A current view of mitochondria damage and the diversity of lipopigment inclusions in neuronal ceroid lipofuscinose type 2 from rectal biopsy.

Neuronal ceroid lipofuscinoses (NCLs) are a growing group of neurodegenerative storage diseases, in which specific features are sought to facilitate the creation of a universal diagnostic algorithm in the future. In our ultrastructural studies, the group of NCLs was represented by the CLN2 disease caused by a defect in the TPP1 gene encoding the enzyme tripeptidyl-peptidase 1. A 3.5-year-old girl was affected by this disease. Due to diagnostic difficulties, the spectrum of clinical, enzymatic, and genetic tests was extended to include analysis of the ultrastructure of cells from a rectal biopsy. The aim of our research was to search for pathognomonic features of CLN2 and to analyse the mitochondrial damage accompanying the disease. In the examined cells of the rectal mucosa, as expected, filamentous deposits of the curvilinear profile (CVP) type were found, which dominated quantitatively. Mixed deposits of the CVP/fingerprint profile (FPP) type were observed less frequently in the examined cells. A form of inclusions of unknown origin, not described so far in CLN2 disease, were wads of osmophilic material (WOMs). They occurred alone or co-formed mixed deposits. In addition, atypically damaged mitochondria were observed in muscularis mucosae. Their deformed cristae had contact with inclusions that looked like CVPs. Considering the confirmed role of the c subunit of the mitochondrial ATP synthase in the formation of filamentous lipopigment deposits in the group of NCLs, we suggest the possible significance of other mitochondrial proteins, such as mitochondrial contact site and cristae organizing system (MICOS), in the formation of these deposits. The presence of WOMs in the context of searching for ultrastructural pathognomonic features in CLN2 disease also requires further research.

TDP-43 pathology in subacute sclerosing panencephalitis.

Subacute sclerosing panencephalitis (SSPE) is a fatal, slowly progressive brain disorder caused by a mutated measles virus. Both subacute inflammatory and neurodegenerative mechanisms appear to play significant roles in the pathogenesis. TAR DNA-binding protein 43 (TDP-43) inclusions are a common co-pathology in several neurodegenerative disorders with diverse pathogenesis. In the present study, we examined brains of 16 autopsied SSPE patients for the presence of TDP-43 pathology and possible associations with tau pathology. Immunohistochemical staining identified TDP-43 inclusions in 31% of SSPE cases. TDP-43 pathology was widely distributed in the brains, most severely in the atrophied cerebral cortex (temporal and parietal), and most frequently as tangle- and thread-like neuronal cytoplasmic inclusions. It was associated with longer disease duration (>4 years) and tau pathology (all TDP-43-positive cases had tau-positive neurofibrillary tangles). This study demonstrates for the first time an association between TDP-43 pathology and SSPE. The co-occurrence of TDP-43 and tau aggregates and correlation with the disease duration suggest that both pathological proteins are involved in the neurodegenerative process induced by viral inflammation.

Incidence and morphology of secondary TDP-43 proteinopathies: Part 2.

Transactivation (TAR) DNA binding protein 43 kDa (TDP-43) inclusions frequently occur as a comorbid pathology in several neurodegenerative disorders, including Alzheimer's disease, Huntington's disease, Lewy body disease, and progressive supranuclear palsy, and may appear in association with nondegenerative neurological etiology, for example neoplastic, paraneoplastic, traumatic, or infectious. Relationships between various pathological proteins and mechanisms associated with TDP-43-induced neurodegeneration are still not fully understood. Thus, overlap of distinct neuropathological mechanisms frequently leads to greater brain atrophy and a more severe clinical course, suggesting the importance of co-pathologies in ante-mortem diagnosing and treatment. The present review aims to discuss the incidence, morphology, and role of TDP-43 pathology in the context of other dominant, hallmark pathologies, referred to as secondary TDP-43 proteinopathies. The previous part (Part 1) focused on common neurodegenerative diseases, including Alzheimer's disease, Huntington's disease, and Lewy body disease, while the present part (Part 2) discusses TDP-43 pathology in rare neurodegenerative diseases and neurological diseases with nondegenerative etiology.

