Quantitative morphological analysis of age structural changes in prostate of experimental animals with ethanol poisoning.

OBJECTIVE: Aim: To find out the age remodeling of the structural components of the prostate gland at alcohol poisoning using quantitative morphological analysis. PATIENTS AND METHODS: Materials and Methods: The structure of the prostate gland of 4 white male rats groups were morphologically investigated. The 1 group included 30 control intact animals aged 8 months, the 2-nd group - 30 rats aged 24 months, the 3-rd group - 30 8-month-old animals with ethanol intoxication, and the 4-th group included 30 24-month-old rats with the specified simulated pathology. Ethanol intoxication was modeled by intragastric administration of 30% ethyl alcohol solution at a dose of 20 ml/kg once daily for 28 days. Rats were euthanized by bloodletting under general thiopental anesthesia 28 days after the beginning of the experiment. The area of glands, the height of glandular epithelial cells, the area of their nuclei and cytoplasm, the nuclear-cytoplasmic ratio in these cells and the stromal-parenchymal ratio in the organ were studied using light microscopy and were determined morphometrically. Morphometric parameters were processed statistically. RESULTS: Results: It was established that with age in the intact prostate of laboratory sexually mature white male rats, the area of glands, the height of glandular epitheliocytes, the area of their nuclei and cytoplasm, with the stability of nuclear-cytoplasmic ratios in the epithelial cells of the glands, significantly decreases, and the stromal-parenchymal ratio in the organ under study increases. Long-term ethanol poisoning leads to pronounced structural changes in the prostate, which is characterized by pronounced atrophy of the glandular epithelium, a decrease in the area of the glands, a decrease in the height of epithelial cells, a violation of nuclear-cytoplasmic relations in them, an increase in stromal-parenchymal ratio, and a prominent growth of the muscle-elastic stroma. The revealed structural changes of the studied components of the prostate dominated in 24-month-old experimental animals. CONCLUSION: Conclusions: Morphological analysis of the prostate gland established that morphometric and morphological changed significantly according to the age and were depend on the ethanol poisoning.

[Qualitative and quantitative characteristics of structures of cerebral cortex structure in young people under conditions of chronic alcohol intoxication]. / Kachestvennaya i kolichestvennaya kharakteristika struktur kory golovnogo mozga u lits molodogo vozrasta v usloviyakh khronicheskoi alkogol'noi intoksikatsii.

OBJECTIVE: To study morphological changes of cerebral cortex in young people under the conditions of chronic alcohol intoxication (CAI). MATERIAL AND METHODS: Morphometric examination of cerebral cortex fragments obtained from 28 persons who died with a CAI diagnosis (average age was 38 years), and 25 subjects who died from other causes, which are not associated with alcohol consumption (average age was 39 years), was carried out. RESULTS: It was shown that neurons of pathological shapes, including hypo- and hyperchromic, pyknotic and «shadow-like¼, were dominant in group of CAI. There was an increase in the glial index and a greater intensity of perivascular and pericellular edema compared to the control group. CONCLUSION: Morphological changes of cerebral cortex under the conditions of CAI are non-specific and largely similar to neurodegenerative alterations in other pathological conditions, senile dementia. Clearer histological criteria for alcoholic encephalopathy are needed, including with the use of immunohistochemical methods.

Acute benzyl alcohol intoxication: An autopsy case report.

INTRODUCTION: The main mechanism of death and the pathological appearance of cases of benzyl alcohol intoxication has not been fully investigated. Autopsy reports of cases of benzyl alcohol intoxication have not been published. CASE PRESENTATION: A 24-year-old man was found in the state of cardiopulmonary arrest at a construction site. He had been performing paint stripping. He was immediately transferred to the hospital, but he did not recover. An autopsy showed focal coloring of the skin without any major caustic injury. A histopathological investigation showed vacuolar degeneration in the epidermis and dermo-epidermal junction, and severe erosion of the tracheal and bronchial mucosa. No pathological changes in the kidney were evident. A neuropathological investigation showed central chromatolysis of neuronal cells in pontine nuclei and grumose degeneration in the cerebellar dentate nucleus. The blood content of benzyl alcohol was 780.0 µg/mL. LESSONS: Present case suggest that multiple pathways of exposure may be associated with more rapid progression in acute benzyl alcohol intoxication, and that early and/or severe involvement of the central nervous system rather than renal dysfunction may be associated with an early death.

Single-dose ethanol intoxication causes acute and lasting neuronal changes in the brain.

