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Acute pancreatitis


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etiology & diagnosis

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Acute pancreatitis

  2. 2. Various etiology 1. Mechanical ampullary obstruction 2. Alcohol 3. Smoking 4. Hypertriglyceridemia 5. Post ERCP 6. Hypercalcemia 7. Genetic mutation 8. Drugs 9. Infection & toxins 10. Trauma 11. Pancreatic divisum 12. Vascular disease 13. Autoimmune 14. others
  3. 3. Machenical ampullary obstruction • Gall stone reflux of bile into the pancreatic duct/ obstruction due to stone or edema Gall stones (including microlithiasis) are most common cause of AP ( 35-40%) • Risk factor – male gender and stone size (3- 5mm)
  4. 4. • A serum ALT value 150 IU/L or more (3 times of normal upper value) carries PPV of 95% for the diagnosis of Billiary pancreatitis • Rule – All pt with first attack of AP should have an USG UA to search for Gall stone, CBD stone or signs of extrahepatic billiary tract obstruction
  5. 5. GB sludge • Billiary sludge is a viscous suspension, may contains microliths • Microscopic analysis of bile in setting of GB sludge often shows cholesterol monohydrate crystal or calcium bilirubinate granuales • Sludge typically found in patients with functional or machenical bile stasis –prolong fasting, with distal bile duct obstruction, TPN
  6. 6. Billiary sludge or microlithiasis • Most patient – asymptomatic • Billiary sludge is commonly found in 20-40% of patient with acute pancreatitis with no obvious cause • In the absence of any other etiology billiary sludge should be suspected as the cause in patients with AP with a transient elevation in Liver test. • Microlithiasis defined as a stone size ≤ 3 mm
  7. 7. • Ceftriaxone can complex with bile to form biliary shudge/ microlithiasis • On ultrasound, sludge appears as a mobile, low-amplitude echo that layers in the most dependent part of the gallbladder and without a DAS
  8. 8. Other causes- Ampullary obstruction • biliary ascariasis • Periampullary diverticula • pancreatic and periampullary tumors • Intraductal papillary mucinous neoplasms (IPMN) of the pancreas
  9. 9. ALCOHOL • Approximately 30 % of cases of AP • Only 5% to 10% of patients who drink alcohol develop AP • Act by increasing the synthesis of enzymes by pancreatic acinar cells (digestive & lysosomal) • Over-sensitization of acini to cholecystokinin • Other machenism – - It triggers proinflammatory pathways such as nuclear factor κB (NF-κB) - Also increases the expression and activity of caspases - Alcohol decreases pancreatic perfusion - Induces sphincter of Oddi spasm - obstructs pancreatic ducts through the precipitation of proteins inside the ducts Med Clin North Am 92:889–923, 2008, Cappell MS
  10. 10. SMOKING cigarette smoking is an independent risk factor for acute and chronic pancreatitis by mechanisms that are unclear
  11. 11. HYPERTRIGLYCERIDEMIA • Serum concentrations above 1000 mg/dL-ppt attacks of acute pancreatitis • A triglyceride level higher than 2000 mg/dL confirms the diagnosis in a setting of AP • Reported in children with inherited disorders of lipoprotein metabolism • Acquired causes – obesity, diabetes mellitus, hypothyroidism, pregnancy, estrogen or tamoxifen therapy, glucocorticoid excess, nephrotic syndrome, and beta blockers
  12. 12. HYPERCALCEMIA • Hypercalcemia of any cause can lead to acute pancreatitis • Proposed mechanisms include deposition of calcium in the pancreatic duct and calcium activation of trypsinogen within the pancreatic parenchyma Mithöfer K, J Gastroenterology. 1995;109(1):239. • Hyperparathyroidism
  13. 13. ERCP • AP is the most common complication after ERCP, occurring in up to 5% of patients • 90% to 95% of patients – mild pancreatitis • An elevation in the serum amylase concentration is common after ERCP occurring in up to 75 % of patients , but acute clinical pancreatitis after ERCP is much less common (5% among those who asymptomatic hyperamylasemia) Gastroenterol Clin North Am. 1990;19(4):793,Pieper-Bigelow C • Important factors are mechanical injury from instrumentation of the pancreatic duct and hydrostatic injury from contrast injection
