2.Acute pancreatitis. Yonas Ademe ppt dox

It describes Causes,diagnosis pathophysiology,severity score systemic and local complication and management of acute pancreatitis

1. Acute pancreatitis Yonas Ademe July, 2016 Oct, 2019 1

2. Introduction Acute pancreatitis is an inflammatory disorder of the pancreas that is characterized by edema and, when severe, necrosis It can be initiated by several factors including gallstones, alcohol, trauma, and infections, and in some cases it is hereditary Most patients present with mild disease (80%) Very often patients develop additional complications such as sepsis, shock, and respiratory and renal failure, resulting in considerable morbidity and mortality 2

3. Cont. The median age at index presentation of acute pancreatitis varies with etiology A lcohol- and drug-induced pancreatitis present in the third or fourth decade compared with gallstone and trauma in the sixth decade The gender difference is probably more related to etiology (in general M>F) I n males alcohol is more often the cause while in females it is gallstones 3

4. E tiology Two factors, biliary tract stone disease and alcoholism , account for 80 - 90% of the cases The remaining 10 - 20% is accounted for either by idiopathic disease or by a variety of miscellaneous causes including trauma , surgery , drugs , heredity , infection and toxins 4

5. Cont. Biliary tract disease Alcohol Trauma External Surgical ERCP Pancreatic duct obstruction Neoplasms Pancreas divisum Ampullary and duodenal lesions Ischemia Hypoperfusion Atheroembolic Vasculitis Drugs T hiazide diuretics, furosemide , sulfonamides, tetracycline, valproic acid, azathioprine , L- asparaginase , 6-mercaptopurine Infections M umps, coxsackievirus , and Mycoplasma pneumoniae Hyperlipidemia Hypercalcemia Hereditary Venom Idiopathic 5

6. Cont. Stone disease A simple mechanical explanation has been proposed whereby elevated intraductal pressure causes rupture of the smaller ductules and leakage of pancreatic juice into the parenchyma Although the pancreatic duct fluid pH is maintained in the range of 8 to 9 by the secretion of bicarbonate, the interstitial pH of 7 within the pancreatic tissue favors activation of proteases when transductal extravasation of fluid occurs These active digestive enzymes then begin autodigestion within the pancreatic acinar cells, leading to pancreatitis 6

7. Cont. Alcohol Between 10 and 15% of individuals with daily intake of between 100 and 150 g of ethanol go on to develop pancreatitis Although some patients show the symptoms of acute pancreatitis after little use or even a single exposure to alcohol, the disease commonly occurs in patients who have consumed alcohol for at least 2 years, and often much longer, up to 10 years In a patient with an exposure history to ethanol and the total absence of other possible causative factors, a first attack of pancreatitis is considered alcohol-related acute pancreatitis It could also be the first manifestation of chronic pancreatitis The disease can become recurrent with continued alcohol abuse 7

8. Cont. Alcohol Ethanol increases overall pancreatic secretion and the protein content of pancreatic juice This can lead to elevation of enzyme proteins that can precipitate within the pancreatic duct Calcium then can precipitate within this protein matrix, causing multiple ductal obstructions, while continued secretion can cause pressure buildup Ethanol increases ductal permeability Making it possible for improperly-activated enzymes to leak out of the pancreatic duct into the surrounding tissue Ethanol causes spasm of the sphincter of Oddi Ethanol is a metabolic toxin to pancreatic acinar cells The acinar cell metabolizes ethanol by oxidative and nonoxidative pathways, and exhibits changes that predispose the cell to autodigestive injury, necroinflammation , and cell death Ethanol transiently decreases pancreatic blood flow, possibly causing focal ischemic injury to the gland 8

9. Cont. Tumors A pancreatic or periampullary tumor should be considered in patients with idiopathic acute pancreatitis, especially in those over 50 years old Crosssectional imaging after the resolution of the acute pancreatitis is required ~ 1 to 2% of patients with acute pancreatitis have pancreatic carcinoma, and an episode of acute pancreatitis can be the first clinical manifestation of a periampullary tumor P ancreatitis possibly results from blockage of secreted juice and its upstream consequences 9

