Splanchnic nerve, efferent somatic nerve – more important Very

PANCREAS extensive Pancreatic disease (inflammatory / malignant)

Doc Medina unreleaving pain

Pancreas- surrounded by lots of somatic nerve

Anatomy Center celiac Ganglion – rendezvous of all pain fibers Celiac G.
Retroperitoneum In absence of opiod drugs  inject 50% ROH over celiac ganglion 
A pistol-shaped organ celiac ganglion blocking 0% pain 2months to 4 months
Extends from duodenum to spleen Advance Pancreatic Ca. very significant
120 grams - Not so much attractive now – due to morphine/ oxycodone.
12-15cm (4-6 in.)
Head, neck, body, tail
Microscopic Anatomy
Uncinate process
 Exocrine tissues – 80% of total mass
 Ducts, vessels, nerves, connective – 18%
Lig of trietz to transverse colon = midgut
4th month of gestation = development  Endocrine tissues – 2% of total mass
Dorsal bud = body and tail  Exocrine – acinar cells, duct cells
Ventral bud = head and uncinate process  Endocrine – alpha, beta, PP, delta cells
Santorini = above drain, kapag madami itong secretions = inc.
Obstruction chance (pancreatic divisum =congenital)  The pancreas is a composite gland containing both exocrine and
30% gyne accessory duct sawirsung = no prob endocrine components
Wirsung = below drain Acini, formed of zymogenic cells around a central lumen, are
5-10% no fusion of duct arranged in lobules.
Each lobule has its own ductule, and many ductules join to form
Sphincterotomy (cut <1cm, 12-1 o’clock) and sphincteroplasty (close intralobular ducts, which then form interlobular ducts that drain
the oddi) into branches of the main pancreatic duct.
“Cut >1cm may cut the pancreatic duct = pancreatitis  Under stimulation of secretin and cholecystokinin (CCK), the
3 o’clock may cut pancreatic duct = pancreatitis zymogenic cells secrete a variety of enzymes:
trypsin (digests proteins)
Rim of Pancreatic Tissue lipase (digests fats)
-You cannot go beyond the groove  devascularized the duodenum amylase (digests carbohydrates), and many others.
Ductular cells produce bicarbonate, which makes the pancreatic
Blood Supply fluid (juice) alkaline.
Pancreatoduodenal artery  Scattered throughout the gland are pancreatic islets (clusters) (of
Celiac artery Langerhans) containing:
SMA beta cells (about 75% of islets; these secrete insulin)
Splenic artery alpha cells (about 20% of islets; these secrete glucagon)
Portal vein delta cells (these secrete somatostatin), and several other
hormone-secreting cells.
Venous drainage accompanies arteries Islets constitute only about 2% of the pancreatic parenchyma.
- IMV, Spleenic V, and SMV  empty at portal vein
-lots of lymphatic extension  many surgeons consider it as a systemic Ductal System
disease. Pancreatic parenchyma – contrast enhance CT – best
Recent standard Ductal problem, Distal Bile Duct, Pancreatic Ducts
All patients with pancreatic CA  mandatory adjuvant chemotherapy 1. Non invasive MRCP
Because of the systemic behavior of the disease (Pancreatic CA) 2. Invasive with therapeutic ERCP
Above reason – extensive lymphatic network.
Ductal px
Lymphatic drainage - Strictures, fibrosis, inflammation
Pancreatoduodenal nodes - Stone
Hepatoduodenal nodes - CA
Celiac nodes - Dilatation
Penaortic nodes
Superior mesenteric nodes Obstruction of Duct – Assessment?
Splenic nodes -choose bet. CT Scan or CP  choose CP

The head of the pancreas drains into pancreaticoduodenal lymph EUS UTS- putting a probe at tip of endoscope
nodes and lymph nodes in the hepatoduodenal ligament, as well as -high frequency probe.
prepyloric and postpyloric lymph nodes. At second part- goes near the major papilla then starts assessment:
The pancreatic body and tail drain into mesocolic lymph nodes Info:
(around the middle colic artery) and lymph nodes along the hepatic assessment of the pancreatic head
and splenic arteries. distalpart of pancreatic ducts
Final drainage occurs into celiac, superior mesenteric, and para- intrapancreatic CBD
aortic and aortocaval lymph nodes pancreaticodoudenal Lymph node
Distances of SMV from tumor
Innervation
Sympa – non secretory
Parasympa – secretion

