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 \200 A multidisciplinary approach is key Reducing fall frequency \200 Drug review . Try to reduce the overall number of medication s. For each drug, weigh the bene \201 ts of continuing with the bene \201 ts of reduction or stopping. Stop if risk is greater than bene \201 t. Reduce if bene \201 t is likely f rom the drug class, but the dose is excessive for that patient. Taper to a stop if withdraw al effect likely, eg benzodiazepine Treatment of orthostatic hypotension (see b \200\230Orthostatic (postural) hypotension \200\231, 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 b \200\230Walking aids \200\231, p.88) Environmental assessment and modi \201 cation (often by OT; see b \200\230Occupational therapy \200\231, p.91) Vision . Ensure glasses are appropriate (avoid vari- or bifocal lenses) \200 Reducing str essors . This involves decision making by the patient or carers. The cognitively able patient can judge risk/bene \201 t and usually modi \201 es risk appropriately, eg limiting walking to indoors, using a walking aid properly and reliab ly, and asking for help if a task (eg getting dressed) is particularly demanding. However: \200 Risk can never be abolished \200 Enforced relative immobility has a cost to health \200 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. I n this case, consider: \200 Osteoporosis detection and treatment \200 Teaching patients how to get up . Usually by a physiotherapist \200 Alarms , eg pullcords in each room or a pendant alarm (worn around the neck). Often these alert a distant call center, which summons more local help (home war den, relative, or ambulance) Supervision . Continual visits to the home (by carers, neighbors, family, and/or voluntary agencies) reduce the duration of a \200\230lie \200\231 post-fall \200 Change of accommodation . This sometimes reduces risk, but is not a panacea. A move from home to a care home rarely reduces risk \200\224 care homes are unfam iliar, often have hard \202 ooring surfaces, and staff cannot provide continuous supervis ion INTERVENTIONS TO PREVENT FALLS 107 Preventing falls in hospital Falls in hospital are common, a product of admitting acutely u nwell older people with chronic comorbidity into an unfamiliar environment. Multifactorial interventions have the best chance of reducing falls: Treat infection, dehydration, and delirium actively \200 Stop incriminated drugs and avoi d starting them \200 Provide good quality footwear, and an accessible walking aid \200 Provide good lighting and a bedside commode for those with urinary or fecal urgency or frequency \200 Keep a call bell close to hand \200 Care for the hig hest risk patients in a bay under continuous staff supervision Interventions that are rarely effective and may be harmful \200 Bedrails (cotsides). Inju ry risk is substantial: limbs snag on unprotected metal bars and patients clamber over the rails, falling even greater distances onto the \202 oor below Restraints. These increase the risk of physical injury, including fractures, pressure sores , and death. Also increase agitation Hip protectors \200 Impact absorptive pads stitched into undergarments \200 Limited evi dence that they are effective in hospitals although there is some evidence in a care home setting Success relies on meticulous use which is dif \201 cult \200\224 they are tricky to put o n, can be uncomfortable, and multiple pairs ( 40 each) are needed if incontinence is a pro blem Further reading Gillespie LD , Robertson MC , Gillespie WJ , et al . ( 2009 ). Intervention s for preventing falls in older people living in the community . Cochrane Database Syst Rev 2 : CD007146 . Oliver D , Connelly JB , Victor CR , et al . ( 2006 ). Strategies to prevent falls and frac tures in hospitals and care homes and effect of cognitive impairment: systematic review and meta-analyzes . BMJ 334 : 82 . 