Neurocognitive Disorders: Delirium and Dementia

This is the chapter where psychiatric nursing and medical nursing stop being separate subjects. A person whose thinking has changed is telling you something about their brain, and the brain is an organ that reports the state of the whole body. Delirium is an acute, fluctuating, potentially reversible disturbance of attention and awareness caused by something physiological — an infection, a drug, a low sodium, a full bladder — and it is a medical emergency that carries a mortality comparable to sepsis or myocardial infarction, yet it is missed in the majority of cases because the commonest form is quiet. Dementia, now called major neurocognitive disorder, is a slow, progressive, and currently incurable loss of cognitive function that is not a normal part of ageing and not a loss of the person. The two overlap constantly: dementia is the single largest risk factor for delirium, and any sudden change in a person who already has dementia is delirium until proven otherwise. Your assessment, your language, and your patience are the interventions.

Section 1Cognition, Ageing and the Three Ds

What “neurocognitive disorder” means now

DSM-5-TR retired the word dementia as a diagnostic heading and replaced it with major neurocognitive disorder, partly because “dementia” carried centuries of stigma and partly because the older term implied memory loss when many of these diseases begin somewhere else entirely. The clinical world still says dementia in conversation, in family education, and in the names of advocacy organisations, and you should too when it aids understanding. What changed is the structure of the definition, and the structure is what you assess.

A neurocognitive disorder is a decline from a previously attained level of performance in one or more of six cognitive domains: complex attention (sustained, divided and selective attention, processing speed); executive function (planning, decision-making, working memory, error correction, mental flexibility); learning and memory (immediate, recent and long-term recall); language (naming, word finding, fluency, comprehension); perceptual-motor ability (visual perception, visuoconstruction, praxis, gnosis); and social cognition (recognition of emotion, theory of mind, behavioural regulation). The decline must be documented by concern from the person, a knowledgeable informant or the clinician, and by objective testing where possible.

The line between major and mild is entirely functional. In major neurocognitive disorder the deficits interfere with independence in everyday activities — the person needs help with paying bills, managing medications, or later with bathing and dressing. In mild neurocognitive disorder the deficits are modest and independence is preserved, though it may take greater effort, lists, alarms and compensatory strategies to maintain it. Mild neurocognitive disorder is the DSM label for what neurology calls mild cognitive impairment, and it matters enormously now, because the newest disease-modifying treatments are only indicated at that stage. Neither diagnosis may be made if the disturbance occurs exclusively during a delirium, and neither may be made if another mental disorder — major depressive disorder, schizophrenia — better explains the findings.

Two facts anchor everything that follows. First, dementia is not normal ageing. Normal ageing slows processing speed and makes name retrieval slower; it does not take away the ability to manage a chequebook, cook a familiar meal, or find the way home. Slowness that is compensated is ageing; loss that costs function is disease, and disease is investigated. Second, dementia is not a loss of personhood. The person is present throughout, including in the late stages when language is gone, and the standard of care is Tom Kitwood’s person-centred care: the goal is not to preserve cognition, which you cannot, but to preserve identity, comfort, attachment, occupation and inclusion, which you can.

The three Ds — and why they are confused with each other

Delirium, dementia and depression produce overlapping presentations in older adults, and distinguishing them is one of the most frequently tested and most consequential judgements in nursing. The distinguishing features are not the presence of confusion, which all three can produce, but onset, course, attention and level of consciousness.

Delirium begins over hours to days, fluctuates markedly across the day with lucid intervals, and its cardinal feature is inattention — the person cannot sustain or shift focus, loses the thread mid-sentence, cannot recite the months backwards. Level of consciousness is altered: hyperalert and agitated, or drowsy and difficult to rouse. It is caused by a physiological insult and is potentially reversible when that insult is treated. Dementia begins insidiously over months to years, progresses steadily rather than fluctuating hour to hour, and leaves consciousness clear until the terminal stages; attention is relatively preserved early, and it is memory, word finding or executive planning that fails first depending on the subtype.

Depression in an older adult can produce what was historically called pseudodementia: onset over weeks, a fairly abrupt and datable start, complaints of memory problems that the person raises themselves and describes vividly, effortful “I do not know” answers rather than confabulation, psychomotor slowing, and a mood disturbance that precedes rather than follows the cognitive change. The tell is the person’s own attitude: a person with early Alzheimer disease commonly minimises the problem while the family is alarmed; a person with depression commonly magnifies it while performing better than they claim once engaged. Cognitive symptoms of depression improve when the depression is treated — though a meaningful proportion of these patients go on to develop a neurodegenerative disorder within a few years, so late-life depression with cognitive symptoms earns follow-up, never dismissal.