Alcohol intoxication at early ages is a risk factor for the development of addictive behavior. To uncover neuronal molecular correlates of acute ethanol intoxication, we used stable-isotope-labeled mice combined with quantitative mass spectrometry to screen more than 2,000 hippocampal proteins, of which 72 changed synaptic abundance up to twofold after ethanol exposure. Among those were mitochondrial proteins and proteins important for neuronal morphology, including MAP6 and ankyrin-G. Based on these candidate proteins, we found acute and lasting molecular, cellular, and behavioral changes following a single intoxication in alcohol-naïve mice. Immunofluorescence analysis revealed a shortening of axon initial segments. Longitudinal two-photon in vivo imaging showed increased synaptic dynamics and mitochondrial trafficking in axons. Knockdown of mitochondrial trafficking in dopaminergic neurons abolished conditioned alcohol preference in Drosophila flies. This study introduces mitochondrial trafficking as a process implicated in reward learning and highlights the potential of high-resolution proteomics to identify cellular mechanisms relevant for addictive behavior.

Morphofunctional State and Circadian Rhythms of the Liver under the Influence of Chronic Alcohol Intoxication and Constant Lighting.

A study of the influence of chronic alcohol intoxication, constant illumination and their combined effects on the morphofunctional state of the rat liver and the circadian rhythms (CR) of the studied parameters of the organism was carried out. It was found that both alcohol and constant illumination caused significant changes in the structure of the liver, as well as in the circadian rhythmicity of micromorphometric parameters of hepatocytes, ALT, and total and direct bilirubin rhythms; however, the combined effects of ethanol and constant illumination had the most significant effect on the studied parameters of the organism. These two factors caused disturbances in the circadian rhythms of the micromorphometric parameters of hepatocytes, disruption of the circadian rhythms of total protein, albumin, AST, ALT, and direct and total bilirubin, as well as disturbances in the expression and rhythmicity of the studied clock genes against a background of the development of an inflammatory process in the liver.

Identification of Dihydromyricetin and Metabolites in Serum and Brain Associated with Acute Anti-Ethanol Intoxicating Effects in Mice.

Dihydromyricetin is a natural bioactive flavonoid with unique GABAA receptor activity with a putative mechanism of action to reduce the intoxication effects of ethanol. Although dihydromyricetin's poor oral bioavailability limits clinical utility, the promise of this mechanism for the treatment of alcohol use disorder warrants further investigation into its specificity and druggable potential. These experiments investigated the bioavailability of dihydromyricetin in the brain and serum associated with acute anti-intoxicating effects in C57BL/6J mice. Dihydromyricetin (50 mg/kg IP) administered 0 or 15-min prior to ethanol (PO 5 g/kg) significantly reduced ethanol-induced loss of righting reflex. Total serum exposures (AUC0→24) of dihydromyricetin (PO 50 mg/kg) via oral (PO) administration were determined to be 2.5 µM × h (male) and 0.7 µM × h (female), while intraperitoneal (IP) administration led to 23.8-fold and 7.2- increases in AUC0→24 in male and female mice, respectively. Electrophysiology studies in α5ß3γ2 GABAA receptors expressed in Xenopus oocytes suggest dihydromyricetin (10 µM) potentiates GABAergic activity (+43.2%), and the metabolite 4-O-methyl-dihydromyricetin (10 µM) negatively modulates GABAergic activity (-12.6%). Our results indicate that administration route and sex significantly impact DHM bioavailability in mice, which is limited by poor absorption and rapid clearance. This correlates with the observed short duration of DHM's anti-intoxicating properties and highlights the need for further investigation into mechanism of DHM's potential anti-intoxicating properties.

The effect of ketoprofen lysine salt on mucosa of rat stomach after ethyl alcohol intoxication.

INTRODUCTION: Ketoprofen is a commonly used nonsteroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic properties. Side effects of ketoprofen occur mainly from the gastrointestinal tract due to the inhibition of cyclooxygenaze-1. Binge drinking at least once a week is reported by 80 million Europeans. On the day after many of them use NSAIDs. This increases the risk for damage of gastric mucosa. AIM: The aim of the study was to check if use of ketoprofen lysine salt (KLS) has any gastroprotective effect on mucosa of rat stomach after ethyl alcohol intoxication. MATERIALS AND METHODS: There were 6 groups of 6 male rats which received: RESULTS: In groups 1, 2 and 3 the histopathologic examination of the stomachs revealed normal picture, without signs of inflammation. In the group 4, 5 and 6 within the mucosa and submucosa there were visible numerous infiltrates of inflammatory cells, consisting mainly of lymphocytes, plasmocytes and eosinophilia. Total leukocyte count was elevated in group 3, 4, 6. There was a significant decrease of blood urea concentration in group 6 vs 2 and significant decrease of serum albumin in group 6 vs 1 and 2, and total protein vs group 1. CONCLUSION: Side effects of ketoprofen occur mainly from the gastrointestinal tract. KLS has no gastroprotective effect after ethanol-gastric injury and does not protect gastric mucosa from damage produced by binge drinking. Therefore it should not be used after drinking distilled spirits.

