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Increased intra-abdominal pressure: is it of any consequence in severe acute pancreatitis?

ABSTRACT: BACKGROUND: Increased intra-abdominal pressure (IAP) is detrimental for the recovery of organ function in trauma and emergency patients. The aim of this study was to assess the correlation between the dynamics of IAP and organ dysfunction in severe acute pancreatitis (SAP). MATERIALS AND METHODS: Management of SAP between 2000 and 2004 was analysed. SAP was classified according to Atlanta 1992. Organ dysfunction, systemic inflammatory response syndrome (SIRS) and outcomes in relation to the IAP were assessed. IAP was measured indirectly. RESULTS: A total of 65 patients, with an average APACHE II score of 6.44, complied with the Atlanta criteria. In all, 34 patients received conservative treatment and 31 were operated. SIRS was observed in 59 cases and multiple organ dysfunction syndrome (MODS) in 61 cases. IAP was significantly higher in the 25 most complicated patients requiring renal replacement therapy (RRT), compared with 40 patients without RRT, 31.72 vs 21.4 cm/H(2)O (p=0.037). IAP interrelated positively with SOFA score (r = + 0.371, p<0.01) and organs involved (r = + 0.356, p<0.01), and negatively with platelet count and enterally provided volume (r = - 0.284, p<0.01; r = - 0.5, p<0.01, respectively). Overall mortality (9.2%) was associated with surgery and sustained increase of the IAP over 25 cm/H(2)O. Our data support the pathophysiological interrelation of elevated IAP and development of organ dysfunction. CONCLUSION: Development of organ dysfunction in SAP could be associated with increased IAP. Grade III increase of IAP should be considered as an indicator for revision of treatment modalities.

SUBMITTER: Pupelis G

PROVIDER: S-EPMC2131680 | biostudies-other | 2006

REPOSITORIES: biostudies-other

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Project description:BackgroundThis study aimed to investigate the microbiol distribution of intra-abdominal infection in patients with acute pancreatitis, and to develop a reliable prediction model to guide the use of antibiotics.MethodsInpatient with acute pancreatitis between January 2015 and June 2020 were enrolled in the study. Participants were divided into the intra-abdominal infection group and non-infection group. Isolated pathogens and antibiotic susceptibility were documented. Characteristics parameters, laboratory results, and outcomes were also compared. Least absolute shrinkage and selection operator (LASSO) regression model was used to select the risk factors associated with intra-abdominal infection in patients with acute pancreatitis. Logistic regression analysis, random forest model, and artificial neural network were also used to validate the performance of the selected predictors in intra-abdominal infection prediction. A novel nomogram based on selected predictors was established to provide individualized risk of developing intra-abdominal infection in patients with acute pancreatitis.ResultsA total amount of 711 participants were enrolled in the study, and of these, 182 (25.6%) had intra-abdominal infection. Of the 247 isolated pathogens, 45 (18.2%) were multidrug-resistant bacteria, and antibiotic susceptibility was lower than that of China Antimicrobial Surveillance Network 2020. The LASSO method identified 5 independent predictors [intra-abdominal pressure (IAP), acute physiology and chronic health evaluation II (APACHE II), computed tomography severity index (CTSI), the severity of pancreatitis, and intensive care unit (ICU) admission] of intra-abdominal infection, which were validated by three different models. The area under the curve was >0.95 for all 5 predictors. A clinically useful nomogram based on these predictors was successfully established.ConclusionsMultidrug-resistant bacteria were quite common in intra-abdominal infection. IAP, APACHE II, CTSI, the severity of pancreatitis, and ICU admission were identified as risk factors and the new nomogram based on these could help clinicians estimate the risk of intra-abdominal infection and optimize antimicrobial prescription for acute pancreatitis patients.

