Acute pancreatitis

Acute Pancreatitis
Acute pancreatitis is an inflammatory condition of the pancreas characterized clinically by abdominal pain and elevated levels of pancreatic enzymes in the blood. 
Two distinct phases of AP have now been identified: early (within 1 week), characterized by the systemic inflammatory response syndrome (SIRS) and / or organ failure; and late (> 1 week), characterized by local complications.
Severe pancreatitis is characterised by organ failure, >3 ranson’s criteria, BISAP score >3 or Apache II>8. Am J Gastroenterol. 2010 Feb;105(2):435-41; quiz 442
BISAP score includes BUN >25 mg/dL, impaired mental status, SIRS, age >60 years, or the presence of a pleural effusion. 
Ransons criteria include 
  • On admission :  WBC > 16,000 , LDH > 350,  AST > 250 , Glucose > 200, Age > 55 yrs.
  • Within 48 hours : Hct fall > 10% , BUN rise > 5mg/dl after fluid resuscitation, Calcium < 8mg/dl, pO2 < 60mmHg , Base deficit > 4 meq/l , Fluid sequestration > 6 litres
  1. Mild AP : absence of organ failure or local complications. 
  2. Moderately severe AP : local complications like pancreatic necrosis or peripancreatic fluid collections, with an absence of persistent organ failure. Patients with moderately severe AP may have transient organ failure, lasting < 48 h.  
  3. Severe pancreatitis: persistent organ failure for >48 hrs, >3 ranson’s criteria, or Apache II>8.  Organ failure had previously been defined as shock (systolic blood pressure < 90 mm Hg), pulmonary insufficiency (PaO 2 < 60 mm Hg), renal failure (creatinine > 2 mg / dl after rehydration), and / or gastro intestinal bleeding ( > 500 ml of blood loss / 24 h) ( 53 ). The Revised Atlanta Criteria now define organ failure as a score of 2 or more for one of these organ systems using the modified Marshall scoring system.
  1. Gallstones — Mechanical ampullary obstruction can be induced by gallstones. An elevated serum alanine aminotransferase (ALT) concentration was the most clinically useful parameter in predicting a gallstone etiology in patients with acute pancreatitis.
  2. Biliary sludge and microlithiasis — Biliary sludge is a viscous suspension in gallbladder bile that may contain small stones. Most patients with biliary sludge are asymptomatic. In the absence of any other etiology, biliary sludge should be suspected in patients with acute pancreatitis with a transient elevation in liver tests.
  3. Alcohol — Alcohol is responsible for approximately 30% of acute pancreatitis in the United States
  4. Hypertriglyceridemia — Serum triglyceride concentrations above 1000 mg/dL can cause acute pancreatitis
  5. Post-ERCP — Asymptomatic hyperamylasemia occurs in 35 to 70% of patients undergoing ERCP. 
  6. Other Causes: Hypercalcemia, Drugs, Infections, Blunt trauma, Pancreatic divisum, Pancreatic ischemia, Vasculitis, sphincter of oddi dysfunction, pancreatic cancer and idiopathic.

Clinical Presentation: Patients with AP typically present with epigastric or left upper quadrant pain. The pain is usually described as constant with radiation to the back, chest, or flanks, but this description is nonspecific. The intensity of the pain is usually severe, but can be variable. The intensity and location of the pain do not correlate with severity. Pain described as dull, colicky, or located in the lower abdominal region is not consistent with AP and suggests an alternative etiology. Abdominal imaging may be helpful to determine the diagnosis of AP in patients with atypical presentations.

