Oxford Handbook of Geriatric Medicine (2 edn)
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Falls and fallers
A fall is an event that results in a person non-intentionally coming to rest at a lower level (usually the floor). Falls are common and important, affecting 1/3 of people living in their own homes each year. They result in fear, injury, dependency, insitutionalization and death. Many can be prevented and their consequences minimized.
Factors influencing fall frequency
Intrinsic factors. Maintaining balance—and avoiding a fall—is a complex, demanding, multisystem skill. It requires muscle strength (power: weight ratio), stable but flexible joints, multiple sensory modalities (eg proprioception, vision, eye sight), and a functional peripheral and central nervous system. Higher level cognitive function permits risk assessment, giving insight into the danger that a planned activity may pose
Extrinsic factors. These include environmental factors, eg lighting, obstacles, the presence of grab rails and the height of steps and furniture, as well as the softness and grip of the floor
Magnitude of ‘stressor’. All people have the susceptibility to fall, and the likelihood of a fall depends on how close to a ‘fall threshold’ a person sits. Older people, especially with disease, sit closer to the threshold, and are more easily and more often pushed over it by stressors. These can be internal (eg transient dizziness due to orthostatic hypotension) or external (eg a gust of wind, or a nudge in a crowded shop); they may be minor or major (no one can avoid ‘falling’ during complete syncope)
If insight is preserved, the older person can to some extent reduce risk, by limiting hazardous behaviours and minimizing stressors (eg walking only inside, avoiding stairs or uneven surfaces, using walking aids or asking for supervision).
Factors influencing fall severity
In older people, the adverse consequences of falling are greater, due to:
Multiple system impairments which lead to less effective saving mechanisms. Falls are more frightening and injury rates per fall are higher
Osteoporosis and increased fracture rates
Secondary injury due to post-fall immobility, including pressure sores, burns, dehydration, and hypostatic pneumonia. Half of older people cannot get up again after a fall
Psychological adverse effects including loss of confidence
Falls are almost always multifactorial. Think:
‘Why today?’ Often because the fall is a manifestation of acute or sub-acute illness, eg sepsis, dehydration or drug adverse effect
‘Why this person?’ Usually because of a combination of intrinsic and extrinsic factors that increase vulnerability to stressors
▶A fall is often a symptom of an underlying serious problem, and is not a part of normal ageing.
The terms simple fall and mechanical fall are used commonly, but they are facile, imprecise, and unhelpful. ‘Simple’ usually refers to the approach adopted by the assessing doctor.
For every fall, identify the intrinsic factors, extrinsic factors, and acute stressors that have led to it
Within each of these categories, think how their influence on the likelihood of future falls can be reduced
Assessment following a fall
Think of fall(s) if a patient presents:
Having ‘tripped’
With a fracture or non-fracture injury
Having been found on the floor
With secondary consequences of falling (eg hypothermia, pneumonia)
Patients who present having fallen are often mis-labelled as having ‘collapsed’, discouraging the necessary search for multiple causal factors.
Practise opportunistic screening—ask all older people who attend primary or secondary care whether they have fallen recently.
History
Obtain a corroborative history if possible. May often need to use very specific, detailed, and directed questions. In many cases, a careful history differentiates between falls due to:
Frailty and unsteadiness
Syncope or near syncope
Acute neurological problems (eg seizures, vertebrobasilar insufficiency)
Gather information about:
Fall circumstances (eg timing, physical environment)
Symptoms before and after the fall
Clarification of symptoms, eg ‘dizzy’ may be vertigo or presyncope
Drugs, including alcohol
Previous falls, fractures and syncope (‘faints’), even as a young adult
Previous ‘near-misses’
Comorbidity (cardiac, stroke, Parkinson's disease, seizures, cognitive impairment, diabetes)
Functional performance (difficulties bathing, dressing, toileting)
Drugs associated with falls
Falls may be caused by any drug that is either directly psychoactive or may lead to systemic hypotension and cerebral hypoperfusion. Polypharmacy (>4 drugs, any type) is an independent risk factor.
The most common drug causes are:
Benzodiazepines and other hypnotics
Antidepressants (tricyclics and serotonin selective reuptake inhibitors (SSRIs)
Antipsychotics
Opiates
Diuretics
Antihypertensives, especially ACE inhibitors and α-blockers
Antiarrhythmics
Anticonvulsants
Skeletal muscle relaxants, eg baclofen, tizanidine
Hypoglycaemics, especially:
Long-acting oral drugs (eg glibenclamide)
Insulin
Examination
This can sometimes be focused if the history is highly suggestive of a particular pathology. But perform at least a brief screening examination of each system.
