Subway Train‐Related Fatalities in New York City: Accident versus Suicide*

Abstract: We examined the characteristics of subway train‐related fatalities in New York City between Jan. 1, 2003 and May 31, 2007 in order to determine which factors are useful in differentiating accident from suicide. Subway train‐related deaths with homicide and undetermined manners also are included. During this period, there were 211 subway train‐related fatalities. The manners of death were: suicide (n = 111), accident (n = 76), undetermined (n = 20), and homicide (n = 4). The causes of death were blunt trauma (n = 206) and electrocution (n = 5). Torso transection and extremity amputation were more frequent in suicides. Antidepressant medications were more frequently detected in suicides, whereas cocaine and ethanol were more frequent in accidents. However, autopsy findings should be weighed in the context of the entire evaluation along with other circumstantial and investigative findings. In unwitnessed deaths where additional information is unavailable or discrepant, the most appropriate manner of death usually is undetermined.     

Sevoflurane concentrations in blood, brain, and lung after sevoflurane-induced death

Sevoflurane concentrations in blood, brain, and lung were measured in an individual apparently dying from sevoflurane inhalation. Sevoflurane is a volatile nonflammable fluorinated methyl isopropyl ether inhaled anesthetic, chemically related to desflurane and isoflurane. The incidence of abuse of sevoflurane is lower than that of other drugs of abuse possibly due to its inaccessibility to the general public and less pleasurable and addicting effects. The dead subject was an anesthetist found prone in bed holding an empty bottle of sevoflurane (Ultane). Serum, urine, and liver were screened for numerous drugs and metabolites using enzyme immunoassays and gas chromatography-mass spectrometry. Analysis did not reveal presence of any drug, including ethanol, other than sevoflurane. Sevoflurane was determined by headspace gas chromatography and revealed concentrations of 15 microg/mL in blood and 130 mg/kg in brain and lung. Autopsy revealed pulmonary edema and frothing in the lung, pathological findings associated with death by sevoflurane or hypoxia. The cause of death was ruled as sevoflurane toxicity and the manner of death as accident.     

Use of "therapeutic complication" as a manner of death

Analyses of deaths due to therapeutic complications (TCs) provide important quality of care information for medical providers. In New York City, 463 deaths were investigated by the Office of Chief Medical Examiner and certified with TC as the manner of death in 2003. The TC manner of death is used for fatalities due to predictable complications of appropriate medical therapy. All death certificates and select autopsy, hospital, and investigation reports were reviewed. Data concerning cause of death, contributing conditions, age, race, and sex were extracted. The types of complications and the causes of death were classified into various types of surgical and nonsurgical categories of complications. These included: postoperative infections, pulmonary emboli, and technical and medication complications. The use of TC as a manner of death has benefits and limitations. Without the TC option, one is forced to certify certain deaths (e.g., penicillin anaphylaxis) either as natural or accident. The TC option allows easy identification and tracking of medical complications for public health purposes and also allows more consistent reporting of natural and medical-accidental deaths. In general, complications that occur during emergency surgeries/procedures for natural disease, tend to be certified with a natural manner. The "but for" test may be used to distinguish natural from TC deaths. There are criteria for distinguishing TC from accidents and homicides. TCs that occur during treatment of a potentially life-threatening injury, are superseded by the manner dictated by the circumstances of the initiating injury. The certification of TC usually does not address errors of omission, clinical judgement/management, or missed diagnoses.     

抗精神病药物致心源性猝死的机制及其法医学意义

精神障碍患者是由各种原因导致脑功能障碍并伴有一系列功能缺失和寿命缩短的群体,其死亡率为普通人群的2~5倍,且服用抗精神病药物导致猝死的发生率明显高于不服药者。大量案例报道和临床资料的回顾性研究表明,精神障碍患者发生心源性猝死风险与服用APs相关。本文简要介绍APs致心源性猝死的机制和危险因素,以期为法医学鉴定提供参考依据。     

Natural,Unexpected Deaths: Reliability of a Presumptive Diagnosis*

Abstract: We retrospectively analyzed 100 deaths because of suspicions and concerns expressed by the family. We compared the preautopsy cause of death, as determined by a thorough review of the clinical data and circumstances, to the autopsy‐derived cause of death. In the majority (91/100), the preautopsy and postautopsy proximate causes of death were in agreement. In 9%, the autopsy provided information that resulted in a proximate cause of death different than anticipated. In four instances, the manner of death also was incorrect and was determined to be an accident rather than the originally presumed natural. No homicide or suicide would have been misclassified. In another nine instances, where the premortem and postmortem proximate causes of death were in agreement, the autopsy provided a specific mechanism of death. With a quality initial medicolegal death investigation, a subset of sudden deaths in adults may be reliably certified without an autopsy.     

