A 68-Year-Old Man with Depression and Acute Renal Failure Due to Rhabdomyolysis Associated with Alcohol Intoxication While Taking Low-Dose Escitalopram: A Case Report.

BACKGROUND Rhabdomyolysis, an uncommon but recognized adverse effect of selective serotonin reuptake inhibitor (SSRI) antidepressants, can precipitate acute renal injury (AKI), especially when combined with risk factors such as alcohol consumption. This report describes a 68-year-old man with acute renal failure due to rhabdomyolysis associated with alcohol intoxication while taking low-dose escitalopram, an SSRI antidepressant. CASE REPORT The patient, with a history of bipolar affective disorder managed with escitalopram, presented with symptoms of general malaise, diarrhea, myalgias, and transient loss of consciousness following substantial ethanol consumption. Laboratory tests indicated severe rhabdomyolysis with a creatine kinase level of 37 672 U/L and myoglobin level >5710 ng/ml, leading to an AKI diagnosis. The discontinuation of escitalopram, along with hydration and renal replacement therapy, facilitated renal recovery. However, the reintroduction of escitalopram resulted in the recurrence of rhabdomyolysis, suggesting a probable causal link, confirmed using the Naranjo Adverse Drug Reaction Probability Scale. CONCLUSIONS This report highlights the importance of identifying the medication history in patients presenting with acute renal failure and rhabdomyolysis and the association with SSRIs, which can be exacerbated by alcohol. This case underscores the importance of vigilant medication history assessment in patients presenting with AKI and rhabdomyolysis, particularly concerning the use of SSRIs like escitalopram, which can pose heightened risks in the context of alcohol use. It highlights the need for clinical caution in managing patients on long-term SSRI therapy, especially when reintroducing such medications after an episode of rhabdomyolysis.

Intoxication and Glasgow coma scale scores in patients with head trauma.

INTRODUCTION: The Glasgow Coma Scale (GCS) is an assessment tool commonly used by emergency department (ED) clinicians to objectively describe level of consciousness, especially in trauma patients. This study aims to assess the effect of drug and alcohol intoxication on GCS scores in cases of traumatic head injury. METHODS: In this retrospective chart review study, data were extracted from The Pennsylvania Trauma Systems Foundation Data Base Collection System. Eligible subjects included trauma patients aged 18 years and older, with head trauma, who presented between January 2019 and August 2023. Subjects were matched to controls who did not test positive for drugs or alcohol, matched by Injury Severity Score (ISS) category. RESULTS: Among 1088 subjects, the mean age was 63 (95% CI 62-64). The mean Injury Severity Score was 21 (95% CI 21-22). The median GCS among all subjects was 14 (IQR 6-15). Cases with alcohol or drug use were matched to controls without alcohol or drug use, and were matched by categories of Injury Severity Score. Cases with alcohol or drug use had lower GCS (median 13; IQR 3-15), compared to cases without alcohol or drug use (median 15; IQR 13-15) (p < 0.0001, Wilcoxon Rank Sum Test). CONCLUSIONS: Among patients with head trauma, intoxicated patients had statistically significant lower GCS scores as compared to matched patients with similar Injury Severity Scores.

Ethanol endometrioma sclerotherapy: safety through 8 years of experience.

