The document provides an overview of acute pancreatitis including: - It begins with anatomy and blood supply of the pancreas. - Pathophysiology involves autodigestion from inappropriately activated pancreatic enzymes. - Etiology is commonly gallstones, alcohol, or idiopathic. - Clinical presentation includes severe abdominal pain and systemic complications can involve multiple organ systems.

1. ACUTE PANCREATITIS

2. Outline
 Anatomy
 Epidemiology
 Pathophysiology
 Etiology
 Clinical Presentation
 Workup
 Severity Scoring System
 Treatment
 Prognosis
 Complications

3. PANCREAS
PANCREAS Greek word with literal meaning ‘pan’
(all/whole) , ‘creas’ (flesh)

4. Anatomy
Pancreas is an
elongated, accessory
digestive gland that lies
retroperitoneally
Transversely it lies
across the posterior
abdominal wall
posterior to the stomach
between duodenum on
the right and the spleen
on the left.

5. Anatomy
Parts of pancreas
• Head
• Neck
• Body
• Tail

6.  HEAD
• The expanded part of the gland
that is embraced by the C
shaped curve of the duodenum
to the right of the superior
mesenteric vessels.
• The head of the pancreas rests
posteriorly on the IVC
Anatomy

7. Anatomy
 NECK
• It is short and overlies the
superior mesenteric
vessels, which form a
groove in its posterior
aspect.
• The anterior surface of
neck, covered with
peritoneum, is adjacent to
the pylorus of the stomach.

8.  BODY
• Continues from the neck
and lies to the left of the
superior mesenteric
vessels,
• Passing over the aorta and
L2 vertebra
• The posterior surface of the
body is devoid of
peritoneum and is in
contact with the aorta,
SMA, left suprarenal gland
and left kidney and renal
vessels

9.  TAIL
• Lies anterior to the
left kidney, where it is
closely related to the
splenic hilum and the
left colic flexure.
• The tip of the tail is
usually blunted and
turned superiorly

10.  Main Pancreatic Duct (WIRSUNG) opens at major duodenal
papilla.
 Accessory pancreatic duct (SANTORINI) usually (60%)
communicates with the main pancreatic duct opens into the
duodenum at the summit of the minor duodenal papilla

11. • Smooth muscle sphincter that control the flow of bile &
pancreatic juice into duodenum :
 - Sphincter of the pancreatic duct
 - Sphincter of the bile duct
 Sphincter of ampulla
 - sphincter of Oddi

12. Blood Supply - Arterial
 -The pancreatic arteries derive mainly from the
branches of the SPLENIC ARTERY
 -The anterior and posterior superior
pancreaticoduodenal arteries, branches of the
gastroduodenal artery
 -The anterior and posterior inferior
pancreaticoduodenal arteries, branches of the SMA.

14. Venous Drainage

15. Lymphatics
 The pancreatic lymphatic
vessels follow the blood
vessel. Most of them end
in the pancreaticosplenic
nodes that lie along the
splenic artery, but some
vessels end in the pyloric
lymph nodes.
 Efferent vessels from
these nodes drain to the
superior mesenteric
lymph nodes or to the
celiac lymph nodes via
the hepatic lymph nodes.

16. Nerve Supply
 The nerves of the
pancreas are
derived from the
vagus and
abdominopelvic
splanchnic nerves.

17. Pancreas - Physiology
FUNCTIONS:
 neutralize chyme
 digestive enzymes
 hormones

18. Physiology
 The pancreas produces :
• An exocrine secretion ( pancreatic juice from the acinar cells)
that enter the duodenum through the main and accessory
pancreatic ducts.
• Endocrine secretion (glucagon & insulin) from the pancreatic
islets (of langerhans) that enter blood.

