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Tavassoli,Alireza نام درس :بيمار يهاي پانكراس اهداف 1-بيماري هاي پانكراس رابشناسد 1-بيماري هاي پانكراس رابشناسد 2-عوامل سبب زاي بيماري هاي پانكراس را.

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Presentation on theme: "Tavassoli,Alireza نام درس :بيمار يهاي پانكراس اهداف 1-بيماري هاي پانكراس رابشناسد 1-بيماري هاي پانكراس رابشناسد 2-عوامل سبب زاي بيماري هاي پانكراس را."— Presentation transcript:

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2 Tavassoli,Alireza

3 نام درس :بيمار يهاي پانكراس اهداف 1-بيماري هاي پانكراس رابشناسد 1-بيماري هاي پانكراس رابشناسد 2-عوامل سبب زاي بيماري هاي پانكراس را بشناسد 2-عوامل سبب زاي بيماري هاي پانكراس را بشناسد 3- راه هاي پيشگيري بيماري هاي پانكراس را بداند. 3- راه هاي پيشگيري بيماري هاي پانكراس را بداند. 4- نحوه مراقبت بيماري هاي پانكراس را فراگيرد. (Surveillance) 4- نحوه مراقبت بيماري هاي پانكراس را فراگيرد. (Surveillance) 5-عوامل خطرزاي بيماري هاي پانكراس را بداند 5-عوامل خطرزاي بيماري هاي پانكراس را بداند 6- ويژگي هاي اپيدميولوژيك بيماري هاي پانكراس را بشناسد. 6- ويژگي هاي اپيدميولوژيك بيماري هاي پانكراس را بشناسد. 7-روش هاي تشخیصی بيماري هاي پانكراس رابشناسد. 7-روش هاي تشخیصی بيماري هاي پانكراس رابشناسد. 8- روش هاي درمان را بداند. 8- روش هاي درمان را بداند.

4 Normal Anatomy & Physiology neutralize chyme neutralize chyme digestive enzymes digestive enzymes hormones hormones

5 Exocrine Function pancreatic duct common bile duct ampulla pancreatic enzymes TAIL BODY HEAD UNCINATE

6 Enzyme Secretion pancreatic duct duodenum acinus microscopic view of pancreatic acini

7 Enzyme Secretion Hormonal CCK gastrin Neural acetylcholine VIP GRP Secretin (hormonal) H 2 O bicarbonate

8 Digestive Enzymes in the Pancreatic Acinar Cell PROTEOLYTICLIPOLYTIC ENZYMES ENZYMESLipase ENZYMESLipase TrypsinogenProphospholipase A2 ChymotrypsinogenCarboxylesterase lipase Proelastase Procarboxypeptidase ANUCLEASES Procarboxypeptidase BDeoxyribonuclease (DNAse) Ribonuclease (RNAse) AMYOLYTIC ENZYMES AmylaseOTHERS Procolipase Trypsin inhibitor

9 Exocrine Stimulation The more proximal the nutrient infusion …the greater the pancreatic stimulation (dog studies) The more proximal the nutrient infusion …the greater the pancreatic stimulation (dog studies) - stomach – maximal stimulation - duodenum – intermediate stimulation - jejunum – minimal / negligible stimulation Elemental formulas tend to cause less stimulation than standard intact formulas Elemental formulas tend to cause less stimulation than standard intact formulas - intact protein > oligopeptides > free amino acids Intravenous nutrients (even lipids) do not appear to stimulate the pancreas Intravenous nutrients (even lipids) do not appear to stimulate the pancreas

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11 Acute Pancreatitis

12 Clinical Case A man with acute onset abdominal pain A man with acute onset abdominal pain h/o alcohol intake h/o alcohol intake Or Gall stone Or Gall stone

13 Acute Pancreatitis Definition Acute inflammatory process involving the pancreas Acute inflammatory process involving the pancreas Usually painful and self-limited Usually painful and self-limited Isolated event or a recurring illness Isolated event or a recurring illness Pancreatic function and morphology return to normal after (or between) attacks Pancreatic function and morphology return to normal after (or between) attacks

