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![Risk factors
• Gall stone and ethanol abuse [about 70-80% of cases]
• In pediatric age group Blunt abdominal trauma, Systemic disease
• Autoimmune / Drug induced in patients with rheumatologic
conditions such as SLE and Sjogren syndrome.](https://image.slidesharecdn.com/acutepancreatitis-240511072547-4c88377e/75/Etiology-and-Management-of-Acute-Pancreatitis-pptx-8-2048.jpg)
![Current management protocol for Necrotic
pancreatitis [based on step-up approach]](https://image.slidesharecdn.com/acutepancreatitis-240511072547-4c88377e/75/Etiology-and-Management-of-Acute-Pancreatitis-pptx-54-2048.jpg)
![Management of pseudocyst
• Observation
• Spontaneous regression in 70% for
pseudocysts < 4cm, located in tail,
and no evidence of pancreatic duct
obstruction OR communication with
MPD.
• Indications for invasive therapy
• Symptomatic patients
• Diagnostic confusion [pseudocyst vs
cystic disease of pancreas]
• Endoscopic approach when
pseudocyst is present < 1cm away
from stomach/duodenum
• Trans gastric drainage
• Transduodenal drainage
• Trans papillary drainage
• If pancreatic duct stricture
endoscopic dilation and stent
placement
• Percutaneous drainage of fistula is
indicated only for septic patients
secondary to pseudocyst infection.](https://image.slidesharecdn.com/acutepancreatitis-240511072547-4c88377e/75/Etiology-and-Management-of-Acute-Pancreatitis-pptx-58-2048.jpg)
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Similar to Etiology and Management of Acute Pancreatitis.pptx
Etiology and Management of Acute Pancreatitis.pptx
- 1.
- 2. Introduction • Most ofthe patients with acute pancreatitis (AP) have milder course • 10-20% of patients have severe, rapid progressive course • Mortality of patients with AP varies from < 1 % in milder cases to 10-50% in severe cases. • Mortality is usually bimodal • Early phase Within first 2 weeks death occurs due to Multiple Organ Dysfunction caused by the intense inflammatory cascade triggered by pancreatic inflammation • Late phase After 2 weeks caused by septic complication.
- 4. Pathophysiology • Exact etiologyis unknown • AP is the final result of abnormal pancreatic enzyme activation inside acinar cells. • Immunolocalization studies have shown that after 15 minutes of pancreatic injury both zymogen granules and lysosome colocalize inside the acinar cells. • The fact that the colocalization occurs before amylase level elevation, pancreatic edema and other markers of pancreatitis are evident suggests that COLOCALIZATION is an early step in the pathophysiologic process of pancreatitis. • Lysosomal enzyme cathepsin B activates trypsin in these colocalization organelles. Trypsin activation leads to acinar cell death.
- 7. Pathophysiology continued.. • Increasedinflammation increased permeability of interstitial fluids Increased microcirculation damage Edema • In severe cases Persistence of inflammation leads to local hemorrhage and pancreatic necrosis. • 80% cases are self limited. In remaining 10%, there is persistence of vicious circle of inflammation-anti inflammation cascade Leads to local and systemic complication ALI and ARDS occurs. • In early phase mortality is due to persistence of inflammatory response.
- 8. Risk factors • Gallstone and ethanol abuse [about 70-80% of cases] • In pediatric age group Blunt abdominal trauma, Systemic disease • Autoimmune / Drug induced in patients with rheumatologic conditions such as SLE and Sjogren syndrome.
- 9. a. Gallstone pancreatitis Obstructivetheory • Obstruction of the pancreatic duct by biliary stones Causes increased pressure inside pancreatic duct alteration of tight junctions via calcineurin signaling Initiation of pancreatitis Reflux theory • Stones impacted in the ampulla of Vater form a common channel that allows bile salt to reflux into the pancreas Bile salt induces direct acinar cell necrosis • 40% of cases of pancreatitis are due to gallstones in US. Overall 3-8% of cases are caused • Mostly, women of age 50-70 years have gallstone pancreatitis.