19. PANCREATITIS
Aseptic inflammation of the pancreas.
PANCREAS
Stroma
Parenchyma
Exocrine
Primary injury causing
PANCREATITIS
Endocrine
Involved secondarily or as
a complication

20. CLINICAL CLASSIFICATION

21. ACUTE PANCREATITIS
 CLINICAL DEFINITION
 An acute condition presenting with abdominal pain-usually
associated with raised blood/urine pancreatic enzymes as a
result of pancreatic inflammation

22. CLASSIFICATION OF ACUTE PANCREATITIS
Atlanta* criteria (1992)
Revised Atlanta criteria
(2012)
 Mild acute pancreatitis (80% cases)
(Acute Interstitial/edematous
pancreatitis)
 Acute Absence of organ failure
 Absence of local complications
 Severe acute pancreatitis(20 % cases)
(Acute Hemorrhagic Necrotizing
(fulminant) pancreatitis)
 Local complications +/-
 Organ failure defined as
 SBP < 90 mm Hg
 PaO2 ≤ 60 mm Hg
 GI bleed ≥ 500 ml/24 hrs
 Cret ≥ 2 mg/dL after rehydration
 Ranson score ≥ 3 or APACHE ≥ 8
 Mild acute pancreatitis
 Absence of organ failure
 Absence of local complications
 Moderately severe acute
pancreatitis
 Local complications +/-
 Transient organ failure(<48 h)
 Severe acute pancreatitis
 Persistent organ failure**(>48 h)
and/or death
*defined as a score of 2 or more for one of these(CVS, Renal, Resp) organ systems using
the modified Marshall scoring system

23. Two Distinct phases of Acute
Pancreatitis
Early Phase(within 1 week) Late Phase (>1 week)
 Characterized by SIRS +/-
organ failure
 Severity assessed by
functional/clinical Severity
Scoring System
(Ranson/Galsgow etc)
 Characterized by local
complication
 Severity assessed by
morphological scoring
system(Balthazar Scoring)

24. Mortality of acute pancreatitis
 The overall mortality remains approximately 5% to
10%
 Rises to >40% if sterile necrosis becomes infected

25. Epidemiology
Gender Predilection
Generally M>F
In males more often related to alcohol
In females more often related to biliary tract
disease
Idiopathic pancreatitis no clear gender
predilection

26. Epidemiology
RACE
Hospitalization rates3 times higher for blacks than
whites
Risk for African Americans aged 35-64 years10 times
higher than for any other group

27. PATHOPHYSIOLOGY
Autodigestion of pancreatic substance by
inappropriately activated pancreatic enzymes
(especially trypsinogen)

28. Acute Pancreatitis Pathophysiology
Pancreatic Ducts
become obstructed
Hypersecretion of the exocrine
enzymes of pancreas
These enzymes enter the bile duct, where
they are activated and with bile back up
into the pancreatic duct
Pancreatitis

29. Acute Pancreatitis Pathophysiology
autodigestion of pancreatic tissue
release of
enzymes into
the circulation
activation
of white
blood cells
local
complications
local
vascular
insufficiency
distant
organ failure

30. MICROBIOLOGY-in infected necrosis
 Commonly polymicrobial infection-60%
 Source:
 gall bladder, colon, small bowel(Transmural) or hematogenous
spread
 INCIDENCE:
 24%(1 week) and 70 %( 3 weeks)
 ORGANISMS:
 E.Coli(35%), klebsiella( 25%), Enterococcus (25%)
 Others….. Staphlyococci, pseudomonas, proteus, enterobacter,
anaerobes, candida(10%)

31. Etiology
Gallstones
45%
Alcohol
35%
Idiopathic
10%
Other
10%

32. MECHANICAL CAUSES OF ACUTE PANCREATITIS
1. GALL STONES  CHOLEDOCHOLITHIASIS(40-70 %)
• Most common biliary tract disease leading to pancreatitis.
• MOA: Ductal obstruction causing ductal hypertension and acinar cell injury
• 5 % of gall stones causes pancreatitis
• M:F=1:3
2. - Ampullary tumor
3. - Sphincter of Oddi dysfunction
4. - Pancreatic head CA(1-2 % )
• 5 % present as AP
5. - Choledochoceles, biliary sludge
6. - Abdominal trauma(1.5 %cases)
• 17 % cases have high enzymes and 5 % have clinical AP
• Penetrating>Blunt
7. - Iatrogenic Injury
• Operative injury - Endoscopic procedures with dye injection

