Therapeutic Effectiveness of Sustained Low‐Efficiency Hemodialysis Plus Hemoperfusion and Continuous Hemofiltration Plus Hemoperfusion for Acute Severe Organophosphate Poisoning

There is no report on the effects of sustained low‐efficiency dialysis (SLED) plus hemoperfusion (HP) (SLED + HP) in patients with acute severe organophosphate (OP) poisoning (ASOPP). This study was designed to compare the therapeutic effectiveness between SLED + HP and continuous hemofiltration (CHF) plus HP (CHF + HP) in patients with ASOPP. In order to assess the two treatment methods, 56 patients with ASOPP were divided into CHF + HP group and SLED + HP group. The biochemical indicators, in‐hospital duration, hemodynamic parameters, Acute Physiology, and Chronic Health Evaluation (APACHE II) score, and survival and mortality rates were compared. In both groups after treatment, the levels of serum creatine kinase isozyme MB, creatine kinase, creatinine, glutamic‐oxalacetic transaminease, and glutamate‐pyruvate transaminase, and the APACHE II scores on the first, second, and seventh day decreased (P < 0.05), whereas the levels of serum acetylcholinesterase increased. The two groups showed no statistical differences in in‐hospital duration, biochemical indicators, APACHE II score, hemodynamic parameters, survival rate, or the mortality rate (P > 0.05). In conclusion, SLED has similar hemodynamic stability to CHF and the two treatment methods have similar effects on ASOPP patients. More importantly, SLED plus HP is relatively economical and convenient for patients with ASOPP in clinical practice.     

术中胃减压对神经内镜经鼻颅底手术后恶心呕吐的影响

目的探讨术中胃减压对行神经内镜经鼻颅底手术患者手术后恶心呕吐(PONV)的影响。方法回顾性分析2019年1—8月在复旦大学附属华山医院神经外科接受神经内镜经鼻颅底手术的357例患者的临床资料。根据术中是否进行胃减压,分为胃减压组(146例)和对照组(211例)。比较两组的临床特征和术后24 h内PONV发生率的差异。对于包括胃减压在内的各因素对行神经内镜经鼻颅底手术患者PONV发生的影响,采用单因素和多因素logistic回归分析法探讨。结果所有患者术后24 h内的PONV发生率为11.8%(42/357)。胃减压组的女性比例[58.2%(85/146)对比46.4%(98/211),P=0.029]和Apfel评分为2~3分的比例[64.4%(94/146)对比50.2%(106/211),P=0.008]均高于对照组,而胃减压组PONV的发生率低于对照组[7.5%(11/146)对比14.7%(31/211),P=0.039]。单因素logistic回归分析结果提示,术中采用脂肪填塞修补脑脊液漏、术中采用黏膜瓣修补脑脊液漏、术中胃减压和术中失血量是神经内镜经鼻颅底手术患者PONV发生的影响因素(均P<0.05)。多因素logistic回归分析结果提示,术中胃减压(OR=0.397,95%CI:0.185~0.852,P=0.018)和术中失血量(OR=1.133,95%CI:1.026~1.250,P=0.013)为神经内镜经鼻颅底手术患者PONV发生的独立影响因素。结论实施术中胃减压可降低神经内镜经鼻颅底手术患者PONV的发生率。     

Lack of therapeutic effects of gabexate mesilate on the hepatic encephalopathy in rats with acute and chronic hepatic failure

Background and Aim: Inflammation plays a pivotal role in liver injury. Gabexate mesilate (GM, a protease inhibitor) inhibits inflammation by blocking various serine proteases. This study examined the effects of GM on hepatic encephalopathy in rats with acute and chronic liver failure. Methods: Acute and chronic liver failure (cirrhosis) were induced by intraperitoneal TAA administration (350 mg/kg/day for 3 days) and common bile duct ligation, respectively, in male Sprague‐Dawley rats. Rats were randomized to receive either GM (50 mg/10 mL/kg) or saline intraperitoneally for 5 days. Severity of encephalopathy was assessed by the Opto‐Varimex animal activity meter and hemodynamic parameters, mean arterial pressure and portal pressure, were measured (only in chronic liver failure rats). Plasma levels of liver biochemistry, ammonia, nitrate/nitrite, interleukins (IL) and tumor necrosis factor (TNF)‐α were determined. Results: In rats with acute liver failure, GM treatment significantly decreased the plasma levels of alanine aminotransferase (P = 0.02), but no significant difference of motor activity, plasma levels of ammonia, IL‐1β, IL‐6, IL‐10 and TNF‐α or survival was found. In chronic liver failure rats, GM significantly lowered the plasma TNF‐α levels (P = 0.04). However, there was no significant difference of motor activity, other biochemical tests or survival found. GM‐treated chronic liver failure rats had higher portal pressure (P = 0.04) but similar mean arterial pressure in comparison with saline‐treated rats. Conclusions: Chronic GM treatment does not have a major effect on hepatic encephalopathy in rats with TAA‐induced acute liver failure and rats with chronic liver failure induced by common bile duct ligation.     