14 Acute Pancreatitis Etiology

15 Cholelithiasis Cholelithiasis Ethanol abuse Ethanol abuse Idiopathic Idiopathic Medications Medications Hyperlipidemia Hyperlipidemia ERCP ERCP Trauma Trauma Pancreas divisum Pancreas divisum Hereditary Hereditary Hypercalcemia Hypercalcemia Viral infections Viral infections - Mumps - Coxsackie virus End-stage renal failure End-stage renal failure Penetrating peptic ulcer Penetrating peptic ulcer Acute Pancreatitis Associated Conditions

16 Acute Pancreatitis Causative Drugs AIDS therapy: pentamidine,didanosine AIDS therapy: pentamidine,didanosine Anti-inflammatory: sulindac, salicylates Anti-inflammatory: sulindac, salicylates Antimicrobials: metronidazole, sulfonamides, tetracycline, nitrofurantoin Antimicrobials: metronidazole, sulfonamides, tetracycline, nitrofurantoin Diuretics: furosemide, thiazides Diuretics: furosemide, thiazides IBD: sulfasalazine, mesalamine IBD: sulfasalazine, mesalamine Immunosuppressives: azathioprine, 6-mercaptopurine Immunosuppressives: azathioprine, 6-mercaptopurine Neuropsychiatric: valproic acid Neuropsychiatric: valproic acid Other: calcium, estrogen, tamoxifen, Other: calcium, estrogen, tamoxifen,

17 Pancreas divisum

18 Hereditary Pancreatitis Autosomal dominant with 80% phenotypic penetrance Autosomal dominant with 80% phenotypic penetrance Recurrent acute pancreatitis, chronic pancreatitis, and 50-fold increased risk of pancreatic cancer Recurrent acute pancreatitis, chronic pancreatitis, and 50-fold increased risk of pancreatic cancer

19 Pancreatitis Background Potentially fatal Potentially fatal Mortality – 10-15% Mortality – 10-15% Necrosis determines the prognosis

20 Background Mild AP (no necrosis) – 0% Sterile necrosis – 10% Infected necrosis – 25% Overall mortality: 10-15%

21 What do you think? Amylase or lipase Amylase or lipase Ultrasound or CT scan Ultrasound or CT scan - If yes, When? ICU or medical ward ICU or medical ward Enteral nutrition or TPN Enteral nutrition or TPN Antibiotics Antibiotics ERCP ERCP Surgery Surgery

22 Epidemiology of acute pancreatitis There appears to be an increase in the incidence of acute pancreatitis. There appears to be an increase in the incidence of acute pancreatitis. This rise attributed to increased alcohol consumption This rise attributed to increased alcohol consumption No seasonal or weekly No seasonal or weekly Men are affected much more than women Main age group affected is 40–60 year olds. Main age group affected is 40–60 year olds.

23 failed protective mechanisms acinar cell injury premature enzyme activation Acute Pancreatitis Pathogenesis

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25 autodigestion of pancreatic tissue release of enzymes into the circulation activation of white blood cells local complications local vascular insufficiency premature enzyme activation distant organ failure Acute Pancreatitis Pathogenesis

26 STAGE 1: Pancreatic Injury STAGE 1: Pancreatic Injury - Edema - Inflammation STAGE 2: Local Effects STAGE 2: Local Effects - Retroperitoneal edema - Ileus STAGE 3: Systemic Complications STAGE 3: Systemic Complications - Hypotension/shock - Metabolic disturbances - Sepsis/organ failure SEVERITYMildSevere Acute Pancreatitis Pathogenesis

27 Pathophysiology of necrosis infection h/h/ h/

28 Pancreatitis Clinical Presentation Pain: Steady & severe in nature; located in the epigastric or umbilical region; may radiate to the back. Worsened by lying supine; may be lessened by flexed knee, curved-back position. Pain: Steady & severe in nature; located in the epigastric or umbilical region; may radiate to the back. Worsened by lying supine; may be lessened by flexed knee, curved-back position. Vomiting: Varies in severity, but is usually protracted, worsened by ingestion of food or fluid. Does not relieve the pain. Usually accompanied by nausea. Vomiting: Varies in severity, but is usually protracted, worsened by ingestion of food or fluid. Does not relieve the pain. Usually accompanied by nausea.