33. METABOLIC CAUSES OF ACUTE PANCREATITIS
1.- ALCOHOLISM (25-35%)
2.- Hyperlipoproteinemia (1-4 %)
• Type I and V hyperlipidemia
• >1000 mg/dL(diagnostic criteria)
3.- Malnutrition
4.- Diabetes, Azotemia,Porphyria
5.- Hypercalcemia/hyperparathyroidism
• Hyper secretion and formation of calcified stones intraductallyAcinar injury
6.- Drugs (2 % cases)(usually mild)
Definite association ( azathioprine, sulfonamaides, sulindac, tetracycline, valproic acid, Didanosine,
Methyldopa,estrogens, furosemide, 6-Mercaptopurine, pentamidine, 5-ASA, steriods,octreotide)
Probable association (thiazides, Flagyl, Methandienone, Nitrofurantoin,
phenformin,piroxicam,procainamide, Colaspase, chlorthalidone, asparagine,cimetidine,cisplatin, cytosine
arabinoside, diphenoxylate, ethacrynic acid)

34. INFECTIVE CAUSES OF ACUTE PANCREATITIS
VIRUSES
• MMR, Dengue virus(complication of dengue hemorrhagic fever,
Coxsackie B, Hepatitis virus, CMV, EBV, Echovirus, VZV, HSV
BACTERIA
• M. tuberculosis, M. avium complex, Mycoplasma, Legionella, Leptospira,
Salmonella, Campylobacter, Yersinia, Brucella, Nocarbia
FUNGI
• Aspergillus
PARASITES
• Clonorchis sinensis, Toxoplasma, Cryptosporidium, Ascaris, Echinococcus
granulosus,
• Fasciola Hepatica, Opistorhcis sp and Dicrocoelium dendriticym
SCORPION AND SNAKE BITE
• Trinidalian scorpion* (Tityus trinitatis)
• MOA: Neurotransmitter discharge from cholinergic nerve terminals, leading to
massive production of pancreatic juice(same MOA in
antiacetylcholinesterase/OPC insecticide)

35. GENETIC CAUSES OF AUTE PANCREATITIS
1. PANCREAS DIVISUM (unfused ducts of Wirsung and Santorini)
• Seen in 20-45 % cases
• MOA(controversial): stenotic minor papillae and atretic duct of santorini
2. ANOMALOUS UNION OF PANCREATICOBILIARY DUCT(annular pancreas)
3. AUTOIMMUNE PANCREATITIs-associated with IBD
4. HEREDITARY PANCREATITIS-
• Autosomal dominant, premature activation of trypsinogen
• Acute pancreatitis in teens
• Chronic in next 2 decades
• 40 % risk of pancreatic cancer by 70 year
5. Celiac disease
6. Cystic fibrosis-CFTR mutation  abnormality of ductal secretion

36. Idiopathic Acute Pancreatitis
 Defined as pancreatitis with no etiology established
after initial laboratory (including lipid and calcium
level,autoimmune markers, viral titers) and imaging
tests (USG and CT in the appropriate patient)
 In some patients an etiology may eventually be found(70 % of
IAP due to microlithiasis), yet in others no definite cause is
ever established.
____________________________________________________
Careful search for the etiology must be made in all cases, and
no more than 20 % of cases should fall into the idiopathic
category

37. Post-ERCP Pancreatitis
 3rd Most common cause of AP(after gallstone and alcohol) i.e. 4%
 Most common complication of ERCP
 INCIDENCE
 2-4 % patients undergoing ERCP develop acute pancreatitis
 Risk of severe AP < 1/500
PREDISPOSING FACTORS
 Sphincter of Oddi dysfunction(risk increases to 30 %)
 H/O recurrent pancreatitis
 Sphincterotomy
 Balloon dilation of sphincter
 Inexperienced endoscopist

