This document provides an overview of the management of acute pancreatitis. It defines acute pancreatitis as the inflammation of the pancreas often associated with pancreatic duct dilation. It discusses the epidemiology, etiology, pathogenesis, clinical forms, investigations, risk assessment, treatment and prognosis of acute pancreatitis. The management involves resuscitation, assessing severity, treating any underlying causes, and monitoring for complications which can include pancreatic necrosis, infection and multi-organ failure. Severity is assessed using scoring systems like Ranson's criteria or CT severity index to determine prognosis and guide management.

1. MANAGEMENT OF ACUTE
PANCREATITIS
DR BASHIR BIN YUNUS
GENERAL SURGERY UNIT
AKTH
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2. OUTLINE
• INTRODUCTION
• Definition
• Epidemiology
• Etiology
• PATHOGENESIS
• CLINICAL FORMS
• MANAGEMENT
• Algorithm
• Investigations and risk assessment
• Treatment
• PROGNOSIS
• COMPLICATIONS
• CURRENT TRENDS
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3. DEFINITION
• It is the inflammation with autodigestion of the pancreas often
associated with varying degree of pancreatic ductal dilatation.
• It is an acute condition presenting with abdominal pain and is usually
associated with raised pancreatic enzyme levels in the blood or urine
as a result of pancreatic inflammation.
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4. EPIDEMIOLOGY
World wide the annual incidence is varies from 5-50 per 100,000
10 fold rise in the western world reflect alcohol use.
Patients age and gender:
Alcohol-induced
30-40years (younger)
Men >> Women
Gallstone-induced
40-60 years (older)
Women >> Men
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5. AETIOLOGY
• Cholelithiasis (50%)
• Alcoholism (25%)
• Post-operative pancreatitis
• Genetic
• Microbial agents
• Endocrine factors
• Cortisone and ATCH
• Hyperparathyroidism and hypercalcemia
• Pregnancy
• Metabolic disorder
• Hyperlipidemia
• Diabetes
• Nutritional factors
• Chemotoxic and iatrogenic causes
• Idiopathic pancreatitis
• Miscellaneous- scorpion bite, worm infestations
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6. PATHOGENESIS
Obstruction- Hypersecretion theory
Common channel theory
Duodenal reflux
Acinar cell derangement
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8. Acinar cell derangement
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9. CLINICAL FORMS OF ACUTE PANCREATITIS
• Mild form
• Moderate
• Severe attack
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10. MILD
• Epigastric pain
 may be the only complaint
Radiates to the back
Relieve by leaning forward (Van Zant Sign)
• Vomiting
may be associated with persistent retching and hiccups
• Constipation is a rule in the initial stage
• Upper abdominal tenderness and guarding
• No organ failure, local or systemic complications
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11. MODERATE
• Local or systemic complications without persistent organ failure
• Organ failure that resolves within 48 h (transient organ failure)
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12. SEVERE
• Patient is much iller
• Pain is severer, Vomiting and retching is more persistent
• The abdominal tenderness, marked guarding, rebound tenderness
and diminished bowel activity
• Full picture of shock may supervene
• Persistent organ failure; single or multiple
• Other features; left pleural effusion, jaundice 20-30%, carpopedal
spasm
• Could assume fulminating pancreatitis(acute haemorrhagic
necrotizing)
Shock is profound and coma or diabetic ketosis
Retroperitoneal Haemorrhage (revealed as Cullen’s sign and grey Turner’s)
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13. CULLEN’S SIGN
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15. MANAGEMENT
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16. Management cont….
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17. Management cont…..
Diagnose
Resuscitate
Assess severity
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18. INVESTIGATIONS
• HEMATOLOGICAL investigations
• RADIOLOGICAL investigations
• Miscellaneous investigations
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19. HEMATOLOGICAL
• BASELINES
• CBC:
• Low Hb: prolonged hemetemesis/melena, internal hemorrhage
• Leucocytosis (10,000-30,000/mcL)-infection, non infectious inflammation
• Low platelets-DIC
• Hct –raised in hemoconcentration
• 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:
• Low sodium/potassium: persistent vomiting
• Hypocalcemia- saponification/fat necrosis
• Serum Protein:
• low protein/ albumin
Diabetes Mellitus AP

20. HEMATOLOGICAL
• ABG’s
• Etiology specific investigations
• Serum fasting lipid profile
• Viral titers
• Serum Calcium (HypercalcemiaAPHypocalcemia)
• Autoimmune markers
• increased serum levels of IgG4
• serum autoantibodies such as anti-nuclear antibody (ANA), anti-lactoferrin
antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF),
Acid-Base Disturbance Etiology
Metabolic (Lactic)acidosis with high anion gap Hypovolemic shock
Cholride-responsive Hypokalemic Hypochloremic metabolic alkalosis
(Urine chloride < 20 mEq/L)
persistent vomiting
Respiratory acidosis ARDS/resp failure

