Oxford Medical Publications Oxford Handbook of Geriatric Medicine

There are structural changes in the brain with age (see ‘The ageing brain and nervous system’, p. 150), but these correlate poorly with cognitive changes. Broadly, intellectual function is maintained until at least 80 years, but processing is slower. Non-critical impairments include forgetfulness, modestly reduced vocabulary, and slower learning of, e.g. languages. These changes are to be expected, their consequences can be managed, and they do not cause significant reduction in functional level.

Three factors support a diagnosis of normal ageing, rather than disease:

• The ability to maintain function in normal life through aids (e.g. aides memoire: lists or calendars) or adaptations (of one’s environment or one’s expectations)

• Very long time scale of decline: 10–30 years, compared with months or a few years in disease

• Relative decline, e.g. the academic who no longer holds his own at the graduates’ reunion

Impairments in cognitive function without dementia

Age-associated memory impairment or benign senescent forgetfulness

Older people learn new information and recall information more slowly, but given time, their performance is unchanged. This is distinct from the impairment in dementia, in that in age-associated memory impairment (AAMI), overall function is unimpaired and usually only less important facts are forgotten. It is often more bothersome to the patient than a concern to relatives (compare dementia, when often the family are much more concerned than the patient).

AAMI can present early (age 40s–50s) when high achievers become frustrated by modest deterioration in speed of new learning. It may be exacerbated by performance anxiety, creating a vicious cycle, and is often helped by psychological strategies to assist memory.

Minimal/mild cognitive impairment (MCI)

Impairments are more broad than memory alone and are felt to be pathological (e.g. 2° to cerebrovascular disease), but the full criteria for a diagnosis of dementia are not met, e.g. because there is not yet significant impact on day-to-day functioning.

Progression to dementia occurs in between 5% (community studies) and 10% (memory clinic studies) annually. Thus, with time, many patients do develop dementia, but many do not, and in some, there is no deterioration.

Diagnosis is important in order to:

• Reassure the patient (by distinguishing from dementia)

• Modify risk factors for progression

• Monitor deterioration such that intervention can begin promptly if progression occurs

Dementia: overview

Dementia is:

• an acquired decline in memory and other cognitive function(s)

• in an alert (i.e. non-delirious) person

• sufficiently severe to affect daily life (home, social function)

All three elements must be present in order to make the diagnosis.

Prevalence ↑ dramatically with age: 1% of 60–65 year olds, >30% of over 85s. Over 50% of care home residents have dementia.

Age-specific incidence is falling (perhaps with improvements in risk factor management), although the national burden continues to ↑ with the ageing population.

Major dementia syndromes (and proportion of cases in older people) include:

• Mixed pathology—(especially Alzheimer’s and vascular) is the most common type in post-mortem studies

• Dementia of Alzheimer type (60%)

• Vascular dementia (30%)

• Other neurodegenerative dementias (15%), e.g. dementia with Lewy bodies, Parkinson’s disease with dementia, frontotemporal dementia

• Reversible dementias (<5%), e.g. drugs, metabolic, subdural, NPH

Diagnostically, there are many false-positive and false-negative cases. Mild to moderate dementia is easy to miss on a cursory, unstructured assessment. Patients labelled incorrectly as having dementia may be deaf, dysphasic, delirious, depressed, or under the influence of drugs.

Triggers for considering a dementia diagnosis

• Delirium (much more common with underlying dementia)

• ‘Unmasking’ of poor cognition after spouse’s death

• Social withdrawal

• Request for social services help

• Poor concordance with prescribed drug therapy

• Domestic crisis (e.g. fire, road traffic accident)

• Spouse/family disproportionately in control or speaking for patient

UK National Dementia Strategy

The first national strategy was published by the UK government in 2009 with focus on accelerating the pace of improvement in dementia care, through local delivery of quality outcomes and local accountability for achieving them. This was updated in 2015 and challenges the UK to achieve global improvements in approaches to dementia across society, as well as health and social care, by 2020.

HOW TO . . . Distinguish delirium from dementia

The most common issue in diagnosing the older patient with confusion (‘brain failure’) is whether the patient has delirium alone, dementia alone, or a delirium superimposed on a pre-existing dementia.

Achieve this by combining information from the history with a physical and mental state examination.

► The history is key. The duration of symptoms is the most important.

Information from medical records, carers, and family will help determine whether dementia was present before the onset of delirium. ‘When was his memory last as good as yours?’ (See Table 9.1.)

Table 9.1 Features distinguishing delirium from dementia

Feature	Delirium	Dementia
Mode of onset	Acute or subacute	Chronic or subacute
Reversibility	Often reversible	Rarely reversible
Fluctuation	Diurnal or hour-to-hour fluctuation common	Generally little diurnal variation, although some deteriorate during the evening; ‘sundowning’. Day-to-day fluctuation more common in Lewy body dementia
Poor attention	Yes (but variable hour to hour)	In severe dementia
Conscious level	Usually affected but may be subtle and variable	Normal
Hallucinations and misinterpretations	Common	Usually occurs late in the disease. Visual hallucinations earlier in the disease, especially when symptoms fluctuate, suggests Lewy body dementia
Fear, agitation, aggression	Common	Uncommon in early stages
Disorganized thought, unreal ideas	Common	Late. Often poverty of thought
Motor signs	Tremor, myoclonus, asterixis common	Late only
Speech	May be dysarthric, dysnomic	Normal
Dysgraphia	Often present	Usually late
Short- and long-term memory	Poor	Long-term memory often normal until late

Dementia: assessment

History is the most important component of assessment. Obtain information from both patient and family/friends. Note the onset, speed of progression, and symptoms. Take a careful drug history, including over-the-counter drugs and recreational drugs (especially alcohol). Also ask about a family history of early dementia and a personal psychiatric history of, e.g. depression.

Usually there is a progressive decline in cognitive function over several years, ending with complete dependency and death (usually due to dehydration, malnutrition, and/or sepsis).

Deterioration may be:

• Insidious and gradual (e.g. Alzheimer’s)

• Stepwise (suggesting stroke/vascular aetiology)

• Abrupt (after a single critical stroke)

• Rapid over weeks/months, suggesting a drug, metabolic, or structural cause (e.g. tumour, subdural)

Abnormalities occur in:

• Retention of new information (e.g. appointments, events, working a new household appliance); short-term memory loss is often severe, with repetitive questioning

• Managing complex tasks (e.g. paying bills, cooking a meal for family)

• Language (word-finding difficulty with circumlocution, inability to hold a conversation)

• Behaviour (e.g. irritability, aggression, poor motivation, wandering)

• Orientation (e.g. getting lost in familiar places)

• Recognition (failure to recognize first acquaintances, then friends or distant family, then close family, e.g. spouse)

• Ability to self-care (grooming, bathing, dressing, continence/toileting)

• Reasoning: poor judgement, irrational or unaccustomed behaviours

• Ability to recognize familiar objects, people, and places (agnosia)

• Ability to carry out complex, coordinated movements (apraxia)

Physical examination

• To determine possible causes of a dementia syndrome, including reversible factors

• Look for vascular disease (cardiovascular, peripheral vascular, and cerebrovascular), neuropathy, parkinsonism, thyroid disease, malignancy, dehydration, (alcoholic) liver disease

• In advanced dementia of any type, primitive reflexes (e.g. grasp, suckling, palmar-mental) and global hyperreflexia with extensor planters may occur

Mental state

• Exclude delirium. Features include agitation, restlessness, poor attention, and fluctuating conscious level (see Appendix, ‘CAM’, p. 706)

• Exclude depression. Features include low affect, poor motivation, and a negative perspective. Perform a GDS (see Appendix, ‘Geriatric Depression Scale’, p. 701)

• Measure cognitive function. Serial testing may be helpful in borderline cases—is there evidence of progression? Many measurement tools are available, e.g. MMSE^™, Montreal Cognitive Assessment (MoCA), Mini-Cog, number of animals named in 1min, clock-drawing test (see ‘Measurement instruments’, pp. 76–77, Appendix, ‘The abbreviated mental test score’, p. 704, and Appendix, ‘Clock-drawing and the Mini-Cog™’, p. 707)

Full neuropsychological assessment (detailed, prolonged assessment by a specialist psychologist) may be helpful in:

• Distinguishing between dementia and depression

• Distinguishing between different subtypes of dementia

• Distinguishing between AAMI and early dementia

• Distinguishing between focal impairments (e.g. aphasic or amnesic syndromes) and dementia

• Measuring progression and response to treatment

Disclosure of dementia diagnosis

Each case should be considered individually, but in general, the diagnosis should be revealed. Disclosure:

• Is consistent with the patient’s right to know (autonomy). Most older people say that they would want to know the diagnosis

• Facilitates medical, financial, and care planning, e.g. ADs, POA, living arrangements

• Allows for consent to treatment and facilitates participation in research

• Facilitates discussion between patient and carer

Arguments against disclosure include a possible depressive reaction, accentuated by a perceived lack of effective treatments. Such a reaction is minimized by sensitive multidisciplinary support that emphasizes the positive therapeutic solutions available.

HOW TO . . . Investigate a patient with dementia

Cases of reversible dementia are uncommon, but their identification is important, as effective treatment may reverse the impairment and prevent progression. Therefore, screen for them.

Blood tests

The following are generally considered useful: FBC, ESR, B₁₂, folate, U, C+E, calcium, LFTs, TSH, CRP, random glucose.

Request syphilis and human immunodeficiency virus (HIV) serology only if there are atypical features or special risks.

