1) Acute pancreatitis is defined as an acute inflammatory process of the pancreas with variable involvement of other tissues. It is diagnosed when a patient presents with abdominal pain consistent with the disease as well as serum amylase or lipase levels over three times the upper limit of normal. 2) Common causes of acute pancreatitis include gallstones, alcohol use, hypertriglyceridemia, endoscopic retrograde cholangiopancreatography (ERCP), trauma, postoperative complications, and certain drugs. 3) Management involves adequate hydration, analgesia, monitoring for organ failure, cautious administration of fluids and insulin, and consideration of endoscopic procedures or surgery in severe cases with complications like necrosis

1. ACUTE PANCREATITIS
DR.RAHUL GARG
M.D.MEDICINE(Std.)
S.N.M.C.,AGRA
DR. RAHUL GARG

2. DEFINITIONS
Atlanta Symposium definition of acute pancreatitis : An acute
inflammatory process of the pancreas with variable
involvement of other regional tissues or remote organ systems.
Acute pancreatitis is best defined clinically by a patient
presenting with two of the following criteria:
(1)Symptoms, such as epigastric pain, consistent with the
disease.
(2)A serum amylase or lipase greater than three times the
upper limit of normal.
(3) Radiologic imaging consistent with the diagnosis, usually
using CT or MRI.

3. CAUSES OF ACUTE PANCREATITS
COMMON CAUSE
•
•
•
•
•
•
•
Gall Stones ( including microlithiasis ) (40%)
Alcohol ( acute and chronic alcoholism (30%)
Hypertriglyceridmia ( mainly over >1000 mg/ dl )
ERCP ( Specially after billary manometry)
Trauma (specially after blunt trauma )
Post – operative ( abdominal and non abdominal)
Drugs (azathioprin, 6 – mp , sulfonamides, estrogen,
anti – HIV protease inhibitor , Vaproic acid
,thiazide,erythromycin,acetaminophen)
• Annular pancreas,Choledochocele

4. CLINICAL FEATURE
 HISTORY
 Abdominal pain :
 Severity
 Character
 Site
 Radiation
 Agg /releaving factor
mild tolerable discomfort
Severe constant incapacitating distress
steady and boring in character
located in epigastrium and
Periumblical region
radiation to back and chest,
lower abdomen flanks.
pain increases when pt in supine
and relieved by sitting with trunk
flexed and knee drawn up
 Nausea/ vomiting / abdominal distention

5. PHYSICAL EXAMINATION




Hypo or hyperthermia(<98.6or>100.4f)
Tachycardia (>90beats/min)
Hypotension and shock (BP<90mmhg)
Jaundice – infrequentely occure due to edema of the head of
pancrease and compression of intrahepatic portion of cbd.
 Erythematous skin nodules – due to subcutaneous fact necrosis
 In 10 – 20% patients pulmonary findings
Basilar rales
atelcectesis
left sided pleural effusion
 Abdominal tenderness and rigidity
 Bowel sound diminished and absent
 Palpable pancreatic pseudocyst in upper abdomen
 In severe necrotizing pancreatitis –
 Cullens sing : faint blue discoloration around umlicus
 Turner,s sing: blue red purpel or grey brown discoloration of the flanks
Sleisenger and Fordtran's Gastrointestinal and Liver Disease ninth edition

6. LABORATORY DIAGNOSIS
PANCREATIC ENZYMES
 Diagnosis of acute pancreatitis relies on at least a three-fold
elevation of amylase or lipase in the blood.
• Serum Amylase(30-180 IU/L)
• It rises within 6 to 12 hours of onset (half-life, 10 hours).
• The serum amylase is usually increased on the first day of
symptoms, and it remains elevated for three to five days in
uncomplicated attacks.
•
Sensitivity is greater than 85%, the serum amylase may be normal
or minimally elevated in fatal pancreatitis, during a mild attack or an
attack superimposed on chronic pancreatitis , or during recovery
from acute pancreatitis also in hypertriglyceridemia-associated
pancreatitis.
• Hyperamylasemia is not specific for pancreatitis because it occurs in
many conditions other than acute pancreatitis.

