The pancreas Adonia haddad - PowerPoint Presentation

Slide1

The pancreas

Adonia

haddad

Slide2

Objectives

Anatomy

/histology/embryology/Physiology

of the pancreas

• Definition and pathophysiology of acute

pancreatitis

• Clinical presentation

• Investigation and Diagnosis

•Complications

•

Management

Quick review of chronic pancreatitis

and neoplasms

Slide3

Anatomy

Retroperitoneal organ ( behind lesser sac and stomach – L1-L2)

15-20 cm in length

Devided

into head / neck/ body / tail

head can be further

subdevided

into : head proper and

uncinate

process

Slide4

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The Head

of pancreas lies within the c shaped concavity of the

duodenum

The

Uncinate

process passes posterior to the superior mesenteric vessels

The neck of the pancreas is anterior to the superior mesenteric vessel .. and posterior to the neck , the superior mesenteric and the splenic veins join to form the portal vein

The tail of the pancreas ends as it passes between layers of the

splenorenal

ligaments

Slide6

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Blood supply

The Head and neck of the pancreas gets it’s supply from the anastomosis of the superior and inferior

pancreatico

-duodenal artery :

Celiac artery -----> Common hepatic branch --



gastrodudenal

artery --

superior

pancreatico

-duodenal artery

Superior mesenteric artery -- inferior

pancreatico

- duodenal artery

Slide8

The body and tail are supplied by small branches from the splenic artery

About 10 branches arise from the splenic artery , but the major branches are

1) the major pancreatic artery

2)the dorsal pancreatic artery

3) the caudal pancreatic artery

Slide9

Venous drainage

Veins from pancreas drains into the superior mesenteric vein and splenic vein

The superior mesenteric vein runs upwards anterior and to the left of the uncinated process and joins the splenic vein behind the neck of the pancreas to form the portal vein

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lymphatic drainage

The head and neck drains into the celiac (through the pyloric nodes) and superior mesenteric lymph nodes

The body and tail are drained by the

pancreatico

-lineal lymph nodes

The pancreatic tissue contains about 70 lymph node

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Nerve supply

Pancreas is rich with sensory nerves

The pancreas is innervated by :

1)parasympathetic (

vagous

) --

 stimulate endocrine and exocrine secretions

2)sympathetic (splanchnic nerves)---



inhibits secretion

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Pancreatic duct anatomy and embryology

There is variation in pancreatic duct anatomy

The pancreas develops from separate ( of endoderm ):

1)ventral buds

2)dorsal buds

Slide16

Duct from smaller ventral bud arises from liver diverticulum , connects directly to CBD

Duct from the larger dorsal bud arises from duodenal bud , drains directly to

dudenu

m

Slide17

-During gestation, the duodenum rotates clockwise on its long axis , and the bile duct and ventral pancreas pass round behind it to fuse with the dorsal pancreas

-5% of individuals the duct draining the dorsal and ventral pancreas fail to fuse , giving rise to pancreas

divisum

Slide18

- most of the duct that drains the dorsal pancreas joins the duct draining

the ventral pancreas

to form the main pancreatic duct ( of

wirsung

), the rest of the dorsal duct

become

the accessory pancreatic duct ( of

satorini

)and enters

the

duodenum proximal to the main duct

Slide19

histology

90% of the pancreatic tissue is composed of exocrine

acinar

tissue , organized into lobules

The main pancreatic duct branches into many ducts which finally end in

acini

Main duct in lined by columnar epithelium , which becomes cuboidal terminally

Acinar

cells are clumped around a central lumen , which communicate with the duct system

Slide20

Endocrine system is known as islets of

langerhan

, consisting of :

1)beta cells : 75% -----

 producing insulin

2)alpha cells : 20% --- producing glucagon

3)delta cells : 5% ---- producing

somatostatin

4)small number of pancreatic polypeptide cells

Beta cells form the inner core , surrounded by other cells

Islets constitute 2% of total pancreatic weight ,, and receive 30%of its blood supply

Slide21

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Physiology

The pancreas secretes 500-800ml/day of alkaline (ph7.5-8.8)enzyme rich juice

Enzymes are synthesized by the

acinar

cells and stored there as

zymo

-gen ( inactive enzymes )granules

Trypsin is

proteolytic

enzyme , released in an inactive form (

trypsinogen

) , only activated by the brush border enzyme of duodenum (

enterokinase

)

