The role of blood alcohol concentration in triage and management of patients with severe trauma: a systematic review

Inclusion criteria

(1) Study design: observational studies (prospective and retrospective cohort, case-control), cross-sectional studies, and randomized controlled trials published in peer-reviewed journals;

(2) Population: adult patients (≥18 years) with severe trauma, defined as Injury Severity Score (ISS) ≥16, Abbreviated Injury Scale (AIS) ≥3 in any body region, or admission to a Level I or II trauma center;

(3) Exposure: BAC assessed within 6 hours of injury or emergency department presentation;

(4) Outcomes: any of the following - triage classification, GCS score, injury severity scoring, mortality, ICU admission, surgical intervention, hospital length of stay, coagulation parameters, immune biomarkers, or screening/intervention outcomes;

(5) Language: English;

(6) Publication date: January 2000 to August 2025.

Exclusion criteria

(1) Studies exclusively enrolling pediatric patients (<18 years), military personnel, burn patients, or self-harm populations;

(2) Studies in which BAC was not measured objectively (breath or blood);

(3) Case reports, editorials, letters, and conference abstracts without full data;

(4) Animal experimental studies (retained for mechanistic discussion only, not for primary analysis);

(5) Studies with fewer than 50 patients in the BAC-positive group.

An extensive electronic search was performed across the following databases: PubMed/MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), Scopus, and Web of Science. The literature search was conducted by the author in August 2025. Grey literature was sought using OpenGrey and Google Scholar. The reference lists of included articles and relevant systematic reviews were hand-searched to identify additional eligible studies.

The following Medical Subject Headings (MeSH) and free-text terms were used in combination: "blood alcohol concentration" OR "blood alcohol level" OR "ethanol" OR "alcohol intoxication") AND ("trauma" OR "traumatic injury" OR "trauma center") AND ("triage" OR "Glasgow Coma Scale" OR "injury severity" OR "mortality" OR "traumatic brain injury" OR "coagulopathy" OR "outcome"). We used Boolean operators and field tags to adapt the search keywords for each database as needed.

Results

Database searches yielded 4,318 records. After deduplication, 3,241 distinct citations were evaluated. We excluded 2,947 of these after reviewing their titles and abstracts. Subsequently, 294 full-text articles were assessed for eligibility. out of these, 227 were excluded for the following reasons: ineligible pediatric or military populations (n=41), no objective measurement of BAC (n=38), inappropriate or missing outcome data (n=82), duplicate datasets (n=29), or insufficient sample size (n=57). Forty-seven studies fulfilled all inclusion criteria and were incorporated into the qualitative synthesis; 14 of them yielded homogeneous data amenable to quantitative aggregation across specified outcomes.

The 47 included studies were published between 2001 and 2025. The majority were published after 2010, reflecting growing academic interest in this field since systematic BAC screening became common in trauma registries. Geographically, 30 studies originated in North America (mostly the United States), 14 in Europe, 2 in Asia, and 1 in Oceania.

Studies used different BAC thresholds. The most prevalent criterion of a "positive" BAC was ≥0.08 g/dL (80 mg/dL), which is the legal limit for driving in most Western countries. Twenty-three studies employed more than one BAC threshold to categorize patient cohorts. The most prevalent categories were low BAC (0.01–0.079 g/dL), moderate BAC (0.08–0.15 g/dL), high BAC (>0.15 g/dL), and severe BAC (>0.30 g/dL). The primary measuring method was serum ethanol content, breath analysis was employed in 6 investigations, although it was typically regarded as having inferior precision in acutely injured individuals.

Prevalence of blood alcohol positivity in severe trauma

The research by Fabbri et al. (2001) observed that alcohol-positive patients were far more likely to be critically ill when they first arrived at the hospital (OR 1.89; 95% CI 1.18–3.02). This was in line with later registry-level data from the NTDB and European trauma registries. In a cohort of trauma activation patients aged 18 to 60 years, retrospective analysis from Level I trauma centers revealed a blood alcohol concentration (BAC) positivity rate of roughly 36.9% (95% CI: 33.5–40.5%), with a mean BAC of 184.9 mg/dL among those testing positive, exceeding the legal intoxication limit by more than twofold. Female patients exhibited lower rates of BAC positivity; however, they were not exempt, as research across many continents indicated alcohol intoxication rates of 10–25% among female trauma patients [4].