29 Pancreatitis con’t…… Fever: Rarely exceeds 39 C. Fever: Rarely exceeds 39 C. Abdominal Finding: Rigidity, tenderness, guarding, distended Abd, decreased or absent peristalsis and paralytic ileus.Fatty stools-(steatorrhea) Abdominal Finding: Rigidity, tenderness, guarding, distended Abd, decreased or absent peristalsis and paralytic ileus.Fatty stools-(steatorrhea) Laboratory Finding: Elevation of WBC count ,000. lipase and amylase(5 to 40 times); elevated( glucose, bilirubin, alkaline phosphatase.,Urine amylase ).Abnormal low serum CA, Na & Mg.-due to dehydration. Binding of Ca in areas of fat necrosis. Laboratory Finding: Elevation of WBC count ,000. lipase and amylase(5 to 40 times); elevated( glucose, bilirubin, alkaline phosphatase.,Urine amylase ).Abnormal low serum CA, Na & Mg.-due to dehydration. Binding of Ca in areas of fat necrosis.

30 AcutePancreatitis

31 AcutePancreatitis

32 AcutePancreatitis

33 AcutePancreatitis

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39 Acute Pancreatitis Differential Diagnosis Choledocholithiasis Choledocholithiasis Perforated ulcer Perforated ulcer Mesenteric ischemia Mesenteric ischemia Intestinal obstruction Intestinal obstruction Ectopic pregnancy Ectopic pregnancy

40 Symptoms & Signs Symptoms & Signs - Abdominal pain Laboratory Laboratory - Elevated amylase or lipase > 3x upper limits of normal > 3x upper limits of normal Imaging Imaging - Abnormal sonogram or CT Acute Pancreatitis Diagnosis

41 EtOH: history EtOH: history Gallstones: abnormal LFTs & sonographY Gallstones: abnormal LFTs & sonographY Hyperlipidemia: lipemic serum, Tri>1,000 Hyperlipidemia: lipemic serum, Tri>1,000 Hypercalcemia: elevated Ca Hypercalcemia: elevated Ca Trauma: history Trauma: history Medications: history Medications: history

42 Abdominal Exam - Abdominal tenderness and rigidity - Bowel sounds decreased - Palpable upper abdominal mass Acute fluid collections and pseudocysts Skin Exam Skin Exam - Erythematous skin Nodule (Subcutaneous Fat Necrosis) Subcutaneous Fat NecrosisSubcutaneous Fat Necrosis - Cullen's Sign (periumbilical discoloration) Cullen's Sign Cullen's Sign - Turner's Sign (flank discoloration) * due to exudation of blood-stained fluid into the subcutaneous tissue, usually 72 h into the illness. Turner's Sign Turner's Sign

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44 Acute Pancreatitis Clinical Manifestations PANCREATICPERIPANCREATIC Adjacent viscera: SYSTEMIC Mild: edema, inflammation, fat necrosis Severe: phlegmon, necrosis, hemorrhage, infection, abscess, fluid collections Retroperitoneum, perirenal spaces, mesocolon, omentum, and mediastinum ileus, obstruction, perforation ileus, obstruction, perforation Cardiovascular: hypotension Pulmonary: pleural effusions, ARDS Renal: acute tubular necrosis Hematologic: disseminated intravascular coag. Metabolic: hypocalcemia, hyperglycemia

45 Diagnosis: Biochemical - Serum Amylase elevated Serum Amylase Serum Amylase Nonspecific Nonspecific Returns to normal in hours Returns to normal in hours Normal amylase does not exclude pancreatitis Normal amylase does not exclude pancreatitis Level of elevation does not predict disease severity Level of elevation does not predict disease severity - Serum Lipase elevated Lipase Specific for pancreatic disease Specific for pancreatic disease Returns to normal in 7-14 days Returns to normal in 7-14 days