38. CLINICAL MANIFESTATION

39. ABDOMINAL PAIN-CARDINAL SYMPTOM
 SITE: usually experienced first in the epigastrium
but may be localized to either upper quadrant or felt diffusely throughout the
abdomen or lower chest
 ONSET: characteristically develops quickly, generally following substantial meal
 SEVERITY: frequently severe, reaching max. intensity within minutes
 NATURE: “boring through”, “knifing” (illimitable agony)
 DURATION: hours-days
 COURSE: constant (refractory to usual doses of analgesics, not relieved by vomiting)
 RADIATION: directly to back(50%), chest or flanks
 AGGRAVATING FACTOR: food/alcohol intake, walking, lying supine.
 RELEIVING FACTOR: sitting or leaning/stooping forward (MUHAMMEDAN
PRAYER SIGN)

40. OTHER MANIFESTATIONS
 Nausea, frequent and effortless vomiting, anorexia,diarrhea
 Due to reflex pylorospasm
 More intense in necrotizing than in edematous pancreatitis
 Persistent retching
 despite empty stomach
 Hiccups
 Due to gastric distension/diaphragmatic irritation
 Fever
 Low grade, seen in infective pancreatitis
 Weakness, Anxiety, Sweating
 Indicates severe attack

41. ABDOMEN EXAMINATION
Tenderness + Rebound tenderness:
 epigastrium/upper abdomen
Guarding(also called “defense
musculaire” )-upper abdomen
Rigidity(involuntary stiffness)-unusual

42. Cutaneous Ecchymosis(1 % cases)*
Acute Hemorrhagic Necrotizing/fulminant
Pancreatitis Periperitoneal/retroperitoneal
Hemorrhage
Methemalbumin formed from digested blood tracks
around
Fascial planes 
hemorrhagic spots
and ecchymosis in
flanks
(GREY TURNER’S
SIGN)**
FALCIFORM
LIGAMENT 
Bluish
Discoloration
around
umbilicus
(CULLEN’S SIGN)
Below inguinal
ligament (FOX SIGN)

43. GREY TURNER1 SIGN CULLEN2 SIGN FOX3 SIGN
1. Named after British surgeon George Grey Turner(1877-1951)
2. Named for Thomas Stephen Cullen (1869-1953), Canadian gynecologist who first
described the sign in ruptured ectopic pregnancy in 1916
3.Named after George Henry Fox(1846-1937), American dermatologist

44. RESPIRATORY MANIFESTATIONS
Left sided* Pleural effusion(10-20%)
+
pulmonary edema
+
pneumonitis
*Due to close approximation of body and tail of pancreas to the left sided
diaphragm

45. SYSTEMIC COMPLICATIONS
 CARDIOVASCULAR
 Shock- hypovolemic and septic
 Arrhythmias/pericardial effusion/sudden death
 ST-T nonspecific changes
 Pulmonary
 Respiratory failure/pneumonia/atelectasis/pleural effusion
 Acute Respiratory Distress Syndrome (ARDS)
 Renal Failure
 Oliguria
 Azotemia
 Renal artery/vein thrombosis
 Hematological
 Hemoconcentation
 Disseminated Intravascular Coagulopathy (DIC)

46. SYSTEMIC COMPLICATIONS
 Metabolic
 Hypocalcemia
 Hyperglycemia
 Hyperlipidemia
 Gastrointestinal
 Peptic Ulcer/Erosive gastritis
 Ileus
 Portal vein or splenic vein thrombosis with varices
 Neurological
 Visual disturbances-Sudden blindness(Purtscher’s retinopathy)
 Confusion,irritability,psychosis
 Fat emboli
 Alcohol withdrawal syndrome
 Encephalopathy
 Miscellaneous
 Subcutaneous fat necrosis
 Intra-abdominal saponification
 Arthralgia

47. LOCAL COMPLICATIONS
 Peripancreatic fluid collections
 Pancreatic necrosis( sterile + infected)
 Pancreatic abscess(Phlegmon)
 Pseudocyst
 Pancreatic ascites
 Pseudoaneurysm