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Physiology  Release of HC03
 centralize sodium cell- near the ducts going to main pancreatic
Pancreas has two main Function duct
Major : Digestion  HC03- bicarbonate
Minor : Endocrine  PH of pancreatic substance – ALKALINE
80% Digestive Electrolyte component of pancreatic juice
-acinar cells : Dots :Zymogen  If in case fistula of pancreas
-storage vesicle  best fluid to be used is Lactated Ringer’s
-inactive digestive enzyme  Replacement of pancreatic fluid losses.
-if stimulated: release ducts  Pancreatic Ducts  Duodenum.  Emanating from fistula/ leak from anastomosis
Somatostatin
Metabolic process of digestion of 3 major substrates: Protein, Fat,  the greatest inhibitor of GI
Carbohydrates  commercially available as Octreotide
 Wherein patient with pancreatic fistula and want to lessen secretion
Endocrine they will inject it.
- Contain one million Islets  Problem is it is costly.

Arrangement of endo and Exo Inorganic Components of Pancreatic juice

Outer- pancreatic acinar. Component
Inner- Islets
*Should be maintained at all times H2O 1500-3000 ml/day

Disrupted by: Sodium 140 mmol/liter

Pancreatic Cancer
Could lead to: Potassium 10 mmol/L
Digestive – Diarrhea/ steatorrhea.
Control of sugar – DM
Chloride 20 mmol /L
Production of digestive enzyme (exocrine fxn)
Start when we eat something Bicarbonate 110 mmol/L

Main stimulus +
+ trypsinogen by enterokinase at 2nd part of duodenum 
domino Effect.
Other proenzymes
CCK
VIP
GRP
Secretin
 These are all stimulus for pancreatic enzyme release for digestion.
Exocrine function
I. Production of digestive enzyme
Amylase (carbohydrate)
Lipase (fat)
Trypsin and chymotrypsin (protein)
Nucleases (DNA/RNA)
Enterokinase activates trypsinogen
Trypsin inhibitor Enterocytes
Shut-off the process when the digestion is already done
*trypsin should always be there:
If not, digestion would take place without fail  auto-
digestion of pancreas  acute pancreatitis
One reason is hereditary pancreatitis
 Genetic patient- gene (Cationic Trypsinogen)
 PRSS1 gene PINK1 gene, CFTR gene
II. Secrete fluids rich in HCO3
Secrete 1-3 L of clear isosmotic alkaline fluids and
electrolytes
Contains Na+, K+, -HCO3 and Cl-
Daily total volume is 2.5L
Secretin (duodenum) stimulates water and HCO3
Basal state enzyme secretion is minimal secondary to
somastatin
Fed state –CCK secretion. Stimulant
Stimulant: CCK, VIP, Ach, GRP and Substance P
Inhibitory: Somatostatin
LR = best fluid for 3rd space loss (severe inflammation)
Endocrine Pancreas
 main cell are islets
 beta cells found in the core
 Outer core is Alpha cells that secret Glucagon
 Opposite effect of insulin Delta cells between the 2, secrete
somatostatin, and pancreas polypeptide cells.
 pancreatic polypeptide- tumors affecting endocrine part of pancreas
 Epsilon cells, contain Leptin and Ghrelin – appetite suppressant.
I. Production of digestive enzyme
A cells,B cells, D cells,PP cells
Regulate blood glucose level
Beta cells:
60-80% produce insulin
Insulin promotes glucose transport, stimulates protein
synthesis
Decrease gluconeogenesis, glycogenolysis, lipolysis
Alpha cells:
5-20% seretes glucagon
Glucagon counter balance insulin by stimulating hepatic
glycogenolysis, ketogenesis and lipolysis
Glucagon inhibits intestinal motility ad gastric acid
secretion
The release of glucagon is stimulated by hypoglycaemia,
stress, CCK
D cells:
Secretes somatostatin w/c have inhibotory effect on most
GIT hormones
PP cells:
Source of pancreatic polypeptide
Decrease exocrine secretions and biliary motility
Used as tumor markers for pancreatic endocrine tumors
Acute Pancreatitis
5000 new cases/yr USA
Over-all mortality – 10%
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 Inflammatory disease involves heart, lung and kidney Organ Failure < 48 hrs; if persist >48 hrs lead to SAP
 2 pathological form:
Interstitial – edematous, PMN infiltrates
Necrotizing – focal of diffuse necrosis of parenchyma, Severe
multiorgan system failure  Severe acute pancreatitis Persistent Organ Failure >48hrs
Etiology: what can happen to pt. with acute pancreatitis?
 Gallstones (40%) resolve spontaneously or;
 Alcohol (30%)
 Idiopathic (15%) (70% secondary to microlithiasis) Leading to:
 Metabolic (5%) Severe Acute Pancretitis
 Anatomical (<5%) Necrotizing pancreatitis
 Mechanical insults (<5%) ERCP, Trauma (1.5%) Infected Necrosis- 10%
 Drugs (<5%)
 Infection (<5%)  only when you are suspecting complication of AP that you will resort
 Hereditary (rare) – autosomal dominant to CT SCAN