When trypsin has been activated , a cascade is established and other

proteolytic

enzymes become activated in turn

Slide24

Enzymes

: (secreted

in there activated form

)

1) lipase -

 digestion of fat

2)amylase - digestion of carbs

Pancreatic secretion is stimulated by :

1)Eating

2)Hormonal mechanisms (CCK , secretin )

3)Neural mechanis

m

( vagal)

Slide25

The endocrine function of the pancreas is important in the regulation of glucose levels in the blood through

1)insulin -



decrease level

2)glucagon -



increase level

Somatostatin

has an inhibitory function of gastrointestinal secretions

Slide26

Acute pancreatitis

Pancreatitis is reversible inflammation of the

pancreas as

a result of

autodigestion

by its own

enzymes (unregulated

activation of trypsin within

pancreatic

acinar

cells

).

• Abdominal

emergency ,

If sever :Mortality rate 20%

Slide27

etiology

Slide28

The Most common cause is an obstruction by small gallbladder stone and chronic alcoholic abuse

Chronic alcoholic abuse causes cell injury by its direct toxicity and alteration of the pancreatic secretion resulting in actual obstruction

Patients who undergo ERCP , 1-3% develop pancreatitis as a consequence of duct

distruption

and the reflux of duodenal enzymes (

enterokinase

) to the

pancrease

Idiopathic pancreatitis should not exceed 20% and it may be caused by biliary

microlithiasis

( stones that are not found) or genes effect which are not yet detected

Slide29

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Pathopysiology

Initial cause ----- >injury ---



1)signaling error

2)

Inflammmation

---

 proteases

1&2 leads to activation of enzymes

Slide31

An initial cause causes injury to the pancreatic ductal cells which results in cell membrane trafficking problem (signaling error)that causes the early activation of pancreatic enzymes and thus ,

distruction

of the pancreatic tissue .

Cell injury causes the release of activated neutrophils which produce

proteolytic

enzymes and activation of zymogens

continued release of activated

proteolytic

enzymes

is responsible

for increased capillary permeability

and rupture

, protein exudation ,then

retropertineal

edema

and

exuadation

(Formation of

pseudocyst

)

Slide32

Due to

exudation

and

hemorrhage

there may

be hypovolemia

and shock

Lipases destroying

peripancreatic

to leading fat necrosis

and

liquefactive

hemorrhagic necrosis can also

develop

The inflammation process includes the production of inflammatory mediators from the macrophages ( IL-6/IL-8/TNF alpha )which act locally ( local inflammation and systematically ( SIRS -- hemodynamic instability) With ,subsequent

multiorgan

failure ,ARDS.DIC,.....

Slide33

Clinical features

• Symptoms:

1. Pain: rapid onset,

epigastric

pain radiating to the back, progressive and reaching maximum intensity within minutes, continuous persisting hours or days, increases when lying supine and decreases when leaning

forward ,refractory

to analgesia.

2. Nausea and vomiting

(may contribute to hypovolemia

)

3.

Fever

4. -Retching and

patient may have anorexia

5. jaundice

Slide34

•

Signs ( PE) :

1.

Epigastric

tenderness

2. Diffuse abdominal tenderness

3. Decrease in bowel sounds (

Adynamic

ileus)

4. Abdominal distention (due to ileus)

5. Fever

6. Dehydration and shock (due to fluid sequestration

)

Abdominal mass (inflammatory pancreatic mass ,or pancreatic abscess, or

pseudocyst

8.

Signs of hemorrhagic pancreatitis (if damage to the blood vessels caused retroperitoneal hemorrhage):

➢ Cullen’s sign [Umbilical

hemoperitoneum

]

➢ Grey-Turner sign [Flank

hemoperitoneum

]

➢ Fox’s sign

[bluish

discoloration of the inguinal ligament]

Slide35

Cullen’s sign Grey-Turner sign

Slide36

Fox’s sign

Due to

necrosis induced hemorrhaging spread

to ST of

of

these

body areas

Slide37

Deferential diagnosis

(

DDX):

1.

