Bilateral peripheral facial nerve palsy in acute poisoning with ethylene glycol

Acute poisonings with polyethylene glycol become more and more frequent. The acute poisoning with polyethylene glycol leads to a considerable metabolic acidosis and acute renal failure. Usually there is no peripheral nervous system involvement. Two cases of the bilateral facial nerve palsy in patients with renal failure due polyethylene glycol poisoning are presented. It seems that it is the first report on the lesions to facial nerve involvement in the course of the acute polyethylene glycol poisoning.     

Mushroom Poisoning in Canada: Report of a Fatal Case

At least 150 cases of mushroom poisoning occur in Canada each year, 75% in the Province of Ontario. Eighty per cent of the total are in children under the age of 9, and most do not require hospitalization. Amanita virosa poisoning is a potentially fatal medical emergency which presents as an acute gastroenteritis, progressing to hepatorenal failure. Treatment consists of elimination of undigested mushrooms, rapid rehydration, management of acute liver and renal failure, and prevention of infection during the recovery phase.     

Acute Paracetamol Poisoning

Of 41 cases of acute paracetamol poisoning one died of gastrointestinal haemorrhage and acute massive necrosis of the liver, three became jaundiced, and 13 others had biochemical evidence of hepatocellular damage. Liver damage is a toxic effect which is present in most patients who ingest more than 15 g. of paracetamol. One patient with liver damage survived renal failure due to acute tubular necrosis. It is suggested that the renal lesion was also the result of paracetamol overdosage.Profound hypoglycaemia and metabolic acidosis may also complicate severe poisoning. Plasma levels of para-aminophenol fall rapidly, and procedures currently used to enhance the elimination of the drug cannot be expected to prevent development of hepatic damage.     

华南常见毒鹅膏菌及其中毒事件分析

根据文献报道和实际调查对华南地区的有毒鹅膏种类进行统计分析,确认了21种常见有毒鹅膏菌,包括急性肝脏损害型的剧毒鹅膏、急性肾脏损害型和神经精神型的毒鹅膏各7种。对2000-2019年20年间发生的有毒鹅膏中毒事件进行统计分析显示,华南地区有毒鹅膏中毒事件共发生45起,163人中毒,60人死亡,病死率为36.8%;毒鹅膏的中毒事件主要发生在3-9月,其中3月份最多。致命鹅膏Amanita exitialis引起的中毒起数、中毒人数和中毒死亡率均占中毒事件总数的70%左右,是华南毒蘑菇中毒的“头号杀手”。本研究对华南地区毒蘑菇中毒的科学精准防控、有效减少中毒事件的发生、以及降低中毒死亡率具有重要意义。     

Carbon monoxide poisoning

Carbon monoxide poisoning is a significant cause of illness and death. Its protean symptoms probably lead to a gross underestimation of its true incidence. Low levels of carbon monoxide aggravate chronic cardiopulmonary problems, and high levels are associated with cardiac arrhythmias and cerebral edema. Patients who survive acute poisoning are at risk of delayed neurologic sequelae. The measurement of carboxyhemoglobin levels does not reveal the tissue levels of carbon monoxide but is useful in determining therapy. Treatment includes the monitoring and management of cardiac arrhythmias and oxygenation. Hyperbaric oxygenation is beneficial, but there are currently no definite criteria for its use.     

Morbidity from Acute Carbon Monoxide Poisoning at Three-year Follow-up

Seventy-four survivors of acute carbon monoxide poisoning were followed up for an average of three years. In eight patients gross neuropsychiatric damage was directly attributable to the poisoning. Three patients had committed suicide and eight had died from other causes. Morbidity and mortality in those deliberately and accidentally poisoned was approximately equal.Of 63 patients alive at follow-up eight showed an improvement and 21 (33.3%) a deterioration of personality after poisoning, and 27 (43%) reported a subsequent impairment of memory. Deterioration of personality and memory impairment were highly correlated. The level of consciousness on admission to hospital in the acute phase of poisoning correlated significantly with the development of gross neuropsychiatric sequelae. These findings emphasize the importance of prompt and efficient treatment of carbon monoxide poisoning and the need to follow-up all cases in the anticipation of a relapsing course or the development of sequelae.     

Outcome of Patients with Carbon Monoxide Poisoning at a Far-East Poison Center

Introduction

Many cases of carbon monoxide poisoning in Taiwan are due to burning charcoal. Nevertheless, few reports have analyzed the mortality rate of these patients who survive to reach a hospital and die despite intensive treatment. Therefore, this study examined the clinical features, physiological markers, and outcomes after carbon monoxide poisoning and the associations between these findings.

Methods

We analyzed the records of 261 patients who were referred for management of carbon monoxide intoxication between 2000 and 2010. Patients were grouped according to status at discharge as alive (survivor, n = 242) or dead (non-survivor, n = 19). Demographic, clinical, laboratory, and mortality data were obtained for analysis.

