Chapter 5
Falls and funny turns
Interventions to prevent falls
HOW TO . . . Distinguish syncope and seizures
HOW TO . . . Manage multifactorial dizziness—clinical example
Orthostatic (postural) hypotension
HOW TO . . . Measure postural blood pressure
Falls and fallers
► A fall is often a symptom of an underlying serious problem and is not a part of normal ageing.
A fall is an event that results in a person non-intentionally coming to rest at a lower level (usually the floor) with or without loss of consciousness. Falls are common and important, affecting one-third of older people living in their own homes each year. They result in fear, injury, dependency, institutionalization, 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 (e.g. proprioception, vision, hearing), 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, e.g. 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 (e.g. transient dizziness due to orthostatic hypotension) or external (e.g. a gust of wind or a nudge in a crowded shop); they may be minor or major (no one can avoid ‘falling’ during syncope)
If insight is preserved, the older person can, to some extent, reduce risk by limiting hazardous behaviours and minimizing stressors (e.g. 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 ↑ fracture rates
• 2° 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 subacute illness, e.g. sepsis, dehydration, or drug adverse effect
• ‘Why this person?’ Usually because of a combination of intrinsic and extrinsic factors that ↑ vulnerability to stressors
Banned terms
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:
• With a fracture or non-fracture injury
• Having been found on the floor
• With 2° consequences of falling (e.g. hypothermia, pneumonia)
Patients who present having fallen are often mislabelled as having ‘collapsed’, discouraging the necessary search for multiple causal factors.
Practise opportunistic screening—ask all older people who attend 1° or 2° 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:
• Acute neurological problems (e.g. seizures, vertebrobasilar insufficiency (VBI))
Gather information about:
• Fall circumstances (e.g. timing, physical environment)
• Symptoms before and after the fall
• Clarification of symptoms, e.g. ‘dizzy’ may be vertigo or presyncope
• Previous falls, fractures, and syncope (‘faints’), even as a young adult
• Comorbidity (cardiac, stroke, Parkinson’s disease, seizures, cognitive impairment, diabetes, incontinence)
• Functional performance (difficulties bathing, dressing, toileting)
Drugs associated with falls
Falls may be caused by any drug that either is 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 selective serotonin reuptake inhibitors (SSRIs)
• Antihypertensives, especially ACE inhibitors and α-blockers
• Skeletal muscle relaxants, e.g. baclofen, tizanidine
• Hypoglycaemics, especially long-acting oral drugs and insulin
Examination
This can sometimes be focused if the history is highly suggestive of a particular pathology; 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
• 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, and cognitive impairment
Tests
The following are considered routine:
• FBC, B12, folate, U, C+E, glycosylated Hb (HbA1c), calcium, phosphate, TFT
• Vitamin D—deficiency is common in older adults, and evidence suggests that replacing may reduce falls/harm from falls
If a specific cause is suspected, then test for it, e.g.:
• 24h 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 (e.g. 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
• Carotid sinus massage (see 
‘HOW TO . . . Perform carotid sinus massage’, p. 121)
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 an 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
National Institute for Health and Care Excellence (2013). Falls in older people: assessing risk and prevention. Clinical guideline CG161. 
http://www.nice.org.uk/CG161.
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, e.g. benzodiazepine
• Treatment of orthostatic hypotension (see ‘Orthostatic (postural) hypotension’, pp. 116–117)
• Strength and balance training. In the frail older person, by a PT, exercise classes, or disciplines such as t’ai chi
• Walking aids. Provide an appropriate aid and teach the patient how to use it (see ‘Walking aids’, pp. 86–88)
• Environmental assessment and modification (a simple checklist can help the family minimize risk; in some cases, a more detailed assessment by an OT is beneficial)
• 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, e.g. limiting walking to indoors, using a walking aid properly and reliably, and asking for help if a task (e.g. getting dressed) is particularly demanding. However:
• 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 PT
• Alarms, e.g. pullcords in each room or a pendant alarm (worn around the neck/wrist). 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 may provide a more suitable physical environment, but it will be unfamiliar 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 (such as FallSafe) 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
Interventions that are rarely effective and may be harmful
• 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 ↑ the risk of physical injury, including fractures, pressure sores, and death. Also ↑ agitation
• Hip protectors are impact-absorptive pads stitched into undergarments. Evidence of efficacy is limited to care home residents and they cause more falls in community-dwelling trials
Further reading
Royal College of Physicians. FallSafe resources. http://www.rcplondon.ac.uk/guidelines-policy/fallsafe-resources-original.
