This document provides an overview of acute pancreatitis including its anatomy, epidemiology, pathophysiology, etiology, clinical presentation, workup, severity scoring, treatment, prognosis, and complications. It begins with definitions of the pancreas' anatomy and functions. It then discusses the disease's worldwide incidence, risk factors, presentations, diagnostic criteria, hematological and radiological evaluations, and key findings on imaging studies like CT scans. The document provides a comprehensive review of acute pancreatitis.

1. Acute Pancreatits
Dr Jawad Ahmed
1st
Year Resident
Surgical D unit
MTI/LRH

2. Outline
• Anatomy
• Epidemiology
• Pathophysiology
• Etiology
• Classification
• Clinical Presentation
• Workup
• Severity Scoring system
• Treatment
• Prognosis
• Complications

3. Anatomy
• Pancrease is a complex lobulated structure.
• Its retroperitoneal organ that lies in an oblique
position, sloping upward from the C-loop of
duodenum to the splenic hilum.
• It has both exocrine and endocrine components.
• Endocrine components is less is less then 1 %
of whole panrease which secret many regulatory
harmones while exocrine portion secret many
digestive anatomy.

5. Epidemiology
• World wide incidence ranges between 5 and 80 per 100,000
population.
• Generally Male > Female
• In males  more often related to alcohol
• In females  more often related to biliary tract disease.
» Geographical
• Highest incidence worldwide is recorded in the United States and
Finland ( 73.4 cases per 100,000)
• Mortality: 2-3% overall mortality from acute pancreatitis
• Physician Visits: 911,000 per year.
• Hospitalizations: Around 230,000 per year
• Deaths: 2500 per year.

6. • The median age of onset depends on the
etiology:
• AIDS related – 31 years
• Vasculitis related – 36 years
• Achohol related – 39 years
• Drug induced etiology – 42 years
• ERCP related – 58 years
• Trauma related – 66 years
• Biliary tract related – 69 years

7. Pathophysiology

8. Etiology
• Gallstones
• Alcohol
• Post-ERCP
• Drugs
• Autoimmune
• Genetic
• Abdominal Trauma
• Post Operative
• Infections
• Metabloic causes  hypercalcemia,
hyperparathyroidism, hypertriglyceridemia
• Miscellanous scorpion bites, worm infestations

9. Clinical Presentation
• Pain ( 95% )
• Acute onset
» Mid-abdominal or mid-epigastric
» Radiates to back (50%)
» Peak intensity in 30 mints
» Last for several hours,
» Severe in intensitiy
» Relieved with sitting or leaning forward
( Muhammedan Prayer Sign)
Aggrevated with food,alcohol, walking or lying supine

10. Other Menifestations
• 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
• Weakness, Anxiety, Sweating
– Indicates severe attack
• Polyarthritis

11. General Physical Examination
• Appearance: well  gravely ill with profound shock, toxicity and
confusion.
• Vitals: Tachypnea(and dyspnea-10%), Tachycardia(65%), Hypotension,
temp  high(76%)/normal/low (acute swinging pyrexia in cholangitis)
• Icterus(28%)
– gallstone pancreatitis or due to edema of pancreatic head.
• Cyanosis
– Improper lung perfusion
• Pallor, cold clammy skin,diaphoretic

12. Abdominal Examination
• Tenderness + Rebound tenderness:
– epigastrium/upper abdomen
• Distension:
– Ileus(BS decreased or absent)
– ascites with shifting dullness
• Mass in epigastrium(usually absent)
– due to inflammation
• Guarding(also called “defense musculaire” )-upper abdomen
– tensing of the abdominal wall muscles to guard inflamed organs within
the abdomen from the pain of pressure upon them(i.e. during palpation)
• Rigidity(involuntary stiffness)-unusual
– Tensing of the abdominal wall muscles to guard inflamed organs even if
patient not touched

13. 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)
(umbllical black
eye)
Below inguinal
ligament
(FOX SIGN)
*Neither sign is pathognomonic of acute
**More commonly, ruddy
erythema in flanks due to
extravasated pancreatic
exudate

14. Differential Diagnosis
GREY TURNER/CULLEN/FOX SIGNs
Acute Pancreatitis
Pancreatic Hemorrhage
Ruptured AAA
Blunt Abdominal Trauma
Ruptured Ectopic Pregnancy
Retroperitoneal Hemorrhage
Coagulopathy
: George Grey Turner Thomas Stephen Cullen

15. Physical Signs

16. Respiratory Examination
• Left sided Pleural Effusion (10-20%)
• Pulmonary edema
• Pneumonitis
– These all can result in
» Reduced Chest movements
» Decreased vocal fremitus/resonance
» Stony dull percussion notes
» Decreased air entry basally bilaterally
» Basal fine mid/end inspiratory crepitation’s that don’t
can with cough.

