logging in or signing up Acute Pancreatitis kwolden Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 135 Category: Education License: All Rights Reserved Like it (0) Dislike it (0) Added: November 16, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Acute Pancreatitis: Acute Pancreatitis Kevin W. Olden, MD Vice Chair, Department of Medicine St. Joseph’s Hospital & Medical CenterThe Pancreas: The PancreasSlide 3: “The pancreas is the mischief maker of the abdomen.” Theodore KocherPancreatic Acinar Cell Secretion Products: Pancreatic Acinar Cell Secretion Products Proenzymes EnzymesCT of the Pancreas: CT of the Pancreas A aorta C vena cava G gallstone I small intestine K left kidney L liver P portal vein S stomach V vertebra Arrows splenic veinSlide 6: Pancreatitis is a complex disorder of the exocrine pancreas, which is characterized by acute acinar cell injury and both regional and systemic inflammatory responses. Pancreatitis is predominantly due to activation of intracellular trypsinogen to trypsin through various pathways PancreatitisEtiology: Etiology Alcoholism Direct injury (25%Cases) Malnutrition Hyperlipidemia Hypersecretion Gallstone Bile reflux (50% Cases) Reflux of activated enzymes Pancreatic ductal hypertension Ischemia Drug induced L-asparaginase, azathioprine, ethanol, steroids Hyperparathyroidism/hypercalcaemia Trauma ERCP/Other proceduresEtiology: Etiology Autoimmune - Hereditary pancreatitis Infectious - Mumps IdiopathicHOW TO DIAGNOSE A CASE OF PANCREATITIS: HOW TO DIAGNOSE A CASE OF PANCREATITISAcute Pancreatitis Epidemiology: Acute Pancreatitis Epidemiology 3.8 – 4.8 / 100,000 Greater than 300,000 hospital staysDefinition: Definition Typical epigastric pain with Increased amylase or lipase (3x greater than normal) or Imaging c/w pancreatitisResearch Question: Research Question Do we need to do amylase and lipase?Symptoms and Signs: Symptoms and Signs Abdominal pain Nausea and vomiting Anorexia Fever Hypovolemia Ileus Abdominal tenderness Left pleural effusion Altered mental status Jaundice ARDS Mortality rate-1% for mild acute pancreatitis 75-90% for severe acute pancreatitis. Overall mortality rate of 15-20%Clinical Investigation: Clinical Investigation Complete blood count Renal function tests Liver function S.amylase - 3-4 times increase (Normal range <115IU) S.lipase - lipase levels may have a slightly greater sensitivity, particularly when measured late (> 24 hours) after initial presentation Serum calcium Arterial blood gasSlide 15: CXR - Basal atelectasis, elevation of diaphragm, pleural effusion AXR - Multiple air fluid interphase, pancreatic calcifications, calcified gall stones, “sentinel loop” sign, “colon cut off” sign, “renal halo” sign US pancreas - Interstitial edema, extra pancreatic fluid collections, gall stones, ascites, dilated CBD Limited value due to presence of intestinal gas CT abdomen Clinical InvestigationSentinel Loop Sign: Sentinel Loop SignColon Cut Off Sign: Colon Cut Off SignWhen to Take a CT: When to Take a CT When the diagnosis is in doubt Patients with persisting organ failure Signs of sepsis Deterioration in clinical status after admission CRP > 110 mg/lt Ranson score > 3, APACHE II score > 8CT Grading: CT Grading [A] Normal pancreas 0 [B] Edematous pancreatitis 1 [C] B plus mild extra pancreatic changes 2 [D] Severe extrapancreatic changes including one fluid collection 3 [E] Multiple or extensive extrapancreatic collections 4 Necrosis CT severity index = CT grade + necrosis scorePrognostication: Prognostication HOW? AND WHY?How ?: How ? Single prognostic factors Multifactor grading systemAtlanta Criteria for Severe Acute Pancreatitis: Atlanta Criteria for Severe Acute PancreatitisRanson’s Criteria: Ranson’s Criteria At Admission Age in years >55years White blood cell count > 16000/mcL Blood glucose > 11 mmol/L (>200 mg/dL) Serum AST > 250 IU/L Serum LDH > 350 IU/L After 48 Hours Haematocrit fall > 10% Increase in BUN by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Hypocalcemia (serum calcium < 2.0 mmol/L (<8.0 mg/dL)) Hypoxemia (P O2 < 60 mmHg) Base deficit > 4Meq/L Estimated fluid sequestration > 6L If the score >=3, severe