目的 采用小RNA(sRNA)测序技术检测清瘟败毒饮干预的脓毒症小鼠24?h脾组织微小RNA(miRNA)的表达变化,从而从非编码基因层面分析清瘟败毒饮抗脓毒性脾功能损伤的可能机制.方法 将45只SPF级健康BALB/C小鼠随机等分为对照组、脓毒症组和清瘟败毒饮组.清瘟败毒饮成分每剂含生石膏15?g、生地黄7.5?g、水牛角15?g、黄连2.5?g、栀子5?g、桔梗5?g、黄芩5?g、知母5?g、赤芍5?g、玄参5?g、连翘5?g、甘草5?g、丹皮5?g、竹叶5?g.脓毒症组和清瘟败毒饮组小鼠腹腔注射脂多糖(LPS)10?mg/kg构建脓毒症模型,对照组腹腔注射等量生理盐水.清瘟败毒饮组于制模前2?d开始给予清瘟败毒饮药液0.3?mL,每1?mL相当于生药1.5?g灌胃,术后继续胃饲,每日2次;对照组及脓毒症组给予等量生理盐水胃饲.术后24?h各组随机取5只小鼠脾组织,每组各取1只小鼠的脾组织于光镜下观察病理学改变,提取其余小鼠脾组织总RNA,采用sRNA测序技术进行miRNA检测,应用生物信息学软件分析脓毒症小鼠脾组织miRNA表达差异及靶基因的预测.?结果 光镜下显示,对照组小鼠脾组织结构正常;脓毒症组小鼠脾组织白髓总体结构稍紊乱,红白髓交界偏模糊,红髓充血明显;清瘟败毒饮组小鼠脾组织紊乱结构较前有所改善.与对照组比较,脓毒症组小鼠脾组织已知miRNA表达上调数为39个,下调数为16个;清瘟败毒饮组小鼠脾组织已知miRNA表达上调数为6个,下调数为24个.经LPS干预后,miR-217-5p、miR-200b-5p、miR-429、miR-148A-3p表达明显上调;经清瘟败毒饮干预后,miR-217-5p、miR-200b-5p、miR-429、miR-148A-3p表达出现一定程度下调.结论 清瘟败毒饮可改善脓毒症小鼠脾组织结构改变,可能通过下调miR-217-5p、miR-200b-5p、miR-429、miR-148A-3p基因表达起到保护脓毒症小鼠脾损伤的作用,可为将来进一步研究提供思路.

目的 探讨乌司他丁联合美罗培南对老年重症肺炎患者炎症介质和氧化应激的影响.方法 选择老年重症肺炎患者90例,采用随机表法分为治疗组与对照组各45例.对照组给予美罗培南治疗,治疗组在美罗培南基础上给予乌司他丁治疗.两组持续治疗14 d.比较两组治疗14 d疗效,治疗前与治疗14 d急性生理与慢性健康评估(APACHE)Ⅱ评分和气道峰压(PIP)、血气分析﹝动脉血氧分压(PaO2)、动脉血氧饱和度(SaO2)和动脉血二氧化碳分压(PaCO2)﹞、炎症介质﹝超敏C反应蛋白(hs-CRP)和乳酸﹞、氧化应激﹝超氧化物歧化酶(SOD)和过氧化脂质(LPO)﹞水平变化.结果 治疗组治疗14 d重症肺炎患者总有效率显著高于对照组(P<0.05).两组治疗14 d APACHEⅡ评分和PIP显著低于治疗前(P<0.05);且治疗组显著低于对照组(P<0.05).两组治疗14 d PaO2和SaO2显著高于治疗前,而PaCO2显著低于治疗前(P<0.05);且治疗组PaO2和SaO2显著高于对照组,而PaCO2显著低于对照组(P<0.05).两组治疗14 d hs-CRP和乳酸水平显著低于治疗前(P<0.05);且治疗组显著低于对照组(P<0.05).两组治疗14 d血清SOD水平显著高于治疗前,而LPO水平显著低于治疗前(P<0.05);且治疗组血清SOD水平显著高于对照组,而LPO水平显著低于对照组(P<0.05).结论 乌司他丁联合美罗培南对老年重症肺炎患者疗效明显,可减轻患者炎症反应,改善患者氧化应激和血气分析.

