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Geriatric medicine

INTRODUCTION AND OVERVIEW

The world’s population is ageing rapidly, particularly in developed countries, where life expectancy is over 80 years for women and just under 80 years for men in many countries. Rapid ageing is occurring in less developed countries too, with the number of people aged over 65 years increasing dramatically in many countries. Consequently, much of general practice now involves care of older people in a range of settings—community, residential and acute-care facilities. It is easy to form the impression that ageing normally involves disease, disability and dependency, but while these are more common with increasing age, they are far from inevitable. Most 90-year-olds are not demented, maintain excellent mobility, are independent in personal, domestic and most community activities of daily living and live in their own home.

AGEING

Some changes with normal ageing are generally towards impaired function—for example, maximum heart rate and exercise capacity are reduced, glomerular filtration rate is lower, there is decline in some aspects of cognition and muscle mass is reduced. An emerging concept in geriatric medicine is that of ‘frailty’, which essentially is a condition in which these normal changes of ageing accumulate and lead to disease, predisposing the person to functional decline. Frailty is not, however, an inevitable part of ageing.

Essentially, most ageing is healthy and most of us age in a mostly healthy way. (Healthy ageing is covered in Ageing.) However, with time the number of organ systems within an individual that begin to age in an unhealthy way increases, so that by age 90 years it is uncommon to exhibit only healthy ageing. Frailty can be seen as a transition stage between healthy and unhealthy ageing. Factors that increase the chance of healthy ageing include genes, physical activity, cognitive stimulation, social engagement, diet and aggressive detection and management of disease risk factors.

EVALUATION OF THE OLDER PERSON

Comprehensive geriatric evaluation requires a detailed assessment of both physical and cognitive status, but also involves assessment of function (basic and more complex tasks), social environment, psychological/psychiatric status, behavioural issues and support systems.

Particular attention needs to be paid to the features of geriatric medical syndromes, including dementia, impaired mobility and falls, incontinence and medication-related issues. There have been several checklists/proformas developed by GP divisions and individual practices to assist this assessment process. These are particularly useful when carrying out routine comprehensive assessments. A suggested checklist is shown in the appendix. Ideally, this information will then be transformed into a problem list with a management plan—an example is shown in Table 57.1. It will be seen that this is best developed as a dynamic process with additional management of the identified problems added as they occur—so a word processed document on computer would be more appropriate than a single hard copy.

TABLE 57.1 Example of a geriatric medical problem list and management plan

PHARMACOLOGICAL ISSUES, INCLUDING POLYPHARMACY

BACKGROUND AND PREVALENCE

Medication issues in older people include polypharmacy (taking a large number of medications), reduced compliance (‘concordance’), drug–drug interactions and adverse drug reactions. Older people consume a disproportionately large number of prescribed drugs, partly because they are more likely to be ill and partly because it can be more difficult to reach a precise diagnosis. On average, an older person in the community takes three prescribed drugs, and this rises to 7–10 in care settings. CAMs and other over-the-counter (OTC) medications are also used extensively by older people. Unfortunately, it is rare for a GP to have a completely accurate list of all the medications their patient consumes—this is partly because the patients themselves cannot always accurately recall them (and may not feel it necessary to mention OTC/CAM medications) and partly because of poor communication from acute-care facilities and specialists. The best way to obtain an accurate list is to visit the patient’s home and ask to see everything they use, or to ask them to put all the medications in a bag and bring them to your office.

Reduced compliance is common at all ages, but is particularly an issue in older people, who take more medications, may not hear or recall or be able to read instructions, may have difficulty opening packages and can be on complicated drug regimens. Fortunately, under-compliance may somewhat protect them from adverse drug reactions, but it does contribute to poorer disease control.

Drug–drug reactions and adverse drug reactions increase with age and with increasing numbers of medications used. Some 3% of all admissions to hospital are primarily due to adverse drug reactions and, if this is expanded to include poor disease control from suboptimal prescribing and compliance, the proportion of admissions rises to over 30%. Drug–drug interactions are almost unavoidable if a person is prescribed more than eight medications, and can cause adverse drug reactions and poor drug efficacy. The problem may be compounded by drug–nutrient or herb–drug interactions, particularly if the ingestion of herbs or nutrients is unknown to the doctor.

AETIOLOGY

A large part of the problem older people have with medication is that their bodies deal with drugs differently (altered pharmacokinetics) and may have a different response from younger people to the same drug concentration (altered pharmacodynamics). Absorption is relatively unaffected by age (much built-in reserve, to meet nutritional needs) but liver metabolism (so-called ‘first pass’ and oxidative cytochrome P-450 metabolism) is reduced, as is renal excretion. Drug distribution is also changed with age—relatively less body water and more body fat affects the peak level and elimination half-life of drugs, which tend to be either predominantly fat soluble (e.g. the benzodiazepines) or water soluble (e.g. digoxin). Protein binding is reduced in the unwell elderly person, leading to more free drug, but this free drug is consequently more available for metabolism and excretion.

Examples of altered pharmacodynamics include a less effective cardiovascular response to low blood pressure, increasing risk of postural hypotension and falls due to medications, and reduced beta-adrenergic receptors reducing the response to and efficacy of beta-blocking agents (older people are effectively already partly beta-blocked).

ASSESSMENT

Always ask older people about their medications and problems they may be experiencing with them. Older people do recognise minor adverse effects well (even though such effects can present atypically) but, surprisingly, have more difficulty recognising more serious adverse events. Sometimes more formal assessment of medication compliance and handling can be useful—pill counts, measuring blood levels of the drug and involving the pharmacist in this process. Poor disease control (e.g. ongoing fitting, depression or hypertension) may indicate poor compliance, and this should be excluded before increasing the medication dose or adding a new medication.

MANAGEMENT

Along with regular medication reviews, there should be a sustained intention to minimise the number of medications an older person takes, but also to ensure that all conditions are being treated effectively. ‘De-prescribing’ is both possible and beneficial, and the basic steps are shown in Box 57.1.¹ Unnecessary medications may include analgesics and laxatives no longer needed, or an antipsychotic for behavioural symptoms that are no longer complicating dementia. Additionally, many prophylactic medications (e.g. statins, bisphosphonates) may no longer be necessary as death approaches (palliative care, end-stage dementia). High-risk medications include anticholinergics (benztropine and benzhexol) and long-acting benzodiazepines.

BOX 57.1 De-prescribing principles ¹

1. Establish an accurate list of all current medications.

2. In partnership with the patient and carer, plan a de-prescribing regimen.

3. Cease all unnecessary medications and, if possible, those causing adverse effects.

4. Cease, if possible, medications with a high likelihood of causing adverse effects.

5. Review and support the patient (and carers) regularly.

6. Update medication list and consider repeating the cycle.

In residential and acute-care settings, medication audits are another approach to improving medication outcomes—for example, the appropriateness of benzodiazepine prescribing can be audited against an evidence-based algorithm and these results then fed back to the prescribing team. Pharmacist and GP can also work as a team to review an individual’s medication in residential and community settings—indeed, annual medication review is now required for those in residential care. Other approaches include academic detailing, and programs such as the National Prescribing Service GP education program in Australia.

IMPORTANT PITFALLS

It is all too easy to become complacent about the number and type of medications older people take, especially when many are commenced in hospital, by other doctors or earlier in life when the medication may well have been appropriate. Such complacency may not serve the patient well.

Also, when a medication is ceased the patient may reintroduce it if not supported and reviewed (e.g. temazepam—cessation in hospital is almost always followed by recommencement after discharge).

Finally, the original condition may re-emerge once a medication is ceased—for example, hypertension may recur if a calcium channel blocker causing swollen legs is ceased. The patient should therefore be monitored, often for up to a year, for this.

PATIENT EDUCATION

The GP may want to have available notices and pamphlets on the importance of correct use of medication and the hazards of unnecessary medications. More detailed brochures can alert patients that any new symptoms may be due to their medications, and to always discuss their medication with their doctor.

CONFUSIONAL STATES: DELIRIUM AND DEMENTIA

DELIRIUM

Background and prevalence

Delirium is an acute-onset confusional state characterised by impairment of cognition—especially attention—with marked fluctuations. There is a hypoactive form, more prevalent in older people, and a hyperactive form, where a person may have difficulty sleeping and may be physically active or even aggressive. Hallucinations (usually visual) and paranoia are common. Delirium affects about 30% of hospitalised elderly people at any one time, with 20% having delirium on admission and up to another 20% developing delirium during their hospitalisation. Prevalence in the community is less, but it must always be considered when there is a sudden change in cognitive status.

Aetiology

Delirium always has a medical cause.² The most common causes include infections, metabolic disturbances (e.g. electrolyte deficiencies, hyperglycaemia, hypercalcaemia) and drugs (adverse effects or drug withdrawal). Other causes include pain, intracerebral lesions, myocardial infarction, organ ischaemia, faecal impaction and epilepsy.

DEMENTIA

Dementia is a chronic, progressive impairment of cognition, including memory, which is usually irreversible and always causes some impairment of function. It affects 5% of those over age 60, but the incidence doubles every 5 years, with around 30% affected by age 80. The average GP is likely to have 5–10 patients with dementia, but this will vary depending on how many elderly patients he/she has.

