This document discusses acute pancreatitis, including its etiology, pathogenesis, clinical presentation, diagnosis, and management. The most common causes of acute pancreatitis are gallstones (30-60% of cases) and alcohol (15-30% of cases). The pathogenesis involves premature activation of pancreatic enzymes within the pancreas, leading to autodigestion and inflammation. Clinical features may include epigastric pain, nausea, vomiting, and signs of systemic inflammatory response. Diagnosis is based on abdominal pain consistent with acute pancreatitis and serum amylase or lipase levels over three times the upper limit of normal. Management involves fluid resuscitation, pain control, nothing by mouth initially, and antibiotics only for proven pancreatic necrosis.

1. ACUTE PANCREATITIS
By:
Dr.NANDHINI

2. ETIOLOGY
 GALL STONES (30% - 60%)
 ALCOHOL(15% - 30%)
 POST ERCP (5% - 10%)
 POST TRAUMATIC (1%)
 DRUGS
 POST OPERATIVE

3. DRUGS
1.Azathioprine 8.Dapsone
2. 6MP 9.INH
3.Asparginase 10.Metronidazole
4.Pentamidine 11. estrogens
5.Didanosine 12.Tamoxifen
6.Valproate 13.Corticosteroids
7.Tetracyclines 14.ACE (-)tors
15. Thiazides

4.  Vascular causes & Vasculitis
 CTD
 Carcinoma head of pancreas
 Infections
Bacterial: mycoplasma, MAC,
Campylobactor, leigionella, Lptospirosis.
Viral: Mumps,Rubella,Varicella,
Coxsackie ,CMV,echo virus.
Parasites: Ascaris, Clonorchis )

5.  Auto immune (type 1&2)
 Scorpion bite
 Malnutrition
 Peritoneal dialysis etc….

6. If recurrent episodes…….
 Metabolic : hypertriglyceridemia,
hypercalcaemia
 Pancreatic divisum
 IPMN
 Heriditary Pancreatitis
 Cystic fibrosis
 Drugs
 Idiopathic

7. PATHOGENESIS
MOST ACEPTED THEORY ---
AUTO DIGESTION
PHASES
1. Enzyme Autoactivation
2.Chemoattraction & sequestration ofPMN and
macrophages releasing CK
3. Local & Systemic effects

9. TRYPSIN
Other Proenzyme activation
Autoactivation
Prophospholipase Pro elastase prekallikrein
Phospholipase elastase kallikrein
Fat necrosis weakens BV clotting .
cascade
HEMORRHAGE

10. Others……
Genetic :
 1. PRSS1(cationictrypsinogengene)
 2.SPINK1(pancreaticsecretorytrypsininhibitor)
 3.CFTR
 4.CTRC(chymotrypsinreceptor gene)
 5.CASR(calciumsensingreceptorgene)
Hypertriglyceridaemia
Hypercalcaemia
Drugs

11. Enzyme activation mechanisms
 Pancreatic duct obstruction
 Primary acinar cell injury
 Defective intracellular transport of Enzymes
Leucocyte sequestration
 Releases chemokines like IL-1ß ,IL-6, TNF, PAF,
SubstanceP.
 Sustains injury
Local and sytemic effects

12. CLINICAL PRESENTATION

13.  Epigastric pain (D/D)
 Nausea,Vomiting
 Abdominal distension
 Cool perpheries
 Blindness (may be transient)
 Respiratory distress
 Hiccoughs

14.  Mild Icterus
 Signs of shock
 SIRS
 Cullens sign
 Grey turners sign
 Fox sign
 Erythematous tender skin nodules
 Evidence of pleural effusion
 Guarding and rigidity
 Sluggish bowel sounds

16. Fox sign

17. Mechanism

18.  Other obsolete signs :
Korte sign
Kamenchick sign
Mayo robsons sign

19. DIAGNOSIS
2 of these 3criteria
 Typical abdominal pain
 3 fold or more raise in serum Amylase or Lipase
 CT findings s/o accute Pancreatitis

20. REVISED ATLANTA
CLASSIFICATION

21. ACUTE PANCREATITIS
Interstitial Necrotising
Acute peripancreatic Acute Necrotic
Fluid collection Collection
after 4wks
Pseudocyst Walled of
Necrosis