 1st week from onset of Severe Abd. Pain forget about CT SCAN - Do
UTZ
 Complications happen after a week

CT Scan progression.
- guide drain infected- Necrotizing pancreatitis
There are only two main causes of Pancreatitis
 Gallstone
 ROH

Most important Dictum > SIZE

Small / large? – small <5m  Significant size Gallstone Pancreatitis
Next thing to do? – submit pt. to surgery

Early beneficial  laparoscopic

Safety done at an early stage

Acute Pancreatitis 2 phases

1st phase - / fluid sequestration
1 wk before onset
massive fluid resuscitation- loss up to 10L P. fluid
fluid resembles LR – 10L on the 1st day/ 1st week
If you fail to do that- acute tubular necrosis

2nd phase – necrotic phase

American College of Gastroenterology
Diagnosis
1) characteristic (severe) abdominal pain
2) serum amylase/lipase exceeding three times the upper limit of
normal
3) characteristic abdominal imaging findings (strong
recommendation, moderate quality of evidence)
Common Dx
 Most important criteria to diagnose clinically as endorse by ACG
1. ABDOMINAL PAIN(SEVERE) *hindi pwede if ‘yong patient can still
walk,etc
2. increase pancreatic enzyme ”amylase and lipase” (3x from the
normal)
3. UTZ findings of acute pancreatitis with stone
Mortality- 10-15%(significant numbers)
Good thing is 80-85% of the time is it resolves spontaneously
little complicated Pancreatitis
ATLANTA CONVENTION (1892)
2 types of pancreatitis
Insterstitial – edematous /(+) Neutrophils
SAP- Severe acute pancreatitis
 presence of necrosis + organ Failure
Moderate type
inflammation + Organ Failure
Fail to manage patient effective
Complicated phase leasd to sepsis
Hospital stay – mortality of pt.
Gallstone
 Common anatomical problem – Functional obstruction in the
common channel
 Distal CBD/ P. Duct – comes from ventral bud
 that’s is why is common channel
 stone stuck into this- Gallstone pancreatitis
Tx: take out the stone, if stone get stuck – endoscopic
sphincterotomy
1.Pancreatitis assoc. w/gallstones (40%)
Common channel between CBD and duct of wirsung was
thought to cause gallstone pancreatitis and pancreatitis
due to other causes
Acinar cell injury secondary to ductal pressures
High proportion of cases with gallstone pancreatitis have
recoverable biliary calcium in the stools
Reflux of bile into the pancreatic duct can induce
pancreatitis (experimental)
Clinical Presentation:
Abdominal pain
Hx of biliary colic
Hx of large quantities alcohol consumption
Hx of recent operative or invasive procedure