These are not mutually exclusive categories. They coexist constantly. Delirium superimposed on dementia is one of the most common presentations on a medical ward, and it is the reason the golden rule exists: any acute change in a person with dementia is delirium until proven otherwise. Depression is also common in early dementia, when insight is preserved enough for the person to grieve what is happening to them. Holding all three possibilities at once, rather than picking one and stopping, is what expert assessment looks like.

Ageism, stigma and the words we use

Two forms of stigma converge on this population. The first is ageism: the assumption that confusion in an older adult is expected, that nothing can be done, that investigating is not worth the trouble. This assumption kills people. Delirium missed because “she is 88 and gets like this” is a urinary tract infection, a subdural haematoma or a hyponatraemia that went untreated. The second is dementia stigma: the belief that the diagnosis ends the person, which drives social withdrawal, delayed help-seeking, and the extraordinary habit clinicians have of talking over people with dementia as though they were furniture.

Language is the correction. Say a person living with dementia, never “a dementia patient”, “a demented woman”, or the appalling institutional shorthand “a pleasantly confused”. Do not describe someone as a “wanderer”, a “feeder”, or a “sundowner”; those words turn a behaviour into an identity and stop the assessment. Do not chart that a person is “difficult”, “non-compliant” or “combative” during care. Chart what happened, what preceded it, and what it appeared to communicate: “Pulled away and shouted ‘stop’ when the shower was started; had declined the shower twice; settled when offered a bed bath with warm towels and her daughter present.” That sentence is assessable and it teaches the next nurse how to succeed. “Combative with care” teaches nothing and guarantees a repeat.

Say it plainly to families as well, because they will have absorbed the same stigma: this is a disease of an organ, like heart failure. It is not a punishment, not a moral failure, not something the person is doing on purpose, and not something they can try harder to overcome. And on the question the public gets most wrong — people living with mental illness and cognitive impairment are far more likely to be the victims of violence, neglect and financial exploitation than the perpetrators of anything. Elder abuse screening belongs in this chapter for exactly that reason.

Section 2Delirium — The Emergency That Looks Like Confusion

What delirium is, and why most of it is missed

Delirium is a disturbance in attention and awareness that develops over a short period, represents an acute change from baseline, fluctuates in severity during the day, is accompanied by at least one additional cognitive disturbance (memory, disorientation, language, visuospatial ability, perception), and is caused by a general medical condition, a substance, a withdrawal state, a toxin, or several of these at once. It is not a psychiatric diagnosis in the ordinary sense. It is brain failure, and it should be treated with the same urgency you would apply to kidney failure appearing overnight.

The numbers justify that urgency. Delirium affects roughly one in five general medical inpatients, up to half of older adults after hip fracture surgery, and the substantial majority of mechanically ventilated intensive care patients. It independently predicts longer stay, functional decline, new nursing-home placement, accelerated long-term cognitive decline, and death — in-hospital mortality figures in the range of a fifth to a third of affected patients are reported across settings. Delirium is not a benign side effect of being sick in hospital; it is a marker and a mediator of harm.

There are three motor subtypes. Hyperactive delirium — restless, agitated, pulling at lines, hallucinating, calling out — accounts for perhaps a quarter of cases and gets attention because it disrupts the ward. Hypoactive delirium — withdrawn, flat, slowed, drowsy, minimally responsive, giving vague answers, sleeping through meals — is the most common form, carries the worse prognosis, and is the one that is routinely missed or charted as “pleasantly confused”, “tired today”, or, disastrously, “depressed”. Mixed delirium alternates between the two. Overall, delirium goes unrecognised in something on the order of two-thirds of cases, and hypoactive delirium is where nearly all of that miss happens. The quiet patient is not the easy patient. The quiet patient is the one to check.

Screening: attention is the test

You cannot diagnose delirium without knowing the person’s baseline, which means you cannot diagnose it without collateral history. Ring the daughter. Ask the group-home staff. Ask the specific question: “Two weeks ago, was he doing his own medications and his own shopping? Was he like this yesterday morning?” A single-question screen validated in practice is the informant question “Do you think he or she has been more confused lately?”, which is far more sensitive than clinician impression alone.

