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Acute pancreatitis
Feb 7, 2019 • Download as PPTX, PDF
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Acute Pancreatitis general surgery undergraduate MBBS Medical School Complication of Acute Pancreatitis
Ranson Criteria Alcohol Pancreatitis Gallstone Cullen sign Grey turner sign Increased serum amylase ERCP
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Rifhan Kamaruddin
CTSeverityIndex:Balthazar+NecrosisScore
CTSeverityIndex

Pancreaticinflammation points
Normalpancreas 0
B Enlargementofthepancreas 1

C Peripancreaticinflammation 2

D 1acuteperipancreaticfluidcollection
E >2acuteperipancreaticfluidcollections 4

Pancreaticnecrosis None 0

<30% 2

30%-50% 4
>50% 6

Maximum10points
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Acute pancreatitis
1. Acute Pancreatitis
2. Outline of Presentation • Anatomy of Pancreas • Aetiology • Pathophysiology • Clinical Approach – History and Physical Examination •
Di!erential Diagnosis • Investigation • Assessment of Severity • Management of Acute Pancreatitis • Complications
3. ANATOMY OF PANCREAS
4. Anatomy • Retroperitoneal organ • In adults- 15cm long & 70-100 weighs • 3 portions- head, body and tail • Relations: Head Neck
Uncinate Body Tail
5.
6.
7. • Main pancreatic duct- Wirsung duct • Acessory duct – Santorini duct
8.
9.
10. Pancreatitis Acute presenting with abdominal pain and is usually associated with raised pancreatic enzyme levels in the blood or
urine as a result of pancreatic inflammation. Chronic
11. Incidence • 3 % of all cases of abdominal pain • Hospital admission rate for is 9.8 per 100 000 population anually • Worldwide, 50 per
100 000 cases anually. • The disease may occur at any age, with a peak in young men and older women.
12. Etiology Two major causes are : • biliary calculi (50–70%) • alcohol abuse (25%) The remaining cases may be due to rare causes or be
idiopathic
13.
14.
15. Gallstone Pancreatitis • Transient blockage of common bile duct reflux of bile into pancreatic duct and impair flow of normal
pancreatic juice premature activation of pancreatic enzymes within duct system.
16. Alcohol Pancreatitis • High risk in: 1. Long standing alcohol intake for at least 2 years or single session of heavy drinking 2.
Consumption >80g/day • What Happened ? 1. Direct toxic e!ect of alcohol in genetically predisposed individuals 2. Viscid secretion of
pancreatic juice formation of protein plugs and impairment of flow
17. Pathophysiology • Premature activation of pancreatic enzymes within the pancreas, leading to a process of autodigestion. •
Anything that injures the acinar cell and impairs the secretion of zymogen granules, or damages the duct epithelium and thus delays
enzymatic secretion, can trigger acute pancreatitis. • Once cellular injury has been initiated, the inflammatory process can lead to
pancreatic oedema, haemorrhage and, eventually, necrosis. • As inflammatory mediators are released into the circulation, systemic
complications can arise.
18.
19. ACUTE PANCREATITIS History and Physical Examination
20. Purpose of History Taking • Pain • Causes • Complications
21. History Taking 1) Abdominal Pain - Remember SOCRATES! • Site: Di!use, upper abdominal pain • Onset: Sudden • Character: Boring
Pain • Radiation: Radiates to the back • Associated factor: Nausea, vomiting, dyspnea • Timing: Pain escalates in intensity and peaks within
10-20 minutes of onset.
22. • Aggravating and relieving factor: Aggravated by breathing with increased chest expansion and relieved by leaning forward. •
Severity: Depending on severity, patient may present in shock
23. 2) History of underlying causes ‘I GET SMASHED’ • Idiopathic (10%) • Gallstone (45%) • Ethanol (35%) • Trauma (10%) • Steroids •
