急性亚硝酸盐中毒29例抢救体会

目的 探讨急性亚硝酸盐中毒的机理、临床特征和急救措施,总结出亚硝酸盐中毒的防治方法.方法 回顾性分析我院2005年5月～2 008年5月共2 9例急性亚硝酸盐中毒的临床资料.结果 29例病人均于24～72小时治愈出院;病人以进食腐烂变质的蔬菜、腌制不久的蔬菜或放置过久的剩菜,食用添加过量的亚硝酸盐的肉制品或将亚硝酸盐误当食盐烹调的食物而引发中毒.结论 亚硝酸盐中毒以综合治疗为主,使用特效解毒剂美兰宜小剂量缓慢给药,大剂量使用氧化还原剂维生素C具有协同治疗作用;加强个人饮食卫生意识,卫生监督,职业培训是预防的关键.     

急性亚硝酸盐中毒23例临床报道

目的探讨急性亚硝酸盐中毒的救治方案。方法分析23例亚硝酸盐中毒病例的临床表现和救治方法。结果 23例中毒患者经迅速催吐、洗胃、导泄清除胃肠道内未吸收毒物,以及应用还原剂亚甲蓝后,均于48～72h出院,抢救成功率达100%。结论亚硝酸盐中毒易误诊,特别是在基层医院,故对疑似病例要尽早检验或谨慎治疗试验明确诊断,诊断明确后应迅速清除胃肠道内部未吸收毒物,及时使用还原剂;美蓝治疗急性亚硝酸盐中毒疗效肯定,但宜小剂量缓慢给药和综合治疗。     

内科疾病处方用药解析(75)

9急性中毒9.8急性亚硝酸盐中毒急性亚硝酸盐中毒是指短时间内摄入大量亚硝酸盐后引起的以血液系统损害为主的全身性疾病,主要表现为高铁血红蛋白血症。亚硝酸盐(常见有亚硝酸钠和亚硝酸钾)为白色或微黄色结晶或颗粒状粉末,无臭味,易溶于水。亚硝酸盐成人口服的最低中毒剂量约为0.1g,口服最低致死剂量为1.0～5.0g。急性亚硝酸盐中毒途径为经口摄入,主     

80例亚硝酸盐中毒临床观察

目的 探讨急性亚硝酸盐中毒的临床特点和预防方法.方法 2010年7月28日急诊抢救80例群体亚硝酸盐中毒患者的临床症状进行回顾性分析.结果 80例患者64例于12 h内,16例经住院观察36～72 h后全部治愈出院.结论 加强卫生监督,个人饮食卫生,可以有效地预防亚硝酸盐中毒的发生,亚甲蓝是治疗亚硝酸盐中毒的首选药物.     

急性亚硝酸盐中毒14例救治成功经验

<正>对亚硝酸盐中毒的报道很多,但近几年仍有反复出现急性亚硝酸盐中毒的情况发生,有的是集体中毒发病,有的是散发中毒发病,部分医师对其了解不多,为了提高对亚硝酸盐中毒的认识,更好地组织和抢救中毒患者,现将我院2007年14例患者集体中毒后救治成功的情况总结分析如下:     

急性亚硝酸盐中毒抢救体会

急性亚硝酸盐中毒主要是由于误服了亚硝酸盐或含有较多的亚硝酸盐的食物所致。亚硝酸盐中毒起病急、病情重，严重者出现休克甚至死亡，因此急性硝酸盐中毒的及时、准确救治至关重要。本文对我院2003年1月至2006年12月救治的19例急性亚硝酸盐中毒病例进行回顾性分析。     

小儿急性亚硝酸盐中毒6例

亚硝酸盐常用于食品加工、防腐以及工业应用,误食即可中毒,病情凶险,病死率高.此外,某些变质蔬菜或腌渍不久的青菜均含有较多硝酸盐,食入后经肠道细菌还原,可转变为亚硝酸盐造成中毒.现将我院儿科抢救6例急性亚硝酸盐中毒病例分析如下:     