17. Neurologic Examination
Mild
Psychosis
 Coma
Toxemi
a
Fat
Embolism
Hypoxi
a
Respirator
y
distress Uremic
encephlopath
y
Hypovolemi
c shock
DI
C

18. Other Manifestations
• Subcutaneous fat necrosis
– Small(<1 cm), red, tender nodules on
extensor skin of legs
• Purtscher retinopathy(on fundoscopy)
– Activation of complement and agglutination
of blood cells within retinal vessels causing
Ischemic injury of retina
– May cause temporary or permanent
blindness

19. Manifestation 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”)
• Flexion of wrist and MCP joints with extension of IP joints
– laryngospasm
– generalized seizures
– Chvostek*(-Weiss) sign
• Depending on calcium level, graded response occur: twitching first at angle of
mouth, then by nose, the eye and the facial muscles
• Positive in 10 % population in absence of hypocalcaemia
– Trousseau** sign of latent tetany
• BP cuff around arm and inflating to 20 mmHg above SBP for 3-5 minutes
• Carpal spasm observed
• More specific and sensitive than chvostek sign(postive even before
tetany/hyperreflxia)

20. Differential Diagnosis
ABDOMINAL CONDITONS
•Perforated peptic ulcer/gastroentritis
•Biliary colic/acute cholecystitis/ Cholangitis
•Mesentric Ischemia
•Ruptured Aortic Anuerysm
•Intestinal Obstruction
•Gastric/colon/pancreatic CA
•Viral Hepatitis
•IBS
SYSTEMIC CONDITIONS
•DKA
THORAX CONDITIONS
•Pneumonia/ARDS
•Pleuritic pain
•MI
GYNECOLOGICAL
CONDITONS
•Ectopic pregnancy
•Salpingtis

21. • A 44-year-old woman comes to the emergency department with severe epigastric pain
• that radiates to her back. The pain was sudden in onset and has remained steady for
• the past several hours. She has associated nausea and vomiting. Past medical history
• is notable for a surgically repaired femoral hernia and appendectomy as a child. The
• patient takes no medications and does not use tobacco, alcohol. or recreational drugs.
• Temperature is 37.2 C (98.9 F). blood pressure is 112170 mm Hg. pulse is 98/min. and
• respirations are 18/mln. BMIIs 35 kg/m'. Examination shows an agitated woman who
• sits leaning forward on the bed. Her skin has no evidence of icterus or excoriations.
• Lungs are clear to auscultation and heart sounds are normal. There is moderate
• tenderness in the epigastrium but no guarding, rebound tenderness, or
• hepatosplenomegaly. Bowel sounds are normal. Laboratory results are as follows:
• Serum chemistries
• Albumin 4.8 g/dl
• Total bilirubin 1.0mg/dl
• Alkaline phosphatase 291 U/L
• Aspartate aminotransferase 133 U/L
• Alanine aminotransferase 172 U/L
• Amylase 2610 U/L
• Lipase 3680 U/L
• Triglycerides 110mg/dl
• Calcium 8.9 mg/dl
• Hemoglobin 12.6 g/L
• Platelets 340,000/mm3
• Leukocytes 14,100/mm3.
•
• Which of the following is the best next step in evaluating the underlying etiology of the patient’s acute conditon
• 1) CT scan of the abdomen
• 2) HIDA scan
• 3) Radiograph of the abdomen
• 4) Abdominal Ultrasound
5) Serologic testing for viral titers.

