Clinical effect of ethanol co-use in patients with acute drug toxicity involving the use of central nervous system depressant recreational drugs.
Level 3 - non-randomized controlled study
Retrospective multicentre comparative cohort study
PubMed 35404314 · doi:10.1097/MEJ.0000000000000932
What was done
A retrospective multicentre cohort study analysed emergency department presentations from the Euro-DEN Plus database from January 2014 to December 2019. The study evaluated 7,644 presentations (out of 43,633 total) involving acute toxicity from central nervous system (CNS) depressant recreational drugs, comparing patients with ethanol co-ingestion (n = 3,811; 49.9%) to those without.
What was found
Patients with ethanol co-use had significantly higher rates of Glasgow Coma Scale ≤8 (34.1% vs. 22.4%; P < 0.001), vomiting (8.1% vs. 4.6%; P < 0.001), anxiety (12% vs. 6.4%; P < 0.001), agitation/aggression (22% vs. 14.7%; P < 0.001), seizures (3.8% vs. 2.4%; P < 0.001), and hypotension (7.5% vs. 4.6%; P < 0.001). They also more frequently required ambulance transport (85.5% vs. 76.5%; P < 0.001), medical treatment (57.3% vs. 48.0%; P < 0.001), hospitalisation (27.7% vs. 18.9%; P < 0.001), and intensive care admission (12.2% vs. 4.0%; P < 0.001). Deep coma (GCS ≤8) was particularly frequent when ethanol was combined with opioids or GHB/GBL. Across the cohort, 53.3% needed medical treatment and 14 died.
Why it matters
Ethanol co-ingestion is present in nearly half of recreational CNS-depressant poisonings and substantially increases clinical severity, including tripling ICU admission rates.
Limits
Retrospective observational design relying on database records. Doses, exact timing of ingestion, toxicological confirmation versus self-report, and adjustment for potential confounders were not detailed in the abstract.
Cited by
- supports Alcohol functions pharmacologically as a central nervous system depressant.