Aetiology

It is not known why one individual develops dementia and another does not. There are genetic mutations that nearly always cause dementia, but this early-onset dementia (in the forties or fifties) is very rare. Risk factors for the much more common late-onset dementia include older age, family history of dementia, apolipoprotein E4 (a carrier of cholesterol), previous head injury, less formal education, lower socioeconomic status and cardiovascular risk factors (hypertension, diabetes, smoking, atrial fibrillation, past cardiac surgery). There are also protective factors, including active leisure activities, physical activity, social contact and marriage, moderate alcohol use, exposure to non-steroidal anti-inflammatory agents, omega-3 fatty acids and use of vitamins E and C. It is also becoming apparent that attentional training, such as mindfulness-based practices, is associated with cell maintenance and neurogenesis in the prefrontal cortex and hippocampus.⁴

The most common cause of dementia is Alzheimer’s disease (AD), usually mixed with cerebrovascular pathology. Pure vascular dementia (that is, with no AD pathology) is uncommon. The emerging concept of ‘cerebral reserve’ may explain this synergism and some protective factors—those with a lesser number of synapses (e.g. from less education or a past head injury) are more prone to the clinical syndrome of dementia once AD pathology develops, especially if they also have cerebrovascular damage (e.g. lacunar infarcts or extensive white matter changes).

Other relatively frequent causes of dementia include dementia with Lewy bodies (DLB) and frontotemporal dementia (FTD). In DLB there is a combination of cognitive impairment, fluctuations, parkinsonism, visual hallucinations and sleep disturbances—but not all features have to be present for the diagnosis to be made. The hallucinations are often of small animals or creatures just outside or coming into the room. Sleep disturbance affects the REM sleep component, with a failure to paralyse muscles during dreams, leading to violent movements. DLB is in the same spectrum as Parkinson’s disease with dementia (PDD)—the main difference is that in PDD the motor changes precede the cognitive changes.

Frontotemporal dementia usually begins with behavioural or language changes with relative preservation of memory initially. The behavioural changes reflect frontal lobe impairment and include disinhibition, apathy, lack of insight, and impaired judgment and reasoning. Language changes can occur with all forms of FTD but there are two language-specific forms, called semantic dementia (language is fluent but the meaning of words is lost) and primary progressive aphasia (language is simply lost, with mutism occurring early in the dementia).

There are over 200 other causes of dementia but these are uncommon. A few are occasionally at least partially reversible (e.g. hypothyroidism, vitamin B₁₂ deficiency, syphilis) and explain why investigations for these are performed. Normal pressure hydrocephalus (characterised by dementia, urinary incontinence and gait disturbance) is also potentially reversible, although many neurosurgeons are reluctant to perform the required shunt, as results are often disappointing.

Pathology

Alzheimer’s disease is characterised by amyloid plaques and neurofibrillary tangles, which begin in the hippocampal/limbic region of the brain and progress throughout the cerebral cortex as the disease progresses. The plaques are composed of the amyloid beta (Ab) peptide, which is a fragment of the amyloid precursor protein (APP), a transmembrane protein whose function is not well understood. This fragment is cleaved off by two enzymes (beta and gamma secretase), and mutations in a component of the gamma secretase as well as mutations in APP cause most of the (rare) early-onset AD. The tangles are composed of hyperphosphorylated tau, a protein which normally stabilises the microtubules that neurons use to transport protein from their nucleus, down axons to the synapse. Which of these two main pathological processes is key to the development and severity of AD is hotly debated—probably both are.

In vascular dementia the pathology is brain tissue damage due to cerebral ischaemia and this can affect any region of the brain, although frontal lobe dysfunction is common, even if the damaged area is distant to the frontal region. There is a spectrum of pathology that can contribute to vascular dementia—a single large critical infarct, multiple large-vessel infarcts, multiple lacunar infarcts, extensive white matter lesions and multiple haemorrhages. Usually this vascular pathology coexists with AD pathology.

Dementia with Lewy bodies (DLB) is characterised by cortical Lewy bodies, which contain alpha-synuclein. Abnormal folding of this protein is thought to be a key precipitant of DLB.

Frontotemporal dementia has a range of pathology, including Pick bodies in one subtype. AD pathology is not found. Recently, a mutation of the progranulin gene has been found in a large proportion of FTD cases—progranulin appears to be a neuronal growth factor. This is associated with an abnormal form of the protein TDP 43 and this can be identified in (post mortem) diagnostic tests.

FIGURE 57.1 Differential diagnosis of dementia and Alzheimer’s disease

Diagnosis

History

The key to diagnosing the dementias is the clinical history, combined with judicious use of specific investigations. AD is characterised by an insidious onset of memory loss—usually at least 1–2 years before presentation—and progressive decline. (Ask: ‘Has there been definite decline in the past 6 months?’) Specific questions may include:

• Does he/she repeat information or questions?

• Does he/she frequently misplace objects or put items away in unusual places?

• Doe he/she forget to turn things off/close things?

• Does he/she forget appointments/arrangements?

• Does he/she forget names of family members?

It is also important to establish whether the cognitive changes are affecting function (e.g. unable to manage finances, unable to operate appliances previously used independently, unable to fix broken items around the house). Cognitive impairment with no effect on function suggests mild cognitive impairment (MCI), which is not dementia, although it is increasingly recognised as a prodromal state.

In vascular dementia there will usually be a history of more sudden episodes of decline associated with other features of cerebral ischaemia events—but not always (e.g. in progressive white matter damage). The history of DLB, FTD and the rarer dementias is driven by enquiring about the specific features described above.

FIGURE 57.2 Brain scan showing Alzheimer’s disease

Examination

Physical examination is necessary and should concentrate on neurological signs—such as parkinsonism in DLB and focal signs in some vascular dementias. The most important reason for performing the physical examination is to detect rarer, potentially reversible, causes of dementia (e.g. thyroid disorders) and comorbidities. Cognitive assessment is essential. The best known screening tool is the MMSE, a 30-item questionnaire that is useful in screening for AD but has less utility with the other dementias. The clock drawing test (CDT) is also useful—the patient is asked to draw a large circle (or the circle can be provided), place the numbers of a clock and then show a requested time with the hands (e.g. 11:10 or 1:50). Errors include incorrect number placement and inability to show the time. Combining the MMSE and the CDT achieves around 90% sensitivity for cognitive impairment—that is, an MMSE score below 26 and an abnormal CDT indicates a 90% chance that the person has significant cognitive impairment.

More-detailed assessment is required in order to characterise the dementia type. In FTD, questioning should concentrate on executive function (e.g. similarities, problem solving) and language (e.g. describe a complex task, name objects, read a paragraph). In DLB there are prominent visuo-spatial deficits, so assessment should include drawing a cube to supplement the CDT and the intersecting pentagons in the MMSE. For vascular dementia, assessment of frontal lobe function is useful but cognitive changes are influenced by the site and extent of the lesions—for instance, if they are in the dominant temporoparietal cortex there may be language changes.

More-detailed neuropsychological assessment usually requires referral to a specialist (geriatrician, psychogeriatrician or neurologist), who may use the expertise of a neuropsychologist.

Investigations

Routine blood tests and neuroimaging should be performed as shown in Box 57.3—mainly to rule out potentially reversible causes of dementia and comorbidities. Increasingly, specialists are ordering tests to ‘rule in’ a diagnosis of dementia and to characterise the type.

The MRI of the brain is moving towards this identification of dementia—for instance, hippocampal atrophy is seen in AD, and frontal atrophy in FTD. The PET scan is only available in a few centres but can be most useful. The FDG PET shows a characteristic pattern in AD (bilateral temporoparietal hypometabolism with sparing of occipital metabolism), whereas sparing of the posterior cingulate metabolism is very much against a diagnosis of AD. In DLB, occipital metabolism is reduced and in FTD frontal and temporal metabolism is down, with characteristic patterns in the language variants. Another PET technique available in even fewer centres is amyloid imaging using PIB or other agents. Absence of amyloid excludes AD, and its presence excludes FTD. Amyloid is frequently found in DLB and vascular dementia. Combining both PET techniques achieves very high diagnostic accuracy.

Management

Prevention

To what extent dementia can be prevented is not fully known, but individual risk reduction is achievable through attention to risk and protective factors. Alzheimer’s Australia has an excellent program that outlines this (‘Mind Your Mind’) and it can obtained from their website or by contacting them directly. Much of the focus is on diet, lifestyle and cardiovascular risk factors—‘what is good for your heart is also good for your mind’. All newly diagnosed people should be advised to follow the recommendations of the program, as should family members. Those with MCI should be particularly encouraged to pursue these practices, although they have not been proved to prevent progression to dementia. At this time, no medication is recommended as a preventative strategy, although two large trials, of Ginkgo biloba (United States and Europe—‘GEM’ and ‘GUIDANCE’) examined this.

