ACUTE PANCREATITIS.pptx

DR sujan pandey
CMC chitwan

1. ACUTE PANCREATITIS DR SUJAN PANDEY SURGERY RESIDENT 1

2. OUTLINE INTRODUCTION DEFINITION EPIDEMIOLOGY ETIOLOGY PATHOPHYSIOLOGY CLINICAL FEATURES INVESTIGATION ASSESSMENT OF SEVERITY OF DISEASE 2

3. INTRODUCTION The name ‘pancreas’ is derived from the greek ‘pan’ (all) and ‘ kreas ’ (flesh ). The average gland weighs between 75 and 125 gm and measures 10 to 20 cm. Retroperitoneal organ that lies in an oblique position, sloping upward from the C-loop of the duodenum to the splenic hilum . Due to its retroperitoneal location, pain associated with pancreatitis often is characterized as penetrating through the back. 3

4. Anatomically divided into 4 parts : ① Head ② neck ③ Body ④ Tail 4

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6. Arterial supply of pancreas 6

7. Main pancreatic duct:wirsung duct Acessory duct: santorini duct 7

8. PANCREATITIS  Inflammation of the pancreatic parenchyma . Types : Acute : Emergency condition . 2. Chronic : Prolonged & frequently lifelong disorder resulting from the development of fibrosis within the pancreas. 8

9. DEFINITION ACUTE PANCREATITIS:  Acute condition of diffuse pancreatic inflammation & autodigestion , presents with abdominal pain, a threefold or greater rise in the serum levels of the pancreatic enzymes amylase and lipase, and or characteristic findings of pancreatic inflammation on contrast enhanced CT. • Reversible inflammation of the pancreas • Ranges from mild to severe. 9

10. EPIDEMIOLOGY Acute pancreatitis accounts for 3% of all cases of abdominal pain among patients admitted to hospital in the UK. The hospital admission rate for acute pancreatitis is 9.8 per year per 100 000 population in the UK, although worldwide, the annual incidence may range from 5 to 50 per 100 000.  Women are affected more the men, but men are more likely to suffer recurrent attacks. 10

11. ETIOLOGY Two major causes are : • Biliary calculi (50–70%) • Alcohol abuse (25 %) The remaining cases may be due to rare causes or be idiopathic. 11

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13.  Mnemonic for the causes of Acute Pancreatitis: ‘I get smashed‘ I diopathic G allstones E thanol T rauma S teroids M umps A utoimmune S corpion / S nakes H yperlipidaemia / H ypercalcaemia E RCP D rugs 13

14. Biliary Pancreatitis : Common channel theory 2 . Incompetent sphincter of Oddi 3 . Obstruction of the pancreatic duct 14

15. Alcoholic Pancreatitis : - Direct toxic effect on the pancreatic acinar cells -Stimulation of the pancreatic secretion -Constriction of the sphincter of Oddi 15

16. PATHOPHYSIOLOGY Exact mechanism of AP not completely known . Most researchers believe that AP begins with the activation of zymogens inside acinar cells, which causes acinar cell injury . Severity of AP may be determined by the events that occur subsequent to acinar cell injury, which include release of cytokines and other chemical mediators of inflammation. 16

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18. Events of pathogenesis of Acute Pancreatitis include: A . Precipitating Initial Events B . Intrapancreatic Events C . Systemic Events 18

19. A. Precipitating Initial Events Acinar Cell Events. When acinar cells are pathologically stimulated, their Lysosomal (L) & Zymogen(Z) contents colocalize , consequently trypsinogen is activated to trypsin by cathespin B. Increased cytosolic Calcium is required . Cathespin B and other contents of these colocalized organelles are released . Cathespin B activates apoptosis by causing cytochrome c to be released from mitochondria. 19

20. Activation of PKC results in a sudden activation of NF Kappa beta Which triggers release of Cytokines Cytokines attract inflammatory response cells which mediate local & syst. inflammation 20

21. Intrapancreatic Events After activation of superoxides (“Respiratory burst”) and release of proteolytic enzymes ( cathespin , elastase and collagenase), activated neutrophils are attracted to focus of tissue injury . Macrophages release TNF- alfa , IL-6 & IL-8 which mediate the local and systemic inflammatory response The inflammatory mediators cause increased pancreatic vascular permeability – leading to edema, hemorrhage & microthrombi Failure of pancreatic microcirculation resulting in pancreatic hypoperfusion & necrosis 21