A primary multiple pleomorphic rhabdomyosarcoma of the heart in an adult dog.

BACKGROUND: Heart tumors are rare in dogs. They can be benign or malignant. Clinical signs depend primarily on the location of the tumor and its effect on blood flow. CASE PRESENTATION: An eleven-year-old crossbreed male dog lethargic and anorectic for previous 3 days was presented to the veterinary clinic. The focused ultrasound assessment with sonograms in trauma (FAST) revealed multiple tumors in the heart which were then confirmed in echocardiographic examination performed by a veterinary cardiologist. Due to the poor general condition and grave prognosis, the dog was humanely euthanized. The autopsy revealed numerous intracardiac tumors in all four heart chambers. No proliferative changes were found in other organs either in thoracic or abdominal cavity. Immunohistochemical examination was performed using formalin-fixed, paraffin-embedded tissue from heart masses. The antibodies against myoglobin, desmin, smooth muscle actin, vimentin, CD34, S100, and pan-cytokeratin (AE1/AE3) were used. Microscopically, the tumor was composed of fascicles of spindle-shaped cells with pale eosinophilic cytoplasm with round, oval, and focally elongated nuclei and one or two prominent nucleoli. The tumor cells showed strong diffuse cytoplasmic immunopositivity for myoglobin and vimentin and focal staining for desmin. Immunostainings for smooth muscle actin-SMA, CD34, pan-cytokeratin, S-100 protein were negative. The immunohistochemical staining pattern confirmed rhabdomyosarcoma. CONCLUSIONS: This is the first description of the primary multiple heart rhabdomyosarcoma in a dog.

Influence of SARS-CoV-2 on Adult Human Neurogenesis.

Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with the onset of neurological and psychiatric symptoms during and after the acute phase of illness. Inflammation and hypoxia induced by SARS-CoV-2 affect brain regions essential for fine motor function, learning, memory, and emotional responses. The mechanisms of these central nervous system symptoms remain largely unknown. While looking for the causes of neurological deficits, we conducted a study on how SARS-CoV-2 affects neurogenesis. In this study, we compared a control group with a group of patients diagnosed with COVID-19. Analysis of the expression of neurogenesis markers showed a decrease in the density of neuronal progenitor cells and newborn neurons in the SARS-CoV-2 group. Analysis of COVID-19 patients revealed increased microglial activation compared with the control group. The unfavorable effect of the inflammatory process in the brain associated with COVID-19 disease increases the concentration of cytokines that negatively affect adult human neurogenesis.

Incidence and morphology of secondary TDP-43 proteinopathies: Part 1.

Transactive response DNA binding protein of 43 kDa (TDP-43) is considered to play an essential role in the pathogenesis of frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Growing body of evidence indicate that pathological TDP-43 inclusions frequently occur in the context of other distinctive hallmark pathologies, referred to as secondary TDP-43 proteinopathies. Comorbid TDP-43 pathology is well-documented in several neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, multiple system atrophy, or progressive supranuclear palsy. It may also appear as a consequence of less obvious disease etiologies, i.e. post-traumatic (chronic traumatic encephalopathy), neoplastic (pilocytic astrocytoma), or post-infectious (post-encephalitic parkinsonism). The aim of the present review was to evaluate the incidence, morphology, and role of TDP-43 pathology in the secondary TDP-43 proteinopathies. This article (Part 1) discussed TDP-43 pathology in more common neurodegenerative diseases, including Alzheimer's disease, Lewy body disease, Huntington's disease, multiple system atrophy, corticobasal degeneration, and progressive supranuclear palsy. A follow-up article (Part 2) will describe abnormal TDP-43 changes in rare neurodegenerative diseases or neurological diseases with nondegenerative etiology.