The Confusion Assessment Method (CAM) is the standard bedside instrument. It requires feature 1 (acute onset and fluctuating course) and feature 2 (inattention), plus either feature 3 (disorganised thinking — rambling, illogical, unpredictable switching) or feature 4 (altered level of consciousness — anything other than alert). Note the structure: 1 and 2 and (3 or 4). Inattention is mandatory and is tested, not guessed — recite the months of the year backwards from December, count backwards from 20, or squeeze my hand every time you hear the letter A in the sequence I read. The 4AT is a faster alternative requiring no special training (alertness, the AMT4 orientation items, months backwards, acute change) with a score of 4 or more suggesting delirium. In intensive care, the CAM-ICU is used with the Richmond Agitation-Sedation Scale (RASS) so that non-verbal, ventilated patients can be assessed; a deeply sedated patient is scored as unassessable rather than as normal.

Screen on admission to establish baseline, then at least once per shift in at-risk patients, because a single normal screen at 10:00 does not exclude a delirium that appears at 22:00. Risk factors that should trigger routine screening include age over 65, pre-existing cognitive impairment, sensory impairment, severe illness, fracture, surgery, polypharmacy, alcohol use, dehydration, and a previous episode of delirium. Predisposing risk plus a precipitating insult produces delirium: a robust 40-year-old needs a huge insult, while a frail 88-year-old with dementia may need only a full bladder.

Months backwards is the cheapest test in nursing. It takes twenty seconds, needs no form, and is abnormal in delirium long before orientation questions fail. If a person cannot get from December to July without losing the thread, you have found inattention — and inattention plus an acute change is a delirium workup, not a note that says “oriented to person only.”

Finding the cause — and the drugs that are usually part of it

Delirium is a syndrome, never a diagnosis you stop at. The nursing task is a structured search for causes, and there are usually several operating together. Two mnemonics survive because they work. PINCH ME — Pain, Infection, Nutrition, Constipation, Hydration, Medication, Environment — is the frontline nursing sweep and catches a remarkable share of ward delirium. DELIRIUM — Drugs, Electrolytes and endocrine, Lack of drugs (withdrawal and uncontrolled pain), Infection, Reduced sensory input, Intracranial events, Urinary and faecal retention, Myocardial and pulmonary causes including hypoxia — is the fuller medical differential.

Do not skip the unglamorous items. Urinary retention and faecal impaction cause delirium regularly and are fixed with a bladder scan and a rectal examination. Hypoxia, hypoglycaemia, hyponatraemia, hypercalcaemia, uraemia, hepatic encephalopathy, thyroid disease, and infection anywhere are standard culprits. Sensory deprivation is a genuine cause: the man who cannot hear because his hearing aid batteries died and cannot see because his glasses are in the property bag is being deprived of the data his brain needs to stay oriented. And pain — particularly untreated pain in a person who cannot report it — is one of the most common reversible precipitants on any surgical or orthopaedic unit.

Medications deserve their own paragraph because they are involved in something like a third of cases and are the cause you can most directly influence. The high-risk classes are anticholinergics (diphenhydramine, hydroxyzine, oxybutynin, tricyclic antidepressants, promethazine, scopolamine), benzodiazepines, opioids — especially meperidine, which should not be used in older adults — corticosteroids, sedative hypnotics such as zolpidem, some antibiotics including fluoroquinolones, H2 blockers, and antiparkinsonian agents. Total anticholinergic burden matters more than any single drug: three “mildly” anticholinergic medications together will do what one strong one does. The Beers Criteria list potentially inappropriate medications in older adults and are the reference to reach for. The most reliably useless drug on a delirium chart is diphenhydramine given for sleep — it is a sedating anticholinergic, and it will make tonight worse.

Prevention first, then non-pharmacological management

Roughly a third of hospital delirium is preventable, and the interventions are nursing interventions. The Hospital Elder Life Program (HELP) bundle is the evidence base: daily orientation and therapeutic cognitive activity; early mobilisation and avoidance of physical restraints and unnecessary lines; a non-pharmacological sleep protocol with quiet hours, dimmed lighting, back rub and warm drinks instead of hypnotics; correction of vision and hearing with the person’s own glasses and hearing aids; and attention to hydration and nutrition. Add pain control, bowel and bladder regimens, familiar objects from home, a visible clock and calendar, consistent staff assignment, and daylight during the day with darkness at night to protect the circadian rhythm.

When delirium is established, the treatment is the cause. Everything else is supportive: a calm low-stimulation environment, one person speaking at a time in short simple sentences, gentle reorientation (which is appropriate in delirium, unlike in advanced dementia), family presence, glasses and hearing aids on, mobilise, remove the tether of unnecessary catheters and telemetry leads, and keep the person hydrated and fed. Physical restraint is not a treatment for delirium — it increases agitation, injury, aspiration, deconditioning, delirium duration and death, and it re-enacts trauma for anyone with an assault history.