BIliary

colic/

Cholecystitis

.

2. Gastritis/Peptic ulcer disease (PUD).

3. Perforated

viscus

.

4. Small bowel obstruction (SBO).

5. Mesenteric ischemia/infarction.

6. Inferior MI/ inferior lobe pneumonia.

7. Ruptured abdominal aortic aneurysm (AAA).

Slide38

Diagnosis

1)Clinical presentation(HX and P.E

)

2)

Lab Studies:

Slide39

Labs

1)LFT

-If Alkaline

phosphatase was high → think of

biliary stones

.

-

If AST > ALT → Think of alcohol.

-

Hyperbilirubinemia

2)CBC

-

LEUKOCYTOSIS

-

HB my be elevated initially due

to

hemoconcentration

, but can drop if hemorrhagic pancreatitis

Slide40

3)Serum pancreatic enzymes

-

Serum amylase concentrations increase in 2 to

12

hrs

After the onset of pancreatitis.

-

levels

of amylase will peak 24 to 72

hrs

Remain

elevated for 3-5 days before returning

to normal

-

levels

are usually 3 times normal (value required

for diagnosis

is1000U/L

-Amylase

is more

sensitive.Lipase

is more

specific as

it remains elevated for longer period

-The

increase in amylase level is not proportional to the severity of the pancreatitis.

Slide41

4)Serum

electrolyte :

patient

may have

hypocalcemia

Fat necrosis consumes

calcium

5) KFT

Hypovolemia may lead to AKI and elevated creatinine

level

6

)Peritoneal

fluid

analysis

if the patient has ascites, you take a sample from the

fluid >>

send it for amylase test if amylase > 100,000/cm3 (+)

for pancreas

so the cause of

ascitis

is acute pancreatitis

.

7

)fat levels

Slide42

RADIOLOGICAL STUDIES

1) CHEST

AND ABDOMINAL X-RAY: to look for

-Pleural

effusion(left) and

Atelactasis

:

1.One of the mechanisms is the

transdiaphragmatic

lymphatic blockage

.

2. formation of a

pancreaticopleural

fistula.

3. Exudation of fluid into the pleural cavity from the

subpleural

diaphragmatic

vessels may also cause pleural effusion.

4.Sentinal loop and colon cut off sign

.

-Gallstones on AXR if radiopaque

Slide43

Air-filled small bowel in

LUQ ..

m.c

sign on X-ray

.

Slide44

Abrupt end of transverse colon

Slide45

2)Ultrasound

(U/S):

• Swollen pancreas with

peripancreatic

collection of pus (

phlegum

) and

fluid may be seen.

• Gallstones or dilated biliary duct may be detected.(Gallstones (only 10% are

radiobaque

)

• specificity 95%, yet its sensitivity ranges between 62% and 95

%

Ultra sound has a major limitation in that it cannot be performed when excessive bowel gas is present, as occurs with an ileus

Slide46

Slide47

3)CT

scan with intravenous

contrast

-

remains the gold standard for diagnosing AP and

its complications(sensitivity

and specificity of CT are 90% and 100%, respectively)

-

Enlarged,

oedematous

pancreas

-

Fuzzy

pancreas borders

-

Fluid around pancreas

-

‘

Fat stranding’ in

retroperitoneum

(fluid density due to

oedema

in fat)

-

Pseudocyst

-

Areas of non-enhancement indicate necrosis (KEEP IN

MIND:Pancreatic

necrosis has two

parts:Parenchymal

liquafative

necrosis and fat

necrosis)

Slide48

Slide49

Slide50

4)ERCP …

Indications:

-

Preoperative

evaluation of patients with suspected

traumatic pancreatitis

to determine whether the pancreatic duct

is disrupted

-

Patients

with jaundice, suspected biliary pancreatitis,

and possible

cholangitis who are not clinically improving by

24 hours

after admission should undergo

endoscopic

sphincterotomy

and stone extraction.

-

Patients older than age 40 years with no identifiable

-cause

to rule out occult common bile duct stones,

pancreatic,or

ampullary

carcinoma or other causes of obstruction

Slide51

5)EUS (Endoscopic

ultrasound

)and

MRCP (Magnetic resonance

cholangiopancreatography

):

-

It’s not widely available.

