Nothing to declare. Probable causes for the change

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1 acute pancreatitis March 25, 2017 C. S PITCHUMONI. MD,MACP,MACG,MPH.FRCP (c) Adjunct Professor of Medicine New York Medical College Professor of Medicine Rutgers university Nothing to declare Lesser sac? Fluid can track down the planes The annual incidence of AP ranges from 13 to 45/100,000 persons, The Epidemiology of Pancreatitis and Pancreatic Cancer D. Yadav and A B. Lowenfels Gastroenterology. 2013; 144: Probable causes for the change 1. Increase in obesity 2. increase in gallstones 3. Increased testing amylase/lipase 4. increased use of CT scan abdomen Diagnosis of Acute pancreatitis Two out of the three features 1.Typical pain of pancreatitis. 2.Elevated ( >3 times) levels of Serum amylase/ lipase. 3.In selected cases imaging study such as contrast enhanced CT scan of abdomen. In delayed presentation, A/L may be normal, When history is difficult to obtain as in demented, disoriented patients. Pain is not typical of pancreatitis Classification of acute pancreatitis 2012: Gut 2013;62:

2 The above clinical classification recognizes the importance of pancreatic necrosis, but overlooks intermediary forms of disease with fluid collections. Bradley.E., International symposium on Acute Pancreatitis. Atlanta Terms used in new classification based on CECT Interstitial edematous pancreatitis: inflammation or stranding in the (peri)pancreatic tissues without tissue necrosis Pancreatic parenchyma enhances,iv contrast Lack of peripancreatic necrosis Necrotizing pancreatitis: Pancreatic parenchymal necrosis and/or peripancreatic necrosis Pancreatic parenchyma areas without enhancement by intravenous contrast and/or Peripancreatic necrosis Acute peripancreatic fluid collection: Peripancreatic fluid occurring in the setting of interstitial edematous pancreatitis; this peripancreatic fluid occurs within the first 4 weeks of interstitial edematous pancreatitis CECT criteria Homongenous fluid adjacent to pancreas confined by peripancreatic fascial planes No recognizable wall CECT contrast enhanced computed tomography The objectives of this presentation ; Management of Severe AP 1. NPO how long? 2. Early feeding, how early, 3. Fluid administration when? how aggressive? what kind? 4. Antibiotics needed or not? 5. Surgery in biliary pancreatitis. Early late, how early? 6. Fluid collection in acute pancreatitis natural history, when to intervene and when not to?. 7. Pancreatic necrosis a. Sterile necrosis conservative Vs Interventional b. Infected 8. Endoscopic interventions in acute complicated pancreatitis. Scope, indications, opportunities, future Initial management 1. Assess hemodynamic status, start resuscitative measures. 2. Risk assessment. 3. Patients with organ failure should be admitted to ICU Prognostic Markers in Acute Pancreatitis: Use anyone Too many: Ransons Imrie BISAP Harmless AP score APACHE II Balthazar CT based Single markers Procalcitonin C Reactive protein Interleukins BISAP (Bed Side Index of Severity) Score BUN > 25 Impaired mental status SIRS 2 or more of the following variables Fever of > 38 C (100.4 F) or < 36 C (96.8 F) Heart rate of > 90 beats per minute Respiratory rate > 20 bpm or arterial carbon dioxide tension (PaCO2) of < 32mm Hg Abnormal white blood cell count (>12,000/µL or < 4,000/µL or >10% immature [band] forms) Age > 60 years Pleural effusions 3 predict pancreatic necrosis And organ failure Mortality prediction similar to APACHE II 2