ECG and CXR

Evidence of heart disease, occult malignancy.

Neuroimaging

Every person with dementia should undergo brain imaging at some stage. Prompt imaging is indicated where there is:

• Early onset (<60 years)

• Sudden onset or brisk decline

• High risk of structural pathology (e.g. known cancer, falls with head injury)

• Focal CNS signs or symptoms

There are patients, usually in late-stage dementia, for whom the benefits of imaging are outweighed by the practical difficulties.

Imaging modality

• CT is the usual imaging modality; dementia protocols allow volumetric assessment of medial temporal structures

• MRI gives superior images and provides additional diagnostic information for selected patients

• SPECT/positron emission tomography (PET) is used rarely, usually in specialist centres, to more reliably differentiate between Alzheimer’s and vascular dementia

Additional testing as clinically indicated

• EEG is used for suspected frontotemporal dementia or Creutzfeldt–Jakob disease (CJD), or where seizure activity is a possibility

• Lumbar puncture where CNS infection is considered

Dementia: common diseases

Alzheimer’s disease (dementia of Alzheimer type)

• The most common cause of a dementia syndrome

• Diagnosis is made clinically, based on the typical history, mental state examination, and unremarkable physical examination

• History—insidious onset, with slow progression over years. Early, profound short-term memory loss progresses to include broad, often global, cognitive dysfunction, behavioural change, and functional impairment. Behavioural problems are common, usually occurring in moderate to severe dementia, but sometimes preceding overt cognitive impairment

• Physical examination—normal

• Neuroimaging—demonstrates no other causes of dementia (e.g. tumour or infarct) and may show disproportionate medial temporal lobe atrophy

• Treatment with acetylcholinesterase inhibitors may be indicated (see ‘Dementia: acetylcholinesterase inhibitors’, pp. 222–223)

• Early-onset Alzheimer’s disease (<65 years) is uncommon, has a stronger genetic component, and is more rapidly progressive

Vascular dementia

• The next most common cause

• History—cognitive impairment may be patchy, compared with the more uniform impairments seen in Alzheimer’s disease. Onset is often associated with stroke, or the deterioration is abrupt or stepwise; however, using ‘multi-infarct dementia’ as a synonym for vascular dementia is imprecise and its use should be discouraged. Frontal lobe, extrapyramidal, and pseudobulbar features and emotional lability are common. Urinary incontinence and falls without other explanation are often early features. Other features may be mostly cortical (mimicking Alzheimer’s disease) or subcortical (e.g. apathy, depression)

• Physical examination often shows:

• Focal neurology suggesting stroke or diffuse cerebrovascular disease (hyperreflexia, extensor plantars, abnormal gait, etc.)

• Other evidence of vascular pathology, e.g. AF, peripheral vascular disease

• Neuroimaging shows either:

• Multiple large-vessel infarcts, or

• A single critical infarct (e.g. thalamus), or

• White matter infarcts or periventricular white matter changes, or

• Microvascular disease, too fine to be seen on neuroimaging, which may cause a significant proportion of vascular dementia, apparent only at post-mortem

Differentiating between Alzheimer’s and vascular dementia

The importance of differentiating between Alzheimer’s and vascular dementia can be overemphasized. Their presentations overlap, and pathologies commonly coexist. Increasingly, it is believed that much of Alzheimer’s disease pathology has a vascular component.

Pragmatically:

• In cases where vascular risk factors and/or signs exist, treat vascular risk factors aggressively, whether or not there is significant cerebrovascular pathology on brain imaging

• A trial of acetylcholinesterase inhibitors is now suggested for both conditions

Dementia and parkinsonism

Dementia with Lewy bodies and Parkinson’s disease with dementia may be considered as extremes of a continuum. In the latter, motor impairments precede cognitive impairments and are more severe. In dementia with Lewy bodies, cognitive and behavioural impairments precede motor phenomena and are more severe. There are frequently additional contributions from Alzheimer’s or vascular pathology. There are believed to be common pathological processes in all these dementia syndromes.

Dementia with Lewy bodies

• Progressive dementia, often with a faster course than other dementias

• Shorter-term fluctuations in cognitive function and alertness

• Prominent auditory or visual hallucinations, often with paranoia and delusions

• Parkinsonism is commonly present, but often not severe

• Typical antipsychotics (e.g. haloperidol) are very poorly tolerated, leading to worsening confusion or deterioration of parkinsonism. Atypical antipsychotics (e.g. risperidone, and especially quetiapine) may be better tolerated, but great caution is advised in their use

• Levodopa or dopamine agonists may worsen confusion

• Anticholinergics (e.g. rivastigmine) are effective, especially for hallucinations and behavioural disturbance

Note that several features are common to both dementia with Lewy bodies and delirium, e.g. fluctuations, effect of drugs, perceptual and psychotic phenomena. When comparing the two, the following is true of dementia with Lewy bodies:

• Onset is insidious and progression gradual

• No precipitating illness (e.g. infection) is found

• Hallucinations are complex and not the result of misperception of stimuli

• Delusions (commonly complex auditory or visual) are well formed and may be persistent

• Orthostatic hypotension and falls frequently occur

• Antipsychotics worsen status (not indicated as a diagnostic trial)

Parkinson’s disease with dementia

• People with Parkinson’s disease are much more likely to develop dementia, especially older people, those in the later stages of the disease, and those who become confused on Parkinson’s medication

• Typical motor features of Parkinson’s disease are present and may be severe

• The presentation and neuropathology are variable and may resemble Alzheimer’s disease, vascular dementia, or dementia with Lewy bodies

• By definition, if features of Parkinson’s precede dementia by more than a year, then the diagnosis is of Parkinson’s disease with dementia, not dementia with Lewy bodies. This applies even if the dementia syndrome is otherwise typical of dementia with Lewy bodies

• Multiple system atrophy, progressive supranuclear palsy, and corticobasal degeneration also present with both parkinsonism and dementia

Minimal cognitive impairment in Parkinson’s disease

Many patients with Parkinson’s disease have subtle impairments of cognition, too mild to justify a diagnosis of dementia. Slowed thinking and deficits in visuospatial, attention, and executive function are commonly seen.

Normal pressure hydrocephalus

NPH classically presents with the triad:

• Gait disturbance (wide-based)

• Incontinence of urine

• Cognitive impairment (psychomotor slowing, apathy, appear depressed)

► Most patients with this triad have other (unrelated) causes or have diffuse cerebrovascular disease.

Assessment

Neuroimaging

• Shows ventricles that are enlarged disproportionately, compared with the degree of cerebral atrophy

• Neuroimaging for unrelated reasons (e.g. TIA) may reveal ventricular enlargement that appears disproportionate to the degree of cerebral atrophy, suggesting possible NPH. In the absence of clinical features of NPH, the diagnosis cannot be supported and the patient may be reassured

Investigation

Lumbar puncture is being used less frequently in favour of external lumbar drainage (ELD) in specialist centres. This involves spinal catheter insertion for a period of up to 3 days, during which large volumes of cerebrospinal fluid (CSF) can be removed and the clinical impact assessed.

Treatment

Ventriculoperitoneal shunting is effective for some, but many do not benefit. Gait is more likely to improve than is cognition.

It is a major procedure, and complications are common, e.g. infection and subdural haematoma. Decision to proceed requires:

• A confident diagnosis (may require specialist neurological review)

• Support of patient and carer for the procedure

• An assessment that the likelihood of benefit is high

Benefit is more likely in those who:

• Have a short history

• Have a known cause—usually trauma or subarachnoid haemorrhage

• Have normal brain substance on neuroimaging

• Have no significant comorbidities. Cerebrovascular disease is especially relevant

• Benefit from large-volume CSF removal

Dementia: less common diseases

Dementia: general management

General

• Modify reversible aggravating factors, commonly multiple but minor (e.g. constipation, low-grade sepsis, mild anaemia, drug side effects)

• Treat depression. SSRIs are much preferred to tricyclics. Repeat cognitive assessment 2–4 months after treatment to determine if cognitive impairment remains

Social

• Encourage physical and mental activity, including social activities (e.g. social clubs, day centres; see ‘Day hospitals’, pp. 22–23)

• Create a safe, caring environment, usually in the patient’s own home. A predictable routine is helpful. OT home assessment identifies hazards, provides visual safety cues, etc.

• Organize carers to assist with ADLs, prompt medication, etc.

• Support caregivers:

• Enquire about caregiver burden and psychiatric symptoms

• Caregiver support groups

• Respite care—usually in care homes, for a few days to 2 weeks

• Sitting services—usually for 2–3h once or twice weekly

• Family support visitor—provides emotional and practical support

• Educate patients and families about the disease and how to cope with its manifestations. This includes appropriate modifications to the home environment and learning to communicate and interact with the patient with dementia. Counselling and support delay admission to care homes

Practical

• Suggest simple interventions to improve coping (e.g. lists, calendars, alarms)

• Simplify medication, and provide dosette boxes or similar, to aid concordance. In the later stages, drugs such as antihypertensives may become pointless, if not harmful (i.e. risk > benefit)

• Support and educate patient and carers about legal and ethical issues including:

• Driving (see ‘HOW TO . . . Manage the driver who has dementia’, p. 219)

• Lasting power of attorney (LPA) (see ‘Making financial decisions’, pp. 658–659)

• Wills (see ‘Making a will’, p. 678)

• Discussion of end-of-life issues (clinically assisted nutrition, comfort versus life prolongation) may be appropriate

HOW TO . . . Manage the driver who has dementia

Road traffic accident and injury risk ↑ with the severity of dementia. In most countries, it is mandatory for the driver to report important health factors to the licensing authority, which will then request further information from the patient’s medical team. Patients and carers should be reminded of this responsibility at diagnosis.