22. MORPHOLOGICAL FEATURES
1. INTERSTITIAL PANCREATITIS
 No necrosis
 Diffuse enhancement

23. 2.ACCUTE PANCREATIC FLUID COLLECTION
(APFC)
 no necrosis
 Peri pancreatic fluid <4wks duration
 No encapsulation
 No intra pancreatic extension

24. 3.Pancreatic pseudocyst
 No necrosis
 >4wks duration
 Well encapsulated
 Homogenous fluid density

25. 4. ACUTE NECROTISING PANCREATITIS
 Parenchymal
or
peri pancreatic necrosis

26. 5.ANC (Acute Necrotic Colletion)
 Necrotic areas
 Heterogenous areas
 Intra or peri pancreatic extension
 Non encapsulated

27. 6.WON(Walled Of Necrosis)
 Necrotic areas
 >4wks duration
 Heterogenic fluid collection
 Well encapsulated
 Intra or peri pancreatic collection

28. SEVERITY
ASSESSMENT

29.  Assessing injury to other organs
1. SOFA score
2. Modified Marshall Scoring System

30. Assessing severity of Pancreatitis
1. BISAP score
2.Ransons score
3. Glasgow score
4. APACHE-II score
5. CT severity Index
6. Modified CT severity Index
7.HAPS score
8.Revised Atlanta Classification

31. SOFA SCORE
Assesses 6 systems i.e,
respiratory
cardiovascular
renal
hepatic
coagulation
neurological

34. MODIFIED MARSHALLSCORING SYSTEM

35. BISAP score
 B – BUN > 22mg%
 I - Impaired mental status
 S - SIRS (Any 2 of 4 criteria)
 A - Age >60 yrs
 P -Pleural effusion

36. RANSON’S score
On Admission With in 48 hrs of
admission WBC >
16,OOOcells/cumm
 AGE >55yrs
 Glucose >200mg/dl
 LDH > 350 IU/L
 AST > 250U/L
 PCV fall > 10%
 Arterial Po2 < 60mm
Hg
 BUN raise > 5mg%
 Calcium < 8 mg/dl
 Base Deficit >
4mEq/L
 Fluidsequestration >
6lit

37. RANSONS SCORE
 11 point scoring system
POINTS ------ MORTALITY
0-2 - 0%
3-4 - 15%
5-6 - 50%
>6 - 70%

38. GLASGOW SCALE
On admission With in 48 hrs
 WBC > 15,000
cells/cumm
 Age > 55yrs
 Glucose > 200
mg/dl
 Arterial Po2 <60
mmHg
 Urea >45 mg/dl
 S.Calcium <8mg/dl
 S.Albumin
<3.2mg/dl
 S.LDH >600U/L
 S.ALT > 200 U/L

39. APACHE – II scoring system
 12 point scoring system
 After 24 hrs of admission into ICU

40. CTSI
 Includes
BALTHAZAR SCORE
&
NECROSIS SCORE

41. BALTHAZAR SCORE
GRADE --- DESCRIPTION --- SCORE
A Normal pancreas 0
B Enlarged pancreas 1
C Inflammatorychanges 2
in pancreas
and peri pancreatic fat
D Ill defined single 3
peripancreatic fluid collection
E ≥2 Ill defined fluid collections 4

42. NECROSIS SCORE
% --- SCORE
NONE 0
≤30% 2
30-50% 4
>50% 6

44. Grading
 0-2 : Mild
 4-6 : Moderate
 8-10 : severe

45. HAPS (Harmless Acute Pancreatitis
Score)
 High PPV
 Used to predict a milder course of illness
 Includes 1.Guarding &/ Rebound
tenderness +/-
2.Creatinine <2mg/dl
3.Hematocrit < 43%(M)
<39.6%(F)
 Score of “0” good prognosis

46. ATLANTA CLASSIFICATION
 MILD : no local complications & organ failure
 MODERATELY SEVERE : transient organ failure
<48hrs +/- local complications
 SEVERE : persistent organ failure (>48hrs) with
local and systemic complications

47. GRADING OF SEVERITY OF
ATTACK
 BISAP score of 3 - 5
 Ransons’ score ≥ 3
 Glassgow score ≥ 3
 APACHE II score ≥ 8
 CTSI (Balthazar) ≥ 6
 Modified CTSI score of 8-10
 Persistent organ failure(RevisedAtlanta)
 CRP >150mg/dl