STUDY QUESTION: What are the complications of transvaginal ethanol sclerotherapy for the treatment of endometriomas? SUMMARY ANSWER: Sclerotherapy is a reliable, minimally invasive method applicable in outpatient procedures but with specific and potential life-threatening complications that need to be identified and prevented. WHAT IS KNOWN ALREADY: There are currently few data on the use of transvaginal ethanol sclerotherapy, and we mainly note septic complications. STUDY DESIGN, SIZE, DURATION: A retrospective observational cohort study was carried out. The study was conducted at an academic hospital and included 126 women aged 31.9 ± 5.5 years (mean ± SD), between November 2013 and June 2021. We analyzed a total of 157 ethanol sclerotherapy treatment (EST), treated by 131 EST procedures, in 126 women. PARTICIPANTS/MATERIALS, SETTING, METHODS: The study included women with an indication for transvaginal ethanol sclerotherapy. Indications were women with at least one endometrioma over 10 mm, isolated or associated with other endometriosis locations, requiring treatment for pain or infertility before assisted reproductive treatment. We followed a standardized transvaginal ethanol sclerotherapy procedure consisting of an ultrasound-guided transvaginal puncture of one or more endometriomas under general anesthesia. The cyst content was completely removed and flushed with saline solution. Ethanol (96%) was injected at 60% of the initial volume of the endometrioma, remained in the cyst for 10 min and was then completely removed. Ethanol loss was defined as a loss of 5 ml or more than 10% of the initial volume of the injected ethanol. Failure was defined by the contraindication of endometrioma puncture because of interposition of the digestive tract, ethanol loss in the previous endometrioma treated (in case of multiple ESTs), failure to aspirate the endometriotic fluid, contraindication to start ethanol injection owing to saline solution leakage, or contraindication to continue ethanol injection owing to suspicions of ethanol leakage at sonography. Intraoperative complications were defined by ethanol loss, positive blood alcohol level, and ethanol intoxication. Postoperative complications were defined by fever, biological inflammatory syndrome, and ovarian abscess. Complications were classified according to the Clavien and Dindo surgical classification, which is a system for classifying postoperative complications in five grades of increasing severity. MAIN RESULTS AND THE ROLE OF CHANCE: We reported a total of 17/157 (10.8%) transvaginal ethanol sclerotherapy failures during 14/131 (10.7%) transvaginal ethanol sclerotherapy procedures in 13/126 (10.3%) women. In the same sets of data, complication was reported for 15/157 (9.5%) transvaginal ethanol sclerotherapy in 13/131 (9.9%) transvaginal ethanol sclerotherapy procedures in 13/126 (10.3%) women. Nine of 126 women (7.1%) had a grade I complication, one (0.8%) had a grade II complication (medical treatment for suspicion of pelvic infection), two (1.6%) had a grade III complication (ovarian abscess) and one (0.8%) had a grade IV complication (ethanol intoxication). We did not observe any grade V complications. LIMITATIONS, REASONS FOR CAUTION: This was a retrospective study and pain assessment not considered. The benefit-risk balance of endometrioma transvaginal ethanol sclerotherapy was not evaluated. WIDER IMPLICATIONS OF THE FINDINGS: Our study is the first to evaluate the complications of transvaginal ethanol sclerotherapy with such a large cohort of women in a standardized protocol. Transvaginal ethanol sclerotherapy seems to be an effective alternative to laparoscopic surgery in the management of endometriomas and limits the alteration of ovarian reserve. Transvaginal ethanol sclerotherapy is a reliable, minimally invasive method applicable on an outpatient basis. The majority of complications are Clavien-Dindo ≤IV, for which preventative measures, or at least early diagnosis and treatment, can be easily performed. The risk of ethanol intoxication is rare, but it is a life-threatening risk that must be avoided by appropriate implementation and promotion of the sclerotherapy procedures. STUDY FUNDING/COMPETING INTEREST(S): None. TRIAL REGISTRATION NUMBER: Aix Marseille University's ethics committee registration number 2021-06-03-01.

Immune biomarkers in non-treatment-seeking heavy drinkers who used a probiotic supplement for 30 days: An open-label pilot study.

Alcohol use disorder (AUD) is associated with significant psychological and economic burdens, as well as physical comorbidities that can lead to death. Previous research has found that probiotics may reduce inflammatory biomarkers in persons with AUD and comorbid conditions such as cirrhosis of the liver. This relationship has not been explored in heavy drinkers without comorbid conditions. In a proof-of-concept study, individuals who were heavy drinkers without known comorbidities received a 30-day course of a daily probiotic supplement in an open-label pilot trial. Eligible participants (N = 16) met NIAAA guidelines for heavy alcohol use and did not report any preexisting medical problems. Blood samples were taken at four timepoints: prior to the probiotic course, at the midpoint, at the end, and after a washout period of at least one month. Immunoassays were conducted on plasma samples to quantify the following inflammatory biomarkers: IL-6, IL-8, IL-10, LBP, MCP-1, sCD14, sCD163, and TNF-α. Linear mixed models were used to test within-subjects changes in biomarker concentrations over the study period, with alcohol use included as a time-varying covariate. Biomarker concentrations did not change significantly. A higher number of heavy drinking days was statistically associated with higher concentrations of IL-6 (F(1,8) = 6.66, p = 0.0326) and IL-8 (F(1,17) = 6.38, p = 0.0218). Greater days since last drink was associated with a lower concentration of MCP-1 (F(1,17) = 5.77, p = 0.028). In summary, biomarker trajectories were associated with alcohol consumption variables, but not probiotic use, in this open-label pilot study. Randomized controlled trials are needed to evaluate fully the potential benefits of probiotics in heavy drinkers without known comorbidities and under conditions of non-abstinence.

