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简介：AbstractImportance:Acute necrotizing encephalopathy (ANE) is a rare disease with high mortality. Plasma exchange (PLEX) has recently been reported to treat ANE of childhood (ANEC), but its efficacy is uncertain.Objective:This study aimed to investigate the effectiveness of PLEX on ANEC.Methods:A retrospective study was conducted in four pediatric intensive care units from December 2014 to December 2020. All patients who were diagnosed with ANEC were included; however, these patients were excluded if their length of stay was less than 24 h. Participants were classified into PLEX and non-PLEX groups.Results:Twenty-nine patients with ANEC were identified, 10 in the PLEX group and 19 in the non-PLEX group. In the PLEX group, C-reactive protein, procalcitonin, alanine aminotransferase, and aspartate aminotransaminase levels were significantly lower after 3 days of treatment than before treatment (13.1 vs. 8.0, P = 0.043; 9.8 vs. 1.5, P = 0.028; 133.4 vs. 31.9, P = 0.028; 282.4 vs. 50.5, P = 0.046, respectively). Nine patients (31.0%, 9/29) died at discharge, and a significantly difference was found between the PLEX group and non-PLEX group [0 vs. 47.4% (9/19), P = 0.011]. The median follow-up period was 27 months, and three patients were lost to follow-up. Thirteen patients (50.0%, 13/26) died at the last follow-up, comprising three (33.3%, 3/9) in the PLEX group and ten (58.8%, 10/17) in the non-PLEX group, but there was no significant difference between the two groups (P = 0.411). Three patients (10.3%, 3/29) fully recovered.Interpretation:PLEX may reduce serum C-reactive protein and procalcitonin levels and improve liver function in the short term. PLEX may improve the prognosis of ANEC, and further studies are needed.

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简介：Hepaticencephalopathy(HE)isasevereneuropsychiatricsyndromethatmostcommonlyoccursindecompensatedlivercirrhosisandincorporatesaspectrumofmanifestationsthatrangesfrommildcognitiveimpairmenttocoma.AlthoughtheetiologyofHEisnotcompletelyunderstood,itisbelievedthatmultipleunderlyingmechanismsareinvolvedinthepathogenesisofHE,andoneofthemainfactorsisthoughttobeammonia;however,theammoniahypothesisinthepathogenesisofHEisincomplete.Recently,ithasbeenincreasinglydemonstratedthatinflammation,includingsystemicinflammation,neuroinflammationandendotoxemia,actsinconcertwithammoniainthepathogenesisofHEincirrhoticpatients.Meanwhile,agoodnumberofstudieshavefoundthatcurrenttherapiesforHE,suchaslactulose,rifaximin,probioticsandthemolecularadsorbentrecirculatingsystem,couldinhibitdifferenttypesofinflammation,therebyimprovingtheneuropsychiatricmanifestationsandpreventingtheprogressionofHEincirrhoticpatients.TheantiinflammatoryeffectsofthesecurrenttherapiesprovideanoveltherapeuticapproachforcirrhoticpatientswithHE.ThepurposeofthisreviewistodescribetheinflammatorymechanismsbehindtheetiologyofHEincirrhosisanddiscussthecurrenttherapiesthattargettheinflammatorypathogenesisofHE.

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简介：摘要IntroductionDelayed encephalopathy due to carbon monoxide (CO) poisoning can even occur in patients with mild symptoms of acute CO poisoning. Some cases taking conventional hyperbaric oxygen (HBO) therapy or steroid-pulse therapy may be insufficient, and AchEI may be effective.Patient concerns and diagnosesWe report two cases of delayed encephalopathy after acute CO poisoning involving two women aged 69 (Case 1) and 60 years (Case 2) whose cognitive function improved with acetylcholinesterase inhibitor (AchEI) treatment. Delayed encephalopathy occurred 25 and 35 days after acute CO poisoning in Case 1 and Case 2, respectively. Both patients demonstrated cognitive impairment, apathy, and hypokinesia on admission.Interventions and outcomesAlthough hyperbaric oxygen therapy did not yield any significant improvements, cognitive dysfunction improved substantially. This was evidenced by an improved Mini-Mental State Examination score from 9 to 28 points in Case 1 and an improved Hasegawa′s dementia rating scale score from 4 to 25 points in Case 2 after administration of an AchEI. In Case 1, we administered galantamine hydrobromide, which was related with improved white matter lesions initially detected on brain magnetic resonance imaging. However, in Case 2 white matter lesions persisted despite AchEI treatment. AchEI treatment may result in improved cognitive and frontal lobe function by increasing low acetylcholine concentrations in the hippocampus and frontal lobe caused by decreased nicotinic acetylcholine receptor levels in delayed encephalopathy after CO poisoning.ConclusionPhysicians should consider AchEIs for patients demonstrating delayed encephalopathy due to CO poisoning.