48. Lab parameters……….
*CBP * Hematocrit
* S. Amylase * BUN
* S. lipase * S.Creatinine
* S. Calcium * CRP
* S. Triglycerides * LFT
*S. Trypsin * Coagulation
* Blood sugar profile

49. ENZYMES
 S.Amylase
 Normal values 23-85U/L
 Sources : parotids, pancreas, fallopian tube,
sweat,
 Types : S-type and P-type (isoenzymes)
 Metabolism : renal & hepatic
 Half life : 7 to 14 hrs
 sensitive & Highly nonspecific

50.  High Amylase levels seen in
*Pancreatic disorders
*Salivary disorders
*Renal failure
*Macroamylasemia
*Intestinal diseases- gut infarction
perforation ,peritonitis,obstruction
* Ruptured ectopic pregnancy
* ectopic production : cancers of pancreas,
thymus, breast, lung ,ovary.
* DKA and other acidotic conditions

51. Amylase
 No corelation b/n severity of pancreatitis and
degree of enzyme elevation
 Usually rises within 24hrs of attack and returns
to normal within 48-72hrs
 After 3-7 days normalises even if inflammation
continues.
 Hence normal levels doesn’t exclude the disease


52.  Amylase – P more specific than serum Amylase

53. Low Amylase levels…………..
 May be seen in
certain pancreatic cancers
Toxaemia of pregnancy

54. Confirmed Pancreatitis with Normal
Amylase levels…..
 Hypertriglyceridemia
(high triglycerides interferes with enzyme assay)
 Some times in patients with Alcoholic pancreatitis

55. S.Lipase
 More specific (95%)
 Remains for longer time in serum than amylase
 Stays even upto 8to 14 days
 useful in patiets who are presenting lately
 Half life about 10to 14hrs
 Level of lipase can’t predict disease severity and
outcome

56.  High serum lipase levels seen in
*Hollow viscus perforation
*Intestinal obstruction
*Intestinal ischemia
 In case of Alcoholic pancreatitis
S. lipase is more elevated than S.Amylase

57. S.CALCIUM
 May be high or low
 Hypercalcemia – cause
 Hypocalcemia - effect of pancreatitis
 Low Calcium levels correlates with severity of
disease
 <7mg/dl with normal albumin levels associated
with tetany have poor prognosis

58. S. TRIGLYCERIDES
 High levels of >900-1000 mg/dl associated with
increased risk
 Estimated in fasting states
 Usually asso. with
Type I ,V Hyperlipidemias

59. Markers of Hemoconcentration
*BUN > 22 mg/dl
*Hematocrit atAdmission >44 %(highNPV)
*S.Creatinine at 48 hrs of Admission
> 1.8mg/dl (high PPV)
 Helpful in assessing fluid status of patient
 Predictors of Pancreatic Necrosis

60.  CRP
Elevated CRP of >150 mg/dl at 48 hrs of
admission suggestive of severe disease.
single important prognostic indicator of severity
 LFT
hyperbilirubinemia >4mg/dl may be seen in 10%
patients assiciated with gall stone associated
pancreatitis
Elevated ALP also seen

61. IMAGING
IN
PANCREATITIS

62. ROLE OF PLAIN X-RAY

63. SIGNS
 Sentinal loop
 Colon cutoff sign
 Renal halo sign
 Loss of psoas shadow
 Gall stone may be seen
 Multiple calcifications in case of accute on chronic
pancreatitis patient
 pleural effusion Lt>Rt

64. COLON CUTOFF SIGN

65.  D/D for Colon Cut Off sign
*Pancreatitis
*IBD
*Mesenteric ischemia
*Carcinoma Colon

66. SENTINAL LOOP SIGN D/D

68. ROLE OF
USG AND DOPPLER

70.  Diffuse Decrease in Pancreatic Echogenicity
(than liver)
 Free fluid
 Increased volume of Pancreas i.e, Bulky Pancreas
(AP diameter >24mm)
 Gall stones
 Parenchymal inhomogenicty may correlate with
necrosis
 Pseudocysts
 Spleenic vien thrombosis etc..

71. ROLE OF CT IN PANCREATITIS

72. MANAGEMENT

73. 1.FLUID RECUSCITATION
 Main stay of therapy
 Initially 15-20ml/kg bolus administered
 Then f/b 3ml/kg/hr infusion should be kept to
maintain urine output of >0.5cc/kg/hr
 Serial evaluations done to assess fluid status
clinically and by measuring BUN & Hematocrit
every 8-12 hrs.

