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ACUTE & CHRONIC

PANCREATITIS
ILA GIT
BY SA3
7TH JUNE
2016

INTRODUCTION
OF ACUTE
PANCREATITIS
PRESENTED BY:
SITI KHADIJAH BINTI MANSOR 10-6-89
PREPARED BY:
SITI ZULAIKHA BINTI SAIAN 10-6-90
SITI SUHAILA BINTI MOHAD SARIF 10-6-91
SITI AISYAH BINTI RUSMAN 10-6-92
SITI NAJWA BINTI KHAMSUL 10-6-84

Acute

pancreatitis (AP)

the

single most frequent gastrointestinal cause of


hospital admissions in the US.

The

risk and etiology of pancreatitis differ with age and


sex, and all pancreatic disorders affect Blacks more
than any other race.

Gallstones

are the most common cause of acute


pancreatitis, and early cholecystectomy eliminates the
risk of future attacks.

CAUSES OF ACUTE
PANCREATITIS
1.
2.
3.
4.
5.

Bile duct stones (50%)


Excess alcohol intake (35%)
Trauma
Rare : viral infections,
hyperparathyroidism, corticosteroid
Idiopathic (20%)

increasing incidence of obesity promotes


gallstone formationthe most common cause of AP.
Increased availability and use of tests to measure
serum levels of pancreatic enzymes detect milder
cases of AP but can also result in over diagnosis
The

Graph shows incidence from 19962005 in White and Black


residents of Allegheny County, PA, US, based on age-group, sex and
etiology.

INCIDENCE IN MALAYSIA
Etiology

Malay

Indian

Total

Alcohol

17

18

Biliary
disease
Viral

14

17

ERCP

Others

Unknown

13

13

Total

31

21

52

DIAGNOSIS OF
ACUTE
PANCREATITIS
PRESENTED BY:
SITI NUR JANNAH BT SHAARI 10-6-97
PREPARED BY:
SITI NUR AFIQAH BT JOHARI 10-6-95
SITI NUR BAIZURI BT HASAN 10-6-96
SYED ALWI BIN SYED HUSIN 10-6-98
SHARIFAH ANITH ATIQA BT SYED ROZHAN 10-6-99

HISTORY
Abdominal
Site:

pain

upper abdomen

Acute

onset

Gradually

intensifies in severity

Duration:

varies

Radiates

to the back

Worsening
Relieve

when drinking alcohol or eating heavy meal

sometimes by sitting upright or leaning

forward
Associated

with nausea, vomiting, anorexia, fever

Dont forget to ask..


History

of previous biliary colic

History

of alcohol consumption

Any

recent operative or other invasive procedures


(e.g. ERCP)

Any

intake of certain medications

Any

viral infection

Family

history of hypertriglyceridemia

EXAMINATION
General examination
Pale
Diaphoretic
Listless
Jaundice

(minority of patients)

Vital signs
Fever
Tachycardia
Hypotension
Tachypnea

Abdominal examination
Abdominal

tenderness

Muscular

guarding (guarding
tends to be more pronounced in
the upper abdomen) and
distention.

Bowel

sounds are often


diminished or absent because of
gastric and transverse colonic
ileus.

Uncommon physical findings


Cullens sign:

bluish discoloration
around the umbilicus resulting from
hemoperitoneum

Grey-Turners sign

: reddish-brown
discoloration along the flanks resulting
from retroperitoneal blood dissecting
along tissue planes.

