Report of eight children with amitraz intoxication

Many pesticides are formulated in organic solvents. An example is amitraz, one of the formamidine groups of pesticidal chemicals. It is commonly used for the treatment of generalized demodicosis in dogs and for the control of ticks and mites in cattle and sheep. In this article, the clinical and laboratory findings of eight children with amitraz intoxication are reviewed. The purpose was to enlighten the findings of amitraz intoxication in children. Of the eight patients, five (62.5%) were boys, three (37.5%) were girls, and the ages ranged from 1 to 4 years. All children accidentally ingested amitraz orally, with no dermal exposure. The most common observed signs were decreased consciousness and bradycardia. Leukocytosis, hyperglycemia, hypernatremia, increased serum aspartate transaminase level, and prolonged partial prothrombin time were diagnosed in children. None of the children had hypothermia, hypotension, or convulsion and none of the patients died. The findings show that the initial signs and symptoms of acute amitraz intoxication appeared severe but they disappeared, with only supportive care needed in most cases within a few days.     

Methylmercury poisoning in Iraqi children: clinical observations over two years

The clinical features of 49 children who had eaten bread contaminated with methylmercury in rural Iraq were reviewed. Symptoms and signs relating to the nervous system--varying degrees of ataxia, weakness, and visual and sensory changes--dominated the clinical picture. The severity of poisoning was related to the blood mercury concentration, as was the degree of recovery. Follow-up over two years showed that children who had had mild or moderate poisoning slowly but steadily improved, some of them recovering normal function, though all had a residual generalized hyperreflexia. In some patients ataxia and motor weakness disappeared. Visual changes also improved, though less completely, and of 17 blind children, only five had recovered partial sight by the end of two years. Seven of the 18 children who suffered very severe poisoning were left physically and mentally incapacitated. The degree of clinical progress shown by these children was better than that shown by some other groups of patients, possibly because the poisoning was relatively acute and mercury consumption was stopped immediately after its effects had become obvious.     

学习障碍儿童临床分析

目的了解学习障碍儿童的临床表现.方法根据学习障碍的诊断标准,采用韦氏儿童智力量表,对95例学习障碍儿童临床表现进行分析.结果学习障碍儿童虽然总智商基本在正常范围内,但言语智商与操作智商之间差异有显著性.结论学习障碍儿童智力构成各要素发展水平均与正常儿童有差异.     

Amitraz poisoning in children

Amitraz is an acaricide and insecticide indicated for the treatment of generalized demodicosis in dogs and for the control of ticks and mites in cattle and sheep. There is little information available in the human literature about the toxicology of the product. In this study, the clinical and laboratory features of amitraz poisoning in 11 children are presented. The age range of the patients was 2-1/2 to 6 years. Accidental ingestion of an improperly stored liquid pesticide was determined in all patients. Unconsciousness (100%), drowsiness (100%), and myosis (84%) were the most common abnormal signs; 45%, 27%, and 18% of patients had bradycardia, respiratory insufficiency, and hypotension, respectively. All of the patients were treated with atropine, gastric lavage, activated charcoal, and supportive care. Although the patients had a prompt response to therapy, three patients required multiple doses of atropine during a 24-h period. This study revealed that clinical poisoning by oral route emerged within 30-90 min and that central nervous system (CNS) depression, which is the most important sign, resolved within 8-1/2-14 h. All cases were discharged.     

蜂蛰伤致儿童中毒24例临床分析

目的总结急性蜂毒中毒致儿童多器官功能障碍的治疗经验。方法综合分析我院1997年至2007年间急性蜂毒中毒患儿24例临床资料。结果24例患儿入院后均呈现不同程度的心、肝、肾功能损害等临床表现。结论治疗蜂毒中毒应尽早采用透析等综合性治疗措施,保护心、肝、肾等多器官功能,促使多器官功能恢复是抢救治疗该病的关键。     

小儿肺炎支原体感染的临床检验特点

目的：总结小儿发生肺炎支原体感染的临床表现以及临床检验特点,提高临床诊断水平。方法对2013年1月～2014年1月收治的156例小儿肺炎支原体感染患者进行临床检验分析,所有患者均接受酶联免疫吸附剂测定（ELISA）肺炎支原体IgM抗体检验（MP-IgM）,被动凝集法检验,以及血常规、尿常规、血生化、血气分析、细菌培养等各项常规检查。结果分析和总结临床检验结果,发现MP-IgM检测法和被动凝集法具有较高的特异性,阳性率分别为39.1%和37.2%,二者差异无统计学意义（P＞0.05）。其他各项常规检查缺乏特异性。结论对可疑肺炎支原体感染患儿应进行早期实验室检查并结合影像学及其临床表现进行综合分析,及早确诊,MP-IgM检测法和被动凝集法具有较高的特异性。     

氟乙酰胺中毒血镁检测及临床意义

目的:探讨氟乙酰胺中毒患儿血镁浓度的变化与其临床价值.方法:将35例氟乙酰胺中毒患儿根据中毒程度分为轻、中、重三组,在其入院24 h内,抽静脉血3 mL进行血镁浓度测定,并与100例正常体检儿的血镁浓度进行比较.结果:氟乙酰胺中毒后血清镁离子水平下降,其下降幅度与中毒程度呈正相关,轻度中毒组与对照组比较差异无统计学意义(P＞0.05),中重度中毒组与对照组比较差异有统计学意义(P＜0.05).结论:硫酸镁对于治疗氟乙酰胺中毒有一定的潜在意义.     

Iron poisoning in children.

