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Conferences and Medical Updates

Cysts and Pancreatitis

A.    Dr Brugge, Harvard
1.    4 types
a)    Serous, mucinous, pseudocyst and IPMN (main and side branch)
2.¬†¬† ¬†Pancreatic cancer ‚Äď 90% PanIN ‚Äď 1 ,2 and 3 pathway and are less than 5 mm in size. ¬†Cannot be detected by current EUS etc.
3.    Pathway is kRAS mutation, then PanIN1 then PanIN2 and then PanIN3 and finally cancer.
4.¬†¬† ¬†IPMN ‚Äď 2 types. ¬†Growth more than 2 mm/year and less than 2 mm/year growth. ¬†2 % malignancy in 5 years if less than 2 mm growth
5.    Risk of cancer is 0.4% year with IPMN
6.    4 types of IPMN
a)    Side branch
b)    Diffuse  main branch
c)    Focal main duct
d)    Mixed duct
7.    Consider IPMN with dilated PD.  IPMN is a villous adenoma
8.    Types of IPMN based on bx
a)    Gastric (best survival)
b)    Intestinal
c)¬†¬† ¬†Pancreatic ‚Äď biliary (worst survival)
d)    Oncocytic
9.    Branched chain IPMN are usually gastric mucosa
10.    Detection in IPMN use CEA, KRAS, cytology
11.    Look at size, growth rate, wall thickness, mural nodule and adjacent mass.
12.¬†¬† ¬†FNA of cyst ‚Äď evacuate cyst and send for 0.3 cc for KRAS, 0.3 for CEA and 0.5 for cytology. ¬†Also cytology of nodule and cytology of mass
13.    Using KRAS and CEA increases sensitivity and specificity to 85%
14.    Molecular analysis : KRAS, GNAS, TP53
15.    Cyst ablation : inject palitaxol after lavage of cyst.  Do this for 2-4 cm cyst in Branched duct IPMN if moderate surgical risk.  If in tail do it only for high risk surgical patient.
16.    EUS guidelines are
a)    If 2-3 cm EUS, cyst fluid analysis to be done every 6 months
b)    If cyst more than 3 cm,recommend surgery and follow up every 3-6 months
1.    Pancreas divisum does not cause pancreatitis. Probably from genetic mutation
2.    Idiopathic pancreatitis is from genetic mutation
3.    Pancreatic SOD are more likely to get recurrent pancreatitis ???
4.    SOD pt should not get ERCP or ES.  Does not help. Most of the patients have psychological issues
5.    ASGE guidelines probably faulty for SOD
6.    Post ERCP pancreatitis (PEP)
a)    Women less than 60, women, suspected SOD, normal Bilirubin, non dilated ducts are all high risk ERCP
b)    Under opacify duct and drain PD
c)    Hydration : give them 2 liters of fluid after ERCP.
d)¬†¬† ¬†Chemoprophylaxis : indomethacin ‚Äď rectal.
e)    Use 100 mg indomethacin rectally
1.    Chronic pancreatic pain : This occurs due to increased nerves in pancreatic cancer.  The nerves produce growth factors that increases the number of nerves and a vicious cycle occurs.  This is also true in pancreatic cancer.
2.    Laproscopic celiac plexus block or EUS guided block.  Do not use x ray block