Assessment of driving ability during a hospital outpatient or GP consultation is often difficult. In some cases, whether a patient is safe to drive will be obvious—either in the very earliest stages of cognitive impairment or in more severe dementia. In other cases, usually of mild (to moderate) cognitive impairment, the following evidence is useful:

• Reports of driving problems, incidents (e.g. near-misses), or accidents. Are relatives/friends concerned to get into the passenger seat? Have they tried but failed to limit or prohibit driving? Some evidence is of less value, e.g. getting lost is a poor indicator of safety

• Reports of how driving patterns have changed, and why. Are journeys now brief, infrequent, and confined to quiet local roads?

• Clinical evidence of major impairment in visuospatial function, attention, or judgement. However, a combination of modest impairments may be as important

• Presence of non-cognitive impairments (e.g. visual, joint function) or other conditions that affect driving safety (e.g. seizures, syncope)

Each case should be reassessed, either at regular intervals or at points prompted by critical incidents. The best assessment of driving ability is by a professional driving assessor, in the patient’s own vehicle on the public roads or in a driving assessment centre (M http://www.rdac.co.uk). Such professionals, often OTs, can deliver the confident, robust opinion that is often required, as well as offering useful practical advice to the cognitively or physically impaired driver. In general:

• It is preferable that the patient, family, and doctor should agree that stopping voluntarily is advisable. Compulsory licence withdrawal by the authority generates great anger and distress

• The issue is best discussed early in the course of the disease, when the patient has best insight

• If driving is safe for the moment, encourage the patient and family to think ahead, to a time when driving cannot be continued—is local public transport sufficient, or will a spouse have to hone long-lost driving skills?

Rarely, a patient continues to drive when clearly unsafe and having been informed that they must stop. In most cases, further clear statements of this, backed up by the threat of medical reporting to the authorities, are sufficient to prompt cessation. If driving continues, the clinician is ethically justified in reporting this to the authorities and will usually have the strong support of the family.

Dementia: risk management and abuse

Risk management is an essential part of care.

• Is there a risk of harm to the patient or to others?

• How great is the risk, over how long is the patient (or other person) exposed to it, and how severe are the consequences of the risk?

► There is no such thing as ‘safe’, only ‘safer’ and risk management demands careful balancing between autonomy/quality of life and safety.

Common risks include:

• Falls. Moving from own home to institutional care is rarely the answer. Supervision is far from continuous in any institution; the environment is less familiar, and the floors are often uncarpeted and unforgiving

• Purposeful walking/wandering. Usually more distressing to carers than presenting risk to the patient

• Aggression by a patient towards carers or family. Usually verbal, but sometimes physical or sexual. May lead to carers refusing to work with patient

• Aggression towards a patient by carers or family. Less easy to identify, as the patient may not complain, through fear or due to cognitive problems. Be concerned if there are unexplained ‘falls’ or unusual patterns of bruising (see ‘Elder abuse’, p. 674)

• Self-neglect. Often with denial. May manifest as poor diet, poor hygiene, etc.

• Fire risk. May be easily modifiable, through removal or modification of kitchen appliances, gas fires, etc. Cigarette smoking is more problematic

• Driving (see ‘HOW TO . . . Manage the driver who has dementia’, p. 219)

• Financial abuse (see ‘Elder abuse’, p. 674)

• Theft or fraud

• Modification of wills

• Misuse or transfer of a patient’s money

Having determined the nature and magnitude of a risk, consider ‘Can the risk be reduced?’ and ‘Should it be reduced?’

Consider whether the patient is competent to make their own decisions about risks or whether you are required to act in the patient’s ‘best interests’.

If risk reduction can be done without impacting on the patient’s independence or enjoyment of life, then go ahead.

If reducing risk involves curtailing liberty or restricting enjoyable activity (walking, living alone), then consider:

• If competent, what is the patient’s attitude to risk?

• If unable to express this, what was his/her premorbid attitude, and what would he/she now want?

• What is the view of carers?

Commonly, discussions around risk occur when a patient is perceived by some (carers, relatives, nursing or therapy staff) to have become unsafe to remain at home. This should prompt multidisciplinary assessment and discussion, including whether a move to institutional care would involve a change of risk patterns, rather than a reduction in overall risk.

Dementia: prevention

Lifestyle interventions

• Physical activity. Physical activity may protect against dementia and should be encouraged for other reasons

• Cognitive activity. Observational studies suggest that games, reading, etc. are protective, but these associations may not be causal, and there are no good randomized controlled trials

• Diet. Again, observational studies suggest benefits from a high fish oil diet, but there is no high-quality prospective evidence. Alcohol intake should be reduced

• Social activity. Likely to be protective

Drugs

Multiple drugs have been proposed (HRT, NSAIDs, antioxidants, antihypertensives, statins), but there is no firm evidence that any should be given for this indication alone.

Usual practice is to encourage physical and mental and social activity (‘use it or lose it’), to optimize BP, and to encourage low-dose aspirin in those with, or at high risk of, cerebrovascular disease.

Dementia: acetylcholinesterase inhibitors

Work by blocking acetylcholinesterase which breaks down acetylcholine, an important neurotransmitter for memory.

Effectiveness

Far from miracle drugs, with very variable response. In general:

• They offer symptomatic benefit through a one-off increment in cognition. The underlying disease continues to progress and some patients stopping the drug may revert to where they would have been without treatment

• Of the dementias, Alzheimer’s disease, dementia with Lewy bodies, and Parkinson’s disease with dementia have the greatest cholinergic deficit, and these are the dementia types known to benefit most from acetylcholinesterase inhibitor treatment

• About half of patients show no benefit; a significant minority show moderate improvements (‘clock turned back a few months’), and for a small minority there is substantial improvement

• In some, there is a worsening in cognition, or onset of agitation that may be temporary or respond to a change in drug

• Early studies focused on effects on cognitive function, and these are overall modest. However, small improvements in cognition can translate into significantly improved day-to-day function, reducing carer burden

• Some evidence that acetylcholinesterase inhibitors can reduce the requirements for home care and can delay placement in nursing home

• Benefit has been demonstrated for mild to moderate dementia, not in severe dementia, although established treatment should not be automatically discontinued as disease advances

Choosing a drug

The three acetylcholinesterase inhibitors currently available are:

• Donepezil

• Galantamine

• Rivastigmine

All should be initiated by a specialist and uptitrated. Effectiveness seems broadly similar. There is most evidence for donepezil in Alzheimer’s disease and it has fewer adverse events than rivastigmine which is probably better for Lewy body dementia. Overall, the evidence for acetylcholinesterase inhibitors is strongest in Alzheimer’s and Lewy body dementia, and weakest in vascular dementia.

HOW TO . . . Treat with acetylcholinesterase inhibitors

Introducing and monitoring acetylcholinesterase inhibitors is a specialist area, usually undertaken by psychogeriatric teams or by geriatricians or neurologists working in the setting of a memory clinic. Increasingly, they are prescribed in 1° care as part of a locally agreed shared care protocol.

In general, acetylcholinesterase inhibitors should not be initiated in inpatient medical or rehabilitation settings, as the effects of environmental changes, physical illness, or drugs may dominate those of the acetylcholinesterase inhibitor, rendering assessment of effect impossible. It is preferable to initiate treatment when the patient is physically well and living in their own home.

Where given for behavioural disturbance or non-cognitive symptoms (e.g. hallucinations), acetylcholinesterase inhibitors may be initiated more urgently in an institutional setting.

Before treatment

• Consider the relative risks and benefits and discuss them with the patient and carer

• Explain that the drugs do not provide a cure and may reasonably be deferred until symptoms worsen

• Consider how concordance can be assured

• Perform an ECG, looking for conduction problems

• Check for relative contraindications, e.g. bradycardia or heart block

Treatment trial

• There are significant side effects, commonly gastrointestinal (nausea, dyspepsia, diarrhoea, anorexia). These occur especially during the dose titration phase at higher doses, are often short-lived

• An acetylcholinesterase inhibitor should be given for an initial treatment period of 2–3 months. If there is no effect at the maximum tolerated dose, the drug should be discontinued. There is probably little benefit from trying other acetylcholinesterase inhibitors if one has failed

Assess impact using

• Clinician’s subjective global assessment, based on the views of the relative(s) or carer(s) and serial clinical observations

• The results of cognitive tests, e.g. MMSE^™, clock-drawing test

Continuing therapy

• If benefit appears to have occurred, the drug should be continued at that dose. Benefit may be absolute or relative—a small decline would be expected during the 2- to 3-month evaluation period, so an absence of deterioration may be attributed to drug benefit

• Acetylcholinesterase inhibitors can be given indefinitely and there is some evidence that withdrawal in advanced disease reduces function

• As more patients are given an acetylcholinesterase inhibitor at an earlier stage of disease, monitoring falls more to 1° care

Dementia: other drug treatments

Memantine

• This is a blocker of N-methyl-d-aspartate (NMDA) receptors that may reduce glutamate-mediated destruction of cholinergic neurons

• It appears to have a beneficial effect in severe dementia of Alzheimer’s or vascular aetiology and may be used in those with behavioural disturbance

• It is well tolerated. Uncommon side effects include hallucinations and worsening confusion

• Avoid in severe renal failure

• Memantine enhances the effect of levodopa and dopamine agonists

Other drugs to prevent progression

No drugs have been proven to slow or halt progression, although dementia is seen as so catastrophic, the following are often used:

• Vascular 2° prevention, e.g. aspirin, lipid-lowering drugs, ACE inhibitors, and other antihypertensives. For patients with vascular dementia and mixed (Alzheimer’s–vascular) dementia, aggressive risk factor modification and tailored drug treatment akin to that following stroke is logical but is without evidence. There is better evidence for 1° prevention, e.g. in those with hypertension

• Vitamin E. High doses are widely used by patients, but evidence is limited

• Ginkgo biloba. A supplement widely used by people with memory impairment or dementia to enhance memory and other cognitive functions, but not convincingly supported by trial evidence. Preparations are expensive, vary in strength, and have antiplatelet activity—caution with anticoagulants

HOW TO . . . Manage patients with dementia in hospital

► Beware iatrogenic deterioration. Modest behavioural deterioration in a patient with moderate dementia at home may lead to hospital admission, with a loss of all familiar routine, physical environment, and caregivers, thus further behavioural decline, administration of sedatives, and further worsened confusion.