Self-Assembled Micelles Improve the Oral Bioavailability of Dihydromyricetin and Anti-Acute Alcoholism Activity.

Dihydromyricetin (DMY) is highly effective in counteracting acute alcohol intoxication. However, its poor aqueous solubility and permeability lead to the low oral bioavailability and limit its clinic application. The aim of this work is to use Solutol®HS15 (HS 15) as surfactant to develop novel micelle to enhance the oral bioavailability of DMY by improving its solubility and permeability. The DMY-loaded Solutol®HS15 micelles (DMY-Ms) were prepared by the thin-film hydration method. The particle size of DMY-Ms was 13.97 ± 0.82 nm with an acceptable polydispersity index of 0.197 ± 0.015. Upon entrapped in micelles, the solubility of DMY in water was increased more than 25-fold. The DMY-Ms had better sustained release property than that of pure DMY. In single-pass intestinal perfusion models, the absorption rate constant (Ka) and permeability coefficient (Papp) of DMY-Ms were 5.5-fold and 3.0-fold than that of pure DMY, respectively. The relative bioavailability of the DMY-Ms (AUC0-∞) was 205% compared with that of pure DMY (AUC0-∞), indicating potential for clinical application. After administering DMY-Ms, there was much lower blood alcohol level and shorter duration of the loss of righting relax (LORR) in drunk animals compared with that treated by pure DMY. In addition, the oral administration of DMY-Ms greatly reduced oxidative stress, and significantly defended liver and gastric mucosa from alcoholic damages in mice with alcohol-induced tissue injury. Taken together, HS 15-based micelle system greatly improves the bioavailability of DMY and represents a promising strategy for the management of acute alcoholism. Graphical abstract.

Microglia depletion and alcohol: Transcriptome and behavioral profiles.

Alcohol abuse induces changes in microglia morphology and immune function, but whether microglia initiate or simply amplify the harmful effects of alcohol exposure is still a matter of debate. Here, we determine microglia function in acute and voluntary drinking behaviors using a colony-stimulating factor 1 receptor inhibitor (PLX5622). We show that microglia depletion does not alter the sedative or hypnotic effects of acute intoxication. Microglia depletion also does not change the escalation or maintenance of chronic voluntary alcohol consumption. Transcriptomic analysis revealed that although many immune genes have been implicated in alcohol abuse, downregulation of microglia genes does not necessitate changes in alcohol intake. Instead, microglia depletion and chronic alcohol result in compensatory upregulation of alcohol-responsive, reactive astrocyte genes, indicating astrocytes may play a role in regulation of these alcohol behaviors. Taken together, our behavioral and transcriptional data indicate that microglia are not the primary effector cell responsible for regulation of acute and voluntary alcohol behaviors. Because microglia depletion did not regulate acute or voluntary alcohol behaviors, we hypothesized that these doses were insufficient to activate microglia and recruit them to an effector phenotype. Therefore, we used a model of repeated immune activation using polyinosinic:polycytidylic acid (poly(I:C)) to activate microglia. Microglia depletion blocked poly(I:C)-induced escalations in alcohol intake, indicating microglia regulate drinking behaviors with sufficient immune activation. By testing the functional role of microglia in alcohol behaviors, we provide insight into when microglia are causal and when they are consequential for the transition from alcohol use to dependence.

NADPH oxidase contributes to oxidative damage and mitochondrial impairment induced by acute ethanol treatment in rat hippocampal neurons.