Pancreatic and biliary system
1. Acute Pancreatitis Number 1 GI diagnosis for hospital admission
2. Incidence of AP is rising
3. Mild AP is 70%, Moderate is 20% and severe is 11%
4. Goal is walled off necrosis in moderate or severe AP
5. Persistent organ failure is more than 2 days of organ dysfunction
6. OF (organ failure) patients were older, worse CT, more intervention was needed. Commonest organ involved was lung, then kidney and then cardiovascular.(SIRS)
7. OF usually in 5-7 days. 20, 40 and 60 mortality depending on 1, 2 and 3 organs with OF
8. Late OF and early OF has no change in mortality
9. OF is worse prognosis then infected necrosis. Infected necrosis 4% mortality, IF plus OF 30% mortality and OF alone 44% mortality.
10. Severity of AP : LOOK AT BUN !!!!3 big studies RISK IS RISING BUN !!!!!! If BUN was more than 20, odds ratio for mortality is 4.6. Any rise in BUN in 24 hours, then OR is 4.3 for mortality. BUN is as good as APACHE.
11. bstay but DOE3-4S NOT CHANGE mortality. LR is better than NS. Give 3-4 L LR in first 24 hours. Do not exceed 4 liters. Monitor UP for more than 0.5 cc//kg/hr. Too much fluid causes abd. Compartment syndrome.
12. IVF is LR with 1 liter in 1 hour, then 3cc/kg/hour (about 200 cc /hr)
13. Pancreatic cysts management : AGA cyst A guidelines have changed.
14. If cyst more than 2 cm is 0.25% lifetime. Risk of transformation is less than 0.5% per year
15. Survellience : no worrisome features, repeat in 1 year, then every 2 years and stop survellience after 5 years.
16. If pancreatic family history of cancer and they have a pancreatic cyst – (or breast cancer),
17. EUS Axios system. (for pseudocyst drainage)
18. Endocuff :to improve polyp detection rate. ADR improves from 28% to 36%
19. POEM is not standard of care yet. Eckardt dysphagia score.
20. Albert Einstein : Difference between stupidity and genius is genius has limits.


·         4% mortality
·         Necrotizing pancreatitis mortality is 12 and if infected then 25% and organ failure for more than 48 hours 25% and if less than 48 hours 1%.
·         2012 Atlanta Revision for acute pancreatitis
·         Mild acute pancreatits or moderately severe acute pancreatitis where organ failure resolves in 48 hours and severe pancreatitis with persistent organ failure for more than 48 hours
·         Do not use Ranson and Apache ii score.
·         DM, obesity, age, fever (SIRS systemic inflammatory response syndrome), and HCT elevated and elevated BUN (even minimally) are predictors of severe pancreatitis in ER
·         BUN is the best marker to follow for mortality.
·         Rising HCT and BUN is an OMINIOUS sign
·         Inflammatory TNF, typsin, PLA2, elastase etc go up
·         Rate of fluid 250-500 cc/hour
·         Fluid must be given in first 12 to 24 hours
·         LR maybe preferred for pancreatits AMJG article
·         If transaminases are more than 3 x then gallstone pancreatitis
·         If bilirubin goes up Рsuggests CBD stone
·         Necrotizing pancreas goes from cement to liquid to similar to pseudocyst.
·         Pseudocyst is outside pancreas but necrosis that is organized Рis in pancreatic bed !!!!  DO NOT PUT DRAIN IN PANCREAS
·         LIMIT LINES
·         Day 7 Рcan do aspiration then patient may have infected necrosis.  INFECTED NECROSIS TREAT WITHOUT SURGERY.
·         Surgery only if clinically  unstable.
·         Necrosis even if infected can be managed with antibiotics
·         Enteral nutrition is the best way to prevent infection
·         NO MORE TPN
·         NJ or NG no difference
·         Do not check residual ! continue TF
·         TF better than eating orally
·         Amylase or lipase bouncing has no meaning