pancreatitis likely If the score < 3, severe pancreatitis is unlikelyApache II: Apache II Total Acute Physiology Score Temperature (°C) Mean arterial pressure (mmHg) Heart rate Respiratory rate Fi O2 Serum HCO3-(mmol/L) Arterial pH Serum sodium (mmol/L) Serum potassium (mmol/L) Serum creatinine Hematocrit (%) WBC (x103/ mm3 ) B. Age Points C. Chronic Health Points Score of 8 or more indicates severe acute pancreatitisSevere Acute Pancreatitis: Severe Acute PancreatitisFeatures that May Predict a Severe Attack Present within 48 hours of Admission to Hospital : Features that May Predict a Severe Attack Present within 48 hours of Admission to Hospital Clinical impression of severity body mass index >30 Pleural effusion on chest radiograph APACHE II score > 8 Clinical impression of severity APACHE II score > 8 Glasgow score 3 or more c reactive protein >150mg/I Persisting organ failure for 48h Multiple or progressive organ failure Initial Assessment 24 – 48 hrs After AdmissionSlide 27: Patient Management Initially, on confirmation of diagnosis admit in ICU General Management: Fluid and electrolyte management by CVP line. Hourly urine out put Monitoring BP, pulse rate, O2 saturation , blood gas analysis to determine ventilatory support. Depending on cardiovascular changes arterial catheters. Strict asepsis NursingNutrition : Nutrition Mild acute pancreatitis Allow oral fluids from day 1 until appetite returns Severe acute pancreatitis Begin fluids as early as 72 hrsFactors Supporting Early Enteral Nutrition: Factors Supporting Early Enteral Nutrition Mucosal integrity is important in ASP Glutamine, arginine, -3 fatty acids, nucleotides have important role in critically ill pts in maintenance of mucosal integrity and immune status Early parenteral nutrition harmfulRole of Antibiotics: Role of Antibiotics Prophylactic antibiotics have shown no decrease in mortality in severe acute pancreatitis. Conditions where antibiotics are justified are: Gas in retroperitoneal space Needle aspiration of necrotic material confirms infection Presence of necrosis – 15 -> 50% CRP of > 120 mg/L Peripancreatic fluid collection APACHE II score of > 6 Organ dysfunctionDrug Treatment: Drug Treatment Cefuroxime or imipenem are the usual drugs of choice Duration: 10-14 days or longer depending on the course of the disease. Use of somatostatin analogues Octreotide 0.5 mgm scEarly ERCP in Acute Pancreatitis due to Gallstone Disease: Early ERCP in Acute Pancreatitis due to Gallstone Disease Early intervention(< 72 hrs) is favored in severe biliary pancreatitis In patients with acute biliary pancreatitis but without obstructive jaundice, early ERCP and papillotomy were not beneficialSlide 33: Biliary origin? Jaundice sepsis? Suspicion of retained stone? Urgent ERCP No ERCP No No Yes Yes Yes Elective ERCP No ERCP NoTiming of Cholecystectomy: Timing of Cholecystectomy In mild pancreatitis, it is advisable to undertake laparoscopic cholecystectomy with intraoperative cholangiogram within 10 days. In severe cases, endoscopic cholangiopancreatography + endoscopic sphincterotomy(<48h) followed by LC once the inflammatory process is resolved.Surgery for Acute Pancreatitis: Surgery for Acute Pancreatitis Pancreatic abscess Pancreatic necrosisIndication for Surgical Management of Necrotizing Pancreatitis and Pancreatic Abscess : Indication for Surgical Management of Necrotizing Pancreatitis and Pancreatic Abscess Clinical Criteria Persistant sepsis No response to intensive care treatment (> 3 days), Persisting or increasing local or systemic complications Surgery in necrotising pancreatitis Debridement with closure over drains Debridement with open packing Debridement with closure over irrigation drains and postoperative lavage.