Erythematous

skin nodules : focal


subcutaneous fat necrosis(size not more
than 1 cm, and the site is on extensor
skin surfaces)

Polyarthritis

INVESTIGATIONS
LABORATORY
CBC
Anemia(hgic),
Liver

leukocytosis (inflammation, infection)

enzymes

ALT

if increases more that 150 U/L probably dto


gallstones

Serum
Low
Blood

electrolytes, BUN, creatinine


Ca2+

glucose, cholesterol, triglycerides

Blood

glucose high dto B-cell injury

ABG
respiratory

distress

Serum
amylas
e

Other
marker
s

LABORATO
RY
STUDIES

Creactiv
e
protein

Serum
lipase

Pancreatic

enzymes (serum amylase and lipase)

Serum

amylase sensitivity of 81-95% but not specific for


pancreatitis

Serum

lipase more preferred dto its improved sensitivity esp


in alcohol-induced pancreatitis, and its prolonged elevation

Rise

2-4 times the upper limit of normal is recommended for

dx
Neither

is useful in monitoring or predicting the severity the


episode of acute pancreatitis

Serum

C-Reactive Protein: best marker for severity

Trypsinogen

and elastase have no significant advantage


over amylase or lipase

IMAGING IN ACUTE
PANCREATITIS
Role:
To clarify

the diagnosis when the clinical picture is

confusing
Help

in determine the possible causes

Assess

severity (Balthazar score)

Determine
Detecting

prognosis

complications

1. Abdominal Ultrasound

Indicated early in acute pancreatitis

Pros

Inexpensive

Excellent for identifying gallbladder pathology

Technique of choice of detecting gallstones (Most common cause of pancreatitis!)

Evaluate bileduct dilation

May visualize masses and follow up of pseudocyst

Cons

Not optimal for pancreas; retroperitoneal location easily obscured by bowel gas
distension

Less sensitive for stones in distal CBD

Limited in early assessment of pancreatitis

2. Abdominal X-ray
Limited

role in acute pancreatitis

Poor

visualization of the pancreas and


retroperitoneum

Most

common radiologic signs associated with


acute pancreatitis include:

Free

The

air in the abdomen, indicating a perforated viscus

colon cut-off sign, and sentinel loop sign, both


indicating inflammatory process damaging
peripancreatic structures

COLON CUT-OFF SIGN


Markedly

distended transverse
colon with air
Absence

flexure

of gas distal to splenic

SENTINEL LOOP SIGN

Mildly dilated, gas-filled segment of small bowel


with or without air fluid level

3. Contrast-Enhanced CT
Standard

imaging of choice

Pros
Aid

in diagnosis and staging of pancreatitis

Evaluate

complications

Evaluate

common bile duct for stones or other obstructions

Assess

severity of acute pancreatitis (CT Severity Index)

Cons
limited

in patients who are allergic to intravenous (IV)


contrast or have renal insufficiency.

CTSI

3. MRI

Increasingly used in diagnosis and management of acute pancreatitis


Pros
alternative

in situations in which CECT is contraindicated

Noninvasive

and no use of IV contrast

Ability

to delineate pancreatic and bile ducts (detect


choledocholithiasis missed on U/S )

Greater

sensitivity than CT in detecting mild pancreatitis

Cons
Expensive
Less

readily available in nontertiary medical centers

SUMMARY

MANAGEMENT OF
ACUTE PANCREATITIS
PRESENTED BY:
SHAFIRA BT SHAHAMEN 10-6-104
PREPARED BY:
SHAHIZAN BT MOHD RASID 10-6-102
SHARIFAH NUR ATIQAH 10-6-103
AIDA NABILAH BT MOHD NASIR 10-6-109
ATIQAH ATHIRAH BT MUSTAFA 10-6-110

Management Algorithm from American College of Gastroenterology

INITIAL MANAGEMENT
Fluid

rehydration

Nutritional

support

Aggressive fluid
Early
AND Aggressive IV fluid hydration must be initiated.
rehydration
How aggressive?
What kind of IV
fluids?
How soon to
start?
Goal with IV fluid
hydration?

If severe hypovolemia present, bolus IV fluids initially


Then keep maintenance rate of 250 500 mL/hr IV
fluids.
Isotonic crystalloid
Lactated Ringers solution may be the preferred
isotonic crystalloid replacement

VERY VERY EARLY


Most beneficial in the first 12-24 h
Decrease BUN

Fluid requirements should be reassessed at frequent


intervals within 6 h of admission and for the next 2448 h.