-

Can detect stones in the CBD along with assessing the pancreatic parenchyma.

Slide52

severity

1)Acute

pancreatitis was divided into two groups as:

(Assessment

of

severity

)

1. Interstitial edematous pancreatitis

which is characterized by acute inflammation of the pancreatic parenchyma

and

peripancreatic

tissues, but without recognizable tissue necrosis

.

2. Necrotizing pancreatitis

-Necrotizing

acute pancreatitis, which is characterized by inflammation associated

with pancreatic

parenchymal necrosis and/or

peripancreatic

necrosis can be complicated

by systemic

inflammatory response syndrome (SIRS) and

multiorgan

dysfunction

syndrome (MODS

)

-This

classification identifies two phases of the disease—early and late

—

and severity of the disease has been classified as mild, moderate, or severe

depending on

the absence or presence of organ failure, fluid collections, and comorbid conditions

Slide53

Ranson

criteria

2)

Ranson

criteria

(not

specific nor

sensitive)

The

modified

Ranson

criteria are used to assess gallstone

pancreatitis

If you have

a patient

with

3 points

or

more, you should immediately admit

him to

the ICU

.

Slide54

3)CT

severity index (CTSI

):

The CTSI is the sum of the scores obtained with the Balthazar score and those obtained with the evaluation of pancreatic necrosis: 0-3: mild acute pancreatitis. 4-6: moderate acute pancreatitis. 7-10: severe acute pancreatitis

.

(A)Normal.

(B) Enlargement.

(C)

Peripancreatic

inflammation.

(D)Single

peripancreatic

fluid collection.

(E)Multiple

peripancreatic

fluid collection

.

4)skin changes as we mentioned in ( signs) part

Slide55

5)APACHE

II [good specificity and sensitivity]:

Needs a calculator → If ≥ 8 →

SEVERE

6)BISAP

: it can be done on bedside with No need for a calculator as APACHE II. [Point for each]:

1) BUN>25

2

) Impaired mental status

3

) SIRS

4)Age>60

5) pleural effusion

.

Slide56

Mortality risks:

• Point/

s→risk

• 0-2→ <2%

• 3-5 → >15 %

Slide57

complications

➢ Early:

1

. Shock and Renal failure

2. Pancreatic ascites and pleural effusion

3. ARDS and Sepsis

4. Severe

HYPOcalcemia

(due to fat saponification, in which fat necrotic

tissue binds to calcium)

5. Superior mesenteric/ Splenic/Portal vein rupture or thrombosis

.

Slide58

➢ Late

1. Pancreatic necrosis

2. Pancreatic Abscess

3. Hemorrhagic pancreatitis

4. Infection

5. Fistula

6.

Pseudocyst

7. Diabetes.

Slide59

1.Acute fluid collection

Occurs early in course of acute pancreatitis less than 4

wks

,adjacent to pancreas with no

fully defined

wall , appear as homogenous fluid density, sterile and mostly resolve

spontanously

Slide60

2. Pancreatic

pseudocysts

-

Defined

as fluid collection over 4 weeks old that is surrounded by a defined wall made up

of fibrous

tissue and surrounding organs. It consists mostly of pancreatic secretions

and inflammatory

exudate .

-

More

than half of all

pseudocysts

are small and resolve within 4 to 6 weeks.

-

After

6 weeks, spontaneous resolution is less likely and surgical intervention is

indicated, usually

in the form of a

cystogastrostomy

,

cystodudonostomy

or

cystojejunostomy

, and aims

to avoid

infection, hemorrhage and rapture.

-

Suspected

it in a patient with acute pancreatitis with unresolved

pain+Palpable

epigastric

mass

.

-Complications

: Rupture +hemorrhage +infection +gastric outlet, duodenal or biliary obstruction

-

CT

scan is the diagnostic imaging of scan (wall thickness, calcifications and number

of

pseudocysts

).

Tx

…Endoscopic drainage(if the

pseudocyst

doesn’t resolve spontaneously within 6 weeks)

Slide61

3. Pancreatic Abscess.

1.Pancreatic

abscesses are defined as a circumscribed,

intraabdominal

collection of pus in proximity to the pancreas,

containing little or no pancreatic necrosis.

