Learn — Substance use disorders

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CAGE questionnaire

The CAGE questionnaire is a four-item bedside screen for problem drinking in which each letter stands for one lifetime question: have you ever felt you should Cut down, have people Annoyed you by criticising your drinking, have you ever felt bad or Guilty about your drinking, and have you ever needed a drink first thing in the morning as an Eye-opener to steady your nerves or shift a hangover. It takes under a minute and needs no equipment, and two or more yes answers is a positive screen that obliges a full assessment for alcohol use disorder rather than being a diagnosis in itself.

The four letters are the memory hook, Cut down, Annoyed, Guilty and Eye-opener, scored one point for each yes, and two or more out of four is positive.
A yes to the eye-opener question is the single most ominous answer, because morning drinking means physical dependence and therefore a real risk of withdrawal once the patient is admitted and cannot drink.
CAGE detects dependence well but misses hazardous and binge drinking, is less sensitive in women, in young people and in older adults, and asks about lifetime experience, so it cannot tell you whether the problem is current.
The WHO Alcohol Use Disorders Identification Test is the ten-item alternative that measures quantity as well as harm: a score of 8 or more indicates hazardous drinking and higher scores suggest dependence, while AUDIT-C is the three-question consumption-only short form.
CAGE-AID substitutes drinking with drinking or drug use so that the same four questions screen for substance use as well.
A screen is not a diagnosis: DSM-5-TR needs two or more of eleven criteria within twelve months for alcohol use disorder, graded mild at two to three, moderate at four to five and severe at six or more, while ICD-11 describes a harmful pattern of use and alcohol dependence.
A WHO standard drink contains about 10 g of pure alcohol, so recording units drunk each week alongside the CAGE score gives the doctor information the four questions cannot.
Relapse prevention drugs are disulfiram 250 mg a day, which blocks aldehyde dehydrogenase so that any alcohol produces violent flushing, vomiting and hypotension; naltrexone 50 mg a day, an opioid antagonist that reduces craving and must never be given to a patient taking opioids; and acamprosate 666 mg three times a day.
Ask the questions matter-of-factly and record the answers as clinical information; the Mental Healthcare Act 2017 counts alcohol and drug use disorders as mental illness, so the rights to confidentiality, dignity and non-discrimination apply in full.

Cannabis (sativa) effects

Cannabis sativa is the hemp plant whose main psychoactive constituent is delta-9-tetrahydrocannabinol, acting on CB1 receptors in the brain, while cannabidiol, the other major constituent, is not intoxicating. Indian preparations differ in strength: bhang is made from the leaves and is weakest, ganja from the flowering tops, and charas is the resin and the most potent, and users describe euphoria, a slowed sense of time, hunger and relaxation followed by drowsiness.

Acute intoxication gives euphoria and talkativeness, an altered sense of time, conjunctival injection, dry mouth, increased appetite, tachycardia, impaired short-term memory, poor coordination and slowed reaction time, which is why driving remains unsafe for hours after use.
Large doses, particularly of charas or of an edible taken by an inexperienced user, can produce acute anxiety, panic, paranoia and a transient psychosis with a clear sensorium that settles over days; fatal overdose from cannabis alone is not described, because the brainstem respiratory centres carry few CB1 receptors.
Regular heavy use from adolescence is associated with an amotivational picture of apathy and falling performance, with cognitive slowing, with chronic bronchitis, and with a dose-related increase in the risk of a psychotic illness in vulnerable people.
Cannabis withdrawal is a recognised DSM-5-TR diagnosis: irritability or anger, anxiety, disturbed sleep with vivid dreams, reduced appetite, restlessness and low mood, beginning within a week of stopping, worst in the first week and settling over one to two weeks.
Cannabinoid hyperemesis syndrome, cycles of severe vomiting in a long-term user relieved only by hot showers and by stopping the drug, is the presentation most often mistaken for a surgical abdomen.
Urine screening detects the metabolite for a few days after occasional use and for several weeks in a daily heavy user, so a positive test proves exposure, not intoxication now.
There is no approved drug for cannabis use disorder: treatment is motivational interviewing, cognitive behavioural therapy and contingency management, with a short course of an antipsychotic only for as long as psychotic symptoms last.
Under the Narcotic Drugs and Psychotropic Substances Act 1985 charas and ganja are controlled substances, while bhang prepared from the leaves and seeds falls outside the Act's definition of cannabis, which is why bhang is sold legally in some states.

Chronic alcoholism — complications

Long-term heavy drinking damages almost every organ, partly through the direct toxicity of ethanol and its metabolite acetaldehyde and partly through the malnutrition and thiamine deficiency that go with it. The nurse meets that damage in five recognisable groups — liver and gut, nervous system, blood, heart, and the fetus of a woman who drinks in pregnancy — and each group contains one emergency that must be recognised on the ward.