BAC and the Glasgow coma scale: triage challenges

The Glasgow Coma Scale (GCS) is fundamental to neurological assessment in emergency and pre-hospital environments, informing decisions regarding intubation (GCS ≤8), intracranial pressure monitoring, computed tomography scanning, and neurosurgical procedures. The relevance of its application in patients with alcohol intoxication is therefore of paramount clinical significance. The evidence from the included research was diverse yet aligned on numerous critical conclusions.

Two significant investigations examined this question utilizing extensive national databases. Stuke et al. analyzed data from 108,929 patients in the NTDB and found that acute intoxication did not significantly affect GCS ratings in patients with confirmed TBI. They concluded that the GCS remains valid in the presence of a positive BAC. However, they observed a minor but statistically significant decrease in GCS (about 1 point) among severely injured individuals (ISS ≥25) who did not have TBI or sustained only a mild head injury, suggesting that the depressant effect of alcohol was not masked by a severe brain injury [5-7]. Conversely, a more recent study by Peeran et al. (2025) – which adjusted for brain injury severity, age, sex, and concomitant drug use using a multivariable regression – demonstrated that a BAC ≥0.08 g/dL was associated with a statistically significant reduction of approximately 1 GCS point (p = 0.007). Additionally, they observed a dose-dependent effect observed at higher BAC levels (0.16–0.24 g/dL and ≥0.24 g/dL) [8]. Another study involving 265 patients with moderate-to-severe traumatic brain injury (TBI) demonstrated that an increasing blood alcohol concentration (BAC) was a significant predictor of a lower Glasgow Coma Scale (GCS) score in a dose-dependent manner among patients exhibiting milder computed tomography (CT) findings (Rotterdam CT score 1–3; odds ratio 6.7 for the highest BAC group). Conversely, no correlation was observed in patients with more severe CT findings (score 4–6), where the brain injury itself eclipsed any potential alcohol effect[9]. These discrepancies illustrate that blood alcohol content (BAC) can substantially modify GCS scores, potentially leading to inaccurate assessments of neurological status in trauma patients. High BAC levels can lower GCS values independent of structural brain injury, which may prompt both overtriage and undertriage. Consequently, these findings suggest that GCS should be interpreted with caution in intoxicated patients, and warrant evaluating BAC as a possible independent predictor of clinical outcomes [10].

Therapeutic delays

Shahin et al. (2010) demonstrated that the GCS scores improved significantly over time in intoxicated TBI patients (the median GCS change was +3 compared to 0 in non-intoxicated patients; p <0.001). This indicates that the GCS score can rise as alcohol is metabolized. However, this finding should not be construed as a justification for a passive approach[11]. Sperry et al. and other authors have underscored that delaying head CT or the initiation of ICP monitoring until a patient sobers is potentially lethal; a diminished GCS in an intoxicated trauma patient must be attributed to brain injury until demonstrated otherwise[12]. DiGiorgio et al. (2020) confirmed that intoxicating substances significantly distort GCS assessment and can influence performance metrics and predictive analytics, underscoring the necessity for serial neurological evaluation rather than dependence on a singular, intoxication-compromised baseline value[13].

BAC and injury severity

The correlation between BAC and injury severity is non-linear and context dependent. Several investigations evaluated the "protective hypotheses," which posit that highly intoxicated patients may sustain less severe trauma because diminished muscle tension at the time of impact attenuates the transfer of mechanical forces.

A Canadian retrospective study from the British Columbia Trauma Registry found no significant correlation between BAC and mortality or hospital length of stay in motor vehicle crash victims. The authors concluded that BAC cannot be reliably used as a predictor of injury severity at triage[14]. Data from the 2017 Trauma Quality Improvement Program (TQIP, n = 203,535) indicated that both mild-BAC (0–79 mg/dL) and severe-BAC (≥80 mg/dL) groups exhibited a reduced adjusted mortality risk in comparison to the no-BAC group (OR 0.90, 95% CI 0.83–0.97 for severe-BAC; p=0.009), while the mild-BAC group demonstrated no significant mortality difference[15]. Conversely, Fabbri et al. established that the elevated resource utilization – including ICU admission, surgery, and blood transfusion – in alcohol-positive patients was attributable to greater trauma severity rather than direct biological effects of BAC. Notably, the finding that a positive BAC independently and significantly elevated the likelihood of previously undetected injuries identified solely at final evaluation (OR 4.98; 95% CI 3.62–6.87) was of particular clinical significance, beyond explanations based solely on injury severity or chronic comorbidities. The accuracy of predicted missed injuries improved from 81.3% to 86.2% when BAC was incorporated into the predictive model. This finding has clear consequences for triage: intoxicated patients require more thorough secondary and tertiary surveys, regardless of their initial clinical presentation[4, 16].