48. MANIFESTAIONS OF
COMPLICATIONS
 Hypocalcaemia
 circumoral numbness or paresthesia (1st symtpom to
develop) /tingling of distal extremities
 carpopedal spasm (=main d'accoucheur- French "hand
of the obstetrician”)
 laryngospasm
 generalized seizures
 Chvostek*(-Weiss) sign
 Trousseau** sign of latent tetany

49. MANIFESTAIONS OF
COMPLICATIONS
Hematemesis/
melena
(5%)
DIC
Peripancreatic
(duodenal)
necrosis
Gastric
erosions

50. Diagnostic criteria
 Most often established by the presence of two of the three
following criteria:
 (i) abdominal pain consistent with the disease,
 (ii) serum amylase and/or lipase greater than three times the
upper limit of normal, and/or
 (iii) characteristic findings from abdominal imaging.
*CT and/or MRI of the pancreas should be reserved for patients
 in whom the diagnosis is unclear(typical pain with normal
enzymes)
 who fail to improve clinically within the first 48–72 h after hospital
admission (e.g., persistent pain, fever, nausea, unable to begin oral
feeding)
 to evaluate complications

51. HEMATOLOGICAL
 BASELINES
 CBC:
 Low Hb: prolonged hemetemesis/melena, internal hemorrhage
 Leucocytosis (10,000-30,000/mcL)-infection, non infectious
inflammation
 Low platelets-DIC
LFT’s:
 raised bilirubin, AST/ALT/LDH, ALP, GGTP- gall stone pancreatitis
 RFT’s:
 raised BUN/cretainine- ATN ARF
 Coagulation profile:
 increased INR-DIC
 BSR:
 > 180 mg/dl-diabetes as a sequelae or cause
 Serum electrolytes:
 Serum Protein:
 low protein/ albumin
Diabetes Mellitus AP

52. HEMATOLOGICAL
 ABG’s
 Etiology specific investigations
 Serum fasting lipid profile
 Viral titers
 Serum Calcium (HypercalcemiaAPHypocalcemia)
 Autoimmune markers
Acid-Base Disturbance Etiology
Metabolic (Lactic)acidosis with high anion gap Hypovolemic shock
Hypokalemic Hypochloremic metabolic alkalosis persistent vomiting
Respiratory acidosis ARDS/resp failure

53. HEMATOLOGICAL
 Pancreatic Enzymes’ Assays
 Serum Amylase:
 ONSET: almost immediately
 PEAK: within several hours
 3-4 times upper limit of normal within 24 hrs (90%)
 RETURN to normal depends on severity(3-5 days)
 Serum Lipase:
 more sensitive/specific than amylase
 Remains elevated longer than amylase(12 days)
 Useful if late presentation
SERUM INDICATOR OF
HIGHEST PROBABILITY
OF DISEASE

54.  Urine Amylase
 More sensitive than serum levels
 Remain elevated for several days after serum levels returned to normal
 Pancreatic-specific amylase(p-amylase)
 Measuring p-amylase instead to total amylase(also includes salivary
amylase) makes diagnosis more specific(88-93%)

55. CONDITIONS ASSOCIATED WITH RAISED SERUM AMYLASE
ABDOMEN
 Small bowel obstruction
 strangulation ileus
 mesenteric ischemia
 Acute appendicitis
 Cholecystitis
 Perforated Duodenal Ulcer
 Gastroenteritis
 Biliary peritonitis
 Spasm of sphincter of Oddi
GYNE
 Ruptured Ectopic pregnancy
 Torsion of an ovarian cyst
OTHERS
 Parotitis (Mumps)
 Macroamylasaemia
 Opioids administration
 Low GFR
 Brain injury(CVA)-
hyperstimulation of pancreas

56. Plain X-ray abdomen erect AP view
Sentinel* loop sign
 Localized isolated Distended gut loop (Ileus) seen
near the site of injured viscus or inflamed organ
 SITE:
 Acute Pancreatitis Left hypochondrium (PROXIMAL
JEJUNUM)
 Acute Appendicitis Right iliac fossa
 Acute Cholecystitis Right Hypochondrium
 Diverticulitis Left iliac fossa
______________________________________________________________
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

