Background Malnutrition is a potentially costly problem in critically ill patients admitted to the intensive care unit (ICU). The aim of this study is to evaluate the relationships between the Onodera’s prognostic nutritional index (OPNI) and intestinal permeability and between OPNI and systemic inflammation in critically ill patients.
Methods This was a cross-sectional study conducted in the general ICU of a university-affiliated hospital. A total of 162 ICU-hospitalized adult patients admitted between May 2018 and December 2019, was included in the study sample. The OPNI was calculated at admission and categorized as ≤40 or >40. We assessed plasma endotoxin and zonulin concentrations as markers of intestinal permeability as well as serum interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hs-CRP) as markers of systemic inflammation upon admission under stringent conditions. The relationships between these markers and OPNI were assessed after adjusting for potential confounders through estimation of a binary logistic regression model.
Results Median (interquartile range) hs-CRP, IL-6 zonulin, and endotoxin were significantly greater in the low OPNI subgroup than in the high OPNI subgroup (all P<0.05). Multivariate analyses showed significant association between serum IL-6 (odds ratio [OR], 0.88; 95% confidence interval [CI], 0.64–0.96), serum hs-CRP (OR, 0.77; 95% CI, 0.53–0.92), plasma endotoxin (OR, 0.81; 95% CI, 0.72–0.93), and plasma zonulin (OR, 0.83; 95% CI, 0.75–0.98) levels with OPNI in the overall population.
Conclusions Our results provide evidence that higher plasma endotoxin, zonulin, IL-6, and hs-CRP levels are associated with progressively lower OPNI in mixed ICU populations, particularly in surgical ICU patients.
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Conventional medical therapies have not been very successful in treating adults with refractory septic shock. The effects of direct hemoperfusion using polymyxin B and veno-arterial extracorporeal membrane oxygenation (ECMO) for refractory septic shock remain uncertain. A 66-year-old man was admitted to the emergency department and suffered from sepsis-induced hemodynamic collapse. For hemodynamic improvement, we performed direct hemoperfusion using polymyxin B. Computed tomography scan of this patient revealed emphysematous pyelonephritis (EPN), for which he underwent emergent nephrectomy with veno-arterial ECMO support. To the best of our knowledge, this is the first report of successful treatment of EPN with refractory septic shock using polymyxin B hemoperfusion and nephrectomy under the support of ECMO.
Severe sepsis and septic shock are the main causes of death in critically ill patients. Early detection and appropriate treatment according to guidelines are crucial for achieving favorable outcomes. Endotoxin is considered to be a main element in the pathogenic induction of gram-negative bacterial sepsis. Polymyxin B hemoperfusion can remove endotoxin and is reported to improve clinical outcomes in patients with intra-abdominal septic shock, but its clinical efficacy for pneumonic septic shock remains unclear. Here, we report a case of a 51-year-old man with pneumonic septic shock caused by Pseudomonas aeruginosa, who recovered through polymyxin B hemoperfusion.
BACKGROUND Bacterial lipopolysaccharide (LPS), an endotoxin, can increase nitric oxide (NO) production by expression of an inducible isoforms of nitric oxide synthase (iNOS). Bacterial infections of the central nervous system dilate cerebral vessels and increase cerebral blood flow. We hypothesized that systemic and intraventricular application of bacterial lipopolysaccharide would increase cerebrospinal fluid (CSF) production due to increase in blood flow to choroid plexus caused by NO-induced vasodilation. METHODS Ventriculocisternal perfusion was used to measure the production of CSF in pentobarbital-anesthetized rats.
The lateral ventricle and cisterna magna were cannulated stereotactically and perfused continuously with artificial CSF with blue dextran 2000 as the indicator. Baseline collections of CSF began after steady state outflow was established; then, endotoxin was administered intravenously or intraventricularly. The baseline rate of CSF production was compared with that measured during 3 hours after endotoxin administration. RESULTS The baseline rate of CSF production was 2.6 0.3 (2.2~3.5)microliter/minute in the rat. There were no significant changes in CSF production rate after intravenous or intraventriculr administration of endotoxin. CONCLUSIONS We could not observe significant changes in CSF production rate with the ventriculocisternal perfusion method of measuring CSF production after intravenous or intraventriculr administration of endotoxin in the rats.
BACKGOUND: Gram negative bacterial lipopolysaccharide (LPS) induces increase in the production of nitric oxide (NO), or a related substance derived from L-arginine in the animal tissue. Recent evidence indicates that airway epithelium may secrete NO or a related compound. It has multiple regulatory roles in the airways. In vitro, the effects of lipopolysaccharide (LPS) on the reactivity of rat' tracheal wall with or without epithelium were examined. METHODS Tracheas were removed from Sprague Dawley rats.
Preparations were mounted for isometric recording in 20ml organ baths at 37degrees C containing Tis-buffered Tyrode solution continuously gassed with 100% O2. Tensions were measured with force displacement transducers and responses were recorded on a polygraph. Cummulative concentration-response curves were constructed for acetylcholine (Ach) in the tracheal strips with or without preincubation of Escherichia coli LPS (100 mcg/ml, 5hrs).
And then effects of NO synthase inhibitors and removal of epithelium were examined. RESULTS In isolated perfused tracheas preincubated by LPS, both removed epithelium and intact epithelium of rat tracheal rings showed decreased Ach-induced contraction. In intact epithelium group, 10 (-5)M L-NAME (N-nitro-L-arginine methyl ester), 10 (-5)M L-arginine or dexamethasone pretreatment was restored in Ach-induced contraction response. But in the removed epithelium group, Ach-induced contraction was potentiated by L-arginine pretreatment and was not restored by the pretreatment of L-NAME and dexamethasone. CONCLUSIONS The results suggest that nitric oxide synthase is induced by endotoxin in the tracheal epithelium, resulting in inhibition of the contractile response.