Functional. Ask the patient to stand from a chair, walk, turn around, walk back and sit back down (‘Get up and go test’). Assess gait, use of walking aids, and hazard appreciation (eg leave an obstacle in the way and see how they negotiate it
Cardiovascular. Always check lying and standing BP. Check pulse rate and rhythm. Listen for murmurs (especially of aortic stenosis)
Musculoskeletal. Assess footwear (stability and grip). Remove footwear and examine the feet. Examine the major joints for deformity, instability, or stiffness
Neurological. To identify stroke, peripheral neuropathy, Parkinson's disease, vestibular disease, myelopathy, cerebellar degeneration, visual impairment, and cognitive impairment
Tests
Vitamin D deficiency is common in older adults, and evidence suggests that replacing it reduces fall, so always check and replace appropriately.
Many other tests are of limited value, but the following are considered routine:
FBC
B12, folate
U, C+E
ECG
Glucose
Calcium, phosphate
TFT
If a specific cause is suspected, then test for it, eg:
24hr ECG in a patient with frequent near-syncope and a resting ECG suggesting conducting system disease
Echocardiogram in a patient with systolic murmur and other features suggesting aortic stenosis (eg slow rising pulse, left ventricular hypertrophy (LVH) on ECG)
Head-up tilt table testing (HUTT) in patients with unexplained syncope, normal resting ECG, and no structural heart disease
However, all tests have false positive rates, and even a ‘true positive’ finding may have no bearing on the patient's presentation. For example, a patient falling due to osteoarthritis and physical frailty will not benefit from echocardiogram that reveals asymptomatic mild aortic stenosis.
▶Use tests selectively, based on your judgement (following careful history and examination) of the likely factors contributing to falls.
Further reading
Interventions to prevent falls
The complexity of treatment reflects the complexity of aetiology:
Older people who fall more often have remediable medical causes
Do not expect to make only one diagnosis or intervention—making minor changes to multiple factors is more powerful
Tailor the intervention to the patient. Assess for relevant risk factors and work to modify each one
A multidisciplinary approach is key
Reducing fall frequency
Drug review. Try to reduce the overall number of medications. For each drug, weigh the benefits of continuing with the benefits of reduction or stopping. Stop if risk is greater than benefit. Reduce if benefit is likely from the drug class, but the dose is excessive for that patient. Taper to a stop if withdrawal effect likely, eg benzodiazepine
Treatment of orthostatic hypotension (see 
‘Orthostatic (postural) hypotension’, p.118)
Strength and balance training. In the frail older person by a physiotherapist, exercise classes, or disciplines such as Tai Chi
Walking aids. Provide an appropriate aid and teach the patient how to use it (see ‘Walking aids’, p.88)
Environmental assessment and modification (often by OT; see ‘Occupational therapy’, p.91)
Vision. Ensure glasses are appropriate (avoid vari- or bifocal lenses)
Reducing stressors. This involves decision making by the patient or carers. The cognitively able patient can judge risk/benefit and usually modifies risk appropriately, eg limiting walking to indoors, using a walking aid properly and reliably, and asking for help if a task (eg getting dressed) is particularly demanding. However:
Risk can never be abolished
Enforced relative immobility has a cost to health
Patient choice is paramount. Most will have clear views about risk and how much lifestyle should change
Institutionalization does not usually reduce risk
Preventing adverse consequences of falls
Despite risk reduction, falls may remain likely. In this case, consider:
Osteoporosis detection and treatment
Teaching patients how to get up. Usually by a physiotherapist
Alarms, eg pullcords in each room or a pendant alarm (worn around the neck). Often these alert a distant call centre, which summons more local help (home warden, relative, or ambulance)
Supervision. Continual visits to the home (by carers, neighbours, family, and/or voluntary agencies) reduce the duration of a ‘lie’ post-fall
Change of accommodation. This sometimes reduces risk, but is not a panacea. A move from home to a care home rarely reduces risk—care homes are unfamiliar, often have hard flooring surfaces, and staff cannot provide continuous supervision
Preventing falls in hospital
Falls in hospital are common, a product of admitting acutely unwell older people with chronic comorbidity into an unfamiliar environment.
