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Acute pancreatitis
This document summarizes the diagnosis, etiology, management, and treatment of acute pancreatitis based on guidelines from the American College of Gastroenterology. It presents a case study of a 47-year-old female diagnosed with gallstone pancreatitis based on abdominal pain, elevated lipase, and ultrasound findings of cholelithiasis. Her case is used to illustrate the guidelines, including IV fluid hydration, no antibiotics given due to mild symptoms resolving in 48 hours, and cholecystectomy before discharge due to gallstone etiology.
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Acute pancreatitis
- 1. Acute Pancreatitis Mini Lecture FaridJalali January 23, 2014
- 2. o Establish theDiagnosis of Acute Pancreatitis o Establish the Etiology of Acute Pancreatitis o Initial Management of Acute Pancreatitis All recommendations are based on the latest ACG Management of Acute Pancreatitis guidelines published in 2013. Objectives
- 3. o Diagnosis ofAcute Pancreatitis requires at least 2 of 3 from the following criteria: o Abdominal pain consistent with acute pancreatitis o Serum amylase or lipase greater than 3 times the upper limit of normal o Characteristic findings on abdominal imaging o CT w/ contrast or MRI should be reserved for patients in whom the diagnosis in unclear or fail to improve within 48-72 hours. A. Diagnosis
- 4. 47 year-old femalewith recent mild alcohol intake and no history of prior gallstones or acute pancreatitis presents to ER with epigastric abdominal pain radiating to the back. Lipase is 500 on admission. o Diagnosis: Met the following 2 of 3 criteria (1) abdominal pain consistent with acute pancreatitis (2) Lipase > 3 times upper limit of normal – therefore, no CT or MR imaging required to establish diagnosis. Case Vignette
- 5. o Transabdominal ultrasoundshould be performed in ALL patient with acute pancreatitis to assess gallstones as etiology of acute pancreatitis. o In absence of gallstones or significant alcohol use, obtain serum triglycerides. o If serum triglycerides > 1,000 mg/dL, consider as etiology of acute pancreatitis. o In patients > 40 years of age, consider pancreatic tumor in absence of other causes. o In patients < 30 years of age and +FH of acute pancreatitis in absence of other causes, consider genetic testing for hereditary pancreatitis. B. Etiology
- 6. o Etiology: Asall patients with acute pancreatitis are recommended to get transabdominal ultrasound, a RUQ ultrasound was done which showed cholelithiasis and CBD dilatation without choledocholithiasis. Likely etiology was gallstone pancreatitis with or without a component of alcohol-induced acute pancreatitis. Case Vignette – cont.
- 7. o Various methodsexist to assess severity of acute pancreatitis. o Next slide describes clinical findings associated with a severe course of acute pancreatitis. o BISAP score is a helpful tool in assessing severity and in-hospital mortality of acute pancreatitis. o BISAP, Ranson’s, APACHE-II and CTSI scores all have similar prognostic accuracy. C. Severity Assessment
- 8. Severity Scoring ofAcute Pancreatitis Bedside index of severity in acute pancreatitis (BISAP) score Presence of organ failure and/or pancreatic necrosis defines Severe Acute Pancreatitis. Patients with high severity of initial presentation and/or presence of end-organ failure (shock, AKI, altered mental status, respiratory failure, ARDS, etc) should be admitted to ICU.
- 9. o Early ANDAggressive IV fluid hydration must be initiated. o How aggressive? o If severe hypovolemia present, bolus IV fluids initially o Then keep maintenance rate of 250 – 500 mL/hr IV fluids o What kind of IV fluids? o Isotonic crystalloid (NS, LR) o LR may be preferred (conditional recommendation) o How soon to start? o Early, early, early !! o Most beneficial in the first 12-24 h o What is my goal with IV fluid hydration? o Decrease BUN (as checked q6h initially) D. Initial Management
- 10. o Management: NPO,IV fluid hydration at 250-500 cc/hr with monitoring BUN q6h with goal of IVF hydration to decrease BUN in the first 12-24 hours. Case Vignette – cont.
- 11. o Do NOT#1: Routine use of prophylactic antibiotics for severe acute pancreatitis is NOT recommended. o Do NOT #2: Use of antibiotics to prevent progression of sterile necrosis to infected necrosis is NOT recommended. o Keep in mind that patients with acute pancreatitis often and early have fever but this does not necessarily mean infected necrosis exists. E. Role of Antibiotics
- 12. o Think ofinfected necrosis if patient with pancreatic or extra-pancreatic necrosis fails to improve after 7-10 days of hospitalization. o In case of infected necrosis, either FNA with gram-stain and culture to narrow antibiotic regimen or empirically treat with antibacterial antibiotics. o Routine antifungal therapy is not recommended unless specifically indicated based on culture and/or gram-stain. E. Role of Antibiotics
- 13. o Antibiotics role:Despite spiking one fever to 101 F, no clinical concern for infected necrosis existed and patient improved clinically within 48 hours. No antibiotics were therefore initiated. Case Vignette – cont.
