What makes substance use a disorder?
A substance use disorder is identified through a pattern of impaired control, functional harm and continued use despite adverse consequences. Identify the substance and the pattern of use, then establish whether the patient is intoxicated, withdrawing or experiencing a complication. These are related clinical states, but they answer different questions and can require different immediate management.
A diagnostic interview explores unsuccessful attempts to cut down, craving, time spent obtaining or using the substance, impaired responsibilities, social consequences, hazardous use and physiological adaptation. The key is the overall pattern rather than a judgement about character. Exam stems usually provide a small set of decisive clues, so organise them into domains before selecting a diagnosis.
| Domain | Examples to look for |
|---|---|
| Impaired control | Craving, unsuccessful reduction, use exceeding intention |
| Social or occupational dysfunction | Neglected duties or continued use despite relationship problems |
| Risky use | Hazardous situations or persistence despite health consequences |
| Physiological adaptation | Tolerance and withdrawal in the appropriate context |
Intoxication concerns the effects of recent exposure; withdrawal follows a reduction or cessation after adaptation. A drug can also cause a psychiatric or medical disorder, such as psychosis, nutritional encephalopathy or organ damage. Do not assume that every confused patient who drinks alcohol has withdrawal: evaluate the time course, examination and alternative causes.
Why does alcohol withdrawal cause excitation?
Alcohol acutely favours inhibitory signalling. With sustained exposure, the nervous system adapts to the persistent depressant effect. When intake falls, this adapted system becomes relatively hyperexcitable. Tremor, anxiety, agitation, sweating and autonomic activation follow. Severe withdrawal can progress to seizures or delirium. The mechanism explains why withdrawal looks different from simple alcohol intoxication.
Risk assessment includes the previous withdrawal history, current symptoms, comorbid illness, nutritional status and the ability to monitor the patient. Previous complicated withdrawal is particularly important. Repeated episodes can increase susceptibility through kindling, so a patient who has previously had withdrawal seizures or delirium should not be assumed to have a mild course merely because early symptoms seem limited.
Typical sequence: tremor and autonomic signs at 6–24 h, withdrawal seizures at 12–48 h, alcoholic hallucinosis at 12–48 h with a clear sensorium, and delirium tremens at 48–96 h. Use the clinical sequence to orient the stem, but avoid treating a rigid hour-by-hour table as diagnostic proof. Timing depends on exposure, dependence and other illness. Ask when use decreased and what has appeared since then. A seizure, worsening agitation or abnormal vital signs changes the management priority regardless of whether it occurs within a memorised window.
How do alcohol hallucinosis and withdrawal delirium differ?
| Feature | Alcohol-related hallucinosis | Alcohol withdrawal delirium |
|---|---|---|
| Consciousness and attention | Relatively clear sensorium is a key clue | Disturbed attention and awareness |
| Psychotic symptoms | Often auditory hallucinations | Hallucinations may accompany global delirium |
| Other features | Assess coexisting withdrawal and psychiatric illness | Agitation, confusion and autonomic instability |
| Priority | Evaluate the cause and safety of psychotic symptoms | Urgent monitored medical treatment |
The key distinction is sensorium, not simply the presence of hallucinations. A patient reporting voices while remaining oriented and attentive does not automatically have delirium tremens. A patient with fluctuating attention, disorientation and physiological instability needs evaluation and treatment as a delirious medical patient. The wording of the mental-status examination often provides the decisive clue.
Withdrawal seizures may occur without an elaborate preceding syndrome. Once a seizure occurs, evaluate other possible causes and manage the withdrawal risk in a monitored setting. Do not assume that hallucinations must always precede seizures or that all alcohol-related complications occur in a fixed order. A short stem may intentionally describe only the complication requiring immediate action.
How is alcohol withdrawal treated?
Benzodiazepines are commonly used for alcohol withdrawal, particularly where seizures or delirium are concerns. Treatment can be guided by symptoms within a suitable monitored protocol. NICE supports a symptom-triggered regimen in settings with appropriate monitoring. The agent and regimen depend on severity, comorbid disease, liver function and the clinical setting rather than on one universal prescription.
- Assess airway, breathing, circulation, glucose, mental status and the risk of complicated withdrawal.
- Choose a setting capable of monitoring the anticipated severity.
- Treat withdrawal with an appropriate medication protocol and reassess the response.
- Give thiamine when indicated and correct nutritional, fluid and electrolyte deficits.
- Investigate coexisting illness and arrange continuing treatment for the underlying alcohol use disorder.
The CIWA-Ar scale helps assess symptom severity in patients able to participate in the assessment. It supports a protocol; it does not replace clinical judgement or the investigation of a delirious patient. If attention, communication or another illness makes scoring unreliable, management must still address the medical state. Do not treat a numerical score as a substitute for direct observation.
Completing withdrawal care does not complete treatment of the disorder. Naltrexone, acamprosate and disulfiram are established medication options for alcohol use disorder in appropriate patients. Selection requires assessment of goals, contraindications and follow-up. The drugs used for ongoing relapse prevention should not be confused with the benzodiazepines used to manage acute withdrawal.
When should you suspect Wernicke encephalopathy?
Wernicke encephalopathy is an acute syndrome caused by thiamine deficiency. The classic features are altered mental status, gait ataxia and ocular abnormalities, including nystagmus or ophthalmoparesis. The complete triad may be absent. Maintain suspicion in a malnourished patient rather than waiting for every feature before giving treatment.