7. • Serum Lipase(0-160 IU/L)
• The sensitivity of serum lipase is similar to that of serum
amylase and is between 85% and 100%.
• Lipase may have greater specificity for pancreatitis than
amylase.
• Serum lipase always is elevated on the first day of illness and
remains elevated longer than does the serum amylase.
• Some believe that serum lipase is preferable to that of
serum amylase , whereas others find no clear advantage .

8. • Secretin-pancreozymin (CCK) test
• Secretin leads to increased output of pancreatic juice and
HCO3; CCK leads to increased output of pancreatic enzymes.
• Sensitive enough to detect occult disease; involves duodenal
intubation and fluoroscopy ,only role in acute on chronic
pancreatitis.
Other Pancreatic Enzymes
• They include PLA2, trypsin/typsinogen, carboxylester lipase,
carboxypeptidase A, colipase, elastase, and ribonuclease.
• None, alone or in combination, are better than serum
amylase or lipase

9. Other blood test• White blood cell count -Increased
• Haematocrit->44 show poor prognosis, moniter daily.
• Serum Creatinine and serum electrolytes
• AST,ALT,alkaline phosphatase, and bilirubin also may
increase .
• MCV- Alcoholic patients tend to have a higher MCV .
• Serum triglyceride levels- increase in acute pancreatitis,
but also with alcohol use, uncontrolled diabetes mellitus,
or defective triglyceride metabolism

10. RADIAOLIGICAL –
Chest X- ray / X – ray abdomen errect
 See for pulmonary complication pleural effusion
 Rule out other diagnosis,specially – a perforation
USG- Specially for diagnosis of gall stone
Helical CT Scan (Contrast Enhanced ,After 48 -72hrs of onset)
 Helpful to know severity and prognosis
 Allows estimation of presence and extend of pancreatic
necrosis.
 Conferm the cinical impression of acute pancreatitis in face of
normal s. Amylase.
 Severe allergy and renal impairment(s.crt>2mg/dl) are
contraindication for contrast use.
 EUS and/or MRCP are better than CT for choledocolithiasis.

11. Markers of Severity within 24 Hours
• BMI>30
• SIRS [temperature >38° or <36°C (>100.4° or 96.8°F), Pulse
>90, Tachypnea >24, WBC >12,000]
• Hemoconcentration (Hct >44%)
• BISAP
• (B) Blood urea nitrogen (BUN) >22 mg%
• (I) Impaired mental status
• (S) SIRS: 2/4 present
• (A) Age >60 years
• (P) Pleural effusion
• Organ Failure

12. Atlanta Criteria for Severe Acute Pancreatitis
Organ Failure
a.
Shock: systolic blood pressure <90 mm Hg
b.
Pulmonary insufficiency: Pao2 ≤60 mm Hg
c.
Renal failure: serum creatinine >2 mg/dL
d.
Gastrointestinal bleeding: >500 mL/24 hr
Local Complications
a.
Necrosis
b.
Abscess
c.
Pseudocyst

13. --
Ranson's Prognostic Criteria
NON-GALLSTONE PANCREATITIS
At Admission
Age >55 yr
White blood cells >16,000/mm3
Blood glucose >200 mg/dL
Serum lactate dehydrogenase
>350 IU/L
Serum aspartate aminotransferase
>250 IU/L
During Initial 48 hr
Hematocrit decrease of >10 %
Blood urea nitrogen increase of
>5 mg/dL
Serum calcium <8 mg/dL
Arterial po2 <60 mm Hg
Serum base deficit >4 mEq/L
Fluid sequestration >6 L
GALLSTONE PANCREATITIS
Age >70 yr
>18,000/mm3
>220 mg/dL
>400 IU/L
>250 IU/L
>10%
>2 mg/dL
<8 mg/dL
NA
>5 mEq/L
>4 L