General supportive measures

It is important to diagnose the presence and type of dementia in the early stages—this can allow planning for the course of the disease and assists the family/caregivers in understanding symptoms. For instance, the sexually explicit repetitive joking of a person with FTD, while not pleasant, can be understood and arrangements made to avoid contact with younger relatives and friends. In later stages, dementia type is less relevant—the very dependent high-level care resident with severe AD has similar symptoms and care needs to the person with severe DLB or FTD.

Not initiating treatment with medication is also a valid option, as current therapies (see below) are only modestly effective. However, pharmacological therapy is becoming a standard of practice (for those dementias responsive to it), with over 50% of people diagnosed with AD receiving such therapy.

For FTD and most of the rarer dementias there is no specific drug therapy, and ‘general supportive measures’ in that therapeutic domain are valid. As described above, for normal pressure hydrocephalus it is not uncommon for the specialist team to elect to not shunt.

Self-help and lifestyle

The preventative strategies described in ‘Mind Your Mind’ are still appropriate in early dementia and should be encouraged. These include physical exercise, engaging in social and leisure activities, a well-balanced diet (rich in omega-3 fatty acids and vitamins C and E, with only modest amounts of saturated fat) and avoiding cardiovascular risk factors (e.g. cease smoking and control diabetes well).

General practitioners can be a powerful motivating force in encouraging individuals to pursue these sage approaches. An individual program can be constructed. This could include:

• walking for 40 minutes

• dining with others at least five times a week

• attending the elderly citizens’ club (or similar) twice a week

• recommencing knitting as a leisure activity

• doing three sudokus a week

• eating a freshly prepared salad five times a week

• moderate use of alcohol—3–5 drinks a week

• taking a daily multivitamin/mineral and omega-3 supplement

• going on an (accompanied) country trip, for a week, within the next year.

Pharmacological

The great advance in dementia therapy has been the development of acetylcholinesterase inhibitors (AChEIs).⁵ In AD, and also in DLB and vascular dementia, there is a deficiency of acetylcholine (ACh). This is due to damage either to the central nucleus (nucleus basilis of Meynert) that produces the enzyme that makes ACh (in AD and DLB) or to the axons within which this enzyme is transported (vascular dementia). The AChEIs boost ACh levels by inhibiting another enzyme, at the synapse, which degrades ACh. These agents include donepezil (Aricept®), galantamine (Reminyl® or Razadyne®) and rivastigmine (Exelon®). They differ somewhat in action, with galantamine also stimulating nicotinic receptors and rivastigmine also inhibiting another enzyme that breaks down ACh (butyrylcholinesterase), but no study has convincingly demonstrated that one agent is superior to others. At this time, only rivastigmine is given more than once daily, but a once-daily patch preparation is marketed in many countries. These agents have predictable cholinergic side effects, including nausea, vomiting, abdominal pain, diarrhoea, anorexia and weight loss. Such symptoms can be significant in about 20% of patients but usually attenuate over 1–2 weeks. More serious and rarer adverse effects include bradycardia, peptic ulceration and precipitation of asthma, so they should not be used in patients with such conditions until the illness is well controlled (e.g. Helicobacter eradication or insertion of a pacemaker).

The efficacy of the AChEIs is significant but modest. On average, there is a stabilisation of cognition for 6–12 months, then a continued decline that would be worse if the agent was ceased. Some do show a clinically apparent improvement and, indeed, the Australian Pharmaceutical Benefits Schedule (PBS) requires that this be demonstrated for subsidised supply to be continued beyond the first 6 months. The scheme requires that these agents only be used in those with mild to moderate AD and that the initial MMSE be above 9 (but lower MMSE is acceptable if due to a non-cognitive cause such as aphasia). The MMSE must improve by two points or more within the first 6 months for subsidised supply to continue. For those with an initial MMSE score above 24, it is harder to show a two-point improvement (ceiling effect), so a baseline ADAS-Cog (another cognitive scale with scores ranging from 0 to 70 and used mainly in research settings) is recommended, with a four-point improvement required. The ADAS-Cog can be performed by some medical specialists and memory clinics, or by some psychologists. Once sufficient initial improvement on one of these scales has been demonstrated, no further scores are required by the PBS (or the DVA equivalent, the RSPB) but the prescriber must confirm, each time a new script is authorised, that the patient still has mild to moderate AD. It is not inappropriate to continue these agents until the end stages of dementia, especially as trials have suggested that they may also have beneficial effects on behaviour and function. Recently, donepezil has gained marketing approval for severe AD, based on recently published trials where it was initiated in those with severe AD.

The other drug with marketing approval for AD is memantine (Ebixa®). It only has marketing approval for moderately severe AD, based on trials where it was used as monotherapy rather than as add-on therapy (to an AChEI). There is trial data, however, to support its use in milder AD and as add-on therapy and, indeed, it is increasingly being used this way. The agent works on a different neurotransmitter system (the glutamatergic system), which is also affected by AD. It has remarkably few side effects. Efficacy has been demonstrated on cognition and behaviour.

None of these agents (AChEIs or memantine) has approval in Australia for other dementias, but in some countries memantine has approval for vascular dementia. There are trial data to support AChEI use in DLB (and in PDD), where there is a cholinergic deficit and where AD pathology is usually also present. No agent has yet proved beneficial in preventing progression from MCI to dementia.

The other pharmacological area of management is the use of atypical antipsychotic agents for the behavioural disturbances (‘challenging neuropsychiatric symptoms’) that can complicate dementia.⁶ Several trials have demonstrated modest efficacy of low doses of risperidone for agitation, aggressive and psychosis complicating more severe dementia, and there is also some (but less) data to support olanzapine and haloperidol. As these agents are usually used for weeks and months rather than days, side-effect profiles must be considered, and the extrapyramidal effects of haloperidol make it usually an inappropriate choice. While quetiapine has some support due to it almost completely lacking extrapyramidal adverse effects, there are almost no data to support its efficacy for this syndrome.

The antipsychotic agents should only be used when non-pharmacological approaches have failed. Adverse effects include an increased risk of cerebrovascular events and death, which affects all agents recommended for these symptoms (all antipsychotics including older agents, and the benzodiazepines). The agents should therefore be used in low doses (risperidone 0.25 mg b.i.d. up to 1 mg b.i.d., olanzapine 2.5 mg daily up to 10 mg daily) and they should be back-titrated and ceased as soon as possible (e.g. target symptom controlled for 1–2 months). Because of their risks, consent for their use should be sought from family and, if feasible, the patient.

Other agents for behavioural disturbance have much less supportive efficacy data and include benzodiazepines (some role for anxiety), antidepressants (appropriate for depression, which not infrequently complicates dementia) and mood stabilisers (e.g. valproate). A psychogeriatrician or geriatrician can be a useful resource if behavioural disturbances are proving difficult to manage.

Complementary therapies

A number of products are purported to have efficacy in those with dementia (usually the dementia type is not specified, or merely for ‘memory problems’). These include:

• Ginkgo biloba—this herbal preparation from the bark of a tree does have some trial evidence of efficacy in dementia. The preparation used in one trial was Egb 761, at doses of 120–240 mg/day. The product is marketed as Tebonin® and efficacy was about half that of the cholinesterase inhibitors. There was no significant toxicity. Other ginkgo preparations vary in content and efficacy has been inadequately trialled.

• brahmi—this preparation has no positive published trial evidence but is often used. It is derived from an Indian plant and recommended dosing is 400 mg daily. Adverse effects include nausea, fatigue and urinary frequency but are insignificantly more frequent than with placebo.

• Curcumin—this component of turmeric, an Indian spice, may be beneficial—consumption was found to be associated with a lower risk of having AD, and in vitro studies support efficacy. There is no significant toxicity but there is no recommended dose.

• polyphenols—these antioxidants are found in a wide range of plant products including berries, tea and also wine. Highest concentrations are in thin-skinned berries (they have a ‘sunscreen’ effect) such as blueberries and pinot noir grapes. Epidemiological studies have associated higher consumption with reduced risk of developing dementia but no prospective study has established therapeutic benefit. A number of commercial preparations include polyphenols.

• vitamins—consumption of vitamins E and C, as food or tablets, has been associated with a lower risk of developing dementia. There is less, but some, evidence for consumption of B-group vitamins including B₆ and folate. One study in severe dementia ⁷ showed that high doses of vitamin E (2000 IU/day) reduced risk of progression to greater dependency or nursing home care, but this has not been replicated. Vitamin E was not effective, in another trial,⁸ in preventing conversion of MCI to dementia, and in the Heart Protection Study⁹ multivitamin supplements did not prevent cognitive decline.

High doses (above 400 IU/day) of vitamin E have been shown in a meta-analysis ¹⁰ to be associated with increased mortality and other adverse events, so daily doses should not exceed this.

• aromatherapy—there is some support in the literature for this for behavioural problems, especially lavender oil. This can be rubbed on or administered as a vapour but be sure that it cannot be inadvertently consumed.

• other environmental therapies—bright light, music, pets and other approaches have been successfully used to modify agitation and aggression, and improve sleep in those with dementia. Music is more effective if items that the person has liked are used (i.e. individualised), and light seems more effective in the morning, or all day, than in the afternoon. One recent study in a residential care facility ⁶ demonstrated that bright light in common areas improved sleep more in those with more severe dementia, adding 16 minutes of sleep each night, on average. This compared very favourably with 4.5 minutes of sleep added by the use of temazepam in one study of older people.

