急性颈脊髓损伤并发抗利尿激素分泌异常综合征的诊断和治疗

目的探讨急性颈脊髓损伤并发抗利尿激素分泌异常综合征的临床特点、诊断和治疗方法。方法回顾性分析8例急性颈脊髓损伤并发抗利尿激素分泌异常综合征患者的临床资料。脊髓损伤分级:FrankelA级5例,B级3例;损伤节段:C4～53例,C5～63例,C6～72例。8例于受伤后3～7d行骨折椎体次全切除椎管减压、自体髂骨植骨融合及颈椎前路钢板内固定术。3例于术前,5例于术后3～7d发生低钠血症,所有患者低钠血症发生后第2～10d确诊SIADH,根据血钠水平,采用控制每日水量、补钠进行治疗。结果7例经10～21d治愈,血钠平均恢复至138(135～142)mmol/L,血浆渗透压、尿渗透压、尿钠均正常;1例C4骨折、FrankelA级者,因截瘫平面上升并发呼吸衰竭死亡。结论急性颈脊髓损伤并发抗利尿激素分泌异常综合征的发病机制与治疗措施不同于普通低钠血症,早期正确的诊治能降低患者病残率和死亡率,严格控制入液量及补钠为主要治疗方法。     

Use of laboratory data to identify risk factors of giant coronary aneurysms due to Kawasaki disease

BACKGROUND: Although some laboratory findings are known to be indicators of the risk of giant coronary aneurysm formation among Kawasaki disease patients, an appropriate cut-off point to predict aneurysm formation is not clear. METHODS: One hundred and five patients with giant coronary aneurysms were selected from the 15th and 16th nationwide surveys of Kawasaki disease in Japan. A total of 2936 patients without Kawasaki disease were recruited from a single hospital as a control group. Odds ratios were calculated for six laboratory data with specific values as cut-off points. Receiver operating characteristic (ROC) curves were observed to determine the most appropriate laboratory tests and cut-off points. RESULTS: Hematocrit, leukocyte count, neutrophil proportion, and hemoglobin had one or more peaks of odds ratio for specific cut-off points, but they did not have a clear cut-off point for the predictor according to the receiver operating characteristic curves. Alanine aminotransferase (ALT) increased the risk of giant coronary aneurysms continuously so no clearly appropriate cut-off point was identified. Serum sodium concentration of 135 mEq/L had a peak of odds ratio, and those with <135 mEq/L had the highest odds ratio (4.78). This value seemed appropriate with a sensitivity of 78% and specificity of 57%, although the predictive positive value was as small as 5%. CONCLUSION: The author's propose that a serum sodium concentration of <135 mEq/L at the patient's first visit to hospital may be a predictor of giant coronary aneurysms due to Kawasaki disease.     

鞍区肿瘤术后中枢性低钠血症的诊断和治疗

目的:探讨鞍区肿瘤术后中枢性低钠血症的诊断及处理方法。方法:对我科近四年鞍区肿瘤术后并发中枢性低钠血症的58例患者进行回顾性分析,术前、手术当日及术后每日定时检测血钠,观察尿量变化,测定中心静脉压,确定低钠血症的类型并给予相应的处理。结果:56例恢复正常,1例死于严重肺部感染,1例自动出院。结论:鞍区肿瘤易出现抗利尿激素分泌不当综合症和脑性耗盐综合症两种类型。前者需限水治疗,后者应予以充分补钠、补水,根据水、钠检测水平治疗。     

加味生脉饮治疗心衰合并低钠血症临床观察

目的 :评价加味生脉饮对心衰合并低钠血症的疗效。方法 :84例心衰合并低钠血症患者随机分为治疗组和对照组。治疗组 4 2例以加味生脉饮为主治疗 ,对照组 4 2例单纯西药治疗。结果 :治疗组心衰控制率、低钠血症改善率及预后均优于对照组 (P <0 0 5 )。结论 :中药对心衰合并低钠血症的治疗具有一定的价值。     

神经外科病人低钠血症的病因分析

目的：本研究通过对神经外科低血钠病人ＡＤＨ与ＡＮＦ放免测定,以及血离子等生化指标的监测,结合补钠实验,进而确定病因,以改进神经外科低钠血症病人的诊断及治疗。方法：随机选１００例低血钠症病人,另选３０例正常人做为对照组。低钠病人逐日监测血钠,血钾,血ＢＵＮ,Ｃｒｅ,２４ｈ尿钠,红细胞压积,血红蛋白浓度。     

The transurethral resection syndrome

The transurethral resection syndrome ("TUR syndrome") is caused by absorption of electrolyte-free irrigating fluid, and consists of symptoms from the circulatory and nervous systems. The clinical picture is inconsistent and the syndrome is easily confused with other acute disorders. Mild forms are common and often go undiagnosed, while severe forms of the TUR syndrome are rare and potentially life-threatening. The pathophysiology is complex but includes four mechanisms: circulatory distress from the rapid absorption of electrolyte-free irrigating fluid, adverse effects of glycine, dilution of the protein and electrolyte concentrations of the body fluids, and disturbance of renal function. The treatment of the TUR syndrome consists of general life support and in specific treatment directed towards hypotension, hyponatraemia and anuria. Methods to lower the uptake of irrigating fluid are widely used and probably reduce the incidence of the TUR syndrome. However, patient safety can be guaranteed only if the absorption is monitored. An irrigating fluid containing tracer amounts of ethanol can be used for this purpose. This permits the uptake of fluid to be indicated by measuring the concentration of ethanol in the patient's exhaled breath.     

Blood-brain barrier disruption and complement activation in the brain following rapid correction of chronic hyponatremia

In previous studies we developed a rat model in which demyelination is reproducibly produced following rapid correction of chronic hyponatremia and demonstrated that the development of demyelination in this model is strongly associated with NMR indices of blood-brain barrier (BBB) disruption. Because complement is toxic to oligodendrocytes, we evaluated the hypothesis that BBB disruption precipitated by correction of hypoosmolality is followed by an influx of complement into the brain, which then contributes to the demyelination that occurs under these conditions. We studied four groups of rats with immunocytochemical analysis using primary antibodies to IgG and the C3d split-fragment of activated complement: (1) normal rats; (2) rats in which hyponatremia was maintained for 7 days; (3) chronically hyponatremic rats in which the plasma [Na(+)] was rapidly corrected with hypertonic saline administration 20 h prior to perfusion; and (4) chronically hyponatremic rats in which the plasma [Na(+)] was rapidly corrected with hypertonic saline administration 5 days prior to perfusion. In normonatremic and uncorrected hyponatremic rats only background staining was observed in areas lacking a BBB and in blood vessel walls, whereas marked increases in IgG and C3d staining were seen in the brains of rats both 20 h and 5 days after rapid correction of hyponatremia. The staining intensity was significantly correlated with the degree of neurological impairment. These results provide evidence for functional BBB disruption following rapid correction of hyponatremia and support the hypothesis that complement activation may be involved in the pathogenesis of osmotic demyelination.