CASC Knowledge Essentials09 · Addictions: dependence, withdrawal and treatment

09 · Addictions: dependence, withdrawal and treatment

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Written by Resident Doctor Committee · Published

9.1 What dependence actually means

ICD-11 requires two of three domains: impaired control, increasing priority of use, and physiological adaptation. The last includes tolerance, withdrawal or relief use. Features usually span 12 months, or at least three months of daily/almost daily use. Tolerance plus withdrawal still count as only one domain.

Term

Meaning

Hazardous use

Increases the chance of harm

Harmful pattern

Has already caused clinically important harm

Dependence

Impaired regulation of use; quantity alone does not establish it

The older Edwards–Gross features remain useful: narrowed drinking repertoire, salience, tolerance, repeated withdrawal, relief drinking, compulsion and rapid reinstatement after abstinence. Relief drinking stops withdrawal symptoms. Feeling normal after a morning drink therefore suggests physiological adaptation.

Units and tools

UK units = mL × ABV% ÷ 1,000. A 750 mL bottle of 13% wine contains 9.75 units; 500 mL of 5% beer contains 2.5. The low-risk guideline is no more than 14 units/week, spread over at least three days. It is not a withdrawal plan for dependence.

Tool

Purpose

AUDIT

Drinking pattern and consequences; 20 or more raises concern for dependence

CAGE

Brief problem-drinking screen

SADQ

Dependence severity

CIWA-Ar

Withdrawal symptoms; cannot establish the cause of confusion

9.2 Alcohol's physical and psychiatric effects

System

Consequences

Liver/GI

Steatosis, hepatitis, cirrhosis, gastritis, pancreatitis, bleeding

Nervous system

Neuropathy, cerebellar dysfunction, withdrawal seizures, thiamine-related injury, cognitive impairment

Cardiovascular

Hypertension, arrhythmia, cardiomyopathy

Nutrition/blood

Malnutrition, vitamin deficiency, macrocytosis

Psychiatric/behavioural

Depression, anxiety, poor sleep, disinhibition, suicide risk, psychosis, violence

Normal bloods do not exclude dependence. GGT, transaminases and MCV may support the history but are not diagnostic. AST may exceed ALT in alcohol-related liver disease. Bilirubin, albumin and INR indicate liver dysfunction rather than simply recent drinking.

Depression: independent or alcohol-related?

Withdrawal anxiety often follows a period without alcohol and improves after drinking. Alcohol-related low mood may improve as withdrawal, sleep and nutrition settle. Depression predating heavy use, recurring independently or persisting during abstinence suggests a primary mood disorder.

NICE suggests reassessment after three–four weeks of abstinence where appropriate. Severe depression, psychosis or suicide risk still needs treatment now. Alcohol use should not exclude access to mental health care; antidepressants do not treat dependence itself.

9.3 Alcohol withdrawal: why stopping can be dangerous

Chronic exposure produces adaptation to alcohol's inhibitory effects. Reduction leaves the nervous system overactive: tremor, anxiety, insomnia, nausea, sweating, tachycardia and hypertension. A falling alcohol level can trigger withdrawal while alcohol remains detectable.

State

Usual timing after reduction/cessation

Features

Uncomplicated withdrawal

Within hours, often 6–24 hours

Tremor/autonomic activation; orientation preserved

Withdrawal seizure

Roughly 6–48 hours

Usually generalised; investigate atypical features

Hallucinosis

During heavy use or around withdrawal

Often threatening auditory hallucinations with relatively clear consciousness

Delirium tremens

Often 48–72 hours, sometimes later

Fluctuating inattention, disorientation, hallucinations and marked autonomic disturbance

Approximate sequence, not fixed deadlines. The figure shows a common 12–48-hour seizure window; seizures can begin around six hours, and delirium tremens can start after 72 hours. Drawn for MRCPsychiatrist. Drawn for MRCPsychiatrist

Previous seizures or delirium tremens, repeated withdrawals, severe dependence and medical illness increase risk. Focal signs, head injury, fever, atypical seizures or persistent impaired consciousness require another explanation.

Delirium tremens versus hallucinosis

Attention and awareness are the key distinction. Fluctuating attention and disorientation indicate delirium; clear consciousness supports hallucinosis. Visual/tactile hallucinations favour delirium tremens and auditory voices favour hallucinosis, but modality alone cannot decide it. Infection, hypoxia, hypoglycaemia, head injury, hepatic encephalopathy and other withdrawal may coexist.

