ACUTE PANCREATITIS

1. ACUTE
PANCREATITIS
PRESENTER : Dr. B.INDUMATHI
MODERATOR: Dr. B.G.MANJUNATH
Dr. KAVITHAA. C

2.  Introduction
 Risk factors and Aetiology
 Pathophysiology
 Clinical manifestations
 Diagnosis
 Investigations
 Assessment of severity of disease
 Treatment
 Complications

3. INTRODUCTION
 Pancreatitis is inflammation of the pancreatic parenchyma.
 For clinical purposes ,it is useful to divide pancreatitis into acute , which presents as
an emergency ,and chronic which is prolonged and frequently lifelong disorder
resulting from the development of fibrosis within the pancreas.
CLASSIFICATION
MARSEILLES’ CLASSIFICATION
1.Acute pancreatitis .
2.Acute relapsing pancreatitis.
3.Chronic relapsing pancreatitis
4.Chronic pancreatitis.

4. ACUTE PANCREATITIS
 It is an acute condition presenting with abdominal pain, a threshold or
greater rise in the serum levels of the pancreatic enzymes amylase or
lipase and /or characteristic findings of pancreatic inflammation on CECT.
EARLY PHASE LATE PHASE
LASTS FOR 2 WEEKS AFTER 2 -3 WEEKS
Oedemtous pancreatitis or sterile necrosis Pancreatic abscess or infective necrosis
Death occurs by Multiorgan failure Sepsis

5. REVISED ATLANTA CLASSIFICATION
DEFINITION DESCRIPTION
ACUTE FLUID COLLECTION
<4 WEEKS AFTER ONSET
EDEMTOUS PANCREATITIS
 Homogenous fluid density
 Confined by normal peripancreatic fascial planes .
 No definable wall encapsulating the collection.
 Adjacent to pancreas
PSEUDOCYST
>4 WEEKS AFTER ONSET
EDEMATOUS PANCREATITIS
 Well circumscribed, usually round /oval
 Homogenous fluid density.
 Well defined wall and completely encapsulated.
 Adjacent to pancreas.
ACUTE NECROTIC COLLECTION
<4 WEEKS AFTER ONSET
NECROTIZING PANCREATITIS
 Heterogenous and nonliquified density.
 No definable wall encapsulating the collection.
 Location : intrapancreatic and /or extrapancreatic.
WALLED -OFF NECROSIS
> 4 WEEKS AFTER ONSET
NECROTIZING PANCREATITIS
 Heterogenous and non liquid density.
 Well defined wall and completely encapsulated .
 Location : intrapancreatic and/ or extrapancreatic.

6. AETIOLOGY
MAJOR CAUSES :
 Biliary tract diseases ( stones ) (50%)-Most common cause
 Alcoholism (25%)
OTHER CAUSES:
 Trauma
 After biliary , gastric , splenic surgery , ERCP .
 Hyperparathyroidism
 Hypercalcemia , hyperlipidemia
 Diabetes

7. AETIOLOGY
 Porphyria
 Drugs ( INH , diuretics , septran , azathioprine , estrogens ,
tetracyclines , valproic acid)-2%
 Autoimmune diseases
 Biliary ascariasis , Clonorchis sinensis
 Mycoplasma pneumoniae
 Infectious mononucleosis
 Pancreatic divisum

8.  Most common cause of acute pancreatitis
 Incidence of Acute pancreatitis in patients with
symptomatic gall stone disease is 3-8%.
 It is seen more frequently in women between 50-70
years of age .
BILIARY OR GALL STONE PANCREATITIS

10. 2 theories
obstructive
Pancreatic duct obstruction
Increased intraductal pressure
Continous secretion of pancreatic enzymes
Pancreaticinjury
reflux
Stones becomes impacted in the ampulla of vater
bile salts reflux into the pancreas
Increased ca in cytoplasm
Direct acinar cell necrosis

11. ALCOHOL INDUCED INJURY
 2nd most common cause
■ More prevalent in young men (30-45
years)
■ Heavy alcohol abuse ( >100 g/day for
atleast 5 years).
■ Alcohol decreases pancreatic
perfusion, induces sphincter of oddi
spasm & obstructs pancreatic ducts
through precipitation of proteins inside
the duct.
Alcohol
triggers proinflammatory pathways
such as nuclear factor kB
Increased TNF ALFA
& IL1
Increased expression
&activity of caspases
Mediate apoptosis

12. ANATOMIC OBSTRUCTION :
 Pancreatic tumors
 parasites ( Ascaris lumbricoides)
 congenital defects (annular pancreas , pancreatic divisum ).
 Abnormal flow of pancreatic juice into the duodenum can result in
pancreatic injury .

