Determining the risk of acute pancreatitis complications based on the patient’s clinical response to the initial infusion

Authors

  • O.Yu. Muryzina State Institution “Dnipropetrovsk Medical Academy of the Ministry of Health of Ukraine”, Dnipro, Ukraine http://orcid.org/0000-0001-6519-2320
  • O.S. Ustiianovych Medical Center “Surgical Clinic Garvis”, Dnipro, Ukraine

DOI:

https://doi.org/10.22141/2224-0586.7.102.2019.180354

Keywords:

acute pancreatitis, acute dehydration, risk stratification, pancreatic necrosis, biliary pancreatitis, fluid resuscitation

Abstract

Background. The strategy of fluid resuscitation in acute pancreatitis (AP) is based on a timely assessment of the patient’s initial volemic status and justified correction of fluid abnormalities that provides for effective systemic and organ circulation and tissue perfusion, thus eliminating pancreatic ischemia and preventing total organ failure, namely development and manifestation of systemic inflammatory response syndrome (SIRS). The goal of this study is to evaluate the risks of a further complicated development of AP based on the results of the clinical response to initial fluid resuscitation. Materials and methods. The results of a cohort prospective observation conducted in 2015–2018 are presented. The clinical data of 61 patients with AP were analyzed, 25 (41 %) women and 36 (59 %) men with average age of 47.1 ± 6.4 years, and average weight of 79.4 ± 5.1 kg. The baseline α-amylase level is 213 ± 34 U/L, urine diastase — 1019 ± 65 U/L. The sample was stratified by the method of random selection: group 1 (alimentary AP) consisted of 53 patients (76.8 %) with varying severity, group 2 (bi-liary AP) included 14 patients (20.3 %). The severity of AP was determined according to Atlanta-2012 classification. Critically decompensated patients were excluded. Results. Upon admission to the intensive care unit, patients suffered from dominating hypovolemia caused by loss of plasma resulting from acute surgical dehydration degree 2 and 3. Subsequently, the development of AP was assessed for all degrees of severity in group 1, namely subgroup I/nonsevere AP: n = 12/23 %, subgroup II/mild AP: n = 26/49 %, subgroup III/severe AP: n = 15/28 %. For noncomplicated course of AP (subgroup I), the normotonic type of dehydration initially developed, whereas in case of severe pancreatic necrosis (subgroup III), the hypertonic type was observed. The clinical response to the initial infusion is associated with the severity of the further course in accordance with the etiological factor of AP and clinically significant (16 ± 2 %, p < 0.01) decrease in heart rate and hematocrit compared to the baseline, but still remaining beyond the upper boundary of the reference range. In the uncomplicated course of AP (subgroup I), organ failure did not develop; moreover, by the end of day 2, both spontaneous diuresis (up to 0.8‒1.0 ml/kg/h), and intestinal peristalsis on the background of enteral nutrition and infusion volume decrease were restored. With moderate severity of AP (subgroup II), manifestations of transient hepatosplanchnic insufficiency dominated with aggravation of SIRS, Acute Physiology And Chronic Health Evaluation (АРАСНЕ) II to 5 points [5; 6], and Multiple Organ Dysfunction Score (MODS) to 1 point [1; 2], combined with critical reduction of the total protein. Remobilization of the deposited fluid was delayed. In severe AP (subgroup III) after starting resuscitation, heart rate and hematocrit exceeded (up to 20 %, p < 0.001) the corresponding values for subgroups I and II; organ failure was aggravated: АРАСНЕ II — up to 8 [7; 10] points, MODS — up to 3 points [2; 4] and progressing SIRS; peristalsis was not restored in a timely manner, there was a delay in the spontaneous recovery of diuresis up to 24‒32 hours, hypoproteinemia increased to 59.2 ± 2.3 g/l, serum creatinine — to 149 ± 14 μmol/l, serum urea — to 9.8 mmol/l. Blood glucose was also elevated to 9.1 mmol/l, even in the absence of diabetes. Mostly hepatosplanchnic insufficiency persisted, foci of sequestration formed, remobilization of the deposited fluid did not occur, causing secondary hypovolemia, hyperhydration of the interstitial space and resistance to conservative treatment. In case of acute biliary pancreatitis, visceral disorders dominated, with inflammation of the biliary tract, biliary hypertension and cholestasis, mainly due to choledocholithiasis. Conclusions. After the initial infusion in the early stage of acute pancreatitis, the complicated and severe course is clinically predicted by secondary systemic abnormalities in the fluid compartments combined with SIRS and transient or persistent, mainly hepatosplanchnic, organ failure of varying severity, which is further aggravated by the formation of sequestered formations preventing proper remobilization of sequestered and deposited fluid.