Acute ptotic myelopathy: cervical compressive myelopathy resulting from prolonged head ptosis after alcohol intoxication.

A 28-year-old man was brought to the emergency department with quadriparesis of acute onset after a bout of binge drinking. Evaluation revealed a mid-cervical myelopathy and magnetic resonance imaging (MRI) showed an acute compressive cervical myelopathy. He also developed rhabdomyolysis, and cervical paraspinal muscles showed MRI hyperintensities. After resolution of rhabdomyolysis and acute kidney injury, he underwent cervical spine fixation. He was found to have acute dropped head syndrome with secondary compressive myelopathy.

Adolescent alcohol and cannabis use as risk factors for head trauma in the Northern Finland Birth Cohort study 1986.

BACKGROUND: The aim of this study was to assess the associations between cannabis use and frequency of alcohol intoxication in adolescence with the risk of traumatic brain injury and craniofacial fractures in early adulthood. Hypothesis was that using alcohol and cannabis in adolescence could increase the risk for head traumas. METHODS: Data from the Northern Finland Birth Cohort 1986 (n = 9432 individuals) were used to investigate the prospective association between the self-reported frequency of alcohol intoxication (n = 6472) and cannabis use (n = 6586) in mid-adolescence and register-based, head trauma diagnoses by ages 32-33 years. To test the robustness of these associations, the statistical models were adjusted for a range of other confounders such as illicit drug use, previous head trauma and self-reported mental health problems. RESULTS: In multivariate analyses, cannabis use was statistically significantly associated with a greater risk of traumatic brain injury among females [hazard ratio (HR) 1.9, 95% confidence interval (CI) 1.1-3.2, P = 0.024). Frequent alcohol intoxication was a statistically significant independent risk factor for both traumatic brain injury (HR 2.6, 95% CI 1.7-3.9, P < 0.001) and craniofacial fractures (HR 2.7, 95% CI 1.6-4.8, P < 0.001) among males. CONCLUSIONS: Cannabis use in adolescence appears to associate independently with elevated risk for traumatic brain injury among females, and frequent alcohol intoxication in adolescence seems to associate with elevated risk of both traumatic brain injury and craniofacial fractures among males.

Binge drinking episode causes acute, specific alterations in systemic and hepatic inflammation-related markers.

BACKGROUND: Frequent binge drinking is a known contributor to alcohol-related harm, but its impact on systemic and hepatic inflammation is not fully understood. We hypothesize that changes in immune markers play a central role in adverse effects of acute alcohol intake, especially in patients with early liver disease. AIM: To investigate the effects of acute alcohol intoxication on inflammation-related markers in hepatic and systemic venous plasma in people with alcohol-related liver disease (ArLD), non-alcoholic fatty liver disease (NAFLD) and healthy controls. METHODS: Thirty-eight participants (13 with ArLD, 15 with NAFLD and 10 healthy controls) received 2.5 mL of 40% ethanol per kg body weight via a nasogastric tube. Seventy-two inflammation-related markers were quantified in plasma from hepatic and systemic venous blood, at baseline, 60 and 180 min after intervention. RESULTS: Alcohol intervention altered the levels of 31 of 72 and 14 of 72 markers in the systemic and hepatic circulation. All changes observed in the hepatic circulation were also identified in the systemic circulation after 180 min. Only FGF21 and IL6 were increased after alcohol intervention, while the remaining 29 markers decreased. Differences in response to acute alcohol between the groups were observed for 8 markers, and FGF21 response was blunted in individuals with steatosis. CONCLUSION: Acute alcohol intoxication induced changes in multiple inflammation-related markers, implicated in alcohol metabolism and hepatocellular damage. Differences identified between marker response to binge drinking in ArLD, NAFLD and healthy controls may provide important clues to disease mechanisms and potential targets for treatment. CLINICAL TRIAL NUMBER: NCT03018990.