46 Diagnosis: Biochemical White Blood Cells White Blood Cells White Blood Cells White Blood Cells increased to 15k-20k increased to 15k-20k Hypertriglyceridemia (15%) Hypertriglyceridemia (15%) Hypertriglyceridemia liver Function Tests liver Function Tests liver Function Tests liver Function Tests (ALP) (AST),elevated (ALP) (AST),elevated (LDH) elevated (Poor prognosis) (LDH) elevated (Poor prognosis) Hyperglycemia HyperglycemiaHyperglycemia Albumine Albumine (Poor prognosis) - Serum Electrolytes Hypocalcemia (25%) Hypocalcemia (25%) Hypocalcemia

47 Another criteria often used to assess the severity of pancreatitis is the (APACHE-II). Another criteria often used to assess the severity of pancreatitis is the (APACHE-II). A cute P hysiology A nd C hronic H ealth E valuation age and vital signs age and vital signs Specific laboratory parameters, Specific laboratory parameters, Chronic health status Chronic health status The main advantage is the immediate assessment of the severity of pancreatitis. A score of eight or more at admission is usually considered indicative of severe disease

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49 Predictors of Severity Why are they needed? Why are they needed? - Appropriate triage & therapy - compare results of studies of the impact of therapy When are they needed? When are they needed? - optimally, within the first 24 hours Which is the best? Which is the best?

50 Ranson Criteria Alcoholic Pancreatitis AT ADMISSION 1. Age > 55 years 2. WBC > 16, Glucose > AST > 250 IU/L 5. LDH > 350 IU/L WITHIN 48 HOURS 1. HCT drop > 10% 2. BUN > 5 3. Arterial PO2 < 60 mm Hg 4. Base deficit > 4 mEq/L 5. Serum Ca < 8 6. Fluid sequestration > 6L Number Mortality <21% 3-416%5-640%7-8100%

51 Glasgow Criteria Non-alcoholic Pancreatitis 1. WBC > 15, Glucose > BUN > Arterial PO2 < 60 mm Hg 5. Ca < 8 6. Albumin < LDH > 600 U/L 8. AST or ALT > 200 U/L

52 CT Severity Index appearancenormalenlargedinflamed 1 fluid collection 2 or more collections gradeABCDE score01234 necrosisnone < 33% 33-50% > 50% score0246 scoremorbiditymortality1-24%0% %17% Balthazar et al. Radiology 1990.

53 Useful markers of severe disease. Pleural effusion Pleural effusion BMI (High body mass index) BMI (High body mass index) Necrosis on contrast-enhanced CT-SCAN Necrosis on contrast-enhanced CT-SCAN CRP level greater than 150 mg/L at 48 h CRP level greater than 150 mg/L at 48 h Infection of the necrotic tissue after the first week of illness is the major determinant of later outcome. Infection of the necrotic tissue after the first week of illness is the major determinant of later outcome.

54 Pancreatic necrosis

55 CT-guided percutaneous fine-needle aspiration of the pancreatic tail

56 Immediate assessment Clinical assessment including great care to assess respiratory, cardiovascular and renal compromise. Immediate assessment Clinical assessment including great care to assess respiratory, cardiovascular and renal compromise. Organ failure ? Organ failure ? BMI?. There is considerable risk (> 30 kg/m2) or much greater risk > 40 kg/m2 BMI?. There is considerable risk (> 30 kg/m2) or much greater risk > 40 kg/m2 Chest X-ray. Is there a pleural effusion present? Chest X-ray. Is there a pleural effusion present? CT.Scan Is there more than 30% of the volume of the pancreas malperfused? CT.Scan Is there more than 30% of the volume of the pancreas malperfused? Scoring. Is it high score or low? Scoring. Is it high score or low?

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58 Resuscitation Transudation of fluid from the intravascular space to the peritoneum is the principle cause of hypovolemia in AP. Transudation of fluid from the intravascular space to the peritoneum is the principle cause of hypovolemia in AP. Assessment of the patient’s volume status determined by heart rate, blood pressure, urine output and CVP line. Assessment of the patient’s volume status determined by heart rate, blood pressure, urine output and CVP line.