10. Cont. Iatrogenic Pancreatitis Acute pancreatitis can be associated with a number of surgical procedures , most commonly those performed on or close to the pancreas P ancreatic biopsy, biliary duct exploration, distal gastrectomy , splenectomy The most common iatrogenic cause is ERCP in which acute pancreatitis occurs after about 5-10% of procedures Due to direct injury and/or intraductal hypertension 10

11. Cont. Hyperlipidemia L ipase can liberate large amounts of toxic fatty acids into the pancreatic microcirculation This could lead to endothelial injury, sludging of blood cells, and consequent ischemic states Hypercalcemia T he mechanism most likely involves hypersecretion and the formation of calcified stones intraductally 11

12. Cont. Idiopathic When gallstones and other etiological factors cannot be identified , there is still the possibility of finding microlithiasis , seen as birefringent crystals, on bile microscopy This occult microlithiasis is probably responsible for up to half of those with idiopathic acute pancreatitis 12

13. Pathophysiology Because the exocrine pancreas produces several enzymes that are potentially injurious to itself, it prevents autodigestion by: I ntracellularly assembling the inactive precursors of these enzymes, called proenzymes or zymogens, which are then transported and secreted outside of the gland Their activation occurs safely in the duodenum, where the brush-border enzyme enteropeptidase (or enterokinase ) activates the trypsinogen , and the resulting trypsin then activates the other zymogens in a cascade reaction Segregating digestive enzymes from the cytoplasmic space within acinar cells by enclosing them within membrane-bound organelles referred to as zymogen granules The synthesis of trypsin inhibitors , which are transported and stored along with the digestive enzyme zymogens 13

14. Cont. It generally is believed that pancreatitis begins with the intrapancreatic activation of digestive enzyme zymogens, acinar cell injury, and activation of transcription factors This in turn leads to the production of proinflammatory factors, acinar cell necrosis, SIRS, and distant organ dysfunction including lung injury that frequently manifests as ARDS The ultimate severity of acute pancreatitis depends on the extent of the systemic inflammatory response 14

15. Cont. 15

16. Cont. I ntra-pancreatic events I nflammatory mediators released from inflammatory cells cause an increased pancreatic vascular permeability, leading to hemorrhage, edema, and microthrombi Fluid may collect in and around the pancreas The failure of the pancreatic microcirculation, a feature of more severe acute pancreatitis, results in pancreatic hypoperfusion and necrosis (evidenced by poor contrast uptake on CT scan) The development of pancreatic necrosis, the breakdown of the intestinal barrier, and the suppression of the immune response through the compensatory inflammatory response contribute to the development of infected pancreatic necrosis, the incidence of which peaks in the third to fourth week 16

17. Cont. Systemic events An important aspect of the pathophysiology of acute pancreatitis is the mechanism by which events occurring in the pancreas induce systemic inflammation and multiorgan failure Organ failure can develop at any stage of acute pancreatitis, associated with an overwhelming proinflammatory response early , or later secondary to the development of infected local complications Organ failure is scored using the Marshall or Sequential Organ Failure Assessment (SOFA) systems Multiple organ failure is defined as two or more organs registering two or more points on these scoring systems The three organ systems most frequently involved are cardiovascular, respiratory , and renal 17

18. Cont. SOFA score in acute pancreatitis 18

19. Complications Local complications Per-pancreatic fluid collections Pancreatic and peri -pancreatic necrosis (sterile or infected) Walled off necrosis (sterile or infected) Pancreatic pseudocyst (sterile or infected ) Involvement of adjacent organs W ith hemorrhage, thrombosis, bowel infarction, OJ, fistula formation, or mechanical obstruction 19

20. Cont. Cont. ( T he revised Atlanta statement ) C ontrast enhanced CT criteria for the diagnosis of the local complications of acute pancreatitis 20 APFC (acute peripancreatic fluid collection) Occurs in the setting of interstitial edematous pancreatitis It is a homogenous collection with fluid density