Multifactorial interventions have the best chance of reducing falls:
Treat infection, dehydration, and delirium actively
Stop incriminated drugs and avoid starting them
Provide good quality footwear, and an accessible walking aid
Provide good lighting and a bedside commode for those with urinary or faecal urgency or frequency
Keep a call bell close to hand
Care for the highest risk patients in a bay under continuous staff supervision
Bedrails (cotsides). Injury risk is substantial: limbs snag on unprotected metal bars and patients clamber over the rails, falling even greater distances onto the floor below
Restraints. These increase the risk of physical injury, including fractures, pressure sores, and death. Also increase agitation
Impact absorptive pads stitched into undergarments
Limited evidence that they are effective in hospitals although there is some evidence in a care home setting
Success relies on meticulous use which is difficult—they are tricky to put on, can be uncomfortable, and multiple pairs (£40 each) are needed if incontinence is a problem
Further reading
Syncope and presyncope
Syncope is a sudden, transient loss of consciousness due to reduced cerebral perfusion. The patient is unresponsive with a loss of postural control (ie slumps or falls). Presyncope is a feeling of light-headedness that would lead to syncope if corrective measures were not taken (usually sitting or lying down).
These conditions:
Are a major cause of morbidity (occurring in a quarter of institutionalized older people), recurrent in 1/3. Risk of syncope increases with advancing age and in the presence of cardiovascular disease
Account for 5% of hospital admissions, and many serious injuries (eg hip fracture)
Cause considerable anxiety and can cause social isolation as sufferers limit activities, in fear of further episodes
Causes
These are many. Older people with decreased physiological reserve are more susceptible to most. They can be subdivided as follows:
Peripheral factors Hypotension may be caused by the upright posture, eating, straining, or coughing; and may be exacerbated by low circulating volume (dehydration), hypotensive drugs or intercurrent sepsis. Orthostatic hypotension is the most common cause of syncope
Vasovagal syncope (‘simple faint’) Common in young and old people. Vagal stimulation (pain, fright, emotion, etc.) leads to hypotension and syncope. Usually, an autonomic prodrome (pale, clammy, light-headed) is followed by nausea or abdominal pain, then syncope. Benign, with no implications for driving. Diagnose with caution in older people with vascular disease, where other causes are more common
Carotid sinus syndrome
Pump problem. Myocardial infarction or ischaemia, arrhythmia (tachy- or bradycardia, eg ventricular tachycardia (VT), supraventricular tachycardia (SVT), fast atrial fibrillation (AF), complete heart block etc.)
Outflow obstruction, eg aortic stenosis
Pulmonary embolism
The main differential is seizure disorder, where the loss of consciousness is due to altered electrical activity in the brain (see ‘Epilepsy’, p.166).
▶ Stroke and TIA very rarely cause syncope, as they cause a focal not a global deficit. Brainstem ischaemia is the rare exception.
History
The history often yields the diagnosis, but accuracy can be difficult to achieve—the patient often remembers little. Witness accounts are valuable and should be sought.
Ensure that the following points are covered:
Situation—was the patient standing (orthostatic hypotension), exercising (ischaemia or arrhythmia), sitting or lying down (likely seizure), eating (post-prandial hypotension), on the toilet (defecation or micturition syncope), coughing (cough syncope), in pain or frightened (vasovagal syncope)?
Prodrome—was there any warning? Palpitations suggest arrhythmia; sweating with palpitations suggests vasovagal syndrome; chest pain suggests ischaemia; light-headedness suggests any cause of hypotension. Gustatory or olfactory aura suggests seizures. However, associations are not absolute, eg arrhythmias often do not cause palpitations
Was there loss of consciousness?—There is much terminology (fall, blackout, ‘funny turn’, collapse etc.), and different patients mean different things by each term. Syncope has occurred if there is loss of consciousness with loss of awareness due to cerebral hypoperfusion; however, many (~30%) patients will have amnesia for the loss of consciousness and simply describe a fall
Description of attack—ideally from an eyewitness. Was the patient deathly pale and clammy (likely systemic and cerebral hypoperfusion)? Were there ictal features (tongue biting, incontinence, twitching)? Prolonged loss of consciousness makes syncope unlikely. A brain deprived of oxygen from any cause is susceptible to seizure; a fit does not necessarily indicate that a seizure disorder is the primary problem. Assess carefully before initiating anticonvulsant therapy
Recovery period—ideally reported by an eyewitness. Rapid recovery often indicates a cardiac cause. Prolonged drowsiness and confusion often follow a seizure
Examination
Full general examination is required. Ensure that the pulse is examined, murmurs sought, and a postural blood pressure is obtained.
