Acute Pancreatitis

Dr.E.Kandasamy @Kumar MDDM

Associate Professor Department of MGE
GMKMC
Acute Pancreatitis
Definition
 Acute inflammatory process involving the
pancreas
 Usually painful and self-limited
 Isolated event or a recurring illness
 Pancreaticfunction andmorphology return to
normal after (or between) attacks
Acute Pancreatitis
Etiology
O th e r
G a lls to n e s
Id i o p a t h i c 10%
45%
10%

E tO H
35%
Causes of
Common Causes 
Acute Pancreatitis
Gallstones (including microlithiasis)
Alcohol (acute and chronic alcoholism)
Hypertriglyceridemia
Endoscopic retrograde cholangiopancreatography (ERCP)
,
Trauma (especially blunt abdominal trauma)
Postoperative (abdominal and nonabdominal operations)
Drugs (azathioprine, 6-mercaptopurine, sulfonamides,
estrogens, tetracycline, valproic acid, anti-HIV
medications)
Sphincter of Oddi dysfunction
Uncommon Causes 
 Vascular causes and vasculitis (ischemic-
hypoperfusion states after cardiac surgery)
Connective tissue disorders and TTP
Cancer of the pancreas
Hypercalcemia
Periampullary diverticulum
Pancreas divisum
Hereditary pancreatitis
 Cystic fibrosis
Renal failure
 Infection
 Ascaris
 Campylobacter
 CMV
 Coxsackie B
 EBV
 Enterovirus
 HIV/AIDS
 Influenza
 MAC
 Measles
 Mumps Rubella
 Mycoplasma
 Rubeola
 Viral Hepatitis
 Varicella
 Autoimmune (e.g., Sjögren's syndrome
Hereditary Pancreatitis
 Autosomal dominant with 80% phenotypic
penetrance
 Recurrent acute pancreatitis, chronic pancreatitis,
and 50-fold increased risk of pancreatic cancer
 Mutation in cationic trypsinogen gene (R122H)
 Other genetic defects
 CFTR
 SPINK1
Acute Pancreatitis
Pathogenesis

acinar cell
injury

premature
enzyme activation

failed protective
mechanisms
Acute Pancreatitis
Pathogenesis
premature enzyme activation

autodigestion of pancreatic tissue

local activation release of

vascular of white enzymes into
insufficiency blood cells the circulation

local distant
complications organ failure
Acute Pancreatitis
Pathogenesis
SEVERITY
Mild  STAGE 1: Pancreatic Injury
 Edema
 Inflammation
 STAGE 2: Local Effects
 Retroperitoneal edema
 Ileus
 STAGE 3: Systemic Complications
 Hypotension/shock
 Metabolic disturbances
 Sepsis/organ failure
Severe
Clinical Presentation
 Clinical
 Continuous mid-epigastric / peri-umbilical abdominal
pain  Radiating to back, lower abdomen or chest
Worse in supine position and relief by sitting with
the trunk flexed and knees drawn up
 Emesis
 Fever
 Aggravated by eating
 Progressive
 Restless and uncomfortable
Clinical Presentation
 More severe cases
 Jaundice
 Ascites
 Pleural effusions – generally left-sided
 Cullen’s sign – bluish peri-umbilical discoloration
 Grey Turner’s sign – bluish discoloration of the flanks
Physical examination
 distressed and anxious patient.
 Low-grade fever,
 tachycardia, and
 hypotension .
 Shock is not unusual and may result from
 (1) hypovolemia secondary to exudation of blood and
plasma proteins into the retroperitoneal space and a "
retroperitoneal burn" due to activated proteolytic enzymes;
 (2) increased formation and release of kinin peptides,
which cause vasodilation and increased vascular
permeability; and
 (3) systemic effects of proteolytic and lipolytic enzymes
released into the circulation
Acute Pancreatitis
Differential Diagnosis
 Choledocholithiasis
 Perforated ulcer
 Mesenteric ischemia
 Intestinal obstruction
 Ectopic pregnancy
Diagnosis – Initial work-up
 Med intake
 Family History
 Alcohol intake
 Viral exposures
 Lipase
 LFTs
 GB US
Diagnosis – Amylase
 Elevates within HOURS and can remain elevated for
4-5 days
 High specificity when using levels >3x normal
 Many false positives (see next slide)
 Most specific = pancreatic isoamylase (fractionated
amylase)
Diagnosis –
 Pancreatic Source
Amylase Elevation
 Unknown Source
 Biliary obstruction  Renal failure
 Bowel obstruction  Head trauma
 Perforated ulcer  Burns
 Appendicitis  Postoperative
 Mesenteric ischemia
 Peritonitis
 Salivary
 Parotitis
 DKA
 Anorexia
 Fallopian tube
 Malignancies
Causes of Increased
Pancreatic Enzymes
Amylase Lipase
Pancreatitis ↑ ↑
Parotitis ↑ Normal
Biliary stone ↑ ↑
Intestinal injury ↑ ↑
Tubo-ovarian
disease ↑ Normal

