Which Patients with Chronic Pancreatitis Are Unlikely to Respond to EUS-Guided Celiac Plexus Blockade (CPB)?

Abstract

Background: Pain from chronic pancreatitis can be debilitating and difficult to treat. EUS-guided CPB has been used for short term palliation of refractory pain in chronic pancreatitis (CP) with marginal efficacy. Ongoing nociceptive input from the pancreas can lead to local neuritis and a state of spinal excitability. The persistence of these changes is collectively termed central sensitization, and is a fundamental aspect in the enhancement of pain sensitivity in chronic pain. More targeted therapies and better patient selection are needed to prevent this “CNS windup” phenomenon. Aim: To evaluate characteristics associated with a clinical response or non-response to EUS-guided CPB in patients with CP and abdominal pain. Patients and Methods: EUS-guided CPB performed from 9/05-6/08 were identified by retrospective chart review. Inclusion criteria included pancreatic pain >3 months and objective evidence of CP, defined by at least one of the following: pancreatic endocrine or exocrine insufficiency, > 5 EUS criteria for CP, suggestive ERCP findings, or histologic evidence of CP. Clinical response to CPB was defined a priori as a >3 point or >50% improvement from baseline VAS pain scores at 2 weeks. Variables analyzed included pre and post procedure pain scores, opioid use, EUS criteria, CPB formulation, alcohol history, illicit drug use, Axis I diagnoses, prior pancreatic surgery or CPB, histologic diagnosis of CP, and extra-pancreatic pain syndromes (IBS, recurrent headaches, neuropathies, chronic back pain, fibromyalgia). Results: EUS-guided CPB were performed on 112 discrete patients from 9/05-6/08. 90 of the 112 patients fulfilled inclusion criteria. 82 patients had complete information: 31 males and 51 females, with average age of 45 years. Only the index CPB cases of each patient were included for analysis. A significant response to CPB occurred in 24 (29%) patients. The mean duration of pain reduction in responders was 48.3 ± 31.7days. Our analysis failed to identify any statistically significant clinical predictors of response to EUS-guided CPB. Patients with co-existing extra-pancreatic pain syndrome were 88% less likely to respond to CPB (OR 0.12, 95% CI 0.02 -0.97, p=0.03). Conclusions: Presence of extra-pancreatic pain syndromes was a significant predictor of nonresponse to EUS-CPB. This may result from sustained central sensitization in this subgroup, rendering therapies directed at the celiac plexus ineffective at palliating pain. Future studies are needed to investigate the role of early CPB utilizing novel neuroinflammatory inhibitors as components in CPB formulations to prevent the development of sensitization.