Acute pancreatitis :

Sudden
Severe abdominal pain
Systemic upset

Varies : Clinically mild to fulminating
disease cause sudden
death
Aetiological factors in acute pancreatitis
Cholelithiasis
Microlithiasis
Alcohol
Trauma (blunt and penetrating)
Endoscopic retrograde cholangiopancrea-
tography
Obstruction (ampullary stenosis, duodenal
diverticulum, neoplasm, parasites)






Hypercalcaemia
Hypertriglyceridaemia (types I and V)
Infection (coxsackievirus, mumps,
Mycoplasma)
Ischaemia (vasculitis, hypotension)
Hypothermia
Cardiopulmonary bypass
Drugs1
Miscellaneous (scorpion bite, hereditary,
pregnancy)
Aetiological factors in acute pancreatitis









Cholelithiasis - pressure pancreatic duct
obstructing stone
Alcohol - interfering the tone of
sphincter of Oddi
- toxin - acinar cells or
- trigger autodigestion.
3 phases :
1. Local inflammation
2. Systemic inflammation
3. Sepsis
pain
vomiting
dehydration
epigastric tenderness
confusion (a result of hypoxia)
hypovolaemic shock
jaundice (10-20%)
Grey - Turner/Cullen sign (discoloration of
the flanks and/or periumbilical area, < 5%).
C
C
C
C
C
C
C
C
Serum amylase/ lipase
Other biochemical tests
Radiology
Ultrasonography
CT
_
_
_
_
_
Early administration of improved a. biotik
Cytokine inhibitors
Endoscopic/ surgical techniques
Treat complication

reduced mortality rate 5% - 10%
4
4
4
4
Critical anatomic areas : 4
1. The glands
2. Relationship pancreas - duodenal loops &
greater curvature and splenic flexure
3. Common bile duct and pancreatic duct
4. Ductal acinar and islets of langerhans

Anatomic abnormalities : 2
1. Pancreas divisum
2. Annular pancreas
Etiology & severity of the attack
ex : alcohol induced pancreatitis
gallstones
4
4
Abdominal pain with
fever or
abdominal mass

Vomiting
constipation
diarrhea
_
_
4
4
4
4
1. Alcohol and gallstones
2. Medications
3. Cancer of the pancreas
4. ERCP
5. Idiopathic pancreatitis
6. Other causes
Duct obstruction
Direct toxic effect on acinar cells
Neurohormonal mechanisms
Vascular insufficiency
Enzyme - cytokine cascade
E
E
E
E
E
Cellular changes only
Edematous pancreatitis
Necrotic and hemorrhagic pancreatitis
Infected necrosis
E
E
E
E
Hormonal pancreatic stimuli
1. Secretion volume and bicarbonate
2. Cholecystokinin (CCK) enzymes

Alcohol p.o / I.V
Vagal or local release CCK
ampullary spasm/ excessive enzym
secretion
for
for
Ransons Signs
Ransons early objective sign (1974)
Alcohol and other Gallstone
0 h Age > 55 y > 70 y
Leukocyte count > 16,000 mm > 18,000 mm
Blood sugar > 200 mg/100 mL > 220 mg/100 mL
LDH > 350 U/L > 250 U/L
AST > 250 U/L > 250 U/L

48 h HCT < 10% < 10%
BUN > 5 mg/100 mL 2 mg/100 mL
Ca
2+
< 8 mg/100 mL < 8 mg/100 mL
P0 < 60 mmHg -
Base deficit > 4 mEq/L > 5 mEq/L
Fluid sequestration > 6000 mL > 4000 mL
Banks Criteria
Banks clinical criteria (1983)

Cardiac Shock, tachycardia > 130, arrhytmia, EcG
changes
Pulmonary Dyspnea, rates P0 < 60, adult respiratory
distress syndrome
Renal Urine output < 50 mL/h, rising BUN or serum
creatinine level
Metabolic Low or falling Ca2+, pH, serum albumin
decrease
Hematologic Falling HCT, diffuse intravascular coagulation
(low platelets, split products)
Neurologic disease On physical (Grey Turner, Cullen) signs or
peritoneal tap
Tense distention Severe ileus, fluid ++
Causes of Hyperamylasemia
Acute Atdominal Emergencies
Penetrating peptic ulcer
Acute cholecystitis with hyperamylasemia
Intestinal obstruction with strangulation
Intestinal infarction
Ruptured aortic aneurysm or dissection
Ruptured ectopic pregnancy
Acute salpingitis
Tonsion of ovarian cyst or carcinoma
Abdominal trauma with hematoma formation
Perforated diverticulitis
Postgastrectomy afferent loop obstruction
Chrohns disease
Causes of Hyperamylasemia
Physiologic
Pregnancy
? Genetic S hyperamylasemia
Protein-Bound Hyperamylasemia
Inborn macroamylasemia attached to albumin or
globulin (macroamylase)
IgA-bound : chronic disease, lymphoma, IPSID
IgG-bound : chronic infections, liver disease
Immune-complex-bound : AIDS, collagen disease,
Sjogrens syndrome
Decreased Excretion of Amylase
Acute and chronic renal failure
Benefits of Treatment Options
Definite benefits Possible benefit Experimental benefit