Ongoing review/monitoring

Ongoing review/monitoring is important for all those with dementia. The disease inevitably progresses and both carers and the patient face new challenges as this occurs. Progress can be quantified with the MMSE repeated 3–6 monthly but other issues should also be enquired about—behaviour, function, comorbidity, medications, caregiver stress, support services. It is helpful to interview the caregiver and the person with dementia separately. Eventually, most people with dementia require residential care, and an aged care assessment team (ACAT) referral is needed to allow this. The ACAT should also be involved earlier to facilitate extra home supports such as through community aged care packages and extended aged care at home (dementia).

Important pitfalls

• In diagnosis, it is easy to incorrectly diagnose vascular dementia because an infarct/lacune is seen on neuroimaging. The history is vital—if it suggests AD, the ischaemic lesion is probably incidental.

• A low MMSE does not diagnose dementia—other causes include poor education, very old age (a normal MMSE at 90 can be 20 or 21) and coming from a culturally and linguistically diverse background. When in doubt, seek a specialist opinion.

• AChEIs should only be used when dementia is diagnosed—not for other cognitive disorders.

• Memantine may not be offered because the doctor feels the family and/or patient cannot afford it.

• Antipsychotic agents are often used too early, without a trial of non-pharmacological management, or for too long (sometimes years). Behavioural disturbances do not usually persist in those with dementia and attempts to cease the agent need to be frequent.

• Caregiver stress is not always adequately recognised or addressed. A well supported caregiver can delay institutionalisation of the person with dementia, improving their quality of life. National Alzheimer’s disease associations are a valuable source of information to assist caregivers, and all caregivers should be aware of them.

Prognosis

The average time course of dementia, from first symptoms to death, is less than 10 years (around 7–8 years for AD, more variable for vascular dementia and shorter for DLB and FTD) but there is much variability. If the diagnosis is correct, sustained improvement is extremely rare—it is only transient when there is a response to an AChEI.

New therapies on the horizon offer great promise for those with AD. These include immunotherapies to remove amyloid inhibitors of the secretases that cleave off Ab and agents to solubilise amyloid. It is likely that these agents will be truly disease modifying or even curative if used early enough.

Patient education

Most Alzheimer’s associations offer a range of fact sheets on their websites (see the Resources list for an example). These cover most of the issues relevant to the person with dementia and their caregivers, and are updated regularly.

INSOMNIA

Insomnia is a subjective lack of sleep associated with daytime tiredness. Poor sleep is a common complaint of older people, with up to 50%, in community surveys, saying they regularly sleep poorly. Sleep does change with age, towards less refreshing and more interrupted sleep, with daytime napping, but insomnia is not inevitable. Poor sleep is even more common in residential and acute-care settings.

AETIOLOGY

There are changes in circadian rhythm with ageing that tend to move older people to earlier retirement to bed, then many hours spent awake in the morning before rising. Thus, sleep time may be normal but the longer time in bed can be perceived as insomnia. Most insomnia in older people is accompanied by pain and/or physical illness and other comorbidities, although it is arguable as to whether these are the cause of the insomnia. Common conditions associated with insomnia are shown in Box 57.4. The main aetiological factor behind insomnia, however, is probably the sleep changes that occur with ageing. It should also be remembered that sleep quality and mental health are intimately related. Although depression is a common cause of insomnia, insomnia is a common cause of depression. Therefore, the assessment of sleep problems should never ignore mental health issues, and the management of mental health issues should always involve behavioural approaches to improve sleep.

BOX 57.4 Conditions that may cause insomnia

• Advanced sleep phase

• Alcohol (initially promotes sleep, then rebound insomnia)

• Antidepressants (some—e.g. SSRIs)

• Anxiety disorders

• Arthritis and other musculoskeletal pain

• Bedding/bed

• Behavioural factors

• Beta-blockers

• Caffeine

• Circadian rhythm sleep disorders

• Delayed sleep phase

• Delirium

• Dementia, including DLB

• Depression

• Diet

• Early retirement to bed

• Environmental factors, especially in institutions

• Gastro-oesophageal reflux

• Lack of exercise

• Lack of exposure to sunlight

• Medications & other substances

• Nicotine

• Nocturia, urinary retention

• Nocturnal angina

• Nocturnal breathlessness

• Noise, light, ambient temperature

• Other painful conditions

• Parkinson’s disease

• Peptic ulceration

• Periodic limb movements

• Physical illness

• Pruritus

• Psychiatric and cognitive disorders

• REM sleep disorders

• Restless legs syndrome

• Time zone change syndrome

• Use of bed for other activities

• Withdrawal from medication (e.g. benzodiazepines)

DIAGNOSTIC APPROACH

The main aim is to establish that the person does indeed have insomnia. This can be established most accurately by having the person keep a sleep diary, detailing time to bed, (estimated) delay in falling asleep, awakening times and naps by day. Occasionally a more formal sleep study is useful—this requires referral to a sleep centre/specialist. A medication review is also important, as prescribed medicines (such as antidepressants and steroids) may cause insomnia.

History and examination

Comorbid conditions should be sought through history and examination, which may need to be quite directive (e.g. ‘Do you drink caffeine later in the day?’ is less useful than ‘Do you drink tea/coffee/chocolate after 4 pm?’).

The examination needs only to be limited—areas to be assessed include tenderness (pain), cardiac (congestive cardiac failure), respiratory (chronic obstructive airways disease) and cognitive function.

MANAGEMENT ¹¹

Prevention, self-help and lifestyle

Insomnia can be both prevented and managed by a range of sleep hygiene techniques as outlined in Box 57.5. The individual should be persuaded to go to bed at a comfortable time (e.g. 11 pm) and rise at a regular time that allows sufficient but not excessive sleep (e.g. 7 am). Long hours spent reading or watching TV in bed should be discouraged. If there is regular daytime napping, this could be reduced by engaging in other activities—e.g. a walk after lunch rather than a nap. Preparation for bed can include a hot (non-caffeinated) beverage and listening to relaxing music (before, not in, bed). At least 30 minutes daily of moderate activity (e.g. a walk), preferably in sunlight, should be encouraged. Often people are relieved to know that if they feel refreshed by 6½ hours sleep nightly, that is all they need—not 8–10 hours, as some of their friends may be requiring. Patients need to be reassured that sleep requirement may change with age.

Insomnia can be transient but if it persists (certainly beyond 2–4 weeks) it should be addressed, especially as it has been associated with adverse health outcomes (see ‘Prognosis’ below).

Pharmacological

When sleep hygiene fails, pharmacological therapy for insomnia should be considered—as an add-on rather than an alternative. There are a range of prescribed hypnosedatives including the benzodiazepines and the benzodiazepine-like ‘Z’ drugs (e.g. zopiclone, zolpidem). All other prescribed drugs (e.g. antidepressants, antipsychotics) and many OTC drugs (antihistamines) are not recommended, because of adverse effects and limited efficacy.

If a benzodiazepine is felt necessary, the preferred agents have relatively short half-lives (e.g. temazepam rather than nitrazepam or flunitrazepam) and should not be used in high dosages (e.g. temazepam 10 mg only—not repeated overnight). This is mainly due to concerns about adverse effects which, for all benzodiazepines, include falls, fractures, motor vehicle accidents and cognitive impairment. The agents are only modestly effective—one study found only 4.5 additional minutes of sleep with temazepam and another no difference from placebo, but most show about 30 minutes per night of extra sleep. Few studies with significant numbers of elderly people have extended beyond 2 weeks and these drugs are only approved for short-term management of insomnia. The patient should be warned of adverse effects when they are begun, and agree to a clear plan to cease them after a short period.

The ‘Z’ drugs have not been demonstrated to be safer and have their own additional adverse effects—zolpidem, for instance, has been associated with abnormal nocturnal activities, including eating and even driving, while asleep. There have been fatal accidents. Again, they should be used only in the short term.

Complementary therapies

Valerian has modest efficacy for insomnia, and is almost devoid of adverse effects. It can be taken as a tablet or a tea.

Melatonin is also useful for insomnia. It may work by re-establishing circadian rhythms, but this is not proven. Adverse effects are rare, although coronary vasospasm has been reported. Dose is 1–2 mg nocte.

Bright light therapy is also useful—see the section on dementia.

ONGOING REVIEW AND MONITORING

The main purpose of ongoing review and monitoring is to ensure that hypnosedative agents are ceased, and to support the patient who (incorrectly) feels certain that they require medication in order to sleep.

IMPORTANT PITFALLS

A complaint of poor sleep alone does not make a diagnosis of insomnia—additional information should be sought.

Sleeping tablets are begun too easily, without the patient (and sometimes the prescriber) being aware of their risks, and the difficulties that can occur in attempting to cease them. Sleep hygiene should always be tried first, and continued even when a hypnosedative is prescribed.

PROGNOSIS

Insomnia is not entirely benign—studies have shown increased mortality in those with chronic insomnia. Bad sleeping habits, once established, can certainly be difficult to change.

