Tourniquet Test for Dengue Diagnosis: Systematic Review and Meta-analysis of Diagnostic Test Accuracy

BackgroundDengue fever is a ubiquitous arboviral infection in tropical and sub-tropical regions, whose incidence has increased over recent decades. In the absence of a rapid point of care test, the clinical diagnosis of dengue is complex. The World Health Organisation has outlined diagnostic criteria for making the diagnosis of dengue infection, which includes the use of the tourniquet test (TT).PurposeTo assess the quality of the evidence supporting the use of the TT and perform a diagnostic accuracy meta-analysis comparing the TT to antibody response measured by ELISA.ConclusionThe tourniquet test is widely used in resource poor settings despite currently available evidence demonstrating only a marginal benefit in making a diagnosis of dengue infection alone.RegistrationThe protocol for this systematic review was registered at PROSPERO: CRD42015020323.     

Oxygen-Derived Free Radicals Mediate Liver Damage in Rats Subjected to Tourniquet Shock

The placement of rubber band tourniquets upon rat hind-limbs for 5 h followed by reperfusion of the extremities results in a severe form of circulatory shock characterized by hypotension and death within 24 h of tourniquet release. Oxidative damage to muscle tissue is an early consequence of hind-limb reperfusion on tourniquet release, yet this local damage does not explain the lethal hypotensive shock state which evolves within the next 24 h. Multiple system organ failure (MSOF), of as of yet unknown causes, is usually described in relation to several shock states. It has been suggested that injured or necrotic tissue may activate neutrophils, platelets, and the coagulation system leading to embolization in remote tissues. Effective decreases in hepatic blood flow have been observed in several forms of sepsis which precedes the biochemical evidence consistent with an ischemic insult of the liver. In support of our original hypothesis, that organ failure has its genesis in a primary perfusion abnormality with secondary ischemic organ injury, herein we have assessed the possibility that oxygen-derived free radicals are generated in the liver of rats after reperfusion of their hind-limbs on release of the tourniquets. We report on the protective effects of allopurinol (ALLO) and a mixture of superoxide dismutase (SOD) catalase (CAT) and dimethylfulfoxide (DMSO) on liver free sulfhydryl content (SH), thiobarbituric acid-reactive substances (TBARS), and on the release of aspartic acid (AsT) and alanine aminotransferase (AIT) activities, and of alkaline phosphatase during a 5 h tourniquet period and after 2 h of reperfusion of the hind-limbs. During the hind-limb ischemic period hepatis tissue SH levels remained essentially constant during the first hour (6.02 ± 0.36 to 5.65 ± 0.20 μmoles/g wet tissue), and decreased significantly, over and above the normal circadian decrease of liver glutathione levels, to 4.02 ± 0.69 μmoles/g wet tissue after the third hour and remained lowered until tourniquet release. A further significant decrease (3.11 ± 0.49 μmoles/g wet tissue) was observed after 2h of reperfusion. TBARS production remained constant during the 5 h hind-limb ischemic period (168.4 ± 37.3 μmoles/g wet tissue) and rose by 55+ to 261.7 ± 55.8 μmoles/g wet tissue after 2 h of tourniquet release. ALLO, but not the SOD-CAT-DMSO combination, protected hepatic SH loss during the hind-limb ischemic insult, yet both offered protection after 2 h of tournoquet release. With regard to TBARS production, ALLO and the SOD-CAT-DMSO mixture had no effect on basal levels during the ischemic period, but both significantly reduced liver TBARS production after the two hour reperfusion period of hind limb reperfusion. Plasma AsT levels rose 8-fold from 99.4 ± 7.2 to 193 ± 17.0 U/L after the 5-hour tourniquet period, and to 844.8 ± 75.1 U/L two hours after hind-limb reperfusion. The plasma levels of AsT were significantly lower in both the ALLO and SOD-CAT-DMSO pre-treated animals. This was not the case with plasma AIT levels which increased 3-fold during the reperfusion period, but which could not be protected with these same pre-treatment protocols. Alkaline phosphatase plasma levels increased 2-fold during the same period. It is concluded that oxidative stress to the liver, as a result of himd-limb ischemia followed by reperfusion, is partly responsible for the MSOF which leads to circulatory derangements and death of rats subjected to this tourniquet shock model.     