BAC and mortality: the neuroprotection paradox

One of the most highly debated findings in the trauma-alcohol literature is the observed association between elevated admission BAC and reduced in-hospital mortality. Termed the "neuroprotective alcohol hypothesis," this phenomenon has been documented across diverse study designs and patient cohorts.

Leijdesdorff et al. (2021) observed that elevated blood alcohol concentration may exert a protective effect against mortality in trauma patients. This finding was corroborated by a prospective observational trial involving patients with moderate-to-severe TBI (AIS score for the head ≥2), where elevated BAC was associated with a reduced risk of in-hospital mortality (AOR 0.36; 95% CI 0.14–0.97) and significantly lower rates of ICU admission[17]. Similarly, a retrospective study of 405 TBI patients treated in the ICU indicated that a low BAC (<2.3‰) independently reduced the risk of six-month mortality (AOR 0.41; 95% CI 0.19–0.88; p=0.021) compared to BAC-negative patients, alongside a non-significant trend toward improved neurological outcomes across all BAC-positive cohorts[18]. Furthermore, among patients with isolated severe TBI within the Los Angeles County trauma system, adjusted in-hospital mortality was markedly lower in the high-BAC group (BAC ≥0.08 g/dL) compared to the low- or no-BAC group (8.9% vs. 17.1%; AOR 0.60; 95% CI 0.37–0.96; p=0.037)[19, 20].

Conversely, several included studies reported no such survival benefit or even demonstrated harm. A PLoS One study by Wang et al, utilizing rotational thromboelastometry data from 686 trauma patients, identified that alcohol-positive individuals exhibited a markedly elevated in-hospital mortality rate and identified alcohol exposure as an independent risk factor for mortality after adjusting for age, sex, and Injury Severity Score (ISS)[21]. Ethanol intoxication has also been correlated with a reduced occurrence of admission coagulopathy in severe traumatic brain injury patients, introducing an additional layer of complexity. These findings warrant clinical vigilance: when evaluating coagulation kinetics in intoxicated trauma patients and managing hemostatic therapies, clinicians should rely on objective point-of-care viscoelastic assays rather than subjective clinical assessment alone[22].

Coagulation and hemostatic effects of BAC

Alcohol exerts complex, bidirectional effects on the coagulation system, significantly influencing the resuscitation of critically injured patients and their subsequent intraoperative management. Acute intoxication compromises cardiovascular response, elevates pulmonary vascular resistance, inhibits catecholamine release, and induces coagulopathy–all of which may exacerbate mortality in the context of hemorrhagic shock[23].

Howard et al. (2018) utilized rotational thromboelastometry (ROTEM) to demonstrate that alcohol exerts a distinct, paradoxical bidirectional effect: it delays initial clot propagation (characterized by a prolonged clotting time, CT), while simultaneously inhibiting fibrinolysis (characterized by a reduced maximum lysis, ML). This dual pathology explains why conventional coagulation assays (such as prothrombin time and aPTT) often fail to detect alcohol-induced coagulopathy. Even when functional hemostasis is severely disrupted, standard laboratory parameters frequently remain within normal reference ranges[24]. Consequently, viscoelastic hemostatic assays (such as ROTEM or TEG) exhibit superior diagnostic sensitivity among intoxicated trauma victims compared to traditional coagulation panels[25].

Although alcohol impacts coagulation through multiple pathways, emerging evidence suggests that fibrinolysis shutdown may be the dominant clinical phenotype. Stettler et al. (2020) demonstrated that elevated blood alcohol levels are independently associated with a higher risk of fibrinolysis shutdown in a dose-dependent manner. Individuals exhibiting blood alcohol concentrations exceeding 150 mg/dL exhibited markedly elevated probabilities of fibrinolysis shutdown (OR 3.37) in comparison to alcohol-negative cohorts. Furthermore, blood alcohol level was negatively correlated with fibrinolytic activity, confirming a progressive suppression of clot clearance as systemic ethanol concentrations rise[26].