(Beger surgery) Minimally invasive surgeryTiming of Surgery: Timing of Surgery Delaying surgery till the second to third week from the onset of disease is ideal Early intervention is unavoidable In the presence of uncertain diagnosis. Complications like hemorrhage associated with pancreatic necrosisSlide 38: Acute Necrotising Pancreatitis ICU Care CECT Focal necrosis Extended necrosis Antibiotics Response Sepsis No response FNAC Infected necrosis Nonsurgical Surgery SurgeryComplications of Pancreatitis: Complications of Pancreatitis Acute Fluid Collections Develops in 30-50% of patients with severe pancreatitis Usually peripancreatic or intrapancreatic Unlike psuedocyst lacks a wall Either regresses or evolves into psuedocyst Pancreatic necrosis or abscessComplications of Pancreatitis: Complications of Pancreatitis Psuedocyst of Pancreas Features Cyst wall lacks epithelial lining. It is predominantly formed by granulation tissue and fibrosis. Most psuedocysts communicate with ductal system. Persistently raised S.amylase levels Most cases regress by themselvesIntervention in Pseudocyst: Intervention in Pseudocyst Symptomatic Enlarging Size > 6 cm Duration more than 6 weeks Infected pseudocysts Complications due to pressure symptoms GOO/obstructive jaundice Haemosuccus pancreaticusTreatment: Treatment Percutaneous drainage - for poor risk patients only Open procedures Distal pancreatectomy Cystogastrostomy Cystoduodenostomy Roux – en – y cystojejunostomy Whipple procedure Endoscopic procedures – stenting Laparoscopic proceduresSlide 43: S. lipase is more useful than amylase in diagnosing acute pancreatitis Prognosticate the patient Single and multiple prognostic factors can be used Identify acute mild and severe pancreatitis Timely resuscitation and invasive monitoring are standard No role for nasogastric tube SummarySlide 44: Early enteral feeding Immune enhancing feeds has a role Prophylactic antibiotics for selected cases Early ERCP in severe biliary pancreatitis Surgery in selected cases of necrotising pancreatitis Delayed surgery is ideal unless indicated for early surgery SummarySlide 45: For patients needing debridement, open surgical techniques remain the "gold standard" of management Debridement with open packing and lavage in early cases Debridement with closed drainage in elective cases Advances in minimally invasive technology hold promise as adjuncts to open procedures in the future SummaryThank You: Thank You You do not have the permission to view this presentation. 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Acute Pancreatitis kwolden Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 135 Category: Education License: All Rights Reserved Like it (0) Dislike it (0) Added: November 16, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Acute Pancreatitis: Acute Pancreatitis Kevin W. Olden, MD Vice Chair, Department of Medicine St. Joseph’s Hospital & Medical CenterThe Pancreas: The PancreasSlide 3: “The pancreas is the mischief maker of the abdomen.” Theodore KocherPancreatic Acinar Cell Secretion Products: Pancreatic Acinar Cell Secretion Products Proenzymes EnzymesCT of the Pancreas: CT of the Pancreas A aorta C vena cava G gallstone I small intestine K left kidney L liver P portal vein S stomach V vertebra Arrows splenic veinSlide 6: Pancreatitis is a complex disorder of the exocrine pancreas, which is characterized by acute acinar cell injury and both regional and systemic inflammatory responses. Pancreatitis is predominantly due to activation of intracellular trypsinogen to trypsin through various pathways PancreatitisEtiology: Etiology Alcoholism Direct injury (25%Cases) Malnutrition Hyperlipidemia Hypersecretion Gallstone Bile reflux (50% Cases) Reflux of activated enzymes Pancreatic ductal hypertension Ischemia Drug induced L-asparaginase, azathioprine, ethanol, steroids Hyperparathyroidism/hypercalcaemia Trauma ERCP/Other proceduresEtiology: Etiology Autoimmune - Hereditary pancreatitis Infectious - Mumps IdiopathicHOW TO DIAGNOSE A CASE OF PANCREATITIS: HOW TO DIAGNOSE A CASE OF PANCREATITISAcute Pancreatitis Epidemiology: Acute Pancreatitis Epidemiology 3.8 – 4.8 / 100,000 Greater than 300,000 hospital staysDefinition: Definition Typical epigastric pain with Increased amylase or lipase (3x greater than normal) or Imaging c/w pancreatitisResearch Question: Research Question Do we need to do amylase and lipase?Symptoms and Signs: Symptoms and Signs Abdominal pain Nausea and vomiting Anorexia Fever Hypovolemia Ileus Abdominal tenderness Left pleural effusion Altered mental status