目的 探讨通心络胶囊联合氯吡格雷对急性脑梗死(ACI)患者康复阶段认知功能及生活质量的影响.方法 选取自2015年12月至2020年12月宁德师范学院附属宁德市医院收治的123例ACI患者为研究对象.按照随机数字表法将患者分为常规组(n=61)与联合组(n=62),其中,常规组患者给予常规基础治疗+氯吡格雷治疗,联合组患者在常规组治疗基础上联合通心络胶囊治疗,比较两组患者的临床总有效率、康复阶段的认知功能[蒙特利尔认知评估量表(MoCA)和简易精神状态量表(MMSE)]及生活质量,并记录两组患者的不良反应发生情况.结果 常规组患者的临床总有效率为75.4％(46/61),明显低于联合组的95.2％(59/62),差异有统计学意义(P<0.05).治疗后,两组患者的MoCA、MMSE评分均升高,联合组高于常规组,差异均有统计学意义(P<0.05).治疗后,两组患者的生活质量评分均升高,联合组高于常规组,差异均有统计学意义(P<0.05).常规组、联合组患者的不良反应发生率分别为14.7％(9/61)、11.3％(7/62),两组间比较,差异无统计学意义(P>0.05).结论 通心络胶囊联合氯吡格雷治疗ACI,能够在一定程度上改善患者康复过程中的认知功能和生活质量,是一种安全、有效的治疗方法.

目的 基于mRNA测序(RNA-seq)技术,采用生物学信息分析软件分析清瘟败毒饮对脓毒症大鼠心肌组织中白细胞介素-17(IL-17)信号转导通路相关基因表达的变化,阐明清瘟败毒饮对脓毒症心肌的保护机制.方法 清洁级健康雄性Wistar大鼠45只,随机分为脓毒症模型组、清瘟败毒饮组和假手术组,每组15只.采用盲肠结扎穿孔术(CLP)制作脓毒症大鼠模型,假手术组仅开腹、关腹与复苏,不进行CLP.清瘟败毒饮组大鼠在制模前2?d给予清瘟败毒饮(组成:生地黄7.5?g,生石膏、水牛角各15?g,黄连2.5?g,栀子、桔梗、黄芩、知母、赤芍、玄参、连翘、甘草、丹皮、竹叶各5?g)胃饲,每日2次,术后继续中药灌胃24?h.3组术毕均予5?mL/kg平衡液肌肉注射.术后24?h取大鼠肌组织提取总RNA,采用RNA-seq技术对mRNA表达量进行检测,并应用京都基因和基因组数据库通路富集方法(KEGG?Pathway)分析清瘟败毒饮对脓毒症大鼠心肌组织IL-17信号通路相关基因表达的影响.结果 RNA-seq检测结果显示,与假手术组相比,脓毒症模型组大鼠心肌组织表达上调的基因有900个,下调的基因有1507个;清瘟败毒饮组大鼠心肌组织表达上调的基因有1288个,下调的基因有1870个.KEGG?Pathway分析结果显示,与假手术组相比,脓毒症模型组大鼠心肌组织IL-17信号通路相关基因表达上调的有10个,下调的有5个;清瘟败毒饮组大鼠心肌组织IL-17信号通路基因表达上调的有11个,下调的有6个.其中脓毒症模型组及清瘟败毒饮组同时上调的基因有7个〔CXC趋化因子配体(CXCL1、CXCL2)、白细胞介素-6(IL-6)、环氧合酶-2(COX-2)、粒细胞集落刺激因子(G-CSF)、基质金属蛋白酶9?(MMP-9)、CCAAT/增强子结合蛋白β(C/EBPβ)〕;同时下调的基因有5个〔转化生长因子激酶1(TAK1)、核转录因子-κB(NF-κB)、泛素特异性蛋白酶25(USP25)、细胞外信号调节激酶(ERK)、天冬氨酸特异性半胱氨酸蛋白酶(CASP)〕;脓毒症模型组上调而清瘟败毒饮组正常表达的基因有2个〔CXCL5、白细胞介素-1β(IL-1β)〕;?脓毒症模型组下调而清瘟败毒饮组正常表达的基因有1个〔热休克蛋白90(HSP90)〕;脓毒症模型组正常表达而清瘟败毒饮组上调的基因有3个〔激活蛋白-1(AP-1)、IκB激酶-β(IKK-β)、CC趋化因子7(CCL7)〕;脓毒症模型组正常表达而清瘟败毒饮组下调的基因有1个(ERK);脓毒症模型组上调而清瘟败毒饮组下调的基因有1个〔IκB激酶-α(IKK-α)〕;脓毒症模型组下调而清瘟败毒饮组上调的基因有1个〔NF-κB抑制因子-α(IκB-α)〕.结论 清瘟败毒饮可通过调节IL-17信号通路相关基因的表达,对脓毒症大鼠心脏起保护作用.

