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百草枯中毒
srf921153




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2004-01-27 23:45user profilesend a private message to userreply to postsearch all posts byselect and copy to clipboard. 
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  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

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2004-01-28 09:40user profilesend a private message to userreply to postsearch all posts byselect and copy to clipboard. 
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死亡率很高的病,抢救数量不多,没太多经验。

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。



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急救与危重病版欢迎您


我的小妹,pp吗?
yisheng




Posts: 121
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2004-01-28 10:18user profilesend a private message to userreply to postsearch all posts byselect and copy to clipboard. 
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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
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2004-01-28 13:10user profilesend a private message to userreply to postsearch all posts byselect and copy to clipboard. 
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百草枯,其化学名称是1,1-二甲-4,4-二氯二吡聢,是一种化学除草剂,广泛应用于农业。百草枯中毒常见于发展中国家,其中是东亚一些国家主要死亡原因之一。百草枯中毒在我国也十分常见。百草枯对肺组织具有较强的亲和力,百草枯进入机体后,肺组织中的浓度是其他组织10-90倍,其损害程度严重于其他组织。百草枯可以使机体产生大量的氧自由基,氧自由基通过脂质过氧化作用,使Ⅰ型、Ⅱ型肺泡细胞的细胞膜和肺间质中血管上皮细胞膜受损。在百草枯中毒早期肺组织的病理变化是,组织细胞水肿,出血,炎症细胞浸润,甚至有肺泡透明膜形成,后期可以有肺纤维化形成、肺小囊形成。百草枯中毒后的预后不好,死亡率与摄入量、血浆浓度有关,最小的致死量是10ml,相当于2g百草枯(20%),死亡时间在摄入后3-720小时,平均为270小时。早期(3-96小时)主要死于急性心功能衰竭,肾功能衰竭和呼吸衰竭等多脏器功能衰竭,晚期(97-720小时)主要死于肺纤维化引起的呼吸衰竭。口服百草枯自杀者的死亡率12%-47%,有合并症则更高。百草枯中毒尚无特效治疗,目前治疗上主要以保护肾脏、肝脏、心脏功能,减轻肺组织损害,抑制肺纤维化,降低多脏器功能衰竭发生。应用清除氧自由基清除剂,如维生素E、C、A等低分子清除剂,超氧化物歧化酶,糖皮质激素和免疫抑制剂等,可以降低氧自由基对组织损害。台湾学者认为环磷酰氨、甲基强的松龙可以降低死亡率。另外,本人正在作一个有关百草枯中毒的基础课题,希望各位兄弟的支持。



一些书籍
xifeng




Posts: 51
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2004-01-28 13:38user profilesend a private message to userreply to postsearch all posts byselect and copy to clipboard. 
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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 Musical Note, radiotherapy (9), hemodialysis, and
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" (NBlack Eye or "dark blue"
(DBlack Eye generally indicates significant PQ ingestion and subsequent poor prognosis
(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
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2004-01-28 22:49user profilesend a private message to userreply to postsearch all posts byselect and copy to clipboard. 
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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
2004-01-29 22:45user profilesend a private message to userreply to postsearch all posts byselect and copy to clipboard. 
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及早反复多次洗胃,及早血液灌流,可联合腹膜透析,加强清除,早用激素控制。出现肾脏衰竭加用血液透析。
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
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2004-02-06 21:04user profilesend a private message to userreply to postsearch all posts byselect and copy to clipboard. 
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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
2004-02-07 16:53user profilesend a private message to userreply to postsearch all posts byselect and copy to clipboard. 
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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
2004-02-14 10:08user profilesend a private message to userreply to postsearch all posts byselect and copy to clipboard. 
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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

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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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