80例亚硝酸盐中毒抢救措施

目的回顾性分析本院急诊科2010年9月8日,对80例亚硝酸盐中毒患者的诊治经过。总结经验,为今后诊断治疗亚硝酸盐中毒患者提供参考。方法对2010年9月8日收治的同一工地80名亚硝酸盐中毒患者进行回顾性分析。结果依据明确的亚硝酸盐接触史,及典型临床表现,可明确诊断,亚甲蓝治疗亚硝酸中毒。结论加强食品安全健康教育,可以有效的防治、杜绝亚硝酸中毒。     

亚硝酸盐集体中毒46例救治体会

急性亚硝酸盐中毒 ,常以集体中毒发病 ,来势凶险。若对其认识不足或处理不当 ,很易造成严重后果。现就本院近期两起亚硝酸盐集体中毒共 46例的救治经验报道如下。1　临床资料第一批中毒 3 3例 ,将亚硝酸盐误作食盐加入饭菜中毒 ,第二批 13例因食用亚硝酸盐卤制的肉食中毒。其中男 2 9例 ,女17例 ;年龄 1～ 73岁。 0 .5～ 2h内全部出现中毒症状。所有患者均有紫绀、头晕、乏力、恶心 ,其中头痛 2 3例 ,呕吐 3 0例 ,嗜睡4例 ,昏迷 2例。取剩余食物、呕吐物经防疫部门测定 ,均含大量亚硝酸盐 ,确诊为亚硝酸盐中毒。2　救治经过立即给予吸氧、催…     

亚硝酸盐中毒的抢救与护理

亚硝酸盐是工业用盐,广泛应用于食品加工防腐、金属表面处理等,因其和食用盐极为近似,近年来亚硝酸盐中毒的报道屡见不鲜.本文曾参与7例亚硝酸盐中毒的抢救及护理,取得了一些经验与教训,现总结如下:     

Evaluation of reagent strips for the rapid diagnosis of nitrite poisoning.

Two commercial urine test strips based on the Griess nitrite-specific diazonium salt reaction, having sulfanilamide and para-arsanilic acid as substrates, respectively, were studied as qualitative tests in the rapid diagnosis of nitrite/nitrate poisoning. Their usefulness was compared to other rapid tests, such as the sulfanilic acid-1 naphthylamin and diphenylamine blue tests. The practical sensitivity limit to nitrites in plasma and in water of both the reagent strips and SA-1NA test was 0.50 micrograms NO2/mL, while the diphenylamine test, which is not nitrite specific, showed a positive reaction to nitrites in plasma and in water above 50 micrograms NO2/mL and 5 micrograms NO2/mL, respectively. The in vitro assays were evaluated in vivo by the sublethal intoxication of a sheep with nitrite, demonstrating that commercial urine test strips may be useful for the rapid diagnosis of nitrite/nitrate poisoning.     

The effect of hyperbaric oxygen on acute experimental sulfide poisoning in the rat

In order to evaluate the efficiency of hyperbaric oxygen in experimental acute sulfide poisoning, we studied the effect of 1 ATA (atmosphere absolute) oxygen and sodium nitrite therapy. We then studied the effect of oxygen at 3 ATA alone and in combination with intraperitoneal sodium nitrite injection on rats poisoned by intraperitoneal injection of LD75 sulfide. Electroencephalogram and heart rate were continuously monitored. We also studied the effect of sodium nitrite and hyperbaric oxygen administered before the poisoning (protective effect). In our experimental set, death of untreated poisoned animals occurred within 5 min. There is a parallel between modification of the EEG pattern and apnea. Respiratory arrest always preceded cardiac arrest. Pure oxygen (1 ATA O2) is effective in preventing death in experimental sulfide poisoning. 3 ATA oxygen was significantly more effective in preventing death than 1 ATA oxygen, or sodium nitrite alone. The best therapeutic regimen was a combination of 3 ATA oxygen and sodium nitrite administration.     