Alcohol use disorder is an important risk setting, but prolonged vomiting, severe malnutrition and bariatric surgery can also create risk. The cause is inadequate thiamine availability, not alcohol exposure alone. This matters in exam stems involving a patient who does not drink alcohol but has restricted nutrition and new neurological findings.
Give parenteral thiamine when Wernicke encephalopathy is suspected, following the clinical protocol, and address associated nutritional deficiencies such as magnesium deficiency. Thiamine should be given before or alongside carbohydrate when feasible. However, do not delay treatment of clinically significant hypoglycaemia while waiting for thiamine; provide glucose promptly and administer thiamine as soon as possible.
How does Korsakoff syndrome differ from Wernicke encephalopathy?
Korsakoff syndrome is characterised by persistent memory impairment, particularly anterograde amnesia, often with confabulation. It can follow Wernicke encephalopathy, especially when deficiency is not treated promptly. Keep the acute encephalopathic presentation separate from the chronic amnestic syndrome: they are linked but are not interchangeable names for every alcohol-associated cognitive problem.
Confabulation means producing inaccurate accounts to fill gaps in memory, without deliberate deception. A patient may converse fluently while being unable to retain new information. The examination should therefore test learning and recall rather than relying on a superficially coherent conversation. The pattern differs from global fluctuating inattention in delirium.
The mammillary bodies, medial thalami and periaqueductal region are important anatomical associations. MRI may support the diagnosis, but it is not a prerequisite for starting treatment in a suspected emergency. For an anatomy-linked question, identify the vulnerable regions; for a treatment question, prioritise thiamine rather than waiting for a scan to make the clinical picture complete.
How do opioid intoxication and withdrawal differ?
| Finding | Opioid toxicity | Opioid withdrawal |
|---|---|---|
| Pupils | Often constricted | Dilated |
| Respiration | Depression is the critical danger | Autonomic activation is typical |
| Mental state | Reduced consciousness or sedation | Restlessness, anxiety and insomnia |
| Other clues | Possible overdose exposure | Yawning, lacrimation, rhinorrhoea, gooseflesh, aches and diarrhoea |
| Immediate approach | Support ventilation and use naloxone when indicated | Assess withdrawal and plan appropriate agonist or supportive treatment |
Opioid overdose is an emergency because respiratory depression can cause death. Ventilatory support and naloxone are central when clinically indicated. Assess the patient rather than relying on pupil size alone; a mixed exposure or other illness can modify the classic appearance. Naloxone reverses opioid effects, and it can also precipitate withdrawal in a dependent patient.
Withdrawal follows cessation or a reduction after dependence, or can be triggered by an antagonist. Its autonomic and gastrointestinal features explain the familiar stem: a restless patient with wide pupils, a runny nose, tearing eyes, yawning, gooseflesh, muscle aches and diarrhoea. Distinguish this from a drowsy patient breathing slowly after exposure.
How is opioid withdrawal managed without losing the long-term goal?
Methadone and buprenorphine are important medication approaches for opioid dependence and withdrawal. Buprenorphine is a partial agonist and can precipitate withdrawal if started while a patient remains under the effect of a full agonist without adequate spontaneous withdrawal. Induction should therefore follow an appropriate assessment and protocol rather than a blanket start time.
The Clinical Opioid Withdrawal Scale, or COWS, supports assessment of the withdrawal state. It differs from CIWA-Ar, which concerns alcohol withdrawal. These tools measure clinical features; a toxicology result establishes exposure imperfectly and does not replace the examination. Use the scale relevant to the substance and the immediate state described in the vignette.
Supportive treatment can address dehydration, gastrointestinal symptoms and aches. Clonidine can reduce autonomic symptoms, but it should not be confused with opioid agonist treatment. A medication relieving one withdrawal feature does not by itself provide continuing treatment for the disorder. Plan follow-up, ongoing medication where appropriate and psychosocial support rather than viewing detoxification as the endpoint.
What cannabis facts are useful for psychiatry revision?
The principal psychoactive cannabinoid, THC, acts mainly through cannabinoid receptors, especially CB1 in the nervous system. Intoxication can cause altered perception, impaired attention, increased appetite, tachycardia, conjunctival redness and dry mouth. Anxiety or psychotic symptoms can occur. Persistent psychosis needs assessment for other substances or a primary psychiatric disorder rather than automatic attribution to a recent positive cannabis history.
Cannabis withdrawal can produce irritability, anxiety, insomnia and reduced appetite. It is a real clinical syndrome, so an option claiming that cannabis never produces withdrawal is incorrect. The diagnostic pattern of a use disorder still depends on control, impairment and consequences. A history of experimentation and a pattern of continued use despite harm are not equivalent descriptions.
Cannabinoid hyperemesis syndrome causes recurrent vomiting in the setting of chronic use. Temporary relief with hot bathing is a useful clue, but sustained resolution requires cessation. Avoid selecting a routine antiemetic as the complete answer when the question asks what addresses the continuing cause. Assess fluid loss and competing causes of vomiting as part of the clinical work-up.
Psychosocial care, including motivational work, cognitive behavioural therapy and contingency management, is central to treatment. Keep these long-term approaches separate from supportive care during intoxication or withdrawal. For revision, connect the substance to its immediate signs, the consequences of stopping, the characteristic complications and the continuing treatment plan.