108 CHAPTER 5 Falls and funny turns Syncope and presyncope Syncope is a sudden, transient loss of consciousness due to reduced cer- ebral perfusion. The patient is unresponsive with a loss of postural control (ie slump s or falls). Presyncope is a feeling of light-headedness that would lead to syncope if corr ective measures were not taken (usually sitting or lying down). These conditions: Are a major cause of morbidity (occurring in a fourth of institutionalized older people), r ecurrent in 1/3. Risk of syncope increases with advancing age and in the presence of cardio vascular 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 susceptib le to most. They can be subdivided as follows: \200 Peripheral factors Hypotension may be caused by the upright posture, eating, straining, or coughing; and may be exacerbated by low circulating volume (dehydrati on), hypotensive drugs or intercurrent sepsis. Orthostatic hypotension is the most common c ause of syncope Vasovagal syncope ( \200\230simple faint \200\231) 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 peo ple with vascular disease, where other causes are more common Carotid sinus syndrome \200 Pump problem . Myocardial infarction or ischaemia, arrhythmia (tachy- or bradycardia, eg ventricular tachycardia (VT), supraventricular tachycardia (SVT) , fast atrial \201 brillation (AF), complete heart block etc.) Out \202 ow obstruction , eg aortic stenosis \200 Pulmonary embolism The main differenti al is seizure disorder, where the loss of consciousness is due to altered electrical activi ty in the brain (see b \200\230Epilepsy \200\231, p.166). 2 Stroke and TIA very rarely cau se syncope, as they cause a focal not a global de \201 cit. Brainstem ischaemia is the rar e exception. History The history often yields the diagnosis, but accuracy can be dif \201 cult to achie ve \200\224 the patient often remembers little. Witness accounts are valuable and should b e sought. Ensure that the following points are covered: Situation \200\224 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 s yncope), in pain or frightened (vasovagal syncope)? SYNCOPE AND PRESYNCOPE 109 Prodrome \200\224 was there any warning? Palpitations suggest arrhythmia; sweating with pa lpitations suggests vasovagal syndrome; chest pain suggests ischaemia; light-headedness sug gests any cause of hypotension. Gustatory or olfactory aura suggests seizures. However, ass ociations are not absolute, eg arrhythmias often do not cause palpitations Was there loss of consciousness? \200\224 There is much terminology (fall, blackout, \200\230funny turn \200\231, 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 (730 % ) patients will have amnesia for the loss of consciousness and simply describe a fall Description of attack \200\224 ideally from an eyewitness. Was the patient deathly pale and clammy (likely systemic and cerebral hypoperfusion)? Were there ictal feat ures (tongue biting, incontinence, twitching)? Prolonged loss of consciousness makes syncop e unlikely. A brain deprived of oxygen from any cause is susceptible to seizure; a \201 t does not necessarily indicate that a seizure disorder is the primary problem. Assess caref ully before initiating anticonvulsant therapy Recovery period \200\224 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, murmur s sought, and a postural blood pressure is obtained. Investigation \200 Bloods \200\224 check for anemia, sepsis, renal disease, myocardial i schaemia \200 ECG \200\224 for all older patients with loss of consciousness or presynco pe. Look speci \201 cally at PR interval, QT interval, trifascicular block (prolonged PR, righ t 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 di agnosis is proving dif \201 cult (lying and standing blood pressures will usually suf \201 ce; tilt testing is a very labor-intensive test, and should not be requested routinely ); brain scan and electroencephalogram (EEG) if seizures suspected; Holter monitor, if look ing for arrhythmias Treatment \200 Treat the cause \200 Often not found, or multifactorial, so treat all re versible factors \200 Review medication (eg diuretics, vasodilators, cholinesterase inhib itors, tricyclic antidepressants) Education about prevention and measures to abort an attack if there is a prodrome. Advise a gainst swimming or bathing alone, and inform about driving restrictions. (Varies from no re striction to a 6-month ban, depending on the type of syncope. See details at M www.dft.gov. uk/ dvla/medical/ataglance.aspx ) 2A signi \201 cant proportion of patients referred to specialist clinics for assess- ment of \200\230syncope \200\231 or \200\230blackout \200\231 are found not to have lost consc iousness, but to have had a fall secondary to gait or balance abnormalities. 