Mechanism of Spontaneous Intracerebral Hemorrhage Formation: An Anatomical Specimens-Based Study.

BACKGROUND: Despite advances in understanding various risk and prognostic factors, spontaneous intracerebral hemorrhage is connected to very high morbidity and mortality, while the therapy is mainly supportive. Understanding of the pathophysiology of initial hematoma expansion is limited due to insufficient clinical data and lack of a suitable animal model. METHODS: We injected 40 anatomic specimens of the basal ganglia with contrast medium, scanned them with a micro-computed tomography scanner and analyzed the results of radiological studies, direct and histological examinations. RESULTS: In 9 cases, micro-computed tomography and histological examinations revealed contrast medium extravasations mimicking intracerebral hematomas. The artificial hematomas spread both proximally and distally along the ruptured perforator and its branches in the perivascular spaces and detached the branches from the adjacent neural tissue leading to destruction of the tissue and secondary extravasations. Moreover, some contrast extravasations skipped to the perivascular spaces of unruptured perforators, created further extravasation sites and aggravated the expansion of the artificial hematoma. There was no subarachnoid extension of any artificial hematoma. CONCLUSIONS: We postulate that a forming basal ganglia intracerebral hematoma spreads initially in the perivascular space, detaches the branches from the neural tissue and causes secondary bleeding. It can also skip to the perivascular space of a nearby perforator. The proposed mechanism of hematoma initiation and formation explains extent of damage to the neural tissue, variability of growth in time and space, creation of secondary bleeding sites, and limited usefulness of surgical interventions. The model is reproducible, the extent of the artificial hematoma can be easily controlled, the rupture sites of the perforating arteries can be determined, and preparation of the model does not require specialized, expensive equipment apart from the micro-computed tomography scanner.

Unruptured intracranial aneurysms: relation between morphology and wall strength.

AIM OF THE STUDY: To determine the morphological features distinguishing small unruptured saccular intracranial aneurysms (sIAs) with high and low wall strength (WS) in post mortem subjects. CLINICAL RATIONALE FOR THE STUDY: Subarachnoid haemorrhage caused by sIA rupture is associated with increased mortality and morbidity. Analysis of the morphology and biomechanical properties of sIAs might facilitate the identification of clinically relevant risk factors for sIA rupture. MATERIAL AND METHODS: Eight single unruptured sIAs were found among eight subjects during 184 post mortem examinations. After assessment of the dimensions, aspect ratio (AR), size ratio (SR), height/width ratio (HW), bottleneck factor (BNF), and shape, sIAs with adjacent cerebral arteries were subjected to quasi-static increasing pressure until the wall of the cerebral artery or sIA ruptured. RESULTS: In three specimens, the sIA ruptured at a significantly lower average pressure than the other cases, in which the rupture occurred within the wall of the adjacent cerebral artery (769 vs. 1,259 mmHg; p = 0.035). The sIAs with low WS, i.e. sIAs that ruptured during experiments, were characterised by significantly increased dome dimensions compared to sIAs with high WS (p < 0.05). At the same time, no significant differences were observed between high and low WS categories regarding AR, SR, HW, and BNF, or the presence of an irregular dome shape. CONCLUSIONS AND CLINICAL IMPLICATIONS: Dome dimension was the only feature that distinguished unruptured sIAs as having low or high WS, and this supports observations that sIAs with increased dome dimensions are characterised by an increased risk of rupture. Thus, dome dimension may be more useful than other morphometric parameters, such as AR, SR, HW and BNF, in assessing the rupture risk assessment of small unruptured sIAs.

Rupture pressure values of cerebral arteries in the presence of unruptured intracranial aneurysm.