Acute barium poisoning is uncommon in clinical practice. It occurs primarily due to the ingestion of soluble barium compounds such as BaCl2 that causes gastroenteritis (vomiting, diarrhea, and abdominal pain), hypokalemia, hypertension, cardiac arrhythmia, and skeletal muscle paralysis. Recently, several related cases of barium poisoning due to food contamination occurred in the vicinity of our hospital. We present the data for these cases and describe a representative case that we managed. On March 13, 2018, several patients presented with symptoms including abdominal cramps, vomiting, diarrhea, partial paralysis (grade 2 to 4 according to the Manual Muscle Testing Grading System) after eating KomPyang, a traditional, charcoal-baked scallion cake made with flour, onions, and meat or vegetable stuffing, at a private roadside booth in Ningde city, Fujian province, China. In the following 24 h, 48 patients with suspected food poisoning were admitted to the hospitals at county level and above, of which 41 were hospitalized. Seven patients were observed in outpatient clinics since they had mild gastrointestinal symptoms and recovered quickly. The Fujian Provincial Center for Disease Control and Prevention (CDC) collected data for these cases. Owing to limited equipment, we could not acquire data for barium concentrations in the urine or blood. The serum potassium level, vital signs, main clinical problems, and ingested dose were considered as the determinants of the severity of barium poisoning. Based on our clinical experience, we classified cases with a blood potassium level <2.5, 2.5 to 3.0, and 3.0 to 3.5 mmol/L as severe, moderate, and mild, respectively. Supplementary Table 1, https://links.lww.com/CM9/A176 summarizes the data for the 21 cases treated at Ningde Hospital (57% [12/21] severe, 19% [4/21] moderate, and 24% [5/21] mild). According to the Registry of Toxic Effects of Chemical Substances (1985), the lowest lethal acute oral dose of BaCl2 is 11.4 mg/kg body weight, and a dose as low as 5.8 mg/kg body weight causes flaccid paralysis, paresthesia, and muscle weakness.[1] For an ordinary 70 kg adult, consumption of food containing ≥0.798 g BaCl2 would be devastating. In this case, the CDC found that all barium-poisoned patients had eaten KomPyang with a meat filling containing 40 g/kg BaCl2. Since the approximate weight of meat filling in one KomPyang is 10 g, each KomPyang contained 0.4 g BaCl2. The average BaCl2 intake in 21 patients was 1.257 g, with a latent period of 3 to 6 h after exposure, and median time in the hospital was 5 days. In Case 20, the patient consumed four KomPyangs at once, and the BaCl2 dose was 1.6 g, which far exceeded the lowest lethal dose. The severity of the poisoning was determined by the quantity of KomPyang eaten. There was a significant positive correlation between the duration of hospitalization and dosage (P < 0.05). Although barium crosses the placenta,[2] it may not be toxic to the human fetus. The pregnant patient in our study [Supplementary Table 1, https://links.lww.com/CM9/A176] delivered a healthy baby months after acute barium poisoning. A 38-year-old man had a sudden attack of abdominal cramps and diarrhea 2 h after eating four KomPyangs. His symptoms included nausea, vomiting, stomach burning, dizziness, and diarrhea followed by heaviness of the limbs and weakness. Owing to life-threatening hypokalemia (1.4 mmol/L potassium), he received symptomatic treatment (continuous oxygen inhalation, intravenous [IV] potassium supplementation, and rehydration). Subsequently, he was transferred to the intensive care unit (ICU) for further treatment. On examination, he was conscious but completely paralyzed. He had a soft neck, no muscle strength (grade 0 according to the Manual Muscle Testing Grading System), insufficient respiration, and diminished neural reflexes with excessive salivation and perspiration. Potassium chloride (IV; 10% KCl) at 15.0 mmol/h coupled with magnesium sulfate (25 g in 250 mL of 5% glucose saline) was administered to precipitate the Ba2+. Approximately 2 h later, the patient became unconscious with shortness of breath, nodding, cyanosis, and profuse facial sweating. Because muscle paralysis leads to respiratory failure, emergency tracheal intubation was performed, and ventilator-assisted breathing was initiated. Subsequently, the potassium level was 1.8 mmol/L, bicarbonate (HCO3−) level was 16.7 mmol/L, and pH was 7.24. In addition to KCl and magnesium sulfate, sodium bicarbonate (125 mL) was administered to correct acidosis. The patient soon regained consciousness and sinus rhythm (95 beats/min), but he could barely nod. In the following hours, the amount and rate of potassium infusion were continuously adjusted according to the urine volume and serum potassium concentration results. About 8 h after ICU admission, the potassium level was normal (5.4 mmol/L), and potassium supplementation was stopped. Rehydration was continued. Two hours later, we disengaged the ventilator and removed the tube. The patient made a miraculous functional recovery without any complications and was discharged after another 3 days. Inadvertent consumption of barium-contaminated food is the leading cause of barium poisoning, and it may occur when BaCl2 is mistakenly used instead of salt, flour, or baking powder. In this case series, the chef unknowingly used BaCl2 instead of potato flour. According to the US CDC, a suspicious dietary history and profound hypokalemia associated with generalized muscle weakness are key indicators of barium poisoning. The clinical manifestations of barium poisoning include gastrointestinal symptoms and hypokalemia which may progress to cardiac arrhythmia, skeletal muscle weakness, and respiratory muscle paralysis caused by the deleterious effects of barium on the potassium channels and sodium-potassium pump.[3] Moreover, hypokalemia is caused by frequent vomiting, severe diarrhea, and overuse of diuretics. As shown in Supplementary Table 1, https://links.lww.com/CM9/A176, every patient with moderate or severe poisoning was hypokalemic to some extent. Additionally, the loss of potassium leads to T-wave morphology, ST-segment depression, and U waves (ST-T-U) changes on electrocardiography and arrhythmia.[4] The laboratory diagnostic criteria consist of elevated urinary barium concentration or detection of barium compounds in environmental samples. Although we lacked the data of urinary or blood barium concentration, the detection of excess BaCl2 in KomPyang clarified the diagnosis. Attention to vital signs and blood biochemistry is the first step in the successful rescue of barium-poisoned patients. For barium ions in the intestines, precipitation by oral administration of sodium sulfate, sodium thiosulfate, or magnesium sulfate is effective. Magnesium ions maintain normal intracellular potassium levels and promote potassium retention in potassium-deficient conditions. Therefore, for patients with hypokalemia, oral magnesium supplementation is recommended (250 mg/kg for children and 300 mg/kg for adults). Although precipitation of barium in blood vessels may theoretically lead to renal failure, there were no abnormalities in creatinine and urea nitrogen or renal failure signs in our cases. Potassium infusion is used clinically to reverse the toxic effects of barium. The highest rate of KCl supplementation in the representative case was 20.0 mmol/h, with a total dose of about 160 mmol (11.2 g) in 8 h. It was remarkable that barium-poisoned people tolerate potassium supplementation and recover quickly upon potassium restoration. Blood chemistry testing should be performed hourly, and attention to changes in electrocardiograms and urine volume will help to prevent rebound hyperkalemia when direct channel block is relieved followed by a backward shift of cellular potassium.[3] Moreover, comprehensive treatments that protect the myocardium, maintain homeostasis, mechanically assist ventilation, and combat arrhythmia are essential for rescuing barium-poisoned patients. The collective cases described in this report highlight the timely and appropriate management of barium-poisoned patients at the Ningde Hospital. Multifaceted treatments that rapidly increase the level of serum potassium ensure the successful rescue of barium-poisoned patients and prevent death. Conflicts of interest None.

