How Reliable are Parenchymal Tissues for the Evaluation of Carbon Monoxide Poisoning? A Pilot Study

Dealing with burnt bodies, the forensic pathologist must first of all answer the question whether the victim was alive at the moment of the fire. This study aims at clarifying whether some human solid tissues may be reliably used for the forensic diagnosis of Co poisoning on burnt bodies providing no collectable blood during the autopsy. From 34 selected cases, both cardiac blood and parenchymal samples were collected to perform CO‐oxymeter, spectrophotometry, and gas chromatography tests: blood CO estimations (blood COHb% and blood[CO]) and parenchymal[CO] values have been compared with special focus on R values. The solid tissues having the best correlations with blood CO amount turned out to be the lung (R 0.84), the liver (R 0.83), the kidney (R 0.79), and the spleen (R 0.92).     

不同来源一氧化碳中毒死亡者血液中COHb含量分析

目的探索一氧化碳中毒存在的个体差异性,分析女性可能存在的抵御一氧化碳中毒的机制。方法收集207例不同来源的一氧化碳中毒死亡者血液,测量COHb含量,将案例按照不同的因素分类进行统计学分析。结果不同一氧化碳的来源对于死者的COHb浓度影响显著,而性别对于COHb浓度影响不显著,少年儿童和老年人有可能对COHb的抵御能力差于成年人。     

Subarachnoid Hemorrhage and Carbon Monoxide Exposure: Accidental Association or Fatal Link?

This case study reports a fatal subarachnoid hemorrhage (SAH) with concomitant accidental carbon monoxide (CO) exposure in 32‐year‐old man. Autopsy results indicated an antemortem aspiration of smoke, and a massive SAH was identified as the cause of death. Intriguingly, the carboxyhemoglobin level was 30%, suggesting that CO could have played a specific role. Intracranial hemorrhages following CO exposure in brain areas and tissues such as the basal ganglia, globus pallidus, or white matter are rare, but well characterized, whereas SAH related to CO exposure has not been previously described. In this case report, the possible role of CO, either as a primary cause or as a facilitating factor, in the pathogenesis of SAH is discussed. In particular, we propose the hypothesis that the excessive vasodilating effects produced by CO on the cerebral endothelium results in consequential loss of microvascular integrity.     

大鼠血液中HbCO随吸入CO浓度和时间的变化

目的研究不同一氧化碳(carbon monoxide,CO)浓度下中毒大鼠的行为学特征、存活时间、碳氧血红蛋白(carboxyhemoglobin,HbCO)饱和度变化规律,为法医学实践中CO中毒死亡案件提供实验依据。方法将160只SD大鼠随机分为4组。自制染毒装置,使大鼠分别在CO浓度为1 250、3 750、6 250 mg/m~3及持续通入CO状态下染毒致死亡。观察不同CO浓度中毒大鼠的行为学特征,记录存活时间,采用分光光度法检测心血HbCO饱和度,并提取脑、心脏、肺、肝等器官进行组织病理学观察。结果 CO中毒大鼠的行为学特征表现为肢体瘫软、反应迟钝。随着CO浓度的升高,大鼠存活时间逐渐缩短,心血HbCO饱和度逐渐升高。在CO浓度为1 250 mg/m~3条件下,发现3例心血HbCO饱和度明显低于致死饱和度,其余各组未发现心血HbCO饱和度低于致死饱和度的情况。结论建立的不同浓度下CO中毒死亡动物模型,操作简单,重复性好,为进一步研究CO中毒及其他吸入性有毒气体的法医学研究奠定了基础。     

Poisoning deaths in Central China (Hubei): A 10-year retrospective study of forensic autopsy cases

A retrospective study of autopsy cases was conducted at the Department of Forensic Medicine, Tongji Medical College (DFM-TMC), in Hubei, China to describe the characteristics of poisoning deaths from 1999 to 2008. A total of 212 poisoning deaths were investigated by DFM-TMC during the 10-year period. The poisoning deaths ranged from 17 cases in 1999 to 27 cases in 2008. Of the 212 cases, 82 deaths (38.7%) were from pesticides, 36 deaths (17.0%) from carbon monoxide, 34 deaths (16.0%) from drugs, 22 deaths (10.4%) from alcohol, 17 deaths (8.0%) from other chemicals, 15 deaths (7.1%) from poisonous plants and animals, and six deaths (2.8%) from heavy metals. Of the 82 pesticide poisoning deaths, 43 (52.4%) cases were caused by rodenticides, mainly tetramine (N = 39). The majority of poisoning deaths were accidents (63.7%), followed by suicides (25.9%) and homicides (3.8%). The manner of death could not be determined in 14 cases (6.6%).     

54例氯化琥珀胆碱中毒案件的法医学分析

目的观察分析氯化琥珀胆碱中毒案件的法医学表现,以期提高氯化琥珀胆碱中毒的检验鉴定。方法收集54例氯化琥珀胆碱中毒案例,通过病理学、毒理学变化及案件特点进行回顾性分析,观察氯化琥珀胆碱中毒的检验鉴定规律。结果氯化琥珀胆碱中毒的病理学表现以急性肺淤血、肺水肿等一般猝死改变为主,部分死者心肌排列紊乱及断裂。死者心血中均检见琥珀胆碱成分,皮肤组织部分检见琥珀胆碱成分。结论氯化琥珀胆碱中毒具有死亡快、手段隐蔽、难以抢救、易漏检等特点。对于猝死案件、死因可疑案件应将氯化琥珀胆碱作为常规检验指标,防止此类案件的未检或漏检。     

Accidental boric acid poisoning following the ingestion of household pesticide

Borate-containing compounds were formerly used as topical antiseptics and were components of many medicinal preparations including skin powders and ointments used for the treatment of burns and diaper rash. These compounds were also used as irrigants for body cavities, including the pleural, vaginal, and rectal cavities. These applications were subsequently discontinued by the medical community when the toxicity and potential lethality of borates were recognized. Although documented cases of borate poisoning are now rare, the chemical is still an active component commonly used in high concentrations in household disinfectants/cleaners, pesticides, and wood preservatives. While the majority of documented borate-related deaths have occurred in infants, the toddler population is currently at risk due to possible exposure to these household products. We present the case of an 18-month-old child who died following the accidental ingestion of a boric acid-containing, commercially available roach pesticide product.     