Over a quarter of UK hospital beds house patients with dementia. Patients with dementia stay in hospital longer than patients with similar problems but without cognitive impairment, and often leave hospital in a worse physical and mental state than when they arrived.

• Where appropriate, manage the patient at home, with a brief but thorough outpatient attendance if there is concern about physical precipitants. Community outreach may be available to help avoid unnecessary admissions

• If hospital admission is required, then, if possible, admit them directly to a dementia-friendly ward where staff are skilled in managing patients with cognitive impairment. This has been shown to improve outcomes, including length of stay

• Try to minimize disorientation by:

• Avoiding admission and ward moves at night

• Avoiding multiple changes of location/ward

• Quiet room with window (so daylight seen)

• Minimal distractions (e.g. turn off background radio/TV)

• Visible clocks and calendars

• Well-labelled facilities, e.g. toilets—images often better

• Regular ward routine

• Encouraging unrestricted family visitation

• Actively ascertain and treat symptoms such as pain or shortness of breath which patients may not spontaneously describe

• Good nursing management of hydration, nutrition, continence (avoid constipation), pressure areas, and falls prevention

• Where psychoactive medication is required, use it sparingly for short courses. Remember that sedation is a side effect and NOT the desired outcome (which is behaviour modification)

• Take time to communicate with the patient and their relatives

• Minimize the length of admission with proactive early discharge planning

Dementia: managing behavioural problems

Behavioural problems include agitation, anxiety, phobias, irritability, purposeful walking (wandering), hoarding, aggression, socially inappropriate behaviour (e.g. sexual disinhibition, inappropriate urination, attention-seeking), hallucinations, and delusions.

These are common in dementia, including Alzheimer’s, and may occur early in the disease. Often it is behavioural problems, rather than cognitive impairment, that lead to institutionalization; managing them successfully may enable a patient to remain in their own home.

General

• Consider whether acute illness (e.g. sepsis), pain (e.g. urinary retention), or changes in drug treatment (e.g. anticholinergics) have contributed, especially if behaviour has deteriorated rapidly

• Consider whether agitation or aggression is a manifestation of depression (consider an SSRI) or of fear (which may respond if care is given in a non-challenging way by a familiar team)

• Medication may not be needed if symptoms are transient, do not cause the patient significant distress, and are not threatening care of the patient in the current environment

Non-drug management

These are preferred and may be sufficient alone.

• Avoid precipitants

• Effective therapies include music, bathing, exercise, pets, art therapy, and aromatherapy

• The environment should be home-like, familiar, and interesting

• Activities may reduce boredom, wandering, and aggression

• Delusions and hallucinations may be helped by distraction and reassurance

• Anxiety may respond to relaxation or a discussion of worries

• Specialist teams (geriatricians or psychiatrists) may be able to offer helpful advice

Drug treatment

The best drug is that which, for that patient with that problem, has worked well previously.

For agitation, anxiety, and irritability:

• Benzodiazepines, e.g. lorazepam, are often successful, but long-term treatment should be avoided due to side effects and dependence

• If depression is prominent, try an SSRI such as citalopram

• If this fails or side effects (usually oversedation) occur, introduce an atypical antipsychotic such as quetiapine—if considered necessary, use the lowest dose for the shortest period possible. Risperidone and olanzapine are now rarely recommended because of the ↑ risk of stroke, IHD, and death

• Haloperidol and phenothiazines are slow-acting and have many side effects so should be avoided in the absence of psychotic symptoms

• Memantine can be used with good effect in extreme agitation

For problematic psychotic symptoms (delusions, hallucinations, paranoia):

• Cholinesterase inhibitors may improve behaviour as well as cognition. They may be given ‘first line’, especially if symptoms are moderate and not acute in onset

• Atypical antipsychotics should be used at the lowest dose that is effective

• Trazodone, an antidepressant, may be useful, especially where sleep disturbance is a problem and aggression is only verbal

• In dementia with Lewy bodies, use antipsychotics with great caution, in low dose, under close supervision, and only when other non-pharmacological and pharmacological measures have been exhausted. Atypical antipsychotics are preferred

Review drug use regularly, being aware of potential side effects such as falls, immobility, or confusion. Behavioural problems are often periodic or provoked, so consider stopping treatment as soon as possible.

Compulsory detention and treatment

Older people in need of medical assessment, treatment, or continuing care commonly lack the capacity to judge the risk and benefit of interventions. They may therefore refuse care when its benefit is clear to others.

In the UK, there are several legal procedures which may support a doctor in the compulsory treatment, admission, or detention of patients.

Mental Capacity Act (2005)

The most commonly used legal support for actions when the patient lacks capacity to make a certain decision (see ‘The Mental Capacity Act 2005’, p. 656). Actions may include:

• Admission to hospital

• Treatment and detention on a ward or within a hospital

• Treatment in the home (e.g. in delirium 2° to infection, but refusing antibiotics)

• Detention in the home (e.g. wandering presents danger to the patient)

Actions should be:

• Justifiable, reasonable, and proportionate to the situation. Based on a consideration of the risks/benefits for that patient, and their likely wishes were they competent. Consider alternatives and always opt for the least restrictive (see ‘Deprivation of Liberty Safeguards’, p. 657)

• Carefully documented and reviewed regularly

Section 5(2) of the Mental Health Act (1983)

• This permits the detention of an inpatient in a general or psychiatric hospital for up to 72h after submission of a report, while their mental health needs are assessed. Outpatients or DH patients do not fall within this section

• It should be considered if a patient is highly resistive to treatment or restraint, formalizing actions taken under common law

• It is sensible to seek the advice of a psychogeriatrician to confirm that it is appropriate, and during the 72h period to perform assessment and help guide further management

• Detention is authorized when the registered medical practitioner in charge of treatment or a fully registered deputy (not pre-registration junior) completes a report (‘Form 12’) and submits it to the duty hospital manager

Section 2 of the Mental Health Act (1983)

• This permits the admission to hospital and detention of a patient for assessment and treatment

• The patient must have a mental disorder that warrants detention in the interests of the patient or for the protection of others

• Application is made by a relative or an approved social worker, and supported by two registered medical practitioners

• The assessment period is up to 28 days and is not renewable

Deprivation of Liberty Safeguards

• This code of practice was published in 2007 and provides supplementary guidance to the Mental Capacity Act (2005). It lays down a framework for when and how Deprivation of Liberty (DoL) may be authorized (see ‘Deprivation of Liberty Safeguards’, p. 657)

• The impetus for these guidelines arose out of a well-publicized case dating back to 1997 in which an autistic patient who was incompetent was detained informally in Bournewood Hospital for assessment. The ‘Bournewood Gap’ was identified as a gap in the law by the European Court of Human Rights. Incompetent patients who were sectioned were subject to stringent rules (Mental Health Act), while ‘informal patients’ held under the common law of necessity did not have similar protective mechanisms and regulations and potentially could be held for indefinite amounts of time

• Deprivation of Liberty Safeguards (DoLS) are applicable in hospitals and care homes. There are detailed requirements about assessment, authorizing detention, renewing, and challenging decisions

• The underlying principle is that a patient should be detained in the least restrictive manner that is practical

• Despite the huge number of patients who potentially come under these legal safeguards in acute geriatric medicine wards, most remain under simple common law. DoLS teams provide assessment and support decision-making and documentation when the deprivation is particularly stringent, long-standing, or is challenged by family or friends

HOW TO . . . Manage the older person refusing treatment

In practice, compulsion is possible only in hospital. Brief interventions against a patient’s will are sometimes possible at home (e.g. restraint to prevent dangerous wandering; forced administration of antibiotics in a sepsis with delirium) but can rarely be sustained because of resource restraints and staff feeling legally and physically vulnerable.

Use guidance from the Mental Capacity Act to admit to acute medical wards in cases of:

• Dementia with acute physical illness

• Delirium with moderate behavioural disturbance

Use the Mental Health Act to admit to psychiatric wards in cases of:

• Dementia, with risk to self, but alternatives must be explored and considered

• Delirium with severe behavioural disturbance (to psychiatric or medical or geriatric ward)

• Psychotic state, severe with risk to self or others, e.g. severe depression with psychosis or risk of self-harm

Compulsory admission is not justified and/or not legal in cases of:

• Physical illness, refusing treatment without psychiatric illness

• Psychotic state or other psychiatric illness of moderate severity, without significant risk to self or others

These are guidelines. If in any doubt, seek emergency advice from the local psychogeriatric team.