Ethanol exacerbates pulmonary complications after burn injury in mice, regardless of frequency of ethanol exposures.

Burn injuries are associated with significant morbidity and mortality, and lungs are the most common organ to fail. Interestingly, patients with alcohol intoxication at the time of burn have worse clinical outcomes, including pulmonary complications. Using a clinically relevant murine model, we have previously reported that episodic ethanol exposure before burn exacerbated lung inflammation. Specifically, intoxicated burned mice had worsened pulmonary responses, including increased leukocyte infiltration and heightened levels of CXCL1 and IL-6. Herein, we examined whether a single binge ethanol exposure before scald burn injury yields similar pulmonary responses. C57BL/6 male mice were given ethanol (1.2 g/kg) 30 min before a 15 % total body surface area burn. These mice were compared to a second cohort given episodic ethanol binge for a total of 6 days (3 days ethanol, 4 days rest, 3 days ethanol) prior to burn injury. 24 h after burn, histopathological examination of lungs were performed. In addition, survival, and levels of infiltrating leukocytes, CXCL1, and IL-6 were quantified. Episodic and single ethanol exposure before burn decreased survival compared to burn only mice and sham vehicle mice, respectively (p < 0.05). However, no difference in survival was observed between burned mice with single and episodic ethanol binge. Examination of H&E-stained lung sections revealed that regardless of ethanol binge frequency, intoxication prior to burn worsened pulmonary inflammation, evidenced by elevated granulocyte accumulation and congestion, relative to burned mice without any ethanol exposure. Levels of infiltrating granulocyte in the lungs were significantly higher in burned mice with both episodic and single ethanol intoxication, compared to burn injury only (p < 0.05). In addition, there was no difference in the granulocyte count between single and ethanol binge mice with burn injury. Neutrophil chemoattractant CXCL1 levels in the lung were similarly increased following single and episodic ethanol exposure prior to burn compared to burn alone (22-fold and 26-fold respectively, p < 0.05). Lastly, we assessed pulmonary IL-6, which revealed that irrespective of frequency, ethanol exposure combined with burn injury raised pro-inflammatory cytokine IL-6 in the lungs relative to burn mice. Again, we did not find any difference in the amount of IL-6 in lungs of burned mice with single and episodic ethanol intoxication. Taken altogether, these data demonstrate that both single and episodic exposure to ethanol prior to burn injury similarly worsens pulmonary inflammation. These results suggest that ethanol-induced exacerbation of the pulmonary responses to burn injury is due to presence of ethanol at the time of injury rather than longer-term effects of ethanol exposure.

Tobacco/nicotine dependence as a risk factor for substance use disorders and related mental health conditions among cancer patients.

BACKGROUND: Cancer patients often face multiple comorbidities and are at risk for various mental health conditions and substance use disorders. Tobacco/nicotine dependence (TND) is a known risk factor for poor health outcomes and has been associated with psychiatric disorders including substance use disorder. However, the specific relationship between TND and the risk of substance use disorder and mental health conditions among cancer patients remains underexplored. This study aimed to assess the association between TND and the risk of comorbid conditions among cancer patients. METHODS: Data were obtained from a database of electronic health records for patients from the University of California health system. The odds for every condition among cancer patients with TND were calculated and compared with those for cancer patients without TND. ORs were adjusted for gender, ethnicity, and race. RESULTS: Three thousand seven hundred and ninety-one cancer patients with TND had 252,619 total conditions, and 51,711 cancer patients without TND had 2,310,880 conditions. After adjusting for confounders, the condition for which TND most exacerbated risk was psychoactive substance-induced organic anxiety disorder (OR = 16.3, p < 0.001). This appeared consistent with the second, third, and fifth most-exacerbated conditions: stimulant use disorder (OR = 12.8, p < 0.001), cocaine induced mental disorder (OR = 11.0, p < 0.001), and cocaine use disorder (OR = 11.0, p < 0.001). Different conditions exacerbated by TND include acute alcoholic intoxication (OR = 11.4, p < 0.001), opioid use disorder (OR = 7.6, p < 0.001), schizoaffective disorder (OR = 7.4, p < 0.001), and cannabis use disorder (OR = 6.3, p < 0.001). CONCLUSIONS: Our findings reveal a strong association between TND and an increased risk of substance use disorder and mental health conditions among cancer patients. Specifically, cancer patients with TND were at an elevated risk for psychoactive substance-induced organic anxiety disorder, stimulant use disorder, and cocaine-related disorders. Additionally, TND was associated with an increased risk of acute alcoholic intoxication, opioid use disorder, schizoaffective disorder, and cannabis use disorder. These findings underscore the need for comprehensive screening and interventions to address TND and comorbid conditions among cancer patients.