Liver disease runs from fatty liver through alcoholic hepatitis to cirrhosis, and its biochemical signature is an AST to ALT ratio of two or more with a raised gamma-glutamyl transferase and a raised mean corpuscular volume.
Gut complications are gastritis, a Mallory-Weiss tear that bleeds after violent retching, acute and chronic pancreatitis, and oesophageal varices, which bleed catastrophically once portal hypertension is established.
Neurological damage includes Wernicke encephalopathy with its triad of confusion, ataxia and ophthalmoplegia, the Korsakoff amnestic syndrome that follows it, symmetrical distal peripheral neuropathy, cerebellar degeneration with a broad-based gait, and alcohol-related dementia.
Blood changes are macrocytic anaemia from folate deficiency and direct marrow suppression, thrombocytopenia, and impaired white cell function that raises the risk of infection.
Heart and vessels: dilated cardiomyopathy, hypertension, atrial fibrillation after a binge, and an increased risk of haemorrhagic stroke.
Metabolic complications are hypoglycaemia, alcoholic ketoacidosis, and low magnesium, potassium and phosphate; magnesium must be corrected or thiamine cannot work.
Alcohol in pregnancy causes fetal alcohol spectrum disorder — growth restriction, microcephaly, a smooth philtrum, a thin upper lip, short palpebral fissures and lifelong intellectual disability — and no amount has been shown to be safe, which makes it a leading preventable cause of intellectual disability.
Long-term drinking raises the risk of cancers of the mouth, pharynx, oesophagus, liver, colon and breast.
Suspected Wernicke encephalopathy is treated with high-dose parenteral thiamine, commonly 500 mg intravenously three times a day for two to three days followed by a lower daily dose, and thiamine always goes in before any glucose.

Alcohol withdrawal symptoms

Alcohol withdrawal is what a physically dependent nervous system does when the drink stops: the chronic suppression of GABA and up-regulation of glutamate are suddenly unopposed, and within six to twelve hours of the last drink the patient becomes tremulous, sweating, anxious, tachycardic and hypertensive. It follows a predictable timetable of tremor, then hallucinosis, then seizures, then delirium tremens, and it is the one withdrawal syndrome that can kill, so it is treated on a schedule rather than on request.

The timetable is the examination answer: tremor, sweating, nausea, anxiety and insomnia at 6 to 12 hours; alcoholic hallucinosis, usually visual, at 12 to 24 hours; generalised tonic-clonic withdrawal seizures at 12 to 48 hours with the peak near 24 hours; and delirium tremens at 48 to 96 hours.
Alcoholic hallucinosis is separated from delirium tremens by the sensorium: in hallucinosis the patient is fully oriented and knows the ward and the day, whereas in delirium tremens consciousness is clouded and the autonomic storm is severe.
The CIWA-Ar scale scores ten items to a maximum of 67; under 8 to 10 usually needs no medication, 8 to 15 is moderate withdrawal, and above 15 signals severe withdrawal with a high risk of seizure and delirium.
Benzodiazepines are the treatment: chlordiazepoxide or diazepam given symptom-triggered against the CIWA-Ar score, switching to lorazepam in liver failure, in the elderly and in the very ill because lorazepam, oxazepam and temazepam are cleared by glucuronidation and do not depend on the failing liver's oxidative pathways.
The named hazard of the treatment is over-sedation with respiratory depression, so the chart that carries the CIWA-Ar score also carries respiratory rate and sedation score; flumazenil is not used to reverse benzodiazepines in a dependent patient because it can precipitate seizures.
Thiamine goes in before glucose in every case, and magnesium and potassium are corrected, because low magnesium keeps the seizure threshold down and prevents thiamine from working.
Withdrawal seizures are typically one or two brief generalised fits without focal features; a focal seizure, a first seizure beyond 48 hours, or status epilepticus means looking for head injury, meningitis, hypoglycaemia or another cause.
The kindling phenomenon means each untreated withdrawal is worse than the last, so a history of previous withdrawal seizures or delirium tremens is the strongest predictor of a severe episode this time.
Never allow an abrupt hospital detoxification without cover, and never let a dependent patient be starved for surgery without a written withdrawal plan.

Delirium tremens

Delirium tremens is the most severe form of alcohol withdrawal: a hyperactive delirium with clouded consciousness that appears 48 to 96 hours after the last drink and usually lasts three to five days. The patient is disoriented and frightened, has a coarse tremor and marked autonomic overactivity with tachycardia, hypertension, fever and drenching sweats, and sees or feels things that are not there, classically small animals or insects on the skin. It is a medical emergency, not a behavioural problem.

