Determining the risk of acute pancreatitis complications based on the patient’s clinical response to the initial infusion
Keywords:acute pancreatitis, acute dehydration, risk stratification, pancreatic necrosis, biliary pancreatitis, fluid resuscitation
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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