Investigation
Bloods—check for anaemia, sepsis, renal disease, myocardial ischaemia
ECG—for all older patients with loss of consciousness or presyncope. Look specifically at PR interval, QT interval, trifascicular block (prolonged PR, right bundle branch block (RBBB) and left anterior fasicular block), ischaemic changes, and LVH
Other tests depend on clinical suspicion, eg tilt test if symptoms sound orthostatic but diagnosis is proving difficult (lying and standing blood pressures will usually suffice; tilt testing is a very labour-intensive test, and should not be requested routinely); brain scan and electroencephalogram (EEG) if seizures suspected; Holter monitor, if looking for arrhythmias
Treatment
Treat the cause
Often not found, or multifactorial, so treat all reversible factors
Review medication (eg diuretics, vasodilators, cholinesterase inhibitors, tricyclic antidepressants)
Education about prevention and measures to abort an attack if there is a prodrome. Advise against swimming or bathing alone, and inform about driving restrictions. (Varies from no restriction to a 6-month ban, depending on the type of syncope. See details at 
www.dft.gov.uk/dvla/medical/ataglance.aspx)
▶A significant proportion of patients referred to specialist clinics for assessment of ‘syncope’ or ‘blackout’ are found not to have lost consciousness, but to have had a fall secondary to gait or balance abnormalities.
This is difficult; consider investigation for both. Remember that hypoxia secondary to syncope can present as fits. Table 5.1 summarizes the key differences
| Syncope | Seiures | |
|---|---|---|
Risk factors | Past history (heart disease, syncope), cardioactive drugs | Past history (stroke, advanced dementia, seizures), electrolyte disturbance |
Situation | Heat, prolonged standing, meals, etc | No associations |
Onset | Nausea, sweating, lightheadedness. Occasionally palpitations, chest pain (indicating dysrhythmia or critical myocardial perfusion) | An aura may occur. A focal seizure may later become generalized |
During event | Often pale, sweaty, absent or very weak carotid pulse; low muscle tone. There may be brief (few seconds) seizure activity | Muscle tone may be raised without prominent movement; muscular activity and movement may become very prominent |
After event | Recovery is usually brisk (few minutes); a brief (minutes) period of confusion may occur. There may be more prolonged (hours) fatigue | Slow recovery to full consciousness, with typically prolonged (minutes to hours) confusion |
Other | Tongue biting possible; incontinence possible | Tongue biting common; lateral bites are more specific; incontinence is common |
Tests | Abnormal ECG (inappropriate bradycardia, prolonged PR interval or higher orders of atrioventricular (AV) block; intraventricular conduction delay) | Abnormal CT brain; abnormal EEG |
| Syncope | Seiures | |
|---|---|---|
Risk factors | Past history (heart disease, syncope), cardioactive drugs | Past history (stroke, advanced dementia, seizures), electrolyte disturbance |
Situation | Heat, prolonged standing, meals, etc | No associations |
Onset | Nausea, sweating, lightheadedness. Occasionally palpitations, chest pain (indicating dysrhythmia or critical myocardial perfusion) | An aura may occur. A focal seizure may later become generalized |
During event | Often pale, sweaty, absent or very weak carotid pulse; low muscle tone. There may be brief (few seconds) seizure activity | Muscle tone may be raised without prominent movement; muscular activity and movement may become very prominent |
After event | Recovery is usually brisk (few minutes); a brief (minutes) period of confusion may occur. There may be more prolonged (hours) fatigue | Slow recovery to full consciousness, with typically prolonged (minutes to hours) confusion |
Other | Tongue biting possible; incontinence possible | Tongue biting common; lateral bites are more specific; incontinence is common |
Tests | Abnormal ECG (inappropriate bradycardia, prolonged PR interval or higher orders of atrioventricular (AV) block; intraventricular conduction delay) | Abnormal CT brain; abnormal EEG |
Balance and dysequilibrium
Balancing is a complex activity, involving many systems.
Input
There must be awareness of the position of the body in space, which comes from:
Peripheral input—information about body position comes from peripheral nerves (proprioception) and mechanoreceptors in the joints. This information is relayed via the posterior column of the spinal cord to the central nervous system (CNS)
Eyes—provide visual cues as to position
Ears—provide input at several levels. The otolithic organs (utricle and saccule) provide information about static head position. The semicircular canals inform about head movement. Auditory cues localize a person with reference to the environment
Assimilation
Information is gathered and assessed in the brain stem and cerebellum.
Output
Messages are then relayed to the eyes, to allow a steady gaze during head movements (the vestibulo-ocular reflex) and to the cortex and the cord to control postural (antigravity) muscles.