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 Pain typically begins 1-4 hours after meal -Precipitation – calcification
Sudden epigastric pain radiating to the back w/ N&V Hallmark- of chronic pancreatitis due to ROH
Severe and steady w/o cramping pain
 PE: lying still in bed, febrile (76%), tachycardia (65%) Smoking – will not cause Pancreatitis but it will aggregate an existing
Abdominal tenderness (68%), distention (65%) pancreatitis.
Severe pancreatic inflammation and necrosis may cause Intake of vegetable only – protective to pancreas
retroperitoneal haemorrhage whick leads to: Severe abdominal pain – Hallmark acute pancreatitis
Large 3rd space fluid loss (5-10%) - Origin of pancreas
Dyspnea (10%) - Usually localized
Jaundice (28%) Typical presentation
Stigmata of chronic liver disease eg. Spider angiomata, PE: take note of Fever present early 76%
gynecomastia and parotid enlargement -this should not make you suspend of an infected pancreatic necrosis
Diminished breath sounds d/t effusion
Jaundice d/t biliary obstruction Early phase
Blood dissection along different planes -patients with acute pancreatitis  fever is common, but it does not
necessitate giving of antibiotics
 Gray Turner’s Sign: Blood extends to the flank tissue resulting  Give only if there is infected pancreatitis documentation
to flank ecchymosis
 Cullen’s sign: Blood dissects up to the falciform ligament and Antibiotics- are only given in the presence of infection
create peri-umbilical ecchymosis How to document- take an aspirate fluid under CT scan
guidance
“Mesentery and omentum with extensive fat necrosis due to acute Subject to Gram Stain
pancreatitis- parang my chalk” If (+) - give antibiotics, only one time
2.Alcohol Pancreatitis (35%) Don’t give all in
Intracellular accumulation of digestive enzymes and their Severe Pancreatic infection
premature activation and release -present with jaundice – sign of chronic obstructive disease 
Increase permeability of ductules, enzymes cause aggrevate condition
parenchymal damage
Increase protein content and decreases bicarbonate level & Acute severe Necrotizing Pancreatitis
trypsin inhibitor  protein plug 2 condition- high mortality
Habitual alcohol Ingestion over 5-15 years 1. Gray turners sign- hemorrhagic P., ecchymosis in flank
Alcohol causes increase in protein concentration into the 2. Cullen – ecchymosis at periumbilical area.
pancreatic juice –precipitation of protein forms a nidus
with subsequent calcification w/c in turn can cause Criteria: American College of Gastroenterologists
duodenal inflammation with some degree of ductal 1. Increased in serum amylase(3x)
obstruction or increase intraductal pressure with spasm of 2. Severe Abdominal Pain
sphincter resulting in pancreatitis *More specific ang Amylase P
3. Lipase is more specific because this remains elevated up to 1 wk.
Alcohol-induced Pancreatitis amylase and lipase are not prognostic. It doesn’t mean that you have
Pancreatic duct obstruction elevated levels and you have very severe disease, it is not the
Increase ampullary resistance case. They will just tell you that you have acute pancreatitis.
Protein deposition
Pancreatic exocrine hypersecretion Diagnostic evaluation:
Ethanol stimulates gastric acid secretion 1.Serum amylase
Activation of secretin – exocrine -increased in 95% of cases: 5% false negative
Impaired trypsin inhibition (no negative feedback) (75% of patients with abdominal pain and increase (3x)amylase have
Acetaldehyde pancreatitis
Injures acinar cells by increasing membrane permeability Amylase P level 3x above
Hypertriglyceridemia Amylase level over 1000 Somogyi-Nelson Units often indicates Biliary
Source of free fatty acids which are cytotoxic tract disease with Pancreatitis
200-500 units indicates alcoholic Pancreatitis
Which is more significant amount or duration? -Other causes of hyperamylasemia
 amount- more significant Acute cholecystitis
The more one consume in one sitting the higher the chance to CBD stones with or without pancreatitis
develop alcohol Pancreatitis Perforated peptic ulcer
If they are persistent acute  chronic pancreatitis Strangulated small bowel
Acute alcoholism
-if one maintains a limit in drinking: men recommended 2; women 1, Cancer of the pancreas
the type of drink doesn’t matter; it’s the amount that matters Mumps
Ruptured ectopic pregnancy
Alcohol type – calcification in case the pt. develops chronic ERCP
pancreatitis Acute appendicitis
Calcification is brought about by obstruction produced by protein
minerals in the pancreatic ducts leading to blockage – increase 2.Lipase
protein -Longer half- life more specific levels remain high for 12 days
<1% of total BW (pancreas) - the level of amylase and lipase has nothing to do with severity and
Protein prod is 13x >liver prognosis

Too much protein is produced

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3.Serum Calcium  Duodenal C -loop may be widened by pancreatic
-Values of < 7.5mg/dL generally indicates poor prognosis and reflects edema
extensive disease process  Pad sign due to smoothing out or obliteration of the duodenal
“Hypocalcemia due to low level of albumin” mucosal folds