In the present state of our knowledge it must be concluded that the outstanding anatomic changes directly attributable to acute iron poisoning are in the gastrointestinal tract and the liver. Both seem to be due to the direct action of iron upon living cells. In the stomach and small bowel the changes appear to be due to the corrosive effect of the iron salt whether in solution or in tablet form. And the anion may indeed play the predominant role as demonstrated by the observation of the severe corrosive changes observed when accumulations of ferrous sulfate tablets occur in areas of the stomach or small bowel. That the mucosal barrier to iron is broken down seems incontrovertible. And it is no longer tenable to assume that the severe complications of iron poisoning are due to the local necroses in the gastrointestinal tract. The liver, being the first parenchymal organ encountered by absorbed iron, is involved to a varying degree. The anatomic changes can progress to frank necrosis in severe cases. And even in those where overt histologic damage is not demonstrable, alterations in biochemical function occur. Anatomic changes in other parenchymal organs are probably largely secondary to dehydration, shock, hemorrhage, and infection. But the possibility of disordered enzyme systems here as well must be borne in mind though so far not demonstrated. In severe cases where hemorrhages play so large a role, albeit infrequently, the specific action of iron in interference with coagulation mechanisms is of the utmost importance. The role of therapy with deferoxamine in production of shock is discussed below. In this connection breakdown of the mucosal barrier with release of apoferritin and ferritin as a hypotensive mechanism has also been suggested by Smith.     

一氧化碳中毒迟发型神经损伤临床特点及预后分析

目的探讨一氧化碳中毒迟发型神经损害临床特点及预后。方法对本院收治的23例一氧化碳中毒迟发型神经损害患者的临床特点及资料进行系统分析,并对预后进行评定。结果在药物对症治疗基础上行高压氧治疗,有效率为95.7%。一氧化碳中毒迟发型神经损害患者预后情况与年龄、昏迷时间、高压氧开始时间、治疗次数,以及并发症等密切相关。结论临床需加强对一氧化碳中毒迟发性神经损伤的认识,高压氧开始时间早及治疗持续时间长,预后越好。     

氟乙酰胺中毒儿童的药代动力学

目的　用气相色谱法测定氟乙酰胺(FAM)中毒儿童的药代动力学。方法　用血液灌流(HP)治疗3例FAM中毒的重症患儿;气相色谱法(GC法)检测FAM血药浓度。结果　在HP治疗后,3例FAM中毒的重度患儿12 h的FAM血药浓度若>90 mg.L-1时,可再用HP治疗。3例患儿HP治疗时的t1/2为(2.43±1.29) h,治疗后0～6 h和6～12 h的t1/2分别为(6.39±4.24) h和(14.90±13.71) h;2例患儿治疗中,当体内FAM的浓度<90 mg.L-1时,t1/2分别为0.70 h和2.00 h。结论 HP治疗FAM中毒患儿安全、有效,机体对FAM的消除呈浓度依赖性。     

Mechanisms of toxicity, clinical features, and management of diquat poisoning: a review

USES: Diquat (1,1'-ethylene-2,2'-bipyridilium) is a nonselective bipyridyl herbicide, related structurally to paraquat, which is used both as a contact herbicide and a preharvest desiccant. In comparison to paraquat, diquat is used much less widely in agriculture. MECHANISMS OF TOXICITY: Diquat is a potent redox cycler and is readily converted to a free radical which, in reaction with molecular oxygen, generates superoxide anions and subsequently other redox products. These products can induce lipid peroxidation in cell membranes, and potentially cause cell death. FEATURES: Over the period 1968-1999, only 30 cases of diquat poisoning were reported in detail in the literature, of which 13 (43%) were fatal. Local and systemic effects have been reported following diquat exposure, with systemic features being invariably associated with ingestion. In severe and usually fatal cases, gastrointestinal mucosal ulceration, paralytic ileus, hypovolemic shock, acute renal failure, and coma have been reported. MANAGEMENT: After rapid confirmation of the diagnosis using a qualitative urine test, gut decontamination may be considered in patients who present within 1 hour of a life-threatening ingestion (>6 g). Supportive measures including fluid and electrolyte replacement should then be employed. Although hemofiltration and hemodialysis are of proven value if renal failure supervenes, there is no clinical evidence that hemodialysis or hemoperfusion removes toxicologically significant amounts of diquat, thereby reducing the risk of organ failure and preventing a fatal outcome in severe cases.     

Clinical features and management of cyanide poisoning

The pathophysiology, clinical features, and management of cyanide toxicity are reviewed and sources of cyanide are listed. Cyanide is a deadly poison that is found in many foods and household and industrial products, including some that are readily available. Cyanide binds with cytochrome oxidase, the enzyme responsible for oxidative phosphorylation, and paralyzes cellular respiration. Because the tissues cannot use oxygen that is delivered, aerobic metabolism ceases. The signs and symptoms of cyanide poisoning reflect the extent of cellular hypoxia. Manifestations may include respiratory abnormalities (progressing from tachypnea and dyspnea to respiratory depression and apnea), hemodynamic instability, metabolic acidosis, and, possibly, local irritant effects after oral ingestion of cyanide. The mainstays of therapy are 100% oxygen and specific antidotes to cyanide. Sequential treatment with amyl nitrite by inhalation, intravenous sodium nitrite 3%, and intravenous sodium thiosulfate 25% is directed toward decreasing the amount of cyanide available for cellular binding. Nitrites convert hemoglobin to methemoglobin, which reacts with cyanide to form cyanomethemoglobin. Sodium thiosulfate serves as a source of sulfur groups, which are needed for conversion of cyanide to thiocyanate, a compound that is relatively less toxic and is excreted renally. Supportive care also is important. Cobalt EDTA, hydroxocobalamin, and aminophenols have also been used but are not considered standard treatments. Cyanide poisoning is a medical emergency that requires prompt recognition and immediate and aggressive treatment.