Acute ethanol treatment induces neurodegeneration in cultured neurons and can lead to brain damage in animal models. Neuronal cells exposed to ethanol showed an increase in reactive oxygen species (ROS), oxidative damage and mitochondrial impairment contributing to synaptic failure. However, the underlying mechanisms of these events are not well understood. Here, we studied the contribution of NADPH oxidase, as a relevant source of ROS production in the brain, to mitochondrial impairment and oxidative stress induced by ethanol. We used primary hippocampal neurons subjected to an acute treatment of ethanol at increasing concentrations (25, 50, and 75 mM, 24 h), and we evaluated ROS production, mitochondrial function, and synaptic vesicle activity. Our studies showed that after ethanol administration, hippocampal neurons presented an increase in ROS levels, mitochondrial dysfunction, calcium handling defects, and synaptic impairment. Interestingly, treatment with the NADPH inhibitor, apocynin, significantly prevented oxidative stress, mitochondrial dysfunction, and the impairment of synaptic vesicle activity induced by ethanol treatment. These results indicate that NADPH oxidase could be a key participant in the molecular mechanism by which alcohol affects the brain.

1,4-Butanediol overdose mimicking toxic alcohol exposure.

Context: 1,4-butanediol (1,4-BD) is a gamma-hydroxybutyrate (GHB) analogue with a similarly narrow therapeutic window that is becoming a more common cause of recreational overdose. Reports of confirmed exposures are limited.Case details: A 44 year-old man who had consumed alcohol subsequently became unconscious after ingesting what was thought to be GHB. The presentation was not entirely consistent with GHB poisoning, including a longer duration of unconsciousness and features that mimicked toxic alcohol exposure including a high anion gap metabolic acidosis (HAGMA) and osmol gap. The patient was treated supportively with intubation, haemodiafiltration and intravenous ethanol until the diagnosis was refined using specific laboratory testing. The concentration of 1,4-BD was the highest reported in the literature and the outcome favourable.Discussion: This case highlights pharmacokinetic issues peculiar to 1,4-BD, including the interaction with ethanol which delays the onset of psychoactive effects from 1,4-BD's metabolite GHB, and dose-dependent pharmacokinetics. In overdose, 1,4-BD can induce a HAGMA and other features of toxic alcohol poisoning. Managing an unconscious patient with these features can prompt certain treatments until the diagnosis is refined, which can require specific laboratory testing to identify the culprit. The actual risk of toxic alcohol and other causes is adjusted on a case-by-case basis from the history of exposure and local epidemiology of substance use and poisoning.

Ipsilateral radial nerve, median nerve, and ulnar nerve injury caused by crush syndrome due to alcohol intoxication: A case report.

RATIONALE: Autologous peripheral nerve injury caused by crush syndrome due to alcohol intoxication is relatively rare, and to our knowledge, the compression of 3 upper limb nerves at the same time has not been reported previously. If a compressive peripheral nerve injury is not treated in a timely manner, it is difficult to recover neurological function, and the prognosis is poor. PATIENT CONCERNS: Here, we present a case of a 50-year-old man with ipsilateral radial nerve, median nerve, and ulnar nerve injuries caused by autogenous compression after drunkenness. DIAGNOSIS: Electromyography and nerve conduction studies suggested peripheral nerve injury in the left upper limb. The diagnosis was injury to the radial nerve, median nerve, and ulnar nerve in the left upper arm. INTERVENTIONS: Exploratory neurolysis surgery of the radial nerve, median nerve, and ulnar nerve was performed in the left upper arm. Postoperative oral neurotrophic drugs were administered, and functional exercise was performed. OUTCOMES: After timely diagnosis and treatment, the strength of the left upper arm muscle recovered, and the prognosis of neurological function was satisfactory during 3 years of follow-up sessions. LESSONS: In the treatment of such patients, a comprehensive understanding of their medical history and a strict physical examination should be performed. Combined with neuroelectrophysiological and imaging examination, the diagnosis can be confirmed. After timely diagnosis and treatment, the prognosis is mostly excellent.

Ethanol Intoxication of Young Children.

Ethanol intoxication of infants and young children can be a challenging diagnosis in the pediatric emergency department, and features of the poisoning may differ in comparison with adolescents. The sources of ethanol exposures in this age are varied and include unintentional, malicious, and iatrogenic etiologies. Young children exposed to ethanol often present with mixed clinical signs and symptoms that may not fit the traditional ethanol or sedative-hypnotic toxidrome. Pediatric ethanol intoxications are often managed supportively, and recovery is usually rapid. The purpose of this review is to describe the sources of ethanol poisoning among children 6 years and younger, highlight presenting symptoms and pharmacokinetic considerations unique to this age group, and review management strategies. In addition, published cases of ethanol poisoning due to ingestion among young infants are compiled for presentation.

