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| This topic has been moved by - emergency , 2004-01-28 09:51 You may read the board announcement or contact board moderators for the reasons. |
| 百草枯中毒 |
| srf921153 Posts: 1 Score: 0 |
请问哪位朋友抢救过百草枯中毒? 我科抢救过2例,第一例因没有经验,很快出现肺纤维化而死亡.在接触第二例时我们很积极,服毒第一天无任何症状,我们就给予做血液灌流,但病情还是发展很快,在第二天就出现呼吸困难、肝肾功能衰竭(转氨酶大于1000,明显全身黄染、无尿)、咽喉部粘膜水肿。我们积极给予药物对症治疗、呼吸支持、及CRRT治疗,但无明显效果。 在文献中有关于洗胃后灌入漂白土、皂土,但我们找了很多资料,均没有发现关于漂白土、皂土的成分和应用方法。哪位朋友能提供帮助? • 【申请上传】British 2001 + British 2003 |
| chenkun 急救与危重病版 丁香园主任 Posts: 1450 Score: 176 |
检索了一下, 洗胃及灌肠液内加入漂白土、皂土或活性炭可使百草枯失活,或在洗胃后灌入15~30%漂白土、7%皂土或活性炭悬液,并给硫酸镁口服以加速排出,每2~4小时一次。口服后2小时内清除毒物疗效最好。 天然存在的矿物土,有不少种类具有吸附能力(或在经过化学处理活化以后)。如漂白土 (亦称富勒氏土,fuller's earth);蒙脱土(montmorillonite,亦称班脱土bentonite),商品常称为膨润土,或简称白土;以及凹凸棒土(简称凹土, attapulgite)等。我国亦有丰富的资源,并有多种产品供应。 蒙脱土的化学组成通式为:Al2(Si4O10)(OH)2·xH2O,或Al2O3.4SiO2·xH2O,其中(SiO2/Al2O3)比率约为4:1。蒙脱土含SiO2(50%~70%)、Al2O3(15%~20%),还含有少量的铁、钙、镁、钠、钾的氧化物。不同产地的成份可有很大差别。蒙脱土的化学结构中有大量的孔隙,能吸附大量水分。天然的蒙脱土含水约50%~60%,在干燥后内部形成大量孔隙,优良者可达其体积的60%~70%,比表面积约为120~140m2/g。它具有良好的吸附性能,能吸附自身重量12%~15%的有机杂质。它还有较强的阳离子交换能力,这与它的化学成分有关。 新开采的蒙脱土相当软,有塑性。呈白色,或带浅黄、浅红、绿、紫等色;是质地致密的鳞片状微晶集合体。具蜡状或油脂光泽。将它经过分选、破碎、干燥、磨粉和筛分等处理而成为产品。 将蒙脱土用盐酸或硫酸处理,可使它活化而将它的吸附能力提高3~5倍。这种产品称为活性白土或酸性白土。将蒙脱土与水调和成浆状,在反应器中加入盐酸(HCl为土量的28%~30%)或硫酸,加热反应2~3小时,将土中的有机物和钙、镁、钠、钾等成分溶去,然后分离除去反应物中的残酸及溶解物,用水洗涤至接近中性(产品中的游离酸含量应小于0.2%),再干燥至水分低于8%,粉碎至200目筛通过90%以上,即为活性白土。 活性白土是白色或米色粉末或颗粒。主要成分是Al2O3.4SiO2.nH2O。表观密度0.55~0.75g/cm3,相对密度2.3~2.5。不溶于水,有油腻感。它的表面有很多不规则的孔穴,比表面积很大,具有良好的吸附性能,可除去动、植物油和矿物油中的不良气味和有色物质,它还有离子交换能力和选择吸附性。活性白土已广泛应用在食品、酿造和化学工业中,将各种油类和有机物脱色精制。 从其机制看来,关键还是吸附作用,因此,活性炭应该是最容易得到的。 但是,中毒患者往往存在严重的消化道腐蚀情况。故CRRT的同时进行积极的血液灌流应该有效且更为合适。供参考。 Click here to open a new window 上边这个网站内容不错,例如: Click here to open a new window • 我的小妹,pp吗? |
| yisheng Posts: 121 Score: 10 |
血浆置换,禁用吸氧,血液透析,支持疗法,除此之外好像别无他法。我们抢救了4例,只活了一例。 • gg征mm |
| xifeng Posts: 51 Score: 7 |
• 一些书籍 |
| xifeng Posts: 51 Score: 7 |
我们治疗的几个病例,死亡率也很高,下面的一篇文章供大家参考 Am. J. Respir. Crit. Care Med., Volume 159, Number 2, February 1999, 357-360 A Prospective Clinical Trial of Pulse Therapy with Glucocorticoid and Cyclophosphamide in Moderate to Severe Paraquat-poisoned Patients JA-LIANG LIN, MEI-LING LEU, YU-CHIH LIU, and GUAN-HSING CHEN Department of Medicine and Poison Center, Chang Gung Memorial Hospital, Lin-Kou Medical Center, Chang Gung Medical College and University, Taipei, Taiwan, Republic of China Paraquat (PQ) is a widely used bipyridyl contact herbicide with a good safety record when used properly. Most cases of PQ poisoning result from PQ suicidal ingestion. There are three degrees of severity in PQ poisoning (1, 2). Mild poisoning can cause oral irritation and gastric upset, and brings complete recovery. Moderate to severe poisoning produces acute renal failure, and in severe cases, hepatitis followed by pulmonary fibrosis, leading to death after 2 to 3 wk. Acute fulminant poisoning results in death within 1 wk from multiple organ failure and cardiovascular collapse. Retrospective studies (3) show that good predictors of outcome may be plasma and urine concentrations within the first 24 h of intoxication. The urine PQ tests taken on admission are reasonable guides to predict the severity of poisoning and have the advantage that a qualitative or semiquantitative result may be easily and rapidly obtained in an emergency situation (5). The results of treatments for PQ poisoning, including absorbents, pharmacological approaches hemoperfusion (10), were disappointing. Although the high-dose cyclophosphamide (CP) and dexamethasone (DX) treatments, including intravenous CP 5 mg/kg/d and