A History of Repeated Alcohol Intoxication Promotes Cognitive Impairment and Gene Expression Signatures of Disease Progression in the 3xTg Mouse Model of Alzheimer's Disease.

The impact of alcohol abuse on Alzheimer's disease (AD) is poorly understood. Here, we show that the onset of neurocognitive impairment in a mouse model of AD is hastened by repeated alcohol intoxication through exposure to alcohol vapor, and we provide a comprehensive gene expression dataset of the prefrontal cortex by the single-nucleus RNA sequencing of 113,242 cells. We observed a broad dysregulation of gene expression that involves neuronal excitability, neurodegeneration, and inflammation, including interferon genes. Several genes previously associated with AD in humans by genome-wide association studies were differentially regulated in specific neuronal populations. The gene expression signatures of AD mice with a history of alcohol intoxication showed greater similarity to the signatures of older AD mice with advanced disease and cognitive impairment than did the gene expression signatures of AD mice not exposed to alcohol, suggesting that alcohol promotes transcriptional changes consistent with AD progression. Our gene expression dataset at the single-cell level provides a unique resource for investigations of the molecular bases of the detrimental role of excessive alcohol intake in AD.

Effects of Acute Ethanol Intoxication on Spinal Cord Injury Outcomes in Female Mice.

Abstract Approximately one in three traumatic spinal cord injuries (SCIs) occurs during or shortly after the consumption of alcohol. A small number of retrospective clinical studies report variable effects of alcohol intoxication on mortality, neurological recovery, and complications after SCI. Some of these studies demonstrate a protective effect of alcohol intoxication on SCI outcomes, whereas others show an increased complication risk. Pre-clinical studies in rat, ferret, and feline SCI models report a detrimental effect of ethanol intoxication on hemorrhage, motor recovery, and biochemical markers of tissue injury. However, no studies to date have investigated the neuropathological consequences of ethanol intoxication at the time of SCI or the reciprocal effect of SCI on ethanol metabolism. Therefore, we combined a pre-clinical mouse model of acute ethanol intoxication and experimental vertebral level T9 contusion SCI to investigate their interactive effects in female mice. We first investigated the effect of SCI on ethanol metabolism and found that T9 SCI does not alter ethanol metabolism. However, we did find that isoflurane anesthesia significantly slowed ethanol metabolism independent of SCI. We also determined how acute ethanol intoxication at the time of SCI alters locomotor recovery and lesion pathology. Using the Basso Mouse Scale (BMS) and CatWalk XT Gait Analysis System, we assessed locomotor recovery for 6 weeks after injury and observed that acute ethanol intoxication at the time of injury did not alter locomotor recovery. We also found no effect of ethanol intoxication on heat hyperalgesia development. There was, however, a detrimental effect of ethanol on tissue sparing after SCI. Therefore, we conclude that acute alcohol intoxication at the time of injury may contribute to the neuropathological consequences of SCI.

Incidences of underlying causes of hypothermia in older patients in the emergency department: a systematic review.