Results

Approximately half of the cases (49.4%) attempted suicide by burning charcoal. Most of the patients were middle-aged adults (33±19 years), and were referred to our hospital in a relatively short period of time (6±10 hours). Carbon monoxide produced many serious complications after exposure: fever (26.1%), hypothermia (9.6%), respiratory failure (34.1%), shock (8.4%), myocardial infarction (8.0%), gastrointestinal upset (34.9%), hepatitis (18.4%), renal failure (25.3%), coma (18.0%) and rhabdomyolysis (21.8%). Furthermore, the non-survivors suffered greater incidences of hypothermia (P<0.001), respiratory failure (P<0.001), shock (P<0.001), hepatitis ((P=0.016), renal failure (P=0.003), coma (P<0.001) than survivors. All patients were treated with high concentration of oxygen therapy using non-rebreather mask. However, hyperbaric oxygen therapy was only used in 18.8% of the patients. In a multivariate-Cox-regression model, it was revealed that shock status was a significant predictor for mortality after carbon monoxide poisoning (OR 8.696, 95% CI 2.053-37.370, P=0.003). Finally, Kaplan-Meier analysis confirmed that patients with shock suffered greater cumulative mortality than without shock (Log-rank test, Chi-square 147.404, P<0.001).

Conclusion

The mortality rate for medically treated carbon monoxide-poisoned patients at our center was 7.3%. Furthermore, the analysis indicates that shock was most strongly associated with higher risk of mortality.     

DNA Pooling Base Genome-Wide Association Study Identifies Variants at NRXN3 Associated with Delayed Encephalopathy after Acute Carbon Monoxide Poisoning

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is more characteristic of anoxic encephalopathy than of other types of anoxia. Those who have the same poisoning degree and are of similar age and gender have a greater risk of getting DEACMP. This has made it clear that there are obvious personal differences. Genetic factors may play a very important role. The authors performed a genome-wide association study involving pooling of DNA obtained from 175 patients and 244 matched acute carbon monoxide poisoning without delayed encephalopathy controls. The Illumina HumanHap 660 Chip array was used for DNA pools. Allele frequencies of all SNPs were compared between delayed encephalopathy after acute carbon monoxide poisoning and control groups and ranked. A total of 123 SNPs gave an OR >1.4. Of these, 46 mapped in or close to known genes. Forty-eight SNPs located in 19 genes were associated with DEACMP after correction for 5% FDR in the genome-wide association of pooled DNA. Two SNPs (rs11845632 and rs2196447) locate in the Neurexin 3 gene were selected for individual genotyping in all samples and another cohort consisted of 234 and 271 controls. There were significant differences in the genotype and allele frequencies of rs11845632 and rs2196447 between the DEACMP group and controls group (all P-values <0.05). This study describes a positive association between Neurexin 3 and controls in the Han Chinese population, and provides genetic evidence to support the susceptibility of DEACMP, which may be the resulting interaction of environmental and genetic factors.     

云南蘑菇中毒事件中的毒蘑菇物种多样性

近年来,云南省每年发生超过500起蘑菇中毒事件,造成2 000余人中毒,约30人死亡,成为我国蘑菇中毒危害最为严重的省份。系统研究蘑菇中毒事件中的毒蘑菇多样性,可以为蘑菇中毒精准防控提供科学依据和技术支撑。本研究对云南省2013年以来开展过科学物种鉴定的223起中毒事件进行了系统分析,发现云南省蘑菇中毒一年四季均有发生,主要集中在6-9月份,中毒事件数和中毒人数7月份达到高峰,而6月份死亡人数最多。地区分布分析发现云南省蘑菇中毒事件涉及14个市州,中毒事件数前5位分别为德宏、玉溪、保山、楚雄和普洱,均位于云南中部及以南地区。223起中毒事件中共成功鉴定出47种毒蘑菇,分属6种中毒类型(急性肝损害型、急性肾衰竭型、横纹肌溶解型、胃肠炎型、神经精神型和光敏性皮炎型)。这些毒蘑菇包含发现于中国的新物种16种,以及2019年以来发现的中国新记录种3种。致命鹅膏Amanita exitialis和亚稀褶红菇Russula subnigricans分别造成19人和9人死亡,是云南省最危险的2种剧毒蘑菇。青褶伞Chlorophyllum molybdites、日本红菇R. japonica、光硬皮马勃Scleroderma cepa、近江粉褶菌Entoloma omiense和发光类脐菇Omphalotus olearius位列胃肠炎型中毒的前5位。热带紫褐裸伞Gymnopilus dilepis、毒歧盖伞近似种Inosperma cf. virosum和兰茂牛肝菌Lanmaoa asiatica位列神经精神型中毒的前3位。叶状耳盘菌Cordierites frondosus是目前云南省造成光敏性皮炎型中毒的唯一物种。     

