
All patients with suspected gastrinoma should be screened for MEN1
Work up: Genetic testing, gastrinoma level, CT abd, EUS, octreotide/DOTA scan
Dx (need both):
- 1st DC any PPI, H2 blocker
- Screening: 1st get fasting serum gastrin >100. If negative, excludes gastrinoma
- If positive, this is not diagnostic
- Confirming test: 24-hour stomach basal acid output > 15.
- Confirming test (MC used): Gastric pH <2 is consistent with gastrinoma. >3 excludes it
- Performed if above tests are unclear: Fasting Secretin test – Check gastrin before, at 5, 10, 15 minutes after secretin given
- Increase in gastrin > 120 above baseline = diagnostic.
Tx:
Medical: 1st give PPI
Surgical:
- If has MEN1, - Surgery usually not performed due to multifocality and metastatic disease spread
- Surgery only indicated here if gastrinoma is identifiable and > 2 cm
- Must do surgery for hyperparathyroidism 1st
- For sporadic cases – Perform surgery, if no evidence of metastatic disease
- Duodenal gastrinoma resection with margins and lymphadenectomy
- 2nd portion whipple
- Pancreatic gastrinoma – Mobilize pancreas, intra-op US, and palpation
- Neck/Body/tail distal pancreatectomy +/- splenectomy. Take peripancreatic nodes
- Head enucleation if <2 cm. > 2 cm whipple. Both need periportal, peri-duodenal, perihepatic lymph node dissection
- Patients with liver mets can undergo surgery only if all of the tumor can be removed
Chemo: 5FU and streptazosin for malignant disease. Palliation is octreotide and PPI.
Mets disease and severe symptoms despite maximum medical tx total gastrectomy. NO VAGOTOMY
Glucagonoma
4 D’s - Diabetes, DVT, Depression, Dermatitis stomatitis, necrolytic migratory rash, anemia, weight loss
Most are malignant.
Most in distal pancreas
Dx: fasting glucagon level
Tx: whipple or distal pancreatectomy with splenectomy; removal of the body and tail of the pancrease to the left of the SMA and SMV. Do lymphadenectomy. Octreotide for symptoms, and zinc, amino acids and fatty acids for skin rash. Chemo same
VIPoma
VIPoma (Verner-Morrison Syndrome)
Watery diarrhea with hypokalemia and achlorhydria (WDHA) or acidosis from diarrhea
Dx: exclude other causes of diarrhea and high VIP level
Most are malignant and distal pancreas.
Tx: resection. Octreotide for symptoms
Somatostatinoma
Somatostatinoma – worst prognosis of all
Diabetes, gallstones, steatorrhea, hypochlorhydria
Most malignant, MC head, MC specific site in ampulla and periampullary area
Dx: fasting somatostatin level
Tx: cholecystectomy with resection. Chemo for malignant same
Whipple performed for:
- Periampullary carcinoid
- Adenocarcinoma in 1st or 2nd portion of duodenum
- Neuroendocrine (gastrinoma, carcinoid, somatostatinoma), in 2nd portion of duodenum
- Distal cholangiocarcinoma (distal to cystic duct)
- Gastrinoma (sporadic) in 2nd portion of duodenum or > 2 cm in pancreatic head
- Pancreatic endocrine neoplasm (insulinoma) in head of pancreas > 2 cm
- Neuroendocrine (gastrinoma, carcinoid, somatostatinoma) > 2 cm in 2nd portion of duodenum
Whipple NOT performed for:
- Lymphoma in 1st or 2nd portion of duochemo-XRT
- Symptomatic duodenal diverticulitis in 2nd portion if biliopancreatic sx: ERCP, stent placement
- Crohn’s affecting duodenum if stricture in 1st or if in 2nd portion gastroJ with vagotomy
Solid pseudopapillary epithelial neoplasm
- Occurs exclusively in young females
- Has some malignant potential
- Resect all of these
Pancreatic lymphoma
Pancreatic lymphoma
Will have B type symptoms, fevers, chills night sweats.
CT will show bulky lymphadenopathy!!!
Will not have weight loss, back pain, obstructive jaundice
Treatment: chemotherapy alone, cyclophosphamide, vincristine, Doxorubicin (Adriamycin), prednisone
Cystic neoplasms of pancreas
-MRCP better characterize duct anatomy (than abdominal CT)
-EUS allows for aspiration for cyst fluid analysis (CEA and Amylase)
-CEA >192 c/w mucinous cyst
-High amylase indicates ductal communication (pseudocyst or IPMN)
Double duct sign on MRCP
simultaneous dilation of common bile duct/ billiard tree and pancreatic duct that suggests biliary obstruction; commonly associated with pancreatic head tumors, particularly periampullary tumors
Next step: ERCP for visualization of biliary tree & pancreatic ducts and bx/ brushings; can also place biliary stent
-Presents with…chronic alcohol use, abdominal pain, jaundice, unintentional weight loss, hepatomegaly, RUQ tenderness
Pancreas cystic lesion flow chart
Pancreatic unresectability
Any metastases, extension into the hepatoduodenal ligament, involvement of major arterial structures, inolvement of nodal or neural structures around the celiac or superior mesenteric artereries
Isolated involvement of the ssuperior mesenteric vein or portal vein can be resected in select patients