Jaundice ARDS Mortality rate-1% for mild acute pancreatitis 75-90% for severe acute pancreatitis. Overall mortality rate of 15-20%Clinical Investigation: Clinical Investigation Complete blood count Renal function tests Liver function S.amylase - 3-4 times increase (Normal range <115IU) S.lipase - lipase levels may have a slightly greater sensitivity, particularly when measured late (> 24 hours) after initial presentation Serum calcium Arterial blood gasSlide 15: CXR - Basal atelectasis, elevation of diaphragm, pleural effusion AXR - Multiple air fluid interphase, pancreatic calcifications, calcified gall stones, “sentinel loop” sign, “colon cut off” sign, “renal halo” sign US pancreas - Interstitial edema, extra pancreatic fluid collections, gall stones, ascites, dilated CBD Limited value due to presence of intestinal gas CT abdomen Clinical InvestigationSentinel Loop Sign: Sentinel Loop SignColon Cut Off Sign: Colon Cut Off SignWhen to Take a CT: When to Take a CT When the diagnosis is in doubt Patients with persisting organ failure Signs of sepsis Deterioration in clinical status after admission CRP > 110 mg/lt Ranson score > 3, APACHE II score > 8CT Grading: CT Grading [A] Normal pancreas 0 [B] Edematous pancreatitis 1 [C] B plus mild extra pancreatic changes 2 [D] Severe extrapancreatic changes including one fluid collection 3 [E] Multiple or extensive extrapancreatic collections 4 Necrosis CT severity index = CT grade + necrosis scorePrognostication: Prognostication HOW? AND WHY?How ?: How ? Single prognostic factors Multifactor grading systemAtlanta Criteria for Severe Acute Pancreatitis: Atlanta Criteria for Severe Acute PancreatitisRanson’s Criteria: Ranson’s Criteria At Admission Age in years >55years White blood cell count > 16000/mcL Blood glucose > 11 mmol/L (>200 mg/dL) Serum AST > 250 IU/L Serum LDH > 350 IU/L After 48 Hours Haematocrit fall > 10% Increase in BUN by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Hypocalcemia (serum calcium < 2.0 mmol/L (<8.0 mg/dL)) Hypoxemia (P O2 < 60 mmHg) Base deficit > 4Meq/L Estimated fluid sequestration > 6L If the score >=3, severe pancreatitis likely If the score < 3, severe pancreatitis is unlikelyApache II: Apache II Total Acute Physiology Score Temperature (°C) Mean arterial pressure (mmHg) Heart rate Respiratory rate Fi O2 Serum HCO3-(mmol/L) Arterial pH Serum sodium (mmol/L) Serum potassium (mmol/L) Serum creatinine Hematocrit (%) WBC (x103/ mm3 ) B. Age Points C. Chronic Health Points Score of 8 or more indicates severe acute pancreatitisSevere Acute Pancreatitis: Severe Acute PancreatitisFeatures that May Predict a Severe Attack Present within 48 hours of Admission to Hospital : Features that May Predict a Severe Attack Present within 48 hours of Admission to Hospital Clinical impression of severity body mass index >30 Pleural effusion on chest radiograph APACHE II score > 8 Clinical impression of severity APACHE II score > 8 Glasgow score 3 or more c reactive protein >150mg/I Persisting organ failure for 48h Multiple or progressive organ failure Initial Assessment 24 – 48 hrs After AdmissionSlide 27: Patient Management Initially, on confirmation of diagnosis admit in ICU General Management: Fluid and electrolyte management by CVP line. Hourly urine out put Monitoring BP, pulse rate, O2 saturation , blood gas analysis to determine ventilatory support. Depending on cardiovascular changes arterial catheters. Strict asepsis NursingNutrition : Nutrition Mild acute pancreatitis Allow oral fluids from day 1 until appetite returns Severe acute pancreatitis Begin fluids as early as 72 hrsFactors Supporting Early Enteral Nutrition: Factors Supporting Early Enteral Nutrition Mucosal integrity is important in ASP Glutamine, arginine, -3 fatty acids, nucleotides have important role in critically ill pts in maintenance of mucosal integrity and immune status Early parenteral nutrition harmfulRole of Antibiotics: Role of Antibiotics Prophylactic antibiotics have shown no decrease in mortality in severe acute pancreatitis. Conditions where antibiotics are justified are: Gas in retroperitoneal space Needle aspiration of necrotic material confirms