Cerebral arteries (CAs) are prone to the saccular aneurysm formation. Since aneurysms may be considered as balloon-like dilations of the locally weakened arterial wall, it should be determined whether the presence of intracranial aneurysm is related to the generalized weakening of CAs. Among 184 consecutive forensic autopsies, eight brains with a single unruptured saccular aneurysm were identified. Aneurysms with adjacent CAs and specific CA segments were excised, namely: the anterior communicating artery complex, and bifurcations of the basilar artery, internal carotid arteries, and middle cerebral arteries. Then, aneurysm and CA specimens were subjected to pressure-inflation tests until rupture occurred at the arterial bifurcation or at the wall of the CA or aneurysm. The same protocol was applied to the control group composed of CAs excised from eight brains without aneurysm. No significant differences were noted between the experimental and control groups, depending on the mean rupture pressure (1054 vs. 1048 mmHg) and rupture site (bifurcation vs. wall) of the analyzed specimens. These findings indicate that the presence of unruptured saccular aneurysm is not related to generalized weakening of CAs among autopsy subjects. Moreover, the CA bifurcations do not represent regions of decreased wall strength.

Integrated Basic Heart and Lung Ultrasound Examination for the Differentiation between Bacterial Pneumonia and Lung Neoplasm in Dogs-A New Diagnostic Algorithm.

The diagnostics of two of the most prevalent lung diseases in dogs, bacterial pneumonia (BP) and lung neoplasm (LN), are challenging as their clinical signs are identical and may also occur in extrapulmonary diseases. This study aims to identify ultrasonographic criteria and develop a lung ultrasound (LUS)-based diagnostic algorithm which could help distinguish between these two conditions. The study is carried out in 66 dyspneic dogs in which a heart disease was excluded using echocardiography. Based on imaging and laboratory diagnostic tests, as well as follow-up, the dogs are classified into LN (35 dogs) and BP (31 dogs) groups. LUS is performed at admission and the presence of seven lung abnormalities (pleural thickening, B-lines, subpleural consolidations, hepatization with or without aeration, nodule sign and mass classified together as a tumor, and free pleural fluid) and classification and regression trees are used to develop an LUS-based diagnostic algorithm. Distribution of all LUS abnormalities except for aerations differs significantly between groups; however, their individual differentiating potential is rather low. Therefore, we combine them in an algorithm which allows for definitive classification of 60 dogs (91%) (32 with LN and 28 with BP) with correct diagnosis of LN and BP in 31 dogs and 27 dogs, respectively.

Activation of the 5-HT7 receptor and MMP-9 signaling module in the hippocampal CA1 region is necessary for the development of depressive-like behavior.

Major depressive disorder is a complex disease resulting from aberrant synaptic plasticity that may be caused by abnormal serotonergic signaling. Using a combination of behavioral, biochemical, and imaging methods, we analyze 5-HT7R/MMP-9 signaling and dendritic spine plasticity in the hippocampus in mice treated with the selective 5-HT7R agonist (LP-211) and in a model of chronic unpredictable stress (CUS)-induced depressive-like behavior. We show that acute 5-HT7R activation induces depressive-like behavior in mice in an MMP-9-dependent manner and that post mortem brain samples from human individuals with depression reveal increased MMP-9 enzymatic activity in the hippocampus. Both pharmacological activation of 5-HT7R and modulation of its downstream effectors as a result of CUS lead to dendritic spine elongation and decreased spine density in this region. Overall, the 5-HT7R/MMP-9 pathway is specifically activated in the CA1 subregion of the hippocampus during chronic stress and is crucial for inducing depressive-like behavior.

Impact of inflammation-related degenerative changes on the wall strength of unruptured intracranial aneurysms: a pilot study.