DIABETES AND THYROID DISORDERS

These are discussed in detail in other sections of this book (see Chs 26 and 29) —the following discussion will briefly cover areas unique to older people.

DIABETES

Diabetes is diagnosed in about 20% of people aged over 65 years, and undiagnosed in up to a further 20%. It is usually type 2, largely due to insulin resistance.

Diagnosis usually follows reporting of symptoms or routine checking of fasting and random glucose levels. Older people may present newly with very high blood sugar levels but rarely with ketoacidosis. Lacticacidosis and non-ketotic coma need to be considered in an unwell elderly person even if diabetes has not yet been diagnosed. Other rarer initial presentations, which can also complicate established diabetes, include malignant cachexia (extreme muscle wasting), femoral neuropathy with marked proximal lower limb weakness and peripheral neuropathy. Diabetes is also a risk factor for dementia.

Management is directed at controlling sugar levels without significant risk of hypoglycaemia, which is poorly tolerated in older people, especially if recurrent. Therefore, target glucose levels may be a little higher (e.g. 8–12 mmol/L). Although the oft-cited UK diabetes study supported some benefits of tighter sugar control, it did not include a population typical of the older diabetic and was not conducted in ways that mimicked usual clinical practice.

Pharmacological management is indicated when diet and other lifestyle changes fail to control sugar levels, and initial therapy is usually with a sulforylurea and/or metformin.¹² Only shorter-acting sulforylureas should be used (e.g. gliclazide)—even glibenclamide (gliburide) has too long a half-life, and therefore too high a risk of inducing hypoglycaemia, in older people. If maximal doses of these fail to achieve control, consideration should be given to adding a ‘glitazone’ such as rosiglitazone, but recent concerns about increased mortality and cardiac adverse events from these agents should be considered. These agents should be avoided if there is heart failure, and the patient should be monitored for fluid accumulation. If oral therapy is failing, insulin should be added. Initially, once-daily longer-acting insulin should be trialled. There is synergism with metformin, which can therefore be continued, but not with the sulfonylureas, which should be ceased. If hypoglycaemia occurs despite insulin dosage adjustments, one of the newer semi-synthetic insulins (e.g. insulin glargine) should be substituted, as these have less risk of causing severe hypoglycaemia.

Other complementary therapies are discussed in Chapter 26, Diabetes in General Practice: the integrative approach by Kerryn Phelps and Craig Hassed.

Diabetic complications should be carefully monitored—the patient should see an eye specialist regularly and urine should be checked for microalbumin. Peripheral sensation should be assessed—a monofilament is useful for this. Older people may have reduced flexibility, impairing regular feet checks—this may require a carer or, less satisfactorily, regular podiatry visits. Diabetic leg ulcers require urgent and comprehensive management, which may include referral to a wound management specialist or a wound/diabetic ‘high-risk foot’ clinic. Cognitive symptoms should lead to an MMSE or other screening tool, and referral to a memory clinic or other memory specialist if indicated.

At the end of life, diabetic control may be less important, although uncontrolled hyperglycaemia does not lead to a quality death and usually some therapy is continued.

THYROID DISORDERS ¹³

In older people, hypothyroidism is usually due to autoimmune thyroid disease (Hashimoto’s thyroidism) but may be due to past radioactive iodine (¹³¹I) therapy, lithium toxicity or to amiodarone—other causes are rare. Hyperthyroidism is usually due to a toxic multinodular goitre or autoimmune (Graves’) disease; again, amiodarone and other sources of iodine should be considered.

The diagnosis can be difficult—often there is only a single major clinical manifestation (e.g. rapid atrial fibrillation or confusion) and the signs of hypothyroidism can be confused with ageing. Unusual presentations are not uncommon (e.g. depression, paranoia or leg ulceration). Fortunately, specific, sensitive blood tests are now available, and are frequently performed. An elevated TSH is usually diagnostic of hypothyroidism (but this is best confirmed with a low free T₄) and a low TSH is usually diagnostic of hyperthyroidism (again, best confirmed with either an elevated free T₄ or free T₃). Autoantibody test results rarely affect clinical management. A thyroid ultrasound can be useful in distinguishing a toxic multinodular goitre from autoimmune thyroiditis.

Referral to an endocrinologist is usually appropriate for further diagnostic tests as well as an initial management plan. Management of both is rarely urgent—occasionally severely unwell patients (e.g. myxoedema coma or ‘madness’) require hospitalisation. Any offending agent (e.g. amiodarone) should be ceased/avoided where possible, but this may not be sufficient to achieve control. Hypothyroidism requires thyroxine therapy but it is vital to start in low doses, to avoid cardiac complications, and increase slowly, using the TSH and symptoms to monitor effectiveness. A starting dose of 25 μg daily, increased by 25 μg every 2–4 weeks, is usually sufficient. Larger initial doses can precipitate coronary ischaemia and death. Hyperthyroidism is usually initially managed with medication—carbimazole or propylthiouracil along with a beta-blocker if there is sympathetic activation. Longer-term management with ¹³¹I is often appropriate in older people, as delayed hypothyroidism is less of a risk in those already of advanced age, and the risks of polypharmacy (see above) lead prescribers to prefer non-drug therapy. Surgery is rarely indicated—except where there is superior mediastinal pressure on the trachea or oesophagus.

Ongoing monitoring is essential—for hypothyroidism the TSH should be checked and the thyroxine dose adjusted, and for thyrotoxicosis (especially after ¹³¹I) emergent hypothyroidism needs to be detected early and treated (with thyroxine).

Thyroid cancer is usually euthyroid and more commonly presents as a mass or as metastatic disease, but should be considered in older people with a neck mass and thyroid dysfunction. Early diagnosis and treatment is vital.

WOUNDS

The management of wounds requires a holistic approach as there are usually many contributing factors to the non-healing wound. Chronic ulcers (wounds present for more than 4 weeks) are particularly troublesome. Not only are they expensive for the individual and the community, but they cause significant psychological and physical morbidity.

IMPORTANT CONDITIONS

Common types of acute wounds include: surgical (not discussed here), traumatic (such as skin tears in the elderly) and burns (not discussed here).

Skin tears are very common in the elderly. The most common cause of chronic leg ulcers is chronic venous insufficiency.

Pressure ulcer incidence is reported to be up to 38% in acute care.¹⁴ In 2006 the Pressure Ulcer Point Prevalence Study (PUPPS) found a prevalence of 26% in public hospitals.

Approximately 15% of individuals with diabetes will develop an ulcer at some point.

AETIOLOGY

Common chronic wounds, according to aetiology, include:

• vascular insufficiency—venous, arterial or vasculitis

• pressure—decubitus ulcers or bedsores

• diabetes related.

PATHOLOGY

• Chronic venous insufficiency causing venous hypertension results in leg oedema, haemosiderin staining and lipodermatosclerosis.

• Peripheral atherosclerosis results in decreased blood supply to the extremities.

• Direct pressure, friction and shear forces and moisture combined in the immobile patient increase the risk of pressure ulcers.

• Patients with diabetes frequently have neuropathy leading to unrecognised trauma, often combined with poor arterial supply and a less effective immune system.

DIAGNOSTIC APPROACH

History

History should aim to identify the aetiology of the wound and current barriers to healing. Factors suggestive of chronic venous insufficiency include varicose veins, previous deep vein thrombosis, surgery or trauma to the limb, obesity, long periods of standing (enquire about employment history) and increased intraabdominal pressure. These wounds frequently commence spontaneously. Risk factors for peripheral vascular disease are as for cardiovascular disease: hypertension, hyperlipidaemia, smoking, family history and diabetes. Enquire about previous amputations. Patients with foot lesions should be questioned regarding causes of neuropathy. Patients with diabetic foot wounds generally have peripheral neuropathy, a history of initiating trauma and often poor arterial supply or infection.

Patients with pressure areas will have reasons for immobility or inability to reduce pressure or neuropathy. Common examples include fractured neck of femur, stroke and spinal lesions. Patients with severe dementia or inability to communicate are also at high risk. Other risk factors for pressure areas include incontinence, temperature abnormality, poor nutritional intake and multiple medical comorbidities.

Skin tears occur in those with frail skin (check for steroid use, warfarin and nutritional status) and are initiated by trauma. Common causes include wheelchair footplates and screws on walking frames.

Pain is common in chronic wounds. This may be background pain or associated with dressing changes or particular dressing products.

Nutritional and hydration status should be reviewed. Adequate vitamin C, zinc and protein are needed for wound healing, and it can be delayed by psychological stress.

Enquire about the current dressing regimen and who applies them. Ideally, gain further history from this person. Also note which dressings have been tried so far and the effects of each.

Examination

General examination should include the cardiovascular system, including peripheral pulses and fluid status.

The common sites of pressure areas if the patient is supine are heels and sacrum. Grade the pressure area (1–4).

• Grade 1 indicates non-blanchable erythema of intact skin.

• Grade 2 is a loss of epidermis and dermis.

• Grade 3 is full thickness skin loss, which may extend to fascia.

• Grade 4 is full thickness skin loss and tissue necrosis down to bone or joint capsule.