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 (i.e. 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 one-third. Risk of syncope ↑ with advancing age and in the presence of cardiovascular disease
• Accounts for up to 5% of hospital attendances and many serious injuries (e.g. 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 ↓ physiological reserve are more susceptible to most. They can be subdivided as follows:
• Peripheral factors. Hypotension may be caused by an 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 hypersensitivity syndrome
• Pump problem. MI or ischaemia, arrhythmia (tachy- or bradycardia, e.g. ventricular tachycardia (VT), supraventricular tachycardia (SVT), fast atrial fibrillation (AF), complete heart block, etc.)
• Outflow obstruction, e.g. aortic stenosis. PE is also a type of outflow obstruction.
The main differential is seizure disorder where loss of consciousness is due to altered electrical activity in the brain (see ‘Epilepsy’, pp. 164–165).
► Stroke and TIA very rarely cause syncope, as they cause a focal, not global, deficit. Brainstem ischaemia is the rare exception.
► 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 2° to gait or balance abnormalities.
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 (postprandial hypotension), on the toilet (defecation or micturition syncope), coughing (cough syncope), or 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, e.g. 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 1° 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 BP 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 fascicular block), ischaemic changes, and LVH
• Other tests depend on clinical suspicion, e.g. tilt test if symptoms sound orthostatic, but diagnosis is proving difficult (lying and standing BPs 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; prolonged ambulatory ECG monitoring or an implantable loop recorder if looking for arrhythmias
Treatment
• Often not found or multifactorial, so treat all reversible factors
• Review medication (e.g. 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 http://www.dft.gov.uk/dvla/medical/ataglance.aspx)
► Transient loss of consciousness (TLOC) may be caused by syncope or seizure.
HOW TO . . . Distinguish syncope and seizures
This is difficult; consider investigation for both. Remember that hypoxia 2° to syncope can present as fits. Table 5.1 summarizes the key differences.
Table 5.1 Differences between syncope and seizures
| Syncope | Seizures | |
| 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, light-headedness. 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 disequilibrium
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 brainstem 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 disequilibrium:
• 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 ↓ visual acuity. Disease (cataracts, glaucoma, etc.) is more common
• Ears—age-related changes ↓ 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—sarcopenia (a syndrome of reduced muscle mass with weakness) due to inactivity, disease, medication (e.g. steroids), or intrinsic 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 BP, exacerbated further by medications.
An approach to disequilibrium
• 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
• Alter the environment (e.g. improve lighting)
• Develop safer ways to mobilize, and ↑ strength, stamina, and balance
• Small adjustments to multiple problems can make a big difference, e.g. when appropriate, combine cataract extraction, a walking aid, vascular 2° prevention, a second stair rail, brighter lighting, and a course of PT
► 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. 560)
• Disequilibrium or unsteadiness (see ‘Balance and disequilibrium’, pp. 110–111)
• Light-headedness—syncope and presyncope (see ‘Syncope and presyncope’, pp. 106–108)
• Mixed—a combination of these sensations
• Other, e.g. 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 (BPPV) (see ‘Vertigo’, p. 560)
• Labyrinthitis (see ‘Vertigo’, p. 560)
• Posterior circulation stroke (see ‘Vertigo’, p. 560)
• Orthostatic hypotension (see ‘Orthostatic (postural) hypotension’, pp. 116–117)
• Carotid sinus hypersensitivity
• Cervical spondylosis (see ‘Cervical spondylosis and myelopathy’, pp. 488–489)
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).