INTRODUCTION: Saccular intracranial aneurysm (sIA) rupture is a serious cerebrovascular event associated with inflammatory destructive processes leading to gradual weakening of the sIA wall. The aim of the present study was to identify the morphological and histological determinants for low wall strength in unruptured sIAs harvested from autopsy subjects. MATERIAL AND METHODS: A total of eight single unruptured sIAs were identified and excised with adjacent cerebral arteries during 8 of 184 postmortem examinations. The dome morphology was assessed for each sIA at a constant pressure of 100 mmHg. Then, after 5 preconditioning cycles which assured muscle fibre relaxation, sIA specimens were subjected to gradually increasing intraluminal pressure at a rate of 20 mmHg/s until rupture of the sIA or cerebral artery was achieved. Micro-structural degenerative changes and inflammatory cell infiltration within the sIA wall were quantitatively analysed after pressurization of the sIA specimens. The microscopic analysis of the slides stained with histological methods (HE, Mallory trichrome, Masson trichrome, orcein) and immunohistochemical methods (LCA, CD3, CD68) was performed. RESULTS: The wall of the sIA ruptured in three specimens, while in the other cases, rupture occurred at the arterial wall. The mean maximal dome size was significantly larger in sIAs with low wall strength, that is, in sIAs that ruptured during pressurization, than in sIAs with high wall strength (6.46 mm vs. 2.43 mm, p = 0.034). Moreover, a significantly higher average percentage of wall hyalinization in sIAs that ruptured than in sIAs that did not rupture was observed (30% vs. 0%, p = 0.006). In contrast, the degree of inflammatory cell infiltration did not differ between the wall strength categories. CONCLUSIONS: Our results support the observations that larger sIAs may be at a higher risk of rupture. Histological analysis revealed that hyalinization corresponds to the weakened regions of the wall of unruptured sIAs.

A rare case of fatal poisoning during long-term therapy with lithium carbonate - chronic poisoning, suicide or psychiatric malpractice? / Rzadki przypadek smiertelnego zatrucia w trakcie dlugotrwalej terapii weglanem litu ­ samobójstwo, przewlekle zatrucie czy blad medyczny psychiatry?

The study aims to present a case of atypical poisoning with lithium carbonate in a 57-year-old woman treated for bipolar affective disorder with lithium carbonate for about 30 years. The patient was admitted to the hospital with significant agitation. An important finding obtained from the family interview was the patient's significant weight loss over the past year. In the hospital, the patient received haloperidol and clonazepam. Laboratory tests showed a very high blood lithium concentration of 3.79 mmol/l [N: 0.6─1.2 mmol/l] and elevated serum concentrations of creatinine (3.6 mg/dl) and urea (110 mg/dl). The patient was transferred to the toxicology department, where hemodialysis was performed and intensive treatment initiated. Despite the rapid decrease in lithium levels, her condition gradually deteriorated. The patient died on the fifth day of hospitalization. The autopsy revealed polycystic kidney disease (PKD). During the preparation of the medico-legal report on the correctness of the medical treatment, it was assumed that the cause of death was lithium carbonate poisoning in the course of advanced chronic kidney disease due to PKD, probably a consequence of long-term lithium therapy. The analysis of medical records revealed that despite her psychiatrist's recommendation, the patient had been refusing the monitoring of lithium levels for the past 18 years. This case demonstrates that both psychiatrists and toxicologists should be aware of possible lithium poisoning upon the deterioration of renal function. Therefore, assessment of renal function should be an integral part of monitoring lithium therapy.

Neuropathological analysis of the brains of fifty-two patients with COVID-19.