Laboratory Studies 2.Ultrasound

 Liver associated enzymes -changes from normal anatomy and vascular landmarks, presence of
Alk PO4, total bilirubin, SGOT, SGPT swelling and loss of tissue plane +PP (100%)
ALT > 150U/L gallstone pancreatitis -PP (75%)
 Serum electrolytes, BUN, Creatinine, Glucose, Calcium and -Endoscopic ultrasound detects stone, ductal flow (more invasive,
Triglycerides more detailed)
 C-reactive protein
24-48 hrs after prognostic value 3.CT scan
Double value= severe pancreatitis -provides a higher resolution than ultrasound ; findings similar to
Acute phase reactant, nonspecific ultrasound
“pwede din sa acute appendicitis” -for severe type or if with complications (infected pancreatic necrosis
or abscess)
Prediction of prognostic indication
Requested to know severity 4. MRCP(magnetic resonance cholangiopancreatography)-
1) Serum Ca+ - lead to severe pancreatic necrosis suspected biliary obstruction, safer, non-invasive and fast
If you don’t know what you are dealing with
It can lead to complication / severe pancreatitis 5. ERCP- not first line; therefore only if:
2) Amylase will not tell you about the large area a. Severe acute section to CBD stone
3) Liver associated enzyme – impacted stone at bile duct from b. Worsening jaundice Complication of procedure pancreatitis
gallbladder stone  all elevated
 If pt. develop jaundice- increase total bilirubin 6. Image- guided aspiration and drainage
4) Glucose differentiate infective necrosis from sterile necrosis
5) BUN and Crea -CT or EUS guided needle aspiration
6) CRP – acute phase – CHON Severity of inflammation Grading/ Scoring with CT Scan
Balthazaar Grading
Once patient develops Grade A – normal
-mass adherent to the colon Grade B – focal or diffuse enlargement
- ---------? After taking out mass Grade C- Intrinsic abnormality, haziness
-inflammation – increase CRP Grade D – single ill-defined phlegm
-decrease albumin – no longer produce albumin- liver produce CRP’s Grade E – multiple ill-defined collection, presence of gas in of
near pancreas
1st imaging Grade A-B = nil
Grade C-E= increase infection and death
Diagnostic evaluation Necrosis – 30% loss of parenchyma –presence of SAP

Transcutaneous Ultrasound Most common-MRCP – parenchyma

Etiology gallstone; presence of swelling and loss of tissue plane. +PP ERCP – Severe abd. Pain + jaundice
(100%), -PP (75%) Early ERCP – done <48hrs – decrease morbidity / mortality
Transcutaneous Ultrasound- 1st modality you will use. -important with ductal obstruction
- disadvantage : operator dependent -jaundice
Edoscopic UTS  detects microlothiasis, periampullary lesion, -Cholangitis
ductal----
In absence of duct involvement
CT Scan X/no ERCP, X/no MRCP
Provides a higher resolution than UTS, findings similar to UTS
For severe type, assess complications Mild acute – moderate
nothing to do at early -image guided aspiration –necrosis in Ct scan
suspicion of organ Failure / Hypotension -sterile/ infected
moderate – severe -only when you have aspirated Fluid surrounding the parenchyma –
Gram stain +/- infection.
Prognostication
Best antibiotic to infected Pancreatitis best penetrance
1.Radiography IMIPINEM (Carbapenems)
-Abdomen (plain film)
 Relatively sensitive[?] 8 criteria to assess acute pancreatitis/ SAP
 Significant findings 1. APACHE
Calcification in the lesser sac and the pancreas 2. B/ SAP scoring- BUN impaired, neutral stat
Gas formation in the lesser sac (abscess formation) 3. Glasgow Scoring - INR age, PE.
-Blurred psoas shadow (retroperitoneal pancreatic necrosis) 4. Japanese Scoring system
- Cut off sign (colonic spasm adjacent to an inflamed pancreas) 5. Necrosis Severity index
-Reversed-3 or inverted-3 sign (local duodenal and jejunal ileus in 6. CT Scan scoring – CT SIS
the area of the head of the pancreas) 7. Doc was not able to recall
“if many calcification = chronic pancreatitis” 8. Pero, may 2 pa daw na assessment tools
-Barium studies - kung wala un ibangDx. Na gamit

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Ranson’s criteria – 48hrs to complete Criteria  Severe acute pancreatitis, necrotizing with infection and bleeding
APACHE – can be used anytime same goes to the other. Early CBDE – ERCP within 48 hours
Laparoscopic cholecystectomy after recovering from
Prognosis: pancreatitis same hospitalization
Ranson’s criteria Drainage- pen rose, closed suction
 signs on admission Peritoneal lavage
>55 years old Embolization after angiography
WBC count >16,000 Antibiotics
Serum Glucose >200 mg/dL (11mmol/L)
LDH >350 IU/mL Treatment:
SGOT >250 IU/ mL  If there are many calcification (parangpulbos) – acute pancreatitis
 criteria during the first 24 hours  Never ever touch the pt. put pt. in ICU
Drop in hct by >10%  Severe – moderate – Admit to ICU
Increased in BUN of 8 mg/dL  Mild – ordinary ward
Ca level <8mg/ dL
PaO2 < 60 mmhg Mild form – NPO always after 3 days if with no abdominal pain – feed
Base deficit > 4mEq/L
3rd space fluid loss >4L – (6000 ml) Severe – NGT feeding < 48hrs