Medication for delirium is for one narrow indication: severe distress or agitation that poses an imminent danger to the person or others and has not responded to non-pharmacological measures. It does not treat delirium, does not shorten it, and is never indicated for hypoactive delirium. Where it is used, a low-dose antipsychotic such as haloperidol is typical, at the lowest effective dose for the shortest possible time, with QT interval and extrapyramidal monitoring, and with a documented plan to stop. Benzodiazepines worsen delirium and are contraindicated except in three situations: alcohol or benzodiazepine withdrawal, neuroleptic malignant syndrome, and catatonia. In alcohol withdrawal delirium, benzodiazepines are the treatment, guided by a CIWA-Ar protocol, and thiamine is given before any glucose load to avoid precipitating Wernicke encephalopathy.

Section 3Major Neurocognitive Disorder — Subtypes, Staging and Assessment

The subtypes, and why the subtype changes your nursing

Alzheimer disease accounts for roughly 60 to 80 percent of dementia. Its pathology is extracellular amyloid-beta plaques and intraneuronal neurofibrillary tangles of hyperphosphorylated tau, with early degeneration of the hippocampus and of the cholinergic neurons of the basal forebrain — the cholinergic deficit that gives us our only symptomatic drugs. Onset is insidious and the course is gradual and relentless. The earliest changes are recent episodic memory (repeated questions, misplaced items, missed appointments), word-finding difficulty, and apathy or withdrawal. As it progresses the classical triad appears: aphasia (language loss), apraxia (inability to perform learned motor tasks such as dressing despite intact strength) and agnosia (failure to recognise objects and, later, faces). Long-term autobiographical memory and emotional memory persist far longer than recent memory, which is why a woman who cannot tell you the year can sing every word of a hymn and can absolutely tell whether you spoke to her kindly.

Vascular neurocognitive disorder is the second most common and is often described as stepwise: plateaus punctuated by sudden drops corresponding to infarcts, though small-vessel disease produces a smoother decline. Executive dysfunction, slowed processing and gait disturbance appear early, often before prominent memory loss, and there are focal neurological signs. This is the one subtype with a genuine prevention strategy — blood pressure control, atrial fibrillation management, glycaemic control, lipid management, smoking cessation — and health teaching here changes trajectories.

Dementia with Lewy bodies is defined by alpha-synuclein inclusions and by four core features: fluctuating cognition with pronounced variation in attention and alertness (which mimics delirium and is frequently mistaken for it), recurrent well-formed visual hallucinations (often of people or animals, and often not distressing), REM sleep behaviour disorder that may precede cognition changes by years, and parkinsonism. Its single most examinable feature is severe neuroleptic sensitivity: a substantial minority of these patients respond to antipsychotics with severe rigidity, immobility, autonomic instability and a neuroleptic malignant syndrome that can be fatal. First-generation agents such as haloperidol are effectively contraindicated. Cholinesterase inhibitors, by contrast, work unusually well here, including for the hallucinations. In Parkinson disease dementia the same pathology is present; the convention is that motor symptoms precede cognitive symptoms by at least a year.

Frontotemporal neurocognitive disorder has a younger onset, commonly between 45 and 65, and it is the subtype most often misdiagnosed as a primary psychiatric illness. In the behavioural variant, memory is relatively preserved while social cognition collapses: disinhibition, tactless or sexually inappropriate remarks, loss of empathy, apathy mistaken for depression, compulsive rituals, and hyperorality with new sweet cravings or eating non-food items. Families describe a personality change, not a memory problem. The language variants (primary progressive aphasia) erode fluency or word meaning. Nursing here is heavily about structure, environmental modification and family support, and about resisting the urge to interpret a symptom of a degenerating frontal lobe as bad character.

Beyond these four, mixed pathology is the rule in advanced age rather than the exception; Alzheimer and vascular changes routinely coexist. Others you will meet include dementia due to traumatic brain injury, HIV infection, Huntington disease, prion disease, and substance-induced neurocognitive disorder including alcohol-related dementia and Korsakoff syndrome — profound anterograde amnesia with confabulation from thiamine deficiency, the chronic sequel of an untreated Wernicke encephalopathy, and therefore a largely preventable disease.

What must never be missed: the reversible contributors

Before anyone is labelled with an irreversible disease, a workup excludes the treatable. Vitamin B12 deficiency, hypothyroidism, neurosyphilis, normal pressure hydrocephalus (the triad remembered as wet, wobbly and wacky — urinary incontinence, gait apraxia and cognitive slowing), chronic subdural haematoma after a fall that may have seemed trivial, obstructive sleep apnoea, severe depression, and above all medications are the classic reversible or partly reversible contributors. Hearing loss deserves particular emphasis: uncorrected hearing loss is one of the largest modifiable risk factors for dementia in the Lancet Commission analysis, and a hearing aid is a cognitive intervention.