Miguel Ángel y el hígado de Noé: ¿Una lección secreta de anatomía? / Michelangelo and Noah's liver: a hidden anatomy lesson?

Miguel Ángel Buonarroti (1475 - 1564) es considerando uno de los más grandes artistas de la historia. Estudió en detalle la anatomía humana a través de la disección de cadáveres, práctica hasta entonces relegada por motivos religiosos. Desde que en el año 1990 el médico Frank Lynn Meshberger publicara su interpretación del fresco "La Creación de Adán" basada en la neuroanatomía, en donde comparaba la imagen de Dios con la de una sección sagital del cerebro humano, muchos autores han encontrado diversas referencias anatómicas ocultas en la obra de Miguel Ángel. En el presente trabajo exponemos el hallazgo de una inédita lección de anatomía hepática oculta en el fresco La Embriaguez de Noé de la Capilla Sixtina.

Michelangelo Buonarroti (1475 - 1564) is considered one of the greatest artists in history. He studied in detail the human anatomy through corpses dissection, practice until then relegated for religious reasons. Since the physician Frank Lynn Meshberger published in 1990 his interpretation of the fresco "The Creation of Adam" based on neuroanatomy, where he compared the image of God with a sagittal section of the human brain, many authors have found various hidden anatomical references in the work of Michelangelo. In the present paper we expose the finding of a hidden lesson on liver anatomy in the fresco The Drunkenness of Noah of the Sistine Chapel.

Function and Mechanism of Myelin Regulation in Alcohol Abuse and Alcoholism.

Excessive alcohol use has adverse effects on the central nervous system (CNS) and can lead to alcohol use disorders (AUDs). Recent studies have suggested that myelin reductions may directly contribute to CNS dysfunctions associated with AUDs. Myelin consists of compact lipid membranes wrapped around axons to provide electrical insulation and trophic support. Regulation of myelin is considered as a new form of neural plasticity due to its profound impacts on the computation of neural networks. In this review, the authors first discuss experimental evidence showing how alcohol exposure causes demyelination in different brain regions, often accompanied by deficits in cognition and emotion. Next, they discuss postulated molecular and cellular mechanisms underlying alcohol's impact on myelin. It is clear that more extensive investigations are needed in this important but underexplored research field in order to gain a better understanding of the myelin-behavior relationship and to develop new treatment strategies for AUDs.

Therapeutic potential of PACAP in alcohol toxicity.

Alcohol addiction is a worldwide concern as its detrimental effects go far beyond the addicted individual and can affect the entire family as well as the community. Considerable effort is being expended in understanding the neurobiological basis of such addiction in hope of developing effective prevention and/or intervention strategies. In addition, organ damage and neurotoxicological effects of alcohol are intensely investigated. Pharmacological approaches, so far, have only provided partial success in prevention or treatment of alcohol use disorder (AUD) including the neurotoxicological consequences of heavy drinking. Pituitary adenylate cyclase-activating polypeptide (PACAP) is an endogenous 38 amino-acid neuropeptide with demonstrated protection against neuronal injury, trauma as well as various endogenous and exogenous toxic agents including alcohol. In this mini-review, following a brief presentation of alcohol addiction and its neurotoxicity, the potential of PACAP as a therapeutic intervention in toxicological consequences of this devastating disorder is discussed.

[HISTOLOGICAL AND IMMUNOHISTOCHEMICAL PROFILE OF THE MYOCARDIUM DURING ALCOHOL INTOXICATION IN THE EXPERIMENT].

The purpose of this study was to identify early structural and conjugated with them molecular changes in the myocardium, stroma and blood vessels under experimental alcohol intoxication, with histological and immunohistological methods. The experiments were carried out on white male rats with initial body weight 180-200gg. Accordingly, specific tasks were carried out 2 series of experiments: I series - acute alcohol intoxication, II series - chronic alcohol intoxication. The study of the both myocardium ventricles at different regimes of ethanol consumption revealed changes in cardiomyocytes and extracellular matrix - basal membrane, connective tissue and vessels. Microcirculation disorder, after 3 hours of ethanol intraperitoneal injection leads to acute myocardial hypoxia, and sarcoplasm vacuolization. Under chronic (30 days) ethanol intoxication, microcirculatory disturbances are aggravate, however, it becomes important the damage of the contractile apparatus in the form of a spectrum of changes: the myolysis, the vacuolization of the sarcoplasm. At the same time, in the wall of small arteries and between myofibrils structures identical to type IV collagen appear. The increase of Vimentin expression, in our experiment, indicates the starting of myocardial damage dynamic mechanisms, realized by the type of focal cardiosclerosis. Data on immunohistochemistry of p53 revealed that under our experimental conditions, the homeostasis of the cardiovascular tissue has changed. The initiation of cardiosclerosis can also be considered as the manifestation of p53 effects, as a factor forming a critical point of intramyocardial regulation disturbance.