21. Cont. Systemic complications  A.    Pulmonary Pneumonia, atelectasis Acute respiratory distress syndrome Pleural effusion B.    Cardiovascular Hypotension/ Hypovolemia Sudden death Nonspecific ST-T wave changes Pericardial effusion D.    Hematologic Hemoconcentration DIC Gastrointestinal hemorrhage E. GIT Peptic ulcer Erosive gastritis Portal vein or splenic vein thrombosis with varices E.    Renal Oliguria Azotemia Renal artery/vein thrombosis 21

22. Cont. Systemic complications F. Metabolic Hyperglycemia Hypocalcemia Hypertriglyceridemia Fat emboli Fat necrosis Intra-abdominal saponification Subcutaneous tissue necrosis G.    Central nervous system Encephalopathy Psychosis Alcohol withdrawal syndrome Sudden blindness ( Purtscher's retinopathy) 22

23. Clinical features 23

24. Cont. The clinical diagnosis of pancreatitis is one of exclusion The other upper abdominal conditions that can be confused with acute pancreatitis include P erforated peptic ulcer A gangrenous small bowel obstruction Acute cholecystitis 24

25. Symptoms All episodes of acute pancreatitis begin with severe pain , generally following a substantial meal The pain is usually epigastric , but can occur anywhere in the abdomen or lower chest It has been described as "knifing" or "boring through" to the back, and may be relieved by the patient leaning forward Pain precedes the onset of nausea and vomiting , with retching often continuing after the stomach has emptied Vomiting does not relieve the pain, which is more intense in necrotizing than in edematous pancreatitis 25

26. Physical findings Vital signs T achycardia, tachypnea , hypotension, and hyperthermia The temperature is usually only mildly elevated in uncomplicated pancreatitis Chest There may be pleural effusion, particularly on the left side Abdomen Voluntary and involuntary guarding can be seen over the epigastric region The bowel sounds are decreased or absent The abdomen may be distended with intraperitoneal fluid In some patients ( about 1% ), the blood from necrotizing pancreatitis may dissect through the soft tissues and manifest as a blueish discoloration around the umbilicus ( Cullen's sign ) or in the flanks ( Grey Turner sign ) 26

27. Cont. 27

28. Diagnosis 28

29. Cont. According to RAC (Revised Atlanta Criteria), the diagnosis of acute pancreatitis requires atleast 2 of the following 3 features: A bdominal pain consistent with acute pancreatitis ( acute onset of a severe constant epigastric pain that often radiates through to the mid back) Serum lipase activity (or amylase activity) atleast 3 times the upper limit of normal Characteristic findings of acute pancreatitis on imaging (usually by contrast-enhanced CT scanning and less commonly MRI or U/S) 29

30. Routine laboratory With increasing severity of disease, the intravascular fluid loss may become life-threatening as a result of sequestration of edematous fluid in the retroperitoneum Hemoconcentration then results in an elevated hematocrit However, there also may be bleeding into the retroperitoneum or the peritoneal cavity The severe fluid loss may lead to prerenal azotemia with elevated BUN and creatinine levels There also may be hyperglycemia , hypoalbuminemia , and hypocalcemia sufficient in some cases to produce tetany 30

31. Serum Markers Because pancreatic acinar cells synthesize, store, and secrete a large number of digestive enzymes (e.g., amylase, lipase, trypsinogen , and elastase ), the levels of these enzymes are elevated in the serum of most pancreatitis patients 31

32. Cont. Amylase Because of the ease of measurement, serum amylase levels are measured most often Serum amylase concentration increases almost immediately with the onset of disease and peaks within several hours and it remains elevated for 3 to 5 days before returning to normal 32

33. Cont. Cont. Drawbacks Hyperamylasemia can also occur as a result of conditions not involving pancreatitis For example, SBO , perforated PUD , or other intra-abdominal inflammatory conditions In contrast, a patient with acute pancreatitis may have a normal serum amylase level, which could be due to several reasons I n patients with hyperlipidemia , values might appear to be normal because of interference by lipids with chemical determination of serum amylase Hemoconcentration can also affect the serum concentration of amylase There is no significant correlation between the magnitude of serum amylase elevation and severity of pancreatitis In fact, a milder form of acute pancreatitis is often associated with higher levels of serum amylase as compared with that in a more severe form of the disease In patients with severe pancreatitis associated with significant necrosis , the pancreas may not have the capacity to release large amounts of enzymes into the circulation Patients with alcoholic pancreatitis, in general, have a smaller increase in serum amylase levels 33