Benzodiazepines are the foundation of withdrawal treatment. Chlordiazepoxide or diazepam are common choices. Lorazepam or oxazepam may be useful when accumulation is a concern, including significant liver impairment. Dosing follows severity, monitoring and local protocol.

Haloperidol may supplement adequate benzodiazepines for persistent disturbance; it is not monotherapy for delirium tremens. Withdrawal seizures need benzodiazepines and assessment; phenytoin does not treat the withdrawal mechanism.

CIWA-Ar requires reliable participation. Severe delirium needs clinical observation and an appropriate inpatient protocol. Opioids and other sedatives increase the respiratory-depression and over-sedation risk.

Persistent psychosis

Alcohol-induced psychotic disorder needs a convincing temporal relationship and symptoms beyond ordinary intoxication/withdrawal. Psychosis predating drinking or persisting through sustained abstinence reopens the differential. Antipsychotics may be needed for dangerous or persistent symptoms, alongside withdrawal treatment and attention to seizure threshold.

9.4 Wernicke's encephalopathy and Korsakoff syndrome

Wernicke's: treat the deficiency urgently

Thiamine deficiency impairs carbohydrate metabolism and injures vulnerable brain regions. Alcohol dependence is one cause; severe malnutrition and prolonged vomiting are others.

The classic triad is altered mental state, eye movement abnormalities and ataxia, but the complete triad is often absent. Nystagmus, gaze palsy, unsteadiness or new confusion in an at-risk person is enough to raise concern. Neither a normal scan nor an incomplete triad justifies delay.

Suspected Wernicke's requires parenteral thiamine; oral absorption may be inadequate. DHSC acute-hospital guidance recommends IV 300–500 mg three times daily for 3–5 days, reviewed daily, with further IV treatment if symptoms persist. Follow local product/route arrangements and correct magnesium deficiency, which can impair response.

Give thiamine before or alongside carbohydrate where possible, but never delay emergency glucose for hypoglycaemia.

Korsakoff: persistent amnesia

The main deficit is forming new memories, with variable retrograde loss. Immediate attention, remote memories and procedural skills may be relatively preserved. Someone can converse fluently yet forget the conversation or a recent meal.

Confabulation is inaccurate memory without deliberate deception; it is not required for diagnosis. Alcohol-related brain damage is broader than Korsakoff syndrome and may include executive and other cognitive deficits. Judge recovery and support needs after physical stabilisation and sustained abstinence.

9.5 Alcohol treatment after withdrawal

Detoxification treats withdrawal; relapse prevention treats the continuing disorder. Medication works alongside psychological treatment and social support.

Medicine

Action

Main cautions

Acamprosate

Supports abstinence through effects on the altered excitatory/inhibitory balance

Diarrhoea; renal clearance makes renal function important

Naltrexone

Opioid antagonism reduces alcohol reward

Nausea, liver cautions, blocked opioid analgesia, precipitated opioid withdrawal

Disulfiram

Inhibits aldehyde dehydrogenase → acetaldehyde accumulates with alcohol

Flushing, headache, nausea, hypotension, potentially severe reactions; liver injury; cardiac/psychiatric contraindications

Acamprosate starts after withdrawal and established abstinence. The usual licensed dose at ≥60 kg is 666 mg three times daily; below 60 kg use the lower weight-based regimen. Renal impairment can make it unsuitable. It does not treat acute withdrawal.

Naltrexone needs an opioid history and a plan for future analgesia. Acamprosate or naltrexone are usual initial medication options. Disulfiram is an alternative when unsuitable or preferred after informed discussion; understanding the reaction and an abstinence goal are essential. Supervised administration can improve adherence.

Disulfiram timing: wait at least 24 hours after the last alcohol. A reaction remains possible for 14 days after stopping, including with alcohol-containing products. Jaundice, fever or systemic illness requires urgent review for liver injury.

9.6 Opioids: withdrawal, overdose and substitution

Overdose and withdrawal look different

Intoxication/overdose

Withdrawal

Reduced consciousness, respiratory depression

Restlessness, anxiety, insomnia

Often small pupils

Dilated pupils, yawning, watery eyes

Reduced gut activity

Cramps, nausea, vomiting, diarrhoea

Potentially fatal hypoxia

Aches, sweating, gooseflesh, rhinorrhoea

Withdrawal generally starts earlier after heroin than methadone; timing depends on dose, route and metabolism. Seizures are unusual in isolated opioid withdrawal: consider alcohol, benzodiazepines, GHB, epilepsy, injury or another medical cause.