DX 24 mg/d for 14 d, had a 75% survival rate after PQ poisoning (11), a subsequent study (12) did not demonstrate the efficacy of this approach. Therefore, the efficiency of high-dose CP and DX in PQ poisoning remains controversial. Recently, pulse therapy with CP and methylprednisolone (MP), including intravenous CP or MP 1 g/d for 2 to 3 d, has been used to treat effectively many patients with severe lung damage from systemic lupus erythematosus (SLE) and Wegener's granulomatosis (13, 14), with greater efficacy and less side effects than those of high doses of CP therapy. In addition, our preliminary report (15) demonstrated that pulse therapy might be effective in treating patients with moderate to severe PQ poisoning. Because the previous study was not prospective and only included a small number of patients, we designed the prospective study to evaluate its efficacy in treating a large group of PQ-poisoned patients. This study was approved by the clinical research committee of Chang Gung Memorial Hospital and had the informed consent of all patients. This prospective study lasted from January 1992 to December 1997. During this period, 142 patients with PQ poisoning were admitted to our hospital within 24 h after ingestion. In urine samples taken on arrival at our emergency department, PQ was immediately detected by the sodium dithionite reaction. The sodium dithionite test is based on the reduction of PQ by sodium thionite under alkaline condition to form its stable blue radical ion. A strong "navy blue" (N (D (5). Patients were classified as having: (1) fulminant poisoning if their urinary dithionite reaction yielded a NB or DB and if they died from multiple organ failure within 1 wk after intoxication; (2) moderate to severe poisoning if the urine PQ tests were NB or DB or if they died from hypoxia and lung fibrosis more than 6 d after intoxication; (3) mild poisoning if the urine PQ tests were colorless or light blue (1). Most plasma PQ concentrations were not checked owing to the limitations of our facilities. Patients with strongly positive urine dithionite tests (NB or DB color) randomly received conventional or pulse therapy for PQ intoxication according to random digit methods. At the end of this study, to avoid bias, the data were collected and analyzed by other doctors who were not aware of the study. A total of 50 patients with moderate to severe PQ poisoning were included in this study. Seventy-one patients with fulminant poisoning and 21 patients with mild poisoning were excluded. To prevent absorption of PQ from the gastrointestinal tract, active charcoal added in magnesium citrate was given through a nasogastric tube after gastric lavage with normal saline. All patients received two courses of 8-h active charcoal hemoperfusion therapy in the emergency room (ER), and dexamethasone 10 mg intravenous injection every 8 h was given for 14 d after admission. In addition, the study group patients received pulse therapy after hemoperfusion at ER. Pulse therapy included 15 g/kg of CP in 5% glucose saline 200 ml and 1 g MP in the other 200 ml 5% glucose saline intravenously infused for 2 h/d. CP was infused for 2 d and MP for 3 d. Blood gas analysis, blood cells count, serum creatinine, chest X-ray, and liver function tests were regularly checked. Definition (12) Acute renal failure was diagnosed if the serum creatinine increased to 1.4 mg/dl (i.e., mean normal value + 2 standard deviations). Hepatitis was diagnosed when aspartate aminotransferase (ST) and alanine aminotransferase (ALT) values were > 70 U/L (normal value is < 35 U/L) or