Micro-scale assessment of bone quality changes in adult cadaveric men with congestive hepatopathy.

Congestive hepatopathy (CH) is a chronic liver disease (CLD) caused by impaired hepatic venous blood outflow, most frequently resulting from congestive heart failure. Although it is known that heart failure and CLDs contribute to increased risk for age-related fractures, an assessment of CH-induced skeletal alterations has not been made to date. The aim of our study was to characterize changes in bone quality in adult male cadavers with pathohistologically confirmed CH compared with controls without liver disease. The anterior mid-transverse part of the fifth lumbar vertebral body was collected from 33 adult male cadavers (age range 43-89 years), divided into the CH group (n = 15) and the control group (n = 18). We evaluated trabecular and cortical micro-architecture and bone mineral content (using micro-computed tomography), bone mechanical competence (using Vickers micro-hardness tester), vertebral cellular indices (osteocyte lacunar network and bone marrow adiposity), and osteocytic sclerostin and connexin 43 expression levels (using immunohistochemistry staining and analysis). Deterioration in trabecular micro-architecture, reduced trabecular and cortical mineral content, and decreased Vickers microhardness were noted in the CH group (p < 0.05). Reduced total number of osteocytes and declined connexin 43 expression levels (p < 0.05) implied that harmed mechanotransduction throughout the osteocyte network might be present in CH. Moreover, elevated expression levels of sclerostin by osteocytes could indicate the role of sclerostin in mediating low bone formation in individuals with CH. Taken together, these micro-scale bone alterations suggest that vertebral strength could be compromised in men with CH, implying that vertebral fracture risk assessment and subsequent therapy may need to be considered in these patients. However, further research is required to confirm the clinical relevance of our findings.

Increased Cortical Porosity, Reduced Cortical Thickness, and Reduced Trabecular and Cortical Microhardness of the Superolateral Femoral Neck Confer the Increased Hip Fracture Risk in Individuals with Type 2 Diabetes.

Individuals with diabetes mellitus type 2 (T2DM) have approximately 30% increased risk of hip fracture; however, the main cause of the elevated fracture risk in those subjects remains unclear. Moreover, micromechanical and microarchitectural properties of the superolateral femoral neck-the common fracture-initiating site-are still unknown. We collected proximal femora of 16 men (eight with T2DM and eight controls; age: 61 ± 10 years) at autopsy. After performing post-mortem bone densitometry (DXA), the superolateral neck was excised and scanned with microcomputed tomography (microCT). We also conducted Vickers microindentation testing. T2DM and control subjects did not differ in age (p = 0.605), body mass index (p = 0.114), and femoral neck bone mineral density (BMD) (p = 0.841). Cortical porosity (Ct.Po) was higher and cortical thickness (Ct.Th) was lower in T2DM (p = 0.044, p = 0.007, respectively). Of trabecular microarchitectural parameters, only structure model index (p = 0.022) was significantly different between T2DM subjects and controls. Control group showed higher cortical (p = 0.002) and trabecular bone microhardness (p = 0.005). Increased Ct.Po and decreased Ct.Th in T2DM subjects increase the propensity to femoral neck fracture. Apart from the deteriorated cortical microarchitecture, decreased cortical and trabecular microhardness suggests altered bone composition of the superolateral femoral neck cortex and trabeculae in T2DM. Significantly deteriorated cortical microarchitecture of the superolateral femoral neck is not recognized by standard DXA measurement of the femoral neck.

Burn index, burn characteristics and carboxyhemoglobin levels in indoor fire-related deaths: Significance and interpretation of the autopsy findings.