Nutritional support
Mild Acute Pancreatitis
Oral feedings can be started immediately if there is no nausea and
vomiting, and abdominal pain has resolved.
Initiation of feeding with a low-fat solid diet appears as safe as a
clear liquid diet

Severe Acute Pancreatitis


Enteral nutrition is recommended to prevent infectious
complications.
Parenteral nutrition should be avoided unless the enteral route is
not available, not tolerated, or not meeting caloric requirements.

Nasogastric delivery and nasojejunal delivery of enteral feeding appear


comparable in efficacy and safety

The Role of Antibiotics in AP


ACG Recommendations
1.

Antibiotics should be given for an extrapancreatic infection, such as cholangitis, catheteracquired infections, bacteremia, urinary tract infections, pneumonia

2.

Routine use of prophylactic antibiotics in patients with severe AP is not recommended

3.

The use of antibiotics in patients with sterile necrosis to prevent the development of infected
necrosis is not recommended

4.

Infected necrosis should be considered in patients with pancreatic or extrapancreatic necrosis


who deteriorate or fail to improve after 710 days of hospitalization. In these patients, either

(i) initial CT-guided fine-needle aspiration (FNA) for Gram stain and culture to guide use of
appropriate antibiotics or
(ii) empiric use of antibiotics after obtaining necessary cultures for infectious agents, without CT
FNA, should be given

The Role of Antibiotics in AP


ACG Recommendations
4. In patients with infected necrosis, antibiotics known to penetrate pancreatic
necrosis, such as carbapenems, quinolones, and metronidazole, may be useful in
delaying or sometimes totally avoiding intervention, thus decreasing morbidity and
mortality
5. Routine administration of antifungal agents along with prophylactic or therapeutic
antibiotics is not recommended

MANAGEMENT OF ACUTE
PANCREATITIS
PRESENTED BY:
IZZATI SHAHIRAH BT SHAHARUDIN
10-6-114
PREPARED BY:
FADZRIN BIN FADHIL 09-6-115
IZZA NADZMI BT OTHMAN 10-6-111
IZZAH ILYANI BT ISMAIL 10-6-112
AIZAT AMIR BIN MOHD ABDUL SALAM 10-6-113

INITIAL ASSESSMENT & RISK


STRATIFICATION SCORE FOR
ICU SETTINGS
(according to the American College of
Gastroenterology updated guidelines)

Recommendations
1- Assessment of hemodynamic status & resuscitative
measures
2- Risk Stratification for Intensive Care Setting
3- Patients with organ failure admission to an intensive
care unit

1- Hemodynamic status
should

be assessed immediately upon


presentation and resuscitative measures
begun as needed
(strong recommendation)

2- Risk assessment
should

be performed to stratify patients into

i-higher-risk categories
ii- lower-risk categories
to assist triage, such as admission to an
intensive care setting.

3- Patients with organ failure


should

be admitted to an intensive care unit


or intermediary care setting whenever
possible.

The

Revised Atlanta Criteria now define organ


failure as a score of 2 or more for one of
these organ systems using the modified
Marshall scoring system.

Management of
post ERCP
pancreatitis

ROLE OF ERCP IN AP
ACG Recommendations
1.

Patients with AP and concurrent acute cholangitis should undergo ERCP within
24 h of admission

2.

ERCP is not needed early in most patients with gallstone pancreatitis who lack
laboratory or clinical evidence of ongoing biliary obstruction

3.

In the absence of cholangitis and/or jaundice, MRCP or EUS rather than diagnostic
ERCP should be used to screen for choledocholithiasis if highly suspected

4.

Pancreatic duct stents and/or post procedure rectal nonsteroidal anti-inflammatory


drug (NSAID) suppositories should be utilized to lower the risk of severe postERCP pancreatitis in high-risk patients

Preventing post-ERCP pancreatitis


Interventions to decrease the risk are:
i.

Guidewire cannulation

ii.

Pancreatic duct stents

iii.

