Pancreatitis

Diagnosis:

· Atlanta Classification (revised working group)- need 2 out of 3

o Abdominal Pain “strongly” suggestive of pancreatitis

o Serum Amylase/Lipase 3x upper limits normal of lab

o Characteristic imaging findings on contrast enhanced CT or US

Determination of Severity: Multiple modalities/tests have been proposed to try and predict course of severity of pancreatitis

· APACHE Score

· CT Severity Index (Balthazar Score)

· Ranson’s Criteria

· Hemoconcentration-

· BISAP Score “Bedside Index for the Severity of Acute Pancreatitis”- validated in separate studies. Has been found in studies to be non-inferior to APACHE, Ransons and CT Severity Index.

o B- BUN>25

o I- Impaired Mental Status (GCS less than 15)

o S- SIRS criteria

o A- Age >60

o P- Pleural Effusion

Causes- limited evaluation should be employed to exclude most common causes of AP

· ETOH –made mostly by history

· Biliary Stones- Obtain RUQ ultrasound in all cases

· Medications- 525 medications are listed in the WHO database with an incidence only around 0.1%-2% of all pancreatitis. Special consideration should be given to “black box” warnings for Valproic acid and exanetide in general IM.

· Triglycerides (usually >1000)

· Genetic/Autoimmune- hot button topic in GI literature

· Miscellaneous (microlithiasis, pancreatic ca, Intraductal Papillary mucinous neoplasm (IPMN),pancreatic divisum, Hypercalcemia from hyperparathyroidism, pregnancy, CFTR et al)

Treatment-

· IVF: aggressive rehydration is mandatory in the acute phase of pancreatitis.

· Many definitions of “adequate” volume resuscitation

§ Urine Output >0.5ml/kg/hr

§ Fluid bolus therapy to achieve hemodynamic stability

§ Then 250-350cc/hr x 48hrs

§ May require mechanical intubation or central venous pressure monitoring

· Analgesia:

· Aggressive parenteral analgesia needed in acute phase

· Decreases oxygen demand in this known hyper-catabolic state.

· Nutrition: often an “afterthought” , in AP this is very important

· Numerous trials have shown that early feeding (within 5-7 days) improves outcomes.

· All type of enteral routes (nasojejunal, nasoduodenal, nasogastric) can be utilized.

· If continues to be intolerant to enteral feedings then TPN should be pursued aggressively after failure of enteral nutrition.

Other Caveats-

o Role of CT is NOT at presentation, can actually worsen pancreatitis in acute phase in certain animal models (never studied in human subjects)

o If you order a CT ORDER THE RIGHT ONE, Ct of the Abd/Pelvis with IV contrast with Pancreatic protocol

o Reason to CT would be if concern for severe disease in 24-48 hrs, or failure to improve

Citations:

1. Acute Pancreatitis Classification Working Group. Revision of the Atlanta Classification of Acute Pancreatitis.

2. Talukdar R, Vege S. Early Mangagement of Severe Acute Pancreatitis. Curr Gastroenterol Rep 2011;13:123-130.

3. Papachristou G, Maussana V, Yadav D et al. Comparison of BISAP, Ranson’s, APACHE II and CTSI in Predicting Organ Failure, Complications, and Mortality in Acute Pancreatitis. Am J Gastroenterol 2010;105:435-441.

4. Khan AS, Latif SU, Eloubeidi MA. Controversies in the Etiologies of Acute Pancreatitis. J Pancreas (Online) 2010;11(6):545-552.
5. Vinklerova I, Prochzka M, Procházka V, Urbanek K. Incidence, Severity, and Etiology of Drug Induced Acute Pancreatitis. Dig Dis Sci 2010;55:2977-2981.

6. Olansky L. Do Incretin-Based Therapies Cause Acute Pancreatitis. J Diabetes Sci Technol 2010;4(1):228-229.

7. Nitsche CJ, Jamieson N, Lerch MM, Mayerle JV. Drug induced pancreatitis. Best Practice and Research Clinical Gastroenterology 2010;24:143-155.

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