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Management of acute pancreatitis

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Management of acute pancreatitis - American College of Gastroenterology Guideline 2013

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Management of acute pancreatitis

  1. 1. MANAGEMENT OF ACUTE PANCREATITIS American College Of Gastroenterology guideline 2013 Dr Subhasish Deb Dept. of General Medicine Burdwan Medical College And Hospital Dr. Subhasish Deb, BMCH
  2. 2. Dr. Subhasish Deb, BMCH
  3. 3. DIAGNOSIS 1. Presence of 2 of the 3 criteria: (i) abdominal pain consistent with the disease, (ii) serum amylase &/or lipase greater than 3 times the UNL (iii) characteristic findings from abdominal imaging 2. CECT and / or MRI of the pancreas should be reserved for patients in whom the diagnosis is unclear or who fail to improve clinically within the first 48 – 72 h after hospital admission Dr. Subhasish Deb, BMCH
  4. 4. AMYLASE VS LIPASE • Limitations in sensitivity, specificity and positive and negative predictive value of serum amylase (serum lipase is preferred). AMYLASE a) rises within a few hours after the onset of symptoms b) returns to normal values within 3 – 5 days (however, it may remain within the normal range on admission in as many as one-fifth of patients) c) Serum amylase concentrations may be normal in alcohol-induced AP and hypertriglyceridemia Dr. Subhasish Deb, BMCH
  5. 5. d) Serum amylase concentrations might be high in the absence of AP in macroamylasaemia (a syndrome characterized by the formation of large molecular complexes between amylase and abnormal immunoglobulins) e) May be high in patients with decreased GFR, in diseases of the salivary glands, and in extrapancreatic abdominal diseases associated with inflammation, including acute appendicitis, cholecystitis, intestinal obstruction or ischemia, peptic ulcer, and gynecological diseases. Dr. Subhasish Deb, BMCH
  6. 6. ETIOLOGY 1. Transabdominal ultrasound should be performed in all patients with acute pancreatitis 2. In the absence of gallstones and / or significant h/o alcohol use, a serum triglyceride should be obtained and considered the etiology if > 1,000 mg / dl 3. In a patient older than 40 years, a pancreatic tumor should be considered as a possible cause of acute pancreatitis 4. Endoscopic investigation in patients with acute idiopathic pancreatitis should be limited, as the risks and benefits of investigation in these patients are unclear 5. Patients with idiopathic pancreatitis should be referred to centers of expertise 6. Genetic testing may be considered in young patients ( < 30 years) if no cause is evident and a family history of pancreatic disease is present Dr. Subhasish Deb, BMCH
  7. 7. • M/c/c – Gall stones followed by alcohol Dr. Subhasish Deb, BMCH
  8. 8. Alcohol and AP The diagnosis should not be entertained unless a person has a history of over 5 years of heavy alcohol consumption  “ Heavy ” alcohol consumption is generally considered to be > 50 g per day, but is often much higher Clinically evident AP occurs in < 5 % of heavy drinkers; thus, there are likely other factors that sensitize individuals to the effects of alcohol, such as genetic factors and tobacco use. Dr. Subhasish Deb, BMCH
  9. 9. Idiopathic AP • IAP is defined as pancreatitis with no etiology established after 1. initial laboratory (including lipid and calcium level) and 2. imaging tests (transabdominal ultrasound and CT in the appropriate patient) Dr. Subhasish Deb, BMCH
  10. 10. INITIAL ASSESSMENT AND RISK STRATIFICATION • Hemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as needed • Risk assessment should be performed to stratify patients into higher- and lower-risk categories to assist triage, such as admission to an intensive care setting • Patients with organ failure should be admitted to an intensive care unit or intermediary care setting whenever possible Dr. Subhasish Deb, BMCH
  11. 11. Dr. Subhasish Deb, BMCH
  12. 12. Organ Failure • Initially defined as: 1. shock (systolic blood pressure < 90 mm Hg) 2. pulmonary insufficiency (PaO2< 60 mm Hg) 3. renal failure (creatinine > 2 mg / dl after rehydration) 4. and / or gastro intestinal bleeding ( > 500 ml of blood loss / 24 h) Organ failure is now defined as a score ≥2 for one of the three scoring systems (cardiovascular, respiratory, and renal) using the modified Marshall scoring system. Dr. Subhasish Deb, BMCH
  13. 13. Local Complications 1. acute fluid collection, 2. pancreatic necrosis, 3. pseudocyst and 4. pancreatic abscess. Dr. Subhasish Deb, BMCH
  14. 14. Pancreatic necrosis • Def: diffuse or focal areas of non viable pancreatic parenchyma > 3 cm in size or > 30% of the pancreas. • Pancreatic necrosis can be: i. sterile or ii. infected • Patients with sterile necrosis can suffer from organ failure and appear as ill clinically as those patients with infected necrosis. • In the absence of pancreatic necrosis, in mild disease the edematous pancreas is defined as interstitial pancreatitis. Dr. Subhasish Deb, BMCH
  15. 15. INITIAL MANAGEMENT 1. Aggressive hydration, defined as 250-500 ml per hour of isotonic crystalloid solution should be provided to all patients, unless cardiovascular and / or renal co-morbidites exist. Early aggressive intravenous hydration is most beneficial the first 12 – 24 h, and may have little benefit beyond. 2. In a patient with severe volume depletion, manifest as hypotension and tachycardia, more rapid repletion (bolus) may be needed . 3. Lactated Ringer’s solution may be the preferred isotonic crystalloid replacement fluid. 4. Fluid requirements should be reassessed at frequent intervals within 6 h of admission and for the next 24 – 48 h. The goal of aggressive hydration should be to decrease the blood urea nitrogen Dr. Subhasish Deb, BMCH