57. SENTINEL LOOP SIGN

58. Plain X-ray abdomen erect AP view
Colon cut-off sign
 Gas filled (Distended) segment of
proximal(mainly transverse) colon
associated with narrowing of the splenic
flexure
 with collapse of descending colon
_______________________________________________________________
_____________________
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

59. COLON CUT-OFF SIGN

60. Plain X-ray abdomen erect AP view
 Renal halo sign
 RATIONALE: peripancreatic inflammatory reaction
extension into pararenal space
 OTHERS
_______________________________________________________________
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis
• Air in the duodenal C-loop
• increased gastrocolic
separation
• Gastric curvature distortion
• To rule out perforated
DU(gas under diaphragm)
• Obliteration of psoas shadow
• Localized ground glass appearance
( localized increased high soft
tissue density)
• Calcified gall stones
• Pancreatic calcification(chronic
pancreatitis)

61. Renal Halo Sign
NORMAL RENAL HALO SIGN

62. Abdominal Ultrasonography
 Not diagnostic
 Should be performed within 24 hours in all patients to
 detect gall stones* as a potential cause
 Rule out acute cholecystits as differential diagnosis
 Detect dilated CBD
 sensitivity-(70-80%)
 THERAPEUTIC:
 USG-guided aspiration for gram staining and culture
 USG-guided pig tail catheter insertion
Gallstone pancreatitis is usually an acute event and resolves when the stone
is removed or passes spontaneously.

63. IV Contrast enhanced Computed Tomography Scan
 Provides over 90 % sensitivity and specificity for the
diagnosis of AP….. BUT
 Routine use in patients with AP is unwarranted, as the
diagnosis is apparent in many patients and most have
a mild, uncomplicated course.

64. IV Contrast enhanced Computed Tomography Scan*
 INDICATIONS-DIAGNOSTIC
 Diagnostic uncertainty (differentiating pancreatitis from
other possible intra-abdominal catastrophes)
 Severe acute pancreatitis- distinguish interstitial from
necrotizing pancreatitis
 Necrosis( non enhancement area > 30 % or 3 cm) done at
72 hrs*
 Systemic complications:
 Progressive deterioration, MOF, sepsis
 Localized complications:
 Altered fat and fascial planes, Fluid collection, pseudocyst,
psduoaneurysm,
 Bowel distension, mesenteric edema, hemorrhage

65. BALTHAZAR CT severity index(CTSI)-1994
___________________________________________________________________
Mild (0-3) moderate (4-6) severe (7-10)
CT Severity Index Inflammation score + Necrosis score

66. Magnetic Resonant Imaging
Suitable alternative to CT in patients with a contrast
allergy and renal insufficiency where T2-weighted
images without gadolinium contrast can diagnose
pancreatic necrosis

67. Magnetic Resonant Cholangiopancreatography
 INDICATION:
 diagnosis of suspected biliary and pancreatic duct
obstruction in the setting of pancreatitis.
 Repeated attacks of idiopathic acute pancreatitis

68. Endoscopic UltraSonography
 INDICATIONS
 Repeated idiopathic acute pancreatitis*
 occult biliary disease- small stones/sludge
_________________________________________
*Endoscopic investigation in patients with acute idiopathic
pancreatitis should be limited, as the risks and benefits of
investigation in these patients are unclear and should be
referred to centers of expertise.