急诊中毒快速检验诊断系统的建立

目的建立急诊中毒的快速检验诊断系统。方法运用中毒诊断专家系统、可见紫外分光光度计、气相色谱仪、薄层色谱扫描仪、气相色谱质谱联用仪、原子吸收光谱仪、动物实验和毒品金标筛选试剂盒建立急诊中毒快速检验诊断系统。结果酒精和一氧化碳中毒检验诊断可在20min内完成,诊断准确度达100%。其他中毒检验诊断可在0.5￣2h内完成。太原地区急诊中毒出现顺序为:安眠镇静药类>乙醇>一氧化碳>其他临床药物>杀虫剂>鼠药>亚硝酸盐>毒品。山西省内中毒死亡原因为一氧化碳>毒鼠强>杀虫剂。结论本研究建立的急诊中毒快速检验诊断系统具有快速、简便、准确、适用面广的特点,可应用于急诊中毒的快速检验诊断。     

Beneficial effect of N-acetylcysteine against organophosphate toxicity in mice

Recent studies showed that oxidative stress could be an important component of the mechanism of organophosphate (OP) compounds toxicity. The aim of present study was to investigate either prophylactic and therapeutic effects of N-acetylcysteine (NAC) against fenthion-induced oxidative stress in mice. Additionally, the effects on survival rates were investigated. Therefore, we determined the changes of the blood levels of glutathione (GSH), malondialdehyde (MDA), nitrite, and nitrate in blood or serum. Additionally, all animals were observed for 6 h and the survival rates were recorded. It was found that fenthion administration increased the levels of MDA, and decreased the levels of GSH, nitrite and nitrate. On the other hand, both prophylactic and therapeutic NAC treatment decreased the levels of MDA, and increased the levels of GSH, nitrite, and nitrate. The results showed that NAC is able to attenuate the fenthion-induced oxidative stress whereby NAC has not only prophylactic but also therapeutic activity in fenthion poisoning. On the other hand, we found that NAC can clearly improve survival rates in mice administered with an acute high dose of fenthion poisoning. In conclusion, NAC can decrease OP-induced oxidative stress and mortality rate, but the exact mechanism of its NAC protective effect needs to be explored further.     

Erythrocyte membrane alterations as the basis of chlorate toxicity

The effects of sodium chlorate and of sodium nitrite on human erythrocytes were studied in vitro. Nitrite rapidly oxidised haemoglobin and glutathione; reduction of methaemoglobin (Hbi) by methylene blue was complete during 3 h of incubation with nitrite. With chlorate, a concentration-dependent lag phase was seen before Hbi was formed. After prolonged incubation, Hbi could no longer be reduced with methylene blue. Several other effects were observed that explain the clinical picture of chlorate poisoning which involves haemolysis followed by disseminated intravascular coagulation and renal failure: increased permeability to cations, increased resistance to hypotonic haemolysis and prolonged filtration time through polycarbonate membranes with cylindrical pores of 5 micron diameter. This suggests an increased membrane rigidity due to membrane protein polymerisation, as demonstrated by SDS polyacrylamide gel electrophoresis. Simultaneously, erythrocyte enzymes were inactivated, primarily glucose-6-phosphate dehydrogenase which is necessary for the therapeutic effect of methylene blue. This explains the inefficacy of methylene blue in the treatment of a case of chlorate poisoning that we observed (Arch. Toxicol., 48 (1981) 281).     