21. 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)
• normal at time of admission in 20% cases
• Compared with lipase, returns more quickly to values below the
upper limit of normal.
• Serum Lipase:
• more sensitive/specific than amylase
• Remains elevated longer than amylase(12 days)
• Useful if late presentation
Raised Amylase  may not AP
Normal Amylase  may be AP
SERUM INDICATOR OF HIGHEST
PROBABILITY OF DISEASE

22. • Pancreatic Enzymes’ Assays
• 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%)

23. 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

24. Plain CXR-PA view
• Left sided Pleural effusion: blunting of costophrenic and cardiophrenic angles + haziness in lower
zones
• Elevated diaphragm on left side
• Linear focal atelactasis of lower lobe of lungs
• ARDS: diffuse alveolar interstitial shadowing
• Pulmonary edema: prominent vascular markings
_________________________________________________________
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

25. 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
• RATIONALE: body's effort to localize the traumatic or inflamed lesions
• ETIOLOGY: Localized paralysis followed by accumulation of gas
• SITE:
• Acute Pancreatitis Left hypochondrium (PROXIMAL JEJUNUM)
• Acute Appendicitis Right iliac fossa
• Acute Cholecystitis Right Hypochondrium
• Diverticulitis Left iliac fossa
*SENTINEL:A soldier stationed as a guard to challenge all comers and prevent a surprise
attack
_______________________________________________________________
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

26. SENTINEL LOOP SIGN

27. 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
• abruptly ending at the area of pancreatic inflammation
• with collapse of descending colon
• RANTIONALE: Extension of inflammatory process from the pancreas into the
phrenicocolic ligament via the transverse mesocolon
• resulting in functional spasm and/or mechanical narrowing of the splenic flexure at
the level where the colon returns to the retroperitoneum.
• Differential DIAGNOSIS:
• IBD
• Carcinoma of colon
• Mesenteric Ischemia
____________________________________________________________________________________
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

28. COLON CUT-OFF SIGN

29. Plain X-ray abdomen erect AP view
• Renal halo sign
• RATIONALE: peripancreatic inflammatory reaction extension into pararenal
space
• ETIOLOGY: water-density (radiolucent-halo)of inflammation in anterior
pararenal space contrasts with perirenal fat; more common on left side
• 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)

30. Renal Halo Sign
NORMAL RENAL HALO SIGN

31. Transcutaneous 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%)
• DEMERIT: overlying gas shadows 2ndary to bowel distension
• THERAPEUTIC:
• USG-guided aspiration for gram staining and culture
• USG-guided pig tail catheter insertion
______________________________________________________________________
________
* Identification of gallstones as the etiology should prompt referral for
cholecystectomy to prevent recurrent attacks and potential biliary sepsis.
Gallstone pancreatitis is usually an acute event and resolves when the stone is

32. 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.

33. 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
_____________________________________________________________
*INVESTIGATION OF CHOICE
**Seldom needed within first 72 hrs after symptom onset unless the
diagnosis is uncertain, because inflammatory changes are often not
radiological present until this time

34. IV Contrast* enhanced Computed Tomography Scan
• INDICATIONS-DIAGNOSTIC
• Initial assessment of prognosis(CT severity index)
• Perfusion CT at 3rd day  area of ischemia predict pancreatic necrosis
• INDICATIONS-THERAPEUTIC:
• CT-guided aspiration of fluid collection/necrotic tissue for gram staining
and culture(sterile vs infected necrosis)
• specimen should be delivered to the laboratory within an hour and
interpreted promptly
• CT-guided pig tail catheter insertion
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*Use of IV contrast may increase risk of complications of pancreatitis and AKI
*Avoided if serum creatinine >1.5 mg/dL
*MRI suitable alternative

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

36. 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

37. Magnetic Resonant Cholangiopancreatography
• INDICATION:
• diagnosis of suspected biliary and pancreatic duct obstruction in the setting of
pancreatitis.
• Repeated attacks of idiopathic acute pancreatitis
• Merit
• used if choledocholithiasis is suspected but there is concern that pancreatitis might
worsen is ERCP is performed
• Provide non-invasive/fast/safe high-quality (Heavily T2–weighted) imaging for
diagnostic and/or severity purposes

38. Endoscopic UltraSonography
• INDICATIONS
• Repeated idiopathic acute pancreatitis*
• occult biliary disease- small stones/sludge
• secretin-stimulated EUS study may reveal resistance to ductal outflow
at the level of the papilla,
• as evidenced by dilatation of the pancreatic duct to a greater extent and
longer duration than in a healthy population
• Age >40 to exclude malignancy
• especially those with prolong or recurrent course
• RATIONALE: 5 % CA pancreas present as AP
_________________________________________
*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.