110 CHAPTER 5 Falls and funny turns HOW TO Distinguish syncope and seizures This is dif \201 cult; consider investigatio n for both. Remember that hypoxia secondary to syncope can present as \201 ts. Table 5.1 summarizes the key differences Table 5.1 Differences between syncope and seizures 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 An aura may occur. A focal seizure may later become generalized Onset Nausea, sweating, lightheadedness. Occasionally palpitations, chest pain (indicating dysrhy thmia or critical myocardial perfusion) Muscle tone may be raised without prominent movement; muscular activity and movement may be come very prominent During event Often pale, sweaty, absent or very weak carotid pulse; low muscle tone. There may be brief (few seconds) seizure activity Slow recovery to full consciousness, with typically prolonged (minutes to hours) confusion After event Recovery is usually brisk (few minutes); a brief (minutes) period of confusion may occur. T here may be more prolonged (hours) fatigue Other Tongue biting possible; incontinence possible Tongue biting common; lateral bites are more speci \201 c; incontinence is common Abnormal CT brain; abnormal EEG Tests Abnormal ECG (inappropriate bradycardia, prolonged PR interval or higher orders of atrioven tricular (AV) block; intraventricular conduction delay) This page intentionally left blank 112 CHAPTER 5 Falls and funny turns 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: \200 Peripheral input \200\224 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) \200 Eyes \200\224 provide visual cues as to position \200 Ears \200\224 provide input at several levels. The otolithic organs (utricle and saccule) provide information about static head position. The semicircular cana ls inform about head movement. Auditory cues localize a person with reference to the enviro nment 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 re \202 ex) and to the cortex and the cord to control postural (anti gravity) muscles. When all this functions well, balance is effortless. A defect(s) in any one contributing system can cause balance problems or dysequilibrium: \200 Peripheral nerves \200\224 neuropathy is more common. Speci \201 cally, it is believed that there is a signi \201 cant age-related loss of proprioceptive function Eyes \200\224 age-related changes decrease visual acuity. Disease (cataracts, glaucoma etc.) is more common Ears \200\224 age-related changes decrease hearing and lead to reduced vestibular function. The older vestibular system is more vulnerable to damage from drugs, t rauma, infection, and ischaemia Joint receptors \200\224 degenerative joint disease (arthritis) is more common in older people CNS \200\224 age-related changes can slow processing. Disease processes (ischaemia, hypertensive damage, dementia, etc.) are more common with age Postural muscles \200\224 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, skeleta l changes may alter the center of gravity, and cardiovascular changes may lead to arrhythmi as or postural change in blood pressure, exacerbated further by medications. BALANCE AND DYSEQUILIBRIUM 113 An approach to dysequilibrium \200 Etiology is usually multifactorial \200 Consider eac h system separately, and optimize its function \200 Look at provoking factors (medication , cardiovascular conditions, environmental hazards etc.) and minimize them Work on prevention: Alter the environment (eg improve lighting) \200 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, comb ine cataract extraction, a walking aid, vascular secondary prevention, a second stair rail, brighter lighting, and a course of physiotherapy 2If falls persist despite simple (but multiple) interventions, refer to a falls clinic. 