69. Endoscopic Retrograde Cholangiopancreatography
INDICATION
 Severe gallstone AP or AP with concurrent acute
cholangitis/biliary obstruction/ biliary sepsis/jaundice (due
to persistent stone)
 ERCP within 24(-72) h of admission
 Sphincterotomy/stent and bile duct clearance reduces
infective complications/mortality

70. SEVERITY SCORING SYSTEMS
ACUTE PANCREATITIS SPECIFIC SCORING SYSTEMS
 Ranson score
 Glagsow score
 Bedside Index for Severity in Acute Pancreatitis(BISAP) score
 Harmless Acute Pancreatitis Score(HAPS)
 Hong Kong Criteria
ACUTE PANCREATITIS NON-SPECIFIC SCORING SYSTEMS
(ICU SCORING SYSTEMS)
 Acute Physiology And Chronic Health Evaluation(APACHE) II score
 Sequential Organ Failure Assessment(SOFA) score

71. RANSON SCORE-1974
(for alcohol pancreatitis)
ON ADMISSION WITHIN 48 HOURS
 Age > 55 yrs
 TLC > 16,000/mm3
 BSR> 200 mg/dL
 AST > 250 IU/L
 LDH > 350 IU/L
 BUN rise >5 mg/dL
 Pa02 < 60 mmHg ( 8 KPa)
 Serum Calcium < 8 mg/dL
 Base deficit > 4 meq/L
 Fluid Sequestration > 6000 mL
 Hct fall > 10 %
NOTE: Disease classified as SEVERE when 3 or more factors are present

72. Revised RANSON SCORE-1979
(for Gallstone pancreatitis)
ON ADMISSION WITHIN 48 HOURS
 Age > 70 years
 TLC > 18000/mm3
 BSR > 220 mg/dL
 AST> 250 IU/L
 LDH >400 IU/L
 BUN rise >5 mg/dL
 Pa02 < 60 mmHg ( 8 KPa)
 Serum Calcium < 8 mg/dL
 Base deficit > 5 meq/L
 Fluid Sequestration > 4 litres
 Hct fall > 10 %
NOTE: Disease classified as SEVERE when 3 or more factors are present

73. RANSON SCORE…….
DRAWBACKS
 One has to measure all 11 signs to achieve the best
predictability of prognosis
 2 full days are needed to complete the profile.
 Difference between gallstone & alcohol etiology
 Only 73 % sensitive and 77 % specific in predicting
mortality

74. Acute Physiology And Chronic Health Evaluation II score-1985

75. APACHE Scoring System
MERIT
 Immediate assessment of the severity of pancreatitis
possible
 Can be used even after 48 hours
 Unlike ALL pancreatic specific scoring systems, APACHE (and
SOFA) also includes clinical features of patient besides
laboratory values
 Best validated

76. DEMERITS OF AP-specific scoring systems(ACG 2013)
 Uniformly cumbersome.
 No laboratory test is practically available or
consistently accurate to predict severity in patients
with AP.
Thus, in the absence of any available test to determine
severity, close examination to assess early fluid losses,
hypovolemic shock, and symptoms suggestive of organ
dysfunction is crucial.

77. MANAGEMENT
 Mild acute pancreatitis
 Conservative Approach
 Admit in general ward
 Non invasive monitoring
 (Moderate)Severe acute pancreatitis
 Aggressive Approach
 Admit in HDU/ICU
 Invasive monitoring
__________________________________________
Recognizing patients with severe acute pancreatitis ASAP is
critical for achieving optimal outcomes

78. Mild Acute Pancreatitis
 mild and self-limiting, needing only brief hospitalization.
 Rehydration by IV fluids
 Frequent non-invasive observation/monitoring(atleast 8
hrly)
 Brief period of fasting till pain/vomiting settles
 No medication required other than analgesics(important) and
anti-emetics
 Antibiotics not indicated in absence of signs or documented
sources of infection
 Avoid Morphine-cause sphincter of Oddi spasm
 Metabolic support
 Correction of electrolyte imbalance

79. Severe Acute Pancreatitis
 P:
 Pain relief
 Proton pump inhibitors-omeprazole
 A
 Admit in HDU/ICU
 Antibiotics
 N
 Nasogastric intubation(if vomiting)
 Nasal oxygen
 Nutrition support
 C
 Calcium gluconate
 CVP line
 Catherisation- Foley
 R
 Rehydration by IV fluids,plasma,blood
 Radiology: CT scan, USG
 Resuscitation when required
 E
 Endotracheal intubation
 Electrolytes management
 ERCP
 A
 Antacids
 S
 Swan-Ganz catheter for CVP and TPN
 Suction-in case of aspiration
 Steroids in case of ARDS
 Supportive therapy for organ failure