14. SEVERITY INDEX IN ACUTE PANCREATITIS
Grade of Acute pancreatitis
Points
A
NORMAL PANCREAS
0
B
PANCREATIC ENLARGMENT ALONE FOCAL OR DIFFUSE WITH
CONTOUR IRREGULARITIES AND INHOMOGENOUS ATTENUATION
1
C
B+PERIPANCREATIC INFLAMMATION
2
D
C+ONE PERIPANCREATIC FLUID COLLECTION
3
E
D+TWO OR MORE PERIPANCREATIC OR RETROPERITONEAL FLUID
COLLECTION OR GAS COLLECTION
4
DEGREE OF PANCREATIC NECROSIS
1
NO – NECROSIS
0
2
NECROSIS OF <33% PANCREASE
2
3
NECROSIS OF 33%-50% OF PANCREASE
4
4
NECROSIS OF > 50% OF PANCREASE
6
CT SEVERITY INDEX ( CT SI )BALTHAZAR SCORE+NECROSIS SCORE
CT GRADE + NECROSIS GRADE
(0 - 4) + ( 0 – 6 )  ( 0 – 10 )

15. Contrast-enhanced computed tomography shows diffuse swelling
of the pancreas (P) with peripancreatic inflammatory changes
(arrows). The pancreas was well perfused without evidence of
necrosis. G, gallbladder.

16. Acute pancreatic necrosis. Contrast-enhanced c t demonstrates focal areas of
decreased perfusion in the pancreatic parenchyma (arrows) with surrounding
peripancreatic inflammation. The necrosis was estimated to involve less than 30%
of the pancreas. G, gallbladder

17. MANAGEMENT;
• Patients with acute pancreatitis require adequate intravenous
hydration and adequate analgesia to eliminate or markedly
reduce pain.
• The patient is usually on npo until any nausea and vomiting
have subsided.
• Opiate dosing is monitored carefully and adjusted on a daily
basis according to ongoing needs.
• Nasogastric intubation is not used routinely because it is not
beneficial in mild pancreatitis.
• It is used only to treat gastric or intestinal ileus or intractable
nausea and vomiting.
• Similarly, proton pump inhibitors or H2-receptor blocking
agents are not beneficial and not used.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease ninth edition

18. • The patient should be carefully monitored for any signs of
early organ failure such as hypotension, vital signs and urinary
output.
• Tachypnea should not be assumed to be due to abdominal
pain; monitoring oxygen saturation and, if needed, blood
gases is advised and oxygen supplementation is mandatory if
there is hypoxemia.
• Any patient who exhibits signs of early organ dysfunction
should be immediately transferred to intensive care
monitoring.

19. FLUID RESUSCITATION;
• The goal is to decrease the hematocrit.
• Laboratory and clinical studies with intravenous dextran to
promote hemodilution have suggested efficacy in preventing
severe disease.
• One of the markers of severity of pancreatitis defined by Ranson
and colleagues is intravascular losses (“fluid sequestration”).
• Requirements of a 70-kg person during the first 48 hours, is should
be at least 250 to 300 mL/hour for 48 hours.
• The rate of volume replacement is more important during the first
24 hours, when a rising hematocrit has been shown to correlate
closely with severe disease.

20. • Maintaining adequate intravascular volume in patients with
severe disease may require 5 to 10 L of fluid such as isotonic
saline daily for the first several days (200 to 400 mL/hour).
• In a patient with unclear cardiac output, a Swan-Ganz catheter
can be useful .
Sleisenger and Fordtran's Gastrointestinal and Liver Disease ninth edition

21. RESPIRATORY CARE;
• Hypoxemia (oxygen saturation <90%) requires
supplemental oxygen.
• Current guidelines recommend the initial routine use of
nasal cannula oxygen to all patients with acute pancreatitis.
• ARDS is the most serious respiratory complication of acute
pancreatitis.
• It generally occurs between the second and seventh day of
illness (but can be present on admission) .
• Chest radiography may show multilobar alveolar infiltrates.
• Treatment is endotracheal intubation with positive endexpiratory pressure ventilation, often with low tidal volumes
to protect the lungs from volutrauma.
• No specific treatment will prevent or resolve ARDS.

22. • Cardiac complications of severe acute pancreatitis include
congestive heart failure, myocardial infarction, cardiac
dysrhythmia, and cardiogenic shock.
• If hypotension persists even with appropriate fluid
resuscitation, intravenous dopamine may help maintain the
systemic blood pressure.
• Dopamine does not impair the microcirculation of the
pancreas as do other vasoconstrictors.