14.  ERCP Induced Pancreatitis (5%)
• Acute pancreatitis occurs more frequently in patients who have
undergone therapeutic procedures compared with diagnostic
procedures .
• It is also more common in patients who have had multiple attempts of
cannulation , sphincter of oddi dysfunction and abnormal
visualization of the secondary pancreatic ducts after injection of
contrast material.

15. METABOLIC FACTORS :
■ HYPERTRIGLYCERIDEMIA :
■ Triglyceride levels > 1000 mg/dl (suspect)
> 2000mg/dl ( confirm)
■ Direct pancreatic injury can be induced by triglyceride metabolites.
■ It is more common in patients with type I,II &V hyperlipidemia .
■ HYPERCALCEMIA :
■ Induces pancreatic injury through the activation of trypsinogen to
trypsin , intraductal precipitation of calcium , leading to ductal
obstruction and subsequent attacks of pancreatitis.
■ Approximately 1.5%- 13% of patients with primary hyperthyroidsm
develop acute pancreatitis.

16. HEREDITARY PANCREATITIS
■ It is characterized by recurrent attacks of severe acute pancreatitis often
beginning in childhood and ultimately leading to chronic pancreatitis.
■ GAIN OF FUNCTION MUTATIONS:
 PRSS1 gene mutations make trypsin resistant to self-inactivation.
■ LOSS OF FUNCTION MUTATIONS:
 SPINK 1gene mutation ( Responsible for coding of trypsin inhibitor).
 Mutations in CFTR gene decreases bicarbonate secretion by pancreatic ductal
cells there by promoting protein plugging , duct obstruction , and the
development of pancreatitis

17. MISCELLANEOUS
 Blunt and penetrating abdominal trauma can be associated with
Acute pancreatitis in 0.2% and 1% of cases respectively.
 Prolonged intra-operative hypotension , excessive pancreatic
manipulation during abdominal surgery can also result in Acute
pancreatitis .
 Pancreatic ischemia in association with acute pancreatic
inflammation can develop after splenic artery embolization .

18. PATHOPHYSIOLOGY

19. PATHOPHYSIOLOGY
Acinar cell death
Apoptosis or necrosis
Induces leak of cathepsin B into the cytosol
PREMATURE ACTIVATION OF TRYPSIN
CATHEPSIN B
TRYPSINOGEN
LYSOSOMES
ZYMOGEN
Zymogen and lysosomes co-localize inside the acinar cells
PANCREATIC INJURY

21. TRYPSIN
Proelastase to
elastase
Causes capillary
rupture
Sequestrated fluid , saponified fat
, blood toxins all together form a
chicken broth fluid
Prolipase to
lipase
Metabolizes TG’s to glycerol+fattyacids .
Fattyacids combine with ca forming
saponified fat

22. Intraacinar pancreatic
enzyme activation
Acinar cell releases pro-inflammatory cytokines
(TNF-ALFA,IL-1,2,6) and anti-inflammatory
antagonists( IL-10,1.),PG’s , lesithinase,PAF,Free
radicles
LOCAL SYSTEMIC
Active neutrophils mediate Acute lung
injury , and induce ARDS
Autodigestion of
normal pancreatic
parenchyma
Increases the
permeability
and damage
the
microcirculati
on leads to
necrosis
SIRS
MODS
DEATH

23.  Toxins released may lead to acute tubular necrosis and so acutr renal
failure.
 Lecithinase reduces the surfactant in the alveoli of lung , and
infection leads to pulmonary insufficiency , ARDS , and respiratory
failure.
 Diffuse oozing in pancreatic bed occurs which utilizes platelets and
causes DIC.