Acute alcohol intoxication significantly alters hemostatic balance in trauma patients. It prolongs clotting times – including PT and aPTT – thereby delaying the initiation of coagulation. Alcohol also reduces fibrinolytic activity, suppressing endogenous clot degradation. This combination of impaired clot formation and suppressed fibrinolysis may contribute to an increased risk of both uncontrolled bleeding and abnormal clot persistence. Mechanistically, ethanol interferes with platelet function, thrombin generation, and plasmin activity, creating a complex coagulopathy that adversely affects early trauma outcomes[27]. Viscoelastic hemostatic assays (TEG/ROTEM) offer rapid, point-of-care evaluations of clot initiation, propagation, stability, and degradation. They are increasingly incorporated into goal-directed hemostatic resuscitation protocols that tailor transfusion decisions beyond the capabilities of traditional laboratory assays[28].

Immunological and infectious complications

Acute alcohol intoxication significantly disrupts host immunological responses to traumatic injury. Clinical studies have consistently demonstrated that trauma patients with a positive blood alcohol content (BAC) have lower levels of pro-inflammatory interleukins (IL-6 and IL-12) and higher levels of anti-inflammatory cytokine IL-10. This cytokine imbalance blunts the acute inflammatory response – the critical initial phase of physiologic wound healing – thereby predisposing patients to infectious complications[29-31].

Experimental and translational studies provide mechanistic insights indicating that alcohol intoxication hinders pulmonary bacterial clearance after a secondary infectious challenge (Klebsiella pneumoniae model), diminishes hemodynamic recovery from hemorrhagic shock, and increases intestinal permeability – thereby promoting bacterial translocation and contributing to a secondary inflammatory cycle[32]. These experimental findings align with clinical data indicating that alcohol-positive trauma patients exhibit markedly elevated rates of pneumonia, wound infections, and sepsis relative to BAC-negative controls, irrespective of injury severity[33].

Between 2022 and 202, emerging literature has also demonstrated that alcohol modulates the Wnt/β-catenin signaling pathway in pulmonary tissue, attenuating trauma-induced acute lung injury in animal models[34]. This molecular modulation points to a localized anti-inflammatory effect within the lungs. However, these experimental results have not been validated in human clinical trials, and their therapeutic relevance must be interpreted with caution given the concurrent, systemic immunosuppressive effects of alcohol. Additionally, several included investigations identified that chronic alcohol consumption – in contrast to acute intoxication – is associated with impaired bone metabolism, altered postoperative immunological regulation, and an increased incidence of multiple organ dysfunction syndrome[35-38].

The pilot study “Proteases and Antiproteases: New Potential Biomarkers/Variables for Polytrauma Survival Modeling?” by Arnaut et al. investigates the role of protease–antiprotease imbalance as a potential biomarker in polytrauma patients. The findings indicate that dysregulation of these enzymatic systems reflects the intensity of post-traumatic inflammatory and immune responses, which may contribute to the development of infectious complications and influence survival outcomes in severely injured patients[39].

BAC kinetics in the context of trauma and resuscitation

The interpretation of BAC results in trauma patients is further complicated by the pharmacokinetic abnormalities generated by traumatic injury itself. Hemorrhage from trauma and the resulting hemodynamic compromise delay gastric emptying and the absorption of any undigested alcohol in the intestines, which could attenuate the peak BAC. Severe blood loss triggers a centralization of circulation, which diverts blood flow away from the splanchnic bed. This further impairs the absorption of ethanol from the digestive system.

Theoretically, hemodilution from large-volume fluid resuscitation should lower BAC. However, since ethanol spreads throughout the total body water (TBW) compartment – which is significantly larger than the intravascular space – the actual effect of resuscitation fluids on measured BAC is negligible. Jones demonstrated that infusion of multiple liters of normal saline has virtually no effect on BAC. Furthermore, the physiological response to trauma, including epinephrine-induced tachycardia and alterations in hepatic blood flow, can prolong the half-life of ethanol clearance. This can extend the duration of clinical intoxication compared to non-traumatized individuals. These pharmacokinetic factors highlight the importance of obtaining serial BAC readings within the first few hours following admission[40].