Pancreatic cyst

·         EUS for all more than 1 cm cyst

Endoscopic Necresectomy
Should only be done in walled off necrosis
CT scan is UNRELIABLE in differentiating between solid and liquid and differentiating between psuedocyst and necrosis
Intervene if patient is infected
Trans gastric or duodenal drainage and needs a large tract. Methods include irrigation or endoscopic necresectomy or combination
First done in 1996
Multigateway approach with 2 tracts created one for egress and one for ingress
Dual drainage – done both by IR and endoscopically on same day.
Fistula is avoided by IR in this situation because when fluid in tail of pancreas low, they pull drain and now the remaining fluid is drained from tail to body to stomach from stent in stomach to the necrosis
SEMS is a huge stent placed in the stomach (metal stent) A newer approach. Not available in USA yet
Chronic Pancreatitis
Most patients nowadays do not drink alcohol
Most patient are smokers
Genetics is a huge contributer
Autoimmune diseases
Bacterial overgrowth, gastroparesis, SIBO, osteoporosis, diabetes occurs in CP
Check fecal elastase -1 fasting TG, stool fecal fat, stool H pylori, Hb, Ca 19-9, B 12, folate, vitamin ADE, celiac, IgG4, ANA
Rx quit smoking, EtoH,
There are 20 genes associated with bad outcome for pancreatitis.
Use non enteric coated PES, antioxidants? pain referral and take care of PD stricture
Pain management in CP – Options are non opiate, opiate, celiac block and spinal stimulator
Type 3C Diabetes
Type 3a, (MODY),
type 3b (genetic insulin resistance donohue syndrome
Type 3d cushings (hormonal defets cushings)
Type 3 e steroids related
Called often brittle DM, difficult to treat, wide BS swings. Normal insulin sensitivity but lower hepatic insulin sensitivity (unsuppressed hepatic glucose production)
Disease state has affected alpha cells (glucagon)
70% have chronic pancreatitis, 8 % HH, 9% pancreatic cancer
RIsk of breast, colon, liver, kidney cancers more common (and esophagus)
Metformin is best drug for it
Avoid DPP4/GLP-1 drugs
Neuroendocrine tumors
Type 1 and 2 MEN
Takes 5-9 years to diagnose after pt has symptoms
Hypergastrinemia Type 1 is atrophic gastritis (autoimmune) and type 2 is ZE syndrome and type 3 is adenoca of the stomach
Duodenal NET (Usually first part of duodenum) and remove endoscopically. If more than 2 cm needs aggressive tumor resection like Whipple
Pancreatic NET – Functional or non functional Eg insulinoma, VIPoma, Gastrinoma, Somatostatinoma
MEN 1 4 gland parathyroid hyerplasia worsens ZES, Gastrinoma can be metastatic and more common in duodenum
Rectal NET – more than 2 cm have a high rate of nodal positivity and 25% liver mets. Prognosis is so bad that surgeons avoid radical surgery.
Cause of death is liver failure, bowel obstruction or ischemia

Pancreatic and Biliary Imaging
First do no harm
IPMN – if it grows 2 mm a year, less than 5% turn to cancer. If growth is more than 2 mm a year, 50% turn into cancer
Risk of IPMN is chronic pancreatitis, previous history of DM, PUD, insulin use
14 x increase in IPMN in last decade
IPMN – main duct do pancreatoscopy. Side branch EUS.
IPMN – 4 types – gastric, intestinal, pancreatic-biliary and oncocytic
70% are gastric, 20% intestinal, 7% pancreatic and 3 % oncocytic
Cyst more than 3 cm, dilatation of main PD, presence of a mural nodule, and if present in main duct vs side branch
Cyst fluid biomarkers that suggest cancer – CEA, RNA, DNA and enzymes. MiRNA 21 is the most imp. one. DNA oncogene k-ras and GNAS occur in 96% of IPMN pt
IPMN less than 1 cm, MRI every 2-3 years. 1-2 cm, MRI every year. If 2-3 cm, EUS every 3-6 months. If more than 3 cm, needs EUS / MRI / Surgery

Cysts of Pancreas

  • 1.2% of general population has it on routine imaging.
  • serous cystadenoma, mucinous cystic neoplasm, IPMN, cystic islet cell tumor, pseudocyst, solid papillary neoplasm
  • IPMN in male, head of pancreas, variable malignancy risk, All other cysts are more common in women.
  • Pseudocyst – may not always have history of pancreatitis. It is 15-30% of all cysts
  • Islet cell tumor – 17% is cystic and more common in MEN 1
  • Serous cystadenoma – usually large, innumerable small cysts with central calcification.¬† There is a macrocystic variant, usually females in 6th or 7 th decade and can be symptomatic, frothy, and very bright on EUS, low malignant potential.
  • Mucinous cystic neoplasm – has ovarian stroma in it, malignant potential and usually in women
  • IPMN – 29% malignant risk in 10 years. Can present as unexplained pancreatitis with dilated PD, jaundice and diabetes. Cancer risk is if size more than 3 cm,mural nodules.¬† Fish mouth appearance of IPMN – with mucous. Amylase in pseudocyst in cystic fluid is more than 250. CEA less than 5 unlikely to be cancer and more than 800 in fluid is probably malignant.
  • PANDA study – DNA analysis of cystic fluid.¬† Moderate accuracy and does not add much to current tests
  • Mucinous cysts – inject with ethanol or paclitaxel.¬† Cyst resolution is 33-79%.¬† 10% pancreatitis risk and 20% abd. pain.
  • Cyst more than 1 cm and symptomatic consider surgery. If more than 1 cm and no symptoms do EUS.
  • If cyst less than 1 cm, repeat imaging in 1 year.