ICU therapy Dextran 60 O-Radical scavengers
Surgery Peritoneal lavage (allopurinol, dismutase,
for complications for 7 days and catalase)
Angiography Antibiotics, Interleukins 10, 11,
for bleeding antifungals TNF- antibody
Octreotide Calcium channel blockers
Gabexate
ERCP and
stone removal
Platelet factor
inhibitor
(Lexipifant)

Differential Diagnosis of Acute Pancreatitis
Ethanol
Gallstones
Choledocholelithiasis
Billiary sludge
Microlithiasis
Mechanical/structural injury
Sphincter of Oddi dysfunction
Pancreas divisum
Trauma
Post-endoscopic retrograde cholangiopancreatography
Pancreatic malignancy
Peptic ulcer disease
Inflammatory bowel disease
Medications
Azathioprine/6-mercaptopurine Dideoxyinosine
Pentamidine
Sulfonamides

L-
Asparaginase
Thiazide diuretics
Differential Diagnosis of Acute Pancreatitis
Metabolic
Hyperlipidemia
Hypercalcemia
Infectious
Viral
Bacterial
Parasitic
Vascular
Vasculitis
Atherosclerosis
Miscellaneous
Scorpion bite
Heretary pancreatitis
Idiopathic pancreatitis
Cystic fibrosis Coronary bypass
Tropical pancreatitis
Prognostic Criteria for Acute Pancreatitis
RANSON CRITERIA SIMPLIFIED GLASGOW CRITERIA
On admission Within 48 hrs of admission
Age > 55 yrs Age > 55 yrs
Leukocyte count > 16,000/ l Leukocyte count > 15,00/ l
Lactate dehydrogenase > 350 IU/liter Lactate dehydrogenase > 600 IU/liter
Glucose > 200 mg/dl Glucose > 180 mg/dl
Aspartate aminotransferase Albumin < 3,2 g/dl
> 250 IU/liter Calcium < 8 mg/dl
Arterial Po2 < 60 mmHg
Serum urea nitrogen > 45 mg/dl
48 hrs after admission
Hematocrit decrease by > 10%
Serum urea nitrogen increase
by > 5 mg/dl
Calcium < 8 mg/dl
Arterial Po2 < 60 mmHg
Base deficit > 4 mEq/liter
Estimated fluid sequenstration > 6 liter

Prognosis
Ranson criteria
simplified Glasgow criteria

Prognostic accuracy : similar
2 or < : mortality < 1 %
3 - 5 : mortality 5 %
6 > : mortality 20 %

Complication
Severe peripancreatic fluid collections
or pancreatic necrosis
infected
Prophylactic antibiotic - controversial
Combination : quinolone & metronidazole


Complications
Pancreatic abscesses
Pseudocyst 10%
Several weeks - pain - compressing organs
eroding mediastinum.

> 5-6 cm 30% - 50% :
rupture, hemorrhage, infection
Persisten (> 6weeks), large, expanding
drained surgical - endoscopie or
percutaneous

Somatostatin analog ocreotide :
risk fistula formation pancreatic secretions
Pulmonary processes
Stress gastritis, renal failure, hypocalemia, delirium,
disseminated fat necrosis
Thrombosis - gastric varices & GI hemorrhage





-
-
Supportive - most cases
crystalloid
Severe cases : volume replection
colloids
nutrition & electrolyte IV NOT ENTERALLY
> 2 - 3 days : TPN
P.E meperidine > morphine

Sphincter of Oddi spasm
NG suctioning - : intractable vomiting

No evidence : routine antibiotics or somatostatin
Reinitiate feeding : Not serum enzym fevels
clinical status
Resolution pain & emergence hunger ready to eat

Gallstone pancreatitis : ERCP sphineterotomy & stone extraction
Note : ERCP worsen pancreatitis.



Mild gallstone : conservativelly
ERCP : after recovery to asses retained bile duct
stones
Risk recurrent gallstone ------- 33%
definitive surgical therapy.