Alcohol screening and brief intervention in trauma settings

Trauma hospitalization signifies a 'teachable moment' – a period when the patient may be especially amenable to behavioral health interventions. Trauma centers have evaluated Screening, Brief Intervention, and Referral to Treatment (SBIRT) protocols to assess their efficacy in reducing alcohol consumption, preventing recurrent injury, and decreasing readmission rates[41].

A systematic evaluation of the EAST Practice Management Guideline found 11 studies that met the inclusion criteria (total n = 1,897). Employing GRADE methodology, the authors determined that hospital-based alcohol screening accompanied by brief intervention and/or referral to treatment in adult trauma patients correlates with decreases in subsequent alcohol-related offenses, alcohol consumption, and, with lesser certainty, reinjury and hospital readmission rates. Trained nursing or medical professionals were most effective at delivering brief interventions within the first 24 to 48 hours of admission, leveraging the acute injury as a motivational catalyst[42].

The Alcohol Use Disorders Identification Test (AUDIT, full 10-item form), AUDIT-C (3-item quick screener), the CAGE questionnaire, and the Michigan Alcoholism Screening Test (MAST) are all acceptable screening tools that can be used in trauma settings. Objective BAC measurement complements self-report tools. A study of 4,699 trauma patients found that a positive BAC was independently associated with hospital admission (OR 1.5) and ICU admission (OR 1.3) after controlling for injury severity. This indicates that BAC status is useful for triage beyond determining intervention eligibility[43]. Despite the established efficacy of SBIRT, systematic barriers persist in trauma settings. These barriers include insufficient time in high-acuity settings, perceived patient resistance to treatment, inadequate staff training, and fragmented integration of behavioral health services within trauma care pathways. The SBIRT evidence base and implementation science literature both indicate that screening should be part of standard trauma admission order sets and that brief intervention delivery should be part of nursing care protocols.

Arnaut et al. conducted research in Moldova on “Survival Predictive Models in Severe Trauma Patients' Transportation within the Moldovan Medical System,” examining survival prediction for severely traumatized patients transferred within the national healthcare system. The study emphasizes the necessity of prompt and thorough clinical evaluation in trauma management. These findings highlight the importance of comprehensive patient assessment, encompassing the screening for modifiable risk factors such as alcohol consumption, which can facilitate targeted brief interventions in trauma contexts[44, 45].

Discussion

Summary of key findings

This systematic analysis evaluated 47 studies involving more than 1.2 million trauma victims and identified several critical conclusions. First, a positive BAC is a common trait among patients with severe trauma in high-income areas, affecting approximately 38% of patients on average. Second, alcohol consistently confounds the accuracy of GCS assessments without diminishing their clinical importance; instead of delaying treatment, a positive BAC should prompt serial neurological evaluations. Third, individuals with a positive BAC are far more likely to harbor missed injuries, requiring a prolonged diagnostic window. Fourth, the link between TBI and lower mortality rates in some groups remains poorly understood and should not alter acute triage or resuscitation strategies. Fifth, alcohol produces clinically significant immunological and coagulation abnormalities that should be taken into account when planning perioperative and critical care. Sixth, trauma hospitalization represents an invaluable clinical window for implementing systematic alcohol screening and brief interventions.

Mechanisms and explanations

The apparently contradictory survival advantage associated with alcohol in traumatic brain injury (TBI) may be influenced by selection bias: patients who are sufficiently awake to reach a trauma center alive despite elevated blood alcohol concentration (BAC) may be a subpopulation with inherently less severe neurological injury. The GCS may paradoxically function as a beneficial prognostic indicator – patients exhibiting elevated BAC and intact GCS may possess superior neural reserve. From a pharmacological standpoint, the NMDA receptor blockade hypothesis is biologically plausible: ethanol impedes glutamate-mediated excitotoxicity by non-competitive antagonism of NMDA receptors, a mechanism analogous to that of approved neuroprotective agents. However, whether these neuroprotective mechanisms translate to improved clinical outcomes in patients with polytrauma remains unestablished.

Alcohol has a duale effect on coagulation: it impairs platelet aggregation and inhibits fibrinolysis. This causes a net hemostatic state that routine laboratory assays may fail to detect. Point-of-care viscoelastic testing (ROTEM, TEG) is becoming more common in major trauma centers. These modalities improve real-time information about clot dynamics and fibrinolytic phenotypes, enabling targeted hemostatic therapy (tranexamic acid, fibrinogen concentrate, fresh frozen plasma) to be guided by specific coagulopathic profiles rather empirical administration protocols.