- 14. o NG versusNJ tube feeding are COMPARABLE in efficacy and safety. o In other words, do NOT delay enteral feeding because NJ tube is not present. o IV nutrition should be avoided unless enteral nutrition is not available, not tolerated, or not meeting caloric requirements. o Enteral feeding is not merely to meet caloric requirements; it also prevents infectious complications. o Timing of enteral feeding? Not mentioned in guidelines, but generally if anticipate patient cannot have PO intake within 48 hours, start enteral feeding with NG or NJ. F. Feeding
- 15. o Enteral feeding:As patient was able to have PO intake within 48 hours, neither NG nor NJ tube feeding was initiated. Case Vignette – cont.
- 16. o Mild acutepancreatitis with gallstones Perform cholecystectomy before discharge o Necrotizing acute pancreatitis with gallstones Delay cholecystectomy until inflammation subsides o Asymptomatic pseudocysts or sterile necrosis do NOT warrant intervention (i.e drainage) regardless of size or location. o Drainage of infected necrosis should be delayed for at least 4 weeks to allow formation of walled-off necrosis. G. Role of Surgery
- 17. o Role ofSurgery: Given evidence of gallstones and mild acute pancreatitis, cholecystectomy was performed before discharge to prevent recurrent episodes of gallstones pancreatitis. Case Vignette – cont.
- 18. o Early andaccurate diagnosis of acute pancreatitis is crucial. o Early treatment of acute pancreatitis with aggressive IV fluid hydration saves lives and is most beneficial in the first 12-24 hours. o Routine prophylactic antibiotic use is not recommended for acute pancreatitis unless presence of infected necrosis is established clinically or by FNA. o Mild acute pancreatitis due to gallstones warrants cholecystectomy before discharge. Summary
- 19. o Scott Tenner MD, MPH,FACG, John Baillie MB, ChB, FRCP, FACG, John DeWitt MD, FACG and Santhi Swaroop Vege MD, FACG. American College of Gastroenterology Guideline: Management of Acute Pancreatitis. Am J Gastroenterol 2013; 108:1400–1415; doi:10.1038/ajg.2013.218; published online 30 July 2013. References
Editor's Notes
- #6 Genetic testing for hereditary pancreatitis is to test for at least three different inheritance patterns for chronic pancreatitis: 1) Autosomal dominant hereditary pancreatitis — This is most often associated with mutations in the serine protease 1 gene (PRSS1) on chromosome 7q35, which encodes trypsin-1 (cationic trypsinogen). Rarely, autosomal-dominant-appearing hereditary pancreatitis is identified in a kindred that does not have an identifiable PRSS1 mutation. 2) Autosomal recessive pancreatitis — Chronic pancreatitis associated with cystic fibrosis is the most common example. Mutations in the serine protease inhibitor Kazal type 1 gene (SPINK1, also called pancreatic secretory trypsin inhibitor gene) also may present in an autosomal recessive pattern. CFTR-associated disorders include chronic pancreatitis with minimal lung disease, and this trait may occur in multiple family members. 3) Complex genetics — Multiple family members may have recurrent acute or chronic pancreatitis associated with a combination of genetic and environmental factors. This is the case for patients with heterozygous SPINK1 mutations, in which the SPINK1 mutation probably acts as a disease modifier, lowering the threshold for developing pancreatitis from other genetic (eg, CFTR mutations) or environmental factors. Some apparently sporadic cases of pancreatitis have complex genetic risk. &lt;number&gt;
- #8 “BISAP, Ranson’s, APACHE-II and CTSI scores all have similar prognostic accuracy.” based on below article: Am J Gastroenterol. 2010 Feb;105(2):435-41; quiz 442. doi: 10.1038/ajg.2009.622. Epub 2009 Oct 27. Comparison of BISAP, Ranson&apos;s, APACHE-II, and CTSI scores in predicting organ failure, complications, and mortality in acute pancreatitis. Papachristou GI, Muddana V, Yadav D, O&apos;Connell M, Sanders MK, Slivka A, Whitcomb DC. &lt;number&gt;