The Lancet Commission’s modifiable risk factors are worth teaching to any family who asks what they can do: less education in early life; hearing loss, high LDL cholesterol, depression, traumatic brain injury, physical inactivity, diabetes, smoking, hypertension, obesity and excessive alcohol in midlife; and social isolation, air pollution and visual loss in later life. Together they account for a substantial share of population dementia risk. That is not a promise of prevention for an individual, and you should not offer it as one, but it is a real answer to a frightened adult child asking what they can change.

Assessment: screening tools, function and staging

Cognitive screening tools are screens, not diagnoses. The Mini-Cog is three-word recall plus a clock drawing test, takes about three minutes, and is ideal for busy settings; an abnormal clock — numbers crowded, hands missing, the whole drawing pushed to one side — is a rich executive and visuospatial finding. The MoCA (Montreal Cognitive Assessment) scores out of 30, is substantially more sensitive than the MMSE for mild impairment because it loads executive function and delayed recall, and adds one point if the person had 12 or fewer years of education. The MMSE also scores out of 30 and remains widely used for tracking; the rough convention is 20 to 24 mild, 13 to 19 moderate, and 12 or below severe impairment. Every one of these tools is biased by education, primary language, literacy, sensory impairment and acute illness — do not screen a person in pain, in delirium, without their glasses, or in a language they do not read, and never report a number without that context.

Function matters more than the score. Assess ADLs with the Katz index — bathing, dressing, toileting, transferring, continence, feeding — and IADLs with the Lawton scale — telephone, shopping, food preparation, housekeeping, laundry, transport, medication management and finances. IADLs fail first, and the two that fail earliest, medications and money, are the two with the most dangerous consequences. A person who cannot reconcile a bank statement is a person at risk of financial exploitation; a person who cannot manage a pill organiser is a person at risk of a double dose of warfarin.

Staging is usually described with the Global Deterioration Scale (GDS) of Reisberg, from stage 1 (no deficit) through stage 3 (mild, subtle work and social difficulty), stage 4 (moderate, needs help with complex tasks and finances), stage 5 (moderately severe, needs help choosing clothing, cannot recall major details), stage 6 (severe, needs help with dressing, bathing and toileting, incontinence appears, personality change) to stage 7 (very severe, speech reduced to a handful of words then none, loss of ambulation, loss of ability to sit up and to smile, rigidity). The FAST scale subdivides those late stages and is used for hospice eligibility. Late-stage dementia is a terminal illness: dysphagia and aspiration pneumonia are the common terminal events, and the palliative conversation belongs long before that point.

Section 4Behaviour Is Communication — Responsive Behaviours, Milieu and De-escalation

Reframing: from “behaviours” to unmet needs

The older literature calls these behavioural and psychological symptoms of dementia; contemporary practice increasingly says responsive behaviours, and the change in wording carries the whole clinical idea. Agitation, calling out, resistance to personal care, exit-seeking, hoarding, sexual disinhibition and aggression are not random products of a diseased brain. They are responses — to pain, to fear, to a full bladder, to a stranger removing your clothes, to noise, to boredom, to being asked a question you cannot answer in front of your family. The need-driven behaviour model holds that the behaviour is the person’s remaining means of communicating a need once language has failed. Your job is translation.

The DICE approach structures that translation. Describe: get the exact behaviour, from the person who saw it, with its context — who, what, when, where, what happened immediately before and after. Investigate: the person (pain, infection, constipation, retention, hunger, thirst, medication change, sensory deficit, depression, fatigue), the caregiver (approach, tone, rushing, task focus, staff change), and the environment (noise, glare, shadows, overstimulation, understimulation, shift change chaos). Create: a plan with the family and team that addresses what you found, non-pharmacological first. Evaluate: did it work, and is it still needed. The PIECES framework covers the same ground under Physical, Intellectual, Emotional, Capabilities, Environment and Social headings.

Pain deserves the first suspicion every time. Untreated pain is among the commonest drivers of agitation in dementia and the person may be unable to say “my hip hurts”. Use an observational tool such as PAINAD, which scores breathing, negative vocalisation, facial expression, body language and consolability. A scheduled analgesic trial — regular paracetamol rather than as-needed — resolves a striking proportion of “behaviour problems” and is a far better first move than an antipsychotic. Constipation and urinary retention come next, and are checked, not assumed.