Poor operative risk : endoscopic sphincterotomy
without cholecyctectomy
Common sequelae of acute pancreatitis
Systemic Local

Manifestation





Complication
Hypovolemia
Hypocalcemia
Hyperglycemia
Coagulopathy
Hepatic dysfunction

Respiratory failure
Cardiovascular
insufficiency
Renal failure
Pain
Nausea and
vomiting
Pancreatic
enlargement
Peripancreatic fluid
Pancreatic infection
Pseudocyst
Gastric outlet
obstruction
Biliary obstruction
ACUTE PANCREATITIS
EDEMATOUS NECROTIZING
(Interstitial) (Hemorrhagic)

INFLAMMATORY
MASS (Phlegmon)


STERILE ABSCESS/ NECROSIS


HEALING CHRONIC INFECTED
PSEUDOCYST ABSCESS/NECROSIS


PSEUDOCYST ABSCESS
Pathologic classification of acute pancreatitis
Hyperamylasemia & abdominal pain
1. Is the hyperamylasemia due to pancreatitis,
another abdominal emergency or concomitant
concidental disease ?
2. Is pancreatitis is present, how severe is the
attack ?
3. What is the etiology of the pancreatitis and
does it need urgent correction ?

Assesment of Severity :
30% severe attack :
hypotension
tachycardia
acidosis
abdominal ileus
hemorrhagic pancreatitis : Grey Turners sign
or Cullens sign
central loop distended bowel
colon cutoff sign
Ransons early objective signs (1974)
Banks clinical criteria (1982) or signs of MOSF
The Apache II physiologic score
4
4
4
Early mortality 2 - 7 days
(extra-abdominal organ failure)

Delayed mortality 7 - 21 days
(intra-abdominal complications)

Infected necrosis or abscess
Non infected continued massive necrosis
Gastrointestinal or intra-abdominal hemorrhage
Cyst formation, ascites and massive pleural effusion

ICU or in-hospital therapy 6-12 months
4
4
4
4
Transient minor complications
Acute diabetes
Peripheral fat necrosis
Retinal changes

SPECIAL TEST
Serologic Test Other than Serum Amylase
serum esterase
phospholipase A 2
salivary (S)
fractionation Serum Amylase
pancreatic P
isoenzym
Serum lipase
Computed Tomography Scan
ERCP
4
4
4




E
E
E
2 definitive treatment periods
Early Treatment
20% severe - ICU - anticipate
extra-abdominal organ system failure
NG suction
nasal O
2

IAO (intake and output)
frequent Serum electrolytes
evaluation metabolic function
E
-
-
-
-
-
in addition : blood reflacement
dextran supp
PE nutrition

Antibiotic : Still uncertain
now appears : is warranted

Ulm (Germany) : bacterial colonization
5
th
day of disease



Administration antibiotik before
imiperem and ciprofloxacin
morbidity & perhaps mortality

Star antibiotics early in the attack
More spesific th/ :
Peritoneal dialysis
antitrypsin (eg. aprotinin or gabexate)
ocreotide(universal inhibitor of secretion) -
spesific centers - not yet gained wide acceptance.

Multicenter trials England & USA :
Cytokines & inhibitors :
PAF inhibitor (lexipafant)
morbidity & mortality



OO
Late Treatment
Continuing Necrosis
failed bacterial contamination septic course :
ICU monitoring, a.biotik th/, TPN continued
CT scans repeated
some centers :
Organ failure develop surgery (necrosectomy)
difference mortality rates (30%)

Infected necrosis or Abscess
Gastrointestinal Hemorrhage
Pancreatic cyst, Ascites and Pleural Effusion
Transient Diabetes
_
_
_
_
_
During the Attack
Stop : alcohol & pancreatitis - producing
drugs hyperlipidemia
After the Attack Has Subsided
Recurrent Attacks
_
_
_
80 % Acute attacks - mild episode 7 - 10 days
1 - 3 % progress to severe or complication
20 % acute attacks - severe

2 - 3% : 72 hours - MOF
prolanged by PD
U
U
30 - 50% severe attack

Mortality Long Island Yewish Medical Centre
13,5 % 1978 - 1982
8 % 1986 - 1990
Scottish and German
5 %

dissappointoments < 5% -10% pat
O
O

U
Diagnosis ditegakkan dari adanya peningkatan
amilase dan terapi ocreotide
Penyakit yang mendasari relatif sama dengan
penelitian lain : DM 4 penderita, batu bilier 3
penderita. Tidak didapatkan alkohol sebagai
penyakit yang mendasari.
Pengobatan dengan ocreotide menunjukkan
hasil baik, namun perlu penelitian lebih lanjut
secara prospektif.