  14. 14. Post ERCP AP • 3 % of patients undergoing diagnostic ERCP • 5 % undergoing therapeutic ERCP • Up to 25 percent undergoing sphincter of Oddi manometric studies Clin Endosc. 2012 Sep;45(3):305-12. Epub 2012 Aug 22. Kahaleh M,
  15. 15. Post-ERCP pancreatitis • factors increase the risk of post-ERCP pancreatitis –  Operator-related factors – Inadequate training Lack of experience  Patient-related factors – Younger age Female sex Normal serum bilirubin Recurrent pancreatitis Prior ERCP-induced pancreatitis Sphincter of Oddi dysfunction
  16. 16. Post ERCP AP  Procedure-related factors – Difficult cannulation, multiple attempts Inadvertent MPD canulation and contrast injection Sphincter of Oddi manometry Precut sphincterotomy Pancreatic sphincterotomy Minor papilla sphincterotomy Biliary balloon sphincteroplasty Ampullectomy Thermal injury from electrocautery- pancreatic orifice edema
  17. 17. Diagnosis • Post-ERCP pancreatitis is typically diagnosed when a patient with signs and symptoms of pancreatitis (eg, abdominal pain and tenderness) has elevated pancreatic enzymes (amylase and lipase) usually within the first 24 to 48 hr after the procedure • Patients who have undergone pancreatogram should be admitted if four-hour amylase (Amylase after 4 hour of procedure) level is greater than 2.5 times the upper limit of reference
  18. 18. Prevention All patients In high-risk patients Unclear efficacy Careful patient selection Pancreatic duct stent placement Nitrates Consider alternative modalities Single-dose rectal indomethacin Protease inhibitors Provider training and experience Intravenous fluid hydration Guide wire-assisted cannulation
  19. 19. GENETIC MUTATIONS • Inherited forms of pancreatitis may present as recurrent acute pancreatitis but eventually progress to chronic pancreatitis -Serine protease 1 gene (PRSS1) -cystic fibrosis gene (CFTR) -serine protease inhibitor Kazal type 1 (SPINK1)
  20. 20. DRUGS Various machenism –  Immunologic reactions - 6-mercaptopurine, aminosalicylates, sulfonamides  Direct toxic - diuretics, sulfonamides  Accumulation of a toxic metabolite - valproic acid, didanosine, pentamidine, tetracycline erythromycin, metronidazole  Ischemia - diuretics, azathioprine  Intravascular thrombosis - estrogen  Increased viscosity of pancreatic juice - diuretics and steroids
  21. 21. Anti cancer drugs • 6- Mercaptopurine • Azathioprine • L- Asparginase • Oxaliplatin • Rarely by Ifosfamide
  22. 22. INFECTIONS • Viruses – Mumps, coxsackievirus, hepatitis B, cytomegalovirus, varicella-zoster, herpes simplex, HIV • Bacteria – Mycoplasma, Legionella, Leptospira, Salmonella • Fungi – Aspergillus • Parasites – Toxoplasma, Cryptosporidium, Ascaris
  23. 23. Miscellaneous Conditions • Blunt and penetrating abdominal trauma can be associated with AP in 0.2% and 1% of cases, respectively • Prolonged intraoperative hypotension and excessive pancreatic manipulation during abdominal surgery can also result in AP • Pancreatic ischemia in association with acute pancreatic inflammation can develop after splenic artery embolization • Other rare causes include scorpion venom stings and perforated duodenal ulcers
  24. 24. Revised Atlanta 2012 ORIGINAL ARTICLE Peter A Banks, Acute Pancreatitis Classification Working Group
  25. 25. Definition of diagnosis of acute pancreatitis • Diagnosis requires any 2 of the following – a. Abdominal pain consistent with acute pancreatitis b. Serum lipase activity (or amylase activity) at least three times greater than the upper limit of normal c. Characteristic findings of acute pancreatitis on contrast-enhanced computed tomography (CECT) and less commonly magnetic resonance imaging (MRI) or transabdominal ultrasonography.