When all this functions well, balance is effortless. A defect(s) in any one contributing system can cause balance problems or dysequilibrium:
Peripheral nerves—neuropathy is more common. Specifically, it is believed that there is a significant age-related loss of proprioceptive function
Eyes—age-related changes decrease visual acuity. Disease (cataracts, glaucoma etc.) is more common
Ears—age-related changes decrease hearing and lead to reduced vestibular function. The older vestibular system is more vulnerable to damage from drugs, trauma, infection, and ischaemia
Joint receptors—degenerative joint disease (arthritis) is more common in older people
CNS—age-related changes can slow processing. Disease processes (ischaemia, hypertensive damage, dementia, etc.) are more common with age
Postural muscles—more likely to be weak, because of inactivity, disease, medication (eg steroids) or the reduced muscle mass of ageing
In the older person, one or more of these defects will occur commonly. In addition, skeletal changes may alter the centre of gravity, and cardiovascular changes may lead to arrhythmias or postural change in blood pressure, exacerbated further by medications.
An approach to dysequilibrium
Aetiology is usually multifactorial
Consider each system separately, and optimize its function
Look at provoking factors (medication, cardiovascular conditions, environmental hazards etc.) and minimize them
Work on prevention:
Alter the environment (eg improve lighting)
With the physiotherapist, develop safer ways to mobilize and increase strength, stamina, and balance
Small adjustments to multiple problems can make a big difference, eg when appropriate, combine cataract extraction, a walking aid, vascular secondary prevention, a second stair rail, brighter lighting, and a course of physiotherapy
▶If falls persist despite simple (but multiple) interventions, refer to a falls clinic.
Dizziness
A brain that has insufficient information to be confident of where it is in space generates a sensation of dizziness. This can be due to reduced sensory inputs, or impairment of their integration. Dizziness is common, occurring in up to 30% of older people.
However, the term dizziness can be used by patients and doctors to mean many different things, including:
Movement (spinning) of the patient or the room—vertigo (see ‘Vertigo’, p.558)
Dysequilibrium or unsteadiness (see ‘Balance and dysequilibrium’, p.112)
Light-headedness—syncope and presyncope (see ‘Syncope and presyncope’, p.108)
Mixed—a combination of these sensations
Other—eg malaise, general weakness, headache
Distinguishing these is the first step in management, as it will indicate possible causal conditions. This relies largely on the history. Discriminatory questions include:
‘Please try to describe exactly what you feel when you are dizzy’
‘Does the room spin, as if you are on a roundabout?’ (Vertigo)
‘Do you feel light-headed, as if you are about to faint?’ (Presyncope)
‘Does it occur when you are lying down?’ (If so, presyncope is unlikely)
‘Does it come on when you move your head?’ (Vertigo more likely)
‘Does it come and go?’ (Chronic, constant symptoms are more likely to be mixed or psychiatric in origin)
Causes
The individual conditions most commonly diagnosed when a patient complains of dizziness are:
Benign paroxysmal positional vertigo (see ‘Vertigo’, p.558)
Labyrinthitis (see ‘Vertigo’, p.558)
Posterior circulation stroke (see ‘Vertigo’, p.558)
Orthostatic hypotension (see ‘Orthostatic (postural) hypotension’, p.118)
Carotid sinus hypersensitivity
Vertebrobasilar insufficiency
Cervical spondylosis (see ‘Cervical spondylosis and myelopathy’, p.486)
Anxiety and depression
In reality, much dizziness is multifactorial, with dysfunction in several systems. This means that precise diagnosis is more difficult (and often not done) and treatment is more complex.
▶Making small improvements to each contributing problem can add up to a big overall improvement (perhaps making the difference between independent living or institutional care).
Mrs A is 85, and has fallen several times. She complains of dizziness, specifically she feels ‘muzzy in the head’, usually when standing. When this occurs, if she sits down promptly it will pass, but often she doesn't make it and her legs ‘just give way’. She also feels ‘muzzy’ in bed sometimes when turning over. Past medical history includes hypertension (she takes atenolol 100mg) and osteoarthritis. She lives alone in unmodernized accommodation.
She is thin and has a kyphotic spine. Pulse is 50/min; supine blood pressure is 130/80, falling to 100/70 on standing. There is limited movement at the hips and cervical spine. Neck movement causes unsteadiness.
Blood tests are normal. ECG shows sinus bradycardia; X-rays show severe degenerative change of the hip joints and cervical spine, with some vertebral wedge fractures.
This is a multifactorial problem. Some of the relevant factors include:
Postural instability: caused by arthritis, kyphosis and low muscle mass
Presyncope: caused by bradycardia and mild postural drop
Possibly benign paroxysmal positional vertigo (BPPV)
Extrinsic factors (eg poor lighting) are almost certainly contributing.