Naloxone restores breathing through opioid antagonism. It can wear off before the opioid, so observation, repeat doses or infusion may be needed. Full alertness is not the immediate target. Take-home naloxone matters particularly after detoxification, hospital or prison, when lost tolerance makes previous doses dangerous.

Methadone versus buprenorphine

Methadone is a full agonist. Long, variable elimination causes accumulation during initiation or escalation. Remember sedation, constipation, respiratory depression and QT prolongation. Alcohol, benzodiazepines and other sedatives amplify overdose risk.

Buprenorphine is a high-affinity partial agonist. Its respiratory-depression ceiling improves safety but does not abolish overdose, especially with sedatives. It displaces full agonists while providing less receptor activation: starting too soon can cause precipitated withdrawal. Standard induction requires objective withdrawal and an appropriate interval; alternative specialist inductions use different protocols.

The lower partial-agonist plateau explains buprenorphine's ceiling; high receptor affinity explains displacement and precipitated withdrawal. Xx684xx, CC0, via Wikimedia Commons. Xx684xx, CC0, via Wikimedia Commons

Both treatments reduce illicit use and improve stability. Choose individually and give an adequate effective dose; an arbitrarily low dose may leave withdrawal and street use untreated. Monitoring and supervised consumption follow risk.

Missed doses and injecting risks

The prescribed dose does not prove current tolerance. Verify the prescription, last dose consumed, missed doses, current sedation/withdrawal and other substances. An unverified full dose risks duplication or overdose. Continue assessment and appropriate treatment while checking: untreated withdrawal can drive self-discharge and street use.

Injecting adds abscesses, cellulitis, thrombosis, endocarditis and blood-borne viruses. Sterile equipment, hepatitis B vaccination and HIV/hepatitis testing address risks that maintenance medication alone cannot remove.

9.7 GHB and GBL: two different emergencies

GHB is a CNS depressant with important GABA-B activity. GBL and 1,4-butanediol become GHB. Variable concentration and a narrow gap between desired and toxic effects make small extra amounts dangerous. Alcohol, opioids and benzodiazepines increase respiratory risk.

State

What to recognise

Intoxication

Amnesia, vomiting, abrupt unconsciousness, respiratory depression

Withdrawal

Begins within hours in dependence, especially with overnight dosing; anxiety/tremor can progress rapidly to delirium

Someone waking after overdose may soon enter withdrawal.

Severe withdrawal causes agitation, hallucinations, seizures, hyperthermia and rhabdomyolysis. It needs acute medical, addiction and toxicology expertise, sometimes intensive care. Benzodiazepines are commonly used; baclofen may be added off-label for its GABA-B action. Doses require specialist supervision, not a universal high-dose schedule.

Chemsex may combine GHB/GBL, stimulants and prolonged sexual activity. Consider impaired consent, assault, infection, exhaustion and interactions according to actual exposure. Abrupt unsupervised cessation is unsafe in dependence.

9.8 Urine drug screens: what the result can and cannot mean

Immunoassays give presumptive detection of selected drugs/metabolites above a threshold. They cannot establish dose, exact timing, impairment, dependence or the cause of psychosis. Cross-reactions and missed compounds cause false positives and negatives. Discuss consequential unexpected results with the laboratory; confirmation may use LC-MS/MS or GC-MS.

Result

Interpretation

Opiates negative

May miss fentanyl, buprenorphine, methadone, nitazenes and others unless included in the panel

Cannabis positive

Can persist beyond intoxication; cannot date use to a particular period of leave

Benzodiazepines negative

Some assays poorly detect particular compounds/metabolites

Routine panel negative

Does not exclude GHB, synthetic cannabinoids or many novel substances

Unexpected positive

Check prescribed medicines, cross-reactivity, timing and confirmation

Detection depends on exposure, renal function and assay threshold. Cannabis may remain detectable for weeks after heavy use; many other drugs for days. There is no universal detection window.

Refusal does not prove use, and a ward agreement does not create legal authority to obtain a sample. Continue assessment of relapse, intoxication, withdrawal and exploitation. DVLA rules distinguish ongoing misuse from stable prescribed substitution; methadone is not an automatic permanent driving bar.