Coronavirus disease 2019 (COVID-19) poses a global challenge to healthcare and society in the early 21st century. We report neuropathological changes in 52 patients aged between 22 years and 88 years (median 58 years) who were infected with the CoV-2 coronavirus. Patients died under various circumstances and had various pre-existing diseases. The inclusion criteria for this study were: positive result for the nasopharyngeal swab for SARS-CoV-2 RNA, diagnosis of pneumonia of SARS-CoV-2 or nucleoproteins of SARS-CoV-2 in pulmonary tissue confirmed by immunohistochemical methods (IHC). Samples from all brain structures and lung specimens were taken for histopathological examinations. Brain and pulmonary samples were stained typically with histological and immunohistochemical methods and small tissue fragments were examined with the transmission electron microscope (TEM). The light and electron microscopy examination confirmed the numerous neuropathological changes in the brains of the patients infected with the CoV-2. Many of these changes were caused by pre-existing diseases of patients and/or by necessary treatment. However, vascular lesions and the inflammatory process seem to be characteristic of the CoV-2 infection. In all of the structures of 52 brains of patients, damage of the vessel walls and morphological feature of the damage to the blood-brain barrier were observed. Lymphocytic and microglial infiltrates, both perivascular and diffuse, were also observed. Hence, the brain changes due to COVID-19 infection, could be called COVID-19 cerebral angiopathy with diffuse inflammation.

A response to Letter to the Editor titled: Valproic acid for myoclonic epilepsy in POLG1 carriers can be fatal.

Dear Dr. Josef Finsterer, Thank you for your careful and thorough reading of our article and for the valuable comments. We agree that valproic acid is harmful in the mitochondrial disease and we want to add that the described case is currently being prosecuted as medical malpractice.

Encephalomyelitis associated with rheumatoid arthritis: a case report.

Encephalitis/encephalomyelitis in the course of rheumatoid arthritis (RA) remains a matter of debate. We present a case of a patient with encephalomyelitis associated with RA confirmed with post-mortem neuropathological examination. A 68-year-old woman with a long-standing, seropositive history of RA presented progressive disturbances of consciousness. Magnetic resonance imaging (MRI) of the brain and cervical spine revealed an increase of signal intensity on T2-weighted and fluid attenuated inversion recovery (FLAIR) images with corresponding restricted diffusion involving cerebral peduncles, pons, medulla oblongata, and cervical spinal cord and mild contrast-enhancement of the right cerebral peduncle. Extensive radiological and laboratory testing, including autoantibodies to paraneoplastic anti-neuronal and neuronal cell surface antigens, were all negative except for elevated rheumatoid factor. Cerebrospinal fluid (CSF) analysis revealed moderate pleocytosis with mononuclear cell predominance, mildly increased protein level, and negative viral PCRs, bacterial cultures, flow cytometry, and neuronal surface antibodies. Despite intensive treatment with corticosteroids, antibiotics, antiviral drugs, and intravenous immunoglobulin the patient died after 3 months of hospitalization. Post-mortem neuropathological examination revealed numerous, disseminated, heterochronous ischaemic lesions, rarely with haemorrhagic transformation, predominantly in the brainstem, and widespread, diffuse microglia and T-cell infiltrations with neuronal loss and astrogliosis, most severe in the frontal and temporal lobes. Mild, perivascular lymphocyte T infiltrations involved particularly small and medium-sized vessels and were associated with brainstem ischaemic lesions. The neuropathological picture confirmed diagnosis of encephalomyelitis, which together with the clinical course suggested association with RA. Concluding, encepha-lomyelitis due to RA remains a challenging, controversial entity that needs further research and the establishment of effective diagnostic and treatment guidelines.

Morphological and ultrastructural changes in Herpes simplex encephalomyelitis: an attempt to determinate the etiological factor.

Herpes simplex encephalomyelitis (HSE) is a rare disease with a high mortality rate. Correct diagnosis is established on the basis of the combination of the clinical and investigative features. Unfortunately, precise diagnosis remains difficult due to several clinical similarities and false negative or inconclusive results of diagnostic tests. Here, we present two cases of HSE together with the morphological and ultrastructural picture. The first case was a 45-year-old man with acute symptoms of encephalitis, and the other one was a 28-year-old woman presenting subacute encephalomyelitis. Both cases had negative serologic and molecular results for Herpes simplex in the blood and cerebrospinal fluid. Brain and spinal cord samples taken from both cases were stained typically with histological and immunohistochemical methods and small tissue fragments were examined with the transmission electron microscope (TEM). Microscopic examination confirmed viral encephalomyelitis in both cases. An electron micrograph showed typical intranuclear viral particles inside of damaged neurons, which together with topography of brain and spinal cord changes suggest HHV-1/HHV-2 in the first case and/or HHV-3 in the other case. Thus, morphological and ultrastructural examinations may be a useful tool to set up correct diagnosis and help to determine the pathogenic factor in patients suspected of viral encephalomyelitis.