- 10. Alcohol and smokinginduced injury • Second most common cause of AP worldwide • 35% of cases of AP • Young men, 30-45 years age group • Of the people who drink heavy alcohol (> 100g/day for at least 5 years), 5-10% of patients develop AP • RR of smokers to non-smokers for developing AP is 4.9:1 • Mechanism of alcohol induced pancreatitis • Multifaceted a. Trigger proinflammatory pathways via upregulation of nuclear factor XB, TNF-α and IL-1 b. Inappropriate basolateral exocytosis of pancreatic zymogens c. Increased autophagy possibly due to dysregulation of cathepsin L and B d. Increased oxidative stress leading to mitochondrial dysfunction e. Activation of pancreatic stellate cells (PSC) causing increased secretion of MMP f. Impaired pancreatic cell repair due to dysregulation in developmental factors PDX1, PTF1a and Notch g. Shift in cell death caused by apoptosis to necrosis by decreasing caspase 3/8 activity and loss of ATP production via mitochondrial depolarization.
- 11. Mechanism of alcoholinduced AP
- 12. Anatomic obstruction • Abnormalflow of pancreatic juice into the duodenum • Usually described in patients with pancreatic tumors, parasites and congenital defects • Pancreatic divisum 5-10% lifetime risk • Occurs due to defect in pancreatic secretion from the minor papilla • Ascaris lumbricoides infection, annular pancreas are also associated with development of AP
- 13. ERCP induced pancreatitis •Up to 5% of cases have AP following ERCP • Mostly occurs in female, young patients with prior history of ERCP induced pancreatitis • Patients undergoing therapeutic procedures have more risk of AP compared to patients undergoing diagnostic procedures • Patients with multiple attempts at cannulation, SOD dysfunction, abnormal visualization of the secondary pancreatic ducts after injection of contrast material have increased risk • Management of ERCP induced pancreatitis • Perform ERCP only when absolutely necessary • Use of indomethacinto prevent ERCP-induced pancreatitis • Use of pancreatic stents • Use of minimal pressure while performing ERCP.
- 14. Drug-induced pancreatitis • Mostcommon agents • Sulfonamides • Metronidazole • Erythromycin • Tetracycline • Didanosine • Thiazides • Furosemide • HMG-CoA reductase inhibitors • Azathioprine • 6-MP • 5-ASA • Sulfasalazine • Valproate • HAART drugs
- 15. Metabolic factors • Hypertriglyceridemiaand Hypercalcemia • Hypertriglyceridemia • Direct pancreatic injury is caused by triglyceride metabolites • More common in patients with triglyceride level more than 1000 mg/dl • Familial hypertriglyceridemia Type I, II and V • Hypertriglyceridemia secondary to hypothyroidism, DM and alcohol does not typically induce AP • Hypercalcemia • Calcium activates trypsinogen into active trypsin AP • Primary hyperparathyroidism Intraductal calcium deposition ductal obstruction and pancreatitis
- 16. Miscellaneous conditions causingAP • Blunt/ penetrating abdominal trauma (0.2/1% respectively) • Prolonged intraoperative hypotension • Excessive pancreatic manipulation during abdominal surgery • Pancreatic ischemia following splenic artery embolization • Scorpion venom • Perforated duodenal ulcers
- 17. Types of acutepancreatitis • Interstitial edematous pancreatitis • Characterized by the inflammation and edema of the pancreatic parenchyma and peripancreatic tissues • Necrotizing pancreatitis • Inflammation and edema of pancreas progresses to pancreatic parenchymal tissue death • Leads to necrotic collection around pancreas containing solid and fluid components • Infection may occur around the necrotic collection leading to infected Acute Necrotic Collection (ANC)
- 20. Clinical features History • Epigastric/periumbilical pain that radiates to the back • Nausea or vomiting • Pain in acute pancreatitis is constant. Any disappearance of pain/ decrease of pain should warrant revision of diagnosis and other illness MUST be considered. Physical examination • Dehydration, poor skin turgor, tachycardia, hypotension and dry mucous membrane are commonly seen in AP. • Abdomen: Normal to rebound tenderness and abdominal rigidity may be seen • Gray Turner and Cullen signs may be seen
- 21. • Concomitant choledocholithiasisor significant edema in head of pancreas may compress the intrapancreatic portion of the CBD jaundice may be seen in such patients • Dullness to percussion and decreased breathing sounds in left (more commonly) or right hemithorax suggests pleural effusion secondary to AP.
- 22. Diagnosis • As perthe revised Atlanta Classification (RAC) • 2/3 of the following • Abdominal pain consistent with AP (acute, persistent, severe, sharp, epigastric often radiating to the back) • A threefold or higher elevation of serum amylase or lipase levels above the upper laboratory limit of normal • Characteristic findings of pancreatitis by imaging • Serum half-life of amylase (10 hours) is shorter than that of lipase (6.9-13.7 hours) and normalizes faster. • In patients who present within first 24-48 hours after symptoms, lipase is more sensitive.