The appearance of the surrounding skin often gives an indication of aetiology. Chronic venous insufficiency causes haemosiderin (brown) staining of the lower third of the leg, lipodermatosclerosis, venous eczema and scaly skin. Deformities of the feet and areas of callus indicate areas of pressure.

The wound itself should be described, including: location, dimensions (including depth), edge, the presence of slough or necrotic tissue, signs of infection or inflammation and the volume and type of exudates.¹⁵

Skin tears may be graded according to the amount of skin lost; the STAR tool by the Silverchain group is useful.¹⁶

Review footwear if implicated in wound formation.

INVESTIGATIONS

Consulting room

An ankle brachial index (using Doppler ultrasound) compares the blood pressure in the dorsalis pedis or posterior tibialis to that in the brachial artery. An index of 1.0 indicates normal arterial supply. A ratio higher than this may indicate calcification of the vessels. A result lower than 0.8 means reduced arterial supply and implies that any application of compression should proceed with caution.

PATHOLOGY

Inflammatory markers, electrolytes, renal function, liver function and albumin may be warranted. Blood sugar level (BSL) and glycosylated haemoglobin are measured in those with diabetes.

A biopsy of the edge of the wound will help determine whether malignancy is present. Culture of biopsy tissue will give more accurate information regarding organisms causing infection. A wound swab will provide information regarding the types of organisms on the surface of the wound, but not necessarily those deeper in the tissue.

Special tests

Vascular imaging of veins and arteries may clarify the aetiology of the wound and outline potential surgical options.

If osteomyelitis is suspected, the best test is MRI—however, the initial starting point is more likely to be X-ray or bone scan.

INTEGRATIVE MANAGEMENT

Prevention

Compression hosiery is not only comfortable, but will reduce the risk of further venous ulcers in those with chronic venous insufficiency.

Peripheral vascular disease may be minimised through control of cardiovascular risk factors.

Pressure area prevention is the cornerstone of management. Braden, Norton and Waterlow scales will stratify the risk of pressure areas. Air mattresses and cushions, gel cushions, bed cradles and orthotic devices have become part of pressure care of the immobile patient. Nursing care such as turning patients and adequate nutrition is still vital.¹⁴

Diabetic patients must be educated regarding footwear, blood sugar level management, and the benefits of regular podiatric care and early recognition of foot trauma.

Non-surgical management

Many wounds will heal eventually if nothing is done other than protective dressings. However, wounds which are due to untreated arterial insufficiency, unrelieved pressure and undiagnosed malignancy are unlikely to heal without intervention.

Self-help/lifestyle

Lifestyle factors such as smoking cessation and ensuring adequate diet and hydration ¹⁷ help wound healing. Exercise is beneficial for venous leg wounds in particular.

Pharmacological

Analgesia may be required. Some medications are known to cause wounds (such as hydroxyurea) or to affect wound healing (such as prednisolone). The indication for these medications should be reviewed.

An appropriate wound dressing should be chosen to prepare the wound bed for healing. A plan for long-term management should then be developed. This will encompass the likelihood of healing or other surrogate goals.

Surgical

Vascular surgery for chronic venous insufficiency and peripheral vascular disease may be required. Skin grafts and flaps may be needed. Occasionally amputation is the only option.

Other medical

Specialist wound clinics generally contain a multidisciplinary team with up-to-date knowledge of the latest wound products and research. Further referral to hyperbaric oxygen may be recommended.

Paramedical

Chronic wounds in the elderly frequently require a multidisciplinary approach. Nursing care is often required for dressing changes, pressure care or diabetic education. Podiatric involvement is vital in the management of diabetic feet and in footwear advice. Dieticians are of particular benefit to those with pressure areas, patients with diabetes and those who are undernourished or obese. Pharmacists with an interest in wound care will be able to advise on wound dressings and costs. Specialised physiotherapists may advise on massage techniques for lymphoedema.

Complementary therapies

Wound dressings are a fast-growing industry.¹⁵ Complementary therapies are also becoming more ‘mainstream’. For example, manuka honey is being developed in new and more user-friendly preparations. Although research is somewhat lacking regarding the true mechanism of action, it is thought to have antimicrobial activity due to the slow release of hydrogen peroxide.¹⁵

Dietary supplements are also now considered virtually mainstream in the management of pressure areas. Commercial products containing arginine (an amino acid), vitamin C and zinc have been proved to aid the healing of pressure areas.¹⁸ Caution is required with the supplementation of zinc, as its benefit is probably only in those with deficiency and the appropriate dosage is not established. High-dose zinc may be associated with nausea and may result in copper deficiency (which can cause anaemia).¹⁹ However, topical zinc oxide preparations may be helpful.²⁰

Horse chestnut is thought to be useful in chronic venous insufficiency. Liver function tests and coagulation profile should be monitored.²¹

Ongoing review/monitoring

The risk of future wounds due to chronic venous insufficiency can be reduced with surgical correction of varicose veins or lifelong use of correctly fitted compression stockings.

Patients with arterial insufficiency should avoid trauma.

Patients with pressure areas frequently have irreversible predisposing conditions. Constant review of pressure areas and scrupulous pressure care are therefore required.

Patients with peripheral neuropathy (diabetes being the most common cause) must inspect their feet daily (or have someone inspect their feet for them). Any trauma must be addressed quickly. Particular attention must be paid to footwear and callus formation (ulcers may form under callus). Regular podiatry review is recommended.

IMPORTANT PITFALLS

Failure to identify the aetiology of the wound, or barrier to healing, is the most important pitfall. For example, if osteomyelitis is present, the overlying ulcer will not heal. Mixed venous and arterial disease is common in the elderly and limits the use of compression. The arterial component is often under-recognised. The principles of moist wound healing do not apply to the dry eschar of digits or heels in ischaemic limbs. These wounds are best kept dry, to limit the risk of infection. Cheaper wound dressings may need to be applied more frequently and slow wound healing, thus increasing the overall cost.

PROGNOSIS

Prognosis is governed by the ability to address the underlying aetiology. Healing may not be possible; substitute goals such as pain relief and exudate management may be more achievable.

PATIENT EDUCATION

Educate regarding wound dressings or compression therapy and the benefits of smoking cessation.

CONTINENCE

Urinary or faecal incontinence is the involuntary or inappropriate loss of urine or faeces. Over 50% of residents of aged care facilities suffer from incontinence and it is one of the major reasons for admission to such a facility. Bladder control problems are thought to treble the cost of care in nursing homes and take up approximately 60% of nursing time. Seventy per cent of incontinence suffers are women, with problems arising after pregnancy and childbirth. Lower urinary tract symptoms increase with age. Incontinence in the elderly frequently has a multifactorial origin. Most importantly, incontinence affects self-esteem, motivation, independence and dignity.

IMPORTANT CONDITIONS

Urinary incontinence:

• Stress incontinence is the leakage of urine with physical exertion such as coughing, laughing, walking or lifting. It commonly affects older women who have oestrogen deficiency or have had children. Being overweight, constipation and chronic cough are also risk factors. Men may have stress incontinence following prostate surgery.

• Urge incontinence occurs when the patient develops a sudden strong urge to urinate; they may not get to the toilet in time. Benign prostatic hypertrophy may cause urge incontinence, but is also associated with detrusor failure (atonic bladder). Detrusor failure is loss of elasticity and may occur with ageing and lower motor neuron lesions. These patients generally have a high residual volume and low voiding pressure.

• Overflow incontinence is the leakage of an overly full bladder that is unable to empty completely. Symptoms include straining to pass urine, a weak stream, feeling that the bladder is not completely empty, no warning to passing urine, passing urine while asleep and frequent urinary tract infections. It may be due to constipation, prostate enlargement, prolapse, damaged innervation of the bladder (such as in stroke, Parkinson’s disease and multiple sclerosis) and medications.

Other:

• Constipation is hardening of faeces and decreased frequency of bowel motions.

• Faecal incontinence is the involuntary loss of faeces. It is commonly associated with constipation, weakened pelvic floor muscles or inadequate sphincter.

BACKGROUND/AETIOLOGY

Continence requires the individual to know where to toilet, be able to get there, be able to hold on to get there and be able to undress and then re-dress. Older people have a reduced bladder capacity, lessened sphincter strength and reduced ability to defer, but environmental factors are often also significant.

The normal bladder empties approximately every 3–4 hours. It has a capacity of 400–600 mL, but feels full at about 200–300 mL. One episode of nocturia is considered normal. A normal bladder does not leak and empties completely.

Normal bowel motions only require a small push to pass. The frequency is from up to three times per day to once every three days.

PATHOLOGY

Sensory urgency is due to a small-capacity bladder or recurrent urinary tract infections.

Overactive bladder (detrusor instability and hyperreflexia) results from spontaneous reflexic detrusor contractions and results in urge incontinence (associated with a sudden strong urge to pass urine). It is often associated with neurological conditions such as Parkinson’s disease, stroke and dementia. Symptoms include urinary frequency and nocturia.

Reduced bladder capacity may result in frequency, nocturia, urgency and urge incontinence (detrusor instability). Hesitancy, slowed stream and terminal dribble may be due to underactive bladder (detrusor failure) or outlet obstruction.