PURPOSE: Hypothermia is a serious condition in older adults. Knowledge of a priori chances of underlying diseases may affect initial management, hence prognosis. This systematic review provided an overview of existing literature on the incidences of underlying causes of hypothermia in older patients at the emergency department. METHODS: MEDLINE, The Cochrane Library, and Embase were searched up to February 1st, 2022. Inclusion criteria were age ≥ 65 years, emergency department setting, and body temperature < 36.0 degrees Celsius. Exclusion criteria were iatrogenic hypothermia, no underlying cause reported, and patient selection based on specific diseases. Title/abstract and full-text were screened and quality was assessed using the Joanna Briggs Institute Critical Appraisal Tool. Data were presented using descriptive statistics and narrative analyses. RESULTS: Forty-one reports were included, including 6 cohort studies and 35 case reports. The 6 studies involved 2173 hypothermic patients, whose age varied from a mean of 67 to a median of 79 years and temperature from a median of 30.8 to a mean of 33.7 degrees Celsius. One study reported about primary hypothermia (incidence of 44%). Acute medical illness was often reported as underlying cause of secondary hypothermia (49-51%). Reported incidences of infection and sepsis ranged from 10 to 32%, of trauma up to 14%, and of alcohol intoxication from 5 to 26%. CONCLUSION: Limited studies have been published regarding this topic, and the overall quality of the evidence was graded as low. Causes that should not be missed include acute medical illness, trauma, alcohol intoxication, primary hypothermia, thyroid failure, and drug-induced hypothermia.

Drug and alcohol intoxication in major trauma: Associations, trends and outcomes over a decade.

OBJECTIVES: Drug and alcohol intoxication is common among injured patients altering trauma presentation and characteristics. However, uncertainty exists regarding the effect of intoxication on injury severity, as well as outcomes. The present study aims to provide an update on substance-use patterns and their association with traumatic presentation and outcome within a contemporary Australian context. METHODS: All major trauma patients captured in our centre's Trauma Registry between July 2010 and June 2020 were included. Demographic, injury characteristic, outcome and substance-use data were collected. Differences in injury severity and characteristics were explored using χ2 tests, while outcomes were modelled using adjusted binomial logistic regression. RESULTS: Among 9700 patients, 9% were drug-intoxicated prior to injury, while 9.4% were alcohol-intoxicated. Drug use almost tripled between 2010 (4.8%) and 2020 (13.3%), while alcohol intoxication fell, from 11.7% to 7.3%, over the same period. Although there were significant differences in trauma mechanism among intoxicated patients, group comparison found no difference in Injury Severity Score for any group. Regarding outcomes, all intoxication resulted in significantly greater odds (odds ratio 1.62-2.41) of ICU admission. No difference in mortality was found among individual substance-use groups; however, polysubstance-intoxicated patients had 3.52 times greater odds of dying (95% confidence interval 1.21-10.23) compared to non-intoxicated patients. CONCLUSION: Within this contemporary Australian population, we demonstrate escalating rates of drug intoxication and declining rates of alcohol intoxication prior to trauma. Intoxication was associated with more frequent violent and non-accidental injury, and despite no difference in severity, it was associated with worse outcomes.

Bottle mix-up: Ethanol intoxication in an infant.

Alcohol intoxication is a common ingestion in pediatrics with close to 10,000 reports to poison control centers annually. Hypoglycemia, neurological depression (ataxia, coma, nystagmus, etc.) and unstable vitals (hypothermia, hypotension, bradycardia, and respiratory depression) are common presentations. The patient is a 3 month old female who was brought into the Emergency Department (ED) for one day of decreased oral intake and inconsolability. Vital signs were reassuring. Physical exam revealed gaze preference to the right with inability to look left, dysconjugate gaze, and hypotonia. Work-up including CT of the head, and urinalysis was unremarkable. Urine drug screen was found to be positive for ethanol with follow up serum ethanol at 162 mg/dL. With conservative management the patient returned to her baseline. On follow-up with her pediatrician, it was elicited that the mother inadvertently used a water bottle of vodka to mix the patient's formula. This case adds to the paucity of literature of abnormal presentations of alcohol intoxication in an infant.

C-L Case Conference: The Case of a 34-Year-Old Male Veteran with Suicidal Ideation in the Context of Alcohol Intoxication.

We describe the case of a 34-year-old male veteran who presents to the emergency department with suicidal ideation while intoxicated on alcohol. From his progression from intoxication through sobriety, this case details changes in his suicide risk during the sobering process. Consultation-liaison psychiatrists present guidance for this clinical scenario based on their experiences and a review of the available literature. The following important concepts for managing suicide risk among patients with alcohol intoxication are considered: evaluating for medical risk, timing the suicide risk assessment, anticipating withdrawal, diagnosing other disorders, and achieving a safe disposition.

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.

Informing the development of diagnostic criteria for differential diagnosis of alcohol-related cognitive impairment (ARCI) among heavy drinkers: A systematic scoping review.