23. METABOLIC COMPLICATION;
• Hyperglycemia may present but usually normalizes as the
inflammatory process subsides.
• Blood sugars fluctuate, and insulin should be administered
cautiously.
• Reduced serum ionized calcium may occur and cause
neuromuscular irritability.
• If hypomagnesemia coexists, magnesium replacement should
restore serum calcium to normal.
• Once the serum magnesium is normal, signs or symptoms of
neuromuscular irritability may require administering
intravenous calcium gluconate as long as the serum potassium
is normal and digitalis is not being given.

24. Prophylactic Antibiotics;
• The majority of organisms detected were gram-negative
aerobic or anaerobic species (Escherichia coli, Enterobacter
aerogenes, Pseudomonas aeruginosa, Proteus species,
Klebsiella pneumoniae, Citrobacter freundii, and Bacteroides
species), with occasional gram positives and rare fungi .
• Imipenem, fluoroquinolones (ciprofloxacin, ofloxacin,
pefloxacin), and metronidazole are the drugs that achieved the
highest inhibitory concentrations in pancreatic tissue, whereas
aminoglycosides did not.
• Recently there is no current recommendation of prophylactic
antibiotic.

25. ENDOSCOPY AND NUTRITION
• Endoscopic early removal of a possibly impacted gallstone in
improving the outcome of gallstone pancreatitis remains a
controversial issue.
• Severe acute gallstone pancreatitis with ascending cholangitis
(jaundice and fever) is an indication for urgent ERCP .
•
Studies demonstrate that enteral nutrition is cheaper and
safer and is preferable in patients with severe acute
pancreatitis.
• It is still unclear, however, when nutrition should be initiated
and for how long it needs to be continued.

26.  Clear fluid diet should be given on 3rd - 6th day and
regular diet from 5th - 7th day.
 The decision to reintroduce oral intake is done by the
following criteria




Resolution of abdominal pain
The patient is hungry
Organ dysfunction if recent has improved
In sever pancreatitis in which much longer restriction of
oral feed needed parenteral neutriton must be
maintained by lipid infusion.

27. OTHER DRUGS;
• Gabexate mesylate is pancreatic protease inhibitor in acute
pancreatitis found no effect on the 90-day mortality rate, but a
reduced incidence of complication.
• The antisecretory hormone somatostatin or its synthetic
analog octreotide(1microgm/kg slow iv 6-8 hrly) have failed to
show evidence of efficacy .
• The use of anti-inflammatory cytokines has lexipafant have not
shown clear efficacy.

28. ROLE OF SURGERY;
•
Cholecystectomy should be performed as soon as the
patient has recovered and the acute inflammatory process
has subsided.
• A second potential role for surgery in pancreatitis is to
debride pancreatic necrosis (necrosectomy) .

29. COMPLICATION;LOCAL
• Necrosis
– Sterile / infected
• Pancreatic fluid collection
– Pancreatic abscess
– Pancreatic pseudocyst
– Pancreatic ascitis
• Involvement of contiguous organ by necrotising
pancreatitis
– Massive intraperitioneal haemorrhage
– Thrombosis of blood vessels
• Obstructive jaundice

30. SYSTEMIC
 Pulmonary




Pleural effusion
Atelectasis
Pneumonitis
ARDS
 Cardiovascular
 Hypotension / hypervolemia
 Sudden death
 Pericardial effusion
 Hematological
 DIC
 GI haemorrhage




Peptic ulcer disease
Erosive gastritis
Hemorrhagic pancreatitis erosion in blood vessel
Portal vein thrombosis

31. SYSTEMIC
 Renal
 Oliguria
 Azotemia
 Renal artery / vein thrombosis
 Metabolic




Hyperglycemia
Hypertriglyceridemia
Hypocalcemia
Purtscher’s retinopathy ( due to occulsion of post retinal
artery by aggregated granulocyte)
 CNS
 Psychosis
 Fat emboli
 Fat necrosis
 Subcutaneous tissue - erythematous nodule

32. THANK YOU…