3 Indications for ICU ( too restrictive) Patients with severe acute pancreatitis Patients with AP and one or more of the following Pulse<40 or >150 BP systolic <80 or mean arterial pressure <60 RR. >35 Serum Na <110 or >170 Serum K <2.0 or >7 PaO2 <50 S.Glucose >800 S. Ca..>15 Anuria, Coma UpToDate 2016 SS Vege Abdominal imaging 1. Routine CECT is unwarranted,the CT may not be helpful, costly,may even delay treatment. 2.If a patient fails to improve after 48 hour or if fever, persistent pain CECT. 3. CECT and MRI equal sensitivity and specificity. 4. MRI/MRCP advantage in estimating CBD size, excluding CBD stone. 5. MRI is helpful in patients with allergy to contrast and renal insufficiency (without gadolinium). Tenner S. et al. American College of Gastroenterology Guideline:management of acute pancreatitis. Am.J.gastroenterol. 2013;108:1400 Initial management of AP.Critical issues during the first 72 hours Preventing severe disease: vigorous IV hydration. Golden period first hours. Aggressive hydration ml per hour of isotonic crystalloid solution,most beneficial in first hour ml/kg If severe depletion (Hypotension and tachycardia)bolus /more rapid infusion. Reassess fluid requirement frequently. Lactated Ringer's solution reduces systemic inflammation compared with saline in patients with acute pancreatitis One liter of Ringer's lactate solution contains: 130 meq of sodium ion = 130 mmol/l 109 meq of chloride ion = 109 mmol/l 28 meq of lactate = 28 mmol/l 4 meq of potassium ion = 4 mmol/l 3 meq of calcium ion = 1.5 mmol/l Ringer's lactate has an osmolarity of 273 mosm/l.the lactate is metabolized into bicarbonate by the liver, which can help correct metabolic acidosis. Ringer lactate may be preferred, ( may be contraindicated in rare hypercalcemic pancreatitis. Contains 3mEq/L calcium). Ringer lactate may reduce incidence of SIRS compared to NS Pain control./ monitoring Opioids are safe and effective. IV opiates. Fentanyl is being increasingly used. ( caution may depress respiratory function ) Patient controlled analgesia Note Morphine does not cause an increase in SOD, or worsen AP. Vital signs Urine output Electrolytes Serum Glucose levels EKG Abdominal compartment syndrome Feedings. NPO,NG,NJ,Oral,IV,TPN?. Or other Early oral feedings when the patient is hungry, pain free. Presence of bowel sounds, Usually 24 to 48 hours. Low residue, low fat, soft diet. Rationale?. If no ileus,nausea or vomiting Enteral feeding rather than parenteral. EF helps to maintain intestinal barrier and prevent translocation of bacteria. EN significantly reduces mortality, multiple organ failure systemic infections, and the need for surgery compared to those who get TPN. Petrow Ms et al. Systematic review Nutritional support in acute pancreatitis. Aliment Pharmacol and Ther. 2008;28:704. Mark PE et al. Meta analysis of parenteral versus enteral nutrition in patients with acute pancreatitis. BMJ.2004;328:

4 Several tests can help differentiate biliary pancreatitis from other causes of AP. Specificity of ALT > 150 IU/L for gallstone AP is 96%. Sensitivity only 48%; a normal ALT does not exclude gallstones as a cause. AST and ALT may be normal in about 11% of patients CT finding of CBD stones sensitivity as high as 80%, CT is often less sensitive than trans abdominal ultrasound. MRCP. EUS. ERCP. Treatment of biliary etiology. EUS/ERCP in early AP. Concurrent acute cholangitis and persistent jaundice and elevated AST?ALT. Suspected biliary etiology with SAP?. MRCP followed by EUS?ERCP Direct EUS followed by ERCP advantages Direct ERCP, sphincterotomy, stent placement. Stone extraction. Endoscopic therapies in AP 1. Endoscopic biliary sphincterotomy. Associated with several risks. Post ERCP pancreatitis, bleeding, infection, peroration. 2. Endoscopic papillary balloon dilatation. Patients with limited number of small stones (<1cm) and minimally dilated bile ducts are ideal candidates. 3. Lithotrypsy. For stones that are difficult to remove because of impaction or large size (typically 10 15MM). Copelan and Kapoor. Choledocholithiasis; diagnosis and management.techniques in vascular and interventional radiology. 2016;18:244 Role of antibiotics in severe acute pancreatitis (SAP). Generally not recommended Aim to prevent superinfection. Not preventive in SAP. Cochrane metaanalysis. Prophylactic antibiotics not indicated in AP regardless of interstitial or necrotizing or disease severity (mild,moderately severe or SAP). Opposing view. JPN guidelines. Tenner et al. Am. Coll. Gastroenterol. Guideline. 2013;108:1400 Acute pancreatitis is a systemic disease with major complications CT scan- Day 1 and Day 10 Patient clinically was worse on day 1 Local Fluid collections pseudocyst Necrosis, sterile and infected Ascites Erosion of adjacent blood vessels GI bleeding Colonic necrosis Abdominal compartment syndrome Systemic Pulmonary Cardiac Renal Multi organ dysfunction CNS, Puertscher s retinopathy Rhabdomyolysis TTP,DIC Arthralgia,bone necrosis Metabolic Hypocalcemia Hypoalbuminemia DKA 4

5 Pancreatic and Peripancreatic Fluid Collections Incidence, location, natural history Pancreatic Fluid Collections Natural History and management options In both acute Interstitial (edematous) and Necrotizing pancreatitis: Nearly 40% of hospitalized patients will have fluid collection. Located pancreatic and or peripancreatic In > 50% of cases fluid collections regress. No explanation for the regression. Regression cannot be predicted Bradley E. Acute Pancreatitis,Principles and Practice *Bollen etal. Br J Surg 2008:95;6-21 ** Cannon etal. Am Coll Surg 2009: 209; Acute Fluid Collection in AP FNA is not required for all peripancreatic fluid collections 1. Fluid collections that lack a discrete capsule Vary in size and shape 2. Occur in 30-50% of patients 3. Resolve spontaneously in 50% 4. Located within the lesser sac or anterior pararenal space Less commonly track into other regions Bradley EL III. Arch Surg 1993;128: Case 4. A 32 year old physician with acute pancreatitis, day 5 after onset of pancreatitis. No abdominal pain. Two months later fluid completely resolved. Ten years later asymptomatic. Localization of fluid collections Lesser Sac Anterior pararenal space Posterior pararenal space In and around the left lobe of liver Spleen Persistence of fluid collection means a pancreatic fistula has developed with a duct. 5