目的 应用RNA-seq技术检测脓毒症大鼠24、48 h肝组织基因的表达变化,分析脓毒性肝损伤可能的机制.方法 随机将30只Wistar大鼠等分为脓毒症组和对照组.脓毒症组采用盲肠结扎穿孔术(CLP)建模,对照组仅行开腹、关腹.两组术毕均肌肉注射平衡液5 mL/kg.术后24、48 h各组随机取5只大鼠取肝组织提取总RNA后采用RNA-seq进行mRNA检测,应用生物信息学软件分析脓毒症大鼠肝组织mRNA随时间变化的表达差异及涉及的相关通路.结果 大鼠建模后24、48 h,相对于对照组,脓毒症大鼠肝脏组织mRNA表达上调数分别为1220个、914个,下调数分别为1741个、822个.其中脓毒症大鼠肝组织随时间变化,NF-κB、信号通路、PPAR信号通路相关mRNA表达差异明显.脓毒症大鼠24h肝组织NF-κB信号通路相关基因正常表达,而48 h转为上调有13个,下调转正常表达有4个,下调转上调有1个,上调转下调有1个,上调转为正常表达有4个,正常表达转为下调有6个,同时上调有7个,同时下调有1个.PPAR信号通路相关的基因从下调转为正常表达有20个,上调转正常表达有3个,正常表达转上调有4个,同时下调有6个,同时上调有5个.结论 肝脏炎症反应、代谢改变可能是脓毒性肝损伤的重要机制之一,可能跟NF-κB、P信号通路、PAR信号通路相关基因表达有关.

