毒蕈中毒8例分析

毒蕈又称毒蘑菇,食用后可导致中毒,常易群体发病,严重者可出现多脏器损害,甚至死亡.因毒蕈所含的毒素种类不同,中毒后患者的临床表现和脏器损害的程度也不尽相同.2006年7月我院收治的集体误食毒蕈中毒后导致多脏器损害的患者8例,现报道如下.     

毒蕈中毒8例分析

毒蕈又称毒蘑菇，食用后可导致中毒，常易群体发病，严重者可出现多脏器损害，甚至死亡。因毒蕈所含的毒素种类不同，中毒后患者的临床表现和脏器损害的程度也不尽相同。2006年7月我院收治的集体误食毒草中毒后导致多脏器损害的患者8例，现报道如下。     

急性砷化氢中毒所致多脏器损害的超声检查

应用超声对急性砷化氢中毒患者的肝脏、胆囊、脾脏、肾、胸腹腔、心脏等脏器进行检查,观察3例急性砷化氢中毒患者各脏器损害的超声表现及治疗后超声改变。结果显示,急性砷化氢中毒后可引起人体多脏器的损害,主要有肝、肾、胸腹腔。提示,超声可以观察急性砷化氢中毒所致的多脏器损伤,并可随诊观察疗效。     

急性一氧化碳中毒致横纹肌溶解症、无尿1例

<正>缺氧是一氧化碳(carbon monoxide, CO)中毒机体损伤的主要原因,一般以中枢神经系统损害为主,同时可导致心、肺等多脏器功能障碍,横纹肌溶解也是急性CO中毒并发症之一^[1]。本文报道1例急性CO中毒患者出现左侧大腿肿胀、横纹肌溶解,同时伴有心、肝、肾等多脏器功能损害,病程持续时间较长、病情复杂。     

急性重度砷化氢中毒继发多脏器损害10例临床分析

目的探讨急性重度砷化氢中毒继发多脏器损害的诊断及治疗方法,达到早期诊断、早期治疗。方法通过临床实践,收集近几年来我院收治的急性砷化氢中毒继发多脏器损害的10例患者的临床资料,结合现场职业卫生学调查综合分析。结果急性重度砷化氢中毒除急性血管内溶血和急性肾功能损害外,还继发心脏、肝脏、胰岛、血管内皮系统等多脏器损害。结论重度砷化氢中毒范围广,较重的病例都继发严重的多脏器损害;适时选择换血治疗是挽救患者生命的重要措施。     

事故性硫化氢急性中毒的临床表现和原因分析

通过对一起急性硫化氢中毒事故原因分析及患者临床观察,提示,加强原始级预防对杜绝事故发生有重要意义;急性硫化氢中毒可导致猝死及中枢神经系统、呼吸系统、心脏、肝脏等多脏器损害。     

急性硫酸二甲酯中毒的护理

硫酸二甲酯（DMS）具有强烈刺激性和腐蚀作用，在常温下可蒸发。工人多数因生产、泄漏或在清洗、检修管道时，个人防护不当、排风装置发生故障或违反操作规程，进而吸入较高浓度DMS导致急性中毒，中毒时受损的主要靶器官是眼和呼吸系统，严重者可发生成人呼吸窘迫综合征、低氧血症而导致中毒性休克，中毒性脑病等多脏器损害。     

有机磷中毒致双眼大泡性角膜病变1例

有机磷中毒在农村比较多见，可以导致全身多脏器的损害，对于眼局部的不可逆性损害，以往有报道因神经毒性造成视神经萎缩，但因有机磷中毒发生大泡性角膜病变者未见报道，现报道1例如下。     

我国汞中毒临床研究概况

汞中毒是古老的常见的职业病,但非职业性中毒亦不少见.以往认为临床上其急性中毒主要表现为口腔疾患和肾脏损害,慢性中毒主要表现为易兴奋症、口腔病变和震颤.随着临床研究深入、病例报道增多,使人们认识到汞是一种损害多脏器的毒物,其靶器官包括神经、呼吸、消化、肾脏、血液、皮肤等,而且都各有其一定的特征性临床表现.本文就国内文献报道作一综述,以供防治研究参考.     

二氯丙烷和三氯丙烷急性中毒的临床救治

急性有机溶剂中毒常导致中枢神经功能损害及急性肾功能衰竭等多脏器功能衰竭,临床表现凶险,病情进展迅速.2008年4月,我们应用血浆置换术结合常规化学毒物中毒救治疗法成功救治1例因误服醇酸漆专用稀释剂导致的急性二氯丙烷和三氯丙烷中毒患者,现报道如下.     