80. Monitoring
CLINICAL INVESTIGATIONS
 Vitals
 Urine Output
 CV pressure
 Baselines
 Serial ABGs
 Serial BSR
 Serum calcium/magnesium

81. EARLY AGRESSIVE IV hydration
Which
fluid?
Lactated Ringer ’s solution may be the preferred isotonic
crystalloid replacement fluid
• Ringer lactate is better electrolyte balance and more pH-
balanced
when? Early aggressive IV hydration is most beneficial during the first 12 –
24 h, and may have little benefit beyond this time period
How
much?
Aggressive hydration, defined as 250 – 500 ml per hour of isotonic
crystalloid solution should be provided to all patients, unless
cardiovascular, renal, or other related comorbid factors exist.
• Fluid requirements should be reassessed at frequent intervals
within 6 h of admission and for the next 24 – 48 h.

82. Antibiotics
 Routine use* NOT recommended(ACG 2013) as
 Prophylaxis in severe AP
 Preventive measure in sterile necrosis to prevent development of
infected necrosis
 Indicated in
 Established infected pancreatic necrosis or
 Extraperitoneal infections
 Cholangitis, catheter-acquired infections, bacteremia, UTIs, pneumonia
 Few antibiotics penetrate due to consistency of pancreatic necrosis
 cefuroxime, or imipenem, or ciprofloxacin plus metronidazole
______________________________________________

83. Nutrition
 In mild AP
 oral feedings can be started immediately if there is no
nausea/vomiting, and the abdominal pain/tenderness/Ileus has
resolved(amylase return to normal, patient feel hunger)
 Initiation of feeding with a small and slowly increasing low-fat (low-
protein) soft diet
 In severe AP
 Enteral route is recommended to prevent infectious complications
 Parenteral nutrition should be avoided, unless enteral route is not
available, not tolerated, or not meeting caloric requirements

84. Route of enteral Nutrition
 Traditionally nasojejunal route has been preferred to avoid
the gastric phase of stimulation BUT
 Nasogastric route appears comparable in efficacy and safety
MERITS OF NASOGASTRIC ROUTE DEMERITS OF NASOGASTRIC ROUTE
NG tube placement is far easier than
nasojejunal tube placement( requiring
interventional radiology or endoscopy, )
Slight increased risk of aspiration

85. Role of Surgery in pancreatitis
 In case of mild gallstone AP, cholecystectomy should be
performed before discharge to prevent a recurrence of
AP
 In case of necrotizing biliary AP, in order to prevent
infection, cholecystectomy is to be deferred until active
inflammation subsides and fluid collections resolve or
stabilize
____________________________________________________
If patient unfit for surgery(comorbid/elderly), biliary
sphincherotomy alone may be effective to reduce further
attacks of AP

86. Sterile necrosis infected necrosis
Asymptomatic Does not mandate
intervention regardless of
size, location and
extension
• Initially treated with
antibiotics
Stable
Symptomatic
(associated with
GOO or bile
obstruction)
minimally invasive
methods of necrosectomy
are preferred to open
necrosectomy
Urgent debridement unstable

87. When to Discharge
 Pain is well controlled with oral analgesia
 Able to tolerate an oral diet that maintains their caloric needs, and
 all complications have been addressed adequately
Follow up
 Routine clinical follow-up care (typically including physical examination and
amylase and lipase assays) is needed to monitor for potential complications
of the pancreatitis
 Within 7-10 days

88. Prognosis
TYPE OF AP MORTALITY
Overall 10-15 %
(Biliary>alcholic)
Mild Acute Pancreatitis(80 % cases) 1 %
Severe Acute Pancreatitis(20 % cases) Severe  20-50 %
<1 week 1/3 cases MOF
>1 week 2/3 cases Sepsis
(+MOF)

89. THANK YOU……….