34. Cont. Cont. Since hyperamylasemia can be observed in many extrapancreatic diseases, measuring pancreatic-specific amylase (p-amylase) rather than total amylase, which also includes salivary amylase (s-amylase), makes the diagnosis more specific (88 to 93%) 34

35. Cont. Lipase Since serum levels of lipase remain elevated for a longer time than total or pancreatic amylase, it is the serum indicator of highest probability of the disease Advantages More specific Remain elevated for a longer time 35

36. Cont. The ideal biochemical marker for prognosis of acute pancreatitis should not only have high specificity and sensitivity, but also should be able to discriminate between mild (edematous) and severe (necrotic) disease on admission While serum enzymes such as amylase and lipase are helpful in the diagnosis of pancreatitis, they have no prognostic value Several recent research studies have suggested additional markers that may have prognostic value, including acute phase proteins such as C-reactive protein (CRP) , α 1 -antitrypsin , phospholipase A 2 , α 2 -macroglobulin, PMN- elastase 36

37. Abdominal ultrasound Possible findings It is the best way to confirm the presence of gallstones in suspected biliary pancreatitis It also can detect extrapancreatic ductal dilations It can reveal pancreatic edema, swelling, and peripancreatic fluid collections However, in about 20% of patients, the ultrasound examination does not provide satisfactory results because of the presence of bowel gas, which may obscure sonographic imaging of the pancreas 37

38. CT (with IV contrast) - CECT The primary purpose of cross-sectional imaging is the diagnosis of local complications ; in particular, the development and extent of pancreatic necrosis and the different collections Indications To diagnose acute pancreatitis When diagnosis is in doubt To diagnose complications Patient not improving (after 72 hours) or deteriorating To guide the insertion of percutaneous drains First episode in patients >40 years without identifiable cause But there is no advantage in using CT scanning to predict the severity of acute pancreatitis 38

39. Cont. CT findings of acute pancreatitis Contrast enhancement Interstitial pancreatitis Since the microcirculation of the pancreas remains intact, the gland shows uniform contrast enhancement Necrotizing pancreatitis Since the microcirculation is disrupted, enhancement of the gland on contrast-enhanced CT scan is considerably decreased Air bubbles The presence of air bubbles on a CT scan is an indication of infected necrosis or pancreatic abscess 39

40. Cont. Based on CECT, 2 distinct types of acute pancreatitis have been described (RAC, 2013) Acute interstitial edematous pancreatitis Acute necrotizing pancreatitis Pancreatic parenchyma necrosis alone Peri -pancreatic necrosis alone Pancreatic parenchyma necrosis and peri -pancreatic necrosis 40

41. Abdominal x-ray 41 Sentinel loop sign Colon cut-off sign

42. Assessment of Severity 42

43. Predicting Severity There are several predictors of severity E arly prognostic signs Ranson’s score Modified Glasgow score APACHE II Bedside Index for Severity of Acute Pancreatitis (BISAP ) Recently proposed These single and combined predictors of severity have an accuracy of around 70% Serum markers At 24 hours after admission a serum C-reactive protein level of >150 mg/ dL predicts severe disease 43

44. Early Prognostic Signs Ranson's score 5 are measured at the time of admission, whereas the remaining 6 are measured within 48 hours of admission Morbidity and mortality of the disease are directly related to the number of signs present ≤2 positive digns : the mortality is generally zero 3-5 positive signs: mortality is increased to 10 to 20% ≥6: the mortality rate increases to more than 50% W hen there are three or more positive criteria, the disease is considered “predicted severe” It is a very good way of assessing severity but the major drawback is that a delay of 48 hours after admission merely for assessment may squander a valuable opportunity to prevent a complication during this time 44