6 Pancreatic Pseudocysts Become defined after 4 weeks of onset of AP. Well circumscribed, round or oval homogenous fluid collection Well defined wall No associated tissue necrosis Cyst fluid usually shows increased amylase-lipase Pseudocyst formation may seal off spontaneous regression >50% Presence or absence of ductal communication- (important to know for Transpapillary drainage) Pseudocysts: When to intervene? > 6 cm in size is no longer the threshold for intervention Total resolution is documented in cysts > 6cm in size Logic dictates that larger the pseudocysts, longer the duration the less likely spontaneous resolution will occur. Pseudocysts (with underlying chronic pancreatitis), PC with thicker wall or known communication with a duct needs intervention Recommendation : close clinical and radiological follow up, action be taken when PC increases in size, becomes symptomatic or complications are suspected. To be differentiated from cystic neoplasms Pre-drainage evaluation of a pseudocyst 1. Exclude a cystic neoplasm. 2. R/O IPMN or a pancreatic cancer. 3. Exclude solid content in a pseudocyst. 4. Delineate the relationship with stomach or duodenum. 5. Exclude vascular structures in the route of approach to the cyst.( Important in patients with portal hypertension). 6. Trans papillary approach is possible only when there is a communication with a pancreatic duct. ERCP/ MRCP needed. Barthet etal Gastrointest Endosc 2008:67; Varadarajulu etal Gastro intest Endoscopy 2007:66; Hookey etal Gastrointest Endosc 2006:63; Pseudocyst Drainage: Role of EUS Baron. J gastrointest Surg 2008:12;369 Baron.Gastro endoscc Clin NA 2007:17;559 Ahlawat etal JOP 2006:7;616 Localizes cyst Determines distance from stomach wall Detects vascular structures 6

7 Necrotizing Pancreatitis Challenges and solutions An overview of current approaches Pancreatic Necrosis Approximately 15% of patients with AP. Focal or diffuse regions of non-viable pancreatic tissue On CECT necrosis is characterized by areas of pancreatic tissue with absent or poor contrast media enhancement (hypoperfusion) or lack of enhancement of the entire gland Infected necrosis generally occurs within 3 weeks of onset of AP. Note mortality in infected pancreatic necrosis is double that of pancreatic abscess. Acute Pancreatitis Timing of Pancreatic Infections % Cases < 7 days 7-14 days days > 21 days Adapted from H. Beger et al., Gastroenterology 1986; 91:433 Case 7:A 78 year old Mexican Lady admitted with Biliary pancreatitis 3 weeks in the hospital Fever, shock, anuria, Follow up CT scan 7

8 How should pancreatic necrosis be managed?. Managed conservatively. Intervention rarely needed in Sterile necrosis Intervention needed only rarely as in multiorgan dysfunction not improving despite maximal therapy in ICU. In infected necrosis delayed necrosectomy and catheter drainage Santvoort et al. A conservative and minimally invasive approach to necrotizing pancreatitis improves outcome. Gastroenterology. 2011:142:1254. Pezelli et al. Practical Guide lines for acute pancreatitis. Pancreatology 2010;10:523. Is necrosectomy obsolete for IPN? A paradigm shift needed? 1960s Explorative laparotomy to total pancreatectomy. 1990s. 100% mortality if IPN is not operated immediately severe IPN benefit from delayed surgical necrosectomy and drainage minimally invasive techniques. Percutaneous catheter, endoscopic transluminal drainage. Followed by video assisted retroperitoneal or endoscopic drainage. Improved outcome over open necrosectomy. Chang Y. WJG. 2014;20:16925 Rosenberg Surg Infect 2015 Walled off Pancreatic necrosis Abdominal Compartment syndrome in acute pancreatitis. (Mentula P et al Arch.Surg. 2010;145: ) intraabdominal pressure results in new onset organ failure A large low-attenuation fluid collection replaces almost entire pancreatic parenchyma. Pancreatic head and tail are markedly displaced by the fluid collection. Destructive pathway similar to compartment syndrome of extremities Occurs when increased Surgical decompression Opening the abdominal wall and abdominal fascia. Early surgical decompression is associated With reduced mortality. 8

9 Learning points 1. An early evaluation of severity of acute pancreatitis should be made clinically and by one of the scoring systems on admission. 2. Initial management. Pain control, adequate,timely, fluid administration. 3. Oral feeding or enteral feeding, seldom TPN. 4. Routine antibiotics not advocated 3. Assessment of Complications. Complicated acute pancreatitis. 1.Fluid collections Most of them resolve,do not needle. 2.Pancreatic pseudocyst if symptomatic, enlarging, Infected, compressing adjacent organs need intervention. 3. Pancreatic necrosis. If sterile usually does not require intervention 4. Pancreatic necrosis if infected intervention endoscopic or surgical. Delay if not avoid surgery. THANK YOU 9