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Diffuse axonal injury (DAI) is caused by acceleration-deceleration forces during trauma that shear white matter tracts. Susceptibility-weighted MRI (SWI) identifies microbleeds that are considered the radiologic hallmark of DAI and are used in clinical prognostication. However, this assumption is limited by a lack of systematic radiologic-pathologic correlation studies. Here, we performed exvivo SWI on three brains from patients who died after severe TBI and assessed axonal injury around SWI microbleeds using immunohistochemistry to the amyloid-beta precursor protein. Axonal injury was present in 64% of microbleeds, indicating a heterogeneous injury response in the white matter.

Cardiac amyloidosis is frequently overlooked, leading to delayed diagnosis and underestimation of its true impact on cardiac mortality. Using CDC WONDER (1999-2020), we identified U.S. decedents aged ≥ 25 years with amyloidosis (ICD-10 E85) as the underlying cause of death and at least one cardiac-related condition as a contributing cause. Age-adjusted mortality rates (AAMRs) per 100,000 population were calculated, and trends were analyzed using Joinpoint regression and autoregressive integrated moving average (ARIMA) forecasting through 2040. Among 16,673 deaths, the AAMR rose from 0.261 in 1999 to 0.608 in 2020, with inflection points in 2012 and 2017 and an overall annual increase of 3.96%. Mortality was higher in men (0.537 vs. 0.210) and Black individuals (0.83 vs. 0.32), with a sharp post-2017 rise, especially among Black decedents. Geographic disparities were also observed, with the highest rates in the Northeast and urban areas. Most deaths occurred in hospitals (43.2%) or at home (31.4%), and mortality rates peaked in those aged 85 and older. Forecasting models project continued increases in AAMR through 2040, reaching approximately 2.0 overall, with especially elevated rates among Black (≈ 5.9) and male (≈ 3.8) decedents. Cardiac mortality in amyloidosis has risen sharply since 2017, likely driven by improved ATTR-CM detection through non-biopsy imaging and guideline adoption. Disparities by sex, race, and geography persist, reflecting uneven diagnostic capacity concentrated in urban and Northeastern centers. Forecasts project continued increases, particularly among Black and male individuals, underscoring the need for more equitable access to diagnosis and treatment.

The City of Tulsa initiated The 1921 Graves Investigation in 2020 in order to recover and identify African American victims of the 1921 Tulsa Race Massacre from unmarked graves. The Tulsa Race Massacre occurred in downtown Tulsa over May 31, 1921, to June 1, 1921, as an act of mob violence, homicide, looting, and arson by white Tulsans against the African American residents of the neighboring Greenwood community. Thirty-nine deaths from both races were documented, and one of the known African American burial sites was in the city cemetery, Oaklawn. Oklahoma statutes regarding disinterment resulted in a recovery plan in which the forensic anthropology lab was established on the cemetery grounds, and lab procedures were adapted for managing fair to poor skeletal preservation, all while accommodating community support and working under media scrutiny. Collaboration between City personnel and the anthropological experts included application of traditional and novel resources to create and operationalize the field laboratory, including adapting a portable building into a functional lab, finding lightweight and opaque remains transport containers, using commonly acquired supplies for new purposes, and modifying analytical techniques for field radiography not previously observed in the literature. These customizations have resulted in the successful implementation of the field laboratory, and the analysis of skeletal remains over five episodes of recoveries and analyses of decedents, as well as a complete deconstruction of the lab at the end of each field season. We present this field laboratory and toolkit assemblage as a resource to the literature of anthropological field analysis.

Background: Studies have reported association between obesity and sudden cardiac death (SCD) but presume cardiac cause without autopsy. Elucidating causes of SCD by weight status may refine prevention strategies. Question: What are the autopsy causes of community sudden death by weight status? Methods: The POstmortem Systematic InvesTigation of SCD (POST SCD) is an ongoing prospective study using autopsy and clinical records to adjudicate arrhythmic (potentially rescuable with ICD) vs. non-arrhythmic (tamponade, stroke) causes among presumed SCDs (pSCDs) meeting WHO criteria in San Francisco County since 2011. Body mass index (BMI) was categorized as underweight (UW; <18.5), healthy (18.5-24.9), overweight (OW; 25-29.9), or obese (OB; >30). Results: Of 1,115 total pSCDs from 2/1/2011-1/1/2024, 322 (29%) were healthy by BMI, 51 (5%) UW, 344 (31%) OW, and 398 (36%) OB. Compared to healthy BMI, OB victims were younger (mean 56 vs 60 years, p<.001), less likely Asian (11% vs 25%, p<.001), more likely Black (23% vs 16%, p<.03), and had more co-morbidities, including hypertension (55% vs 38%, p<.001), diabetes (28% vs 14%, p<.001), dyslipidemia (30% vs 16%, p<.001), diagnosed coronary artery disease (CAD; 15% vs 9%, p<.01), and chronic kidney disease (11% vs 4%, p<.01). UW pSCDs had similar demographics and co-morbidities as healthy BMI cases. The proportion of pSCDs attributable to arrhythmic causes increased with higher BMI: 27% (UW) to 49% (Healthy) to 58% (OW) to 60% (OB), p<.001. Compared to healthy, OB had more CAD (37% vs 26%, p<.01), cardiac hypertrophy (11% vs 6%, p<.05), and pulmonary embolism (7% vs 2%, p<.01) causes of pSCD. UW BMI victims had more non-cardiac causes (67% vs 49%, p<.01), including infection (16% vs 5%, p<.01) and respiratory failure (10% vs <1%, p<.001). Among arrhythmic deaths, OB cases had fewer normal heart/primary electrical disease causes vs healthy (3% vs 10%, p<.01), but other causes were similar across BMI classes. Conclusions: In this 13-year countywide postmortem study, OB and OW sudden deaths had higher likelihood of arrhythmic causes while UW had more non-cardiac causes than pSCDs with healthy BMI. Among arrhythmic deaths, causes were similar by weight status, but OB victims had more cardiac pathology and pre-existing comorbidities. Awareness of non-cardiac causes in UW and redoubled efforts to screen and treat cardiac risk factors in OB individuals may mitigate sudden death risk at each end of the weight spectrum.