  16. 16. Rationale for rapid hydration • Despite dozens of randomized trials, no medication has been shown to be effective in treating AP. • The rationale for early aggressive hydration in AP arises from observation of the frequent hypovolemia that occurs from multiple factors: i. including vomiting, ii. reduced oral intake, iii. third spacing of fluids, iv. increased respiratory losses and v. diaphoresis. vi. In addition, researchers hypothesize that a combination of microangiopathic effects and edema of the inflamed pancreas decreases blood flow, leading to increased cellular death, necrosis, and ongoing release of pancreatic enzymes activating numerous cascades. Dr. Subhasish Deb, BMCH
  17. 17. Why RL? • benefits to using the more pH-balanced lactated Ringer ’ s solution for fluid resuscitation compared with normal saline. Low pH activates the trypsinogen, makes the acinar cells more susceptible to injury and increases the severity of established AP in experimental studies. Although both are isotonic crystalloid solutions, normal saline given in large volumes may lead to the development of a non-anion gap, hyperchloremic metabolic acidosis. Dr. Subhasish Deb, BMCH
  18. 18. ERCP IN AP 1. Patients with acute pancreatitis and concurrent acute cholangitis should undergo ERCP within 24 h of admission. 2. ERCP is not needed in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction. 3. In the absence of cholangitis and / or jaundice, MRCP or endoscopic ultrasound (EUS) rather than diagnostic ERCP should be used to screen for choledocholithiasis if highly suspected. 4. Pancreatic duct stents and / or postprocedure rectal nonsteroidal anti-infl ammatory drug (NSAID) suppositories should be utilized to prevent severe post- ERCP pancreatitis in high-risk patients Dr. Subhasish Deb, BMCH
  19. 19. ROLE OF ANITIOTICS IN AP 1. Antibiotics should be given for an extrapancreatic infection, such as cholangitis, catheter-acquired infections, bacteremia, urinary tract infections, pneumonia . 2. Routine use of prophylactic antibiotics in patients with severe acute pancreatitis is not recommended . 3. The use of antibiotics in patients with sterile necrosis to prevent the development of infected necrosis is not recommended . 4. Infected necrosis should be considered in patients with pancreatic or extrapancreatic necrosis who deteriorate or fail to improve after 7 – 10 days of hospitalization. In these patients, either – (i) initial CT-guided FNA for Gram stain and culture to guide use of appropriate antibiotics or – (ii) empiric use of antibiotics without CT FNA should be given. Dr. Subhasish Deb, BMCH
  20. 20. 5. In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis, such as carbapenems, quinolones, and metronidazole, may be useful in delaying or sometimes totally avoiding intervention, thus decreasing morbidity and mortality . 6. Routine administration of antifungal agents along with prophylactic or therapeutic antibiotics is not recommended Dr. Subhasish Deb, BMCH
  21. 21. NUTRITION IN AP • In mild AP, oral feedings can be started immediately if there is no nausea and vomiting, and abdominal pain has resolved . • In mild AP, initiation of feeding with a low-fat solid diet appears as safe as a clear liquid diet . • In severe AP, enteral nutrition is recommended to prevent infectious complications. Parenteral nutrition should be avoided unless the enteral route is not available, not tolerated, or not meeting caloric requirements . • Nasogastric delivery and nasojejunal delivery of enteral feeding appear comparable in efficacy and safety. Dr. Subhasish Deb, BMCH
  22. 22. • The need to place the pancreas at rest until complete resolution of AP no longer seems imperative. • Long held assumption that the inflamed pancreas requires prolonged rest by fasting does not appear to be supported by clinical and laboratory observations. • TPN is associated with infections and other line related complications. Enteral feeding maintains gut mucosal barrier, prevents disruption and translocation of bacteria that seed pancreatic necrosis. Dr. Subhasish Deb, BMCH
  23. 23. ROLE OF SURGERY IN AP • In patients with mild AP, found to have gallstones in the gallbladder, a cholecystectomy should be performed before discharge to prevent a recurrence of AP • In a patient with necrotizing biliary AP, in order to prevent infection, cholecystectomy is to be deferred until active inflammation subsides and fluid collections resolve or stabilize . • The presence of asymptomatic pseudocysts and pancreatic and / or extrapancreatic necrosis do not warrant intervention, regardless of size, location, and / or extension . • In stable patients with infected necrosis, surgical, radiologic, and / or endoscopic drainage should be delayed preferably for more than 4 weeks to allow liquefication of the contents and the development of a fibrous wall around the necrosis . • In symptomatic patients with infected necrosis, minimally invasive methods of necrosectomy are preferred to open necrosectomy . Dr. Subhasish Deb, BMCH
  24. 24. THANKYOU Dr. Subhasish Deb, BMCH

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