POLG gene mutation. Clinico-neuropathological study.

We present a female patient with a mutation of the POLG gene (POLG DNA polymerase gamma, catalytic subunit; *174763) in which the clinical course suggested a mitochondrial disease, a neuropathological examination identified the syndrome more closely, and a genetic test confirmed the disease. Apart from the morphological lesions typical of Alpers-Huttenlocher syndrome, rarely observed symmetrical degenerative changes in the accessory olivary nuclei were found. It was unusual in the clinical course of the disease that pancreatitis was diagnosed before symptoms of liver failure appeared.

Effects of ethyl alcohol on injuries severity according to injury severity scales in pedestrian fatal injury in traffic crashes.

INTRODUCTION: The dominant cause of injuries in traffic crashes. A significant portion of them affects victims under the influence of ethyl alcohol. The goal of the studies was to assess the correlation between the state of sobriety and the severity of injuries expressed by injury severity scales in fatal pedestrian victims of traffic crashes. Research Material and Method: The data were obtained from the Warsaw Medical University's Department of Forensic Medicine. The analysis covered the data for 2009-2013 and included 200 fatal pedestrian victims hit by passenger cars. The assessment of the effect of risk factors on injury severity expressed in terms of injury severity scales such as Life Threat Indicator (LTI), International Classification based Injury Severity Score (ICISS), Injury Severity Score (ISS) and New Injury Severity Score (NISS), was made using adequately selected methods of statistical analysis. RESULTS: As alcohol concentration increases in women, the values of LTI, ICISS-10 and ICISS-15 decrease, which denotes more severe injuries. In the ISS and NISS, the effect of alcohol concentration on the severity of injuries turned out to be negligible. However, these injuries are significantly heavier in women than in men. According to all the scales used, the older the victims, the milder injuries cause their death. CONCLUSIONS: The studies show that ethyl alcohol concentration may harm injury severity, especially in the case of women. The assessment of the severity of injuries in traffic crash victims is significantly influenced by their age and gender. The more risk factors the scale takes into consideration, the more precise is the assessment.

The effect of ethyl alcohol on the severity of injuries in fatal pedestrian victims of traffic crashes.

INTRODUCTION: A substantial percentage of traffic crashes involve people under the influence of ethyl alcohol. In such circumstances, we speak of the possible effect of ethanol upon trauma outcomes. The present research aimed to assess the state of sobriety fatal pedestrian victims and the correlation between the level of sobriety and the severity of injuries. RESEARCH MATERIAL AND METHOD: The data was obtained from the Warsaw Medical University's Department of Forensic Medicine. The analysis covered the data for the period of 2009-2013; it encompassed 158 fatal pedestrian victims hit by passenger cars. The appropriate methods of statistical analysis were applied. RESULTS: The majority of the fatal pedestrian victims were individuals under the influence of ethyl alcohol (72.15%). Significant correlations were observed between the concentration of ethyl alcohol and the victims' gender (p<0.0001) and age (p = 0.0026). The analysis showed that pedestrians under the influence of ethyl alcohol more often died on the scene (78.95%). CONCLUSIONS: Pedestrians under the influence of ethyl alcohol are a significant group of victims of traffic crashes. Ethyl alcohol is not an independent factor affecting the severity of injuries. A higher percentage of pedestrian victims die on the scene, especially in rural areas.