Oxygen-Derived Free Radicals Mediate Liver Damage in Rats Subjected to Tourniquet Shock

The placement of rubber band tourniquets upon rat hind-limbs for 5 h followed by reperfusion of the extremities results in a severe form of circulatory shock characterized by hypotension and death within 24 h of tourniquet release. Oxidative damage to muscle tissue is an early consequence of hind-limb reperfusion on tourniquet release, yet this local damage does not explain the lethal hypotensive shock state which evolves within the next 24 h. Multiple system organ failure (MSOF), of as of yet unknown causes, is usually described in relation to several shock states. It has been suggested that injured or necrotic tissue may activate neutrophils, platelets, and the coagulation system leading to embolization in remote tissues. Effective decreases in hepatic blood flow have been observed in several forms of sepsis which precedes the biochemical evidence consistent with an ischemic insult of the liver. In support of our original hypothesis, that organ failure has its genesis in a primary perfusion abnormality with secondary ischemic organ injury, herein we have assessed the possibility that oxygen-derived free radicals are generated in the liver of rats after reperfusion of their hind-limbs on release of the tourniquets. We report on the protective effects of allopurinol (ALLO) and a mixture of superoxide dismutase (SOD) catalase (CAT) and dimethylfulfoxide (DMSO) on liver free sulfhydryl content (SH), thiobarbituric acid-reactive substances (TBARS), and on the release of aspartic acid (AsT) and alanine aminotransferase (AIT) activities, and of alkaline phosphatase during a 5 h tourniquet period and after 2 h of reperfusion of the hind-limbs. During the hind-limb ischemic period hepatis tissue SH levels remained essentially constant during the first hour (6.02 ± 0.36 to 5.65 ± 0.20 μmoles/g wet tissue), and decreased significantly, over and above the normal circadian decrease of liver glutathione levels, to 4.02 ± 0.69 μmoles/g wet tissue after the third hour and remained lowered until tourniquet release. A further significant decrease (3.11 ± 0.49 μmoles/g wet tissue) was observed after 2h of reperfusion. TBARS production remained constant during the 5 h hind-limb ischemic period (168.4 ± 37.3 μmoles/g wet tissue) and rose by 55+ to 261.7 ± 55.8 μmoles/g wet tissue after 2 h of tourniquet release. ALLO, but not the SOD-CAT-DMSO combination, protected hepatic SH loss during the hind-limb ischemic insult, yet both offered protection after 2 h of tournoquet release. With regard to TBARS production, ALLO and the SOD-CAT-DMSO mixture had no effect on basal levels during the ischemic period, but both significantly reduced liver TBARS production after the two hour reperfusion period of hind limb reperfusion. Plasma AsT levels rose 8-fold from 99.4 ± 7.2 to 193 ± 17.0 U/L after the 5-hour tourniquet period, and to 844.8 ± 75.1 U/L two hours after hind-limb reperfusion. The plasma levels of AsT were significantly lower in both the ALLO and SOD-CAT-DMSO pre-treated animals. This was not the case with plasma AIT levels which increased 3-fold during the reperfusion period, but which could not be protected with these same pre-treatment protocols. Alkaline phosphatase plasma levels increased 2-fold during the same period. It is concluded that oxidative stress to the liver, as a result of himd-limb ischemia followed by reperfusion, is partly responsible for the MSOF which leads to circulatory derangements and death of rats subjected to this tourniquet shock model.     