Approach this problem by listing each contributing factor, and identifying what can be done to improve it. For example:
| Contributing factor | Management |
|---|---|
Osteoarthritis | Optimize analgesia Consider referral for joint replacement Physiotherapy (provision of walking aids; strength and balance training) |
Kyphosis | Consider bisphosphonate, calcium and vitamin D to prevent progression Walking aids will improve balance |
Low muscle mass | Take a dietary history Consider nutritional supplements Physiotherapy; encourage exercise |
Bradycardia and postural drop | Consider stopping (or reducing) atenolol Monitor blood pressure |
BPPV | Epley's manoeuvre (see |
Environment | Occupational therapy review to: Provide grab rails and perching stool Improve lighting and flooring ‘De-clutter’ the home |
| Contributing factor | Management |
|---|---|
Osteoarthritis | Optimize analgesia Consider referral for joint replacement Physiotherapy (provision of walking aids; strength and balance training) |
Kyphosis | Consider bisphosphonate, calcium and vitamin D to prevent progression Walking aids will improve balance |
Low muscle mass | Take a dietary history Consider nutritional supplements Physiotherapy; encourage exercise |
Bradycardia and postural drop | Consider stopping (or reducing) atenolol Monitor blood pressure |
BPPV | Epley's manoeuvre (see |
Environment | Occupational therapy review to: Provide grab rails and perching stool Improve lighting and flooring ‘De-clutter’ the home |
Drop attacks
This term refers to unexplained falls with no prodrome, no (or very brief) loss of consciousness, and rapid recovery. The proportion of falls due to ‘drop attack’ increases with age.
There are several causes, including:
Cardiac arrhythmia
Carotid sinus syndrome
Orthostatic hypotension
Vasovagal syndrome
Vertebrobasilar insufficiency (see ‘Vertebrobasilar insufficiency (VBI)’, p.117)
Weak legs (eg cauda equina syndrome)
The first four causes listed usually lead to syncope or presyncope, with identifiable prior symptoms (eg dizziness, pallor); those episodes would not be termed ‘drop attacks’. However, such prior symptoms are not universal, and may not be recollected, leading to a ‘drop attack’ presentation.
In most cases, following appropriate assessment, cause(s) can be identified, and effective treatment(s) begun.
▶Making a diagnosis of ‘drop attack’ alone is not satisfactory; assess more completely, and where possible determine the likely underlying cause(s).
Vertebrobasilar insufficiency (VBI)
A collection of symptoms attributed to transient compromise of the vertebrobasilar circulation. There is often associated compromise of the anterior cerebral circulation.
Symptoms
These arise from functional impairment of the midbrain, cerebellum, or occipital cortex, and can include:
Abrupt onset, recurrent dizziness, or vertigo
Nausea and/or vomiting
Ataxia
Visual disruption (diplopia, nystagmus)
Dysarthria
Limb paraesthesia
Causes
Impairment of the posterior cerebral circulation leads to VBI:
Atherosclerosis of the vertebral or basilar arteries
Vertebral artery compression by cervical spine osteophytes (due to degenerative joint disease), at times triggered by neck movement
Obstructing tumour
Diagnosis
This is based mainly on the history, supported if necessary by investigations. Invasive tests such as angiography are very rarely indicated
Check for vascular risk factors (see ‘Predisposing factors’, p.182)
Cervical spine X-ray may show osteophytes, although these are common and very non-specific
CT brain may demonstrate tumour or ischaemic change. MRI is more sensitive for posterior circulation ischaemic change
MR angiography may reveal occlusive vertebral artery disease
Doppler ultrasound (rarely) to examine vertebral artery flow
Treatment
Vascular secondary prevention measures (see ‘Vascular secondary prevention’, p.308)
Where there is demonstrated posterior circulation stenosis, vessel stenting may be performed in some centres
Limiting neck movements, if these are a precipitant for symptoms, can be useful. Soft collars can be worn, and act mainly as a reminder to the patient to avoid rapid head turns
There is no evidence that anticoagulants are effective
Orthostatic (postural) hypotension
Orthostatic hypotension is common. About 20% of community-dwelling and 50% of institutionalized older people are affected.
