MANAGEMENT AND EVALUATION OF PANCREATIC CYST
A. Dr Brugge, Harvard
1. 4 types
a) Serous, mucinous, pseudocyst and IPMN (main and side branch)
2. Pancreatic cancer – 90% PanIN – 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 – 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)
c) Pancreatic – biliary (worst survival)
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 – 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
XI. SPHINCTEROTOMY OF PANCREAS
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 – rectal.
e) Use 100 mg indomethacin rectally
XII. CELIAC NEUROLYSIS
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. www.gastro.org/guidelines
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 – suggests CBD stone
· Necrotizing pancreas goes from cement to liquid to similar to pseudocyst.
· CT CANNOT TELL DIFFERENCE BETWEEN PSEUDOCYST OR NECROSIS
· Pseudocyst is outside pancreas but necrosis that is organized – is in pancreatic bed !!!! DO NOT PUT DRAIN IN PANCREAS
· DO NOT — — USE BROAD SPECTRUM ANTIBIOTICS
· LIMIT LINES
· Day 7 – can do aspiration then patient may have infected necrosis. INFECTED NECROSIS TREAT WITHOUT SURGERY.
· REPEAT ASPIRATION IF INFECTION SUSPECTED EVERY 5-7 DAYS
· 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
· EUS for all more than 1 cm cyst
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
Most patients nowadays do not drink alcohol
Most patient are smokers
Genetics is a huge contributer
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
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
Screening for Pancreatic Cancer
Familial Pancreatic Cancer