Previous research shows that even expert-level recovery teams can miss osteological evidence. The present research examined recovery rates and distances using dispersed nonhuman (pig [Sus scrofa], white-tailed deer [Odocoileus virginianus], and mule deer [O. hemionus]) bones with different taphonomic color alteration. Searching was done by a Special Emergency Response Team of the Massachusetts State Police during researcher-guided walk-throughs in a simulated outdoor surface scene. The authors hypothesized that sun-bleached bones would be recognized from the greatest distances due to their starker contrast from natural leaf litter as opposed to control bones or those with soil/decomposition staining. The control sample was unaltered, dry bone without significant staining, and the stained bones had variable brown color from decomposition and/or shallow burial. The sun-bleached bones were spotted at an average distance of 8.76 m ± 7.75 m, while soil/decomposition-stained bones were spotted at 4.09 m ± 2.79 m and the control sample at 6.73 m ± 5.40 m. As determined by a two-way ANOVA test, the interaction between bone color and distance was significant (p < 0.001). Sun-bleached bones had a 100.0% recovery rate (60/60), control bones 96.7% (58/60), and soil/decomposition-stained bones 70.0% (42/60). In addition, bone type also had a statistically significant effect on distance (p < 0.001), and therefore the likelihood of being recovered. Even expert-level recovery teams can miss osteological evidence during surface searches, with natural bone camouflage factoring into recovery success rates. As a result, increased training and education surrounding taphonomically altered bones is necessary for all personnel involved in forensic surface searching.

Benzimidazole opioids, isotonitazene (ITZ), and metonitazene (MTZ) and their associated metabolites, 5-aminoisotonitazene (5-AI), 4'-hydroxy nitazene (4'-HN), N-desethyl isotonitazene (N-DI), and N-desethyl metonitazene (N-DM), were evaluated in human postmortem casework. A total of twenty-seven cases that previously tested positive for ITZ (n = 11) and MTZ (n = 16) in routine case analysis were retested for the presence of metabolites in blood and urine specimens by solid-phase extraction and LC/MS/MS. N-DI was the most prevalent metabolite detected in ITZ cases, present in six blood and four urine samples. N-DM was the most prevalent MTZ metabolite, primarily found in urine. 4'-HN was detected in both ITZ and MTZ cases. Fentanyl was the most prevalent co-finding, and all cases were classified as mixed drug intoxications except for two blunt force traumas. Due to the reported potency of N-DI and prevalence of metabolite detection in these cases, this study encourages the addition of nitazene metabolites to routine testing scopes.

Potassium thiocyanate is a long-discontinued weak antihypertensive and an uncommonly encountered toxic agent. We report a 52-year-old man who presented to the emergency department with a sudden onset of altered mental status, vomiting, and seizures after a suspected toxic ingestion. Clinical laboratory tests showed a falsely elevated serum chloride (>200mmol/L) with other normal electrolytes, resulting in a significant negative anion gap. An endoscopy showed gastric mucosa edema and hyperemia. Repeated electroencephalograms showed moderate to severe encephalopathy. He remained symptomatic until his death 9 days later. An autopsy found hypoxic-ischemic changes in the brain. Toxicological analysis on antemortem blood collected 93 to 95 hours after apparent ingestion revealed a thiocyanate concentration of 260μg/mL and cyanide concentration of 0.21μg/mL. Toxicology on postmortem specimens revealed thiocyanate concentrations of 78μg/mL in cardiac blood, 75μg/mL in peripheral blood, 16μg/g in brain, 49μg/g in kidney, 37μg/g in liver, and 21μg/g in skeletal muscle. Further investigation found an internet order for potassium thiocyanate in the days before ingestion. This case report raises the awareness of thiocyanate as a potentially re-emerging toxin and pseudohalide that can interfere with clinical laboratory testing and present as falsely elevated serum chloride (pseudohyperchloremia).