The reasoning
Alcohol use disorder = impaired control, increasing priority of drinking over other activities, and persistence despite harm, ± neuroadaptation (tolerance, withdrawal). Screen with AUDIT/CAGE; quantify units, pattern, and morning drinking (relief drinking = dependence marker).
The neurobiology that predicts withdrawal
Alcohol is a GABA‑A agonist + NMDA antagonist (net CNS depressant). Chronic use → downregulated GABA, upregulated glutamate/NMDA. Abrupt cessation unmasks a hyperexcitable, hyperglutamatergic, hyperadrenergic state → the withdrawal syndrome (tremor, autonomic arousal, seizures, delirium). This mechanism is the rationale for benzodiazepine treatment.
Risk stratification (do this every time) 🚩
The strongest predictor of severe withdrawal is a prior history of withdrawal seizures or delirium tremens (kindling). Also: heavy daily intake, prior detoxifications, comorbid illness, deranged electrolytes. Identify high‑risk patients before cessation.
Management orientation
Assisted withdrawal with benzodiazepines (symptom‑triggered via CIWA‑Ar, or fixed‑dose with a long‑acting agent; shorter‑acting lorazepam in hepatic impairment); parenteral thiamine before glucose; correct Mg²⁺/K⁺. Relapse prevention: psychosocial + acamprosate/naltrexone (or disulfiram in selected, supervised patients).
Pitfalls
- Not risk‑stratifying withdrawal; missing the kindling history.
- Giving glucose before thiamine (can precipitate Wernicke's).
Pearls
- 🎯 Prior DTs/withdrawal seizures = high‑risk withdrawal — plan proactively.
- 🩺 GABA↓/NMDA↑ neuroadaptation explains both the syndrome and the benzodiazepine fix.
Next → The emergency end of that spectrum (Concept 42).