Simvastatin effects on portal‐systemic collaterals of portal hypertensive rats

Background and Aim: Portal‐systemic collateral vascular resistance and vasoconstrictor responsiveness are crucial in portal hypertension and variceal bleeding control. Statins enhance vasodilators production, but their influence on collaterals is unknown. This study aimed to survey the effect of simvastatin on collaterals. Methods: Partially portal vein‐ligated rats received oral simvastatin (20 mg/kg/day) or distilled water from ?2 to +7 day of ligation. After hemodynamic measurements on the eighth postoperative day, baseline perfusion pressure (i.e. an index of collateral vascular resistance) and arginine vasopressin (AVP, 0.1 nM–0.1 µM) responsiveness were evaluated with an in situ perfusion model for collateral vascular beds. RT‐PCR of endothelial NO synthase (eNOS), inducible NOS (iNOS), cyclooxygenase‐1 (COX‐1), COX‐2, thromboxane A₂ synthase (TXA₂‐S) and prostacyclin synthase genes was performed in parallel groups for splenorenal shunt (SRS), the most prominent intra‐abdominal collateral vessel. To determine the acute effects of simvastatin, collateral AVP response was assessed with vehicle or simvastatin. SRS RT‐PCR of eNOS, iNOS, COX‐1, COX‐2 and TXA₂‐S, and measurements of perfusate nitrite/nitrate, 6‐keto‐PGF1_α and TXB₂ levels were performed in parallel groups without AVP. Results: Acute simvastatin administration enhanced SRS eNOS expression and elevated perfusate nitrite/nitrate and 6‐keto‐PGF1_α concentrations. Chronic simvastatin treatment reduced baseline collateral vascular resistance and portal pressure and enhanced SRS eNOS, COX‐2 and TXA₂‐S mRNA expression. Neither acute nor chronic simvastatin administration influenced collateral AVP responsiveness. Conclusion: Simvastatin reduces portal‐systemic collateral vascular resistance and portal pressure in portal hypertensive rats. This may be related to the enhanced portal‐systemic collateral vascular NO and prostacyclin activities.     

Impact of the Tokyo guidelines on the management of patients with acute calculous cholecystitis

Background and Aim: Prompt treatments for acute calculous cholecystitis can reduce both mortality and morbidity. The aim of this retrospective study was to assess the impact of the Tokyo guidelines on management of patients with acute cholecystitis. Methods: The records of patients admitted due to acute calculous cholecystitis were collected between January 2007 and June 2008. Exclusion criteria included acalculous, hepatobiliary malignancy, younger than 18 years old and mortality unrelated to cholecystitis. These 235 patients were classified into three groups; grade I, grade II and grade III, according to the severity grading in the Tokyo guidelines for acute cholecystitis. They were further classified into two subgroups; those compatible with and incompatible with managements suggested in the Tokyo guidelines, for comparison. Results: Lower levels of platelets, lower blood pressure, higher levels of C‐reactive protein, blood urine nitrogen, prothrombin time, bilirubin, alkaline phosphatase, and more incidences of positive microorganisms cultured in bile or blood, were found in patients as the severity of disease progressed. Shorter mean length of hospital stay was compatible with the Tokyo guidelines, but no significant differences in outcomes, including incidences of survival, post‐surgery complications and mortality, were found between the two subgroups. Conclusion: No significant benefit of the application of the Tokyo guidelines in the management of patients was found between the two subgroups except for reduced mean length of hospital stay. The application of the Tokyo guidelines for improving the outcomes of patients with acute cholecystitis needs further investigation and evaluation.     

Medical students' experience of vaginal examinations of anaesthetised women

Medical students usually initially learn vaginal examination (VE) by examining consenting anaesthetised women. To assess their experience of this practice, a questionnaire was distributed to all 66 fifth-year students at the Wellington School of Medicine in 2005—53 students responded. Although 184 women were available to approach for consent, only 141 were approached—students claimed insufficient time as their major difficulty. All male students discussed consent with women only in the 2 hours preoperatively, whereas nine (28%) of the female students sought consent earlier on the day or the day before. Of the 114 women asked, 97 gave written consent, but the VE was conducted in only 76 women mostly because the supervising gynaecologist claimed time constraints or was uninterested. Four other women were examined when consent was uncertain and two without consent. All but one of the students considered the experience educationally valuable. Eleven responding students did not perform a VE, and if the 13 nonresponders also did not, more than one-third of students lack this educational opportunity prior to their final year. In conclusion, some students require more commitment to seeking consent, and some gynaecologists may need to better facilitate this learning opportunity so that the consent agreed with the woman and student is more often respected.