Psychosis

Psychotic symptoms, e.g. delusions and hallucinations, are common in older people, particularly in those who are acutely unwell, hospitalized, or in care homes. Symptoms range from benign and non-distressing to those that cause anxiety among patients and caregivers, and often indicate important, treatable disease.

What is psychosis?

A state of severe impairment of assessment of reality. The results include:

• Distortions of perception, e.g. illusions (misperceptions—distortions of actual perceptions) and hallucinations (perceptions not the result of external stimulus)

• Distortions of thought content, i.e. delusions—beliefs held with great conviction despite contrary evidence. These are usually 2°, i.e. a response to abnormal occurrences such as hallucinations or low mood

Causes of psychotic symptoms in older people

The most common causes are ‘organic’. In order of frequency:

• Dementia

• Depression

• Delirium

• Drugs, e.g. levodopa

• Other neurological causes, e.g. cerebrovascular disease, brain tumour

Less common causes are ‘functional’ or ‘non-organic’, e.g.:

• Persistence into late life of chronic schizophrenia

• Delusional disorder of later life (‘late-onset schizophrenia-like psychosis’)

• Psychotic presentation of affective disorder (mania or depression)

Treatment of patients with psychotic symptoms

• Can usually be managed on the general medical wards or at home, but early specialist psychogeriatric team support is advised

• Avoid reinforcing a patient’s paranoid beliefs: do not avoid contact, do not seek rapid transfer from the ward, etc.

• Make a diagnosis and treat the underlying cause, e.g. stop drugs leading to delirium

• Attend to hearing and visual impairments

• Treat underlying mood disorder

• In dementia, especially Alzheimer’s and dementia with Lewy bodies, consider acetylcholinesterase inhibitors

• If symptoms are distressing and persistent, consider the use of antipsychotics, e.g. haloperidol, risperidone, olanzapine; usually after specialist advice. Be cautious in patients who may have dementia with Lewy bodies

• On discharge, offer opportunities for social interaction and practical home support

Delirium: diagnosis

Delirium is a syndrome of disturbance of consciousness accompanied by change in cognition not accounted for by pre-existing dementia. The term delirium (acute confusional state) refers to an acute brain syndrome, effectively acute brain failure, characterized by impairment of consciousness (however slight).

Beware sloppy language—the term confusion means only that: muddled thinking or an inability to think clearly. It is an important symptom of acute ‘organic’ brain disorders such as delirium but is not confined to them, i.e. low specificity. It may also be seen in depression, dementia, and less commonly in some 1° psychotic disorders. Use the term confusion when describing a presentation, but never as a diagnosis.

Key features

• A disturbance of consciousness (↓ clarity of awareness of the environment). May be hypoactive, hyperactive, or mixed (see Box 9.1). ↓ ability to focus, shift, or sustain attention. Distractability. Lose thread of conversation. Leads to uncertainty about time of day. Impairment is often not obvious, especially if onset gradual; but, after recovery, memory for the period will be poor. This feature is not seen in early dementia or in 1° psychotic disorders

• Change in cognition. Often widespread, e.g. memory impairment (often recent memory), disorientation (time, place; person less common), language disturbance (e.g. dysgraphia, dysnomia), perceptual impairment (misinterpretations, e.g. slamming door = gunshot), illusions (usually visual, e.g. bedclothes animated), hallucinations. Thinking may be slow and muddled, but is often rich in content

• Acute onset and fluctuates. Usual onset over hours or a few days. Sometimes changes are subacute (weeks to a few months) and may be misdiagnosed as dementia. Severity varies during the day, e.g. ‘sundowning’ is a syndrome of worsening confusion in the later part of the day or at night

Other features (not essential to make the diagnosis)

These include:

• Disturbance of the sleep–wake cycle. May be complete reversal

• Disturbed psychomotor behaviour. May be ‘up’ (restless, picking, wandering) or ‘down’ (slow, immobile)

• Emotional disturbance, e.g. fear, depression, anger, euphoria, lability. Fear and aggression may be a consequence of threatening hallucinations or delusions. The patient may call out, scream, or moan continually. In an institutional setting, this may be problematic, especially at night. At a lesser level, the patient may appear simply perplexed and bewildered

• Delusions (often persecutory) are common, but usually transient and poorly elaborated

• Poor insight is typical

Box 9.1 Pitfalls in diagnosis

Making the diagnosis can be difficult, but early identification is vital as early treatment will improve prognosis. Delirium is a varied syndrome. As well as fluctuating day-to-day or hour-to-hour, it is variable in nature, manifesting distinctly in different patients, or in the same patient at different times. For example, two patterns (ends of a spectrum) have been described:

• Hyperactive or ‘up’: oversensitive to stimuli, psychomotor agitation, repeatedly getting out of bed, noisy, psychotic symptoms, aggression

• Hypoactive or ‘down’: psychomotor retardation, lethargy, quiet, paucity of speech, few psychotic symptoms. This variety is more commonly not recognized and has a worse prognosis

• A mixed picture can also occur

Delirium may be misdiagnosed when it is not present (e.g. in deaf, or blind or dysphasic patients). More commonly, the diagnosis is not made when it is present. Therefore, screening tests (typically the AMTS, and see Appendix, ‘CAM’, p. 706) are valuable and should be performed in all cases when delirium is possible—certainly at the time of admission, and during admission if changes in clinical condition occur.

Usually there is evidence of the medical condition that has led to delirium. Although this is not necessary to make the diagnosis, it is necessary to treat it effectively.

Ensure you document your assessment and diagnosis well.

Delirium: causes

A particular case is often multifactorial, i.e. several factors (individually modest and alone insufficient) combine to push a patient across a threshold to frank delirium. Chronic factors (e.g. overt or incipient dementia) may maintain a person closer to that threshold, and impaired homeostasis of older age ↑ the systemic—and cerebral—effects of illness.

Delirium is therefore especially likely to occur in very elderly people, in the physically frail, or if there is pre-existing dementia, defective hearing or vision, or brain damage of any kind, e.g. idiopathic Parkinson’s disease. In these cases, more minor acute illnesses may cause delirium.

Factors that may contribute to delirium

► Usually, there is evidence from either the history or examination or simple tests, of the factor(s) that have contributed to delirium.

These factors include:

• Infection. Viral or bacterial. Not necessarily severe, especially in those with MCI, dementia, or other contributory factors. Common sources are chest, urine, skin (cellulitis). Remember other infections, e.g. CNS, endocarditis, biliary infection, diverticulitis, pancreatitis, abdominal perforation, and abdominal or pelvic collection

• Drug intoxication. Especially anticholinergics, anxiolytics/hypnotics, anticonvulsants, opiates (see Box 9.2)

• Disorders of electrolyte/fluid balance, e.g. dehydration, uraemia, hypo-/hypernatraemia, hypercalcaemia. Modest degrees of hyponatraemia (>130mmol/L) are unlikely to be the sole cause of delirium

• Alcohol or drug withdrawal

• Organ failure, e.g. cardiac, respiratory, liver

• Endocrine. High or low blood sugar, hypo- or hyperthyroid

• Epileptic. Post-ictal state following unrecognized seizures. Consider if there has been an unwitnessed ‘collapse’, with amnesia, and any ictal features (incontinence, tongue biting). If conscious level is low, consider ongoing ictal activity or even non-convulsive status

• Intracranial pathology, e.g. head injury, space-occupying lesion, ↑ intracranial pressure of whatever cause, infection, pre-existing cognitive impairment, or acute/chronic cerebrovascular disease

• Pain

• Constipation/urinary retention

• Surgery, trauma, any anaesthesia

These factors may be accentuated on admission to hospital by environmental disorientation, a lack of information, sensory over- or under-stimulation, impersonal setting, changes in staff or wards, poorly understood investigations and treatments, and being away from a familiar home and family/carers.

Box 9.2 Drugs causing delirium

Drug-induced delirium is common. Incidence of delirium is closely associated with anticholinergic activity (anticholinergic burden scales exist; see Further reading below). Many more drugs are less frequently associated with delirious reactions:

• Anticholinergics (used for either urinary or gastrointestinal effects, e.g. oxybutynin, hyoscine)

• Antipsychotic drugs (‘neuroleptics’), e.g. chlorpromazine, trifluoperazine

• Antihistamines, e.g. chlorphenamine

• Hypnotics/anxiolytics, e.g. benzodiazepines, ‘Z-drugs’ (zolpidem)

• Antidepressant drugs, especially tricyclics

• Anticonvulsant drugs, e.g. phenytoin, carbamazepine

• Opiates and opiate-like drugs, including codeine, dihydrocodeine, and tramadol

• Corticosteroids, including prednisolone

• Lithium

• H2 receptor blockers, e.g. ranitidine (rarely)

• L-dopa (co-beneldopa, co-careldopa), dopamine agonists. Caution in treating parkinsonism in patients with Lewy body dementia

• Digoxin

‘Recreational’ drugs that may cause delirium include alcohol, marijuana, LSD, amphetamines, cocaine, opiates, and inhalants.

A drug may be the ‘final straw’ that leads to overt delirium. For example, a dry, septic patient who has tolerated co-codamol when well may become delirious when it is again administered in hospital.