Mumps • Autoimmune • Scorpion / Snake • Hyperlipidemia • ERCP • Drugs (10%)
24. 3) History of Complications Systemic : • ARDS • Renal Failure • Shock, arrythmias • Metabolic: hypocalcemia, hyperglycemia •
Encephalopathy
25. Local : • Mostly develop silently • Pancreatic abscess – high grade fever • Pseudocyst • Pancreatic e!usion
26. Physical Examination: Acute Pancreatitis • Elevation of body temperature is o"en is acute pancreatitis
27. • Abdominal Examination 1. Inspection: abdominal distension 2. Palpation: • Hepatomegaly • Tenderness • Cullen sign • Gray turner
sign • Peritoneal signs • Rigidity • Guarding
28.
29. • Percussion : Dullness suggesting ascites • Auscultation: auscultate the abdomen for hypoactive or an absent bowel sounds or an
abdominal bruit. Ileus is common in pancreatitis. • Ausculation of lungs: 10-20% of patients have pulmonary findings, commonly le" sided
findings. 1. Basilar rales 2. Atelectasis 3. Pleural e!usion
30. Presented by Siti Nur Rifhan Kamaruddin DIFFERENTIAL DIAGNOSIS INVESTIGATIONS SEVERITY SCORING
31. Di!erential Diagnosis For Mild Acute Pain For Severe Acute Pain Acute Cholecystitis Fecal Peritonitis due to Perforated Colon Peptic
Ulcer Disease Ruptured Abdominal Aortic Aneurysm Inferior Myocardial Infarction Ruptured Ectopic Pregnancy Acute Appendicitis
Massive Bowel Infarction
32. INVESTIGATIONS
33. Investigations • The diagnosis if made on basis of clinical presentation, an elevated serum Amylase level and characteristic Imaging
features. • Biological : - Serum Amylase increase 3x than normal or more than 1000IU/mL (Peak within the first 24hours a"er onset of
Symptom) - Serum Lipase has longer half life thus more useful in delayed cases. - Serum Lipase: more sensitive & specific for Pancreatitis
than Amylase
34. Other Causes of Increased Serum Amylase : • Renal Failure • Liver Cirrhosis • Peritonitis • GIT Inflammation • Ruptured Ectopic
Pregnancy/Salphingitis • Salivary Gland Inflammation (Parotitis)
35. Other Blood Tests.. Full Blood Count Elevated Leucocytes count for Ranson’s Criteria and to predict prognosis LFT To asses cause of
Pancreatitis/obstructive jaundice BUSE To determine level of dehydration Random Blood Glucose Damage to beta cells interferes with
insulin production causing Hyperglycemia (in severe cases) Serum Calcium Hypocalcaemia suggests saponification
36. Role of Imaging in Acute Pancreatitis • To clarify diagnosis when the clinical picture is confusing • To determine possible causes • To
assess severity (Balthazar Score) and thus to determine prognosis • To detect complications
37. Imaging : Ultrasound • Trans abdominal USG : Does not establish a diagnosis. • USG should be performed within 24 hours in ALL
patients - To detect gallstones - To rule out Acute Cholecystitis - To determine whether the common bile duct is dilated • To evaluate
change on pancreas i.e. edema, mass in Pancreas
38. • Transverse Transbadominal Ultrasound shows a swollen pancreatic body with ill- defined heterogeneous hypoechoic pattern.
39. ERCP • Diagnostic and therapeutic • To look for Gallstones, CBD stones or CBD dilatation • In patient with severe acute gallstone
pancreatitis & signs of on going biliary obstruction and cholangitis – an urgent ERCP should be sought.
40. ERCP : Gallstone Pancreatitis
41. Plain Abdominal X-Ray • Plain erect chest & abdominal X-ray are not diagnostic of Acute Pancreatitis but are useful in di!erential
diagnosis. • Non specific findings in Pancreatitis : Generalized or local ileus (Sentinel Loop), a colon cut o! sign, and calcified gallstones. •
Erect CXR. Look for pleural e!usion. In severe cases, a di!use alveolar shadowing (Acute Respiratory Distress Syndrome)
42. A focal dilated proximal jejunal loop in the le" upper quadrant. A focal area of adynamic ileus close to an intraabdominal