If 0-2 minimal mortality SAP – put tube in jejunum – gives feeding <24hrs
If 3-4 of the criteria is positive, 10-20% mortality -will not stimulate pancreas
If 5-6, 50% mortality -bypass 2nd part of duodenum
If 7 or greater of the criteria is positive, 100% mortality -provide nutrition in severe w/ in 24hrs
*Ranson’s criteria is only valid at 48 hrs after onset. Sensitivity 73%
specificity 77% for predicting mortality Best modified – low residue ex. Peptameal
- Include: Fa (medium chain)
How to interpret Ranson’s - Easily absorbed
 Mortality 100% - 3 of the FF: significant For SAP
specificity 60-70%; sensitivity 70% - Early ERCP
Apache – 88% more sensitive - CT – declaration
 If apache >8 – pt. will develop SAP Tx – is becoming less invasive
Ex. Infected P. necrosis – can place CT guide / laparoscopic drain in
Severe Acute Pancreatitis case pt does not improve:
(Atlanta Classification) Open up pt and gently remove necrotic part (necrosectomy)
-Evidence of organ failure
Systolic BP <90mmHg Very essential in immune acute pancraetitis
PaO2 < 60 mmHg -you have to drain / peritoneal lavage wash the paracolic /
Creatinine < 2mg/dL paranephric
GI bleed >500 cc per day Post drain – cigarette drain, close suction drain
Criteria of SAP Essential component
 Simple obstructive Take out the GB
 Ransons>3
 Apache >8 Complication severe >17%, (necrotizing)32% mortality
 30% mortality – if organ Failure (bleeding)mortality >60%
 Imaging
CT Scan ACG Guidelines
Necrosis >50% of the gland 1) Diagnosis based on symptoms and labs
Extensive peripancreatic fluid collection 2) Resuscitate within12-24hrs
(+) gas within the pancreas or adjacent soft tissue 3) ICU admission with SIRS/organ failure
--All mothers are predictors of poor outcome in CT scan 4) ERCP (+) cholangitis
CT Scan Predictors 5) No routine prophylactic antibiotics
- Gas in the pancreas 6) Oral feeding/ enteral feeding priority
- Extensive pancreatic fluid 7) Treatment (sx, rx, endo) postponed 4 weeks to permit wall
- >30% necrosis formation

Local complications Summary of ACGE

Abscess 1stwk – resuscitate
Necrosis Fluid
Pseudocyst Nutrition
Admission in ICU
Treatment: SIRS – severity – presents >48hrs SAP
 Mild to moderate acute pancreatitis
IV hydration Definitive Tx:
Pain medication (Demerol relax sphincter of Oddi) Stone: stable pt. - delay management for 1wk to clearly see active
NGT suction ( not routine for vomiting pt. only) demarcation
Antibiotics  Cefuroxime, not used as prophylactic antibiotic - See viable from non-viable tissues
Laparoscopic cholecystectomy/ open - If no-viable  do necrosectomy
Laparoscopic IOC, post-op ES  patient with Gallstone
pancreatitis kapag nawala lang ang pain or asymptomatic

6
CT scan done after a day / two 4) Lobularity
-repeat CT Scan different finding 5) Irregular main pancreatic duct (MPD)
-delayed ct scan – was able to deliberate necrotic part 6) Dilation of MPD
-serve as guide 7) Hyperechoic margins of MPD
Early Sx / able to remove broken part – 1wk
Days after procedure pt still have no improvement? – repeat ct scan  MRCP
baka meron pang natira Suspected biliary obstruction, safer, non-invasive and fast
ERCP
Delay is a safe option- as to really which is necrotic. Not first line, performed only if:
a) SAP sec. To CBD stone
Persistent of signs / insult b) worsening jaundice
Lead to recurrence/ recurrent acute P.(continued drinking/ROH)
Chronic P. Image guided aspiration and drainage
Could lead to P. CA Differentiated infected necrosis from sterile necrosis
CT or EUS guided needle aspiration
Chronic pancreatitis
8/100,000 per year (USA) Treatment:
Parenchymal fibrosis, ductal stricture, atrophy of acinar and 1. Analgesics
islet tissue 2. Endocrine and exocrine replacement
(M.C) Chronic calcific (alcoholic), chronic obstructive 3. Abstinence form alcohol
(pancreatic carcinoma), inflammatory (autoimmune and 4. (main) Surgery- more than 6mm drainage; less than 6mm--
sclerosing pancreatitis) (subgroups) resection (last resort)
Fibrosis, (hallmark) calcification of small ducts, intraductal *Puestow procedure
protein plugging -operative mortality- 0-4%
Alcohol related sec to ductal plugging -relief of pain 80-90% 5 yr ffup
Gallstone disease does not result in chronic pancreatitis * Resection – small ducts, poor long term results
Steatorrhea- loss of exocrine fxn about 90% *Celiac plexus block- limited success - after 4 months limited
DM - endocrine part 80% lost alpha and beta cell damage need success, sa may aorta = 60% ethanol inject
insulin
Roux en Y – gastrointestinal continuity
Classification of Chronic Pancreatitis
1. Fibrosis
2. Ductal stricture/ bleeding (description?)
3. Atrophy
- ULDM/ UC steatorrhea – atrophy of acinar / interstitial T.?