24. CLINICAL MANIFESTATIONS
 PAIN :
 Acute onsent
 Epigastric or periumbilical
 Radiates to back .
 Peak intensity in 30 min .
 Lasts for several hours.
 Relieved by leaning forward .(MUHAMMEDAN PRAYER SIGN)
 Nausea and vomiting .
 Dehydration , poor skin turgor ,dry mucous membrane.
 tachycardia , hypotension , oliguria.
 Severely dehydrated and older patients may also develop mental status changes.
 Hemetemesis/Malena due to duodenal necrosis , gastric erosions ,decreased
coaguability /DIC.
 Paralytic ileus is common .

26.  PHYSICAL EXAMINATION :
 Normal or reveals only mild epigastric tenderness ( Mild pancreatitis).
 Significant abdominal distention , associated with generalized rebound
tenderness and abdominal rigidity ( Severe pancreatitis ).
 GREY TURNER SIGN : haemorrhagic spots and echymosis in the flanks
 CULLENS SIGN : peri-umbilical echymosis
 FOX SIGN : echymosis below the inguinal ligament
 Patients with concomitant choledocholithiasis or significant edema in the
head of the pancreas that compresses the intrapancreatic portion of the
CBD can present with JAUNDICE.
 Dull note on percussion .

28. FOX SIGN

29. DIAGNOSIS
 The cornerstone of the diagnosis of Acute pancreatitis is the clinical
findings plus an elevation of pancreatic enzyme levels in the plasma.
 A threefold or higher elevation of amylase and lipase levels confirms the
diagnosis .
 Serum lipase levels is a most sensitive and specific marker for diagnosis of
Acute pancreatitis.
 Serum amylase levels can be elevated in a number of conditions such as
peptic ulcer diseases , mesenteric ischemia , salpingitis , and
macroamylasemia ,salivary gland tumors.
 The elevation of alanine aminotransferase levels and high pancreatic
enzyme levels has a positive predictive value of 95% in the diagnosis of
acute biliary pancreatitis .

30.  Patients with Acute pancreatitis are typically hyperglycemic .
 Leukocytosis , abnormal elevation of liver enzymes.
 Amylase creatinine clearance ratio is increased :
 Urine amylase/serum amylase × serum creatinine /urine creatinine ×100
 Normal value is 1-4 %.
 >6 signifies acute pancreatitis.
 Serum lactescence : (related to triglyceride metabolism )
 Most specific in hereditary hyperlipidemia or alcohol pancreatitis.
 Serum trypsin is the most accurate indicator but is not commonly used.
 Arterial P02 and PCO2 level to assess the pulmonary insufficiency
(ARDS).

31.  Peritoneal tap fluid shows high amylase ,lipase and protein level .
 Serum calcium levels – decreased .
 Total count , hematocrit ,platelet count , coagulation profile .
 Blood urea and serum creatinine.
 CRP
 Trypsinogen activation polypeptide (TAP) assay in serum and urine
reveals the severity of the acute pancreatitis.

32. IMAGING STUDIES
■ Plain X ray shows :
 Sentinel loop of dilated proximal small bowel.
 Distention of transverse colon with collapse of descending colon
(COLON CUT OFF SIGN ).
 Air fluid level due to ileus.
 Renal halo sign.
 Obliteration of psoas shadow .
 Localized ground glass appearance.

33. SENTINEL LOOP SIGN

34. COLON CUT OFF SIGN

35. IMAGING STUDIES
IMAGING USE IN ACUTE PANCREATITIS DRAWBACKS
1.USG High sensitivity (95%) in diagnosing gall
stones .
Its use is limited by intra-abdominal fat and
increased intestinal gas as a result of ileus
2.CECT Its evaluates the viability of pancreatic
parenchyma ,amount of peripancreatic
inflammation & presence of intra-abdominal
free air or fluid collections .
In renal failure patients it is contraindicated
3.CT It identifies any fluid collections or extra-
luminal air.
It cannot evaluate for pancreatic necrosis vascular
complications.
4.MRI To evaluate the extent of necrosis
,inflammation and presence of free fluid .
Differenciates between fluid and solid debris.
Its costs and availability and the fact that patients
requiring imaging are critically ill and need to be
intensive care units limits its applicability in acute
phase .