Sundowning — late-afternoon and evening escalation — is best understood as a collision of fatigue, circadian disruption, low light with shadows and misperception, hunger, and the noisiest, most understaffed hour on the unit. Manage it before it starts: bright light and activity during the day, an earlier and calmer evening routine, the largest meal at midday, closed blinds and lights on before dusk to eliminate shadows, no caffeine after midday, no naps late in the afternoon, familiar music, and consistent staff at that hour.

The dialogue — what to say and why it lands

The single most useful skill in this chapter is what comes out of your mouth in the first ten seconds. Approach from the front, never from behind or from the side where you appear suddenly. Get to eye level — standing over someone reads as threat. Use the person’s preferred name, introduce yourself every time without testing whether they remember you, keep your hands visible, and speak in short sentences with one idea each. Ask one question at a time and wait — processing may take ten or fifteen seconds, and filling that silence with a second question resets the clock. Offer closed or two-option choices (“the blue sweater or the green one?”) rather than open ones (“what would you like to wear?”). Announce every touch before it happens. Break tasks into single steps and use hand-under-hand guidance so the person retains control of the movement.

Three responses reliably escalate, and students use all three from the best of motives. The first is quizzing: “Do you remember me? What did you have for lunch? Do you know what year it is?” Every question is a test the person will fail, and failure in front of family produces shame and then anger. The second is arguing with the reality: correcting a false belief that is emotionally true. The third is the sentence “calm down”, which tells a frightened person that their feeling is unacceptable and reliably makes it worse.

What replaces them is validation — responding to the emotion rather than to the factual content. Naomi Feil’s validation therapy and the wider practice of emotion-focused responding hold that behind “I have to go home, my mother is waiting” is a feeling of being unsafe and unmoored, and that feeling is entirely real even though the mother died forty years ago. Reorientation is appropriate in delirium and in early dementia where insight remains. In moderate to advanced dementia it is repeatedly cruel: each correction delivers the news of a bereavement for the first time. The middle ground the profession has settled on is this — never lie to gain compliance or for staff convenience, never construct an elaborate false world, but do not force a truth whose only effect is to re-traumatise. Answer the emotion, then redirect to something meaningful.

De-escalation, restraint law, trauma-informed care and delegation

De-escalation always precedes restriction, and the principle is the least restrictive intervention that maintains safety. The sequence: recognise early warning signs (pacing, rising volume, clenched hands, refusing food, scanning the room); reduce stimulation and clear the audience; assign one staff member to speak; keep more than an arm’s length and never corner yourself or the person; keep your voice lower and slower than theirs; name the feeling and offer help; and offer real choices — a walk, a drink, a quiet room, a phone call to a daughter, a PRN analgesic. Offer, do not demand. If a person is escalating and something you tried is not working, change what you are doing rather than repeating it louder.

Restraint and seclusion are last-resort emergency measures for imminent serious harm when less restrictive measures have failed, and they are governed by regulation, not preference. They are never used for punishment, discipline, coercion or staff convenience, never as a substitute for adequate staffing, and never as a standing solution to a care plan nobody has written. An order from a licensed independent practitioner is required, and PRN or standing orders for restraint are prohibited. A face-to-face evaluation within one hour of initiation is required for violent or self-destructive behaviour. Orders are time-limited and renewable — up to 4 hours for adults 18 and over, 2 hours for ages 9 to 17 and 1 hour for children under 9. Monitoring is continuous, with documented attention to circulation, skin integrity, airway, hydration, nutrition, toileting and range of motion. Release occurs at the earliest moment behavioural criteria are met, and both the person and the team are debriefed afterwards. Note also that a side rail raised to stop a person voluntarily leaving the bed is a restraint, whatever it is called on the order set, and that in delirium and dementia physical restraint predictably increases falls, injury, agitation and death.

Trauma-informed care is not optional here, because dementia can strip away the defences that kept old trauma contained, and because the tasks of personal care — undressing, bathing, being held, being moved by strangers, being confined — map with uncomfortable precision onto the mechanics of assault. Assume a trauma history may be present in anyone. Ask the family, in a neutral way, whether there is anything from the person’s past that makes bathing, bedtime, darkness, uniforms or being touched frightening. Then build it into the care plan: announce and explain before every touch, offer a same-gender caregiver, keep the person covered, go slowly, stop when asked and come back, and treat “no” as information rather than an obstacle. A veteran who becomes terrified in a dark room at night is not agitated; he is somewhere else.