Delirium: clinical assessment

History and examination

• Most factors leading to a presentation with delirium can be identified by taking a history and examining the patient. Even confused, forgetful patients report ongoing symptoms (e.g. pain, dysuria) if asked

• Always obtain a collateral history, paying careful regard to recent minor/major symptoms (e.g. cough), as well as drug history, and an exploration of the nature and duration of memory/cognitive symptoms

• Always assess cognition objectively, e.g. using the AMTS or clock-drawing test. This may yield surprising results (better or worse than expected) and permits tracking of progress

• If a patient is non-compliant with examination, use distraction (e.g. chatting while examining) or complete the examination in sections. Sedation will only rarely be necessary

• Focus the examination on important areas—is there evidence of infection (examine all lung areas, abdomen) or of new focal neurology? Is the patient dehydrated or overloaded?

• Repeat vital signs regularly, especially temperature

• Check arterial oxygen saturation off oxygen—even modest hypoxaemia (sats ≤95%) may indicate important cardiopulmonary pathology

Investigation

• One contributing factor may be obvious (e.g. UTI), but do not assume that this is the sole—or even the most important—factor, until others have been excluded

• All patients should have some baseline tests (see Box 9.3). These will vary according to the clinical picture, the availability of tests, and whether a clear cause is already apparent

• If the cause remains unclear despite a careful history, examination, and ‘simple’ tests, then repeat clinical assessment, consider less common causes, and consider more advanced tests such as CT/MRI brain, EEG, or CSF examination

Box 9.3 Baseline investigations in delirium

• FBC, ESR. Evidence of infection, anaemia (unlikely on its own to cause delirium)

• U, C+E. Hypo-/hypernatraemia, dehydration, renal impairment

• Glucose. Hypo-/hyperglycaemia. The sugar may now be normal—but what was it an hour/day ago?

• LFTs and amylase

• TFTs. Hypo- or- hyperthyroidism are common and treatable. Both may contribute to a presentation of delirium

• CRP. A very useful test but may be normal early in the course of infection

• Calcium and phosphate

• CXR. Clinical examination is relatively insensitive to early/localized pathology, e.g. infection

• ECG. Silent ischaemia/infarction common in older people. Consider troponin

• Urinalysis ± urine microscopy and culture. Asymptomatic bacteriuria is common; a positive dipstick may not therefore explain a patient’s delirium. Look for additional causes

• Blood culture. Always send before starting antibiotics. Occult bacteraemia is common

• Blood gases. Hypoxaemia or hypercapnia may contribute to delirium

• Drug levels, e.g. digoxin, lithium

Delirium: treatment issues

► Initiate treatment early—delirium is a medical emergency.

Where to treat?

In all cases, the patient should be thoroughly assessed by appropriately trained clinicians who have access to baseline investigations. If further investigations are required (e.g. CT), assessment at an acute hospital may be appropriate. Outside an acute hospital—in a domestic setting, care home, community or psychiatric hospital—the medical team must balance the benefits of advanced diagnostics, treatment, and monitoring with the possible detrimental effect of transfer. There is place for a ‘treat at home’ approach which may improve outcomes, provided that:

• The dominant cause is clear

• Effective treatment can be given

• Appropriate care and supervision can be assured

Keep the admission brief. With appropriate support and monitoring, discharge home or transfer to a less acute environment can often be achieved early before complete resolution.

The underlying cause

► Making the diagnosis of delirium is half the job. The second part is eliciting and treating the cause(s).

• Use targeted antibiotics. Broad-spectrum antibiotics, with the associated risk of Clostridium colitis, should be reserved for patients with severe sepsis of unknown origin

• Always check the drug chart. Consider each drug in turn—at this time, does risk equal or exceed benefit? If so, stop the drug, at least temporarily

• Ensure adequate fluid and nutrition. The patient may not be dry or malnourished on admission (though they commonly are) but may soon become so

• If alcohol dependency or severe malnutrition is known or suspected, high-dose parenteral vitamin B supplements may be needed

• Occasionally, the cause of delirium is not apparent. In such cases:

• Initiate general supportive measures (fluid, pressure care, nutrition, etc.)

• Continually re-examine and consider more advanced tests

Competency

Patients with delirium are not usually competent to direct treatment. The law allows assessment and treatment in their best interests. This may include:

• Holding within a ward or hospital if a patient attempts to leave

• Temporary restraint (e.g. while drugs are administered)

• Covert administration of essential drugs

Clear explanations should be given to staff and family of the need for such interventions, and their ethical and legal justification. Document clearly in the medical notes why the team considers that such measures are necessary. Reassess competence continually. Once the acute illness is over, a ‘Deprivation of liberty assessment’ may be needed (see ‘Deprivation of Liberty Safeguards’, p. 657).

Delirium: non-drug management

Delirious patients feel ill, frightened, bemused, and disorientated. There are problems with attention, memory, and perception. Therefore, do what you can to make life easier for the patient:

• Provide a quiet environment free from worrying sounds; appropriate clothes; quality lighting, at an appropriate level for the time of day; a clock or outside view to aid orientation

• Optimize visual and auditory acuity by providing spectacles and hearing aids that work

• Reassure the patient repeatedly and calmly

• Explain who you are and what you wish to do, and confirm understanding

• Patients will sense a doctor’s manner, particularly aggression or frustration. At all times, appear relaxed, unhurried, and pleasant

• Use non-verbal communication—sit down, smile, and appear friendly rather than professional

• Do not argue or correct delusions—the product will be aggravation and lesser compliance

• Educate visitors who are heightening emotion—ask them to modify their behaviour or even ask them to leave

• Explain to relatives and enlist their help in supervising, feeding, and bringing in items familiar to the patient

Physical restraint

Restraint is terrifying and has adverse mental and physical sequelae. It is only rarely needed but is sometimes (inappropriately) used as a substitute for supervision and guidance by an experienced carer/nurse.

In cases of severe aggression, where parenteral drugs are required, brief immobilization of the patient using the minimum force necessary may, on balance, be in the patient’s best interests.

Recovery phase

► Patterns of recovery from delirium vary. Most patients recover completely in a few days; some take much longer, but some never return to baseline cognitive and/or physical function. Delirium can ‘unmask’ a previously unrecognized dementia. In those whose functional status declines significantly, remember that full recovery may take weeks or months—beware making irreversible decisions (e.g. home versus residential care)— before the final functional level is known.

Once a patient is admitted, multiple barriers to discharge often appear:

• Carers and family will fear that recent deterioration will persist and may resist discharge

• Care packages may be cancelled, taking weeks to restart

• Therapists may assess function as suboptimal in the unfamiliar hospital environment, judging that discharge is unsafe

Therefore, once the acute event has been diagnosed and treatment begun, encourage the team to begin promptly to plan for home. Delay in discharge leads to ↑ prescription of psychotropic drugs, institutionalization, and care home placement.

Delirium: drug treatments

Drugs are needed only when the agitation that accompanies delirium is:

• Causing significant patient distress

• Threatening the safety of the patient or others

• Interfering with medical treatment (e.g. pulling out of iv lines, aggression preventing clinical examination)

Having decided that drug treatment is in the patient’s interests, remember that:

• Drugs should complement, not replace, non-drug approaches

• The correct dose is the minimum effective dose

• The response (adverse and beneficial) and prescription must be reviewed regularly

• It is preferable to use only one drug, starting at low dose, and ↑ the dose incrementally at intervals of 30–60min

• Delirium can resolve quickly, so avoid regular prescription—each dose should be as needed (PRN).

The relative merits of differing drug classes and drugs are debated, but a reasonable consensus is presented in ‘HOW TO . . . Prescribe sedating drugs in delirium’, p. 241.

In cases where behaviour remains problematic, seek urgent advice from the local psychogeriatric team.

HOW TO . . . Prescribe sedating drugs in delirium

Short-acting benzodiazepines (e.g. lorazepam)

• Have recently replaced antipsychotics as first-line treatments. Useful if sleep disturbance is prominent or for severe distress or agitation

• Short-acting benzodiazepines are preferred, e.g. lorazepam po, im, or sublingual, repeated as necessary/tolerated

• Dependence and tolerance are possible, so review regularly and discontinue as soon as possible. Avoid inclusion on ‘to take out’ (TTOs), if possible

• Long-acting benzodiazepines are especially useful for the treatment of delirium caused by alcohol or benzodiazepine withdrawal. Use chlordiazepoxide in reducing dose

• In extreme cases only (e.g. severe distress/agitation, with imminent danger to self/others), consider giving a small iv dose of a short-acting benzodiazepine (e.g. midazolam), carefully titrated to response. Monitor closely both clinically and with oximetry—the major risk is respiratory depression

Typical antipsychotics (e.g. haloperidol)

• Compared with low-potency antipsychotics, there are fewer side effects (e.g. sedation, hypotension, anticholinergic)

• Begin with a small dose, e.g. 0.5mg po, as tablet or liquid, prn. Repeat doses after 1–2h, and ↑ the dose size as needed and tolerated. Total daily oral dose is usually 0.5–4mg

• Response is idiosyncratic—some patients are very sensitive to low doses, others only to very large doses

• In older people, the half-life of haloperidol may be as long as 60h. Dosing can be cumulative. Failure to titrate the dose correctly may render the patient semi-conscious for days

• The oral liquid formulation of haloperidol is colourless and odourless, aiding covert administration (e.g. in a drink) if required

• In the very agitated, consider haloperidol 1–2mg im repeated after 1h (~2:1 oral to intramuscular dose equivalence)

• The incidence of extrapyramidal side effects is high. Avoid haloperidol in dementia with Lewy bodies and Parkinson’s

Atypical antipsychotics (e.g. olanzapine, risperidone)

• Should be used second line following concerns of ↑ risk of stroke/cardiac events

• Risperidone liquid can be diluted in water, black coffee, or orange juice

Combination treatment

Benzodiazepines and antipsychotic medications are sometimes combined in the management of delirium symptoms, generally under specialist advice.