36. IMAGING USES IN ACUTE PANCREATITIS DRAWBACKS
5.EUS Sensitive in identifying choledocholithiasis. It allows
examination of the biliary tree & pancreas with no
risk of worsening of the pancreatitis.
6.ERCP 1. For suspected gall stone pancreatitis.
2. Can be used selectively as a therapeutic measure
It may actually
worsen the
symptoms because
of manipulation.
7.MRCP 1. In recurrent or unexplained pancreatitis because it
allows complete visualization of the biliary tree
and pancreatic duct injury .

39. ASSESSMENT OF SEVERITY OF DISEASE
SCORING
SYSTEMS
PARAMETERS MERITS DRAWBACKS
1.RANSON 11 Parameters obtained at time of
admission or 48hours later.
It is mainly used to rule out severe
pancreatitis or to predict the
severity of the disease.
It does not predict the severity of
disease at the time of admission
because 6 parameters are assessed
only after 48hrs.
2.APACHE II Age , previous health status , and
12 routine physiological
measurements.
It can be used on admission and
repeated at any time
It is complex, not specific for AP
and based on patients age which
easily upgrades the AP severity
score.

40. Ranson Prognostic Criteria
Non – Gallstone Pancreatitis Gallstone pancreatitis
Ranson score ≥ 3 defines severe pancreatitis.
AT PRESENTATION AFTER 48 HOURS OF
ADMISSION
• Age > 55 years • Hematocrit decrease
>10%
• Blood glucose levels
>200 mg /dl.
• Serum calcium level <
8mg/dl
• White blood cell count >
16,000 cells/mm3
• Base deficit > 4 mEq/L
• Lactate dehydrogenase
level >350IU/litre
• Blood urea nitrogen
increases >5mg/dl
• Aspartate
aminotransferase level
>250 IU/litre
• Fluid requirement > 6
litres
• PaO2 <60 mm hg
AT PRESENTION AFTER 48 HOURS OF
ADMISSION
Age >70 years Hematocrit decreases > 10%
Blood glucose levels >220
mg/dl
Serum calcium level <8
mg/dl
White blood cell count >
18,000 cells /mm3
Base deficit >5 mEq/L
Lactate dehydrogenase
>400IU/litre
Blood urea nitrogen >2mg/dl
Aspartate aminotransferase
level >250 IU/litre
Fluid requirement >4 litres
PaO2 ; Not available

41. ■ 2012 REVISED ATLANTA CLASSIFICATION
COMPLICATIONS MILD MODERATE SEVERE
Local complications NO YES YES
SYSTEMIC COMPLICATIONS
Transient organ failure NO YES YES
Persistent organ failure NO NO YES
Exacerbation of preexisting comorbidity NO YES YES

42. Glasgow – Imrie prognostic criteria
ON ADMISSION WITHIN 48 HOURS
Age >55 years Serum calcium < 2 mmol/L
TC >15,000/cu mm Serum albumin < 3.2 gm/dl
PaO2 <60 mm hg LDH > 600 U/L
Blood urea > 16 mmol/L AST/ALT >600 U/L
Blood Sugar > 200 mg% (no h/o diabetes)

44. BALTHAZAR CT SEVERITY INDEX
FEATURE POINTS
PANCREATIC INFLAMMATION
Normal pancreas 0
Focal or diffuse pancreatic enlargement 1
Intrinsic pancreatic alterations with peripancreatic fat and
inflammatory changes
2
Single fluid collection or phlegmon 3
Two or more fluid collections or gas , in or adjacent to the
pancreas
4
PANCREATIC NECROSIS
None 0
≤30% 2
30%-50% 4
>50 6
CTSI MORTAL
ITY
MORBID
ITY
0-3 3% 8%
4-6 6% 35%
7-10 17% 92%