45. Cont. Ranson’s score 45

46. Cont. Glasgow score 46

47. Cont. Acute physiology and chronic health evaluation (APACHE-II) score A ssesses severity on the basis of quantitative measures of abnormalities of multiple variables, including vital signs and specific laboratory parameters, coupled with the age and chronic health status of the patient The main advantage of this scoring system is the immediate assessment of the severity of pancreatitis A score of ≥8 at admission is usually considered indicative of severe disease 47

48. Cont. BISAP I t has the advantage of simplicity and can be performed within the first 24 hours of admission Criteria Age >60 years Presence of SIRS Impaired mental status (GCS <15 ) Pleural effusion BUN >25 mg/ dL 0 to 2 points: lower mortality (<2%) 3 to 5 points: higher mortality (>15%) 48

49. Classification of severity The key determinants of severity are: L ocal complications (absent, sterile, or infected) S ystemic complications (absent, transient organ failure ( <48 hours ), persistent organ failure (>48 hours)) The wide spectrum of pancreatitis severity was not captured in the previous binary classifications (mild or severe) Two classification systems have recently been proposed: The three grades (mild, moderately severe, and severe ) of the Revised Atlanta Criteria ( RAC) T he four categories (mild, moderate, severe, critical) of the Determinants Based Classification (DBC) 49

50. Cont. Revised Atlanta Classification (2013) Mild No local or systemic complications No organ failure Moderately severe Local or systemic complications without persistent organ failure Transient organ failure Severe Persistent organ failure 50

51. Cont. Determinants Based Classification (2012) Mild No ( peri )pancreatic necrosis AND organ failure Moderate S terile ( peri )pancreatic necrosis AND/OR transient organ failure Severe Infected ( peri )pancreatic necrosis OR persistent organ failure Critical Infected ( peri )pancreatic necrosis AND persistent organ failure 51

52. Cont. 52

53. Treatment 53

54. Principles Regardless of severity, hospitalization of the patient with suspected acute pancreatitis for observation and diagnostic study is usually mandatory Upon confirmation of the diagnosis, patients with moderate to severe disease should be transferred to the ICU for observation and maximal support 54

55. Cont. Principles of treatment General supportive care O ral food and fluid restriction R eplacement of fluids and electrolytes Nutritional support Control of pain ?Antibiotics Most experts’ recommendation when signs of infection are present Close monitoring 55

56. Cont. General supportive care Patients with any sign of severity should be admitted to the ICU Specific complications of the disease process should be carefully looked for and appropriately managed For example, the presence of ARDS usually requires assisted ventilation with positive end-expiratory pressure The lung injury is caused by the systemic release of phospholipase A 2 and other enzymes that directly damage alveolar tissue and pulmonary capillaries 56

57. Cont. R estriction of oral food and fluids (resting the pancreas) Nasogastric suction and H 2 -blockers have routinely been used in this connection, based on the reasoning that even the smallest amount of gastric acid reaching the duodenum could stimulate pancreatic secretion However, these measures are of little value 57

58. Cont. Fluid therapy Fluid balance can become dangerously disturbed even in mild acute pancreatitis because of fluid sequestration, vomiting, and sudoresis While there are proponents for vigorous fluid therapy (5–10 mL/kg/ hr ), especially in the first 24 hours, and for specific resuscitation goals, it is probably best to resuscitate with a balanced crystalloid and aim to restore normal blood volume, BP, and urine output In one study, lactated Ringer’s solution was superior to normal saline in reducing the systemic inflammatory response Caution needs to be exercised in those with cardiac and renal disease and in the elderly, where the risks of over-resuscitation are greater 58

59. Cont. Nutritional support It is no longer acceptable to “rest the pancreas” by avoiding enteral nutrition Parenteral nutrition is now known to be more expensive, riskier, and not more effective than enteral nutrition and should only be offered if the patient’s calculated nutritional requirements cannot be achieved by the enteral route A delay in commencing enteral nutrition may contribute to the development of intestinal ileus and feeding intolerance Early initiation of enteral nutrition (within the first 24 hours of admission) is not superior to delaying an oral diet until 72 hours If feeding is not tolerated over 48 to 72 hours, then nasogastric tube feedings can be started and increased in step-wise fashion over 2 to 3 days A low-fat, low-protein diet is advocated as the initial form of nutrition following an attack of acute pancreatitis 59