Stopping treatment

Once behaviour has improved, consider stepwise dose reduction, aiming to stop the drug as soon as possible without prompting relapse.

Confusion and alcohol

It is an error to consider alcohol abuse as exclusively a disease of younger people. Even if the clinician remembers to ask about alcohol, they are often deceived by the patient who is embarrassed. ↓ alcohol metabolism means that older people should probably be recommended lower ‘safe’ drinking levels than younger adults. ↓ balance and cognitive reserve may mean that even very small doses of alcohol can have detrimental effects.

Alcohol withdrawal—occurs when habitual excess alcohol intake is stopped, e.g. when a patient is admitted to hospital. Agitation and confusion can occur along with physical signs such as diarrhoea, fever, and hypertension. Visual or tactile hallucinations or illusions can occur.

Delirium tremens—severe form of alcohol withdrawal with a high mortality. There are delusions, tremor, autonomic hyperactivity, and sometimes seizures.

Wernicke’s encephalopathy—triad of confusion, ataxia, and ophthalmoplegia. May respond to prompt thiamine administration, but many go on to develop Korsakoff’s syndrome.

Korsakoff’s syndrome—irreversible brain damage caused by thiamine deficiency, most commonly seen in alcoholism. May follow an episode of Wernicke’s encephalopathy or develop gradually. Amnesia and confabulation occur with lack of insight and apathy. Ataxia and tremor may also be found.

Alcohol dementia syndrome—a dementia almost indistinguishable from Alzheimer’s, can occur without the typical features of Korsakoff–Wernicke syndrome.

Managing alcohol withdrawal in hospital

• Make the diagnosis

• If necessary (not routinely—heavy drinkers get withdrawal symptoms in about half of cases), use a decreasing-dose schedule of benzodiazepine, e.g. chlordiazepoxide to control symptoms and behaviour. Clomethiazole should not be used in older patients.

• Always prescribe B vitamins—either parenterally or po (multivitamins plus thiamine)

• Offer support

Squalor syndrome

Also referred to as senile self-neglect (inappropriately derogatory) or Diogenes syndrome.

Clinical features

• Affected people, usually elderly, live in conditions of severe self-neglect, are socially withdrawn, and lack insight into the unusual nature of their behaviours and effects on others

• Financial problems are rare

• Homes are typically dirty, their upkeep neglected, and are often the repository for hoarded rubbish. This often causes distress and anxiety to neighbours, social and health professionals, much more so than to the patient themselves. Thus they come to the attention of many agencies—health, social, and public (e.g. environmental health)

The syndrome is not uncommon. Diagnosis is made when the clinical features listed exist, without major psychiatric illness (dementia, depression) to explain it. The best guess is that the syndrome is an unusual manifestation of long-standing personality disorder and that isolated frontal lobe dysfunction commonly plays a part.

Risk factors

• Borderline personality (‘eccentricity’)

• Early dementia or depression

• Recent bereavement (commonly spouse)

• Lack of close family

• Social isolation

• Sensory impairment (often visual)

Management

• This should include identification and treatment of contributing psychiatric illness and 2° physical illness, e.g. malnutrition

• Patients often decline ongoing social support. Psychiatric day care may maintain more mainstream behaviour for a time, but relapse is common. Institutional care is a long-term solution, if accepted

• Usually such people are competent to decide to maintain their unusual lifestyle and to decline offers of support

• Caring for them can be frustrating, but adverse consequences for the patient are often surprisingly few, and a watching brief is usually sufficient, with prompt intervention when decompensation occurs

Depression: presentation

The most common psychiatric illness in older people. Probably 10–15% prevalence over 65 years, severe in 3%.

Risk factors for depression include:

• Disability and illness (especially if serious)

• Care home residents

• Bereavement. Reactive depression is more common in older people, who suffer more bereavement, illness, and other life events. The reaction may be understandable, but there is benefit from treatment (see ‘Bereavement’, p. 640)

• Social isolation

• Chronic pain

• Sensory impairment (e.g. hearing or sight)

Comorbidity may mask or precipitate depression and may be:

• Physical (Parkinson’s, stroke, cancer, or post-acute illness)

• Psychiatric (dementia)

Depression is underdiagnosed in older people, for the following reasons:

• Perception that depression carries a social stigma, so not volunteering symptoms

• Presentation with symptoms suggesting physical, rather than psychiatric, disease (e.g. weight loss, rather than sadness)

• Perception that low mood is a normal part of ageing (e.g. ‘Of course she is depressed—she is in a nursing home with chronic disability and pain’)

► Have a low threshold for opportunistic screening.

HOW TO . . . Distinguish dementia from a depressive pseudodementia

Pseudodementia is a depression that presents with poor memory and concentration and impaired functional capacity, e.g. for ADLs. Also known as dementia of depression.

It is usually distinguishable from dementia, because:

• The history is often short and the onset relatively abrupt

• Patients often complain about poor memory and are despairing

• Assessment of cognition often results in ‘don’t know’ responses

• Memories are often accessible with ‘hints’ or cues from the assessor—they remain ‘stored’

• There is often a past history of depression, or an identifiable precipitant

The prognosis is variable. In some, mood and cognition respond to antidepressants. However, many go on to develop dementia, usually of Alzheimer type.

Coexistence of depression and dementia

• Both depression and dementia are relatively common and may coexist coincidentally

• Over 20% of people with an early dementia may be depressed, suggesting a depressive reaction to the onset of dementia—especially common and understandable if insight is preserved

• This is quite different from pseudodementia (where there is no actual dementia)

General guidance

• Treat depression whatever the cause—whether a ‘true’ pseudodementia or a combination of dementia and depression

• Avoid mislabelling a depressed patient as also having dementia—the management and prognoses are very different

• Always screen for depression when assessing patients with cognitive disorders, including short-term memory loss alone

Depression: clinical features

Sadness

Commonly denied, and not necessary in order to make a diagnosis of depression. Tearfulness is uncommon, especially in men. Also ask about biological symptoms, anhedonia (inability to enjoy—ask ‘What do you enjoy or look forward to?’), and depressive thoughts (guilt, worthlessness, low self-esteem, self-blame, suicidal thoughts, hopelessness, and helplessness).

Anorexia and weight loss

Common to both depression and serious physical illness. In the patient who presents in this way, without evidence of a physical cause after clinical examination and basic tests, it is a matter of judgement whether and when an antidepressant trial should begin, and whether more invasive tests should be delayed pending the results of that therapeutic trial (see ‘HOW TO . . . Manage weight loss in older patients’, p. 355).

Sleep disturbance

Typically early morning wakening, but a full sleep history is useful, as early wakening may be appropriate, e.g. if sleeping during the day. Some older people do sleep much less than when younger—the key is whether they wake refreshed or wake anxious and fearful, keen to return to sleep but unable to do so (see ‘Sleep and insomnia’, pp. 174–175).

Disturbance of behaviour

May include attention-seeking, aggression, irritability, cries for help (e.g. intentional falls), self-neglect, malnutrition, and social withdrawal.

Cognitive impairment

Poor attention and concentration may result in impairments in several cognitive domains, typically memory. If severe, this may manifest as a ‘depressive pseudodementia’.

Suicidal ideation and self-harm

Should always be taken seriously, as completed suicide is relatively common in older people, especially those with physical illness. Self-harm (e.g. drug overdose) may be medically trivial, but psychiatrically very serious, and should mandate psychiatric referral. Parasuicide—a ‘cry for help’ or ‘manipulative’ self-harm event—is very rare; most older people who self-harm are at least moderately depressed.

Physical slowness

Exclude physical causes, including parkinsonism, cerebrovascular disease, and hypothyroidism. May manifest as ↑ dependence or ‘failure to cope’. May be severe, with very reduced mobility or total immobility—the depressed, bed-bound, motionless, anorexic patient must be treated as an emergency.

Somatization

This expression of psychological problems as physical symptoms is common, as is hypochondriasis (disproportionate concern over health). In the patient presenting with somatization or hypochondriasis, the risks are of failing to investigate and treat when a true physical illness is present, or conversely of failing to appreciate that antidepressant treatment is actually what is needed.

HOW TO . . . Assess depression

Depression rating scales

For example, GDS (see Appendix, ‘Geriatric Depression Scale’, p. 701), which is known to be valid in community and hospital settings and maintains specificity in mild to moderate dementia.

Two or three simple questions can be effective screening tools. Simply asking ‘Do you feel low?’ has reasonable sensitivity and specificity for depression.

Psychiatric history and examination

Physical history and examination

Targeting evidence of physical illness contributing to, or mimicking, depression, and contraindications to drug treatments.

Cognitive assessment screen

For example, MoCA, clock-drawing test. Is there coexisting cognitive impairment? If so, does it improve with treatment for depression, i.e. pseudodementia? (see ‘HOW TO . . . Distinguish dementia from a depressive pseudodementia’, p. 245.)