The diagnosis of AP is most often established by the presence of at least two of three criteria: abdominal pain, serum amylase and or lipase greater than three times the upper limit of normal and characteristic findings from abdominal imaging. CT/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 or to evaluate complications. MRI has a higher sensitivity for the diagnosis of early acute pancreatitis as compared with contrast-enhanced abdominal CT scan and can better characterize the pancreatic and bile ducts and complications of acute pancreatitis. Am J Gastroenterol. 2007 May;102(5):997-1004.
  • Amylase and Lipase: Compared with lipase, serum amylase returns more quickly to values below the upper limit of normal. Serum amylase concentrations may be normal in alcohol-induced AP and hypertriglyceridemia. Serum amylase concentrations might be high in the absence of AP in macroamylasaemia or in patients with decreased glomerular filtration rate. Lipase is also found to be elevated in a variety of nonpancreatic diseases, such as DKA, renal disease, appendicitis and cholecystitis.
  • Serum lipase is more specific than serum amylase. Lipase elevations occur earlier and last longer as compared with elevations in amylase. 
  • Other Labs: check triglycerides, CMP and liver tests.
  • Gallstones: Abdominal ultrasound should be performed in all patients with acute pancreatitis. If ultrasound is negative and clinical suspicion is high, additional testing should be considered with MRCP/EUS to rule out choledocholithiasis.
  • Alcohol: Plain film/CT scan for pancreatic calcification; blood glucose for diabetes; 72 hour fecal fat for steatorrhea; exclude other causes of acute pancreatitis
  • In patients with unexplained pancreatitis who are at risk for underlying malignancy (age older than 40) and or worrisome clinical features including weight loss and new onset of diabetes, CT with pancreas protocol or MRI with MRCP should be obtained.  
  • In patients with recurrent episodes of pancreatitis, EUS and/or ERCP should be considered. MRCP or MRI of abdomen could be a reasonable alternative. 
Patients with pancreatitis may have leukocytosis and an elevated hematocrit from hemoconcentration due to extravasation of intravascular fluid into third spaces. Metabolic abnormalities including elevated blood urea nitrogen (BUN), hypocalcemia, hyperglycemia, and hypoglycemia may also occur.
Predictor of severity:
AGA guidelines suggest that Prediction of severe disease be performed using the APACHE II system (using a cutoff of ≥8).