目的:观察重症患者配合中医中药治疗疗效.方法:本次观察病例为2018年11月～2019年12月福建医科大学附属宁德市医院与宁德东侨御启堂中医综合门诊部共同配合收治的73例各种重症患者,根据就诊顺序分成对照组37例和观察组36例患者,对照组采用常规西医治疗,观察组在此基础上配合中医中药治疗,对比两组最终临床治疗效果.结果:通过配合中医中药治疗后的观察组患者治疗总有效率、临床症状改善时间、并发症发生率控制效果及生存质量均显著优于采用单独常规西药治疗的对照组,组间数据差异明显统计学意义存在(P<0.05).结论:在各种重症患者治疗中配合中医中药进行治疗,可有效提高临床治疗效果,增强患者身体抗病能力,使患者的临床症状得到尽早改善,从而提高患者的生存质量.

目的 分析重度脑外伤患者血清铁蛋白水平与格拉斯哥昏迷评分(GCS)、病死率的关系.方法 选择医院2018年6月-2019年9月收治的重度脑外伤患者127例为研究对象,依据患者GCS评分分为低分组56例和高分组71例.比较2组GCS评分、血清铁蛋白及血脂水平,分析血清铁蛋白水平与GCS评分、ICU病死率及血脂的关系.结果 高分组GCS评分、血清铁蛋白水平及总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇水平(LDL-C)均高于低分组,高密度脂蛋白胆固醇(HDL-C)水平低于低分组,差异均有统计学意义(P<0.05).重度脑外伤患者血清铁蛋白水平与GCS评分、病死率、TC、TG、LDL-C呈正相关(P<0.05),而与HDL-C呈负相关(P<0.05).结论 重度脑外伤患者的血清铁蛋白水平异常升高,可能提示不良预后.

目的:研究ICU中右美托咪定联合舒芬太尼静脉镇痛对脊柱手术后患者睡眠质量的作用效果.方法:选取2017年2月至2019年2月福建医科大学附属宁德市医院重症医学科收治的ICU脊柱手术患者94例作为研究对象,按照抽签法分为观察组和对照组,每组47例.观察组采用右美托咪定联合舒芬太尼静脉镇痛,对照组采用单纯应用右美托咪定,比较各时点疼痛评分、镇静评分与睡眠质量.结果:术前1周2组睡眠质量比较,差异无统计学意义(P>0.05);术后1周观察组平均睡眠时间较对照组长,睡眠障碍指数较对照组低;术后1h、6h、12h与48h患者疼痛评分较对照组低,镇静评分较对照组高,差异有统计学意义(P<0.05).结论:对ICU脊柱手术患者采用右美托咪定联合舒芬太尼静脉镇痛能提高睡眠质量,缓解疼痛且提高镇静效果,值得推荐.