An important, treatable cause of dizziness, syncope, near-syncope, immobility, falls and fracture. Less frequently leads to visual disruption, lethargy, neck- or backache
Often most marked after meals, exercise, at night, and in a warm environment, and abruptly precipitated by increased intrathoracic pressure (cough, defecation, or micturition)
Often episodic (coincidence of precipitants) and covert (ask direct questions; walk or stand the patient and look for it). May occur several minutes after standing
Diagnosis
Thresholds are arbitrary. A fall in BP of ≥20mmHg systolic or 10mmHg diastolic on standing from supine is said to be significant. Severity of symptoms often does not correlate well with objective BP change.
Causes
Drugs (including vasodilators, diuretics, negative inotropes or chronotropes (eg β-blockers, calcium channel blockers), antidepressants, antipsychotics, opiates, levodopa, alcohol)
Chronic hypertension (↓ baroreflex sensitivity and LV compliance)
Volume depletion (dehydration, acute haemorrhage)
Sepsis (vasodilation)
Autonomic failure (pure, diabetic, Parkinson's disease, etc.)
Prolonged bed rest
Adrenal insufficiency
Raised intrathoracic pressure (bowel or bladder evacuation, cough)
Treatment
Treat the cause. Stop, reduce, or substitute drugs incrementally
Reduce consequences of falls (eg pendant alarms)
Modify behaviour: stand slowly and stepwise; lie down at prodrome
If salt or water deplete (eg diuretics, diarrhoea), supplement with:
Na (liberal salting at table or NaCl tabs, eg Slow Sodium® 5–10g/day)
Water (oral or intravenous (iv fluid as isotonic dextrose or saline))
Consider starting drugs if non-drug measures fail:
Fludrocortisone (0.1–0.2mg/day)
α-agonists, eg midodrine (2.5mg three times daily (tds), titrated to maximum 40mg/day); unlicensed in UK; contraindicated in ischaemic heart disease (IHD)
Desmopressin 5–20micrograms nocte, intranasal
In all cases, monitor electrolytes and for heart failure and supine hypertension. Caution if supine BP rises >180mmHg systolic. Dependent oedema alone is not a reason to stop treatment
The following may help:
Full-length compression stockings
Head-up tilt to bed (decreases nocturnal natriuresis)
Caffeine (strong coffee with meals) or NSAIDs (→ fluid retention)
Erythropoietin or octreotide
Postprandial hypotension
Significant when associated with symptoms and fall in BP ≥20mmHg within 75min of meals. A modest fall is normal (and usually asymptomatic) in older people. Often more severe and symptomatic in hypertensive people with orthostatic hypotension or autonomic failure.
Diagnosis
Measure BP before meals and at 30min and 60min after meal. Symptoms and causes overlap with orthostatic hypotension.
Treatment
Avoid hypotensive drugs and alcohol with meals
Lie down or sit after meals
Reduce osmotic load of meals (small frequent meals, low simple carbohydrates, high fibre/water content)
Caffeine, fludrocortisone, non-steroidal anti-inflammatory drugs (NSAIDs) and octreotide are used rarely
Lay the patient flat for ≥5min
Measure lying blood pressure with a manual sphygmomanometer
Stand the patient upright rapidly, if necessary with assistance
Check BP promptly (within 30sec of standing)
Whilst standing, repeat systolic BP measurement continually—at least every 30sec for >2min
Record:
Supine BP
Nadir of systolic and diastolic BP
Symptoms
Note that:
Lying-to-standing measurements are more sensitive than sitting-to-standing or lying-to-sitting. The latter are sometimes all that is possible for less mobile patients, even with assistance, but sensitivity can be improved by hanging the legs over the side of the bed
Consider repeat assessment at different times of day—OH is more common after a meal and when relatively fluid depleted (early morning)
Automatic (oscillometric) BP devices (eg ‘Dinamap’) should not be used—they cannot repeat measurements rapidly, nor track a rapidly changing BP
Consider referral to a falls clinic for prolonged tilt table testing if symptoms suggest syncope or near-syncope after more prolonged standing
Carotid sinus syndrome
Carotid sinus syndrome (CSS) is episodic, symptomatic bradycardia and/or hypotension due to a hypersensitive carotid baroreceptor reflex, resulting in syncope or near-syncope. It is an important and potentially treatable cause of falls.
CSS is common in older patients, and rarely occurs under 50 years. Series report a prevalence of 2% in healthy older people, and up to 35% of fallers >80 years. It is a condition that has been identified recently, and not all physicians are convinced that we fully understand the normal responses of older people to carotid sinus massage or the significance of the spectrum of abnormal results.
