Reducing the Incidence and Severity of Post Ercp Pancreatitis

Abstract

Acute pancreatitis remains the commonest complication of ERCP (endoscopic retrograde cholangiopancreatography) with published incidence rates that have changed little over 30 years despite significant advances in endoscope and ERCP accessory technology and the introduction of structured ERCP training. Technique related risk factors for post ERCP pancreatitis have been recognised for many years and have been recently refined via large prospective audits. These studies have also revealed the importance of patient related factors and highlighted the high incidence of post ERCP pancreatitis in women being investigated for acalculus biliary pain or idiopathic recurrent acute pancreatitis. Sphincter of Oddi hypertension is often found to be present in this group of patients. Methods of preventing post ERCP pancreatitis have been sought for many years and numerous drugs have been tried using a variety of regimes with heterogeneous groups of patients. At present pancreatic duct stenting looks to be the most efficacious prophylactic method but is not for the beginner endoscopist. It is possible, however, by using a simple strategy to minimise the incidence of post ERCP pancreatitis and modulate its severity.

Botulinum toxin may predict the outcome of endoscopic sphincterotomy in episodic functional post-cholecystectomy biliary pain

“…None of these has superseded sphincter of Oddi manometry (SOM) as the "gold standard" investigation. Unfortunately in patients with SOH SOM is associated with post SOM pancreatitis rates between 3% and 31% and deaths have been reported [6,9]. Moreover, SOH is commonly associated with other functional disorders and therefore a manometric diagnosis of SOH does not guarantee that SOH is the cause of the patient's symptoms.…”

Pancreatits after endoscopic retrograde cholangio-pancreatography

“…More severe forms of PEP are obvious and rarely escape notice. Up to 75% of asymptomatic patients have elevations in serum amylase and lipase after diagnostic or therapeutic ERCP, whereas, others develop significant abdominal pain without hyperamylasemia; neither of these entities are diagnosed as clinical pancreatitis [2,3] . Other patients fall into an overlap group, with pain that is consistent with pancreatitis but with borderline elevation of serum markers of pancreatitis or with substantial elevations of serum markers of pancreatitis combined with minimal pain that does not clearly indicate pancreatitis; these patients may be variably considered as having, or as not having, pancreatitis.…”

Prophylactic Pancreatic Stents: Does Size Matter? A Comparison of 4-Fr and 5-Fr Stents in Reference to Post-ERCP Pancreatitis and Migration Rate

“…This may lead to intracellular activation of proteolytic enzymes, with enhanced local inflammation as indicated by increased levels of cytokines (IL 1, 8, and 6) [12]. Pharmacologic prophylaxis in an attempt to block the initial insult and inflammatory response has been disappointing [5,13,14]. The suggested mechanisms for impaired drainage include papillary edema and/or spasm [15].…”