Chronic Pancreatitis

  • Pain occurs from PD obstruction or ischemia of pancreas or pseudocyst formation or inflammation or duodenal and CBD obstruction.
  • Mx from enzymes, analgesics, octreotide, antioxidants, nerve blocks, endoscopic therapy, ESWL and surgery.
  • Pancreatic surgery – islet autotransplantation.
  • Endoscopic treatment involves ESWL, EUS and ERCP.¬† Pancreatic and biliary sphincterotomy.¬† Often needs a screw dilator, shock wave lithotripsy and then stone extraction
  • Pancreatic stone extraction – less than 30-40% extraction rate

Screening for Pancreatic Cancer

  • 85% pancreatic cancer not respectable at presentation.¬† Back pain, jaundice and anorexia is associated with irresectable disease
  • PJ patients have 36% chance of pancreatic cancer
  • HNPCC pts have <5% of pancreatic ca
  • Hereditary pancreatitis have 40% chance of PaC
  • New onset DM less than 3 years associated with PaC
  • New onset DM past age of 50, identify a unique biomarker for PaCDM
  • Type 2 DM – usually onset associated with weight gain.¬† However, if type 2 DM associated with weight loss can be suggestive of PaC

Pancreatic Imaging

  • CT angio Pancreas or MRI pancreas
  • 8 ml/second, advanced 3 D imaging and ASIR (suppresses noise an advanced algorithm) (adaptive statistical iterative reconstruction)
  • In Mayo, they start 2 IV and inject 4 ml/sec in each arm
  • MRI – diffusion restriction technique

Familial Pancreatic Cancer

  • 2 or more patients with pancreatic cancer in family.
  • 10% of all pancreatic cancers are familial.
  • High risk FPC.¬† Families with > 3 members with cancer.
  • Hereditary Pancreatic cancer BRCA1/2, p16 mutations or FAMMM, Lynch syndrome, PJ syndrome, hereditary pancreatitis (cationic trypsinogen gene)
  • Hereditary breach and ovarian cancer HBOC BRCA 1 and BRCA2
  • PJ syndrome higher risk of colon cancer and should be monitored for pancreatic cancer also.¬† Moreover risk of gastric cancer, ovarian, breast, cervical and endometrial cancer
  • FAMM (familial atypical multiple mole melanoma). p16/CDKN2A gene.¬† They have atypical melanocytic nevi, autosomal dominant
  • Lynch – SB cancer, ureter cancer, renal pelvis cancer, brain, ovary and pancreatic cancer.¬† Age 50 1.3% and Age 70 4% risk of pancreatic cancer
  • HBOC syndrome – autosomal dominant.¬† Some patient family may have pancreatic cancer but no breast or ovarian cancer !!!!
  • BRCA mutation in Jewish patients.
  • PALB-2 Multiple family members with pancreatic cancer.¬† Also increased risk of breast cancer
  • Johns Hopkins, Mayo clinic, Creighton Univ, Mt Sinai, Anderson CC,¬† – sites for familial¬† cancers
  • Screening with EUS, dedicated MRI / MRCP or dedicated pancreatic protocol CT, aggressive evaluation of cysts. ????prophylactic pancreatectomy.
  • PanINs lesions – intraepithelial neoplasia (similar to colon cancer from adenoma).¬† High grade PanIN3 and more dense, different Kras mutations.
  • Thus 2 ways to develop pancreatic cancer PanIN or IPMN.
  • 3 D reconstruction for pancreatic neoplasm
  • MRI has no radiation advantage.
  • EUS not widely available and high inter observer variability.¬† Requires extra training.
  • Start screening at 50 or 10 years younger.¬† PJ start at 35