Stress incontinence is due to weakened pelvic floor musculature or intrinsic sphincter failure.

Comorbidities are likely to contribute in the elderly patient. General poor health, frailty, poor mobility, cognitive deficits or renal or cardiac dysfunction may affect continence. Cortical micturition centres exert an inhibitory effect on the sacral reflex arc and may be damaged in neurological and dementing illnesses.

It is generally thought that there is no reduction in bowel movement frequency with normal ageing. The elderly community probably overestimates constipation. However, severe constipation is the most common cause of faecal incontinence, with watery stool flowing around the hard faeces. Constipation has many potential causes; those common in the elderly include inadequate fluid or dietary fibre, immobility, medication, bowel pathology, neurological conditions such as stroke and Parkinson’s disease causing slow-transit bowel and poor toileting habits. Inadequate sphincter function due to poor pelvic floor or neurological condition may also result in faecal incontinence.

DIAGNOSTIC APPROACH

History

Enquire about lower urinary tract symptoms: frequency, urgency, nocturia, voiding difficulties, dysuria, haematuria, urge incontinence, stress incontinence, overflow incontinence and functional incontinence.

Consider reversible causes: delirium, urinary tract infection, atrophic vaginitis in women, psychological (severe depression, neurosis), pharmacological, excess fluid intake or output, restricted mobility or environment, stool impaction.²²

Medical conditions that may affect continence include neurological conditions (especially multiple sclerosis, stroke and Parkinson’s disease), dementia, diabetes, cardiac failure and those that impair mobility. Gynaecological and urological history (including surgery), obstetric and menstrual history, sexual history and previous continence assessments should be taken.

Regarding constipation and faecal incontinence, the history should include the relevant past surgical history. Diet, fluid intake, mobility, duration of constipation, frequency of bowel actions, character of the stool, pain, straining and laxative use are also vital.²³

Consider impact on quality of life—for example, limitation of social activities, sleep disturbance.

Examination

Abdominal examination including per rectal examination: note the size and texture of the prostate in men, and anal tone. The vaginal examination in women should check for urine excoriation, senile changes, infection, prolapse and pelvic floor strength.

Stress incontinence can be checked by asking the patient to stand and cough (ensure there is adequate protection on the floor, to prevent embarrassment). This can also be checked in the supine position when examining.

Check mobility and cognitive function.

The patient may manage urinary incontinence—for example, more frequent or regular voiding, use of continence aids. Laxatives are also available over the counter—many patients may self-medicate. Unfortunately, continence problems may worsen if no changes are made.

Self-help

Eating adequate fibre (fruit, vegetables, lentils and high-fibre breakfast cereal) and fluid (approximately 2 L per day if there are no contraindications) can help avoid constipation. Stopping smoking (reduces coughing) and losing weight also help to reduce incontinence.

If caring for a confused incontinent person, consider labelling the toilet with a sign or picture, keep a light on in the toilet, keep a regular daily routine for eating, walking and toileting. Offer the toilet at predicted toileting times (for example, after breakfast) or times of unsettled behaviour. Ensure that clothing is easy to remove. Encourage double voiding. Restrict fluids after 7 pm.

An occupational therapy assessment of toilet facilities may help with issues such as aids to sitting and standing to void.

Lifestyle

• Exercise and weight reduction.

• Reduce or eliminate caffeine.

• Lifestyle can be inhibited by incontinence—ensuring that the patient is ‘socially continent’ with the use of continence aids is valuable.

Pharmacology

A medication review should be undertaken and altered as appropriate. Drugs may induce urinary incontinence.

• Alpha-blockers reduce urethral resistance.

• Opioids result in constipation.

• Anticonvulsants may cause confusion and ataxia.

• Calcium channel blockers may cause constipation and urinary retention.

• Loop diuretics increase urgency.²²

Cholinesterase inhibitors (donepezil, galantamine, rivastigmine) are reported to increase urinary frequency and perhaps urinary incontinence. There is now evidence that anticholinergic treatment for urinary incontinence in this situation may be helpful—although it does seem illogical.²²

Topical oestrogen (cream applied to the vaginal entrance or using vaginal applicators) may improve symptoms of urgency and stress incontinence and help prevent future episodes of cystitis.

Antibiotics should be used to treat urinary tract infections and should be accompanied by probiotic support.

Detrusor instability is best managed with anticholinergics, such as oxybutynin. Newer agents such as solifenacin succinate are claimed to be more specific to muscarinic receptors in the bladder and thus have fewer of the systemic anticholinergic side effects, such as confusion and dry mouth. Anticholinergics should not be used in those with previous closed angle glaucoma or atonic bladder, or those with any cause of increased post-void residual volume.

Botulinum A toxin injections into the bladder neck or detrusor have also been reported to manage detrusor instability.

Benign prostatic hypertrophy may be managed with alpha-1 blockers; androgen blockade is used in cases with clinically enlarged prostate.²²

Sensory urgency may benefit from a urine alkaliniser, which helps reduce the irritability of the urine.

Treatment of autonomic dysfunction is appropriate if present in nocturnal polyuria. Desmopressin is reported to help, but is not generally recommended in the elderly, due to the risk of hyponatraemia.

Aperients can be used in the short-term to manage constipation. Options include stimulants such as senna, psyllium, bulking agents and osmotic agents. Enemas and suppositories may be needed for impaction.

Surgical/other medical

Referral to a specialist continence clinic for multidisciplinary assessment is appropriate, especially if lower urinary tract symptoms have not responded to conventional treatment such as bowel management, bladder training, pelvic floor exercises and anticholinergic medication. Geriatricians, physiotherapists, urologists, urogynaecologists, gynaecologists, gastroenterologists and colorectal surgeons may be needed. Surgical opinion may be required if other measures have failed. Operations include prostate surgery, surgical correction of prolapse and sphincter repair.

Paramedical

• Continence physiotherapy for training of the pelvic floor—may use aids such as electrostimulation, pressure biofeedback or weighted vaginal cones.

• Continence nursing for education and advice regarding continence aids such as pads, pants, bedpads and chairpads, protective bedding, condom drainage and catheters; also skin care and odour management.

• Occupational therapists may advise regarding raised toilet seats, commodes and urinals.

• Dietician for dietary advice.

• Faecal impaction causing faecal incontinence being mistaken for diarrhoea.

• Urinary incontinence due to overflow from urinary retention.

• Applying too much barrier cream or talcum powder—will transfer to the continence pad, restricting absorption.

PROGNOSIS

Not all cases of incontinence may be treatable, but many will be manageable. An incontinent individual may be able to be ‘socially continent’ or ‘dependently’ continent.

PATIENT EDUCATION

• Bladder retraining is aimed at increasing the storage capacity of the bladder for management of urge incontinence.

• Pelvic floor exercises.

• Intermittent self-catheterisation or managing a permanent indwelling catheter, for management of overflow incontinence.

• Appropriate defecation techniques and normal bowel habit—for example, when sitting on the toilet, place the elbows on the knees, lean forward with a straight back and put feet on a stool. Passing a bowel action should take less than one minute. Wipe from front to back. The strongest urge to defecate will occur approximately 30 minutes after eating, particularly breakfast. A hot drink may also stimulate a bowel movement.

CARDIOVASCULAR

Important cardiac conditions in the elderly include ischaemic heart disease, heart failure, valvular heart disease and arrhythmia, especially atrial fibrillation.

BACKGROUND/AETIOLOGY

Important risk factors for ischaemic heart disease are: age, gender, hypertension, dyslipidaemia, smoking, poor mental health and diabetes mellitus. Heart failure can be divided into ischaemic and non-ischaemic causes. Common non-ischaemic causes are hypertension and valve disease.

PATHOLOGY

Ischaemic heart disease (IHD) results from coronary atherosclerosis and usually becomes symptomatic once a stenosis occupies 70% or more of the vessel lumen. Elderly patients often have significant vessel calcification, which can increase the difficulty of interventional procedures.

Heart failure may be caused by:

• systolic dysfunction—characterised by reduced left ventricular contraction

• diastolic dysfunction—characterised by impairment of left ventricular relaxation and raised left atrial pressure

• a combination of systolic and diastolic dysfunction.

Risk factors for diastolic heart failure are increasing age, female gender, hypertension and diabetes mellitus.

Degenerative valvular disease is a common finding in the elderly. Calcific, degenerative aortic stenosis (AS) is the most common valvular disease. Mitral valve disease is also common and may result from degenerative processes causing prolapse and flail leaflets, ischaemic papillary muscle dysfunction or dilatation of the mitral annulus due to cardiac enlargement.

Atrial fibrillation (AF) is frequently found in elderly patients. Left atrial enlargement, left ventricular hypertrophy and left ventricular dysfunction are associated with an increased likelihood of AF. Sinus node and atrioventricular (AV) node dysfunction increase with age due to degeneration of the conduction system. AV node blocking agents such as beta-blockers, calcium channel blocker and digoxin can exacerbate AV node disease.