Tourniquet shock in rats: effects of allopurinol on biochemical changes of the gastrocnemius muscle subjected to ischemia followed by reperfusion

Recent data suggest that oxygen free radicals are implicated in the pathogenesis of ischemic injury. This study evaluates the effects of allopurinol, a xanthine oxidase (XO) inhibitor, on malonaldehyde generation, free sulfhydryl levels, oxygen consumption, and water contents of rat gastrocnemius muscles of female Sprague-Dawley rats subjected to tourniquet shock and after hind-limb reperfusion. Serum lactic dehydrogenase isozyme patterns after ligature release were also examined. Our results show that the four muscle parameters were not altered during 5 hr of ischemia, but that on hind-limb reperfusion, malonaldehyde production, SH levels, O2 consumption, and water contents were significantly altered in the control animals, but not in those pretreated with allopurinol. LDH serum patterns of the untreated animals showed the presence of all five isoforms; these were much less evident in the drug-protected rats. Our data suggest that following ischemia, the affected muscles are unable to recover their normal function when reperfusion is resumed. The subsequent damage is probably due to the generation of cytotoxic superoxide radicals formed during the XO-catalyzed transformation of hypoxanthine to uric acid on tissue reoxygenation. The severity of tissue damage is related to the duration of the ischemic episode possibly due to hypoxanthine accumulation during ischemia.     

右美托咪定对下肢手术患者止血带诱发肢体缺血-再灌注损伤的影响

目的:探讨右美托咪定对下肢手术患者因止血带诱发肢体缺血-再灌注损伤的影响。方法:选取2015年1月-2016年5月我院行下肢手术治疗的患者90例,按照数字随机法分为观察组及对照组,每组各45例。两组均给予蛛网膜下腔阻滞联合硬膜外麻醉,观察组在穿刺成功15 min内静脉输注1μg/kg的右美托咪定,维持剂量0.5μg/kg·h直至手术结束,对照组患者则给予同等剂量的生理盐水。对比两组止血带前(T0)、止血带充气30 min(T1)、止血带充气1 h(T2)、止血带释放后30 min(T3)、止血带释放后1 h(T4)时的超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)、平均动脉压(MAP)、心率(HR)水平以及不良反应发生情况。结果:T3、T4时点观察组SOD水平显著高于对照组,MDA水平显著低于对照组(P0.05)。T1、T2、T3、T4时点观察组TNF-α水平显著低于对照组,T4时点IL-6水平也显著低于对照组(P0.05)。T1、T2时点观察组MAP、HR水平均显著低于对照组(P0.05)。观察组术中止血带疼痛、高血压发生率均显著低于对照组(P0.05)。结论:右美托咪定可显著抑制下肢手术患者止血带诱发氧化应激反应以及炎症反应,进而降低肢体缺血-再灌注损伤,具有较好的安全性。     

全膝关节置换术中不同止血带使用方法的疗效比较及对患者凝血功能、炎症反应和生活质量的影响

摘要 目的：探讨全膝关节置换术（TKA）中不同止血带使用方法的疗效比较及对患者凝血功能、炎症反应和生活质量的影响。方法：选取2019年1月至2022年2月间来我院接受治疗的256例TKA患者,根据止血带使用方法的不同将患者分为A组（n=124,全程使用止血带）和B组（n=132,安装假体至切口缝合包扎完毕间使用止血带）。对比两组临床指标、凝血功能指标、炎症因子指标和生活质量评分。结果：两组术中出血量组间对比差异无统计学意义（P>0.05）。B组的下肢深静脉血栓的发生率低于A组,美国特种外科医院（HSS）评分高于A组,视觉疼痛模拟量表（VAS）评分低于A组（P<0.05）。两组术后1 d 纤维蛋白原含量（FIB）升高,且B组低于A组（P<0.05）。凝血酶原时间（PT）、凝血酶时间（TT）、活化部分凝血酶时间（APTT）均缩短,且B组大于A组（P<0.05）。两组术后1 d白介素-1β（IL-1β）、白介素-6（IL-6）、白介素-8（IL-8）、C反应蛋白（CRP）均升高,且B组低于A组（P<0.05）。两组术后3个月健康调查量表（SF-36）各维度评分均升高,且B组高于A组（P<0.05）。结论：TKA术中安装假体至切口缝合包扎完毕间使用止血带,可减轻对机体炎症反应、凝血功能的影响,有助于膝关节功能恢复,改善患者术后生活质量。