Delegation on a unit like this is a constant judgement. Assistive personnel may assist with bathing, dressing, grooming, toileting schedules and transfers; ambulate and mobilise; set up and assist with meals for a patient the nurse has assessed as safe to swallow; obtain vital signs, intake and output and weights; provide orientation cues, familiar music and simple activities; sit with a person on constant observation; and — critically — report changes. What may not be delegated is the nursing process itself: the initial and ongoing assessment, interpretation of a CAM or 4AT screen, the swallowing evaluation, patient and family teaching, evaluation of the response to any intervention, clinical judgement about a change in condition, and the decision to initiate restraint. Teach assistive personnel exactly what to report and how fast: “Tell me immediately if she seems more sleepy or more confused than she was this morning, if she has not passed urine this shift, or if she pushes your hand away during care.” That instruction is often what catches the delirium.

Section 5Medications, Emergencies and the Care Partner

Drugs that target cognition — mechanism and monitoring

Cholinesterase inhibitors — donepezil, rivastigmine and galantamine — block acetylcholinesterase so that the acetylcholine still being produced by a shrinking cholinergic system persists longer in the synapse. Benefit is symptomatic and modest: a slowing of decline measured in months, not a cure, and families must be told this plainly so that stopping the drug later is not experienced as abandonment. Donepezil is used at all stages, rivastigmine is available as a patch and is also indicated in Parkinson disease dementia, and cholinesterase inhibitors are particularly useful in Lewy body dementia including for hallucinations.

Their adverse effects are entirely predictable from cholinergic excess: nausea, vomiting, diarrhoea, anorexia and weight loss; increased gastric acid with risk of ulcer and bleeding, especially with NSAIDs; urinary frequency; vivid dreams and insomnia (give donepezil in the morning if dreams disturb sleep); muscle cramps; and the cardiovascular one that matters most — bradycardia, heart block, syncope and consequent falls and fractures. Check an apical pulse before administration; hold and notify the provider if it is under 60. Titrate slowly, weigh regularly, and screen the whole medication list for anticholinergics, because prescribing oxybutynin alongside donepezil is prescribing two drugs to cancel each other out while collecting the side effects of both.

Memantine works differently: it is a moderate-affinity, uncompetitive NMDA receptor antagonist that dampens pathological glutamate signalling and the excitotoxicity it causes, while leaving physiological signalling largely intact. It is indicated in moderate to severe Alzheimer disease, alone or combined with a cholinesterase inhibitor, is generally better tolerated, and has dizziness, headache, constipation and confusion as its main adverse effects. It is renally cleared, so dose reduction is required in significant renal impairment. Titrate up weekly.

The anti-amyloid monoclonal antibodies, lecanemab and donanemab, are the first disease-modifying agents. They are intravenous infusions, indicated only in mild cognitive impairment or mild dementia due to Alzheimer disease with amyloid confirmed by PET or cerebrospinal fluid or an approved blood biomarker — they are not for moderate or severe disease. They slow decline modestly. Their defining safety issue is ARIA, amyloid-related imaging abnormalities: ARIA-E (vasogenic oedema and effusion) and ARIA-H (microhaemorrhage and superficial siderosis). Most ARIA is asymptomatic and detected on scheduled surveillance MRI, but it can present with headache, confusion, dizziness, visual change, nausea, gait difficulty or seizure — and any of those in a person on these agents is an urgent call, not a wait-and-see. Risk is markedly higher in APOE epsilon-4 homozygotes, so genotyping precedes treatment, and anticoagulation raises the stakes of a haemorrhage considerably. Infusion reactions are common with lecanemab. Nursing responsibilities: verify the MRI schedule is being kept, teach the family the ARIA symptom list before the first dose, and hold and escalate rather than infuse through a new neurological symptom.

Medicating behaviour — the boxed warning and what to do instead

There is no drug for the behaviour of dementia in the way students hope there is. Antipsychotics carry a boxed warning of increased mortality when used in older adults with dementia-related psychosis, applying to both first- and second-generation agents, with an increase in death of roughly 1.6 to 1.7 times over a short course, driven by cardiac events, pneumonia and stroke. None of the older agents is approved for that indication. Where a trial is justified — severe distress, psychosis or aggression that is dangerous and has not responded to a documented non-pharmacological plan — the rules are informed discussion with the person where possible and the surrogate decision-maker, a documented target symptom, the lowest effective dose, a defined review date, and an active plan to taper and stop. Deprescribing is a nursing advocacy role: ask at every admission and every care conference why each psychotropic is still there and what it is for. Brexpiprazole now carries an approval for agitation in Alzheimer dementia and still carries the class mortality warning; pimavanserin is approved for Parkinson disease psychosis.