DIAGNOSTIC APPROACH

History

History is vital; however, elderly patients frequently present atypically. While the classic IHD presentation may occur, elderly patients may present without pain or with dyspnoea alone. A comprehensive cardiac history should still include questions regarding chest pain, ‘indigestion’, breathlessness, exercise tolerance and classic symptoms of cardiac failure, palpitations, syncope and presyncope. Questions regarding concomitant acute illness, such as pneumonia, are important as these are frequent precipitants of acute cardiac presentations such as heart failure or AF.

Examination

Full cardiovascular examination including pulse (rate and rhythm), fluid status and heart sounds. Postural blood pressure and heart rate are also relevant. The blood pressure and heart rate should be taken initially when lying or sitting and then on standing. After waiting for 3–5 minutes, the blood pressure and heart rate should be repeated. A blood pressure drop of more than 15–20 mmHg is significant. The heart rate should increase to compensate for the initial drop in blood pressure.

INVESTIGATIONS

Consulting room:

• 12-lead electrocardiogram.

Pathology:

• Full blood count (anaemia and platelet count), electrolytes and renal function, cardiac enzymes (creatine kinase and troponin) if suspect acute coronary syndrome.

• Thyroid function tests.

Special tests:

• Further investigations may be appropriate, such as a stress test (exercise or pharmacological ECG, echocardiogram or nuclear myocardial perfusion scan) to investigate ischaemia. An echocardiogram will identify cardiac function and valve pathology. A Holter monitor will record any arrhythmia, but sensitivity is low.

Therapies available for elderly patients in the management of IHD are the same as those for younger patients: antiplatelet therapy (aspirin and/or clopidogrel), statin, beta-blocker, angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker, nitrates.

Medications for heart failure include ACE inhibitors (angiotensin receptor blockers), beta-blockers if euvolaemic (carvedilol, bisoprolol, metoprolol XL), diuretics (for symptom control only).

There is currently no effective pharmacological management for chronic valvular disease.

The best management of AF includes management of the cause. A rate control strategy (beta-blocker or non-dihydropyridine calcium channel blocker ± digoxin) is generally sufficient as it is safer than rhythm control and has similar outcomes. Patients over the age of 75 years with an additional risk factor, such as left ventricular systolic dysfunction, hypertension, diabetes mellitus or previous stroke, benefit from the addition of warfarin therapy. The CHADS2 score helps to assess risk.²⁴ The benefits of anticoagulation must be considered in the context of the patient’s comorbidities. Some studies have suggested that the rate of severe bleeding complication is not as significant as perhaps perceived.²⁵

Complementary therapies

See Chapter 25, Cardiovascular in General Practice: the integrative approach by Kerryn Phelps and Craig Hassed.

Surgical

Several interventions are available for cardiac disease, including percutaneous intervention (angioplasty/stenting) or coronary artery bypass surgery for IHD; revascularisation for ischaemic cardiac failure and biventricular pacemakers for those with dyssynchronous ventricular contraction.

Aortic valve replacement is the only effective treatment for symptomatic severe aortic stenosis. Age is not a barrier to treatment. Surgery should be considered for severe symptomatic mitral regurgitation. Valve repair is preferred over replacement.

Paramedical

Coronary care units are beneficial to the elderly in the acute coronary syndrome setting. Multidisciplinary cardiac rehabilitation and chronic disease community nursing are especially helpful in the management of heart failure. Advice from a dietician may assist with coronary risk factors such as hyperlipidaemia or obesity.

ONGOING REVIEW

Monitoring of symptomatic status, cardiac risk factors, fluid balance and tolerance of medications is necessary. Review patients for the appropriateness of new technologies and drugs.

IMPORTANT PITFALLS

Elderly people may not always present with classic symptoms of ischaemic chest pain. They may present with dyspnoea, syncope or confusion.

Digoxin should be considered a second-line or add-on therapy in the rate control of AF. This is due to the narrow therapeutic range and significant side effects.

Vasodilators such as calcium channel blockers and ACE inhibitors should be used with caution in severe aortic stenosis. Caution should be exercised with beta-blockers in severe aortic stenosis.

Non-steroidal anti-inflammatory drugs may exacerbate heart failure, an additional reason to avoid these agents in the elderly.

Ankle oedema has many potential aetiologies in the elderly, including dependent oedema, venous insufficiency, hypoproteinaemia and heart failure. Unless other signs of heart failure are present, diuretics should be avoided as side effects may outweigh benefit. Leg elevation and compression therapy may be more appropriate.

PROGNOSIS

The goal of therapy in many elderly individuals with cardiac disease is symptom control. There is limited evidence for most treatments specific to the very elderly population.

PATIENT EDUCATION

Some patients with heart failure may be able to follow a management plan based on regular weigh-ins and adjustment of diuretics. Patients taking anginine should be informed of how to take it safely and to sit down when doing so, to avoid problems with hypotension.

PAIN IN THE ELDERLY POPULATION

Pain is an ‘unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. The inability to communicate verbally does not negate the possibility that a patient is experiencing pain and is in need of appropriate pain relieving treatment’ (International Association for the Study of Pain). Up to 50% of older community dwellers and 80% of those in residential care suffer from persistent pain.²⁶

Chronic pain is ‘without apparent biological value and persists beyond normal tissue healing time’ (IASP). Conditions common in the elderly include arthropathy, postherpetic neuralgia (PHN), polymyalgia rheumatica, peripheral vascular disease and cancer.

BACKGROUND/AETIOLOGY

Nociception is the sensation evoked by noxious stimulation of the neural system. Older patients have higher pain thresholds, which may mean they present later for conditions such as acute myocardial ischaemia and peritonitis. However, pain tolerance decreases with age. Older adults appear to be more vulnerable to developing severe and persistent pain. This implies that those older patients who do have pain are more likely to have severe and persistent pain.

PATHOLOGY

Animal and human studies suggest a reduced plasticity of the nocioceptive system and prolonged dysfunction following tissue injury, inflammation or nerve injury in the elderly. Older patients therefore will not recognise mild pain until there is significant damage and will be less likely to recover from it.

Cell-mediated immunity is impaired with ageing, placing the elderly at risk of reactivation of Herpes zoster and development of PHN.²⁷

DIAGNOSTIC APPROACH

Identify and treat the cause of the pain and associated symptoms, if possible. Select the appropriate modes of therapy for pain relief. Review and modify therapy.

History

Identify the onset, cause and time frame, factors that increase and decrease the pain, severity and impact on lifestyle.²⁸ Gain an understanding of which treatment modalities have already been tried, and their effectiveness. Watch for ‘red flags’ indicating serious underlying pathology, such as thoracic pain, pain associated with incontinence or gait disturbance or back pain in someone with known malignancy.

Examination

Use a pain intensity scale to quantify the pain. Examples include verbal descriptor scale and numeric rating scale. Pain scales for those with dementia, or those who cannot verbalise, include: pain assessment in advanced dementia (PAINAD) and the Abbey pain scale. Although these scales are not particularly useful when comparing patients, they are useful for assessing management strategies in an individual.

Look for a zoster-type rash if indicated.

INVESTIGATIONS

These will be guided by the history and examination. Consider inflammatory markers and prostate-specific antigen (in men) in new-onset back pain—serious pathology would be malignancy or discitis. Arrange or review imaging of the area. For example, MRI spinal cord if ‘red flags’ for spinal cord compression are present.

INTEGRATIVE MANAGEMENT

Prevention

Appropriate treatment of acute pain syndromes and acute illness may help reduce the risk of a pain syndrome becoming chronic. Prevention of Varicella zoster virus infection and immunisation against Herpes zoster may decrease the incidence of this condition in the future.²⁷

For mild to moderate pain, simple analgesics such as paracetamol are preferred.²⁸ Glucosamine and paracetamol may provide enough relief for many patients suffering from osteoarthritis pain. Long-term use of non-steroidal anti-inflammatory agents is best avoided in the elderly due to the side-effect profile (gastrointestinal upset, renal failure, fluid retention, hypertension). COX-2 inhibitors have similar issues.

For moderate to severe pain, agents such as codeine or tramadol may be considered. However, side effects including constipation and confusion should be taken into consideration in the elderly. Tramadol is generally avoided in the elderly population due to the incidence of delirium.

Newer transdermal patches of fentanyl or buprenorphine have the advantages of steady-state medication delivery and less frequent dosing ²⁸; however, side effects including delirium may limit their use. Initiation at low dose, and slow titration, are appropriate in the elderly.

Opioids such as oxycodone and morphine may be required in the elderly patient with severe pain. Constipation, nausea and confusion are common unwanted effects. A long-acting oxycodone for background relief and a short-acting oxycodone for breakthrough pain are usually prescribed. A low dose should be used initially in the elderly, due to pharmacokinetic and pharmacodynamic changes related to ageing, caused by altered organ function and volumes of distribution. Initially the dose should be reviewed frequently.²⁹ Aperients are generally prescribed at the same time as opioids, to avoid constipation.

In neuropathic pain syndromes, such as PHN, the combination of opioid and gabapentin or pregabalin is often helpful; tricyclic antidepressants (TCA) and tramadol have also been shown to be of use.³⁰ However, these agents may cause confusion in the elderly and the TCAs have undesirable potential cardiac side effects. Topical capsaicin and lignocaine also show promise.²⁷,³⁰