BACKGROUND: Early detection and diagnosis of alcohol-related cognitive impairment (ARCI) among heavy drinkers is crucial to facilitating appropriate referral and treatment. However, there is lack of consensus in defining diagnostic criteria for ARCI. Uncertainty in attributing a diagnosis of suspected ARCI commonly arises in clinical practice and opportunities to intervene are missed. A systematic scoping review approach was taken to (i) summarise evidence relating to screening or diagnostic criteria used in clinical studies to detect ARCI; and (ii) to determine the extent of the research available about cognitive assessment tools used in 'point-of-care' screening or assessment of patients with suspected non-Korsakoff Syndrome forms of ARCI. METHODS: We searched Medline, PsycINFO, Cinahl and the Web of Science, screened reference lists and carried out forward and backwards citation searching to identify clinical studies about screening, diagnosis or assessment of patients with suspected ARCI. RESULTS: In total, only 7 studies met our primary objective and reported on modifications to existing definitions or diagnostic criteria for ARCI. These studies revealed a lack of coordinated research and progress towards the development and standardisation of diagnostic criteria for ARCI. Cognitive screening tools are commonly used in practice to support a diagnosis of ARCI, and as a secondary objective we included an additional 12 studies, which covered a range of settings and patient populations relevant to screening, diagnosis or assessment in acute, secondary or community 'point-of-care' settings. Across two studies with a defined ARCI patient sample and a further four studies with an alcohol use disorder patient sample, the accuracy, validity and/or reliability of seven different cognitive assessment tools were examined. The remaining seven studies reported descriptive findings, demonstrating the lack of evidence available to draw conclusions about which tools are most appropriate for screening patients with suspected ARCI. CONCLUSION: This review confirms the scarcity of evidence available on the screening, diagnosis or assessment of patients with suspected ARCI. The lack of evidence is an important barrier to the development of clear guidelines for diagnosing ARCI, which would ultimately improve the real-world management and treatment of patients with ARCI.

Elevated creatinine kinase levels amongst Dutch adolescents with acute alcohol intoxication.

This study aims to explore the prevalence of creatinine kinase elevation amongst a sample of Dutch adolescents admitted for acute alcohol intoxication. The data on all admitted adolescents < 18 years old with acute alcohol intoxication between 2008 and 2021 were collected from a Dutch major district general hospital, Reinier de Graaf Gasthuis, in Delft. Overall, 495 adolescents who were treated for symptoms of acute alcohol intoxication during this period were included in the study. When evaluating the blood samples of the included patients, elevated creatinine kinase levels were found in 60% of the cases, with a mean of 254 U/I (normal value ≤ 145 U/I). A confirmed diagnosis of rhabdomyolysis (increase in CK > fivefold the upper limit of normal) was present in 4.4% of cases. Moreover, using a linear regression this study found that a higher blood alcohol concentration was associated with higher creatinine kinase levels, when adjusted for positive drug screenings amongst the adolescents with acute alcohol intoxication (p = 0.027; ß = 66.88; 95% CI 7.68 - 126.08).    Conclusions: This is the first study focusing on how acute alcohol intoxication affects adolescents' muscle tissue. The results could potentially help to prevent alcohol use within the sports world. It could also aid understanding of how acute alcohol intoxication influences the breakdown of adolescents' muscle tissue. What is Known: • Alcohol, alongside pharmaceutical agents and illicit drugs, is a significant cause of rhabdomyolysis (increase in creatinine kinase > fivefold the upper limit of normal). • Creatinine kinase elevation in alcohol intoxicated patients may be as a result of direct "muscular" toxicity" (myotoxicity) or from prolonged immobilization and ischemic compression induced by coma. What is New: • Our retrospective cohort study is a pioneer in addressing the effect of acute alcohol intoxication amongst adolescents (< 18 years) upon muscle tissue (creatinine kinase level) within a large population. When evaluating the blood samples of the included population, elevated creatinine kinase levels were found in 60% of the cases, with a mean of 254 U/I (normal value ≤ 145 U/I). • There is an association between alcohol intoxication and elevated creatinine kinase levels amongst adolescents. Future research is needed to further understand the pathophysiology and causality of this interaction.