Amitasha Sinha1, Rukshana Cader2, Venkata S Akshintala3, Susan M Hutfless4, Atif Zaheer5, Vinshi N Khan6, Mouen A Khashab7, Anne Marie Lennon8, Anthony N Kalloo9, Vikesh K Singh10. 1. Department of Internal Medicine, Division of Gastroenterology and Hepatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: amitashasinha@gmail.com. 2. Department of Internal Medicine, Division of Gastroenterology and Hepatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: rcader@me.com. 3. Department of Internal Medicine, Division of Gastroenterology and Hepatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: findsandeep.amc@gmail.com. 4. Department of Internal Medicine, Division of Gastroenterology and Hepatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: shutfle1@jhmi.edu. 5. Pancreatitis Center, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Department of Radiology and Radiological Science, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: azaheer1@jhmi.edu. 6. Department of Internal Medicine, Division of Gastroenterology and Hepatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: vinshinazkhan86@gmail.com. 7. Department of Internal Medicine, Division of Gastroenterology and Hepatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: mkhasha1@jhmi.edu. 8. Department of Internal Medicine, Division of Gastroenterology and Hepatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: amlennon@jhmi.edu. 9. Pancreatitis Center, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Department of Internal Medicine, Division of Gastroenterology and Hepatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: akalloo@jhmi.edu. 10. Pancreatitis Center, Johns Hopkins Medical Institutions, Baltimore, MD, USA; Department of Internal Medicine, Division of Gastroenterology and Hepatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA. Electronic address: vsingh1@jhmi.edu.
Abstract
BACKGROUND: Early systemic inflammatory response syndrome (SIRS) has been associated with severe non-iatrogenic acute pancreatitis. The aims of this study were to determine whether early SIRS could be used to predict severe post-ERCP pancreatitis (PEP) and to determine the effect of prophylactic-pancreatic stenting (PS) on SIRS and severe PEP. METHODS: Between 1/2000 and 6/2012, all patients admitted for PEP after an outpatient ERCP and who had ≥1 abdominal CT scan during hospitalization were retrospectively evaluated. The presence of SIRS was assessed between 0 and 24 h and 24 and 48 h after the time of ERCP completion. SIRS was evaluated as a predictor of severe PEP using area under receiver operating characteristic (AUROC) curve analysis. RESULTS: There were 113 patients with PEP of whom 22 (19.5%) had severe PEP. SIRS was present in 44 (38.9%) and 33 (29.2%) patients between 0 and 24 h and 24 and 48 h, respectively. SIRS between 24 and 48 h had a higher predictive accuracy for severe PEP compared to SIRS between 0 and 24 h (AUROC = 0.7 vs. 0.5, p = 0.002). The prevalence of SIRS between 24 and 48 h was significantly less among the 19 patients who underwent PS (11% vs. 37%, p = 0.03). There was no difference between the prophylactic stenting and no stenting groups with regards to acute fluid collection(s), pancreatic necrosis, organ failure or mortality during hospitalization. CONCLUSIONS: SIRS between 24 and 48 h after ERCP is an accurate, easy to obtain, and inexpensive predictor of severe PEP. PS is associated with a decreased prevalence of SIRS between 24 and 48 h after ERCP.
BACKGROUND: Early systemic inflammatory response syndrome (SIRS) has been associated with severe non-iatrogenic acute pancreatitis. The aims of this study were to determine whether early SIRS could be used to predict severe post-ERCP pancreatitis (PEP) and to determine the effect of prophylactic-pancreatic stenting (PS) on SIRS and severe PEP. METHODS: Between 1/2000 and 6/2012, all patients admitted for PEP after an outpatient ERCP and who had ≥1 abdominal CT scan during hospitalization were retrospectively evaluated. The presence of SIRS was assessed between 0 and 24 h and 24 and 48 h after the time of ERCP completion. SIRS was evaluated as a predictor of severe PEP using area under receiver operating characteristic (AUROC) curve analysis. RESULTS: There were 113 patients with PEP of whom 22 (19.5%) had severe PEP. SIRS was present in 44 (38.9%) and 33 (29.2%) patients between 0 and 24 h and 24 and 48 h, respectively. SIRS between 24 and 48 h had a higher predictive accuracy for severe PEP compared to SIRS between 0 and 24 h (AUROC = 0.7 vs. 0.5, p = 0.002). The prevalence of SIRS between 24 and 48 h was significantly less among the 19 patients who underwent PS (11% vs. 37%, p = 0.03). There was no difference between the prophylactic stenting and no stenting groups with regards to acute fluid collection(s), pancreatic necrosis, organ failure or mortality during hospitalization. CONCLUSIONS: SIRS between 24 and 48 h after ERCP is an accurate, easy to obtain, and inexpensive predictor of severe PEP. PS is associated with a decreased prevalence of SIRS between 24 and 48 h after ERCP.