Onset at 48 to 96 hours separates delirium tremens from early withdrawal at 6 to 12 hours and from withdrawal seizures at 12 to 48 hours; the seizure usually comes before the delirium, not after it.
The diagnostic core is clouding of consciousness with disorientation and fluctuating attention on top of the autonomic storm; a patient who hallucinates while remaining fully oriented has alcoholic hallucinosis instead.
Hallucinations are typically visual and tactile, with small animals, insects and formication, and they are entirely real to the patient, who may act on them by trying to climb out of bed or escape the ward.
Mortality is now under 5% with prompt benzodiazepine treatment and good supportive care, but it rises steeply when the delirium is missed or when untreated infection, injury, pancreatitis or electrolyte disturbance is hiding underneath.
Benzodiazepines are the only drugs shown to reduce mortality: intravenous diazepam or lorazepam, front-loaded and then given symptom-triggered against CIWA-Ar or a sedation score, with lorazepam preferred in liver failure and in the elderly, and the named hazard is respiratory depression, so respiratory rate and oxygen saturation are monitored throughout.
Haloperidol is an adjunct only, added for distressing hallucinations after adequate benzodiazepine cover, because antipsychotics lower the seizure threshold and prolong the QT interval; they must never be the sole treatment.
Supportive care decides the outcome: parenteral thiamine before glucose, correction of magnesium, potassium and phosphate, careful replacement of the litres lost in sweat, and an active search for the pneumonia, subdural haematoma, pancreatitis or hepatic encephalopathy underneath.
Nurse the patient in a quiet, well-lit room with consistent staff, reorient at every contact, keep the floor clear and the bed low, and have someone sit with the patient; physical restraint under the Mental Healthcare Act 2017 is a last resort used only to prevent imminent harm, in the least restrictive form, authorised, recorded, and with the nominated representative informed.
The strongest predictors of delirium tremens are a previous episode, previous withdrawal seizures, a high CIWA-Ar score early, older age and a concurrent acute illness.

Opioid dependence

Opioid dependence is a pattern of heroin or pharmaceutical opioid use in which control is lost: the drug takes precedence over other activities, tolerance rises so that more is needed for the same effect, and stopping produces a stereotyped withdrawal syndrome. ICD-11 requires the pattern over at least twelve months, or continuously for at least one month, while DSM-5-TR covers the same ground as opioid use disorder, graded by how many of eleven criteria are met.

Withdrawal from a short-acting opioid such as heroin begins 8 to 12 hours after the last dose, peaks at 36 to 72 hours and settles by 5 to 7 days, whereas methadone withdrawal begins at 24 to 48 hours and lasts 10 to 14 days.
The withdrawal picture is the mirror image of intoxication: yawning, lacrimation, rhinorrhoea, dilated pupils, gooseflesh, muscle and joint pain, abdominal cramps, vomiting, diarrhoea, insomnia, restlessness and intense craving, scored objectively on the Clinical Opiate Withdrawal Scale.
Opioid withdrawal is agonising but not usually life-threatening in an otherwise healthy adult, with two exceptions: in the neonate it causes seizures, and in pregnancy abrupt withdrawal risks fetal distress and pregnancy loss, so a pregnant woman is maintained on buprenorphine or methadone and never detoxified abruptly.
Opioid substitution therapy is the evidence-based treatment: buprenorphine, a partial agonist given sublingually with a ceiling effect on respiratory depression, or methadone, a full agonist given as supervised daily liquid; buprenorphine is started only once the patient is in moderate withdrawal or it will precipitate withdrawal, and methadone prolongs the QT interval.
Naltrexone 50 mg a day is the antagonist option for an abstinent patient and must not be started until 7 to 10 days opioid-free, or it precipitates severe withdrawal; the buprenorphine and naloxone combination tablet exists to deter injection.
Overdose is recognised by the triad of pinpoint pupils, a respiratory rate under 12 and unrousable coma, and naloxone 0.4 to 2 mg intravenously, intramuscularly or intranasally reverses it within minutes but wears off in about 30 to 90 minutes, so the patient is observed for hours and may need repeated doses.
Injecting brings HIV, hepatitis B and hepatitis C, abscess, cellulitis, infective endocarditis and venous thrombosis, so harm reduction with sterile needles and syringes, testing, immunisation and take-home naloxone is offered even to a patient who is not ready to stop.
In India opioid substitution therapy is delivered through government-approved centres on the National Drug Dependence Treatment Centre model, with the National Action Plan for Drug Demand Reduction covering prevention and rehabilitation, while the opioid drugs themselves are controlled under the Narcotic Drugs and Psychotropic Substances Act 1985.
Language is part of the treatment: describe the person as having opioid dependence rather than as an addict, because stigma is a documented reason patients do not come back for the second dose.

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