急性乙醇中毒性肌病——病例报道并文献复习

目的 提高对急性乙醇中毒性肌病的认识。方法 对3例急性乙醇中毒性肌病的临床和实验室检查资料进行收集和分析,并结合相关文献进行复习。结果 3例均于饮酒后发病,并具有急性肌肿胀、肌无力、肌酶显著增高的临床特点。肿胀部位B型超声波检查对了解肌肉受损范围及程度是一项无创伤的及有价值的检查方法。镇静、止痛,局部制动,补液、利尿、碱化尿液及抗脂质过氧化剂有利于本病的恢复。结论 横纹肌溶解症预后相对较好,早期诊断及及时治疗,可使临床症状及血清酶学改变在短期内好转及下降,并有助于预防其严重并发症急性肾功能衰竭发生。     

Tri-phenyl Phosphate Poisoning: Should It be a Prescribed Disease?

A man subsequently confirmed as a case of muscular dystrophyclaimed he was suffering from prescribed disease No. 11 (poisoningby tri-cresyl phosphate) and prescribed disease No. 12 (poisoningby tri-phenyl phosphate), under the National Insurance (IndustrialInjuries Act) 1965. Although he withdrew his claim, the justificationfor including tri-phenyl phosphate in the list of prescribeddiseases was critically examined. Experimental work showed considerabledifference in animal specificity with these two aryl phosphates—thehen (the most suitable experimental animal with the clinicalpicture of delayed neurotoxicity similar to that in man) beingsensitive to tri-cresyl phosphate and insensitive to tri-phenylphosphate, whilst the reverse was true in the case of the monkey.The threshold limit value (TLV) of tri-phenyl phosphate (TPP)is 30 times that of tri-cresyl phosphate (TCP). It had previouslybeen reported that a group of men working for a period of over10 years with TPP at atmospheric levels of more than 30 timesthat of the tri-cresyl phosphate TLV and reaching peaks at timesof over 400 times, showed no clinical effects. No human caseof poisoning with tri-phenyl phosphate on its own has ever beenreported Requests for reprints should be addressed to: Dr Alan A. Morgan, 37 Holcombe Road, Ilford, Essex IG1 4XF     

Summary review of the health effects associated with phenol

Phenol, a monohydroxy derivative of benzene, occurs naturally in animal waste and by decomposition of organic wastes. It is also produced by man, originally by fractional distillation of coal tar, but more recently by cumene hydroperoxidation and toluene oxidation. As a result of large production volume and natural sources, occupational and environmental exposure to phenol is likely. Phenol poisoning can occur by skin absorption, vapor inhalation, or ingestion, and, regardless of route of exposure, can result in detrimental health effects. Acute toxicity has been observed in man and experimental animals, resulting in muscle weakness, convulsions, and coma. In addition, studies have shown that although teratogenic effects have not been associated with exposure to phenol by either inhalation or oral route, high doses of phenol are fetotoxic. This paper addresses these studies and others in an attempt to determine if human health is at risk to those levels of phenol present in the environment and workplace. However, because data are limited, further research is necessary to analyze the mutagenic and carcinogenic potential of this chemical.     

Sources, symptoms, and signs of arsenic poisoning

Arsenic poisoning continues to be a serious medical problem that may easily be overlooked or misdiagnosed. The broad constellation of symptoms and signs in arsenic poisoning, along with changing sources of this toxin, contributes to misdiagnosis. A re-examination of current potential sources was carried out. Sources were determined in 17 of 20 documented cases of arsenic poisoning. Fourteen cases resulted from ingestion of a single, commonly available, arsenic-containing ant killer. In contrast to earlier reports, this survey found that agricultural and industrial sources were relatively uncommon. A peculiar posturing of the hand is commonly seen in the early stages of arsenic poisoning prior to the development of Mee's lines or palmar hyperkeratosis. An illustrative case is reported that resulted from intermittent self-administration of an arsenic-containing ant killer in order to maintain a state of chronic invalidism.     

Effects of Chronic Dieldrin Ingestion on the Muscular Efficiency of Rats

Several cases of dieldrin poisoning were reported amongst sprayers following repeated exposure to this insecticide. The symptoms developed by some of the most severe cases of poisoning included epileptiform convulsions.

The effect of dieldrin on muscular efficiency of rats was studied. A state of chronic toxicity was produced by maintaining two groups of rats on a diet containing 25 p.p.m. and 50 p.p.m. of dieldrin respectively. A third group receiving a diet containing no dieldrin acted as a control. Muscular efficiency was measured by training the rats to pull weights of increasing magnitude in a 250 cm. runway. The time taken to pull the weights through the standard distance was recorded.

Dieldrin appeared to have no effect on body weight, food intake, or learning, but muscular efficiency (as measured here) seemed to be affected by this compound. A progressive deterioration in muscular efficiency was observed, and was related to the amount of dieldrin administered. Although the nature of the deterioration cannot be deduced from this study, the results obtained here suggest possible lines of investigating the early effects on human beings of exposure to dieldrin.