Normally, in response to increased arterial BP, baroreceptors in the carotid sinus act via the sympathetic nervous system to slow and weaken the pulse, lowering blood pressure. This reflex typically blunts with age, but in CSS, it is exaggerated, probably centrally. This hypersensitivity is associated with increasing age, atheroma and the use of drugs that affect the sinoatrial node (eg β-blockers, digoxin, and calcium channel blockers).
Typical triggers
Neck turning (looking up or around)
Tight collars
Straining (including cough, micturition and defecation)
Meals, ie post-prandial
Prolonged standing
Often, however, no trigger is identified.
Subtypes
Cardioinhibitory (sinus pause of >3sec)
Vasodepressor (BP fall >50mmHg)
Mixed (both sinus pause and BP fall)
Diagnosis
The diagnosis is made when all three of the following factors are present:
Unexplained attributable symptoms
A sinus pause of >3sec and/or systolic BP fall of >50mmHg in response to 5 sec of carotid sinus massage (see ‘HOW TO. . . . Perform carotid sinus massage’, p.123)
Symptoms are reproduced by carotid sinus massage
CSS is often associated with other disorders (vasovagal syndrome and orthostatic hypotension), probably due to shared pathogenesis (autonomic dysfunction). This makes management more challenging.
Treatment
Stop aggravating drugs where possible
Pure cardioinhibitory carotid sinus hypersensitivity responds well to AV sequential pacing, resolving symptoms in up to 80%
Vasodepressor related symptoms are harder to treat (pathogenesis is less well understood), but may respond to increasing circulating volume with fludrocortisone or midodrine (not licensed), as for orthostatic hypotension
As this is a potentially hazardous procedure:
Perform it in conditions that optimize test sensitivity—eg on a tilt table, at a 70–80° tilt, massaging on the right hand side
Ensure that resuscitation facilities are available (full cardiac arrest trolley, another health professional close by, telephone)
Check for contraindications—do not perform after recent MI (increased sensitivity), in cerebrovascular disease, or if there is a bruit present unless carotid Doppler is normal
Advise the patient about possible side effects—arrhythmias (most common if taking digoxin) and neurological symptoms (usually transient, occurring in about 0.14% of tests)
The patient should be relaxed, with the head turned to the left, lying on a couch with the body resting at 45° (or on a tilt table at 70–80°)
Attach the patient to a cardiac monitor with printing facility (to provide documentary evidence of asystole). The fall in BP is usually too brief to be detected by conventional (sphygmomanometric) methods, but continuous (‘beat-to-beat’) blood pressure monitoring (using, eg Portapres or Finapres devices) enables the detection of pure vasodepressor CSS
Identify the carotid sinus—the point of maximal carotid pulsation in the neck
Massage with steady pressure in a circular motion for 5–10sec
Look for asystole and/or hypotension during massage or shortly (seconds) afterwards
If clinical suspicion is high, and the result of right-sided massage is negative, repeat on the left side
Falls clinics
The assessment and secondary prevention of falls are complex processes best performed by an experienced MDT with expert knowledge, functioning within a ‘falls clinic’.
Falls clinics have become much more common, initially a result of trials showing the power of multidisciplinary interventions to reduce falls in community-dwelling older people. More recently, the NSF has required universal UK provision.
The team structure, diagnostic approach, and delivery of care varies enormously, but there are broadly two complementary approaches taken by falls clinics:
Focus on identifying and reducing syncope and near-syncope, with careful drug review and a low threshold to further investigation including tilt table testing and arrhythmia detection
More global approach in which cardiovascular evaluation is an important but minor part of the assessment
Reflecting the differing approaches, some clinics (often those practising a more medical model) take place in outpatient clinics, while others occur in DHs and are more routinely multidisciplinary.
Falls clinics are often led and delivered by non-physician health professionals such as experienced nurses, occupational therapists, and physiotherapists. Screening for modifiable medical factors should be a routine part of all assessments, with referral to a medical specialist (eg GP with a special interest (GPSI) or geriatrician) if such factors are identified.
Referral criteria
Falls are so common that health services would be swamped if all who had fallen were referred. Instead, refer those with more sinister features suggesting a likelihood of recurrent falls, injury or an underlying remediable medical cause. Referral criteria might include:
Recurrent (≥2) falls
Loss of consciousness, syncope, or near-syncope
Injury, especially fracture or facial injury (the latter suggesting poor saving mechanisms or loss of consciousness)
Polypharmacy (≥4 drugs)
Sources of patients include:
ED (assess most people with non-operatively managed fractures)
Acute orthopaedic units (hip and other operatively managed fractures)
GP or community nurse
Medical wards
Self-presenting. Some services advertise directly, via posters and other media