  26. 26. Imaging when: for diagnosis • If abdominal pain suggests strongly that acute pancreatitis is present, but the serum amylase and/or lipase activity is less than three times the upper limit of normal, as may be the case with delayed presentation, imaging will be required to confirm the diagnosis
  27. 27. Definition of onset of acute pancreatitis • The onset of acute pancreatitis is defined as the time of onset of severe abdominal pain at first during entire course of disease (not the time of admission to the hospital).
  28. 28. Definition of types of acute pancreatitis • Acute pancreatitis can be subdivided into two types – 1. Interstitial oedematous pancreatitis 2. Necrotising pancreatitis.
  29. 29. Interstitial oedematous pancreatitis • Defined as diffuse (or occasionally localised) enlargement of the pancreas due to inflammatory oedema.
  30. 30. CECT: Interstitial oedematous pancreatitis • Pancreatic enlargement due to edema • pancreatic parenchyma shows relatively homogeneous enhancement, and the peripancreatic fat stranding • There may also be some peripancreatic fluid
  31. 31. Outcome: AIOP • The clinical symptoms of interstitial oedematous pancreatitis usually resolve within the first week
  32. 32. Necrotising pancreatitis • Defined as pancreatic inflamation associated with necrosis of the pancreatic parenchyma, the peripancreatic tissue or both • Necrotising pancreatitis most commonly manifests as necrosis involving both the pancreas and peripancreatic tissues and less commonly as necrosis of only the peripancreatic tissue, and rarely of the pancreatic parenchyma alone
  33. 33. Necrotising pancreatitis • The impairment of pancreatic perfusion and signs of peripancreatic necrosis evolve over several days – early CECT may underestimate the eventual extent of pancreatic and peripancreatic necrosis. • After the first week of the disease, a non- enhancing area of pancreatic parenchyma should be considered to be pancreatic parenchymal necrosis.
  34. 34. Necrotising pancreatitis • The natural history of pancreatic and peripancreatic necrosis is variable, because it may remain solid or liquefy, remain sterile or become infected, persist, or disappear over time.
  35. 35. Infected pancreatic necrosis • Pancreatic and peripancreatic necrosis can remain sterile or become infected • No absolute correlation between the extent of necrosis and the risk of infection and duration of symptoms • Rare during the first week • The diagnosis of infected pancreatic necrosis is important because of the need for antibiotic treatment and likely active intervention
  36. 36. Infected pancreatic necrosis • The presence of infection can be presumed – When there is extraluminal gas in the pancreatic and/or peripancreatic tissues on CECT OR When percutaneous, image-guided, fine-needle aspiration (FNA) is positive for bacteria and/or fungi on Gram stain and culture
  37. 37. Fate of PN Necrosis Liquefaction Suppuration (PUS)
  38. 38. The original Atlanta Classification proposed the term ‘pancreatic abscess’ to define a ‘localised collection of purulent material without significant pancreatic/peripancreatic necrosis’ This finding is extremely uncommon, and because the term is confusing and has not been adopted widely, the term ‘pancreatic abscess’ is not used in the current classification
  39. 39. Infected pancreatic necrosis • The development of secondary infection in pancreatic necrosis is associated with increased morbidity and mortality
  40. 40. A 47-year-old man with acute necrotising pancreatitis complicated by infected pancreatic necrosis. There is a heterogeneous, acute necrotic collection (ANC) in the pancreatic and peripancreatic area (white arrows pointing at the borders of the ANC) with presence of gas bubbles (white arrowheads), usually a pathognomonic sign of infection of the necrosis
  41. 41. ? Infection from where • Translocation of bacteria • Percutaneous procedure- FNA, PCD • Endoscopic intervention- internal drainage • Rarely -Worms causing acute pancreatitis
  43. 43. Definition of organ failure • Three organ systems should be assessed to define organ failure: respiratory, cardiovascular and renal • Organ failure is defined as a score of 2 or more for one of these three organ systems using the Modified Marshall Scoring System (MMSS)
  44. 44. Local complication of acute pancreatitis Local complications are – 1. Acute peripancreatic fluid collection (AFC) 2. Pancreatic pseudocyst (PP) 3. Acute necrotic collection (ANC) 4. Walled-off necrosis (WOPN)
  45. 45. Local complication • Other local complications of acute pancreatitis include gastric outlet dysfunction, splenic and portal vein thrombosis, and colonic necrosis.
