Causes of Death in the Presence of Law Enforcement in Johnson County, Iowa, 2011-2020.

Objectives. To examine sudden and unexpected or trauma-related deaths that occurred in the presence of law enforcement in Johnson County, Iowa, between 2011 and 2020. Methods. We identified deaths in the presence of law enforcement using definitions from the National Association of Medical Examiners. We obtained data, including demographics, cause and manner of death, toxicology results, and circumstances and location of event leading to death, from comprehensive medical examiner investigative reports. Results. There were 165 deaths that occurred in the presence of law enforcement: 114 were from a known disease, and 51 were either trauma related or the sudden, unexpected initial presentation of a previously unrecognized disease. Three deaths occurred in the context of physical restraint by law enforcement. Suicide was the leading manner of death among trauma-related deaths; the means of suicide was predictable based on in-custody (hanging) or precustody (firearm) circumstances. Conclusions. Our findings highlight the potential role of medical examiners and coroners in improving completeness of data on reporting death in the presence of law enforcement to public health agencies. (Am J Public Health. 2024;114(6):642-650. https://doi.org/10.2105/AJPH.2024.307616).

Ventilatory response to CO2 in patients with epilepsy.

OBJECTIVE: Severe periictal respiratory depression is thought to be linked to risk of sudden unexpected death in epilepsy (SUDEP) but its determinants are largely unknown. Interindividual differences in the interictal ventilatory response to CO2 (hypercapnic ventilatory response [HCVR] or central respiratory CO2 chemosensitivity) may identify patients who are at increased risk for severe periictal hypoventilation. HCVR has not been studied previously in patients with epilepsy; therefore we evaluated a method to measure it at bedside in an epilepsy monitoring unit (EMU) and examined its relationship to postictal hypercapnia following generalized convulsive seizures (GCSs). METHODS: Interictal HCVR was measured by a respiratory gas analyzer using a modified rebreathing technique. Minute ventilation (VE ), tidal volume, respiratory rate, end tidal (ET) CO2 and O2 were recorded continuously. Dyspnea during the test was assessed using a validated scale. The HCVR slope (ΔVE /ΔETCO2 ) for each subject was determined by linear regression. During the video-electroencephalography (EEG) study, subjects underwent continuous respiratory monitoring, including measurement of chest and abdominal movement, oronasal airflow, transcutaneous (tc) CO2 , and capillary oxygen saturation (SPO2 ). RESULTS: Sixty-eight subjects completed HCVR testing in 151 ± (standard deviation) 58 seconds, without any serious adverse events. HCVR slope ranged from -0.94 to 5.39 (median 1.71) L/min/mm Hg. HCVR slope correlated with the degree of unpleasantness and intensity of dyspnea and was inversely related to baseline ETCO2 . Both the duration and magnitude of postictal tcCO2 rise following GCSs were inversely correlated with HCVR slope. SIGNIFICANCE: Measurement of the HCVR is well tolerated and can be performed rapidly and safely at the bedside in the EMU. A subset of individuals has a very low sensitivity to CO2 , and this group is more likely to have a prolonged increase in postictal CO2 after GCS. Low interictal HCVR may increase the risk of severe respiratory depression and SUDEP after GCS and warrants further study.

3,4-Methylenedioxymethamphetamine (MDMA, Ecstasy) Intoxication in a Young Adult with Giant Coronary Aneurysms from Kawasaki Disease.

Kawasaki disease is an acute vasculitis of unknown etiology that usually occurs in children less than five years old. Coronary artery aneurysm due to arteritis is the most common cardiac complication. Chronic aneurysms are associated with an increased risk of developing luminal thrombosis and ischemic myocardial injury. We present a case of an 18-year-old male with a history of Kawasaki disease complicated by chronic giant aneurysms of the right and left coronary arteries. Serial echocardiographic studies and treadmill electrocardiogram stress tests as recent as 1.5 years before death revealed excellent cardiac function by clinical criteria. The decedent sustained a witnessed collapse after ingesting 3,4-methylenedioxymethamphetamine (MDMA) and ethanol. He was pronounced dead in the emergency department after unsuccessful resuscitative efforts. Autopsy revealed large aneurysms of the three main epicardial coronary arteries with extensive foci of severe stenosis by intimal fibrosis and organizing thrombus. Microscopic examination revealed multifocal severe myocyte hypertrophy. There were remote microinfarcts in the anterior and posterior aspects of the left ventricle and a recent, healing microinfarct in the posterior aspect of the left ventricle. Toxicology examination of postmortem femoral blood revealed MDMA, ethanol, and amiodarone. This case illustrates the residual, lasting effects of cardiac disease due to Kawasaki disease and a potential complication in the setting of use of an illicit stimulant, MDMA, an amphetamine derivative that produces sympathetic activation and cardiovascular effects including tachycardia, vasoconstriction, dysrhythmias, and coronary artery spasm. Kawasaki disease-related abnormalities of the heart likely resulted in a lower threshold for developing a fatal cardiac dysrhythmia under the circumstance of stimulant use.