46.  APACHE-II (Acute Physiology and Chronic Health Evaluation ).
 Sum of the 12 individual variable points + age points + chronic
health points.
 Physiologic variables :
i. Temperature vii. Serum Na(mMol/L)
ii. Mean arterial pressure viii. Serum K (mMol/L)
iii. Heart rate ix. Serum Creatinine (mg/dl)
iv. Respiratory rate x. Hct (%)
v. Oxygenation xi. WBC
vi. Arterial Ph xii. Glasgow coma score

47. SCORING SYSTEMS IN ACUTE PANCREATITIS
CUTOFF FOR PREDICTED SEVERE ACUTE
PANCREATITIS
APACHE II ≥ 8 In first 24 hours
BISAP ≥ 3 In first 24 hours
Modified Glasgow (or Imrie) ≥ 3 In first 48 hours
Ranson ≥ 3 In first 48 hours
Urea at admission >60 mmol/L
C-reactive protein >150U/L within 48 - 72 hours

48. Differential diagnosis
 Perforated duodenal ulcer.
 Cholecystitis .
 Mesenteric ischemia.
 Ruptured aortic aneurysm.
 Ectopic pregnancy .
 Salpingitis .
 Intestinal obstruction.
 Diabetic ketoacidosis.

49. TREATMENT
 EARLY SUPPORTIVE MEASURES :
 1.Pain management :
 In the majority of Acute pancreatitis patients , intense abdominal
pain is the presenting symptom in the emergency department.
 A specific pain treatment regimen for acute pancreatitis is not
available .
 Analgesia especially narcotics (pethidine ).

50. 2. FLUID THERAPY :
 The cornerstone of the treatment of Acute pancreatitis is aggressive fluid
resuscitation with isotonic crystalloid solution.
 Main aim is to correct or preferably prevent intravascular hypovolemia
and maintain microcirculation of the pancreas.
 Uncontrolled aggressive fluid therapy may induce morbidity and even
mortality , so careful monitoring of the response to fluid resuscitation is
necessary ( HR , MAP , and urine output 0.5 to 1 mL/kg/h).
 The recent update of the IAP/APA treatment guideline for AP
recommends the use of RL with an infusion rate of 5 to 10 mL/kg/L
until resuscitation goals are reached , monitored by vital parameters and
urine production

51.  NUTRITION THERAPY :
 Oral feeding may be impossible because of persistent ileus , pain , or
intubation .
 In addition , 20% of patients with severe AP develop recurrent pain
shortly after the oral route has been restarted.
 The main options are enteral feeding and total parenteral nutrition.
 Demerits of TPN : mucosal atrophy , decreased intestinal blood flow
, increased risk of bacterial overgrowth in the small bowel , antegrade
colonization with colonic bacteria , and increased bacterial
translocation ,central line infections and metabolic complications
(hyperglycemia , electrolyte imbalance )
 Whenever possible, enteral nutrition should be used rather than TPN .

52.  ANTIBIOTICS:
 3rd generation cephalosporins , imipenem , meropenem , cefuroxamine are
used even though it has no role but it is commonly used to reduce the
anticipated sepsis.
 INDICATIONS :
 In severe infected necrosis with proved culture.
 Prophylactic antibiotic therapy , in severe pancreatitis .
 In biliary pancreatitis with biliary stones and cholangitis.
 Pancreatic abscess formation .
 Clinically disease is rapidly progressing with deterioration.
*No role in early pancreatitis.

53.  Calcium gluconate 10% 10ml IV 8th hourly is given as patient will be
hypocalcaemic.
 IV Ranitidine 50mg 6th hourly or IV Omeprazole 40mg BD or IV
Pantoprazole 80 mg BD to prevent stress ulcers and erosive bleeding.
 Somatostatin /octreotide is often used to reduce pancreatic secretion
 Steroid injection in initial phase of shock is beneficial . It is also used
in respiratory distress and ARDS.