22. 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 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

23. Famous People who hadFamous People who had APAP
• Alexander the Great
• Ludwig von Beethoven
• Dizzie Gillespie
• Maximilian Schell
• Matthew Perry
• John Ashcroft
Acute

24. WORKUP
• HEMATOLOGICAL
investigations
• RADIOLOGICAL
investigations
• Miscellaneous investigations

25. 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

26. Hematological
• ABG’s
• Acid-Base Disturbance Etiology
• Metabolic (lactic) acidosis with high anion gap Hypovolumic shock
• Chloride responsive Hypokalemic Hypochloremic Persistant Vomiting
metabolic alkalosis.
Respiratory Acidosis ARDS/Resp Failure
• 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),

27. Hematological
• Pancreatic Enzyme’s Assay
– Serum Amylase:
• ONSET: almost immediately
• PEAK: within several hours
– Serum Lipase:
• more sensitive/specific than amylase
• Remains elevated longer than amylase(12
days)
• Useful if late presentation
– 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 INDICATOR OF HIGHEST

28. • 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%)

29. Plain X-ray abdomen erect AP view
• Xray erect abdomen is non-diagnostic and non-specific but there
are some signs which may be found in acute pancreatitis.
• Sentinel loop sign
• Localized isolated distended gut loop ( ileus) seen near th site of inflammed
organ
• Colon cutoff sign
• Gas filled ( distended) segment of proximal ( mainly transverse) colon
associated with narrowing of the splenic flexure.
• Renal Halo sign
• Peripancreatic inflammatory reaction with extension into pararenal space.

30. Sentinel Loop Sign

31. Colon Cut off Sign

32. Renal Halo Sign

33. Abdominal U/S
• 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

34. Contrast enhanced CT 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.
• When do I Order a CT scan ???
• If the patient has
• Signs of severe acute pancreatitis
• No signs of clinical improvement after several days.
• Diagnostic dilemma
• Infection suspected
• Temp > 101 F
• Positive blood cultures
What Kind of CT??
Dynamic with rapid bolus of IV contrast ( CT with pancreatic
protocols )
What are you looking for on CT??
Necrosis: Lack of enhancment with contrast
Fluid collections
Alternate diagnosis.

35. CT scan Findings
• Pancreas
• Pancreatic enlargement
• Decreased density due to edema
• Intrapancreatic fluid collections
• Blurring of gland margins due to inflammation
• Peripancreatic
• Fluid collections and stranding densities
• Thickening of retroperitoneal fat
* It may take up to 72h for inflammatory changes to become apparent on
CT *
Acute

36. CT Scan FindingsCT Scan Findings
Tail
Indistinct
Intraperitoneal
fluid
PANC
Acute
LIVE
R

37. Severe Pancreatitis
Peripancreatic edema
and inflammation
Unenhancing
Necrosis
PANC
Acute
LIVE
R
GB

38. Acute

39. Therapeutic Indications of CT
– 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

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

41. MRCP
• 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

42. Endoscopic US
• 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.

43. ERCP
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

44. Clinical Severity Scoring
Systems
ACUTE PANCREATITIS SPECIFIC SCORING
SYSTEMS
–Ranson score
– Atlanta Score
–POP score ( Panreatic outcome Prediction 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

45. Radiographic Severity Scoring
System
• Baltazor scoring system
• CT severity Index

46. Ranson’ score

47. Atlanta Score

51. Management Questions
Acute
• When should patients admitted with AP be monitored
in an ICU or step-down unit?
• Should patients with SAP receive prophylactic abx?
• What is the optimal mode and timing of nutritional
support for the patient with SAP?
• What are the indications for surgery in AP; optimal timing for
intervention, and roles for less invasive approaches including
percutaneous drainage and laparoscopy?