inflammatory process The sentinel loop sign may aid in localizing the source of inflammation. Sentinel Loop in upper abdomen may
indicate Pancreatitis
43. -Colon Cut-o! Sign describes gaseous distension seen in proximal colon - Associated with narrowing of splenic flexure in cases of
Acute Pancreatitis - This Appearance results from inflammatory process extending from Pancreas into the phrenicolic ligament via
transverse mesocolon
44. CT Scan • Not necessary for all patients. • May reveal pseudo cyst or abscess (complication of acute pancreatitis) • A contrast-enhanced
CT is indicated in following : If there is diagnostic uncertainty In Pt. with severe acute Pancreatitis to distinguish interstitial from
necrotizing pancreatitis. In Pt. with organ failure, signs of sepsis or progressive clinical deterioration When a localized complication is
suspected I.e. fluid collection, pseudo cyst.
45. CT Anatomy Pancreatic Level
46. CT shows significant swelling & Inflammation of the Pancreas
47. Morphologic Types of Acute Pancreatitis THE REVISED ATLANTA CLASSIFICATION 1) Interstitial Edematous Pancreatitis 2) Necrotizing
Pancreatitis • Parenchymal necrosis • Peripancreatic necrosis • Combined Type
48. Interstitial Edematous Pancreatitis • Pancreatic Enlargement due to edema • Pancreatic Parenchyma shows relatively homogenous
enhancement & peripancreatic fat stranding • Outcome : Symptoms usually resolve within first week
49. - Inflammation associated pancreatic parenchymal necrosis orperipancreatic necrosis - Cause impairment of pancreatic perfusion -
Impairment evolve over several days - Early CECT may underestimate extent of disease Necrotizing Pancreatitis (5-10%)
50. Pancreatic Fluid Collection : Revised Atlanta 2012 85% 15%
51. Local Complications should be suspected if : Persistence or recurrence of abd. pain Secondary increases in Serum Pancreas
activity Increasing organ dysfunction Development of clinical signs of Sepsis i.e. fever, leucocytosis Prompt CECT to be done in these
cases. Pancreatic Fluid Collection : REVISED ATLANTA 2012 •Acute Peripancreatic Fluid Collection (APFC) •Pancreatic Pseudocyst (PP)
•Acute Necrotic Collection (ANC) •Walled-o! Necrosis (WOPN)
52. 1) Acute Peripancreatic Fluid Collection (APFC) • Peripancreatic Fluid associated with IEP with no necrosis • Usually seen within first 4
weeks • Homogenous collection of fluid • Usually resolve spontaneously • When a localised APFC persists > 4 weeks – develop into a
Pseudocyst
53. 2) Pancreatic Pseudo cyst • Encapsulated collection of fluid with a well defined inflammatory wall usually outside the pancreas • With
minimal or no necrosis • Usually round or oval • Appears a"er 4 weeks of onset IEP -Note the two round, homogenous fluid collection with
a well defined borders - White stars denote normal enhancing pancreas
54. 3) Acute Necrotic Collection (ANC) • A collection containing of both fluid & necrosis • < 4 weeks • Occurs only in setting of NP • Single or
multiple heterogeneous collection • No defined wall -Note enhancement of entire pancreatic Parenchyma (Whitestars) - Note the
heterogeneous, non-liquid component in retroperitoneum (White arrows pointing at the borders of ANC)
55. 4) Walled-o! Necrosis (WON) • A mature, encapsulated collection of pancreatic /peripancreatic necrosis • that has developed a well-
defined inflammatory wall • Appears >4 weeks a"er onset of NP • Heterogeneous with liquid & non-liquid density -Note the Area of non-
liquid components of high attenuation (black arrows) in the collection - It has a well defined, enhancing wall (White arrows)
56. - Homogenous, low attenuation fluid density - NO solid component Pseudocyst (PC) vs. Walled-o! Necrosis (WON) -Heterogeneous
with liquid and solid densities
57. SUMMARY: Local Complications of AP
