Early aggressive intravenous hydration is recommended for acute pancreatitis treatment although randomized trials have not documented benefit. We performed a randomized trial of aggressive vs. standard hydration in the initial management of mild acute pancreatitis.
Sixty patients with acute pancreatitis without systemic inflammatory response syndrome (SIRS) or organ failure were randomized within 4 h of diagnosis to aggressive (20 ml/kg bolus followed by 3 ml/kg/h) vs. standard (10 ml/kg bolus followed by 1.5 mg/kg/h) hydration with Lactated Ringer’s solution. Patients were assessed at 12-h intervals. At each interval, in both groups, if hematocrit, blood urea nitrogen (BUN), or creatinine was increased, a bolus of 20 ml/kg followed by 3 ml/kg/h was given; if labs were decreased and epigastric pain was decreased (measured on 0–10 visual analog scale), hydration was then given at 1.5 ml/kg/h and clear liquid diet was started. The primary endpoint, clinical improvement within 36 h, was defined as the combination of decreased hematocrit, BUN, and creatinine; improved pain; and tolerance of oral diet.
The mean age of the patients was 45 years and only 14 (23%) had comorbidities. A higher proportion of patients treated with aggressive vs. standard hydration showed clinical improvement at 36 h: 70 vs. 42% (P=0.03). The rate of clinical improvement was greater with aggressive vs. standard hydration by Cox regression analysis: adjusted hazard ratio=2.32, 95% confidence interval 1.21–4.45. Persistent SIRS occurred less commonly with aggressive hydration (7.4 vs. 21.1%; adjusted odds ratio (OR)=0.12, 0.02–0.94) as did hemoconcentration (11.1 vs. 36.4%, adjusted OR=0.08, 0.01–0.49). No patients developed signs of volume overload.
Early aggressive intravenous hydration with Lactated Ringer’s solution hastens clinical improvement in patients with mild acute pancreatitis.
1Division of Gastroenterology, University of Southern California, Keck School of Medicine, Los Angeles, California, USA
2Department of Preventive Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA
3Department of Surgery, University of Southern California, Keck School of Medicine, Los Angeles, California, USA
4Department of Emergency Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA
5Section of Digestive Diseases, Yale School of Medicine, New Haven, Connecticut, USA
6VA Connecticut Healthcare System, West Haven, Connecticut, USA
Correspondence: James L Buxbaum, MD, Division of Gastroenterology, University of Southern California, Keck School of Medicine, D & T Building Room B4H100, 1983 Marengo St, South Pasadena, Los Angeles, California 90033-1370, USA. E-mail: firstname.lastname@example.org
Received 01 September 2016; accepted 01 January 2017
Guarantor of the article: James Buxbaum, MD.
Specific author contributions: Concept and design: J.B., T.K., C.L., P.J. and K.D.; acquisition of data: J.B., M.Q., B.D., N.J., D.W., T.K., P.J. and K.D.; statistical analysis and interpretation of data: J.B., B.D., M.Q., C.L. and L.L.; drafting and revision of manuscript: J.B., M.Q., B.D., N.J., C.L., D.M., T.K., P.J., K.D. and L.L.
Financial support: This publication was supported by NIH/NCRR SC CTSI Grant Number UL1TR000130. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH.
Potential competing interests: None.
SUPPLEMENTARY MATERIAL is linked to the online version of the paper at http://www.nature.com/ajg