Acid-sensing ion channel 1 and nitric oxide synthase are in adjacent layers in the wall of rat and human cerebral arteries.

Extracellular acidification activates a family of proteins known as acid-sensing ion channels (ASICs). One ASIC subtype, ASIC type 1 (ASIC1), may play an important role in synaptic plasticity, memory, fear conditioning and ischemic brain injury. ASIC1 is found primarily in neurons, but one report showed its expression in isolated mouse cerebrovascular cells. In this study, we sought to determine if ASIC1 is present in intact rat and human major cerebral arteries. A potential physiological significance of such a finding is suggested by studies showing that nitric oxide (NO), which acts as a powerful vasodilator, may modulate proton-gated currents in cultured cells expressing ASIC1s. Because both constitutive NO synthesizing enzymes, neuronal nitric oxide synthase (nNOS) and endothelial NOS (eNOS), are expressed in cerebral arteries we also studied the anatomical relationship between ASIC1 and nNOS or eNOS in both rat and human cerebral arteries. Western blot analysis demonstrated ASIC1 in cerebral arteries from both species. Immunofluorescent histochemistry and confocal microscopy also showed that ASIC1-immunoreactivity (IR), colocalized with the smooth muscle marker alpha-smooth muscle actin (SMA), was present in the anterior cerebral artery (ACA), middle cerebral artery (MCA), posterior cerebral artery (PCA) and basilar artery (BA) of rat and human. Expression of ASIC1 in cerebral arteries is consistent with a role for ASIC1 in modulating cerebrovascular tone both in rat and human. Potential interactions between smooth muscle ASIC1 and nNOS or eNOS were supported by the presence of nNOS-IR in the neighboring adventitial layer and the presence of nNOS-IR and eNOS-IR in the adjacent endothelial layer of the cerebral arteries.

Autopsy after traumatic death--a shifting paradigm.

OBJECTIVE: The role of autopsy in evaluating missed injury after traumatic death is well established and discussed in the literature. The frequency of incidental findings in trauma patients has not been reported. We believe that incidental findings are under recognized and reported by trauma surgeons. PATIENTS AND METHODS: This prospective, descriptive, cohort study was conducted at a Level 1 trauma center in a rural state. Four hundred ninety-six deaths over a 4-y period were identified from the trauma registry. Two hundred four complete autopsies were available for review. One thousand eighteen traumatic diagnoses were identified from 204 autopsies and corresponding medical records by trauma surgeons blinded to patient identity. The surgeons recorded missed diagnoses, incidental diagnoses identified at autopsy, and diagnoses known at the time of death confirmed by autopsy. RESULTS: The surgeons had a κ-score of 0.82-0.84. Forty-two patients (21% of patients) had 68 severe missed injuries; 67 patients (33% of patients) had 94 minor missed injuries. Twenty-eight patients (14%) had significant incidental findings including premature atherosclerosis, multiple endocrine neoplasia, tuberculosis, and others. CONCLUSIONS: The autopsy after traumatic death is more than a mechanism of quality control and teaching. A high proportion of patients will have incidental findings important to family members, and have public health importance. Systems need to be developed to review autopsy results with attention to identifying and communicating incidental findings. Given the incidence of significant missed injuries and incidental findings, the autopsy continues to have an important role in health care.

Nitroxidergic innervation of human cerebral arteries.

A dense network of nerves containing neuronal nitric oxide synthase is present in cerebral vessels from experimental animals. The nerves may regulate cerebrovascular tone, protect the brain from stroke, and contribute to cluster headaches in humans; but studies in humans have shown only modest nitroxidergic innervation of cerebral vessels. We tested the hypothesis that nerve fibers containing neuronal nitric oxide synthase richly innervate human cerebral arteries. We used immunohistochemical techniques at post mortem and found dense neuronal nitric oxide synthase nerve staining in human cerebral vessel walls consistent with participation of nitroxidergic fibers in human physiological and pathophysiological processes.

Thymocytes, pre-B cells, and organ changes in a mouse model of chronic ethanol ingestion--absence of subset-specific glucocorticoid-induced immune cell loss.