Rectal NSAIDs

Treatment of post ERCP pancreatitis


Role of endoscopist:

Volume of fluid
resuscitation

Frequency and type of


narcotic analgesia

SURGICAL
INTERVENTIONS
IN ACUTE PANCREATITIS
PRESENTED BY:
AINI HAFIZAH BT SALLEH 10-6-121
PREPARED BY:
AIZURA BT ABD AZIZ 10-6-115
AFIFUL FIDAIY BIN HASLAN 10-6-116
AISYAH BT JAAFAR 10-6-119
FAIZUL ADLAN BIN ANUAR 10-6-122

1.

ROLE OF SURGERY IN ACUTE


PANCREATITIS (ACG
In patients with mild AP, found to have gallstones in the GB, a cholecystectomy should be performed
Recommendations
2013)
before discharge to prevent a recurrence of AP.

2.

In a pt with necrotizing biliary AP, in order to prevent infection, cholecystectomy is to be deferred until
active inflammation subsides & fluid collections resolve / stabilize.

3.

The presence of asymptomatic pseudocysts & pancreatic and/or extrapancreatic necrosis do not
warrant intervention, regardless of size, location and/or extension.

4.

In stable pts with infected necrosis, surgical, radiologic and/or endoscopic drainage should be delayed
preferably for more than 4 weeks to allow liquefaction of the contents & the development of a fibrous
wall around the necrosis (walled-off necrosis).

5.

In symptomatic patients w infected necrosis, minimally invasive methods of necrosectomy are preferred
to open necrosectomy.

PANCREATIC PSEUDOCYST

Def: a localized fluid collection that is rich in amylase


& other pancreatic enzymes & is surrounded by a wall
of fibrous tissue that is not lined by epithelium.

Should be suspected when a pt with AP fails


to resolve pain / recover after a week of Rx or
symptoms recur after improving!!
20-50% regress spontaneously w/in 6-7 weeks.
Acute complications:

Chronic complications:

1. Bleeding (usually from


splenic artery
pseudoaneurysm)
2. Infection
3. Rupture

1. Gastric outlet obstruction,


2. Biliary obstruction,
3. Thrombosis of the splenic
or portal vein with
development of gastric
varices

Mx of Pancreatic Pseudocyst

Imaging:

Transabdominal US hypoechoic / anechoic collections w low


level echoes are often seen dependent representing debris

CT scan well-circumscribed usually round or oval


peripancreatic fluid collections of homogenously low
attenuation, usually surrounded by well defined enhancing
wall.

Rx options:

1.

Observation: IV fluids, analgesics, antibiotics wait for ~ 6


weeks for spontaneous resolution & to allow maturation of the
wall so to be fit for surgical interventions.

2.

Drainage procedure:

Indications: size > 5cm, symptomatic, presence of complications

CT or US-guided external/percutaneous drainage

Surgical drainage: (take biopsy of cyst wall to exclude


cystadenocarcinoma)

Cystogastrostomy
Cystojejunostomy
Cystoduodenostomy

3. Endoscopic drainage:
less invasive, avoids the need for external drain, high long term
success rate

Transpapillary approach with ERCP

Transgastric / transduodenal approach

4. Other interventions:

Pseudocyst in tail of pancreas resection

Infected pseudocyst percutaneous external drainage with IV


antibiotics

Pseudocyst with bleeding into the cyst angiogram &


embolization

MANAGEMENT OF BILIARY
PANCREATITIS DUE TO GALL
BLADDER STONE

Overview of Biliary
Pancreatitis
Definition:

Gallstones obstructing pancreatic duct


causing the juice to attack its own tissues.

Signs

and Symptoms:
severe upper abdominal pain.
jaundice
nausea
vomiting
fatty stool production.
weight loss.

How do we approach such


case?
Investigation:
MRCP/CT

(gold)

ALP
AST
Pancreatic
US

Guided

Amylase

Algorithm

HAEMORRHAGIC
PANCREATITIS
Debridement

of necrotic tissues (necrosectomy)

o Endoscopic

approach

o Transgastric,
o Laparoscopic

transduodenal, transpapillary

debridement

o Retroperitoneal

approach

Retroperitoneal debridement

Endoscopic transgastric
necrosectomy

SURGERY OF
PANCREATIC
ABSCESS

What is pancreatic abscess?


