PANKREATITIS AKUT

Dr.H.ALI IMRON YUSUF,SpPD

SMF ILMU PENYAKIT DALAM

RSUD Dr.H.ABDUL MOELOEK
BANDAR LAMPUNG
 PANKREATITIS
Y I REAKSI RADANG PANKREA S.
KLINIS AKUT DITANDAI NYERI
PERUT AKUT DISERTAI KENAIKAN
ENZIM DLM DARAH DAN URIN.
PERJALANAN PEYAKIT BERVARIASI,
RINGAN SAMPAI BERAT YG FATAL.
Aetiological factors in acute pancreatitis
Cholelithiasis
Microlithiasis
Alcohol
Trauma (blunt and penetrating)
Endoscopic retrograde cholangiopancrea-
tography
Obstruction (ampullary stenosis, duodenal
diverticulum, neoplasm, parasites)
Aetiological factors in acute pancreatitis

Hypercalcaemia
Hypertriglyceridaemia (types I and V)
Infection (coxsackievirus, mumps,
Mycoplasma)
Ischaemia (vasculitis, hypotension)
Hypothermia
Cardiopulmonary bypass
Drugs1
Miscellaneous (scorpion bite, hereditary,
pregnancy)
 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%).
 Abdominal pain with
fever or

abdominal mass

Vomiting
constipation

diarrhea
 Serum amylase/ lipase
Other biochemical tests

Radiology
Ultrasonography

CT
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

Acute pancreatitis :
Sudden
Severe abdominal pain
Systemic upset

Varies : Clinically mild to fulminating

disease cause sudden
death
 Early administration of improved a. biotik

Cytokine inhibitors

Endoscopic/ surgical techniques

Treat complication

reduced mortality rate 5% - 10%

 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
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

 Cellular changes only

Edematous pancreatitis

Necrotic and hemorrhagic pancreatitis

Infected necrosis
Hormonal pancreatic stimuli

1. Secretion for volume and bicarbonate

2. Cholecystokinin (CCK) for enzymes

Alcohol p.o / I.V

Vagal or local release CCK
ampullary spasm/ excessive enzym
secretion
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
Ca2+ < 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 Hypovolemia Pain

Hypocalcemia Nausea and
Hyperglycemia vomiting
Coagulopathy Pancreatic
Hepatic dysfunction enlargement
Peripancreatic fluid
Complication Respiratory failure Pancreatic infection
Cardiovascular Pseudocyst
insufficiency Gastric outlet
Renal failure obstruction
Biliary obstruction
 Pathologic classification of acute pancreatitis
ACUTE PANCREATITIS

EDEMATOUS NECROTIZING
(Interstitial) (Hemorrhagic)

INFLAMMATORY
MASS (Phlegmon)

STERILE ABSCESS/ NECROSIS

HEALING CHRONIC INFECTED

PSEUDOCYST ABSCESS/NECROSIS

PSEUDOCYST ABSCESS
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
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
 2 definitive treatment periods
Early Treatment
20% severe - ICU - anticipate
extra-abdominal organ system failure
NG suction
nasal O2
IAO (intake and output)
frequent Serum electrolytes
evaluation metabolic function
in addition : blood reflacement
dextran supp
PE nutrition

Antibiotic : Still uncertain

now appears : is warranted

Ulm (Germany) : bacterial colonization

5th 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
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
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
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.