Increased levels of urinary nitrite and nitrotyrosine in Yusho victims 40 years after accidental poisoning with polychlorinated biphenyls in Nagasaki, Japan

Forty years have passed since the accidental poisoning with polychlorinated biphenyls (PCB) in Japan in 1968, named Yusho. High concentrations of PCB are still detected in the serum of the Yusho victims. PCB produces superoxide (O(2) (-)) in the metabolic process and we reported high concentrations of serum nitrite, a stable metabolite reflecting nitric oxide (NO), in the Yusho victims. NO reacts with O(2) (-) and immediately produces peroxynitrite (ONOO(-)). ONOO(-) causes nitration of tyrosine residues and produces nitrotyrosine (NT). Therefore, we measured urinary concentrations of nitrite and NT in the victims and age-matched controls. The mean urinary concentrations of nitrite and NT were significantly higher than in the controls. There was a positive correlation between urinary nitrite and NT in the Yusho victims. Furthermore, there was a positive correlation between the ratio of urinary NT to nitrite and serum PCB concentrations in the Yusho victims. It was considered that the emergence of some ailments could be presumed to have been caused by high levels of urinary nitrite and NT in the Yusho victims.     

The protective effect of alpha-tocopherol characterized by erythron system indices in rats with chronic nitrite intoxication

The effect of alpha-tocopherol administered in a dose of 15 and 150 mg/kg on the erythron system was studied in rats subjected to chronic nitrite intoxication. The chronic poisoning with sodium nitrite led to three-phase changes in the concentration of erythrocytes (RBC count) and hemoglobin and to activation of the erythropoiesis and erythrophagocytosis processes. The introduction of alpha-tocopherol on the background of intoxication with sodium nitrite prevents from the development of erythropenia, causes erythrocytosis (in large doses), decreases the degree of cytoarchitectonic changes, and reduces the erythropoiesis and erythrophagocytosis activity.     

The treatment of experimental cyanide poisoning by hemiglobin formation

Summary Following the observation that some aminophenols produce hemiglobin rather rapidly in vivo and in vitro and with regard to the need of rapid hemiglobin formation in the treatment of cyanide poisoning, o-aminophenol hydrochloride was tried in cyanide poisoning of mice and dogs.In mice o-aminophenol was found to produce hemiglobin more rapidly than an equally effective dose of nitrite.The injection of o-aminophenol hydrochloride saved 95% of the mice injected subcutaneously with two DL₅₀ of potassium cyanide. Only 60% of these mice survived if an optimal dose of sodium nitrite was injected.Dogs which had received four DL₅₀ of potassium cyanide were kept alive if the treatment with o-aminophenol began at the moment the corneal reflex disappeared.Whereas the intravenous injection of nitrite was found to lower the arterial pressure quickly for a long time, o-aminophenol did not affect the blood pressure in dogs.Briefly presented at a meeting of the Deutsche Pharmakologische Gesellschaft in Bad Nauheim on Oct. 8, 1964 (Kiese andWeger).     

Severe keloids caused by hydrogen cyanide injury: a case report

The purpose of this study was to report severe keloids caused by hydrogen cyanide injury. Hydrogen cyanide poisoning is still a problem as an occupational disease in China. We report a 37-year-old man with severe hydrogen cyanide poisoning. The patient fell on the floor after inhalation of hydrogen cyanide and was burned on his back by hydrocyanic acid. Sequential treatment included amyl nitrite by inhalation, intravenous sodium nitrite 3%, and intravenous sodium thiosulfate 25%. Other treatment consisted of incision of the trachea, mannitol and furosemide, antibiotics, and nutrient support measures. The patient also received hyperbaric oxygen therapy; during the first treatment, he became apneic and cardiopulmonary resuscitation was supplied in the hyperbaric oxygen chamber. He eventually recovered, but a large amount of keloids developed on his back and buttocks.     

Comparison of nitrite treatment and stroma-free methemoglobin solution as antidotes for cyanide poisoning in a rat model

The standard nitrite/thiosulfate regimen for cyanide poisoning was tested in our rat model. By modifying the treatment regimen and the nitrite solution an effective antidote against an LD90 of cyanide could be produced. However, this treatment was effective against two times the LD90 only when administered ten minutes prior to cyanide injection. These results are in marked contrast to our results with stroma-free methemoglobin solutions (SFMS) which showed SFMS to be a highly effective antidote against four times the LD90 when administered 30 seconds after an intravenous injection of cyanide. SFMS proved to be an effective antidote for two times the LD90 when administered up to sixty seconds after the cessation of respiration.