infection Presence of necrosis – 15 -> 50% CRP of > 120 mg/L Peripancreatic fluid collection APACHE II score of > 6 Organ dysfunctionDrug Treatment: Drug Treatment Cefuroxime or imipenem are the usual drugs of choice Duration: 10-14 days or longer depending on the course of the disease. Use of somatostatin analogues Octreotide 0.5 mgm scEarly ERCP in Acute Pancreatitis due to Gallstone Disease: Early ERCP in Acute Pancreatitis due to Gallstone Disease Early intervention(< 72 hrs) is favored in severe biliary pancreatitis In patients with acute biliary pancreatitis but without obstructive jaundice, early ERCP and papillotomy were not beneficialSlide 33: Biliary origin? Jaundice sepsis? Suspicion of retained stone? Urgent ERCP No ERCP No No Yes Yes Yes Elective ERCP No ERCP NoTiming of Cholecystectomy: Timing of Cholecystectomy In mild pancreatitis, it is advisable to undertake laparoscopic cholecystectomy with intraoperative cholangiogram within 10 days. In severe cases, endoscopic cholangiopancreatography + endoscopic sphincterotomy(<48h) followed by LC once the inflammatory process is resolved.Surgery for Acute Pancreatitis: Surgery for Acute Pancreatitis Pancreatic abscess Pancreatic necrosisIndication for Surgical Management of Necrotizing Pancreatitis and Pancreatic Abscess : Indication for Surgical Management of Necrotizing Pancreatitis and Pancreatic Abscess Clinical Criteria Persistant sepsis No response to intensive care treatment (> 3 days), Persisting or increasing local or systemic complications Surgery in necrotising pancreatitis Debridement with closure over drains Debridement with open packing Debridement with closure over irrigation drains and postoperative lavage.(Beger surgery) Minimally invasive surgeryTiming of Surgery: Timing of Surgery Delaying surgery till the second to third week from the onset of disease is ideal Early intervention is unavoidable In the presence of uncertain diagnosis. Complications like hemorrhage associated with pancreatic necrosisSlide 38: Acute Necrotising Pancreatitis ICU Care CECT Focal necrosis Extended necrosis Antibiotics Response Sepsis No response FNAC Infected necrosis Nonsurgical Surgery SurgeryComplications of Pancreatitis: Complications of Pancreatitis Acute Fluid Collections Develops in 30-50% of patients with severe pancreatitis Usually peripancreatic or intrapancreatic Unlike psuedocyst lacks a wall Either regresses or evolves into psuedocyst Pancreatic necrosis or abscessComplications of Pancreatitis: Complications of Pancreatitis Psuedocyst of Pancreas Features Cyst wall lacks epithelial lining. It is predominantly formed by granulation tissue and fibrosis. Most psuedocysts communicate with ductal system. Persistently raised S.amylase levels Most cases regress by themselvesIntervention in Pseudocyst: Intervention in Pseudocyst Symptomatic Enlarging Size > 6 cm Duration more than 6 weeks Infected pseudocysts Complications due to pressure symptoms GOO/obstructive jaundice Haemosuccus pancreaticusTreatment: Treatment Percutaneous drainage - for poor risk patients only Open procedures Distal pancreatectomy Cystogastrostomy Cystoduodenostomy Roux – en – y cystojejunostomy Whipple procedure Endoscopic procedures – stenting Laparoscopic proceduresSlide 43: S. lipase is more useful than amylase in diagnosing acute pancreatitis Prognosticate the patient Single and multiple prognostic factors can be used Identify acute mild and severe pancreatitis Timely resuscitation and invasive monitoring are standard No role for nasogastric tube SummarySlide 44: Early enteral feeding Immune enhancing feeds has a role Prophylactic antibiotics for selected cases Early ERCP in severe biliary pancreatitis Surgery in selected cases of necrotising pancreatitis Delayed surgery is ideal unless indicated for early surgery SummarySlide 45: For patients needing debridement, open surgical techniques remain the "gold standard" of management Debridement with open packing and lavage in early cases Debridement with closed drainage in elective cases Advances in minimally invasive technology hold promise as adjuncts to open procedures in the future SummaryThank You: Thank You