BACKGROUND: The well-known immune deficiency of the chronic alcoholic dictates the need for a long-term rodent ethanol administration model to evaluate the baseline immunologic effects of chronic ethanol abuse, and investigate the genetic determinants of those effects. Much published work with rodents has shown clearly that acute ethanol administration and short-term ethanol-containing liquid diets both cause elevated corticosterone and can cause significant thymocyte, pre-B cell and peripheral lymphocyte losses. Such losses may mask more subtle alterations in immune homeostasis, and in any case are generally short-lived compared with the span of chronic ethanol abuse. Thus, it is important to have a model in which long-term immune alterations can be studied free of corticosteroid-induced cell losses. METHODS: We have utilized chronic 20% (w/v) ethanol in water administration to several mouse strains for prolonged periods of time and evaluated serum corticosterone, immunologic stress parameters, and other organ changes by standard methods. RESULTS: We now confirm earlier reports that chronic ethanol in water administration to mice does not produce net elevations of corticosterone, although diurnal variation is altered. Importantly, there is neither selective loss of immune cell populations known to be corticosteroid sensitive, CD4+CD8+ thymocytes and pre-B cells, nor are changes observed in the histologic appearance of the thymus. Nonetheless, there are significant chronic ethanol effects in other tissues, including reduced heart weight, mild hepatic steatosis, alterations of gut flora, increased serum peptidoglycan, and as published elsewhere, immune system abnormalities. CONCLUSIONS: This model of ethanol administration is convenient, sustainable for up to 1 year, demonstrably feasible in several mouse strains, permits good weight gains in most strains, and results in significant changes in a number of organs. The administration method also will permit modeling of long-term steady abuse punctuated by major binges, and is suitable for supplementation studies using water soluble additives. Overall, the method is useful for a wide range of studies requiring a chronic low-stress method of ethanol administration.

"Med-X": a medical examiner surveillance model for bioterrorism and infectious disease mortality.

We created a model surveillance system (Med-X) designed to enable medical examiners and coroners to recognize fatal infections of public health importance and deaths due to bioterrorism. All individuals who died in New Mexico and fell under medical examiner jurisdiction between November 23, 2000, and November 22, 2002, were prospectively evaluated using sets of surveillance symptoms and autopsy-based pathologic syndromes. All infectious disease deaths were evaluated to identify the specific causative agent. Of 6104 jurisdictional cases, 250 (4.1%) met Med-X criteria, of which 141 (56.4%) had a target pathologic syndrome. Ultimately, 127 (51%) of the 250 cases were due to infections. The causative organism was identified for 103 (81%) of the infectious disease deaths, of which 60 (58.3%) were notifiable conditions in New Mexico. Flu-like symptoms, fever and respiratory symptoms, and encephalopathy or new-onset seizures had predictive values positive for fatal infections of 65%, 72%, and 50%, respectively, and are useful as autopsy performance criteria. Before the development of surveillance criteria, 37 (14.8%) of the cases ordinarily would not have been autopsied resulting in a 1% increase in autopsy workload. Med-X is an effective method of detecting infectious disease deaths among medical examiner cases. Uniform criteria for performing medical examiner autopsies and reporting cases to public health authorities enhance surveillance for notifiable infectious diseases and increase the likelihood of recognizing deaths related to bioterrorism.

Ruptured cerebral artery aneurysm and bacterial meningitis in a man with osteogenesis imperfecta.

This report describes a 38-year-old man with osteogenesis imperfecta who died of a ruptured cerebral artery aneurysm and bacterial meningitis. He had multiple long bone fractures in the past, and approximately 4 months before death, he had surgery to relieve symptoms of basilar impression. The surgery was complicated by a postoperative wound infection. For the next 4 months, he had intermittent headaches and vomiting. He was found dead in his bed at home. At autopsy, he had a ruptured anterior communicating artery aneurysm and bacterial meningitis. Cerebrospinal fluid and blood cultures had growth of Staphylococcus aureus. Osteogenesis imperfecta is a disorder of type I collagen. Type I collagen is present in many tissues, including blood vessels. The etiology of cerebral artery aneurysm formation is multifactorial. Some patients with cerebral artery aneurysms have been shown to have abnormalities in type III collagen. There has not been a reported relationship made between abnormalities in type I collagen and aneurysms. Meningitis can also result in cerebral artery aneurysms, but they are usually due to Aspergillus or Mycobacterium species. The case we report is unique; cerebral artery aneurysm formation may have been due to osteogenesis imperfecta and/or bacterial meningitis.

Accuracy of cause of death determination without forensic autopsy examination.

Medical examiners and coroners commonly determine cause and manner of death without an autopsy examination. Some death certificates generated in this way may not state the correct cause and manner of death. From the case files of the Department of Forensic Medicine in Sydney, Australia, the authors retrospectively reviewed investigative information of all cases in a 6-month period that were initially considered natural deaths (429). The authors, blinded to autopsy results, accepted 261 cases as appropriate for certification without autopsy and assigned a cause of death to each. Per standard local practice, all cases had been autopsied. The actual causes of death as determined by autopsy were then revealed and compared with the presumed causes of death. Most presumed and actual causes of death were cardiovascular (94% and 80%, respectively). The majority of presumed causes of death were listed as ASCVD as the cases lacked features of a more specific cardiovascular process. A large majority of cases had a presumed cause of death of ischemic heart disease based on individual case details. The actual causes of death demonstrated a large breadth of cardiovascular and noncardiovascular disease processes, even though ischemic heart disease accounted for 62% of deaths. The presumed cause of death was completely wrong in 28% of cases. A nonnatural manner of death was present in 3% of cases. This study demonstrates that experienced forensic pathologists may generate erroneous death certificates for cases that are not autopsied.