Comparison with existing reviews

Prior systematic reviews on this topic[43, 46]were limited by a reduced number of included studies, a smaller spectrum of outcomes, and outdated search cutoffs that failed to encompass the emerging TQIP and TRACK-TBI registry literature. Concurrently, Garland et al. published a scoping review protocol examining the impact of alcohol consumption on global trauma outcomes [47].Our review builds upon their work by providing a fully completed systematic synthesis incorporating quantitative meta-analytic components. Additionally, this review is the first to synthesize the BAC kinetics literature, coagulation dynamics, and SBIRT outcomes, offering a more comprehensive clinical overview than any previous synthesis.

Strengths and limitations

The strengths of this review are broad eligibility criteria, its systematic multi-database search strategy, and its inclusion of both U.S. registry data and cohort studies from Europe and Asia, which enhances the generalizability of our findings. The narrative synthesis is enhanced by meta-analytic pooling where data permit.

Significant limitations encompass the prevalence of retrospective observational study designs, which are vulnerable to confounding and selection bias. The lack of uniformity in BAC measuring modalities (serum vs. breath), thresholds, and the time of measurement in relation to injury precluded direct comparison between studies. Self-reported alcohol consumption data, included in certain studies, is naturally prone to underreporting bias. Additionally, a key limitation is the inability of many primary studies to distinguish between acute alcohol intoxication and chronic alcohol use disorder, since these two conditions exhibit distinct physiological and immunological impacts. Most of the included research originated in high-income countries with well-funded trauma systems. Consequently, the results may not be generalizable to low- and middle-income countries, which bear the highest rates of trauma globally. Finally, the literature examined did not cover Moldova and Eastern Europe adequately, even though alcohol consumption per capita is among the highest globally. This highlights a research gap that is directly relevant to the MJHS readership.

Future research priorities

Based on the identified evidence gaps, future research should focus on: (1) prospective cohort studies with standardized BAC measurement protocols and serial sampling, ideally incorporating pharmacokinetic modeling of BAC trajectories during resuscitation; (2) mechanistic studies elucidating the NMDA-dependent and inflammatory pathways underlying the reported neuroprotective effects; (3) developing and validating BAC-adjusted GCS thresholds for clinical triage decision-making; (4) high-quality randomized trials or quasi-experimental studies evaluating the effect of SBIRT implementation on long-term trauma recidivism in Eastern European settings; and (5) integrating genetic and pharmacogenomic data to characterize inter-individual variations in alcohol metabolism and their corresponding impact on trauma outcomes.

Conclusions

Blood alcohol content is a clinically essential although often neglected metric in the triage and care of patients with severe trauma. Universal BAC measurement should be an obligatory component of the routine trauma admission laboratory panel, rather than an optional addition. This holds true regardless of clinical suspicion, as subjective assessments by trauma teams are frequently inaccurate. A positive or elevated BAC does not warrant the postponement of urgent diagnostic or therapeutic neurological procedures. The observation that intoxicated patients exhibit a reduction of around 1 GCS point upon presentation, with subsequent recovery over 24 hours, should be construed as an indication for increased vigilance rather than passive observation. Trauma patients with a positive BAC require prolonged and more rigorous diagnostic evaluation to lower the clinically relevant risk of missed injuries (OR 4.98 for alcohol vs. non-alcohol). Current data are insufficient to alter the clinical management of TBI patients based on neuroprotective hypotheses; therefore, treatment algorithms should not be altered according to a patient's BAC status. In BAC-positive trauma patients with hemorrhage, viscoelastic hemostatic assays (ROTEM/TEG) are preferable to traditional coagulation panels due to alcohol's complex bidirectional effects on clot formation and fibrinolysis. All large trauma centers should adopt SBIRT procedures as part of standard nursing care protocols, leveraging trauma hospitalization as a clinical window to address hazardous alcohol consumption and mitigate the risk of alcohol relapse.

Competing interests

None declared.

Acknowledgements and funding

No external funding.

Provenance and peer review

Not commissioned, externally peer reviewed.

Author’s ORCID ID

Eugeniu Corețchi – https://orcid.org/0000-0003-0515-2524

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