     

Inclusion Body Myositis: A Case of Bilateral Extremity Weakness

Inflammatory myopathy is a common cause of bilateral muscular weakness in adults. Although not as common as polymyositis, inclusion body myositis (IBM) is a form of inflammatory myopathy characterized by chronic progressive muscle inflammation and often goes undiagnosed and untreated. IBM patients most commonly present with proximal lower extremity weakness and may have normal creatine kinase (CK) levels. A high level of clinical suspicion is required for prompt and accurate diagnosis of IBM, which is diagnosed definitively with a muscle biopsy. The patient described in this case report is a 68-year-old man who initially presented with both bilateral symmetric proximal lower extremity and distal upper extremity weakness. IBM was suspected through history, electromyography, and definitively diagnosed with muscle biopsy. The patient was subsequently initiated on prednisone therapy and physical therapy, with improvement in muscular strength after 2 months. In patients presenting with bilateral extremity weakness and normal CK level, the diagnosis of IBM should be included in the differential diagnosis and muscle biopsy performed for appropriate cases.     

Oliva vidua fulminans, a marine mollusc, responsible for five fatal cases of neurotoxic food poisoning in Sabah, Malaysia

This is the first report in which a marine mollusc, Oliva vidua fulminans (olives), generally not known to be poisonous, was responsible for death in five children after consuming boiled olives with tamarind. The onset of symptoms was rapid 10 to 20 min after consumption of the olives. Signs and symptoms included nausea, vomiting, abdominal pain, tingling sensation around the lips, numbness around the mouth, drowsiness, lethargy and generalized weakness with paraesthesia in the limbs. The five deaths occurred within 3 to 4 hours after eating the poisoned olives and resulted from respiratory failure. Left-over olives from the affected household and freshly collected live olives had a toxicity of 14,200 mouse units (M.U.) and 15,000 M.U. per 100 g meat respectively. No other common chemical poison and organophosphorus insecticides were detected. The neurotoxic agent was acid and heat stable and was toxic at pH less than 4. Its action was similar to that of paralytic shellfish poisoning which was caused by toxins from certain dinoflagellates.     

117例百草枯中毒患者预后与相关影响因素的分析

目的 通过分析百草枯中毒患者的预后及其相关影响因素,明确决定预后的重要因素,为急性百草枯中毒患者的病情评估、预后判断及治疗方案制定提供参考依据,并为探索更加有效的治疗手段建立基础.方法 纳入2010年6月～2011年11月期间因口服百草枯中毒就诊于某院急诊科的117例患者,入院时检测治疗前血浆百草枯浓度并给予洗胃、导泻、血液灌流、免疫抑制剂和抗氧化等治疗.采用Kaplan-Meirer单因素分析及Cox回归模型分析来判断年龄、口服剂量、服毒至洗胃时间、服毒至血液灌流时间、血液灌流次数、治疗前血中百草枯浓度等6项相关因素与患者预后的关系.结果 117例患者随访1月后有54人死亡,死亡率46.15％;死亡组与存活组两组间除口服百草枯剂量、治疗前血浆百草枯浓度以及血液灌流次数的差异有统计学意义(P＜0.05)外,在年龄、服毒至洗胃时间、服毒至血液灌流时间上差异均无统计学意义(P＞0.05);采用生存分析发现服毒剂量和血浆百草枯浓度两项指标对患者预后有显著影响,差异有统计学意义(P＜0.05).结论 百草枯口服剂量及血浆百草枯浓度是决定百草枯中毒患者是否能够存活的独立预后因素,而其他4项指标不能改变百草枯中毒患者的预后.     

A review of the health effects of ingested asbestos.

Occupational studies indicate that a human health hazard may exist for ingested asbestos since the death rates due to digestive system cancers are elevated in asbestos workers. This finding may be related to the swallowing of asbestos that was inhaled and cleared from the respiratory system via the respiratory clearance mechanism. Published animal ingestion experiments have serious shortcomings in their design and execution which make their interpretation very difficult. Animal ingestion and human autopsy studies suggest that asbestos fibers may penetrate the digestive tract and migrate to other locations in the body.     

Multidose activated charcoal in the treatment of carbamazepine overdose with seizures: a case report

Serious complications after carbamazepine poisoning, such as coma, seizures, respiratory failure, cardiac conduction abnormalities, and death are more likely with serum levels greater than 170 micromol L(-1). We report a case of a single massive carbamazepine overdose in a 19-year-old male, following attempted suicide, without prior history of seizure disorder. On admission, three hours after ingestion, serum carbamazepine concentration was 179 micromol L(-1) and Glasgow Coma Scale scored 6. The patient was intubated and treated with multiple doses of activated charcoal for 48 hours. Twelve hours after ingestion, two repeated generalised myoclonic seizures were noted when serum carbamazepine levels peaked at 181 micromol L(-1), and were successfully treated with diazepam. Carbamazepine serum level fell within the therapeutic range 63 hours after ingestion and the patient was discharged without any long-term sequelae. As there is no antidote for carbamazepine poisoning, supportive treatment remains the only, but usually potent option.