HOW TO . . . Manage multifactorial dizziness—clinical example
History
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 does not 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.
Examination
She is thin and has a kyphotic spine. Pulse is 50/min; supine BP is 130/80, falling to 100/70 on standing. There is limited movement at the hips and cervical spine. Neck movement causes unsteadiness.
Investigations
Blood tests are normal. ECG shows sinus bradycardia; X-rays show severe degenerative changes of the hip joints and cervical spine, with some vertebral wedge fractures.
Diagnosis and treatment plan
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
• Extrinsic factors (e.g. 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, see Table 5.2.
Table 5.2 Management of dizziness
| Contributing factor | Management |
| Osteoarthritis |
Consider referral for joint replacement PT (provision of walking aids; strength and balance training) |
| Kyphosis |
Consider bisphosphonate, calcium, and vitamin D to prevent progression |
| Low muscle mass | |
| Bradycardia and postural drop | |
| BPPV | Epley’s manoeuvre (see ‘HOW TO . . . Perform Epley’s manoeuvre’, p. 564) |
| Environment | OT review to:
• Provide grab rails and perching stool |
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’ ↑ with age.
There are several causes, including:
• Carotid sinus syndrome (CSS)
• VBI (see Box 5.1)
• Weak legs (e.g. cauda equina syndrome)
The first four causes listed usually lead to syncope or presyncope, with identifiable prior symptoms (e.g. 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, the 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).
Box 5.1 Vertebrobasilar insufficiency
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
• Visual disruption (diplopia, nystagmus)
Causes
Impairment of the posterior cerebral circulation leads to VBI:
• Atherosclerosis of vertebral or basilar arteries
• Vertebral artery compression by cervical spine osteophytes (due to degenerative joint disease), at times triggered by neck movement
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. 180)
• Cervical spine X-ray may show osteophytes, although these are common and very non-specific
• CT brain may demonstrate a tumour or ischaemic change. MRI is more sensitive for posterior circulation ischaemic change
• CT angiography may reveal occlusive vertebral artery disease
• Doppler ultrasound (rarely) to examine vertebral artery flow
Treatment
• Vascular 2° prevention measures (see ‘Vascular secondary prevention’, p. 310)
• 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
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 ache, or backache
• Often most marked after meals, exercise, at night, and in a warm environment, and abruptly precipitated by ↑ 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 (e.g. β-blockers, calcium channel blockers), antidepressants, antipsychotics, opiates, levodopa, alcohol)
• Chronic hypertension (↓ baroreflex sensitivity and LV compliance)
• Volume depletion (dehydration, acute haemorrhage)
• Autonomic failure (pure, diabetes, Parkinson’s disease, etc.)
• Raised intrathoracic pressure (bowel or bladder evacuation, cough)
Treatment
• Treat the cause. Stop, reduce, or substitute drugs incrementally
• Reduce consequences of falls (e.g. pendant alarms)
• Modify behaviour—stand slowly and stepwise; lie down at prodrome
• If still salt- or water-deplete, supplement with:
• Sodium (liberal salting at table or sodium chloride (NaCl) tablets)
• Water (oral or intravenous fluids)
• Consider starting drugs if non-drug measures fail:
• Fludrocortisone (0.1–0.2mg/day)
• α-agonists, e.g. midodrine (2.5mg three times daily (tds), titrated to a maximum of 40mg/day); unlicensed in the UK; contraindicated in vascular disease
• Desmopressin 5–20 micrograms nocte, intranasal (used rarely in older patients as causes electrolyte imbalances)
• 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
• Full-length compression stockings
• Head-up tilt to bed (↓ nocturnal natriuresis)
• Caffeine (strong coffee with meals) or non-steroidal anti-inflammatory drugs (NSAIDs) with extreme caution (→ fluid retention)
• Erythropoietin or octreotide
Situational hypotension
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
• 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
• Reduce osmotic load of meals (small frequent meals, low simple carbohydrates, high fibre/water content)
• Caffeine, fludrocortisone, NSAIDs, and octreotide are used rarely
Others