目的 探讨8％枸橼酸钠液对股静脉双腔导管封管的效果.方法 将120例股静脉双腔导管置管行血液灌流患者随机分为观察组和对照组各60例,两组给予相同的置管方法,观察组给予8％枸橼酸钠液封管,对照组给予肝素钠封管;比较枸橼酸钠和肝素钠封管后短期凝血指标以及导管使用情况.结果 观察组使用8％枸橼酸钠封管优于对照组(P＜0.05);观察组导管使用情况优于对照组(P＜0.05).结论 8％枸橼酸钠对股静脉双腔导管封管对凝血相关指标影响小,出血风险小,值得临床广泛使用.

目的 研究不同固定方式在深静脉置管中的应用价值.方法 方便选取该院2013年1月—2016年4月收治的深静脉置管患者900例为对象进行分组.其中翼固定组均为2014年10月之前病例,采用固定翼固定;直接局部缝线固定组均为2014年10月(含当月)之后病例,采用无翼直接局部缝线方法固定.比较两组患者穿刺点感染率、导管脱出发生率;患者舒适度评分、疼痛评分、深静脉置管时间.结果 无翼直接局部缝线组跟翼固定组比较,前者穿刺点7、14、21 d感染率分别为2.22％、4.44％、6.67％,而后者穿刺点7、14、21 d感染率分别为11.11％、22.22％、24.44％;前者导管总脱出发生率为2.22％,后者导管总脱出率为13.33％(P<0.05);无翼直接局部缝线固定组与翼固定组患者舒适度评分分别为(9.51±1.41)分、(8.39±1.77)分,而疼痛评分分别为(1.51±0.21)分、(3.39±0.57)分,深静脉置管时间分别为(45.62±3.21)d、(32.61±1.59)d(P<0.05).结论 不同固定方式在深静脉置管中的应用均有一定价值,但无翼直接局部缝线方法固效果优于用翼固定,可有效提高固定的稳定性,减少导管脱出发生率,减少局部感染的发生,有利于提升患者舒适度,减轻痛苦,延长置管时间,值得推广.

目的:探析酪酸梭菌肠球菌三联活菌结合早期肠内营养对危重症颅脑损伤患者肠道免疫及感染的治疗效果.方法:129例在笔者所在医院进行治疗的颅脑损伤中的危重症患者,分为单一组(n=64)和试验组(n=65),单一组给予单纯的早期肠内营养治疗,试验组则在其基础上联合应用酪酸梭菌肠球菌三联活菌治疗,观察其治疗效果及各项指标变化.结果:经治疗1周后,试验组患者IL-6、CRP及白细胞计数的等各项指标水平均明显低于单一组,差异有统计学意义(P<0.05),且试验组患者的GCS评分较高,入住ICU时间及肠道功能恢复时间也较单一组短,感染发生率及病死率与单一组相比较低,差异有统计学意义(P<0.05).结论:针对颅脑损伤中的危重症患者给予酪酸梭菌肠球菌三联活菌+早期肠内营养进行联合治疗后效果显著.

目的 探讨恶性肿瘤伴脓毒血症患者的降钙素原(PCT)、白介素6(IL-6)、C-反应蛋白(CRP)、白细胞计数(WBC)和血沉(ESR)等炎症指标及预后.方法 选取2016年7月至2017年2月间同济医学院附属同济医院收治的73例恶性肿瘤伴脓毒血症感染患者为观察组,选取同期住院的60例非肿瘤脓毒血症患者为对照组.检测并比较两组患者的PCT、IL-6、CRP、WBC和ESR水平,评估两组患者的急性生理与慢性健康状况评分Ⅱ(APACHEⅡ)和序贯器官衰竭评估(SOFA)状况.结果 观察组患者的IL-6、CRP和ESR水平均比对照组患者高,WBC较对照组患者低,差异均有统计学意义(均P ＜0.05).但两组患者PCT水平无明显变化,差异无统计学意义(P＞0.05).结论 恶性肿瘤伴脓毒血症患者可通过联合检测PCT、IL-6、CRP、WBC和ESR水平判断感染情况,其中PCT不受肿瘤干扰,对早期诊断、指导临床应用抗菌素及评估预后有重要意义.

目的:探讨对蜂蜇伤合并急性肾损伤患者实施连续性肾脏替代治疗的方法和临床效果.方法:选取2015年4月-2016年4月笔者所在医院收治的蜂蜇伤合并急性肾损伤患者60例,对其实施连续性肾脏替代治疗,观察患者的治疗效果.结果:患者治疗后的生命体征及生化指标均显著优于治疗前,差异有统计学意义(P<0.05),总并发症发生率仅为13.33%.结论:对蜂蜇伤合并急性肾损伤患者实施连续性肾脏替代治疗的效果显著,且安全有效,值得临床进行推广.