代谢组学在一氧化碳中毒研究的应用和展望

一氧化碳中毒是常见的以中枢神经系统损害为主的全身性疾病。一氧化碳作为一个脂溶性分子,进入细胞内造成组织缺氧。一氧化碳是否可以诱导产生其他特定的生物学效应,还需要我们去研究。代谢组学是继基因组学、转录组学、蛋白质组学后的又一新兴学科,在肿瘤、糖尿病、冠心病、肥胖症、脑卒中等多种临床疾病的相关研究中显示出巨大的潜力。将代谢组学技术应用到一氧化碳中毒研究中,可以加深对一氧化碳中毒发病机制的认识,丰富早期诊断方法,改善治疗效果的监测手段。但代谢组学技术在一氧化碳中毒研究中的应用仍是凤毛麟角,我们在此对代谢组学在一氧化碳中毒研究中应用及前景作一展望。     

The role of hepatic glycogen stores in anaerobic metabolism in rats

Plasma levels of lactate and oxypurines markedly increased in both fed and fasted rats exposed to three acute anoxic states, cyanide poisoning, carbon monoxide poisoning and inhalation of oxygen-deficient gas, suggesting that the transition of aerobic to anaerobic metabolism occurred similarly in both groups. Plasma glucose level of fed rats increased 1.8-2.5 times after exposure to anoxia, whereas a remarkable hypoglycemia was induced by the exposure of fasted rats to anoxia. Hepatic glycogen stores in fed rats induced hyperglycemia, while exhaustion of the stores in fasted rats resulted in severe hypoglycemia during acute anoxia.     

七叶皂苷钠对一氧化碳中毒迟发性脑病大鼠模型细胞凋亡 及调控凋亡基因表达的影响

目的:探讨七叶皂苷钠对一氧化碳中毒迟发性脑病大鼠模型细胞凋亡及Caspase-3表达的影响。方法:将30只大鼠随机分为正常对照组、一氧化碳中毒迟发性脑病大鼠模型对照组和七叶皂苷钠治疗组,原位末端标记法(TUNEL)检测细胞凋亡,免疫组化法检测Caspase-3的表达。结果:治疗组大鼠脑细胞凋亡率及Caspase-3表达较迟发性脑病对照组显著降低(P<0.01)。结论:七叶皂苷钠对一氧化碳中毒迟发性脑病的脑保护作用机制可能与干预脑细胞凋亡相关基因表达并减少神经细胞凋亡有关。     

A Resting-State Functional Magnetic Resonance Imaging Study of Acute Carbon Monoxide Poisoning in Humans

The objective of this study was to evaluate the brain function characteristics of carbon monoxide poisoning patients using resting-state functional magnetic resonance imaging (fMRI) method. For this purpose, 12 carbon monoxide poisoning patients and healthy controls were subjected to resting-state fMRI scans separately. A regional homogeneity (ReHo) approach was used to analyze the brain function in carbon monoxide poisoning patients. Compared with control group, the value of ReHo in carbon monoxide poisoning group showed distinct decrease in bilateral superior frontal gyrus, middle frontal gyrus, right cuneus, left middle temporal gyrus, right insula, and cerebellum. Therefore, it was concluded that the brain functions in carbon monoxide poisoning patients were abnormal under the resting-state. The cuneate lobe function may indicate the degree of brain hypoxia and strengthening the cerebellar function training may promote the rehabilitation process.     

急性一氧化碳中毒131例临床分析

目的：探讨急性一氧化碳中毒（ACOP）患者的发病特点、临床表现及其对预后的影响。方法：回顾性分析2006年1月一2011年12月我院收治的131例ACOP患者,将其按病情的严重程度分为轻、中、重度3组,比较各组的发病原因和临床表现。结果：接触时间、基础疾病、血清肌酸激酶（CK）、昏迷时间在3组间差异有显著性（P〈0．01）,年龄、性别、中毒原因方面3组间差异无显著性（P〉0．05）。迟发性脑病组和无迟发性脑病组在年龄、基础疾病、并发症、接触时间、昏迷时间、CK方面差异有显著性（P〈0．01）;而在性别、中毒原因方面差异无显著性（P〉0．05）。结论：对于ACOP患者而言,接触时间长、伴有基础疾病、昏迷时间长、CK高不仅提示病情的严重程度,更是迟发性脑病的易患因素。而高压氧治疗是ACOP的首选及有效的治疗方法。     

The role of reactive oxygen species and oxidative stress in carbon monoxide toxicity: An in-depth analysis

Abstract

The underlying mechanism of the central nervous system (CNS) injury after acute carbon monoxide (CO) poisoning is interlaced with multiple factors including apoptosis, abnormal inflammatory responses, hypoxia, and ischemia/reperfusion-like problems. One of the current hypotheses with regard to the molecular mechanism of CO poisoning is the oxidative injury induced by reactive oxygen species, free radicals, and neuronal nitric oxide. Up to now, the relevant mechanism of this injury remains poorly understood. The weakening of antioxidant systems and the increase of lipid peroxidation in the CNS have been implicated, however. Accordingly, in this review, we will highlight the relationship between oxidative stress and CO poisoning from the perspective of forensic toxicology and molecular toxicology.     