74.  Decrease in serial BUN & Hematocrit ensues
adequate resuscitation
 Adjust fluid rates of infusion in patients with co
morbid cardiac , pulmonary , renal illnesses
 Increasing BUN & Hematocrit inspite of
aggressive fluid therapy can be treated with
repeated volume challenge with 2L crystalloid
bolus f/b increase in infusion rate by 1.5ml/kg/hr
.

75.  If still unresponsive transfer to intensive unit for
careful hemodynamic monitering.
 Fluid of choice is Lactated Ringer which reduces
systemic inflammation and preffered over Normal
Saline

76. 2. Pain Management
 Opiates like Buprenorphine is DOC
 Pethidine can be given alternatively
 Meperidine 100to 150mg IM can be given every
4th hrly if necessary
 NSAID of choice is Metimazole
 Morphine is contraindicated.

77. 3.NBM
 NPO is no longer advisable
 Usually kept for 2-3 days with ryles tube
aspiration
 As soon as possible oral fluids are allowed even
enzymes are elevated
 Initially with soft liquids
 Later with low fat diet preferred
 Maintains barrier integrity and decreases
bacterial translocation

78. 4. Role of Antibiotics
 Prophylactic therapy has no role
 Mild disease doesn’t needs antibiotics at all
 For severe pancreatitis i.e, with necrosis may
benefit
 Definitive role is seen with proven cases of
infected Necrosis
 Antibiotics of choice are CARBAPENUMS

79.  IMIPENUM 5oomg 8th hrly given
 Alternatively Cefuroxime 1.5g IV TID
f/b 250mg oral BD for 14 days
 Meropenum and
combination of Ciprofloxacin and Metronidazole
doesn’t appear to reduce frequency of infected
necrosis and MODS

80. 5.Supportive therapy
 FFP transfusions in case of DIC
 Ionotropes for cardiac support
 Mechanical ventilation for ARDS
 Hemofilteration etc….

81. In Spl situations like……
 1. Gall stone pancreatitis :
*should undergo ERCP within
24-48hrs of admission to prevent
recurrence
*cholecystectomy may be done on
later date

82.  2.Hypertriglyceridemia :
*Initially treated with Insulin ,
Heparin, plasmapheresis
* later hypolipidemic drugs like
Fibrates , Niacin can be used.
 3. ERCP induced Pancreatitis:
*Rectal Indomethacin , Allopurinol ,
newer drug Ulinastatin , aggressive
hydration with ringered lactate can
prevent this .

83. COMPLICATIONS

84. SYSTEMIC LOCAL
 Pleural effusion
 ARDS
 Atelectasis
 Hypotension
 arrythmias
 Pericardial effusion
 DIC
 ATN
 Renal vein /artery thrombosis
 Hyperglycemia
 Encephalopathy
 Purtscher’s retinopathy
 Subcutaneous fat necrosis
 Acute fluid collection
 Necrosis
(sterile/infected)
 Pseudocyts
 Pancreatic abscess
 Portal / spleenic vein
thrombosis
 Pseudoaneurysm

85. PURTSCHER’S RETINOPATHY

86. NECROSIS
 May be sterile(60%) or
infected(40%)
 Prophylactic antibiotics no role
 Infected necrosis can be suspected by clinical
deterioration with persistant MODS
 Aspirated under CT guidance sent for gram’s and
culture

87. Pseudocyst
 Emperical antibiotic therapy with Imipenum can
be started
 Step up approach
 Requires 4wks for epithelisation and maturation
 Resolve spontaneously with in 6wks
 May or may not communicate with ductal system

88. SURGEON’S ROLE
 1. Necrosis - necrosectomy
*indications :
worsening sepsis in case of
infected necrosis
 2.pseudocyst –
>6cm lasting for 12 wks producing
pressure symptoms warrants
surgery

90. Prognosis
 Risk of chronic pancreatitis after an attack of
accute alcoholic pancreatitis
is 13% in 10 yrs
& 16% in 20 yrs

91. Follow up care
 Aimed towards assessment of risk of
DM
Exocrine Pancreatic insufficiency
etc..

92. THANK U