52. When do I transfer to unit?
Acute
• Severe pancreatitis
• Multi-organ failure
• Pulmonary
• Renal
• Consider it if you are placing the
patient on antibiotics and/or
ordering a CT to evaluate non-
improvement

53. Management
Acute
Mild-Moderate
•NPO with IVF (crystalloid)
• Colloid (blood if Hct <25, albumin if serum alb <2)
•Closely follow
•Generous narcotic
•NGT decompression
• if frequent emesis or evidence of ileus on plain films
•Start clear liquids when pain/anorexia resolve
•DO NOT follow amylase and lipase levels

54. • A 44-year-old woman comes to the emergency department with severe epigastric pain
• that radiates to her back. The pain was sudden in onset and has remained steady for
• the past several hours. She has associated nausea and vomiting. The
• patient takes no medications and does not use tobacco, alcohol. or recreational drugs.
• Temperature is 37.2 C (98.9 F). blood pressure is 112170 mm Hg. pulse is 98/min. and
• respirations are 18/mln. BMIIs 35 kg/m'. Examination shows an agitated woman who
• sits leaning forward on the bed. Her skin has no evidence of icterus or excoriations.There is moderate
• tenderness in the epigastrium but no guarding, rebound tenderness, or
• hepatosplenomegaly. Bowel sounds are normal. Laboratory results are as follows:
• Serum chemistries
• Albumin 4.8 g/dl
• Total bilirubin 1.0mg/dl
• Alkaline phosphatase 271 U/L
• Aspartate aminotransferase 133 U/L
• Alanine aminotransferase 172 U/L
• Amylase 2610 U/L
• Lipase 3680 U/L
• Triglycerides 110mg/dl
• Calcium 8.9 mg/dl
• Hemoglobin 12.6 g/L
• Platelets 340,000/mm3
• Leukocytes 14,100/mm3.
• Diagnosis of Acute pancreatits was made. He was started on IV fluid and analagesic. His condition didn’t
improved. CT scan was done which showed 35% necrosis. What is the next best step in the management of this
patient.
• A) Necrosectomy
• B) IV antibiotics
• C) Percutaneous aspiration
• D) IV steroids

55. When Do I start Antibiotics?
Acute
• Acute pancreatitis with infection ~ 10%
• 30-50% of those with necrosis get infection
• Prophylactic antibiotics
• Controversial
• No benefit in mild acoholic pancreatitis
• Imipenem or meropenem in necrotizing pancreatitis
• Selective gut decontamination may be beneficial
• Abx do not appear to promote fungal infection
• General recommendations for use:
• Biliary pancreatitis with signs of cholangitis
• > 30% necrosis on CT scan

56. When can Patient Eat?
Nutritional issues in AP
• It is no longer acceptable to rest the pancrease by avoiding nutrition.
• TNP vs Enteral feeding ?
– No TPN per meta-analysis unless the calculated nutritional
requirements cannot be achieved by enteral route only.
– Enteral feeding should be commenced after initial fluid resuscitation and
within first 24 hours of admission.
– NJ feeding better then NG feeding but first start with NG feeding.
– If there is feeding intolerance with NG then the tube can be advanced to
the jejunum by endoscopy or floroscopy.
• Early initiation of enteral nutriton in severe AP
– Tube feed if anticipate NPO > 1week
– Reduce microbial translocation
– Enhance gut mucosal blood flow
– Promote gut mucosal surface immunity
– These all reduce incidence of infected necrosis

58. 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

59. Complications of AP
Localized Collection:
Systemic collection

61. Management of Pancreatic Complications
• Infected necrosis
• Organisms on gram
stain after aspirate
• Surgical drainage
• Trans-gastric drainage
• Try to delay
necrosectomy 2-3wk
for demarcation of
necrosis
• Pancreatic
abscess
• CT or EUS guided
drainage
• Walled collection of
pus
• Similar to
management of
pseudocyst

62. Pseudocyst
Acute
• Collection of pancreatic fluid
enclosed by non-epithelialized wall
of granulation tissue
• Complicates 5-10% cases of AP
• ~ 4 weeks after insult
• 25-50% resolve spontaneously

63. Complications of Pseudocyst
Acute
• Infection - 14%
• Rupture - 6.8%
• Hemorrhage - 6.5%
• Common bile duct obstruction - 6.3%
• GI obstruction - 2.6%

64. Management of Pseudocyst

65. Pseudocyst Drainage Techniques
• Endoscopic
• Surgical
• RadiologicPC
Acute
PC
Liver
Stom

66. Endoscopic Cystogastromy

67. When to discharge Pateint?
• Pain is well controlled with oral analgesia
• Able to tolerate an oral diet that maintains
their caloric needs.
• All complications have been addressed
adequately.

68. Laproscopic cyst gastrostomy
Acute

69. Any QuestionAny Question