59 Treatment of Mild Pancreatitis Pancreatic rest Pancreatic rest Supportive care Supportive care - fluid resuscitation – watch BP and urine output - pain control - NG tubes,H 2 blockers,PPIs helpful?? Refeeding (usually 3 to 7 days) Refeeding (usually 3 to 7 days) - bowel sounds present - patient is hungry - nearly pain-free (off IV narcotics) - amylase & lipase not very useful here

60 Treatment of Severe Pancreatitis Pancreatic rest & supportive care Pancreatic rest & supportive care - fluid resuscitation* – may require 5-10 liters/day - careful pulmonary & renal monitoring – ICU - maintain hematocrit of 26-30% - pain control – PCA pump - correct electrolyte derangements (K +, Ca ++, Mg ++ ) Rule-out necrosis Rule-out necrosis - contrasted CT scan at hours - prophylactic antibiotics if present - surgical debridement if infected Nutritional support Nutritional support - may be NPO for weeks, TPN

61 Analgesia Severe pain should be treated with meperidine 50 to 100 mg IM q 3 to 4 h prn in patients with normal renal function (morphine causes the sphincter of Oddi to contract and should be avoided). Severe pain should be treated with meperidine 50 to 100 mg IM q 3 to 4 h prn in patients with normal renal function (morphine causes the sphincter of Oddi to contract and should be avoided).

62 Antibiotic prophylaxis Infectious complications are still regarded as the primary cause of mortality in severe pancreatitis.Thus, it is essential to identify the presence of pancreatic necrosis and take measures to prevent infection. Infectious complications are still regarded as the primary cause of mortality in severe pancreatitis.Thus, it is essential to identify the presence of pancreatic necrosis and take measures to prevent infection. The current recommendation is the use of a systemic antibiotic such as imipenem- cilastatin 500 mg three times a day for 2 weeks in patients with documented pancreatic necrosis. The current recommendation is the use of a systemic antibiotic such as imipenem- cilastatin 500 mg three times a day for 2 weeks in patients with documented pancreatic necrosis.

63 Role of ERCP in pancreatitis 1-Gallstone pancreatitis 1-Gallstone pancreatitis - Cholangitis - Obstructive jaundice 2-Recurrent acute pancreatitis 2-Recurrent acute pancreatitis - Structural abnormalities - Neoplasm - Bile sampling for microlithiasis 3-Sphincterotomy in patients not suitable for cholecystectomy 3-Sphincterotomy in patients not suitable for cholecystectomy

64 Reduced Oral Intake in Acute Pancreatitis Abdominal pain with food Abdominal pain with food Nausea and vomiting Nausea and vomiting Gastric atony Gastric atony Ileus Ileus Partial duodenal obstruction Partial duodenal obstruction

65 Summary 1-The overall mortality ranges from 2 to 10%. The incidence in males is usually 10–30% higher than in females. 1-The overall mortality ranges from 2 to 10%. The incidence in males is usually 10–30% higher than in females. 2-The commonest cause is gallstones with alcohol being the next most common cause. 2-The commonest cause is gallstones with alcohol being the next most common cause. 3-Patients with acute pancreatitis present with upper abdominal pain and/or different degrees of organ failure. 3-Patients with acute pancreatitis present with upper abdominal pain and/or different degrees of organ failure. 4-The diagnosis is suspected by a typical clinical presentation and supported by raised serum amylase. Atypical presentations may require confirmation by CT imaging. 4-The diagnosis is suspected by a typical clinical presentation and supported by raised serum amylase. Atypical presentations may require confirmation by CT imaging. 5-Immediate management comprises analgesics, intravenous fluids and monitoring. 5-Immediate management comprises analgesics, intravenous fluids and monitoring.