22. Systemic Events Organ failure can develop at any stage of acute pancreatitis . The development pancreatic necrosis, the breakdown of the interstitial barrier and suppression of immune response contribute to the development of infected pancreatic necrosis . This may associated with late development of SIRS or MODS Organ failure is scored using the Marshall or Sequential Organ Failure Assessment system(SOFA). The 3 organ system most frequently involved are Cardiovascular, Respiratory an Renal. 22

23. SIRS 23

24. Having a persistent SIRS throughout hospital admission, having a transient SIRS, or never meeting SIRS criteria has been associated with mortality rates of 25%, 8%, and 0%, respectively. 24

25. MODIFIED MARSHALL SCORE 25

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27. DIAGNOSIS A . Clinical presentation B . Investigation c.Imaging 27

28. Revised Atlanta Criteria Diagnosis of acute pancreatitis, which states that acute pancreatitis requires at least 2 of the following three criteria : 1) Abdominal pain and physical exam consistent with pancreatitis 2) lipase or amylase levels three times the upper limit of normal and 3 ) imaging (CT, MRI, ultrasound) findings that are consistent with acute pancreatitis. 28

29. CLINICAL PRESENTATION  History and Physical Examination :   Abdominal Pain – ( SOCRATES) • Site: Diffuse, upper abdominal pain ( epigastric ) • 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. 29

30. 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( Tachypnea, tachycardia and hypotension may be present  ) 30

31. Physical Examination Elevation of body temperature is often in acute pancreatitis . In gallstone pancreatitis icterus may be present . 31

32. Abdominal Examination 1 . Inspection : abdominal distension ( ileus,ascites ) 2 . Palpation : Hepatomegaly Tenderness ( epigastric region) Cullen sign Gray turner sign FOX’S sign Guarding/Rigidity 32

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34. Percussion : shifting dullness suggesting ascites Auscultation : hypoactive or an absent bowel sounds . Ileus is common in pancreatitis. Ausculation of lungs : 10-20% of patients have pulmonary findings, commonly left sided findings. Basilar rales Atelectasis Pleural effusion 34

35. Differential Diagnosis Perforated viscus (DU) Acute cholecystits , Biliary colic Acute intestinal obstruction Esophageal rupture Mesenteric vascular obstruction Renal colic Dissecting aortic aneurysm Myocardial infarction Basal pneumonia Diabetic ketoacidosis 35

36. INVESTIGATIONS Serum Amylase : Sensitivity : 72% Specificity : 99% Released within 6-12 hours of the onset, & Remains elevated for 3-5 days. Elevation ˃ 3X normal is significant. Undergoes renal clearance. After its serum levels decline, its urinary level remains elevated. Its level doesn't correlate with the disease activity. 36

37. Other Causes of Increased Serum Amylase Renal Failure Liver Cirrhosis Peritonitis GIT Inflammation Mesentric ischemia Ruptured Ectopic Pregnancy/ Salphingitis Salivary Gland Inflammation ( Parotitis ) 37

38. Serum Lipase : More pancreatic-specific than s. Amylase. Sensitivity : about 100% , Specificity : 96% Remains elevated longer than amylase (7 to 14 days). Useful in patients presenting late to the physician. S . Amylase tends to be higher in gallstone pancreatitis S . Lipase tend to be higher in alcoholic pancreatitis 38

39. 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 . Random Blood Glucose: Damage to beta cells interferes with insulin production causing Hyperglycemia (in severe cases ) Serum Calcium : Hypocalcaemia suggests saponification 39

40. Serum albumin is low in 10% of patients and indicates severe pancreatitis. Markedly elevated LDH (>500U/dl) suggests poor prognosis. Serial assessment of C-reactive is a good indicator of progress . ABGs show hypoxia. 40

41. IMAGING  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 41

42. Chest x-ray Not diagnostic of AP but are useful in differential diagnosis . Non specific findings in Pancreatitis : Generalized or local ileus (Sentinel Loop), a colon cut off sign, and calcified gallstones. Erect CXR : Look for pleural effusion. In severe cases, a diffuse alveolar shadowing (Acute Respiratory Distress Syndrome) 42