Postmortem detection of isopropanol in ketoacidosis

Isopropanol (IPA) detected in deaths because of diabetic ketoacidosis (DKA) or alcoholic ketoacidosis (AKA) may cause concern for IPA poisoning. This study addressed this concern in a 15-year retrospective review of 260 deaths in which concentrations of acetone and IPA, as well as their ratios, were compared in DKA (175 cases), AKA (79 cases), and IPA intoxication (six cases). The results demonstrated the frequency of detecting IPA in ketoacidosis when there was no evidence of IPA ingestion. IPA was detectable in 77% of DKA cases with quantifiable concentrations averaging 15.1 ± 13.0 mg/dL; 52% of AKA cases with quantifiable concentrations averaging 18.5 ± 22.1 mg/dL; and in cases of IPA intoxication, averaging 326 ± 260 mg/dL. There was weak correlation of IPA production with postmortem interval in DKA only (r = -0.48). Although IPA concentrations were much higher with ingestion, potentially toxic concentrations were achievable in DKA without known ingestion.     

死后生物化学在糖尿病酮症酸中毒法医学诊断中的应用

糖尿病酮症酸中毒是糖尿病患者一种处于高糖、高酮状态并且导致代谢失代偿的危险并发症。这类死者常规法医学检查无特异性表现,需要进行死后生物化学指标分析。死后生物化学是一种采集死者体液进行生物化学检测,从而判断死者生前的代谢状态进而明确死因的检查方法。本文综述了糖尿病酮症酸中毒死亡的基本情况、法医学检查表现,并着重阐述运用于诊断糖尿病酮症酸中毒的死后生化指标,从而总结糖尿病酮症酸中毒死亡的法医学诊断思路。     

Vitality and wound-age estimation in forensic pathology:review and future prospects

Determining the age of a wound is challenging in forensic pathology,but it can contribute to the reconstruction of crime scenes and lead to arrest of suspects.F...     

The Role of Postmortem Cardiac Markers in the Diagnosis of Acute Myocardial Infarction*

Abstract: Sudden cardiac deaths because of acute myocardial infarction (MI) constitute a significant percentage of the caseload for death investigators, coroners, and forensic pathologists. Clinicians use cardiac markers, highly sensitive and specific for myocardial damage, to screen living patients for acute MI; however, to this point, the utility of these markers in the autopsy setting has not been fully established. The current study included 10 decedents, five who died of acute MI, and five subjects who died of noncardiac disease. Samples of pericardial fluid and blood from multiple sites were tested for creatine kinase, creatinine kinase MB, and troponin‐I. Three main conclusions were drawn: the levels of cardiac markers from all patients are significantly higher than the reference range for living patients, there are significant differences in cardiac marker levels between samples from different anatomic locations, and only three cardiac marker/anatomic site combinations were significantly different between the control and study groups.     

Sudden cardiac death in young adults: environmental risk factors and genetic aspects of premature atherosclerosis

Familial hypercholesterolemia (FH) is a genetic disorder that may lead to premature coronary heart disease (CHD) and sudden cardiac death (SCD). Mutations in the LDLR or APOB genes cause FH. We have screened the LDLR and the ligand-binding region of APOB genes in 52 cases of SCD. Deceased patients were younger than 40 years of age and were suspected of having FH. The LDLR and APOB genes were examined via PCR, high-resolution melting, and DNA sequencing. Therein, it was observed that 7.7% of the screened patients exhibited a rare sequence variant in the LDLR gene, with 5.7% suspected of being pathogenic mutations. Lipid profiles and genetic testing for FH could be considered when autopsy reveals significant atherosclerosis of the coronary arteries in young adults. First-degree family members are advised to seek medical advice and testing to determine their own risks of atherosclerosis to prevent premature CHD and SCD.