when total bilirubin was > 3.0 mg/dl (normal value is < 1.4 mg/dl). Hypoxia was diagnosed if a patient had an arterial blood gas analysis of PaO2 < 70 mm Hg at room air. Data Analysis The differences between groups were compared with Student's t tests. To clarify the effects of the pulse therapy on the clinical course of the patients, we compared the outcome of patients in the two groups by a chi-square test with Fisher exact test. A p value less than 0.05 was considered significant. All data were presented as mean ± SD. Seventy-one patients with fulminant PQ poisoning who died within 1 wk after intoxication were excluded (Table 1). Fifty patients were enrolled in the study. Most were young adults. All were suicidal and had ingested liquid PQ concentrate (24%). Twenty-two patients received pulse and conventional therapies in the study group and 28 received conventional therapy only in the control group. Age, sex, and clinical conditions were equally represented in both groups (Table 2). There were no significant differences in age, sex, time elapsed from ingestion to arrival at ER, the beginning of hemoperfusion, and severity of PQ poisoning between the study group and control group. The prevalence rates of acute renal failure, hepatitis, and hypoxia at the third day after PQ ingestion were not significantly different between the two groups (Table 2). The clinical course and biochemical data of both groups of patients are presented in Table 3. The peak serum creatinine and total bilirubin concentrations of the study group were significantly lower than in the control group (serum creatinine: 2.5 ± 1.8 mg/dl versus 5.3 ± 4.1 mg/dl, p = 0.0040; total bilirubin: 2.6 ± 4.8 mg/dl versus 7.2 ± 8.6 mg/dl, p = 0.046). Otherwise, the lowest PaO2 of the study group was marginally significantly higher than that of the control group (67.9 ± 27.3 mm Hg versus 52.2 ± 29.4 mm Hg, p = 0.0584). The mortality rate of the study group (4 of 22, 18.2%) was lower than that of the control group (16 of 28, 57.1%; chi-square test, p = 0.0052; corrected by Fisher test, p = 0.0084). All fatalities in these two groups were caused by progression of respiratory failure. The pulse therapy group included eight patients (8 of 22, 36.4%) with leukopenia (white blood cell count [WBC] < 3,000), which was considered to be a side effect of pulse therapy. They spontaneously recovered 1 wk later without mortality. Leukopenia was the only major complication. Other complications, including hair loss and acne, were noted in some patients after pulse therapy. Our results, similar to our preliminary report (15), suggest that pulse therapy with CP and MP may improve the survival rate of patients with moderate to severe PQ poisoning. However, our preliminary report was not a prospective study and only included a small number of patients. The current prospective, controlled study with a large group of patients may yield a more definite conclusion in treatments for PQ poisoning. Comparison to previous studies (11, 12), excluding patients with fulminant paraquat poisoning from our study, clarifies the efficacy of pulse therapy in treating patients with moderate to severe paraquat poisoning. This may be the reason why our study demonstrated greater efficacy than others. In addition, the pulse therapy may also have improved the survival rate of our patients, although the exact mechanism is unknown. In a previous work (16) which was confirmed by a subsequent study (17), we found that the respiratory function and arterial blood oxygen concentrations of PQ-poisoned survivors with lung fibrosis could