• Collapse at initiation or during defecation or micturition are commonly due to hypotension, and a similar management approach should be adopted
• Hypotension in response to cough can also occur—direct management towards reducing cough and optimizing BP
HOW TO . . . Measure postural blood pressure
1. Lay the patient flat for ≥5min
2. Measure lying BP with a manual sphygmomanometer
3. Stand the patient upright rapidly, if necessary with assistance
4. Check BP promptly (within 30s of standing)
5. While standing, repeat systolic BP measurement continually—at least every 30s for >3min or confirmation of a significant drop
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 the day—orthostatic hypotension is more common after a meal and when relatively fluid-depleted (early morning)
• Automatic BP devices 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
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 ↑ arterial BP, baroreceptors in the carotid sinus act via the sympathetic nervous system to slow and weaken the pulse, lowering the BP. This reflex typically blunts with age, but in CSS, it is exaggerated, probably centrally. This hypersensitivity is associated with ↑ age, atheroma, and the use of drugs that affect the sinoatrial node (e.g. β-blockers, digoxin, and calcium channel blockers).
Typical triggers
• Neck turning (looking up or around)
• Straining (including cough, micturition, and defecation)
Often, however, no trigger is identified.
Subtypes
• Cardioinhibitory (sinus pause of >3s)
• Vasodepressor (BP fall of >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 >3s and/or systolic BP fall of >50mmHg in response to 5s of carotid sinus massage (see ‘HOW TO . . . Perform carotid sinus massage’, p. 121)
• 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 ↑ circulating volume with fludrocortisone or midodrine (not licensed), as for orthostatic hypotension
HOW TO . . . Perform carotid sinus massage
1. As this is a potentially hazardous procedure:
• Perform it in conditions that optimize test sensitivity, e.g. on a tilt table, at a 70–80° tilt, massaging on the right-hand side
• Ensure that resuscitation facilities are available
2. Check for contraindications—do not perform after recent MI (↑ sensitivity). Concerns about carotid atheroma are probably overplayed; large studies have shown carotid sinus massage to be safe and well tolerated
3. Advise the patient about possible side effects—arrhythmias (most common if taking digoxin) and neurological symptoms (usually transient, occurring in about 0.1% of tests)
4. 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°)
5. 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’) BP monitoring enables the detection of pure vasodepressor CSS
6. Identify the carotid sinus—the point of maximal carotid pulsation in the neck
7. Massage with steady pressure in a circular motion for 5–10s
8. Look for asystole and/or hypotension during massage or shortly (seconds) afterwards
9. If clinical suspicion is high, and the result of right-sided massage is negative, repeat on the left side
Falls services
The assessment and 2° prevention of falls are multifactorial processes requiring a systematic approach. This is frequently appropriate in 1° and 2° care settings and can be delivered effectively by any trained member of the MDT. More complex cases may benefit from assessment within a specialist setting such as a geriatric or falls clinic.
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 cause. Referral criteria might include:
• Loss of consciousness, syncope, or near-syncope
• Injury, especially fracture or facial injury (the latter suggesting poor saving mechanisms or loss of consciousness)
Sources of patients include:
• ED (assess most people with non-operatively managed fractures)
• Acute orthopaedic units (hip and other operatively managed fractures)
• Self-presenting. Some services advertise directly, via posters and other media
Service structure
The team structure, diagnostic approach, and delivery of care vary enormously. Falls clinics are often led and delivered by non-physician health professionals such as experienced nurses, OTs, and PTs.
A systematic review of possible contributing factors is essential and will usually include:
• Cardiovascular examination (including postural BP)
• Routine bloods (including FBC, U, C+E, haematinics, vitamin D)
Screening for modifiable medical factors should be a routine part of all assessments, with referral to a medical specialist (e.g. GPSI or geriatrician) if such factors are identified.