5 Types of Pancreatitis
1. Chronic calcific- ROH P.
2. Chronic obstructive – tumor or stones
3. Inflammatory – sclerosing cholangitis
4.
Clinical Manifestations
 unrelenting epigastric pain
 nausea
 loss of appetite, weight loss
 steatorrhea (90%)
 diabetes (80%)  difficult to control
Diagnostic Evaluation:
1) Amylase/ Lipase- normal
2) Low albumin/ Malnutrition
3) Sudan staining of stool 72 hours collection, consume 100g fat TUMOR
per day, stool fat excretion >7g per day (steatorrhea or fat Pancreatic Pseudocysts
malabsorption) most common complication of acute and chronic pancreatitis,
trauma—2-10%
Imaging studies: located within substance, adjacent distant
1) Plain film fluid-filled pancreatic secretions from duct system
2) ERCP/MRCP-ductal anatomy, size (small vs large ducts), (not true cyst) lacks epithelial lining, walls composed of
stricture, cancer  small – resect; large - drain adjacent organ, fibrosis and inflammatory granulation tissue
3) CT scan (Dx. Of choice) single or multiple fluid collection
presence of calcification in the pancreas virtually establishes size: 2-3 cm :head (1/3) tail (2/3)
the diagnosis type of fluid collection very important
-complications, planning surgery, endoscopy fluid rich in amylase and other enzymes
-sensitivity 75-90%, specific 85-100% disruption of pancreatic duct secondary to alcohol or
gallstone disease
Endoscopic Ultrasonography (EUS) in children, trauma are frequently associated
Criteria:
1) stones “Pain, jaundice, fever, mass 50%, address due to complication:
2) Visible side branches -Infection, obstruction, bleeding, rupture
3) Cyst

7
Clinical Manifestations: Blacks
Pain (80-90%), fever, ileus --y/o, median age 69y/o
Pain radiating to the back
Jaundice Risk factors
Early satiety, N/V, weightless  Smoking – 30% of cases of pancreatic cancer
Tenderness, palpable mass (50%)  Obesity, especially central, has been associated with a higher
Bleeding, rupture, infection or obstruction incidence of pancreatic cancer
 Fruits and vegetables rich in folate and lycopenes. Red meat.
Diagnosis Processed kinds, Coffee consumption
1) Amylase, lipase, CEA, fluid viscosity  Diabetes Mellitus of at least 5-years duration have a two-
2) CT scan (90-100%) fold increased risk of developing pancreatic carcinoma
3) Ultrasound
4) MRI- solid component drainage Multicenter study of more than 2000 patients with chronic
5) ERCP- planning drainage pancreatitis showed a 26-fold increase in the risk of developing
pancreatic cancer. 4% of patients who has chronic pancreatitis for
Treatment 20 yrs’ duration developing pancreatic cancer
Surgery (best) The risk of pancreatic cancer is even higher with hereditary
To prevent complication such as infection, severe pancraetitis
haemorrhage, rupture of adjacent viscus
Pseudocyst rarely resolve once thick fibrous wall has Prognosis
developed At the time of diagnosis, 52% of all patients have distant
Pseudocyst that persist 4-6 wks are unlikely to resolve disease and 26% have regional spread
spontaneously and should be treated surgically The relative 1-year survival rate for pancreatic cancer is only
concern about malignancy 26% and the overall 5-year survivial is 6%
symptomatic In patients able to undergo a successful resection (about
20%of the patients), median survival time ranges from 12-19
4 main treatment options: months, and the 5-year survival rate is 15-20%
1) Percutaneous drainage The best predictors of long term survival after surgery are a
2) Endoscopic drainage tumor diameter of less than 3 cm, no nodal involvement,
3) Laparotomy with internal drainage negative resection margins, and diploid tumor
4) Laparoscopic internal drainage deosyribonuceic acid (DNA) content