目的 探讨分析恙虫病误诊误治临床情况.方法 选取我院收治的1例恙虫病患者为研究对象,总结分析恙虫病的临床表现、诊断及治疗,并对该例患者误诊为重症肺炎的原因进行分析.结果 恙虫病症状复杂,且不典型,容易出现误诊误治,但多数有典型体征,即皮肤见典型焦痂,需考虑本病.结论 恙虫病病情复杂,详细询问病史及体检对恙虫病早期诊断有重要意义,避免误诊误治.

目的 探讨肝素钠在感染相关性血小板减少的病例输注血小板治疗中是否可以减少血小板的消耗或者延缓血小板的消耗.方法 将符合入选标准的患者随机分成两组,研究组在血小板中加入肝素钠(按10单位血小板:10mg肝素钠),对照组中无添加任何试剂,观察两组输血后12 h内及输血后24 h内血小板计数的变化,通过体重校准后再用SPSS软件进行t检验.结果 12h内的研究组与对照组间对比P＜0.05,差异有统计学意义,24 h内组间对比P＞0.05,差异无统计学意义.结论 感染相关的血小板减少患者,在输血小板中加入小剂量的肝素钠有减少血小板消耗的作用或者是延缓血小板消耗有一定的临床意义.

目的：探讨血液灌流( hemoperfusion，HP)联合连续性静-静脉血液滤过(CVVH)治疗重症胰腺炎( severe acute pancreatitis、SAP)的临床疗效。方法将59例SAP 患者随机分为治疗组(A 组)和对照组(B 组),A 组30例采用内科综合治疗+HP +CVVH 治疗；B 组29例采用内科综合治疗+CVVH。观察治疗前后临床症状体征及白细胞(WBC)、血淀粉酶(AMY)、血糖( Glu)、肝肾功能、内毒素(LPS)、肿瘤坏死因子α( TNF-α)、白细胞介素6(IL-6)、白细胞介素8( IL-8)结果。结果两组患者WBC、AMY、Glu 和ALT 在治疗后7天均有不同程度的降低,其中治疗组更明显,差异有统计学意义( P<0.01)；Cr 在A 、B组明显降低,但差异无统计学意义( P >0.05)；A 组治疗后AMY 低于B 组(115.12±45.02) U/ L vs(164.31±39.42) U/ L ( P<0.01)。两组治疗后血清LPS、TNF-α、IL-6、IL-8水平均明显下降,与治疗前比较差异有统计学意义(均P<0.01)。两组间治疗后IL-6、IL-8比较差异有统计学意义( P<0.01)。结论 HP联合CVVH治疗SAP 能迅速改善临床症状体征,显著降低WBC、AMY、Glu、LPS、TNF-α、IL-6、IL-8水平,提高患者存活率。

<正>重度有机磷农药中毒病情凶险,死亡率可达8.55%～58.6%。为提高抢救成功率,福建省宁德市医院自2007年5月至2010年6月在常规救治的基

临床资料 例1:患者,男,15岁,以摔伤后神志不清3小时为代诉入院.入院诊断:摔伤,颅脑外伤,右侧额、颞、顶叶多发性硬膜外血肿,蝶窦积血,双肺挫裂伤,右侧血气胸,呼吸衰竭,部分代偿性酸中毒.立即气管插管,接呼吸机通气,其SPO2由入院80%上升到90%,逐步加用PEEP,SPO2逐步上升到97%.气管插管保留4天,期间患者有不耐管和一过性低血压现象.

病历资料 患者,男,56岁,以"发热咳嗽4天,腹痛、腹泻2天",于6月4日入院.入院4天以前,患者无明显诱因出现发热,自测体温高达38.6℃,热型不详,干咳,偶有胸闷,活动后气促,伴头晕、心悸,全身乏力,食欲不振,四肢肌肉酸痛.入院2天前,患者出现阵发性、非放射性腹痛,排5次淡红色水样大便,每次150～200ml,排便后腹痛无缓解.发病2天以来,小便呈淡红色,量较平时少(具体量不详),就诊于我院.门诊以"发热原因待查"收入传染科.