- 23. • Conditions causingrise in level of serum amylase
- 24. • Acute pancreatitispatients have • Hyperglycemia • Leukocytosis • Abnormal LFT • Elevation of alanine aminotransferase levels in the serum in context of AP confirmed by high pancreatic enzyme levels has a PPV of 95% in the diagnosis of acute biliary pancreatitis.
- 25. Imaging studies • Notmandatory for diagnosis, but may be helpful in determining the need for intervention in severe AP or elucidating an elusive etiology • Abdominal X-ray • Non-specific • Findings include air-fluid levels suggestive of ileus • Cutoff colon sign D/t colonic spasm at the splenic flexure • Sentinel loop sign • Widening of C-loop of duodenum D/t severe pancreatic head edema
- 26. Colon ‘cut-off’ signrefers to mild distension of transverse colon with collapsed descending colon.
- 27. • USG • Limitedby the intraabdominal fat and increased intestinal gas • USG is done to diagnose gallstones • Elevated Liver enzymes, pancreatic enzymes and gall stones is 97% sensitive and 100% specific for acute biliary pancreatitis • CECT abdomen-pelvis • Best modality for evaluation of pancreas • Indications for CT include • Diagnostic uncertainty • Confirmation of severity based on clinical predictors • Failure to respond to conservative treatment • Clinical deterioration • CT evaluation is done in portal venous phase (65-70 seconds after contrast) • CT comments on • Pancreatic parenchyma • Amount of peripancreatic inflammation • Presence of intraabdominal air/ collection • CT scan can detect necrotizing pancreatitis from 72-96 hours after the onset of symptoms • If diagnostic uncertainty, it can be performed at the time of admission.
- 28. • Abdominal MRI •Evaluating the extent of necrosis, inflammation, and presence of free fluid • Costly • MRI requiring patients are often times critically ill and ICU restricted. Hence, use of MRI in AP is limited. • MRCP however is important in evaluation of patients with unexplained or recurrent pancreatitis because it allows complete non-invasive visualization of the biliary and pancreatic duct anatomy. • Intravenous (IV) administration of secretin can be injected prior to imaging to stimulate pancreatic juice secretion, thereby causing a transient distention of the pancreatic duct. This helps in visualizing difficult pancreatic ducts
- 29. EUS role inAP • Evaluation of persistent choledocholithiasis • Routine ERCP may not reveal evidence of infection, and in fact may increase the severity of the disease • EUS>>ERCP for identifying choledocholithiasis • EUS allows examination of biliary tree and pancreas with no risk of worsening of the pancreatitis
- 30. Assessment of severityof Disease • Ranson scoring • Ranson and colleagues in 1974 identified 11 parameters (at the time of admission and after 48 hours) to predict the severity of disease • Mortality correlates with the number of positive parameters • If > 3 parameters are fulfilled, we define as severe pancreatitis • Disadvantage is that severity of the disease is not identified at the time of admission at assessed 48 hours later • PPV 50%, NPV 90% • APACHE II (Acute physiology and chronic health evaluation) • A GENERAL MEASURE OF SEVERITY OF THE DISEASE • >8 SCORE defines severe pancreatitis • PPV of 43%, NPV 89%
- 31. Assessment of severityof Disease • Ranson scoring @After 48 hours Pa F C ks Ha Bi Bi
- 32. Assessment of severityof Disease • CT severity index
- 33. Assessment of severityof Disease • Most of the prognostic indices have been hindered by the complexity, need for imaging and inability to be calculated at the time of admission • SIRS has been advocated as a tool to replace other scoring systems SIRS Criteria Mortality prediction (%) Meeting SIRS criteria 25 Transient SIRS 8 No SIRS 0
- 34. CRP and AP •CRP peaks 48-72 hours after onset of pancreatitis • Elevated CRP correlates with the severity of disease • A CRP level of > 150 mg/ml or higher defines severe pancreatitis
- 35.