114 CHAPTER 5 Falls and funny turns Dizziness A brain that has insuf \201 cient information to be con \201 dent of where it i s in space generates a sensation of dizziness. This can be due to reduced sensory inputs, o r impairment of their integration. Dizziness is common, occurring in up to 30 % of older pe ople. However, the term dizziness can be used by patients and doctors to mean many different things, including: \200 Movement (spinning) of the patient or the roo m \200\224 vertigo (see b \200\230Vertigo \200\231, p.558) Dysequilibrium or unsteadiness (see b \200\230Balance and dysequilibrium \200\231, p.112) Light-headedness \200\224 syncope and presyncope (see b \200\230Syncope and presyncope \200\231, p.108) Mixed \200\224 a combination of these sensations \200 Other \200\224 eg malaise, genera l weakness, headache Distinguishing these is the \201 rst step in management, as it will indicate possible causal conditions. This relies largely on the history. Discriminatory que stions include: \200 \200\230Please try to describe exactly what you feel when you are d izzy \200\231 \200 \200\230Does the room spin, as if you are on a roundabout? \200\231 ( Vertigo) \200 \200\230Do you feel light-headed, as if you are about to faint? \200\231 ( Presyncope) \200 \200\230Does it occur when you are lying down? \200\231 (If so, presync ope is unlikely) \200 \200\230Does it come on when you move your head? \200\231 (Vertigo more likely) \200 \200\230Does it come and go? \200\231 (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 dizzin ess are: \200 Benign paroxysmal positional vertigo (see b \200\230Vertigo \200\231, p.55 8) \200 Labyrinthitis (see b \200\230Vertigo \200\231, p.558) \200 Posterior circulati on stroke (see b \200\230Vertigo \200\231, p.558) \200 Orthostatic hypotension (see b \200\230Orthostatic (postural) hypotension \200\231, p.118) Carotid sinus hypersensitivity \200 Vertebrobasilar insuf \201 ciency \200 Cervical sp ondylosis (see b \200\230Cervical spondylosis and myelopathy \200\231, p.486) Anxiety and depression In reality, much dizziness is multifactorial, with dysfunction in se veral systems. This means that precise diagnosis is more dif \201 cult (and often not done ) and treatment is more complex. 2Making small improvements to each contributing problem ca n add up to a big overall improvement (perhaps making the difference between independent li ving or institutional care). DIZZINESS 115 HOW TO Manage multifactorial dizziness \200\224 clinical example History Mrs A is 85, and has fallen several times. She complains of dizziness, speci \201 - cally she feels \200\230muzzy in the head \200\231, usually when standing. When this occ urs, if she sits down promptly it will pass, but often she doesn \200\231t make it and her legs \200\230just give way \200\231. She also feels \200\230muzzy \200\231 in bed sometim es 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 blood pres- sure is 130/80, falling to 100/70 on standing. There is limited movement at the hips and cervica l spine. Neck movement causes unsteadiness. Investigations Blood tests are normal. ECG shows sinus bradycardia; X-rays show severe dege nerative change 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: \200 Postural instability: caused by arthritis, kyphosis and low muscle mass \200 Presyncope: caused by bradycardia and mild postural drop \200 Possibly benign parox ysmal positional vertigo (BPPV) \200 Extrinsic factors (eg poor lighting) are almost cert ainly contributing. Approach this problem by listing each contributing factor, and identi- fying what can be done to improve it. For example: Contributing factor Management Osteoarthritis Optimize analgesia Consider referral for joint replacement Physiotherapy (provision of walk ing aids; strength and balance training) Kyphosis Consider bisphosphonate, calcium and vitamin D to prevent progression Walking aids will imp rove 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 Epley \200\231s maneuver (s ee b \200\230 HOW TO Perform Epley \200\231s maneuver \200\231, p.562) BPPV Environment Occupational therapy review to: - Provide grab rails and perching stool - Improve lighting and \202 ooring - \200\230De-clutter \200\231 the home 116 CHAPTER 5 Falls and funny turns Drop attacks This term refers to unexplained falls with no prodrome, no (or very brief) los s of consciousness, and rapid recovery. The proportion of falls due to \200\230drop attack \200\231 