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References

Aggarwal A, Manrai M, Kochhar R. Fluid resuscitation in acute pancreatitis. World J Gastroenterol.2014;20(48):18092–103. doi:10.3748/wjg.v20.i48.18092.

Phillip V, Steiner JM, Algül H. Early phase of acute pancreatitis: Assessment and management. World J Gastrointest Pathophysiol. 2014;5(3):158-68. doi: https://dx.doi.org/ 10.4291/wjgp. v5.i3.158.

Krishna SG, Kamboj AK, Hart PA et al. The changing epidemiology of acute pancreatitis hospitalizations: a decade of trends and the impact of chronic pancreatitis. Pancreas. 2017;46 (4): 482–8. doi: 10.1097/MPA.0000000000000783.

Muryzina OYu, Ustiianovych OSt. Liver and volmic disorders in patients with different forms of acute pancreatitis after initiation of infusion therapy [Ridy`nni volemichni porushennya u paciyentiv iz rizny`my` formamy` gostrogo pankreaty`tu pislya provedennya startovoyi infuzijnoyi terapiyi]. Emergency medicine [Medicina neotložnyh sostoânij]. 2018; 5 (92):156‒61. doi: 10.22141/2224-0586.5.92.2018.143252. Ukranian.

Garber A, Frakes C, Arora Z, Chahal P. Mechanisms and management of acute pancreatitis. Gastroenterol Res Pract. 2018:6218798. doi: 10.1155/2018/6218798.

Lankisch P.G., Apte M., Banks P.A. Acute pancreatitis. Lancet. 2015; 386(9988): 85–96. doi: 10.1016/S0140-6736(14)60649-8

Koutroumpakis E., Slivka A., Furlan A. et al. Management and outcomes of acute pancreatitis patients over the last decade: a US tertiary-center experience. Pancreatology. 2017;17:32–40.

Hamada Sh., Masamune A., Shimosegawa T. Transition of early-phase treatment for acute pancreatitis: An analysis of nationwide epidemiological survey. World J Gastroenterol. 2017: 23(16):2826‒31. doi: 10.3748/wjg.v23.i16.2826.

Crockett SD, Wani S, Gardner TB, Falck-Ytter Y, Barkun AN. American Gastroenterological Association Institute Guideline on Initial Management of Acute Pancreatitis.Gastroenterology. 2018;154(4):1096-101. doi: 10.1053/j.gastro.2018.01.032.

Pintado MC, Trascasa M, Arenillas C, de Zárate YO, Pardo A, Blandino Ortiz A, de Pablo R. New Atlanta Classification of acute pancreatitis in intensive care unit: Complications and prognosis. Eur J Intern Med. 2016;30:82-7. doi: 10.1016/j.ejim.2016.01.007.