60. Cont. Pain Management Pain is the cardinal symptom of acute pancreatitis, and its relief is a clinical priority The severe pain of acute pancreatitis prevents the patient from resting, and results in ongoing cholinergic discharge, which stimulates gastric and pancreatic secretion Because of unpredictable absorption, analgesia should be administered intravenously, at least at the outset and before oral intake has been established There is a lack of high-quality evidence to guide the choice of analgesic Those with mild pain can usually be managed with a NSAIDs T hose with more severe pain are best managed with opioid analgesia ( (e.g ., buprenorphine, meperidine) Morphine is to be avoided, due to its potential to cause sphincter of Oddi spasm 60

61. Cont. Antibiotics Although the use of broad-spectrum antibiotics to treat established infection in acute pancreatitis is a well-established practice, there has been considerable controversy surrounding the use of prophylactic antibiotics The overuse of antibiotics has been associated with a documented rise in fungal infections and resistant organisms Overall , it appears that the most recent and generally better designed studies do not support the use of prophylactic antibiotics to reduce the frequency of pancreatic infectious complications, surgical intervention, and death 61

62. Management of Organ Failure The early identification of organ dysfunction and failure is important because it is a key determinant of severity and outcome The responsiveness of organ failure to resuscitation over the first 48 hours is an important prognostic clue T hose that respond have transient organ failure and have a better outlook than those who do not respond and have persistent organ failure Organ failure that develops later in the disease course is usually secondary to infection of a local complication and should be managed accordingly 62

63. Management of Local Complications The decisions regarding how and when to intervene are often difficult While guided by the information gained by cross-sectional imaging, the decision to intervene is based on the clinical status and trajectory of the patient and the response to maximal intensive care support In practice, intervention is delayed in order to allow demarcation and to reduce the risk of bleeding, disseminated infection, and collateral damage to adjacent organs by an intervention Appreciation of this has resulted in a notable trend toward delayed intervention, now uncommon before 3 to 4 weeks from the onset of symptoms 63

64. Cont. Indication A deteriorating patient with suspected infected local complication Step-up approach Percutaneous catheter drainage Minimally invasive interventions Open surgery 64

65. Cont. Percutaneous catheter drainage An important emerging approach in patients with suspected infected collections Preemptive drainage with one or more catheters often produces improvement or stabilization of the patient’s overall clinical status In this way, drainage “buys time” and allows the lesion to become more walled off and safer to treat It may be the only intervention required in a third to a half of patients Fine-needle aspiration is now rarely used to confirm infection because the insertion of a needle at the time of planned drainage allows confirmation of the suspected infection 65

66. Cont. M inimally invasive interventions A proportion of patients do require further treatment when they fail to respond to percutaneous catheter drainage and there is a wide array of minimally invasive options to choose from: V ideo-assisted retroperitoneal debridement E ndoscopic transgastric necrosectomy 66

67. Cont. Cont. Video-assisted retroperitoneal debridement 67

68. Cont. Cont. Endoscopic transgastric necrosectomy 68

69. Cont. Open surgical intervention Indications Acute abdomen (perforation or ischemia) Failed “step-up approach” for further debridement/ drainage Severe abdominal compartment syndrome (rarely ) Timing of intervention Early surgery is more difficult & dangerous Surgical intervention should be undertaken as late as possible after the onset (preferably 3- 4 weeks) When the necrotic process has stopped extending When there is clear demarcation between viable and nonviable tissues When infected necrotic tissue has become organized and “walled off ’ 69

70. Cont. Cont. Options Necrosectomy + Wide tube drainage Necrosectomy + Planned relaparatomy Pancreatectomy Approach Pancreas is exposed by dividing gastrocolic ligament and entering the lesser sac If inflammatory changes obliterate the lesser sac, then via dividing transverse mesocolon 70