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简介：摘要BackgroundDelayed encephalopathy (DE) is the most severe complication after acute carbon monoxide (CO) poisoning, which seriously affects the outcome of patients and leads to a high disability rate. Prior studies have shown that hyperbaric oxygen (HBO2) therapy is therapeutic for DE due to reducing immune-mediated neuropathology and thus improving cognitive performance.MethodsIn our present perspective study, five DE patients were treated regularly with HBO2 therapy. The mini-mental state examination (MMSE) and Barthel index (BI) were intermittently collected during their hospitalization for mental and physical status evaluation, the peripheral bloods were serially sampled to determine the concentration changes of circulating stem cells, as well as corresponding BDNF and neural markers.ResultsMMSE and BI showed series of improvements after multiple HBO2 therapies. The CD34+/CD90+ and CD34+/CD133+ dual positive cells, which were categorized as circulating stem cells, were observed an overall up-regulation since the beginning of the DE onset upon the application of HBO2 therapy. Characteristic neurotrophin BDNF, neural markers such as nestin and synaptophysin (SYP) were also up-regulated after exposure of HBO2. Conclusion The application of HBO2 therapy is of significance in improving the cognition of DE patients, along with mobilized circulating stem cells.ConclusionWe primarily infer that the CD34+/CD90+ and CD34+/CD133+ cells were mobilized by HBO2 exposure and have played a positive role in cognition improvement on DE patients by up-regulation of BDNF, nestin and SYP. The altering amount of circulating stem cells mobilized in peripheral blood could be a potential marker on predicting the outcome of DE.

简介：摘要：总结我院1例肝性脑病躁动患者的护理措施

简介：AbstractBackground:Sepsis, a serious condition with high mortality, usually causes sepsis associated encephalopathy (SAE) that involves neuronal cell death. However, the cell death programs involved and their underlying mechanisms are not clear. This study aimed to explore the regulatory mechanisms of different cell death programs in SAE.Methods:A neonatal rat model of SAE was established by cecal ligation and perforation. Survival rate and vital signs (mean arterial pressure and heart rate) were monitored, nerve reflexes were evaluated, and cortical pathological changes were observed by hematoxylin and eosin staining. The expression of pyroptosis, apoptosis, and necroptosis (PANoptosis)-related proteins, mitogen-activated protein kinase (MAPK), and its upstream regulator toll-like receptor 9 (TLR9) were detected. The expression of TLR9 in neurons was observed by immunofluorescence staining. The ultrastructure of neurons was observed by transmission electron microscope.Results:First, PANoptosis was found in cortical nerve cells of the SAE rats. Meanwhile, the subunits of MAPKs, p38 MAPK, Jun N-terminal kinase, and extracellular signal-regulated kinase (ERK) were activated. After pharmacologically inhibiting each of the subunits, only p38 MAPK was found to be associated with PANoptosis. Furthermore, blocking the p38 MAPK signaling pathway activated necroptosis but inhibited apoptosis and pyroptosis. When necroptosis was pharmacologically inhibited, apoptosis and pyroptosis were reactivated. Finally, we found that the expression of TLR9, a regulator of MAPKs, was significantly increased in this model. After down-regulation of TLR9, p38 MAPK, and ERK signaling pathways were inhibited, which led to the inhibition of PANoptosis. Further analysis found that down-regulation of TLR9 improved the survival rate and reduced the pathological changes in SAE rats.Conclusions:Our study showed that the programs comprising PANoptosis are activated simultaneously in SAE rats. TLR9 activated PANoptosis through the p38 MAPK signaling pathway. TLR9 may work as a potential target for SAE treatment.

简介：摘要：目的 分析一例胆总管囊肿患儿二次术后出现Wernicke脑病的原因及护理对策。方法 ​2020年6月我院收治一例胆总管囊肿患儿，因术后出现肠梗阻症状行二次手术后患儿出现神志淡漠、反应迟钝、四肢活动欠佳、言语不清，症状逐渐加重甚至意识模糊，通过循证查询Wernicke脑病发生原因及机制，回顾性分析患儿的临床资料、辅助检查结果、临床表现、治疗及护理措施等，总结该特殊病例的发病原因及护理要点、难点。结果 此例患儿二次手术后第二天逐渐出现意识障碍，言语不清，共济失调症状，经维生素