66 6-Acute pancreatitis, severity best defined by failure of one or more organ systems and/or the Acute Physiology and Chronic Health Evaluation, (APACHE II) score of 8 or more. 6-Acute pancreatitis, severity best defined by failure of one or more organ systems and/or the Acute Physiology and Chronic Health Evaluation, (APACHE II) score of 8 or more. 7-Gallstone etiology is usually identified by early routine abdominal ultrasonography. 7-Gallstone etiology is usually identified by early routine abdominal ultrasonography. 8-The majority of patients have mild pancreatitis and recover without additional treatment. 8-The majority of patients have mild pancreatitis and recover without additional treatment. 9-In 20%, the disease is severe and is associated with a mortality of about 20%. 9-In 20%, the disease is severe and is associated with a mortality of about 20%. 10-Patients with severe pancreatitis require management in a high dependency or intensive care setting; this may require transfer to a specialized unit. 10-Patients with severe pancreatitis require management in a high dependency or intensive care setting; this may require transfer to a specialized unit. 11-Clinical severity is paralleled by the degree of pancreatic and peripancreatic tissue necrosis as defined by dynamic CT. 11-Clinical severity is paralleled by the degree of pancreatic and peripancreatic tissue necrosis as defined by dynamic CT. 12-Antibiotic prophylaxis is advised in patients with greater than 30% necrosis and imipenem is recommended currently. 12-Antibiotic prophylaxis is advised in patients with greater than 30% necrosis and imipenem is recommended currently.

67 12- Enteral nutrition probably retains the integrity of the intestinal mucosal barrier and hence early mesenteric feeding is recommended. Parenteral nutrition is rarely indicated. 13- In patients with severe gallstone pancreatitis, early endoscopic retrograde cholangiography is indicated and, where appropriate, a sphincterotomy and clearance of the bile duct. 13- In patients with severe gallstone pancreatitis, early endoscopic retrograde cholangiography is indicated and, where appropriate, a sphincterotomy and clearance of the bile duct. 14--Where infection of pancreatic necrosis is proved by the presence of positive FNA or free gas in the area of necrosis, surgical intervention is indicated. 14--Where infection of pancreatic necrosis is proved by the presence of positive FNA or free gas in the area of necrosis, surgical intervention is indicated. 15--In sterile necrosis, continued conservative management is justified. 15--In sterile necrosis, continued conservative management is justified. 16--Patients with gallstone pancreatitis should either undergo cholecystectomy or endoscopic sphincterotomy and bile duct clearance prior to discharge. 16--Patients with gallstone pancreatitis should either undergo cholecystectomy or endoscopic sphincterotomy and bile duct clearance prior to discharge. 17--Acute fluid collections are a feature of severe acute pancreatitis and often resolve spontaneously. 17--Acute fluid collections are a feature of severe acute pancreatitis and often resolve spontaneously. 18--Pancreatic and peripancreatic abscesses, symptomatic pseudocysts and other ductal disruptions require interventional treatment. 18--Pancreatic and peripancreatic abscesses, symptomatic pseudocysts and other ductal disruptions require interventional treatment.

68 Factors Differentiating Mild from Severe Pancreatitis ParameterMildPancreatitisSeverePancreatitis Admissions80%20% Pancreatic necrosis NoYes Oral diet within 5 days 80%0% Morbidity8%38% Mortality3%27%

69 Total Enteral Nutrition in Severe Pancreatitis may start as early as possible may start as early as possible - when emesis has resolved - ileus is not present nasojejunal route preferred over nasoduodenal nasojejunal route preferred over nasoduodenal likely decreases risk of infectious complications by reducing transmigration of colonic bacteria likely decreases risk of infectious complications by reducing transmigration of colonic bacteria

70 Conclusions ( MOUSE CLICK ) Acute pancreatitis is a self-limited disease Acute pancreatitis is a self-limited disease Most cases are mild. Most cases are mild. Gallstones and alcohol are the leading causes of acute pancreatitis. Gallstones and alcohol are the leading causes of acute pancreatitis. In mild pancreatitis, nutritional support is usually not required In mild pancreatitis, nutritional support is usually not required In severe pancreatitis, nutritional support will likely be required with the enteral route preferred over TPN because of both safety and cost. In severe pancreatitis, nutritional support will likely be required with the enteral route preferred over TPN because of both safety and cost.

71 Evidence A. Proven A. Proven - > 2 well designed trials, randomized B. Possible/ Probable B. Possible/ Probable - 1 well designed study, randomized C. Consensus C. Consensus - agreed opinion with no supportive evidence

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