  46. 46. Local complication Local complications should be suspected – - There is persistence or recurrence of abdominal pain, - Secondary increases in serum pancreatic enzyme activity, - Increasing organ dysfunction, - Development of clinical signs of sepsis, such as fever and leucocytosis. Prompt CECT to be done in these cases
  47. 47. CECT • The morphologic description of local complications is necessary for accurate diagnosis However Local complications alone, do not define the severity of acute pancreatitis.
  48. 48. APFC (Acute Peripancreatic Fluid Collection) • Peripancreatic fluid associated with interstitial oedematous pancreatitis with no associated peripancreatic necrosis, usually seen within the first 4 weeks after onset of interstitial oedematous pancreatitis.
  49. 49. CECT: APFC • Occurs in the setting of interstitial oedematous pancreatitis • Homogeneous collection with fluid density • Confined by normal peripancreatic fascial planes • No definable wall encapsulating the collection • Adjacent to pancreas (no intrapancreatic extension)
  50. 50. acute interstitial oedematous pancreatitis and acute peripancreatic fluid collection (APFC) in the left anterior pararenal space. The pancreas enhances completely, is thickened, and has a heterogeneous appearance due to oedema. APFC has fluid density without an encapsulating wall
  51. 51. A follow up CT shows complete resolution of the APFC with minimal residual peripancreatic fat stranding.
  52. 52. APFC • Most acute fluid collections remain sterile and usually resolve spontaneously without intervention • When a localised APFC persists beyond 4 weeks, it is likely to develop into a pancreatic pseudocyst
  53. 53. PSEUDOCYST OF PANCREASE An encapsulated collection of fluid with a well defined inflammatory wall usually outside the pancreas with minimal or no necrosis, usually appears more than 4 weeks after onset of interstitial oedematous pancreatitis
  54. 54. CECT : PP • Well circumscribed, usually round or oval • Homogeneous fluid density • No solid component • Well defined wall, completely encapsulated • Maturation usually requires >4 weeks after onset of acute pancreatitis; occurs after interstitial oedematous pancreatitis
  55. 55. A 40-year-old man with two pseudocysts in the lesser sac 6 weeks after an episode of acute interstitial pancreatitis on CT (A, B).Note the round to oval, low-attenuated, homogeneous fluid collection with a well defined enhancing rim (white arrows pointing at the borders of the pseudocysts), but absence of areas of greater attenuation indicative of non-liquid components. White stars denote normalenhancing pancreas
  56. 56. PP • If aspiration of cyst content is performed, there is usually a markedly increased amylase activity • A pancreatic pseudocyst is thought to arise from disruption of the main pancreatic duct or its intra- pancreatic branches without any recognisable pancreatic parenchymal necrosis • Although CECT is the imaging modality used most commonly to describe pseudocysts, MRI or ultrasonography may be required to confirm the absence of solid content in the collection.