Blood tests

• FBC (anaemia leading to lethargy; high mean corpuscular volume (MCV) in alcohol excess)

• ESR (malignancy, vasculitis)

• B₁₂ and folate (low levels may contribute to depression or result from anorexia)

• U, C+E (uraemia, dehydration)

• Calcium (hypercalcaemia leading to depression and fatigue)

• Thyroid function (hypothyroidism, and occasionally hyperthyroidism, may present as depression)

• Liver function (malignancy, alcohol excess)

Depression: non-drug management

Depression is undertreated as well as under-diagnosed. Treatment should be started promptly.

Supportive treatment

• Includes counselling and relief of loneliness

• Treat physical symptoms and pain

• Address rational anxieties, e.g. financial, housing, physical dependency

• Consider stopping contributory drugs (β-blockers, benzodiazepines, levodopa, opiates, steroids)

Psychotherapy

As effective as antidepressants for mild to moderate depression and is without physical side effects. For severe depression, should be combined with drug treatment. Cognitive behavioural therapy has the most evidence. Is resource-intensive and often has limited availability and/or long waiting lists.

Electroconvulsive therapy

Electroconvulsive therapy (ECT) offers a safe, rapid, and reasonably certain response in cases where:

• Rapid response is necessary

• Patients with depression have been intolerant to, or have not responded to, drug treatment

• When depression is very severe and manifests as psychosis, severe physical retardation, depressive stupor, or food/fluid refusal

Relative contraindications include coronary, cerebrovascular, and pulmonary disease.

Specialist referral

Consider psychogeriatric assessment if:

• Treatment is unsuccessful after 6–8 weeks

• Depression is severe, e.g. with delusions

• The diagnosis is unclear, e.g. when depression and significant cognitive impairment coexist

• A patient is refusing treatment or otherwise threatening self-harm

• There are questions of competency

• ECT is being considered

Depression: drug treatments

Drug treatment is generally effective, well tolerated, and non-addictive, although patients often believe otherwise.

► There is significant stigma associated with taking antidepressants, which is more prevalent in older age populations, and this may need to be explored and addressed.

General

• In reactive depression, consider saying ‘This won’t stop you feeling sad, that’s understandable, but it will help you to cope better with those feelings’

• Inform the patient that response takes time but is usual

• No antidepressant class has been shown to be more effective, so choice depends on side effects, speed of onset, response to previous treatment, drug interactions, and associated conditions, e.g. anxiety or pain

Selective serotonin reuptake inhibitors

For example: citalopram or sertraline.

• Now generally the first class of antidepressant prescribed

• Compared with tricyclic antidepressants such as amitriptyline, they are less sedating, have fewer anticholinergic and cardiotoxic side effects, have fewer drug interactions, and are much safer in overdose

• Symptomatic response commonly starts after 2 weeks but may take up to 8 weeks

• Common side effects include gastrointestinal symptoms (nausea and diarrhoea), postural hypotension, anxiety, and restlessness, and hyponatraemia. Hyponatraemia is usually moderate (sodium >125mmol/L) and asymptomatic, and especially common in combination with diuretics

• Rarely causes serotonin syndrome (see ‘Neuroleptic malignant syndrome’, p. 167)

• Start at low doses to minimize side effects and build up, as needed, to give a useful response

• If there is no response to an adequate dose of one SSRI, there is little point trying another. Instead, switch class

Serotonin antagonist

For example: mirtazapine.

• An atypical antidepressant which tends to cause weight gain (so may be particularly useful in malnourished)

• It has fewer anticholinergic side effects but is more sedating than tricyclics (so consider when a degree of sedation is desirable)

• Also less commonly complicated by hyponatraemia than SSRIs

Serotonin and noradrenaline reuptake inhibitors (SNRIs)

For example: venlafaxine or duloxetine.

• For severe depression or when poor response to SSRIs after 6 weeks

• Also useful for anxiety and obsessive–compulsive disorder

• May cause less orthostatic hypotension than the SSRIs, but other side effects similar

Tricyclic antidepressants

For example: amitriptyline, nortriptyline.

• Much less prescribed than previously

• They still have a role, e.g.:

• If anticholinergic effects are desirable (urge incontinence)

• When there is neuropathic or other pain that may respond to its co-analgesic effect

• In depression resistant to other drugs

• The 2° amines (e.g. nortriptyline) are preferred, causing less orthostatic hypotension than tertiary amines (e.g. amitriptyline, imipramine). Anticholinergic side effects are less troublesome if doses start low and are ↑ weekly

Monoamine oxidase inhibitors

For example: moclobemide.

• Occasionally used, under expert guidance, but dietary and drug interactions are problematic

• Treatment should be continued for up to a year. If depression has been severe and/or recurrent, consider continuing indefinitely

Stopping drugs

Withdrawal reactions (anxiety, mania, delirium, insomnia, gastrointestinal side effects, headache, giddiness) may occur if drugs are stopped abruptly after 8 weeks or more. Therefore, reduce the dose gradually, over 4 weeks. In those on long-term treatment, reduce over several months.

Switching drugs

‘Cross-tapering’ is generally advised, i.e. the incremental reduction of the ‘old’ drug, and incremental ↑ of the ‘new’ drug usually over 2–3 weeks. Rarely, a washout period between drugs is required (e.g. before MAOIs).

Suicide and attempted suicide

Older people, especially men, have a higher risk of completed (rather than attempted) suicide than all other groups. Following an attempted suicide, further attempts—and successful suicide—are common.

Risk factors include being ♂, single (i.e. unmarried, divorced/separated, or widowed), being socially isolated, having financial problems, having made previous attempts, and recent bereavement. Unlike younger people, the substantial majority of older people who attempt suicide are psychiatrically unwell at the time of the attempt; most are depressed. Many seek contact with medical services prior to the attempt, although they may not express depressive or suicidal thoughts at that visit.

Suicidal behaviours may be overt or covert.

Overt behaviours include:

• Intentional drug overdoses (opiates, antidepressants, paracetamol, benzodiazepines; more common in women)

• Self-injury (hanging, shooting, jumping, drowning; more common in men)

Covert suicide is relatively more common in older people and includes

• Social withdrawal

• Severe self-neglect

• Refusal of food, fluid, or medication

This may manifest in subtle ways that encourage extensive investigation to exclude physical illness, while the psychiatric problem goes unrecognized and untreated.

Suicidal ideation is more common in institutional settings (acute and rehabilitation hospital wards, and care homes) and in people with acute or chronic physical illness. Risk factors here include depression, chronic pain, sleep disturbance, functional impairment, drug abuse, and psychotropic drug prescription. At their mildest, suicidal ideas manifest as common and relatively benign doubts about whether life is worth living. At their most worrying, they are carefully considered, well formulated, and strongly held beliefs that death is preferable to life, and how that could be achieved.

Assessment of the ‘severity’ of an attempt requires an effort to determine perceived risk from the patient’s perspective at the time of the attempt. This may not parallel the medical seriousness. Consider:

• Degree of planning versus impulsivity

• Likelihood of interruption during attempt

• Reaction to interruption to attempt (disappointment or relief?)

• Suicide note and its contents

• Planning for future (e.g. making of will, contents of suicide note)

• Personal view of suicide as a reasonable ‘life choice’

Specialist referral. Always in cases of attempted suicide, suicidal ideation, or ‘covert suicide’. Probably not in cases of non-persistent or poorly formulated views that life is not worth living.

Psychiatry

Age-associated memory impairment or benign senescent forgetfulness

Minimal/mild cognitive impairment (MCI)

Triggers for considering a dementia diagnosis

UK National Dementia Strategy

HOW TO . . . Distinguish delirium from dementia

Physical examination

Mental state

Disclosure of dementia diagnosis

HOW TO . . . Investigate a patient with dementia

Blood tests

ECG and CXR

Neuroimaging

Imaging modality

Additional testing as clinically indicated

Alzheimer’s disease (dementia of Alzheimer type)

Vascular dementia

Differentiating between Alzheimer’s and vascular dementia

Dementia with Lewy bodies

Parkinson’s disease with dementia

Assessment

Neuroimaging

Investigation

Treatment

Further reading

Frontotemporal dementia

Dementia and infection

Dementia and drugs/toxins

General

Social

Practical

HOW TO . . . Manage the driver who has dementia

Further reading

Lifestyle interventions

Drugs

Effectiveness

Choosing a drug

HOW TO . . . Treat with acetylcholinesterase inhibitors

Before treatment

Treatment trial

Assess impact using

Continuing therapy

Memantine

Other drugs to prevent progression

HOW TO . . . Manage patients with dementia in hospital

General

Non-drug management

Drug treatment

Mental Capacity Act (2005)

Section 5(2) of the Mental Health Act (1983)

Section 2 of the Mental Health Act (1983)

HOW TO . . . Manage the older person refusing treatment

What is psychosis?

Causes of psychotic symptoms in older people

Treatment of patients with psychotic symptoms

Key features

Other features (not essential to make the diagnosis)

Box 9.1 Pitfalls in diagnosis

Factors that may contribute to delirium

Box 9.2 Drugs causing delirium

Further reading

History and examination

Investigation

Box 9.3 Baseline investigations in delirium

Where to treat?

The underlying cause

Competency

Physical restraint

Recovery phase

HOW TO . . . Prescribe sedating drugs in delirium

Short-acting benzodiazepines (e.g. lorazepam)

Typical antipsychotics (e.g. haloperidol)

Atypical antipsychotics (e.g. olanzapine, risperidone)

Combination treatment

Stopping treatment

Managing alcohol withdrawal in hospital

Clinical features

Risk factors

Management

HOW TO . . . Distinguish dementia from a depressive pseudodementia