71. Cont. Cont. Major post- nectrosectomy complications Postoperative bleeding Early (<24 hr ): due to colonic or peri -pancreatic artery bleeding Late (>24 hr ): due to bleeding pseudo aneurysm (splenic , gastroduodenal, pancreaticoduodenal, and dorsal pancreatic arteries) Pancreatic fistulas ( pancreatico -enteric or pancreatico -cutaneous ) Exocrine and/or endocrine insufficiency Mortality could reach to 10-20% 71

72. Cont. Sterile Necrosis Patients with no systemic complications, local compressive effects, or concerns about secondary infections S upportive care Patients who develops systemic complications, and in whom a secondary infection is suspected A CT-guided FNA should be performed and if there is no infection, the patient can be managed medically Patients who appear to be very ill, have high APACHE-II and Ranson's scores, and show evidence of systemic toxicity including shock These patients need aggressive débridement 72

73. Cont. Infected necrosis Infection of pancreatic & peripancreatic necrosis complicates 30-70% of acute necrotizing pancreatitis It commonly occurs during the 3 rd -4 th week but may occur at anytime It is a serious complication of acute pancreatitis and is the most common cause of death It is caused most often by translocated enteric bacteria, and is seen commonly in necrotizing rather than interstitial pancreatitis 73

74. Cont. Pancreatic pseudocyst The management of an acute non-infected pseudocyst is usually conservative, as about half of these will resolve spontaneously Indications for intervention Symptomatic Persisting pain or the inability to eat Complication ( e.g , infection, bleeding, rupture, mass effect) S ize and duration (>6 cm, after 6 weeks and enlarging ) Intervention EUS-guided internal drainage into stomach or duodenum or transpapillary stenting is the preferred approach Surgical drainage Percutaneous drainage should be avoided because of the risk of external pancreatic fistula 74

75. Cont. Pancreatic abscess A pancreatic abscess occurs 2 to 6 weeks after the initial attack, in contrast to infected necrosis, which occurs in the first few hours or days The mechanism of delayed infection is not clear, but the treatment consists of external drainage , whether established by surgical, minimally invasive, or percutaneous catheter-based methods 75

76. Treatment of Biliary Pancreatitis Most patients pass the offending gallstone(s) during the early hours of acute pancreatitis, but have additional stones capable of inducing future episodes This raises the question of the timing of surgical or endoscopic clearance of gallstones General consensus favors either urgent intervention (cholecystectomy) within the first 48 to 72 hours of admission, or briefly delayed intervention (after 72 hours, but during the initial hospitalization) to give an inflamed pancreas time to recover Index cholecytectomy can almost always be accomplished laparoscopically 76

77. Cont. I ndex cholecystectomy is not suitable for all patients, particularly some who have had local pancreatic complications, which includes a large inflammatory mass that extends into the porta hepatis These patients may require an interval cholecystectomy after resolution of the inflammatory process If surgery is required for the management of local complications, then a cholecystectomy is often performed at that time 77

78. Cont. Surgical options Cholecystectomy and operative CBD clearance is probably the best treatment for otherwise healthy patients with obstructive pancreatitis On-table cholangiography Patients who are at high risk for surgical intervention are best treated by endoscopic sphincterotomy , with clearance of stones by ERCP 78

79. Cont. ERCP More recent evidence has suggested that early (within 24 or 48 hours of admission ) ERCP confers no benefit in the absence of concomitant cholangitis , as the offending common duct stone usually passes before ERCP can be performed ( rate of detection of residual stones is only 5% ) T he risks of increasing the severity of pancreatitis , cholangitis , bleeding , and perforation are high If there is persistent cholestasis, an MRCP can be used to detect a common duct stone and can be used as a prerequisite for attempting an ERCP 79

80. Acute pancreatitis and diabetes P rediabetes and diabetes are common after acute pancreatitis and occur in nearly 40% of patients after hospital discharge The prevalence of newly diagnosed diabetes is much higher after acute pancreatitis (23%) than the prevalence of diabetes in the general population (4–9 %) Interestingly , the severity of acute pancreatitis appears to have minimal effect on risk of diabetes 80

81. Cont . The risk of diabetes increases by at least twofold after 5 years as compared with 12 months The implication is that patients recovered from an attack of acute pancreatitis may need follow-up and screening for glucose intolerance 81

82. E nd! 82