Renal failure ↑ ↑
Macroamylasemia ↑ Normal
Diagnosis – Lipase
 The preferred test for diagnosis
 Begins to increase 4-8H after onset of symptoms
and peaks at 24H
 Remains elevated for days
 Sensitivity 86-100% and Specificity 60-99%
 >3X normal S&S ~100%
Diagnosis – Imaging
 CT
 Excellent pancreas imaging
 Recommended in all patients with persisting organ
failure, sepsis or deterioration in clinical status (6-10
days after admission)
 Search for necrosis – will be present at least 4 days
after onset of symptoms; if ordered too early it will
underestimate severity
 Follow-up months after presentation as clinically
warranted for CT severity index of >3
Diagnosis - Imaging
 ERCP / EUS
 Diagnostic and Therapeutic
 Can see and treat:
 Ductal dilatation
 Strictures
 Filling defects / GS
 Masses / Biopsy
Diagnosis – Imaging
 ERCP indications (should be done in the first 72hr)
 GS etiology with severe pancreatitis – needs sphincterotomy
 Cholangitis
 Jaundice
 Dilated CBD
 If no GS found sphincterotomy is indicated anyway
 Poor surgical candidate for laparoscopic cholecystectomy
 Clinical course not improving sufficiently to allow timely laparoscopic
cholecystectomy and intraoperative cholangiogram
 Pregnant patient
 Uncertainty regarding biliary etiology of pancreatitis
Acute Pancreatitis
Prognosis
Severity Scoring Systems
 Ranson and Glasgow Criteria (1974)
 based on clinical & laboratory parameters
 scored in first 24-48 hours of admission
 poor positive predictors (better negative predictors)
 APACHE Scoring System
 can yield a score in first 24 hours
 APACHE II suffers from poor positive predictive value
 APACHE III is better at mortality prediction at > 24 hours
 Computed Tomography Severity Index
 much better diagnostic and predictive tool
 optimally useful at 48-96 hours after symptom onset
Ranson Criteria
Alcoholic Pancreatitis

AT ADMISSION WITHIN 48 HOURS

1. Age > 55 years 1. HCT drop > 10
2. WBC > 16,000 2. BUN > 5
3. Glucose > 200 3. Arterial PO2 < 60 mm Hg
4. LDH > 350 IU/L 4. Base deficit > 4 mEq/L
5. AST > 250 IU/L 5. Serum Ca < 8
6. Fluid sequestration > 6L

Number <2 3-4 5-6 7-8

Mortality 1% 16% 40% 100%
Glasgow Criteria
Non-alcoholic Pancreatitis
1. WBC > 15,000
2. Glucose > 180
3. BUN > 16
4. Arterial PO2 < 60 mm Hg
5. Ca < 8
6. Albumin < 3.2
7. LDH > 600 U/L
8. AST or ALT > 200 U/L
 CT Severity Index
1 fluid 2 or more
appearance normal enlarged inflamed
collection collections

grade A B C D E

score 0 1 2 3 4

necrosis none < 33% 33-50% > 50%

score 0 2 4 6

score morbidity mortality

1-2 4% 0%
7-10 92% 17%

Balthazar et al. Radiology 1990.

Severe Acute
Scoring systems

Pancreatitis
  3 Ranson criteria
  8 APACHE II points
  5 CT points
 Organ failure
 shock (SBP < 90 mmHg)
 pulmonary edema / ARDS (PaO2
<
60
mm
H
g
)
 renal failure (Cr > 2.0 mg/dl)
 Local complications
 fluid collections  pseudocysts
 necrosis (mortality 15% if sterile, 30-35% if infected)
 abscess
Management
 Mainly supportive
 Hydration, pain relief, and pancreatic rest
 NPO – to decrease pancreatic secretion
 Remember stress ulcer prophylaxis always
 Look for complications
 Management - Feedings
 Enteral nutrition is preferred
 There is a push for nasojejunal feeds however
nasogastric feeds have been shown to be effective in
80% of cases¶
 NGTs should be used with caution in patients with
AMS however
 More risk with TPN / IL but if cannot feed enterally >5
days may be needed

¶ Eatock FC. Nasogastric feeding in severe acute pancreatitis. Radiology 1994: 193,
297-306.
Management – Necrosis
 All severe pancreatitis should be managed in the ICU

 Necrosis associated Infection generally requires

debridement (surgical or IR) best outcomes are
reports associated with >30 after admission
Complications – Local
 Necrosis
 Sterile
 Infected - abscess
 Pseudocyst
 Ascites
 Intraperitoneal hemorrhage
 Thrombosis
 Bowel infarction
 Obstructive jaundice
Complications
 Pulmonary
– Systemic
 Gastrointestinal
 Pleural effusions  PUD
 Atelectasis  Erosive gastritis
 Mediastinal abscess  Blood vessel erosion
 ARDS  Portal vein thrombosis
 Cardiovascular  Renal
 Hypotension  Oliguria
 Sudden death  Azotemia
 Pericardial effusion  Renal artery/vein throbosis
 Hematologic  ATN
 DIC
Complications – Long Term
 Chronic Pancreatitis
 Abdominal Pain
 Steatorrhea
 Exocrine insufficiency (pancreas has a 90% reserve for
the secretion of digestive enzymes)
 DM, i.e.Endocrine Insufficiency
 Pseudocyst