- 37. Treatment-Fluid therapy • Regardlessof the severity, the cornerstone of treating AP is aggressive fluid resuscitation with isotonic crystalloid solution, pain control, early nutrition • Rate of fluid should be individualized and adjusted as per age, comorbidities, vital signs, mental status, skin turgor and urine output. • Non-responsive patients to fluid therapy or have significant renal, cardiac or respiratory comorbidities often require invasive monitoring with central venous access and a Foley catheter. • RL is the fluid of choice
- 38. • Intravascular volumedepletion from fluid sequestration associated with pancreatic, peripancreatic and systemic edema is characteristic of patients with acute pancreatitis • IV repletion should begin as soon as the diagnosis of acute pancreatitis is made. • Recommendations for fluid therapy in AP • As per American Pancreatic Association/ International Association of Pancreatology, fluid given should be a crystalloid 5-10 ml/kg/h until the resuscitation goals are met • Resuscitation goals include HR <120 bpm, MAP of 65-85 mmHg, Urine output >0.5-1 ml/kg/hr
- 39. Nutrition in acutepancreatitis • Nutrition is paramount • Acute pancreatitis is a state of intense inflammatory response resulting in a catabolic state, increasing the caloric and nutritional requirements • Reduced intestinal vascular perfusion in AP results in gut mucosal damage bacterial translocation and entry into portal circulation and portal lymphatics Organ failure, sepsis and secondary pancreatic infection and peripancretic necrosis • Early nutrition reduces the bacterial migration, replenishes nutritional requirements, increases GI blood flow, preserves integrity of bowel mucosa and stimulates GI motility.
- 40. • Persistent ileus,pain, intubation may cause oral feeding impossible. Pain may also recur when the oral route is resumed • Nutritional support pathway • Enteral feeding • TPN • Whenever possible, enteral nutrition should be used rather than a TPN • TPN should be used only when there is intolerance to enteral feeding • NJ feeding tube is currently favored • It is unnecessary to wait until the pain has resolved before resuming diet in patients with pancreatitis. • It is recommended to begin initiating enteral feeding within 24-72 hours • Low fat soft diet is the diet of choice. • Patients unable to tolerate oral feed NJ/ NG feeding • Unable to feed within 72 hours Start TPN
- 41. Antibiotics and pancreatitis •Prophylactic antibiotics do not decrease the frequency of surgical intervention, infected necrosis OR mortality in patients with severe pancreatitis • Use of antibiotics in pancreatitis is associated with increase in Gram Positive Cocci infection Staphylococcus aureus and Candida. • Use antibiotics only in • Pre-existing infections • Radiologic findings suggestive of infected peripancreatic fluid collection
- 42.
- 44. Laparoscopic cholecystectomy after pancreatitis •If no definitive management of gallstone induced pancreatitis is done, 30% will recur • Laparoscopic cholecystectomy is indicated for all patients with mild acute biliary pancreatitis • Early laparoscopic cholecystectomy (laparoscopy during the initial admission to the hospital) is safe procedure that decreases recurrence of the disease. • IOC, MRCP or EUS helps in exclusion of the choledocholithiasis. • For severe cases Conservative management for at least 6 weeks f/b laparoscopic cholecystectomy.
- 45. ERCP and Acutepancreatitis • Do NOT use ERCP during any form of pancreatitis • ERCP is indicated only in cholangitis, persistent bile duct obstruction • In old age patients who have poor performance status OR several comorbidities, ERCP with sphincterotomy is a safe alternative to prevent recurrent biliary pancreatitis
- 46.
- 47. Sterile and infectedperipancreatic fluid collection • 30-57% of patients with AP have peripancreatic fluid collection • Peripancreatic fluid collection are not surrounded or encased by epithelium or fibrotic capsule • Usually self resolving, may become infected • Evidence of gas within a fluid collection on imaging and acute decompensation/ failure to improve after 14 days suggests infective contamination • CT guided fluid sampling must be done • Drainage and IV antibiotics (carbapenem, quinolones, cephalosporins) are indicated.
- 48.
- 49. Pancreatic necrosis andinfected necrosis • Pancreatic necrosis is defined as Non-viable pancreatic parenchyma OR peripancreatic fat • Can be focal necrosis OR diffuse necrosis of pancreas • CECT is the most reliable tool to diagnose ANC. Areas of low attenuation are seen (<40-50 HU is seen) in such conditions. • Normal pancreatic attenuation= 100-150 HU • In autopsy studies, about 80% of patients with death secondary to AP had necrotic pancreas. Hence, timely identification is paramount. • Main complication of ANC is infection. Amount of necrosis is proportional to the risk of infection. • Mostly infection occurs due to translocation of the enteric flora E coli, Klebsiella, Pseudomonas and Enterococcus
- 50. When to suspectpancreatic necrosis? • Prolonged fever • Elevated WBC • Progressive clinical deterioration • Sepsis/SIRS/ Organ failure (> 7 days from the day of onset of AP) • On CT scan, presence of air in pancreas confirms Necrotic Pancreatitis
- 51. Management of Necrotizingpancreatitis • If Necrosis of pancreas is suspected, FNAC is done Culture is done if a positive Gram stain/ culture is present, diagnosis is established as “infected necrosis of the pancreas”. • Indications for intervention • Persistent pain • Failure to improve clinically with conservative management • Symptomatic biliary/ enteric obstruction • Documented infected necrotic collection with clinical deterioration
- 52. Management of Necrotizingpancreatitis • Once the infection is demonstrated IV antibiotics • Antibiotics Carbapenem, quinolones, Metronidazole, 3rd generation Cephalosporins and piperacillin
- 53. • Step upapproach • Percutaneous drainage followed by minimally invasive video-assisted retroperitoneal debridement • In 2018, a companion study
- 54. Current management protocolfor Necrotic pancreatitis [based on step-up approach]
- 55.