  57. 57. PP • A pseudocyst may also arise in the setting of acute necrotising pancreatitis as a result of a ‘disconnected duct syndrome’, whereby pancreatic parenchymal necrosis of the neck or body of the gland isolates a still viable distal pancreatic remnant • A pseudocyst may be evident many weeks after operative necrosectomy due to localised leakage of the disconnected duct into the necrosectomy cavity
  58. 58. ANC (acute necrotic collection) • During first 4 week, a collection containing variable amounts of both fluid and necrosis associated with necrotising pancreatitis • The necrosis can involve the pancreatic parenchyma and/or the peripancreatic tissues
  59. 59. CECT: ANC • Occurs only in the setting of acute necrotising pancreatitis • Single Or multiple loculated Heterogeneous collection and non-liquid density of varying degrees in different locations (some appear homogeneous early in their course) • No definable wall encapsulating the collection • Location—intrapancreatic and/or extrapancreatic
  60. 60. Acute necrotic collections (ANC) in a 44-year-old man with acute necrotising pancreatitis involving only the peripancreatictissues. Note enhancement of the entire pancreatic parenchyma (whitestars) and the heterogeneous, non-liquid peripancreatic components in the retroperitoneum (white arrows pointing at the borders of the ANC).
  61. 61. The ANC in the same patient as (A) but imaged a few weeks later demonstrate a heterogeneous collection with areas of fat (black arrowheads) surrounded by fluid density, and areas which have a slightly greater attenuation (black arrows) than seen in collections without necrosis White arrows denote border of ANC; white stars denote enhancement of pancreatic parenchyma
  62. 62. ANC • An ANC may be associated with disruption of the main pancreatic duct within the zone of parenchymal necrosis and can become infected • Sequential imaging may be useful to characterise acute collections • Within the first week of the disease, it may be difficult to differentiate an APFC from an ANC, as both types of collections may appear as areas with fluid density
  63. 63. ANC • After the first week, the distinction between these two important types of collections becomes clear, such that at this stage of necrosis, a peripancreatic collection associated with pancreatic parenchymal necrosis can be properly termed an ANC and not an APFC • MRI, USG or EUS may be helpful to confirm the presence of solid content in the collection.
  64. 64. WON • A mature, encapsulated collection of pancreatic and/or peripancreatic necrosis that has developed a well defined inflammatory wall, usually appears >4 weeks after onset of necrotising pancreatitis.
  65. 65. CECT: WON • Heterogeneous with liquid and non-liquid density with varying degrees of loculations (some may appear homogeneous) • Well defined wall, that is, completely encapsulated • Location—intrapancreatic and/or extrapancreatic • Maturation usually requires 4 weeks after onset of acute necrotising pancreatitis
  66. 66. A heterogeneous, fully encapsulated collection is noted in the pancreatic and peripancreatic area Non-liquid components of high attenuation (black arrowheads) in the collection are noted. The collection has a thin, well defined, and enhancing wall (thick white arrows).
  67. 67. A heterogeneous, fully encapsulated collection is noted in the pancreatic and peripancreatic area. A largely liquefied collection in the bed of the pancreas is observed with non-liquid components representing areas of trapped fat (black arrowheads).
  68. 68. T2-weighted MRI showing the true heterogeneity of the collection. Black arrowheads denote areas of necrotic debris surrounded by fluid (white on T2- weighted image).
  69. 69. WON • WON derives from necrotic pancreatic parenchyma and/or necrotic peripancreatic tissues and may be infected, may be multiple, and may be present at sites distant from the pancreas • CECT may not readily distinguish solid from liquid content and, for this reason, WOPN may be misdiagnosed as a pancreatic pseudocyst • MRI, USG or EUS may be required for this distinction.
  70. 70. Definition of systemic complications • Exacerbation of pre-existing co-morbidity, such as coronary artery disease or chronic lung disease, precipitated by the acute pancreatitis is defined as a systemic complication.