  1. Management of severe acute pancreatitis is changing fundamentally. ‘Less is more’ is the new paradigm in acute pancreatitis – less antibiotics, less fluids, less surgery, which should eventually lead to less morbidity and mortality. 
  2. Aggressive hydration, defined as 250-500 ml per hour of isotonic crystalloid solution should be provided to all patients, unless cardiovascular and / or renal comorbidites exist. Early aggressive intravenous hydration is most beneficial the first 12 – 24 h, and may have little benefit beyond. Over resuscitation will lead to significant gut edema, intra-abdominal hypertension/abdominal compartment syndrome, and renal failure.  
  3. 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 and hematocrit. Do not blindly hydrate as part of protocol, if the patient is euvolemic. The goal is to restore euvolemia. Adequate fluid resuscitation can be assessed by improvement in vital signs, decrease in  Hct and BUN if they are high on admission and adequate urine output. 
  4. Patients who have ESRD on dialysis and severe CHF might not need too much fluids.  The rationale for early aggressive hydration in AP arises from observation of the frequent hypovolemia that occurs from multiple factors affecting patients with AP, including vomiting, reduced oral intake, third spacing of fluids, increased respiratory losses, and diaphoresis.  
  5. 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. Inflammation also increases vascular permeability, leading to increased third space fluid losses and worsening of pancreatic hypoperfusion that leads to increased pancreatic parenchymal necrosis and cell death. Early aggressive intravenous fluid resuscitation provides micro- and macro circulatory support to prevent serious complications such as pancreatic necrosis  
  6. Lactated Ringer’s solution may be the preferred isotonic crystalloid replacement fluid (conditional recommendation, moderate quality of evidence).  
  7. It is important to recognize that aggressive early hydration will require caution for certain groups of patients, such as the elderly, or those with a history of cardiac and / or renal disease in order to avoid complications such as volume overload, pulmonary edema, and abdominal compartment syndrome. (  Fluid resuscitation and nutritional support during severe acute pancreatitis in the past: what have we learned and how can we do better? Clin Nutr 2006 ; 25 : 497 – 504 .
  8. Patients with acute pancreatitis and concurrent acute cholangitis should undergo ERCP within 24 h of admission.  
  9. 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  
  10. Opiates are safely tolerated for pain control in acute pancreatitis. 
  11. Routine use of prophylactic antibiotics in patients with severe acute pancreatitis is not recommended. 
  12. 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 CT-guided fine-needle aspiration for Gram stain and culture to guide use of appropriate antibiotics or empiric use of antibiotics after obtaining necessary cultures for infectious agents should be given. Subsequently, if cultures are negative, antibiotics should be stopped.  
  13. In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis, such as carbapenems, quinolones, and metronidazole and high dose cephalosporins, may be useful in delaying or sometimes totally avoiding intervention. 
  14.  In mild to moderate AP, oral feedings can be started immediately if there is no nausea and vomiting, abdominal pain has resolved and markers are trending down. Recent data also suggest that immediate feeding is not detrimental in mild pancreatitis, regardless of symptom resolution and markers. Clin Nutr. 2007 Dec;26(6):758-63  
  15. Post pyloric feeds: In severe AP, enteral nutrition is recommended to prevent infectious complications. Nasogastric delivery and nasojejunal delivery of enteral feeding appear comparable in efficacy and safety. ( Crit Care 2013, 17:R120, (J Clin Gastroenterol. 2006 May-Jun;40(5):431-4, ( Pancreas. 2012 Jan;41(1):153-9 ), ( Am J Gastroenterol. 2005 Feb;100(2):432-9 )
  16. TPN: Parenteral nutrition should be avoided unless the enteral route is not available, not tolerated, or not meeting caloric requirements. As enteral feeding maintains the gut mucosal barrier, prevents disruption, and prevents the translocation of bacteria that seed pancreatic necrosis, enteral nutrition may prevent infected necrosis. A recent metaanalysis describing 8 randomized controlled clinical trials involving 381 patients found a decrease in infectious complications, organ failure, and mortality in patients with severe AP who were provided enteral nutrition as compared with total parenteral nutrition.  ( Intern Med 2012 ; 51 : 523 – 30 ), ( BMJ. 2004 Jun 12;328(7453):1407 )  , ( Cochrane Database Syst Rev. 2010 Jan 20;(1):CD002837 )
  17. In patients with mild AP, found to have gallstones in the gallbladder, a cholecystectomy should be performed before discharge to prevent a recurrence 
  18. 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. 
  19. 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 (walled-off necrosis). The concept that urgent surgery is required in patients found to have infected necrosis is no longer valid.  
  20. In symptomatic patients with infected necrosis, minimally invasive methods of necrosectomy are preferred to open necrosectomy.  Minimally invasive approaches to pancreatic necrosectomy including laproscopic surgery either from an anterior or retroperitoneal approach, percutaneous, radiologic catheter drainage or debridement, video-assisted or small incision-based left retroperitoneal debridement, and endoscopy are increasingly becoming the standard of care. Percutaneous drainage without necrosectomy may be the most frequently used minimally invasive method for managing fluid collections complicating necrotizing AP  
  21. The presence of asymptomatic pseudocysts and pancreatic or extrapancreatic necrosis do not warrant intervention, regardless of size, location and extension. 
  22. Pancreatitis induced by hypertriglycerides: In most cases, it is transient and returns to near normal within two to three days. If persistent, it can be treated by apheresis/plasma exchange. Insulin also can be used to decrease serum triglyceride levels by enhancing lipoprotein lipase activity. Oral gemfibrozil should be started simultaneously. 
  23. Pancreatic necrosis seen on CT may or may not be infected. So, don’t start antibiotics if there are no signs of any infection. CRP might have some utility here. The use of antibiotics in patients with sterile necrosis to prevent the development of infected necrosis is not recommended. There is no correlation between the extent of necrosis and the risk of infection. (strong recommendation, moderate quality of evidence).  
  24. Pancreatic necrosis usually develops between days 7-10. 
  25. Pancreatic pseudocyst is usually seen after 6 weeks. The amylase activity within these pseudocysts may be extremely high, and leakage into the blood may be associated with marked hyperamylasaemia.  
  26. Things that do not improve outcome in acute pancreatitis is resting the pancreas with NG suction and acid suppression. 
  27. ERCP is not needed in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction (strong recommendation, low quality of evidence). In the majority of patients with gallstone pancreatitis, the common bile duct stone passes to the duodenum. Routine ERCP is not appropriate unless there is a high suspicion of a persistent common bile duct stone, manifested by an elevation in the bilirubin. Patients with mild AP, with normal bilirubin, can undergo laparoscopic cholecystectomy with intraoperative cholangiography, and any remaining bile duct stones can be dealt with by postoperative or intraoperative ERCP.  





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