54. SPECIAL CONSIDERATIONS
 ERCP WITH OR WITHOUT SPHINCTOROTOMY:
 INDICATIONS :
 Patients with severe acute biliary pancreatitis with cholangitis .
 Persistent bile duct obstruction demonstrated by other imaging
modalities such as EUS .
 Older patients with poor performance status or severe comorbidities
that preclude surgery.
 Recurrent biliary pancreatitis

55. LAPROSCOPIC CHOLECYSTECTOMY :
 INDICATIONS :
 Mild acute biliary pancreatitis.(exception :old people &those with poor
performance status).
 Early laproscopic cholecystectomy defined as laproscopic
cholecystectomy during the initial admission to the hospital , is a safe
procedure that decrease the recurrence of the disease .
 Current recommendations suggest conservative management for atleast 6
weeks before laproscopic cholecystectomy is done .

56. SURGERY
 Indications for surgical intervention ( 10%)
 1. If condition of patient deteriorates in spite of good conservative
treatment.
 If there is formation of pancreatic abscess , or infected necrosis.
 In severe necrotizing pancreatitis .

57. Algorithm for the evaluation and management of acute pancreatitis
1. Diagnosis
 History of abdominal pain consistent with acute pancreatitis
 >3x elevation of pancreatic enzymes
 CT scan if required to confirm diagnosis
2. Initial assessment/management (first 4 hrs)
 Analgesia
 Fluid resuscitation
 Predict severity of pancreatitis
i. Ranson’s criteria
ii. HAPS score
 Assess systemic response
i. SIRS score
ii. SOFA (organ failure)

58. 3. Reassessment/management (4 to 6 hrs)
 Assess response to fluid resuscitation
 Determine etiology
a. Ultrasound for gallstones/sludge
b. History of alcohol consumption
c. Laboratory evaluation of other causes
 MRCP and/or Urgent ERCP if concomitant cholangitis is present
-- not for cholestasis or predicted severe disease per se
 Transfer to ICU or specialist center as needed
a. Deterioration or failure to respond to initial management
b. Intensive support for persistent organ failure
 Commence enteral nutrition
 No prophylactic antibiotics or probiotics

59. 4. Conservative management and monitoring (at least daily)
 Clinical evaluation
 Daily C-reactive protein
 Classify severity (mild, moderate, severe, critical)
 Detect intolerance of NG EN
i. Advance tube for NJ feeding if needed
ii. Consider supplemental parenteral nutrition by day 4
5. Indications for “pancreatic protocol CT scan” (rarely in first week)
 For significant clinical deterioration and elevated CRP
 For suspicion of local pancreatic complications
 For suspected bowel ischemia
 For acute bleeding (CTa) (if stable enough and consider embolization)
 For abdominal compartment syndrome

60. COMPLICATIONS
■ LOCAL
 Acute fluid collection .
 Sterile pancreatic necrosis.
 Infected pancreatic necrosis.
 Pancreatic abscess .
 Pseudocyst.
 Pancreatic ascites.
 Portal/splenic vein thrombosis.
 Pseudoaneurysm.

61. ■ SYSTEMIC COMPLICATIONS
 PULMONARY:
i. ARDS.
ii. Pleural effusion.
 CARDIOVASCULAR:
i. Shock
ii. Arrhythmias
 HEMATOLOGIC:
i. Hemoconcentration
ii. Disseminated intravascular coagulation.
 GI HEMORRHAGE:
i. Peptic ulcer.
ii. Erosive gastritis.

62.  RENAL :
i. Oliguria
ii. Azotemia
iii. Renal artery/vein thrombosis.
 METABOLIC:
i. Hyperglycemia
ii. Hypocalcemia
iii. Hypertriglyceridemia.
 NEUROLOGICAL:
i. Visual disturbances.
ii. Confusion ,irritability.
iii. Encephalopathy

63. REFERENCES
 SABISTON TEXTBOOK OF SURGERY 20TH EDITION
 BAILEY & LOVE’S SHORT PRACTICE OF SURGERY
 SCHWARTZ PRINCIPLES OF SURGERY
 SHACKELFORD’S SURGERY OF THE ALIMENTARY
CANAL
 SRB’S MANUAL OF SURGERY
 ROBBINS PATHOLOGY