58. CT Severity Index: Balthazar + Necrosis Score A B C D E
59. Assessment of Severity Ranson Score Glasgow Scale APACHE II Score
60. Severity: RANSON’S SCORE To predict severity of acute pancreatitis. On Admission (LEGAL) L – Leucocytes >16000 E – Enzyme AST >
250 G – Glucose > 200 A – Age > 55 L – LDH > 350 During Next 48 Hours (C.HOBBS) C – Calcium 8mg/dl H – Hematocrit fall of >10% O2– Pa02
< 60mmHG B – Base deficit > 4mmol/L B – BUN rise > 5 S – Sequestration (Fluid) > 6 litres 3 or more factors present – SEVERE
61. Glasgow Scale 3 OR MORE FACTORS PRESENT - SEVERE
62. APACHE II SCORE Score > 8 : Severe Acute Pancreatitis
63. Management of Acute Pancreatitis Presented By Fariza Asilah Ahmad Rahim
64. Mild Acute Pancreatitis 1. Nil by mouth 2. Fluid resuscitation : 4 pints 3. Analgesia : IM Tramal 50mg TDS 4. Treat underlying cause 5.
No role for antibiotics
65. Severe Acute Pancreatitis • Admission to intensive care or high- dependency unit 1. Oxygen supplementation 2. Analgesia 3.
Aggressive fluid rehydration 4. Monitor vital signs 5. Monitor haematological & biochemical parameters
66. 6. Nasogastric drainage 7. Antibiotic prophylaxis –imipenem, cefuroxime 8. CT scan 9. ERCP within 72 hours 10. Supportive therapy
for organ failure 11. Nutritional support
67. Complications of Acute Pancreatitis
68. SYSTEMIC • Cardiovascular - shock - arrhythmia • Pulmonary - ARDS • Renal failure • Haematological - DIC • Gastrointestinal - Ileus
69. SYSTEMIC • Metabolic - Hypocalcaemia - Hyperglycaemia - Hyperlipidaemia • Neurological - Visual disturbance - Confusion -
Encephalopathy • Miscellaneous - Arthralgia
70. • Acute fluid collection • Sterile pancreatic necrosis • Infected pancreatic necrosis • Pacreatic abscess • Pseudocyst LOCAL
71. • Pancreatic ascites • Pleural e!usion • Portal or systemic vein thrombosis • Pseudocyst LOCAL
72. Complications & their Management Acute fluid collection No intervention unless pressure e!ect Aspirate under US or CT
guidance OR Transgastric drainage under EUS guidance Pancreatic necrosis No intervention
73. Infected pancreatic necrosis Aspirate under CT guidance Percutaneous drainage Prophylactic antibiotic
74. If patient deteriorates Necrosectomy Closed continuous lavage Closed drainage Open packing Closure and relaparotomy
75. Pancreatic abscess Percutaneous drainage Antibiotic cover Pancreatic ascites Drainage Parenteral or jejunal feeding
76. Pancreatic e!usion Percutaneous drainage under CT guidance Portal or systemic vein thrombosis Aspirin in the early
process
77. Pseudocyst Percutaneous transgastric cystogastrotomy and place double-pigtail drain Endoscopic under EUS guidance and
place tube drain Surgical drainage – internal drainage into gastric or jejunum lumen
78. Cystogastrotomy
79. Reference BAILEY, H., LOVE, R. J. M., MANN, C. V., & RUSSELL, R. C. G. (1992). Bailey and Love's short practice of surgery. London,
Chapman & Hall Medical. COLLEDGE, N. R., WALKER, B. R., RALSTON, S., & DAVIDSON, S. (2010). Davidson's principles and practice of
medicine. Edinburgh, Churchill Livingstone/Elsevier.

Editor's Notes
1. Normal Amylase : 85Normal Lipase : The 3rd criteria is only required to establish diagnosis if the first
two criteria are not met. Imaging is of utmost importance for the detection of complications and to
help guide the treatment.
2. Normal Amylase : 85Amylase /Lipase only 40-60% sensitive for Pancreatitis, Amylase 70-80% specific,
80-90%specific
3. IEP : Di!use or lozalised enlargment of pancrease d/t inflammatory edemaNP:
4. Assessment of Clinical Parameters ( Vital Signs, Electrolytes, ABG)Point Allocated in accordance to
agePoint added for co-morbid disease or chronic health Pt A + B + C > 8 : severe acute Pancreatitis

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