- 56. Pseudocyst of pancreas •5-15% of patients with acute peripancreatic fluid collection (APFC) have pseudocyst • Pseudocyst is composed of collagen and granulation tissue and is not lined by epithelium • Pseudocyst typically develops at least 4- 8 weeks later after APFC • Nonspecific complains of patients • Persistent pain, Early satiety, nausea, weight loss, Elevated pancreatic enzymes in plasma suggest the diagnosis • CT/MRI Support the diagnosis • EUS with FNA is indicated in patients with diagnostic uncertainty. • High levels of amylase with absence of mucin and low CEA suggests characteristic feature of pseudocyst
- 57. Classification of pseudocystof pancreas
- 58. Management of pseudocyst •Observation • Spontaneous regression in 70% for pseudocysts < 4cm, located in tail, and no evidence of pancreatic duct obstruction OR communication with MPD. • Indications for invasive therapy • Symptomatic patients • Diagnostic confusion [pseudocyst vs cystic disease of pancreas] • Endoscopic approach when pseudocyst is present < 1cm away from stomach/duodenum • Trans gastric drainage • Transduodenal drainage • Trans papillary drainage • If pancreatic duct stricture endoscopic dilation and stent placement • Percutaneous drainage of fistula is indicated only for septic patients secondary to pseudocyst infection.
- 59. Management of pseudocyst •Surgery indications • Pancreatic pseudocyst not treatable by endoscopy due to complex anatomy • Failure to respond to endoscopic treatment • Management depends upon the location of the cyst • Tail Cystogastrostomy • Jejunum Cystojejunostomy • Head Cystoduodenostomy • For pseudocysts not present near the contact of stomach/ duodenum Roux-en-Y Cystoduodenostomy • Cyst drainage is obtained in > 90% following surgery • Recurrence 12%
- 60. Complications of pseudocyst •Bleeding • Pancreaticopleural fistula • Bile duct and duodenal obstruction • Rupture into abdominal cavity • Infection
- 62. Pancreatic ascites andPancreaticopleural fistula (PPF) • Complete disruption of the pancreatic duct can cause fluid accumulation. • Patient with AP who develop significant abdominal distention and free intraabdominal fluid Suspect pancreatic ascites • Management • Drainage with endoscopic placement of stent across the disruption • Failed cases surgical treatment consisting of distal resection and closure of proximal stump. • Posterior rupture of MPD leads to development of PPF • Dyspnea, chest pain, cough, abdominal pain are usual presenting complaints • Diagnosis by CXR, Thoracentesis, CT scan • Usually left sided pleural effusion • Amylase of pleural fluid > 50,000 IU • PPF is a/w pseudocyst in about 70% patients • Management • Chest drainage • Parenteral nutritional support • Administration of octreotide • If persistent • Endoscopic sphincterotomy • Stent placement • Failure to heal • Surgical treatment similar to pancreatic ascites
- 63. Vascular complications Pseudoaneurysm • SplenicA, SMA, Cystic A, GDA pseudoaneurysm • Pancreatitis elastase pseudoaneurysm formation • Rupture causes massive bleeding • Hypotension and tachycardia, sudden onset abdominal pain may suggest rupture • Management involves embolization/ ligation Vascular thrombosis • Splenic vein, Portal vein thrombosis • Splenomegaly and gastric varices may occur due to splenic vein thrombosis/ portal HTN • Management • Thrombolytics • Conservative management • If recurrent UGI bleeding due to venous HT Splenectomy
- 64. Pancreatocutaneous fistula • 0.4%of patients with acute pancreatitis may have Pancreatocutaneous fistula • May be coexistent with other complications • Treatment is conservative, yet patients may require surgical debridement