Diesel fumes do kill: a case of fatal carbon monoxide poisoning directly attributed to diesel fuel exhaust with a 10-year retrospective case and literature review*

While it is known that diesel fuel combustion engines produce much lower concentrations of carbon monoxide (CO) than gasoline engines, these emissions could certainly generate lethal ambient concentrations given a sufficient amount of time in an enclosed space and under suitable environmental conditions. The authors report a case of CO poisoning which was initially referred for autopsy as a presumed natural death of a truck driver found in the secure cab of a running diesel tractor trailer truck. Completion of the preliminary investigation ascribed death to complications of ischemic heart disease (IHD), pending toxicological analysis that included quantification of CO. When the toxicology results showed lethal blood COHbg, the cause of death was re-certified as CO intoxication secondary to inhalation of (diesel) vehicular exhaust fumes. Because of the unique source of fatal CO intoxication in this case, the contributory IHD and the possible contaminants in the putrefied blood, a 10-year retrospective review was conducted on all nonfire related CO deaths autopsied (n = 94) at the Office of the Chief Medical Examiner in Louisville, KY from 1994 to 2003. For validation of the COHbg detection method used by the Kentucky Office of Forensic Toxicology (KYOFT), blood samples from these cases along with controls were submitted to three laboratories using various analytical methods yielding no statistically significant differences. Lastly, an extensive literature review produced no scientifically reported cases of fatal CO poisoning attributed to diesel fuel exhaust.     

Concentration of carbon monoxide (CO) in postmortem human tissues: effect of environmental CO exposure

We studied how carbon monoxide (CO) is distributed within the human body through quantitation of CO concentrations in postmortem tissue samples from fatalities including possible CO exposure. Stored, frozen tissues were diced, sonicated in water, and 0.01-8.0 mg wet weight (ww) tissues were incubated with sulfosalicylic acid in CO-purged, septum-sealed vials. CO released into the headspace was quantitated by reduction gas chromatography. Mean tissue CO concentrations (pmol/mg ww) from subjects diagnosed to have no known CO exposure (control, N=14), died from fire (N=13), and CO asphyxiation (N=7), respectively, were: adipose (2;13;9), brain (3;13;65), muscle (15;97;297), heart (30;99;371), kidney (22;432;709, lung (54;690;2638), spleen (73;1366;3548), and blood (162;2238;5070). Carboxyhemoglobin concentrations were 1.4%, 25.2%, and 69.1% of total hemoglobin, respectively. We conclude that measurements of CO concentration in a variety of tissues can be used as markers for the degree of exogenous CO exposure and the identification of possible causes of death.     

甲维盐中毒死亡小鼠体内的分布及死后再分布

目的研究甲氨基阿维菌素苯甲酸盐(简称甲维盐)中毒死亡小鼠的致死血浓度、靶器官组织、毒物蓄积库和死后毒物再分布的特征。方法采用灌胃法建立中毒小鼠模型,动态观察急性中毒组、亚急性中毒组小鼠的主要中毒症状和临床死亡时间。观察中毒死后小鼠各器官组织病理形态学改变,应用酶联免疫吸附试验测定死后0、24、48、72h甲维盐体内分布及死后再分布,采用高效液相色谱法测定中毒小鼠的致死血浓度和死后各时间点的血中甲维盐浓度。结果中毒小鼠均在灌胃后15~30 min内依次出现神经、呼吸系统症状。急性中毒组小鼠的临床死亡时间为(45.8±7.9)min,亚急性中毒组为(8.0±1.4)d。甲维盐的急性致死血浓度范围为447.164 0~524.463 5 mg/L。光镜及荧光显微镜下各器官组织均见明显的病理改变;小鼠中毒死后72 h内,血、心、肝、脾、肺、肾及脑甲维盐浓度变化具有规律性(P0.05)。结论甲维盐中毒作用的主要靶器官为心、肝、肾、肺、脑和接触部位(胃),其主要蓄积库为肾、肝,甲维盐在小鼠体内存在死后再分布现象。     

The forensic deaths caused by pesticide poisoning between the years 2006 and 2009 in Izmir, Turkey

Pesticide poisoning is still a significant health problem in Turkey. We conducted a retrospective study of autopsy cases at Izmir Branch of the Council of Forensic Medicine to describe the characteristics of deaths caused by pesticide poisoning between 2006 and 2009. The distributions of the cases according to gender and age were as follows: men 74.1% (n = 40, mean [±SD] age, 44.7 ± 14.1), women 25.9% (n = 14, mean [±SD] age, 39.2 ± 18.9). The majority of pesticide-poisoning deaths were suicides (n = 43, 80%) followed by accidents (n = 4, 8%) and homicide (n = 1, 2%). The manner of death could not be determined in six cases (11%). Suicides mostly occurred at home (n = 26, 63%) (p < 0.05). Methomyl was the most frequent pesticide (n = 9, 17%) among the all cases. This study reported that most of the pesticides found in poisoning cases were highly hazardous types. Combined efforts of medical professionals and law makers are needed for enacting strict laws against highly hazardous pesticides.