Two absolute cautions. In Lewy body dementia and Parkinson disease dementia, avoid antipsychotics, and avoid first-generation agents such as haloperidol entirely — the neuroleptic sensitivity reaction produces severe rigidity, autonomic collapse and neuroleptic malignant syndrome, and it can kill. And avoid benzodiazepines as a routine calming strategy: they cause falls, oversedation, aspiration, worse confusion, paradoxical disinhibition and dependence, and they lengthen delirium. Their legitimate uses remain alcohol and benzodiazepine withdrawal, neuroleptic malignant syndrome and catatonia. Also avoid diphenhydramine and hydroxyzine for sleep or agitation, zolpidem, and anticholinergic bladder agents where alternatives exist. For depression in dementia, sertraline and citalopram are reasonable, with citalopram limited to 20 mg daily over the age of 60 because of QT prolongation, and paroxetine avoided for its anticholinergic load. Antidepressant benefit takes 2 to 6 weeks, which a family watching for a change within days needs told plainly. Know the extrapyramidal effects by their timing too: acute dystonia within hours to days, drug-induced parkinsonism (tremor, rigidity, bradykinesia, masked face, shuffling gait) over days to weeks and regularly misread in an older adult as Parkinson disease, akathisia at any point, and tardive dyskinesia after months to years.

Care partners, capacity, safety and escalation

The family member who brings the person to you is also your patient. Dementia care partners have measurably elevated rates of depression, anxiety, sleep deprivation, physical illness and mortality, and the burden is highest in spouses and in the adult daughter who is usually doing most of it. Assess it directly — the Zarit Burden Interview is one tool, but the question “How are you sleeping?” opens the same door. Connect people to respite, adult day programmes, the Alzheimer’s Association 24-hour helpline, caregiver support groups and, where warranted, treatment for the caregiver’s own depression. Teach the specific skills too: routine, simplification, environmental cues, how to answer the same question ten times, and permission to accept help. And screen for elder abuse and neglect — physical, emotional, sexual, financial and neglect — using an unhurried private interview; exhausted, unsupported caregiving is itself a risk factor for harm, and nurses are mandatory reporters in every jurisdiction in which they practise.

Capacity is clinical, situational and fluctuating: the ability to understand relevant information, appreciate how it applies to oneself, reason about options, and communicate a consistent choice for a specific decision at a specific time. Competence is a legal determination made by a court. A person with mild dementia may lack the capacity to manage complex finances while retaining full capacity to decide who visits, what to eat, and whether to accept an antibiotic. Assume capacity, assess it for the decision in front of you, and support it rather than substituting for it: simplify, use the person’s best hour of the day, involve a trusted person, and re-ask. Capacity lost for one decision does not remove the right to be consulted about the rest, and it does not by itself authorise care the person is actively refusing. Suspected abuse, neglect or financial exploitation of an older or dependent adult is a mandatory report. Early diagnosis is the window for advance care planning — a healthcare proxy or durable power of attorney, an advance directive, POLST or MOLST forms, financial and driving discussions — and it should happen while the person can still author their own future.

Safety planning is concrete. Driving must be raised honestly and early, with local reporting requirements followed. Firearm access is asked about directly and secured. Ask about suicide just as directly, because risk is elevated in the year after a dementia diagnosis while insight is still intact, and where it is present secure stockpiled medications along with the firearms and involve the mental health team. Cooking with a gas hob, medication self-administration, scam and financial exploitation vulnerability, wandering and getting lost, hot water temperature and night-time falls all need a plan. Wandering technology, identification jewellery, alarmed doors and a photograph readily available for police are practical measures. Later, the conversation moves to palliative care and hospice: advanced dementia is a terminal illness, comfort-focused care is appropriate, hospitalisation itself carries risk, and pain, dyspnoea and mouth care become the whole of good nursing.

Finally, escalate properly. Use SBAR and lead with the change from baseline, because “more confused” buried in paragraph three does not get a response. Situation: “This is Sam, nurse on 4 West. Mrs Okafor in 412 has an acute change in mental status.” Background: “She is 82, day 2 after a hip fracture repair, baseline lives alone and manages her own medications, no history of dementia. She received oxybutynin and diphenhydramine overnight.” Assessment: “CAM is positive — acute onset, fluctuating, cannot say the months backwards past September, drowsy but rousable. Temperature 38.2 degrees Celsius, heart rate 112, blood pressure 96 over 58, oxygen saturation 91 percent on room air, bladder scan 480 millilitres, no bowel movement in four days, glucose 6.1. Pain score by PAINAD is 6.” Recommendation: “I think this is delirium with possible sepsis and urinary retention. I would like you to see her now. Can I get orders for urinalysis and culture, blood cultures, a full blood count and electrolytes, in-and-out catheterisation, scheduled analgesia, and can we stop the diphenhydramine and oxybutynin?”

Words worth knowing