INTRODUCTION: The Burn Index (BI) is a significant clinical prognostic parameter for patients with burns. It simultaneously considers major mortality risk factors: age and burns extensivity. Despite the inability to distinguish between ante- and post-mortem burns, their characteristics on autopsy might indicate if a significant thermal injury occurred before the onset of death. We investigated whether autopsy BI, burn extensivity, and severity could tell whether burns were the concurrent cause of fire-related death (FRD), even if the body remained in a fire. MATERIAL AND METHODS: Ten-year retrospective study analyzed FRD that occurred at the scene in a confined space. Soot aspiration was the main inclusion criterion. Autopsy reports were reviewed for demographic data, burn characteristics (degree, Total Body Surface Area burned- TBSA), coronary artery disease, and blood ethanol. We calculated the BI as a sum of the victim's age and percentage of TBSA affected by 2nd, 3rd and 4th-degree burns. Cases were divided into two groups: those with COHb≤ 30% and with COHb> 30%. Subjects with burned TBSA≤ 40% were analyzed separately afterward. RESULTS: The study included 53 males (71.6%) and 21 females (28.4%). No significant difference in age was observed between groups (p > 0.05). COHb≤ 30% had 33, and COHb> 30% had 41 victims. BI and burns extensivity (TBSA) had significant negative correlation with COHb values (ρ = -0.581, p < 0.01 and ρ = -0.439, p < 0.01, respectively). Both were significantly higher in subjects with COHb≤ 30% compared to those with COHb> 30% (140.7 ± 29.57 vs. 95.49 ± 38.49, p < 0.01 and 98 (13-100) vs. 30 (0-100), p < 0.01, BI and TBSA respectively). BI had excellent and TBSA fair performance for detection of subjects with COHb≤ 30% on ROC curve analysis (AUCs 0.821, p < 0.001 and 0.765, p < 0.001), with optimal cut-off values: BI≥ 107 (sensitivity 81.3%, specificity 70.7%) and TBSA≥ 45 (sensitivity 84.8%, specificity 70.7%). On logistic regression analysis BI≥ 107 was independently associated with COHb≤ 30% values (aOR 6; 95%CI 1.55-23.37). The same holds for the presence of 3rd-degree burns (aOR 5.9; 95%CI 1.45-23.99). In the subgroup of subjects with TBSA≤ 40% burned, those with COHb≤ 50% were significantly older than victims with COHb> 50% (p < 0.05). Here BI≥ 85 was a particularly good predictor for detection of subjects with COHb≤ 50% (AUC=0.913, p < 0.001, 95% CI 0.813-1.00; sensitivity 90.9%, specificity 81%). CONCLUSION: The BI≥ 107, TBSA≥ 45% burned, and 3rd-degree burns observed on autopsy point to a significantly higher odds that limited CO intoxication occurred, and burns should be considered a concurrent cause of indoor FRD. When less than 40% of TBSA was affected, BI≥ 85 indicated sub-lethal CO poisoning.

Guillain-Barré syndrome as a fatal complication of SARS-CoV-2 infection - An autopsy case.

We presented a case of a 57-year-old female, who was tested positive for SARS-CoV-2 infection and was admitted to a hospital seven days later with signs of early pneumonia. The second day after her admission to the hospital, and nine days after the first positive PCR test, examination showed progressive ascendant weakness of the arms and legs with persisting paresthesia, lab tests showed increased concentration of proteins in the cerebrospinal fluid with albumino-cytological dissociation. She was diagnosed with Guillain-Barré syndrome (GBS). She was on low-flow oxygen support of 3 L/min, with good oxygen saturation (97-99%), without clinical or radiological progression of pneumonia. After receiving a negative PCR test for COVID-19 (11 days after the initial, positive test), four days after admission, she was set to be transferred to a specialized neurology clinic, however, she died unexpectedly during admission. The autopsy showed light to moderate lung edema, signs of moderate to severe coronary atherosclerosis and early myocardial ischemia. Histochemical and immunohistochemical staining of the peripheral nerves sampled from the cervical and brachial plexuses, showed foci of demyelination as well as infiltration with inflammatory cells, predominantly macrophages, and lymphocytes to a lesser degree. It was concluded that the causes of death were a breathing disorder and the paralysis of the diaphragm due to inflammatory polyneuropathy caused by GBS, initiated by SARS-CoV-2 infection. With the lack of similar autopsy cases, we believe that the presented case could be a valuable addition to the understanding of GBS development in SARS-CoV-2 related cases.

Three-dimensional mapping of cortical porosity and thickness along the superolateral femoral neck in older women.

Although several studies have analyzed inter-individual differences in the femoral neck cortical microstructure, intra-individual variations have not been comprehensively evaluated. By using microCT, we mapped cortical pore volume fraction (Ct.Po) and thickness (Ct.Th) along the superolateral femoral neck in 14 older women (age: 77.1 ± 9.8 years) to identify subregions and segments with high porosity and/or low thickness-potential "critical" spots where a fracture could start. We showed that Ct.Po and Ct.Th significantly differed between basicervical, midcervical, and subcapital subregions of the femoral neck (p < 0.001), where the subcapital subregion showed the lowest mean Ct.Th and the highest mean Ct.Po. These cortical parameters also varied substantially with age and with the location of the analyzed microsegments along the individual's neck (p < 0.001), showing multiple microsegments with high porosity and/or low thickness. Although the highest ratio of these microsegments was found in the subcapital subregion, they were also present at other examined subregions, which may provide an anatomical basis for explaining the fracture initiation at various sites of the superolateral neck. Given that fractures likely start at structurally and mechanically weaker spots, intra-individual variability in Ct.Po and Ct.Th should be considered and the average values for the entire femoral neck should be interpreted with caution.