Unerwartete Kohlenmonoxid‐Gefahren

Unexpected carbon monoxide poisonings The poisonous gas carbon monoxide (CO) is not only produced as a result of combustion processes but can also be inhaled during the operation of barbecues, the smoking of water pipes, or in wood pellet stores. Inhalation of carbon monoxide can lead to life‐threatening or chronic poisoning. The present article provides information on the formation and effects of CO in domestic settings, and gives advice on how instances of poisoning can be avoided.     

HBO治疗对急性CO中毒后海马不同分区神经细胞凋亡的作用研究

目的:通过研究高压氧(HBO)治疗急性CO中毒大鼠海马不同分区神经细胞凋亡情况,探讨HBO治疗急性CO中毒的应用及机理。方法:利用雄性SD大鼠,建立急性CO中毒模型。应用免疫组织化学以及免疫荧光的方法,测定在染毒和CO中毒HBO治疗后1 d、3 d、7 d、14 d和21d Bcl-2、caspase-3、Neu N、BAX和MMP-9的表达水平的变化。结果:海马CA3区神经细胞对急性CO中毒与HBO治疗比CA1和CA2区更加敏感;急性CO中毒后,海马各区神经细胞凋亡程度随1 d、3 d、7 d、14 d和21 d时间延长而加重;BAX、caspase-3和Bcl-2等凋亡相关因子的表达水平与MMP-9的变化趋势一致:在1d开始增多,3d达到最大值,7d开始减少,14 d与21 d与正常组类似;CO中毒大鼠进行HBO治疗后,海马各区MMP-9、BAX、caspase-3和Bcl-2的表达水平明显降低;且HBO治疗7 d后,海马各区这些凋亡相关因子的表达降低最为明显。结论:海马CA3区神经细胞对急性CO中毒及HBO治疗敏感;海马神经细胞凋亡可能与神经细胞表达MMP-9降解神经细胞周围的基质,表达BAX、caspase-3和Bcl-2等凋亡相关因子促进凋亡发生有关;HBO治疗可降低MMP-9以及BAX、caspase-3和Bcl-2等凋亡因子的表达,抑制神经细胞的凋亡;HBO治疗7d对神经细胞凋亡的抑制作用最明显。     

复方丹参对急性汞中毒家兔的保护作用及其机制

目的:探讨复方丹参对急性汞中毒家兔的保护作用及其机制。方法:采用皮下注射1%氯化高汞(Hg-Cl2,1.7ml/kg)溶液,复制家兔急性汞中毒的动物模型。动态观察血尿素氮(BUN)、血浆铜蓝蛋白(CP)、乳酸脱氢酶(LDH)、酸性磷酸酶(ACP)、丙二醛(MDA)及红细胞超氧化物歧化酶(SOD)含量的变化;检测肾皮质、肺、肝、心及脾脏组织匀浆MDA、SOD的含量;同时检测尿蛋白和尿沉渣;并与丹参处理组和生理盐水对照组比较。结果:注射HgCl2后0.5h和9.5h分别给予复方丹参注射液2ml/kg,可使BUN、CP、LDH、ACP及MDA含量降低,且可防止SOD减少,各项指标与汞中毒组比较均有统计学意义(P0.05,P0.01);尿蛋白和尿沉渣中的管型也明显减少。结论:急性汞中毒后不仅损害肾脏,而且累及多个器官组织。复方丹参能通过稳膜作用减轻或在一定程度上防止急性汞中毒过程的进行性加剧。     

Should patients with renal failure associated with myeloma be dialysed?

In a study of renal function in multiple myeloma seven patients presented with renal failure and three developed it 16-106 months after diagnosis. All were dialysed. Infection with dehydration was a precipitating factor in all seven cases of acute or acute on chronic renal failure. Of these, two patients recovered normal renal function and one other was left with permanent renal impairment but no longer required dialysis. Results from the seven patients with acute renal failure and for the three with more chronic features support the practice of dialysis for all patients who present with renal failure. Dialysis is not indicated for those patients with progressive myelomatous disease. The study showed no evidence that chemotherapy permitted recovery from established renal failure. The prognosis in this elderly group is heavily dependent on the presence of cardiovascular or other degenerative disease.     

Renal failure in otherwise uncomplicated acute viral hepatitis.

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.