Pancreatic abscess is a late complication
of acute necrotizing pancreatitis, occurring
more than 4 weeks after the initial attack.
A pancreatic abscess is a collection of pus
resulting from tissue necrosis, liquefaction,
and infection.

Surgical Treatment
EUS-guided necrosectomy is the standard
treatment for pancreatic necrosis and
abscess.
CT-guided drainage is the next best strategy
when a good transluminal window is not
available for EUS-guided transgastric
drainage.

CHRONIC
PANCREATITIS
PRESENTED BY:
FATIN KHAIRANNI BT AHMAD KHAIRUDDIN 10 6 - 128
PREPARED BY:
FATHIN AZIZAH BT MOHAMAD BASRI 10 6 123
FATIMAH AMIRA BT ZUHAIRI 10 6 125
FATIMATUL SYAHIRAH BT MOHD BADLI SHAH 10 6 126
FATIMAH NADHIRAH BT ABDULLAH ALWI 10 6 127

DEFINITION
A continuing, chronic, inflammatory process
of the pancreas, characterized by irreversible
morphologic changes

ETIOLOGY

Autoimmune pancreatitis

Increased circulating levels of gamma globulin, the presence


of autoantibodies, and a possible association with other
autoimmune diseases

Alcoholic chronic pancreatitis

The most common cause of pancreatitis (60%). A theory


suggests that the persistent demands of metabolizing
alcohol cause oxidative stress within the pancreas and may
lead to cellular injury and organ damage

Hereditary pancreatitis
An autosomal dominant disorder accounting for
about 1% of cases.

Cystic fibrosis in pancreatitis


The most common genetic abnormalities, is an
autosomal recessive disorder accounting for a small
percent of patients with chronic pancreatitis

Idiopathic

CLINICAL PICTURE
Abdominal

pain :

character : dull aching

worsens after eating

site : epigastric

radiation : to the back

Type B : prolonged, severe pain

Steatorrhea

(oily,
smelly stool)

Weight

loss

Gastroparesis

diarrhea

Type A : short relapsing episodes


lasting days to weeks, separated by
pain-free intervals

&

(type B is associated with worse quality of


life, greater healthcare need and
disability)

May be caused by :
Maldigestion
Fear of eating
multifactorial
Anorexia
Nausea
Vomiting
*severe / rapid weight loss is a red
flag for pancreatic cancer

INVESTIGATIONS
LABORATORY

Blood test

RADIOLOGY

Liver function test

Ultrasound

Renal function test

CT scan

Serum amylase and


lipase

ERCP

MRCP

Abdomen ultrasound

Serum trypsinogen

Fecal test

ESR

Serum amylase and lipase


not that relevant in chronic
pancreatitis as theyre only
high in acute pancreatitis
Low concentrations of serum
trypsin - relatively specific for
advanced chronic pancreatitis,
but not sensitive enough
Steatorrhea is seen in patients
with advanced chronic
pancreatitis

Ultrasound is the best initial


test and has sensitivity of
70%-80%
CT scan is good for assessing
complications
ERCP and MRCP can be used to
detect duct obstruction
MRCP is safer and safer than
ERCP, but less sensitive

TREATMENT
GOALS :
The goals of medical treatment are as follows:
Modify behaviors that may exacerbate the natural history of the
disease
Enable the pancreas to heal itself
Determine the cause of abdominal pain and alleviate it
Detect pancreatic exocrine insufficiency and restore digestion and
absorption to normal
Diagnose and treat endocrine insufficiency

Lifestyle
modification
Cessation of
tobacco
smoking,
Cessation of
alcohol intake

Endoscopic
treatment

Diet
Low fat diet,
High in protein
and carbohydrate

Surgical
treatment
pancreatic duct
drainage,
pancreatic
resection

Hospitalization
depends on the
severity of the
patient.