2.Contains enteric bacteria

3.For pancreatic abscess, the treatment consists of

adequate drainage

and antibiotic coverage .

4.Drainage

can be achieved either by

image-guided placement

of percutaneous drains or a formal

surgical debridement

.

Slide62

4. Pancreatic necrosis

1. Pancreatic necrosis is defined as diffuse or focal area(s) of

nonviable pancreatic

parenchyma, often associated with

peripancreatic

fat necrosis.

2. . CT is diagnostic in more than 90% of the cases. Focal or diffuse

well circumscribed

areas of

nonenhanced

pancreatic parenchyma larger than 3

cm, or

involving more than 30% of the gland, are required for CT diagnosis .

3. Infected pancreatic necrosis is an indication for

surgical debridement(pancreatic

necrostomy

). Therefore, the clinical

differentiation between

sterile and infected pancreatic necrosis is essential.

4. Because clinical and laboratory findings in these two groups can

be identical

, the distinction is best made by cultures and Gram stains from

percutaneously

attained needle aspirates.

5. Sterile necrotic pancreatitis can be managed conservatively

Slide63

managment

• Patients with Interstitial edematous pancreatitis(80 % cases) are treated

conservatively ((

90% of cases will resolve)

incluiding

1- Early aggressive fluid and electrolyte resuscitation(in the first 12-24hrs

) • 250-500cc/

hr

Isotonic crystalloids are the preferred fluid(lactated ringer is the

prefered

crystalloids) Adjust

fluid therapy at frequent interval

withn

6

hrs

of admission and for the next 24-48

hrs

(vital signs

, urine

output, BUN ,Creatinine ,hematocrit).

2. NPO , NGT, parenteral

antiemetics

(such as promethazine and

ondansetron

) (in

pt

with ,nausea and

vomiting)

3. Oxygen supply and serial monitoring of po2 and ABG

4- Analgesia :opiates

5-nutritional support :

-

IN mild AP ,oral feeding can be started immediately if there is no nausea and vomiting ,

abd

pain is resolving

starting

with low fat solid diet is as save as clear liquid diet

-

IN sever AP enteral feeding (feeding through NGT )is recommended to prevent gut failure and

infectious complications(Enteral

feeds have the advantage of maintaining the integrity of the intestinal mucosa

and decreasing

bacterial translocation)

Slide64

6.Inhibit

pancreatic enzymatic secretions :

Somatostatin

analogue : octerotide, H2-blockers

7.Antibiotics

Pancreatitis is a sterile inflammation unless complicated

by infection

, The use and efficacy of prophylactic antibiotic therapy

in acute

pancreatitis has long been a point of controversy

Slide65

8- Role of ERCP and

cholycystectomy

-In

pt

with gallstone pancreatitis and

Juandice

/cholangitis ,

urgent ERCP

(within first 72

hrs

of symptoms onset) is recommended

.

-

In patients with mild gallstone pancreatitis,

cholecystectomy should

be performed during the index hospitalization

Slide66

Chronic pancreatitis

Prolonged and

frequently lifelong

disorder

resulting from

development of

fibrosis within pancreas

(irreversible morphological

changes

)

Note: Splenic vein thrombosis is a complication of both acute and chronic pancreatitis

Slide67

neoplasms

95% of pancreatic neoplasm are malignant pancreatic cancer . The remaining are endocrine tumors

Other pancreatic tumors are like cystic tumors and

gastrinomas

(

zollinger

Ellison syndrome)

Affects people in seventh decade and has a slight male preponderance

Cancers :

1)ductal adenocarcinomas 85%

2)

acinar

adenocarcinoma 5%

Investigations: tumor markers CA19-9,, CA50//ultrasound//cholangiography//cytology//

mri

angiography

Slide68

Staging by spiral

ct

/

mri

angiography … use

tnm

method

Manegment

: surgical with chemo-radiotherapy .. Standard operation of radical

pancreaticoduodenectomy

(

whipple’s

procedure) entails block resection of the head of the pancreas , the distal half of the stomach , the duodenum , gallbladder . CBD

Please go back and read more about

chronic pancreatitis and

neoplasms if it is necessary



Slide69

THANK YOU