gradually improve to nearly normal after 3 mo follow-up, even if the lung fibrosis persisted. Hence, the severe inflammation, not the fibrosis, of lung may play the predominant role in the lethal hypoxia of patients with PQ poisoning during the subacute period of intoxication. If the PQ-induced lung inflammation can be attenuated, the survival rate of PQ intoxication may be improved, especially in patients with moderate to severe PQ poisoning. Pulse therapy with MP is known as a strong anti-inflammation treatment in clinical practice (13, 14). CP exerts a wide range of immunomodulatory effects that influence virtually all components of the cellular and humoral immune response and reduce the severity of inflammation (18). In addition, CP-induced leukopenia may contribute to reduce pulmonary inflammatory changes of PQ-poisoned patients (11). Hence, the efficacy of pulse therapy may be due to improvement of the PQ-induced severe inflammatory changes of lungs and reduction of the severity of hypoxia. Although CP may induce pulmonary toxicity in clinical practice, the frequency is only 1% or less (19) and most reports are from patients with malignant disease who received multiple agents (20). There were no severe complications in the study group patients, which suggests that the pulse therapy is safe and well tolerated. Lack of plasma PQ level in our patients is the limitation of this study, but the plasma PQ level falls very quickly after poisoning; an error of an hour or two in the estimate of time of ingestion can move a patient from the 30% to the 70% survival curve (21). In addition, practical experience suggests that such inaccuracies are not uncommon (21). Because previous studies (5) showed that plasma and urine tests within the first 24 h of intoxication were good predictors of outcome and prognosis, the urine dithionite test is a reasonable indicator of the severity of PQ poisoning of our patients. In addition, it can be performed easily and quickly in any situation and no specific equipment is needed. In conclusion, our results demonstrate that pulse therapy with CP and MP may be effective in treating patients with moderate to severe PQ poisoning, but not in treating patients with fulminant PQ poisoning. Further double-blinded controlled studies are required to confirm this observation. • 打死你我也弄不明白的几个科学问题 |
| ygl69 Posts: 27 Score: 6 |
我接触过好几例,第一例,经验不足,先是消化道腐烂,然后肺纤维化,无可奈何(是小青年赌气自杀)。第二例,也是一个小青年自杀,有了前一次的教训,及早的行血液滤过,以及激素的应用,但还是死于肺纤维化,并且很快出现了肝肾衰竭,可怕。每一次抢救,大家有关吸氧的争论很多,因为书上都说它能促进肺纤维化,但是我在想,当他的氧饱和度过低,还是应该先保证,毕竟可以多存在世上几天。不知你们有没有抢救成功的经验? ygl69 edited on 2004-01-28 22:53 • 2000-2003医师执业资格考试全部真题下载 |
| wylily Posts: 39 Score: 16 |
血液灌流的活性炭也可服用。 晚期行生命支持,严重氧分压下降,还是可以吸氧的。吸氧的争论源于:百草枯中毒的动物在低氧条件下存活延长。 百草枯中毒,死亡率极高。国内的一些文章,多标榜经过××治疗,效果如何如何好,仔细分析,均存在如下问题: 没有对中毒的程度进行科学的分级,缺少可比性,此为研究大忌。 百草枯的研究在60-70年代较多,在NEW ENGLAND JOURNAL OF MEDICINE 有报道,有分级,当时已有冲击治疗。台湾也有多篇研究报告,曾在“胸科”发表也进行分级,发现使用甲强龙和CTX冲击效果较好。当时该期杂志编辑还写了编者意见以示赞许。临床上有的患者存在肝功能严重损害,对此类患者使用CTX似有加重肝损的风险。 wylily edited on 2004-01-29 22:48 • 教师节专贴---老师,谢谢您! |
| 普通绿茶 Posts: 74 Score: 10 |
我们那里基本上是死亡率100% 死于MODS • 一道今年高考语文题的爆笑答案-爆笑!! |
| yisheng Posts: 121 Score: 10 |
所以,我认为应该像毒鼠强那样禁止生产。 • 2000-2003年中西医结合医师资格考试真题选编 |
| wzhxm4 Posts: 20 Score: 2 |
我以前见过好几例,但都死了,死因主要为多脏器衰竭,以呼吸及肾功能损害为主。该病没有特殊的解毒剂,比较好的方法是百草枯中毒后即刻用泥土混水服用,因为百草枯与泥土混合后毒性大为降低。国外百草枯运用比较广就因为其入土后的低毒性,这种方法一般基层医院医生不知道罢了。如果毒性吸收后再予抢救那就看病人运气了! • 2000-2003医师执业资格考试全部真题下载 |
| vancom 丁香园准中级站友 Posts: 404 Score: 93 |
http://www.dxy.cn/bbs/post/view?bid=112&id=339928&sty=3&keywords=%B0%D9%B2%DD%BF%DD • 中医执业医师考真题,就是不太全 |
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