Percutaneous catheter drainage Clinical Manifestation

Establish diagnosis, temporizing measure 1) wt.loss (most common)
54% failure, 63% recurrence 2) Pain (dull and aching, epigastric and radiates to the back,
High risk of infecting the cyst aggravated by eating and lying down) due to obstruction to the
Procedure for infected cyst pancreatic duct and perineural invaeion
Contraindicated in poor compliance strictures of MPD, bloody 3) Progressive jaundice – 75% (cancer of the head of the
and solid cysts pancreas)
4) Anorexia and weakness (50%)
Endoscopic drainage 5) Pruritus
Transpapillary or transmural 6) Hepatomegaly/ splenomegaly
Axios stent- FDA approved stent 7) Enlarged palpable gallbladder not tender and w/o fever is
Transpapillary- requires cyst communication with pancreatic reliable diagnostic criteria for malignant choledochal
duct, 80% success rate, 10-14% recurrence rate obstruction
Transmural- find bulge, cut through gastric wall or duodenum, 8) Diabetes (20%)
89% success, 6-18% recurrence, 20% complication (bleeding) 9) Gastric outlet obstruction secondary to distorted duodenum –
15%
Surgical Drainage 10) Acute pancreatitis – rare 5% Lymphadenopathy –
 Procedure of choice Virchow’s node, sister Mary Joseph node, Blumper’s shelf
 Mortality is 3% 11) DVT and migratory thrombophlebitis
 Success rate 90%
 Complication 24% Pancreatic Carcinoma
 Laparoscopic approach – favoreddue to high success rate and Marked weight loss and jaundice
low morbidity
Diagnostic Evaluation
Pancreatic Tumor 1) Liver function test
Background 2) Ultrasound of the biliary tree
8% cancer death USA 3) CT Scan
4th leading cause of death 4) ERCP- double duct sign (90% sensitive)
75% (head), 15-20% (body), 10% (tail) 5) (for obstructive jaundice, can provide relief by placing a
Surgery remains the only cure stent, biopsy)( if CT scan can’t delinate the malignancy)
Unknown cause, smoking, chronic pancreatitis, K-RAS, 6) MRCP – safer, cheaper, less invasive
CDKN2 gene, p53, p16, BRCA-2, Smad 4 7) Endoscopic ultrasound – staging involvement of vessel by
Preoperative chemotheraphy tumor biopsy
8) PET Scan – occult metastasis
Epidemiology 9) Chest Xray – pulmonary metastasis
46,420 cases in USA 2014 (ACS) 10) Bone scan – bone pain
13th in incidence. 8th in cancer death

8
ERCP (double duct = CBD and pancreatic)
Pancreatic CA has fairly characteristic appearance on ERCP w/
pancreatic ductal obstruction often combine with bile duct
obstruction

Treatment
1.Prior to surgery
 Nutrition
 Preoperative cardiopulmonary and renal function
 Biliary drainage

2.Wipple’s surgery
 The only definitive and potentially curative treatment of
periampullary CA. it is performed for localize CA of the ampulla,
duodenum and CBD in good risk patient and done to pancreatic
CA if no evidence of spread to liver
 Expose the portal vein and remove the gallbladder
 Cholecystojejunostomy , Choledochojejunostomy,
Gastrojejunostomy
 Preserve the pylorus
 With feeding jejunostomy (enteral feeding)

3.For unresectable lesions

The average survival time is 6 mos.

 Procedures that can be done

Cholecystojejunostomy
Gastrojejunostomy
Endoscopic stenting/ transhepatic
Choledochojejunostomy
Intraoperative infection of celiac plexus w/ 95% alcohol
for relief of pain, NSAID, narcotics

“chemotherapy and radiation under investigation”

Distal pancreatectomy = advance stage, sometimes with intestinal
obstruction involve transverse colon

Neoadjuvant Chemotherapy

 Down-staging significantly reduced median tumor size from 3.1

cm to 1.7 cm and serum CA19-9 levels from 96.3 U/mL to 20.0
U/mL.
 Median survival was 40.1 months, mdian disease-free survival
was 23.2 months, and overall five-year survival was 42.9%
 Recent publications (Feb 2016) shows that ACT increases both
local recurrence-free survival and distant recurrence-free
survival, with a corresponding befit in overall survival.
 By contrast, adjuvant chemoradiation theraphy (ACRT) provides
a benefit in local recurrence-free survival but not in distant
recurrence free survival or overall survival.

Transcribed by: JMAR

Encoded by: MJG and JAC
Scavengers2.0“TheReclusers”