Project description:Background/Aims:Severe acute pancreatitis (SAP) is associated with intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS), but treatment of these conditions is difficult. We studied a rat model of SAP + IAH to determine the effect of oral administration of Clostridium butyricum and butyrate (its major metabolite) on intestinal barrier functions. Methods:A total of 48 rats were assigned to four groups, with 12 rats per group: Sham, SAP+IAH, SAP+IAH+C. butyricum, and SAP + IAH + butyrate. SAP was induced by sodium taurocholate infusion into the biliopancreatic duct, intra-abdominal pressure (IAP), mortality was measured 24 h later, and then rats were euthanized. The plasma levels of several markers [amylase, diamine oxidase (DAO), fluorescein isothiocyanate (FITC)-dextran, tumor necrosis factor alpha (TNF-?), interleukin (IL)-6, IL-1?, IL-12, lipopolysaccharide (LPS)] and fecal butyric acid level were determined. The pancreas and intestine were examined using histology, and RT-PCR and Western blotting of intestinal tissues were used to measure the expression of six markers {tight junction proteins [zonula occludens protein-1 (ZO-1), claudin-1, claudin-2, occluding], matrix metalloproteinase 9 [MMP9], and TNF-?}. The gut flora of the rats was examined by 16S rRNA sequencing. Results:Induction of SAP + IAH altered several functions of the intestinal barrier, and enhanced intestinal permeability, decreased the levels of ZO-1, claudin-1, occludin, the richness and diversity of the microflora community, the relative abundance (RA) of Firmicutes, and the number of probiotic organisms. However, induction of SAP+IAH increased the expression of claudin-2, MMP9, and TNF-?, and the RA of Proteobacteria and pathogens in the feces. Rats that received oral C. butyricum or butyrate had reduced intestinal injury and plasma levels of DAO, LPS, and inflammatory cytokines. Conclusion:This study of rats with SAP+IAH indicated that oral dosing of C. butyricum or butyrate reduced intestinal injury, possibly by altering the functions of the intestinal mucosal barrier.

Project description:BackgroundThe intra-abdominal pressure (IAP) is an important clinical parameter that can significantly change during respiration. Currently, IAP is recorded at end-expiration (IAPee), while continuous IAP changes during respiration (?IAP) are ignored. Herein, a novel concept of considering continuous IAP changes during respiration is presented.MethodsBased on the geometric mean of the IAP waveform (MIAP), a mathematical model was developed for calculating respiratory-integrated MIAP (i.e. MIAPri=IAPee+i??IAP), where 'i' is the decimal fraction of the inspiratory time, and where ?IAP can be calculated as the difference between the IAP at end-inspiration (IAPei) minus IAPee. The effect of various parameters on IAPee and MIAPri was evaluated with a mathematical model and validated afterwards in six mechanically ventilated patients. The MIAP of the patients was also calculated using a CiMON monitor (Pulsion Medical Systems, Munich, Germany). Several other parameters were recorded and used for comparison.ResultsThe human study confirmed the mathematical modelling, showing that MIAPri correlates well with MIAP (R2 = 0.99); MIAPri was significantly higher than IAPee under all conditions that were used to examine the effects of changes in IAPee, the inspiratory/expiratory (I:E) ratio, and ?IAP (P <0.001). Univariate Pearson regression analysis showed significant correlations between MIAPri and IAPei (R = 0.99), IAPee (R = 0.99), and ?IAP (R = 0.78) (P <0.001); multivariate regression analysis confirmed that IAPee (mainly affected by the level of positive end-expiratory pressure, PEEP), ?IAP, and the I:E ratio are independent variables (P <0.001) determining MIAP. According to the results of a regression analysis, MIAP can also be calculated asMIAP=-0.3+IAPee+0.4??IAP+0.5?IE.ConclusionsWe believe that the novel concept of MIAP is a better representation of IAP (especially in mechanically ventilated patients) because MIAP takes into account the IAP changes during respiration. The MIAP can be estimated by the MIAPri equation. Since MIAPri is almost always greater than the classic IAP, this may have implications on end-organ function during intra-abdominal hypertension. Further clinical studies are necessary to evaluate the physiological effects of MIAP.

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Increased intra-abdominal pressure: is it of any consequence in severe acute pancreatitis?

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