increases with age. There are several causes, including: Cardiac arrhythmia \200 Carotid sinus syndrome \200 Orthostatic hypotension \200 Vaso vagal syndrome \200 Vertebrobasilar insuf \201 ciency (see b \200\230Vertebrobasilar in sufficiency (VBI) \200\231, p.117) Weak legs (eg cauda equina syndrome) The \201 rst four causes listed usually lead to sync ope or presyncope, with identi \201 able prior symptoms (eg dizziness, pallor); those epis odes would not be termed \200\230drop attacks \200\231. However, such prior symptoms are n ot uni- versal, and may not be recollected, leading to a \200\230drop attack \200\231 pres entation. In most cases, following appropriate assessment, cause(s) can be identi \201 ed, and effective treatment(s) begun. 2Making a diagnosis of \200\230drop att ack \200\231 alone is not satisfactory; assess more completely, and where possible determin e the likely underlying cause(s). DROP ATTACKS 117 Vertebrobasilar insuf \201 ciency (VBI) A collection of symptoms attributed to transient c ompromise of the vertebrobasilar circulation. There is often associated compromise of the a nterior cerebral circulation. Symptoms These arise from functional impairment of the midbrain, cerebellum, or occipital c ortex, and can include: \200 Abrupt onset, recurrent dizziness, or vertigo \200 Nausea and/or vomiting \200 Ataxia \200 Visual disruption (diplopia, nystagmus) \200 Dysarth ria \200 Limb paraesthesia Causes Impairment of the posterior cerebral circulation leads to VBI: \200 Atherosclerosis of the vertebral or basilar arteries \200 Vertebral artery compression by cervical spine osteophytes (due to degenerative joint disease), at times tr iggered by neck movement Obstructing tumor Diagnosis This is based mainly on the history, supported if necessary by investiga- tions. Invasive tests such as angiography are very rarely indicated \200 Check for vascular risk factors (see b \200\230Predisposing factors \200\231, p.182) \200 Cer vical spine X-ray may show osteophytes, although these are common and very non-speci \201 c CT brain may demonstrate tumor or ischaemic change. MRI is more sensitive for posterior circulation ischaemic change MR angiography may reveal occlusive vertebral artery disease \200 Doppler ultrasound (rar ely) to examine vertebral artery \202 ow Treatment \200 Vascular secondary prevention m easures (see b \200\230Vascular secondary prevention \200\231, p.308) Where there is demonstrated posterior circulation stenosis, vessel stenting may be performed in some centers 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 avo id rapid head turns There is no evidence that anticoagulants are effective 118 CHAPTER 5 Falls and funny turns Orthostatic (postural) hypotension Orthostatic hypotension is common. About 20 % of communi ty-dwelling and 50 % of institutionalized older people are affected. \200 An important, t reatable 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 stan ding Diagnosis Thresholds are arbitrary. A fall in BP of (cid:116) 20mmHg systolic or 10mmHg dia stolic on standing from supine is said to be signi \201 cant. Severity of symp- toms often does not correlate well with objective BP change. Causes \200 Drugs (including vasodilators, diuretics, negative inotropes or chronotropes (eg B -blockers, calcium channel blockers), antidepressants, antipsychotics, opiates, levod opa, alcohol) Chronic hypertension ( d barore \202 ex sensitivity and LV compliance) \200 Volume deple tion (dehydration, acute hemorrhage) \200 Sepsis (vasodilation) \200 Autonomic failure (pure, diabetic, Parkinson \200\231s disease, etc.) \200 Prolonged bed rest \200 Adrena l insuf \201 ciency \200 Raised intrathoracic pressure (bowel or bladder evacuation, cou gh) Treatment \200 Treat the cause. Stop, reduce, or substitute drugs incrementally \200 Re duce consequences of falls (eg pendant alarms) \200 Modify behavior: stand slowly and ste pwise; lie down at prodrome \200 If salt or water deplete (eg diuretics, diarrhea), suppl ement with: \200 Na (liberal salting at table or NaCl tabs, eg Slow Sodium 5 \200\22310g/day) Water (oral or intravenous (iv \202 uid as isotonic dextrose or saline)) Consider starting drugs if non-drug measures fail: Fludrocortisone (0.1 \200\2230.2mg/day) \200 A -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 \200\22320micrograms nocte, intranasal \200 In all cases, monitor electrol ytes and for heart failure and supine hypertension. Caution if supine BP rises > 180mmHg sy stolic. Dependent oedema alone is not a reason to stop treatment ORTHOSTATIC (POSTURAL) HYPOTENSION 119 The following may help: Full-length compression stockings \200 Head-up tilt to bed (decreases nocturnal natriures is) \200 Caffeine (strong coffee with meals) or NSAIDs ( l \202 uid retention) \200 E rythropoietin or octreotide 120 CHAPTER 5 Falls and funny turns Postprandial hypotension Signi \201 cant when associated with symptoms and fall in BP (cid :116) 20mmHg within 75min of meals. A modest fall is normal (and usually asymptomatic) in o lder people. Often more severe and symptomatic in hypertensive people with orthostatic hypo tension or autonomic failure. Diagnosis Measure BP before meals and at 30min and 60min after meal. Symptoms and causes ov erlap with orthostatic hypotension. Treatment \200 Avoid hypotensive drugs and alcohol with meals \200 Lie down or sit afte r meals \200 Reduce osmotic load of meals (small frequent meals, low simple carbohydrates, high \201 bre/water content) Caffeine, \202 udrocortisone, non-steroidal anti-in \202 ammatory drugs (NSAIDs) and octreotide are used rarely POSTPRANDIAL HYPOTENSION 121 HOW TO Measure postural blood pressure 1 Lay the patient \202 at for (cid:116) 5min 2 Measure lying blood pressure with a manual sphygmomanometer 3 Stand the patient upright rapidly, if necessary with assistance 4 Check BP promptly (within 30sec of standing) 5 Whil st standing, repeat systolic BP measurement continually \200\224 at least every 30sec for > 2min 6 Record: Supine BP \200 Nadir of systolic and diastolic BP \200 Symptoms Note that: \200 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 mob ile patients, even with assistance, but sensitivity can be improved by hanging the legs ove r the side of the bed Consider repeat assessment at different times of day \200\224 OH is more common after a me al and when relatively \202 uid depleted (early morning) Automatic (oscillometric) BP devices (eg \200\230Dinamap \200\231) should not be used \200\224 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 122 CHAPTER 5 Falls and funny turns Carotid sinus syndrome Carotid sinus syndrome (CSS) is episodic, symptomatic bradycardia an d/ or hypotension due to a hypersensitive carotid baroreceptor re \202 ex, resulting in sy ncope 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 prevalen ce of 2 % in healthy older people, and up to 35 % of fallers > 80 years. It is a condition that has been identi \201 ed recently, and not all physicians are convinced that we fully understand the normal responses of older people to carotid sinus massage or the signi \201 cance 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 re \202 ex typically blunts with age, but in CSS, it is exaggerated, probably centrally. T his hypersensitivity is associated with increasing age, atheroma and the use of drugs that affect the sinoatrial node (eg B -blockers, digoxin, and calcium channel blockers). Typical triggers \200 Neck turning (looking up or around) \200 Tight collars \200 Str aining (including cough, micturition and defecation) \200 Meals, ie post-prandial \200 Prolonged standing Often, however, no trigger is identi \201 ed. Subtypes \200 Cardioinhibitory (sinus pause of > 3sec) \200 Vasodepressor (BP fall > 50 mmHg) \200 Mixed (both sinus pause and BP fall) Diagnosis The diagnosis is made when all three of the following factors are present: \200 Unexplained attributable symptoms \200 A sinus pause of > 3sec and/or systolic BP fall o f > 50mmHg in response to 5 sec of carotid sinus massage (see b \200\230HOW TO Per form carotid sinus massage \200\231, p.123) Symptoms are reproduced by carotid sinus massage CSS is often associated with other disorde rs (vasovagal syndrome and orthostatic hypotension), probably due to shared pathogenesis (a utonomic dysfunction). This makes management more challenging. Treatment \200 Stop aggravating drugs where possible \200 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 \202 udrocortisone or midodrine (no t licensed), as for orthostatic hypotension CAROTID SINUS SYNDROME 123 HOW TO Perform carotid sinus massage 1 As this is a potentially hazardous procedure: Perform it in conditions that optimize test sensitivity \200\224 eg on a tilt table, at a 70 \200\22380 tilt, massaging on the right hand side Ensure that resuscitation facilities are available (full cardiac arrest trolley, another health professional close by, telephone) 2 Check for contraindications \200\224 do not perform after recent MI (increased sensitivity), in cerebrovascular disease, or if there is a bruit present unless carotid Doppler is normal 3 Advise the patient about possible side effects \200\224 arrhythmias (most common if taki ng digoxin) and neurological symptoms (usually transient, occurring in about 0.14 % of test s) 4 The patient should be relaxed, with the head turned to the left, lying on a couch with th e body resting at 45 (or on a tilt table at 70 \200\22380 ) 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 detect ed by conventional (sphygmomanometric) methods, but continuous ( \200\230beat-to-beat \200 \231) blood pressure monitoring (using, eg Portapres or Finapres devices) enables the detec tion of pure vasodepressor CSS 6 Identify the carotid sinus \200\224 the point of maximal carotid pulsation in the neck 7 Massage with steady pressure in a circular motion for 5 \200\22310sec 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 124 CHAPTER 5 Falls and funny turns Falls clinics The assessment and secondary prevention of falls are complex processes best p erformed by an experienced MDT with expert knowledge, func- tioning within a \200\230falls clinic \200\231. 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: \200 Focus on identifyin g and reducing syncope and near-syncope, with careful drug review and a low threshold to fu rther investigation including tilt table testing and arrhythmia detection More global approach in which cardiovascular evaluation is an important but minor part of the assessment Re \202 ecting the differing approaches, some clinics (often those practicing a more medic al model) take place in outpatient clinics, while others occur in DHs and are more routinel y multidisciplinary. Falls clinics are often led and delivered by non-physician health professionals such as exp erienced nurses, occupational therapists, and physiotherapists. Screening for modi \201 ab le 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 ident i \201 ed. 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 sug- gesting a likel ihood of recurrent falls, injury or an underlying remediable medical cause. Referral criter ia might include: \200 Recurrent ( (cid:116) 2) falls \200 Loss of consciousness , sync ope, or near-syncope \200 Injury , especially fracture or facial injury (the latter sugge sting poor saving mechanisms or loss of consciousness) Polypharmacy ( (cid:116) 4 drugs) Sources of patients include: \200 ED (assess most peopl e with non-operatively managed fractures) \200 Acute orthopedic units (hip and other oper atively managed fractures) \200 GP or community nurse \200 Medical wards \200 Self-pr esenting . Some services advertise directly, via posters and other media Further reading Gillespie LD , Robertson MC , Gillespie WJ , et al . ( 2009 ). Intervention s for preventing falls in older people living in the community . Cochrane Database Syst Rev 2 : CD007146 . 125 Chapter 6 Drugs Pharmacology in older patients 126 Prescribing \200\230rules \200\231 128 Taking a drug hi story 130 HOW TO Improve concordance 132 Drug sensitivity 134 Adverse drug reactions 135 ACE inhibitors 136 HOW TO Start ACE inhibitors 137 Amiodarone 138 HOW TO Manage amiodarone-induced thyroid dysfunction 139 Analgesia 140 HOW TO Manage pain in older patients 141 Steroids 142 Warfarin 144 HOW TO Initiate warfarin 146 HOW TO Manage drug-induced skin rashes 147 Proton pump inhibitors 148 Herbal medicines 149 Breaking the rules 150 126 CHAPTER 6 Drugs Pharmacology in older patients Perhaps the most common intervention performed by physicians is to write a prescription. Older patients will have more conditions requiring medication; polypharmacy is