Importance of effusion of blood under the dura mater in forensic medicine: A STROBE - compliant retrospective study.

Subdural hemorrhage is commonly associated with mechanical brain injury and has a correspondingly high mortality rate. Subdural hematomas may immediately provoke symptoms or may be initially asymptomatic, with further symptoms evolving rapidly and fatally.The data regarding forensic autopsy of victims were obtained from The State Forensic Medicine Service of Lithuania between the years 2013 and 2016. A retrospective study was performed including 110 patients, whose cause of death was subdural hemorrhage. 95% confidence intervals were calculated.It was calculated, that in cases of sudden death, after subdural hemorrhage was diagnosed, a higher concentration of ethyl alcohol in blood (mean 2.22 ±â€Š1.3%) demanded a smaller amount of blood under the dura matter (mean 81.6 ±â€Š60.5 g) in order for the patient to die. It was also noted that hospitalized patients with subdural hemorrhage had a smaller concentration of blood ethyl alcohol (mean 1.33 ±â€Š1%) and a larger amount of blood under the dura (mean 135.6 ±â€Š82.9 g).Due to the toxic effect of ethyl alcohol, even a small amount (81.6 ±â€Š60.5 g) of blood under the dura matter can determine a sudden death.

[Clinical pathomorphology and tanatogenesis of various forms of alcoholic intoxication]. / Klinicheskaia patomorfologiia i tanatogenez razlichnykh form alkogol'noi intoksikatsii.

The objective of the present study was to identify the clinical and pathomorphological changes in the internal organs for the elucidation of the cause of death associated with various forms of alcoholic intoxication (chronic alcoholic intoxication, poisoning with surrogate alcohols, etc.). The analysis of the clinical conditions resulting from alcohol abuse has demonstrated that the principal pathology underlying the fatal outcome is complemented by a variety of non-lethal somatic disorders aggravating the patients' condition and enhancing its severity. The clinicians are known to give more attention to the accompanying somatic complications than to the cause underlying the main pathology (alcoholism). Such attitude in the absence of the adequate treatment of the alcohol dependency is neither clinically efficient nor economically appropriate. Poisoning with surrogate alcohols is characterized by the pulmonary-cerebral variant of tanatogenesis in the combination with hypercoagulation and the erosive processes in the gastrointestinal tract whereas death from alcoholic intoxication is usually associated with heart tanatogenesis.

Bath-related Deaths in Korea between 2008-2015.

BACKGROUND: The diagnostic criteria for bathtub drownings are not standardized, and the risk factors associated with bath-related deaths are unclear. METHODS: We analyzed a Korean nationwide database of bath-related deaths that occurred between January 2008 and December 2015. Eighty-four cases were enrolled after reviewing 31,123 autopsy records. RESULTS: The subjects' ages ranged from 18 to 91 years, with a mean age ± standard deviation of 61.3 ± 16.0 years. Bath-related deaths in the winter were approximately 4.6-fold greater than those in the summer. Of the 84 subjects, the primary cause of death in 57 (67.9%) was drowning in the bath; 24 (28.6%) drowned of other causes such as natural diseases, and 3 (3.6%) died of acute alcohol intoxication. We analyzed water-inhalation signs to establish criteria for bathtub drowning diagnosis. There were significantly higher incidences of hyperinflated lungs, water in the sphenoid sinus and stomach/duodenal contents, and Paltauf's spots (subpleural hemorrhage) in bathtub-drowned subjects compared to non-drowned individuals (P < 0.01). Multiple signs of water inhalation were significantly associated with bathtub drowning (P < 0.01). The two leading contributory causes of bath-related death were cardiovascular diseases and alcohol intoxication (binge drinking before bathing). CONCLUSION: The diagnosis of bath-related deaths could present considerable medico-legal problems; therefore, a comprehensive autopsy with a thorough scene investigation can clarify the cause of death in these situations. Preventive strategies for reducing such deaths should target alcohol drinking before bathing and long soaking times in bathtubs, especially among elderly individuals with preexisting cardiovascular diseases.