39. 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
NOT INDICATED
• Not needed early in most patients with gallstone pancreatitis who lack
laboratory or clinical evidence of ongoing biliary obstruction
• As most of gallstones causing AP readily pass to duodenum and are lost in stool
• MRCP or EUS recommended if CBD stone still suspected
• as risk of post-ERCP pancreatitis is greater with normal calibre bile duct and normal
bilirubin
• MRCP /EUS as accurate as diagnostic ERCP

40. ASSESSMENT OF SEVERITY
• Early identification of patient at risk of severe pancreatitis and serious
complication thereby decrease mortality.
• Haemodynamic status should be assessed immediately upon
presentation and resuscitative measures begun as needed
• Ranson’s scoring system
• Glasgow scoring system
• Apache II scoring system
• Contrast enhance CTScan
• C-reactive protein
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41. RANSON’S SCORING SYSTEM
• 11 Parameters, 5 on admission, 6 within 48hours. ≥3 factors indicate
severe acute pancreatitis
• ON ADMISSION
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42. RANSON SCORE-1974
(for alcohol pancreatitis)
ON ADMISSION
• Age > 55 yrs
• TLC > 16,000/mm3
• BSR> 200 mg/dL
• AST > 250 IU/L
• LDH > 350 IU/L
WITHIN 48 HOURS
• 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

43. Revised RANSON SCORE-1979
(for Gallstone pancreatitis)
ON ADMISSION
• Age > 70 years
• TLC > 18000/mm3
• BSR > 220 mg/dL
• AST> 250 IU/L
• LDH >400 IU/L
WITHIN 48 HOURS
• 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

44. RANSON SCORE
Ranson
score
Mortality rate SEVERITY Interpretation
0-2 ≈ 0-2 % i.e. minimal mortality Mild AP Admit in regular ward
3-5 10-20 %
Severe AP
Admit in ICU/HDU
6-7 40 % Associated with more systemic
complications
>7 >50 % Same as above
SCORING SYSTEM SENSITIVITY SPECIFICITY
Ranson Criteria 73% 77%
APACHE II 77% 84%
CRP 73% 71%

45. 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.
• A delay of 48 hours after admission merely for assessment may squander
a valuable opportunity to prevent a complication during this time.
• Best used within the initial 48 hours of hospitalization and have not
been validated for later time intervals.
• Threshold for abnormal valve depends on whether cause is gallstone
or alcohol
• Only 73 % sensitive and 77 % specific in predicting mortality

46. TREATMENT OF MILD/MODERATE
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47. Mild/moderate 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
• Little physiological justification for prolonged NPO
• No medication required other than analgesics(important) and anti-emetics
• Antibiotics not indicated in absence of signs or documented sources of infection
• Pain results in ongoing cholinergic discharge, stimulating gastric and pancreatic
secretions
• Analgesics: WHO analgesic ladder-1986
• Avoid Morphine-cause sphincter of Oddi spasm
• Metabolic support
• Correction of electrolyte imbalance

48. Severe Acute Pancreatitis
• P:
• Pain relief
• Proton pump inhibitors-omeprazole
• Peritoneal lavage
• 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
• Ranitidine(for stress ulcer)
• 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
• Inotropes
• Hemofiltration
• Ventilator(PEEP)

49. Monitoring
CLINICAL
• Vitals
• UOP
• CV pressure
INVESTIGATIONS
• Baselines
• Serial ABGs
• Serial BSR
• Serum calcium/magnesium

50. Role of Surgery in AP
• In case of mild gallstone AP, cholecystectomy should be performed before
discharge to prevent a recurrence of AP
• Within 48-72 hour od admission or briefly delay intervention(after 72 hrs but during
same admission
• Along with intraoperative cholangiography and any remaining CBD stones can be
dealt with intra/post operative ERCP or
• Along with preoperative EUS or MRCP
• 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
• Cholecysectomy done for recurrent AP (IAP) with no stones/sludge on USG
and no significant elevation of LFTs is associated with >50 % recurrence of
AP
_________________________________________________________
If patient unfit for surgery(comorbid/elderly), biliary sphincherotomy alone
may be effective to reduce further attacks of AP

51. Sterile necrosis infected necrosis
Asymptomatic doesnot mandate
intervention regardless of
size, location and extension
surgical, radiologic, and/or
endoscopic drainage should be
delayed preferably for more
than 4 weeks
• to allow liquefaction of
the contents and the
development of a
fibrous wall around the
necrosis
• 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
Minimally invasive approach: laparoscopic surgery(ant or retroperitoneal approach),
percutaneous radiologic catheter drainage or debridement, video-assisted or small incision-
based left retroperitoneal debridement, and endoscopy

52. 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, especially pseudocysts.
• Within 7-10 days

53. PROGNOSIS
• Mortality rate for all patient with acute pancreatitis is about 10%
• Necrotizing pancreatitis associated with infection has mortality of
20%
• Earlier diagnosis of infection and aggressive intervention may lower
this figure.
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54. COMPLICATIONS
• Pancreatic abscess
• Pancreatic pseudocyst
• Pancreatic fistula
• Acute renal failure
• Diabetic ketosis
• Gastric erosion
• Intestinal obstruction
• Splenic rupture
• Hypocalcaemia and tetany
• Hypomagnesaemia
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55. CURRENT TREND
• Treatment with platelet-activating factor (PAF) antagonists appears
to ameliorate the severity of acute pancreatitis and reduction in
organ failure.
Lexipafant
• Interleukin 1 antagonist and IL-10 administration may prove beneficial
to patient with severe disease, still under trial.
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56. REFERENCES
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