Zhao G, Zhang JG, Wu HS, Tao J, Qin Q, Deng SC, Liu Y, Liu L, Wang B, Tian K, Li X, Zhu S, Wang CY . Effects of different resuscitation fluid on severe acute pancreatitis. World J Gastroenterol. 2013;19(13):2044–52. doi: 10.3748/wjg.v19.i13.2044.

van Dijk, S.M., Hallensleben, N.D.L., van Santvoort, H.C. et al. Acute pancreatitis: recent advances through randomised trials. Gut. 2017;66(11):2024–32. doi: 10.1136/gutjnl-2016-313595.

de-Madaria, E., Soler-Sala, G., Sanchez-Paya J. Lopez-Font I, Martínez J, Gómez-Escolar L, Sempere L, Sánchez-Fortún C, Pérez-Mateo M. Influence of fluid therapy on the prognosis of acute pancreatitis: a prospective cohort study. Am J Gastroenterol. 2011;106 (10):1843–50. doi: 10.1038/ajg.2011.236.

Lipinski M, Rydzewska-Rosolowska A, Rydzewski A, Rydzewska G. Fluid resuscitation in acute pancreatitis: Normal saline or lactated Ringer's solution? World J Gastroenterol. 2015 Aug 21;21(31):9367‒72. doi: 10.3748/wjg.v21.i31.9367.

Kiat TTJ, Gunasekaran SK, Junnarkar SP, Low JK, Woon W, Shelat VG. Are traditional scoring systems for severity stratification of acute pancreatitis sufficient? Ann Hepatobiliary Pancreat Surg. 2018;22(2):105‒15. doi: 10.14701/ahbps.2018.22.2.105.

Lee KJ, Kim HM, Choi JS, Kim YJ, Kim YS, Cho JH. Comparison of Predictive Systems in Severe Acute Pancreatitis According to the Revised Atlanta Classification. Pancreas. 2016;45(1):46-50. doi: 10.1097/MPA.0000000000000433.

Yang CJ, Chen J, Phillips AR, Windsor JA, Petrov MS. Predictors of severe and critical acute pancreatitis: a systematic review. Dig Liver Dis. 2014;46(5):446-51. doi: 10.1016/j.dld. 2014.01.158.

Koutroumpakis E, Wu BU, Bakker OJ, Dudekula A, Singh VK, Besselink MG, Yadav D, Mounzer R, van Santvoort HC, Whitcomb DC, Gooszen HG, Banks PA, Papachristou GI. Admission Hematocrit and Rise in Blood Urea Nitrogen at 24 h Outperform other Laboratory Markers in Predicting Persistent Organ Failure and Pancreatic Necrosis in Acute Pancreatitis: A Post Hoc Analysis of Three Large Prospective Databases. Am J Gastroenterol. 2015;110(12):1707‒16. doi: 10.1038/ajg.2015.370.

Qiu Q, Nian YJ, Guo Y, Tang L, Lu N, Wen LZ, Wang B, Chen DF4, Liu KJ. Development and validation of three machine-learning models for predicting multiple organ failure in moderately severe and severe acute pancreatitis. BMC Gastroenterol. 2019;19(1):118. doi: 10.1186/s12876-019-1016-y.

Jin Z, Xu L, Wang X, Yang D. Risk Factors for Worsening of Acute Pancreatitis in Patients Admitted with Mild Acute Pancreatitis. Med Sci Monit. 2017;23:1026-32.

Gurusamy KS, Debray TPA, Rompianesi G. Prognostic models for predicting the severity and mortality in people with acute pancreatitis. Cochrane Database Syst Rev 2018; Issue 5. Art. No.: CD013026. doI: 10.1002/14651858.CD013026.

Żorniak M, Beyer G, Mayerle J. Risk Stratification and Early Conservative Treatment of Acute Pancreatitis. Visc Med. 2019;35(2):82-9. doi: 10.1159/000497290.

Published

2019-11-25

How to Cite

Muryzina, O., & Ustiianovych, O. (2019). Determining the risk of acute pancreatitis complications based on the patient’s clinical response to the initial infusion. EMERGENCY MEDICINE, (7.102), 18–25. https://doi.org/10.22141/2224-0586.7.102.2019.180354

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Section

Original Researches