  71. 71. Phases of acute pancreatitis • two overlapping phases in this dynamic disease process with two peaks of mortality: early and late • The early phase, which usually lasts for the first week, is followed by a second late phase which can run a protracted course from weeks to months
  72. 72. Early phase • During the early phase, systemic disturbances result from the host response to local pancreatic injury • This early phase is usually over by the end of the first week but may extend into the second week • Cytokine cascades are activated by the pancreatic inflammation which manifest clinically as the systemic inflammatory response syndrome • When SIRS is persistent, there is an increased risk of developing organ failure
  73. 73. SIRS Signs of systemic inflammatory response syndrome (SIRS) SIRS—defined by presence of two or more criteria of following Heart rate >90 beats/min Core temperature <36°C or >38°C White blood count <4000 or >12000/mm3 Respirations >20/min or PCO2 <32 mm Hg
  74. 74. Early phase • During the early phase, organ failure described as “ transient OF” and “persistent OF” • ‘Transient organ failure’ if the organ failure resolves within 48 h with supportive Rx • ‘Persistent organ failure’ if organ failure persists for >48 hrs • If organ failure affects more than one organ system, it is termed multiple organ failure (MOF).
  75. 75. Late phase • The late phase is characterised by persistence of systemic signs of inflammation or by the presence of local complications • Late phase occurs only in patients with moderately severe or severe acute pancreatitis • Local complications evolve during the late phase • It is important to distinguish the different morphologic characteristics of the local complications by radiologic imaging, because these local complications may have direct implications for management
  76. 76. Definition of severity of acute pancreatitis • First, on admission, it is important to identify patients with potentially severe acute pancreatitis who require aggressive early treatment • Second, in a secondary care setting, clinicians need to identify such patients for possible transfer to specialist care • Third, for specialists who receive such referrals, there are advantages to stratifying these patients into subgroups based on the presence of persistent organ failure and local or systemic complications
  77. 77. Why not early CECT • First, the presence and extent of pancreatic and peripancreatic necrosis may not be defined clearly on imaging during the first few days of disease. When necessary, a CECT 5–7 days after admission is more reliable in establishing the presence and extent of pancreatic necrosis • Second, the extent of morphologic changes and necrosis is not directly proportional to the severity of organ failure • Third, even if imaging during the first week identifies the presence of peripancreatic fluid collections or pancreatic necrosis, in general no treatments are required for these conditions at that time.
  78. 78. CTSI (balthazar’s) • CTSI Depends on degree of pancreatic imflamation and percentage of pancreatic necrosis
  79. 79. Computed Tomography Severity Index (CTSI) for Acute Pancreatitis Features points Pancreatic Inflammation Normal pancreas 0 Focal or diffuse pancreatic enlargement 1 Intrinsic pancreatic alterations with peripancreatic 2 fat inflammatory changes Single fluid collection/or phlegmon 3 Two or more fluid collections or gas, in or 4 adjacent to the pancreas Pancreatic Necrosis None 0 ≤30% 2 30%-50% 4 >50% 6
  80. 80. CTSI CTSI Morbidity Mortality 0-3 8% 3% 4-6 35% 6% 7-10 92% 17%
  81. 81. Take home msg • Gall stone and alcohol consist most common cause accounting 70-75% of all cause • All pt with first attack of AP should have an USG UA to search for Gall stone, CBD stone or signs of extrahepatic billiary tract obstruction • AP is the most common complication after ERCP, occurring in up to 5% of patients • Post ERCP pancreatitis requires high suspicion for the diagnosis , need to be suspected & evaluated if any inadvertent event occurs during the procedure.
  82. 82. Take home msg • Acute pancreatitis is an evolving, dynamic condition and that the severity may change during the course of the disease • AP has got two peak of mortality in early phase due to MOF and in late phase due to infective complications • The accurate description of local complications, including the presence of fluid or necrosis in or around the pancreas, the presence or absence of infection is necessary to decide need for an intervention
  83. 83. Take home msg • Although local complications may be identified during the early phase, they are not the predominant determinants of severity • Extent of morphologic changes is not directly proportional to the severity of organ failure • The definition of severe or moderately severe acute pancreatitis in the early phase depends on the presence and duration of organ failure
  84. 84. THANK YOU….