common. In the developed world: The over 65s typically make up around 14 % of the population yet consume 40 % of the drug budget 66 % of the over 65s, and 87 % of the over 75s are on regular medication 34 % of the over 75s are on three or more drugs \200 Care home patients are on an average of eight medications Good prescribing habits are essential for any medical practitioner, b ut especially for the geriatrician. Administration challenges include: \200 Packaging may make tablets hard to access \200 \224 childproof bottles and tablets in blister packets can be impossible to open with arthritic hands or poor vision Labels may be too small to read with failing vision \200 Tablets may be large and dif \201 cult to swallow (eg co-amoxiclav) or have an unpleasant taste (eg potassium supplements) Liquid formulations can be useful, but accurate dosage becomes harder (especially where manual dexterity is compromised) Any tablet needs around 60mL of water to wash it down and prevent adherence to the oesophag eal mucosa \200\224 a large volume for a frail older person. Some tablets (eg bisphosphona tes) require even larger volumes Multiple tablets, with different instructions (eg before/after food) are easily muddled up, or taken in a suboptimal way Some routes (eg topical to back) may be impossible without assistance Absorption \200 Many factors are different in older patients (increased gastric pH, delay ed gastric emptying, reduced intestinal motility and blood \202 ow etc.) Despite this, absorption of drugs is largely unchanged with age \200\224 exceptions include iron and calcium, which are absorbed more slowly Distribution \200 Some older people have a very low lean body mass, so if the therapeutic index for a drug is narrow (eg digoxin) the dose should be adjusted There is often an increased proportion of fat compared with water. This reduces the volume of distribution for water-soluble drugs giving a higher initial con centration (eg digoxin). It also leads to accumulation of fat-soluble drugs, prolonging eli mination and effect (eg diazepam) \200 There is reduced plasma protein binding of drugs w ith age, which increases the free fraction of protein-bound drugs such as warfarin and furosemide PHARMACOLOGY IN OLDER PATIENTS 127 Hepatic metabolism \200 Speci \201 c hepatic metabolic pathways (eg conjugation) are una ffected by age Reducing hepatic mass and blood \202 ow can impact on overall function which slows metabo lism of drugs (eg theophylline, paracetamol, diazepam, nifedipine) Drugs that undergo extensive \201 rst pass metabolism (eg propranolol, nitrates) are most affected by the reduced hepatic function Many factors interact with liver metabolism (eg nutritional state, acute illness, smoking, other medications, etc.) Renal excretion \200 Renal function declines with age (see b \200\230The ageing kidney \200\231, p.384), which has a profound impact on the handling of drugs that are predominantly handled renally Drugs, or drugs with active metabolites, that are mainly excreted in the urine include digo xin, gentamicin, lithium, furosemide, and tetracyclines Where there is a narrow therapeutic index (eg digoxin, aminoglycosides) then dose adjustment for renal impairment is required (see UK British Nati onal Formulary ( BNF ) Appendix 3) \200 Impaired renal function is exacerbated by dehydra tion and urinary sepsis \200\224 both common in older patients 128 CHAPTER 6 Drugs Prescribing \200\230rules \200\231 1. Is it indicated? Treatment of new symptom Some sympt oms trigger a re \202 ex prescription (eg constipation \200\224 laxatives; dizziness \200\224 prochlorperazine). Before starting a medication, consider: \200 What is the diag nosis? (eg dizziness due to postural drop) \200 Can something be stopped? (eg opioid anal gesia causing constipation) \200 Are there any non-drug measures? (eg increase \201 bre for constipation) Optimizing disease management For example: a diagnosis of cardiac failur e should trigger consideration of loop diuretics, spironolactone, ACE inhibitors, and B -bl ockers. \200 Ensure the diagnosis is secure before committing the patient to multiple drugs (may be dif \201 cult where there is no clear diagnostic gold standard, eg with TIAs)