43. A focal dilated proximal jejunal loop in LUQ SENTINEL LOOP SIGN COLON CUT OFF SIGN 43

44. 44 PLEURAL EFFUSION

45. USG 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 i n Pancreas 45

46. Transverse Transbadominal Ultrasound shows a swollen pancreatic body with ill- defined heterogeneous hypoechoic pattern. 46

47. USG cannnot clearly delineate extrapancretic spread of pancreatic inflammation or identify necrosis within the pancreas; these important findings are the best seen by CECT. 47

48. CT SCAN Gold standard. Done 72 hours after acute attack.  48

49. A contrast-enhanced CT is indicated in following : If there is diagnostic uncertainty severe acute Pancreatitis to distinguish interstitial from necrotizing pancreatitis . In Pt. with organ failure(MODS), signs of sepsis or progressive clinical deterioration Local complication is suspected I.e. fluid collection, pseudo cyst. 49

50.   Peripancreatic stranding (arrow). Multiple gallstones in the gallbladder Peripancreatic stranding (arrow). Multiple gallstones in the gallbladder 50

51. Pancreatic edema with peri -pancreatic inflammatory changes. 51

52. Contrast-enhanced CT: acute necrotising pancreatitis. Pancreatic area of reduced enhancement, peripancreatic edema and stranding of the fatty tissue 52

53. Pancreatic Necrosis. Lack of gland enhancement following IV contrast administration is diagnostic. 53

54. Pancreatic abscess. Large, relatively well-circumscribed heterogeneous collection containing gas bubbles inferior to the pancreatic head. 54

55.  Pancreatic pseudocyst 55

56. ERCP Diagnostic and therapeutic T o 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. 56

57. ERCP 57

58. ERCP IN ACUTE PANCREATITIS 58

59. ERCP: GALLSTONE PANCREATITIS 59

60. MRCP Both enhanced and non enhanced ,has a strong correlation with contrast-enhanced CT in acute pancreatitis. Greater sensitivity compared to CT to detect mild acute pancreatitis. Better categorize fluid collection ,necrosis, abscess,hemorrhage and pseudocyst . Delineates the pancreatic and bile ducts. 60

61. MRCP 61

62. ASSESSMENT OF SEVERITY OF DISEASE Ranson Prognostic criteria B . Acute Physiology And Chronic Health Evaluation (APACHE II)score C . Computed Tomography Severity Index (CTSI) D . Atlanta Criteria for Acute Pancreatitis 62

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64. Acute Physiology and Chronic Health Evaluation (APACHE II) Score : Based on patient’s age, previous health status and 12 routine physiologic measurements. The main advantage is that it can be used on admission and repeated at any time. APACHE II score of 8 or higher defines severe pancreatitis . APACHE II has a positive predictive value of 43% and a negative predictive value of 89 %. 64

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66.  Atlanta Criteria for Acute Pancreatitis Organ Failure, as Defined by Shock (SBP <90mm Hg) Pulmonary insufficiency (PaO2 <60 mm Hg) Renal failure ( creatinine level >2 mg/dl after fluid resuscitation) Gastrointestinal bleeding (>500 ml/24 hrs ) Systemic Complication DIC ( platelet ≤10,000) Fibrinogen <1 g/L Fibrin split products >80 mcg/dl Metabolic disturbance (calcium level ≤7.5 mg/dl ) Local Complications Necrosis Abscess Pseudocyst 66

67. Based on the severity of the disease A cute pancreatitis is divided into the following types; In mild acute pancreatitis , there is the absence of local or systemic complications and organ failure. In moderately severe acute pancreatitis are local complications with or without organic failure for less than 48 hours. In severe acute pancreatitis , there is persistent organ failure for more than 48 hours with the involvement of one or more than one organ. 67

68. C –REACTIVE PROTEIN I nflammatory marker , peaks 48 to 72 hours after the onset of pancreatitis . C orrelates with the severity of the disease . A CRP level of >=150 mg/mL defines severe pancreatitis. The major limitation is that it cannot be used on admission; sensitivity decreases if CRP levels are measured within 48 hours after the onset of symptoms . In addition to CRP, a number of studies have shown. Biochemical markers (e.g., serum levels of procalcitonin , IL-6 , IL- 1 , elastase ) that correlate with the severity of the disease. 68

69. REFERENCE SABISTON 21TH EDITION BAILEY AND LOVE 27 TH EDITION SCHWARTZ’S 10 TH EDITION 69

70. THANK YOU 70