Prevention of post-ERCP pancreatitis

Abstract

Post-procedure pancreatitis is the most common complication of endoscopic retrograde cholangio pancreatography (ERCP) and carries a high morbidity and mortality occurring in at least 3%-5% of all procedures. We reviewed the available literature searching for "ERCP" and "pancreatitis" and "post-ERCP pancreatitis". in PubMed and Medline. This review looks at the diagnosis, risk factors, causes and methods of preventing post-procedure pancreatitis. These include the evidence for patient selection, endoscopic techniques and pharmacological prophylaxis of ERCP induced pancreatitis. Selecting the right patient for the procedure by a risk benefits assessment is the best way of avoiding unnecessary ERCPs. Risk is particularly high in young women with sphincter of Oddi dysfunction (SOD). Many of the trials reviewed have rather few numbers of subjects and hence difficult to appraise. Meta-analyses have helped screen for promising modalities of prophylaxis. At present, evidence is emerging that pancreatic stenting of patients with SOD and rectally administered nonsteroidal anti-inflammatory drugs in a large unselected trial reduce the risk of post-procedure pancreatitis. A recent meta-analysis have demonstrated that rectally administered indomethecin, just before or after ERCP is associated with significantly lower rate of pancreatitis compared with placebo [OR = 0.49 (0.34-0.71); P = 0.0002]. Number needed to treat was 20. It is likely that one of these prophylactic measures will begin to be increasingly practised in high risk groups.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved. Key words: Acute pancreatitis; Endoscopic retrograde cholangio pancreatographyCore tip: Select patients carefully, and give high risk patients rectal indomethacin.Wong LL, Tsai HH. Prevention of post-ERCP pancreatitis.

Chinese expert consensus on perioperative medications for endoscopic retrograde cholangiopancreatography (ERCP)

“…Numerous studies have shown that NSAIDs can effectively inhibit the activity of phospholipase A 2 and reduce the incidence of PEP . Recent RCTs and meta‐analyses have shown that NSAIDs can significantly reduce the incidence of PEP in high‐risk patients.…”

“…Recent RCTs and meta‐analyses have shown that NSAIDs can significantly reduce the incidence of PEP in high‐risk patients. The route of administration and dosage have also been evaluated, showing that rectal administration of NSAIDs within 30 minutes before or after ERCP is effective in preventing PEP, while its oral or intramuscular administration is not . A meta‐analysis of 24 clinical studies concluded that indomethacin and diclofenac could significantly reduce the incidence of mild PEP, although there was no significant reduction in moderate‐to‐severe PEP.…”

“…Numerous studies have shown that NSAIDs can effectively inhibit the activity of phospholipase A 2 and reduce the incidence of PEP. 49 Recent RCTs and meta-analyses have shown that NSAIDs can significantly reduce the incidence of PEP in high-risk patients. The route of administration and dosage have also been evaluated, showing that rectal administration of NSAIDs within 30 minutes before or after ERCP is effective in preventing PEP, while its oral or intramuscular administration is not.…”

Combination of two-hour post-endoscopic retrograde cholangiopancreatography amylase levels and cannulation times is useful for predicting post-endoscopic retrograde cholangiopancreatography pancreatitis

“…Andriulli et al[3] conducted a systematic review of 21 selected surveys involving 16855 patients exhibiting a 3.5% incidence of PEP and observed that 0.11% of those patients died. Although many PEP prophylactic treatments have been reported[4-6], only prompt aggressive intravenous hydration is reportedly effective at reducing morbidity and mortality[7-10]. Therefore, early PEP identification is important, as it facilitates early intervention and may prevent disease progression and death.…”

The management of the patient with acute pancreatitis: from evidence to clinical practice

“…They may also generate toxic metabolites (like nucleoside reverse transcriptase inhibitors) or induce hypetriglyceridemia (like estrogens), or give an immuno-mediate reaction (like sulfonamides). 17 Drugs inducing pancreatitis are classified in four classes: Ia (drugs with at least one case report, evidence of a positive re-challenge, and exclusion of other causes of AP, such as codeine, cytarabine, dapsone, enalapril, furosemide, isoniazid, mesalamine, metronidazole, pentamidine, pravastatin, simvastatin, sulfamethoxazole, sulindac, tetracycline, valproic acid), Ib (the same but without exclusion of other causes of AP such as amiodarone, azathioprine, dexamethasone, lamivudine, losartan, 6-MP, premarin, trimethoprim-sulfamethoxazole), II (at least four case reports with a consistent latency period for at least 75% of the cases, for example: acetaminophen, clozapine, erythromycin, estrogen, propofol, tamoxifen), III (at least two case reports but without re-challenge data or a consistent latency period, like alendronate, carbamazepine, ceftriaxone, clarithromycin, cyclosporin, hydrochlorothiazide, ribavirin, metformin, minocycline, naproxen, prednisone, prednisolone), and IV (one case report without re-challenge data, for example ampicillin, cisplatin, colchicine, cyclophosphamide, diclofenac, doxorubicin, interleukin-2, octreotide, propoxyphene, rifampin, risperidone, sertraline, tacrolimus, vincristine). The management of the patient with acute pancreatitis Acute pancreatitis has also been reported during therapies with interferon (both in the standard and pegylated form) in patients with chronic hepatitis B and C (in these cases in association with ribavirin), may be due to immune modulation effects of the drug.…”