Signs Again, early signs are sensitive, but not speci \201 c (eg tachycardia, pulmo- nary crepitations, peripheral oedema). Later signs are more speci \201 c, but not sensitive (eg elevated JVP \200\224 98 % speci \201 c, 17 % sensitive; gallop rhythm \200\224 99 % sp eci \201 c and 24 % sensitive) 2Overall, clinical features tend to be sensitive OR speci \201 c, but not both. The multiple pathology of older patients poses a particular challenge in diagnosis. Clinical suspicion should then be supported by investigation before embarkin g on a trial of treatment. HEART FAILURE: ASSESSMENT 289 HOW TO Investigate a patient with suspected heart failure Use investigations to support a clinical diagnosis and establish cause. \200 ECG \200 \224 abnormal in over 90 % of cases (Q waves, T wave/ST segment changes, LVH, bundle branch block, AF). Consider Holter monitor if paroxysmal symptoms CXR \200\224 look for cardiac enlargement (although this is absent with acute onset eg pos t MI or PE), upper lobe blood diversion, \202 uid in the horizontal \201 ssure, Kerley B lines, bat wing pulmonary oedema, pleural effusions (usually bilateral; R > L if unilater al), any other cause for breathlessness 2Combination of a normal CXR and ECG makes heart failure very unlikely indeed. \200 Blood tests \200\224 FBC (? anemic), biochemistry (? renal function, sodium low in severe heart failure), glucose and lipids (CHD risk factors), liver function (? congestion), thyroid function. BNP if available (see Box 10.2 ) Echocardiography \200\224 echo should be done for all with suspected heart failure (NICE g uidelines) to help con \201 rm diagnosis, establish cause and grade disease severity. Look s for LV function (systolic and diastolic \200\224see b \200\230Diastolic heart failure \200\231, p.296), estimates ejection fraction, looks for evidence of valve disease, cardiom yopathy, regional wall abnormalities from IHD, pericardial disease, intracardiac shunts, LV aneurysms or cardiac thrombus. Open access echo (ie direct GP referral) has improved the n umber of patients who have an echo, but the results are only as good as the echo technician and there can be problems with interpreting results (eg diastolic problems). Overall, only 25 % of those referred for echo have LV systolic dysfunction Pulmonary function tests \200\224 may help distinguish cardiac from respiratory breathlessness (peak expiratory \202 ow rate (PEFR) and forced expiratory vol ume in one second (FEV 1 ) reduced in heart failure, but less than in COPD). Remember many patients have both 290 CHAPTER 10 Cardiovascular Box 10.2 B-type natriuretic peptide (BNP) Three types of natriuretic peptide known, with effects on heart, kidneys and the nervous sy stem. B-type is found mainly in the heart and increases with pressure overload of the heart , acting as a biochemical marker for heart failure. BNP concentration correlates with the s everity of heart disease \200\224 very high levels carry a poor prognosis. In addition a n egative value makes a diagnosis of heart failure extremely unlikely (negative predictive va lue of 96 % ). Problems \200 What is a high level? Different assays produce different numbers, and there is a continuum of results making a diagnostic cut-off necessary \200 What is the gold st andard for diagnosis in order to evaluate the test? (Echo has limitations) BNP level does not help distinguish systolic from diastolic heart failure Drug treatment can affect levels, eg reduced by ACE inhibitors \200 False positives can b e caused by COPD, PE, age > 70, diabetes, LVH, previous MI, tachycardia, renal impairment, and liver cirrhosis Cost-effectiveness unknown \200 Limited clinical trial evidence \200 Signi \201 cance of a high level in an asymptomatic patient is unclear and it is not currently recommended for screening Currently not widely available in the UK 2Overall, a \200\230negative \200\231 (ie very lo w) result in a breathless patient makes heart failure very unlikely, and other causes shoul d be sought. NICE recommends measuring BNP in patients with suspected heart failure without previous MI in order to help preselect patients for echocardiog- raphy and specialist revi ew. ACUTE HEART FAILURE 291 Acute heart failure Treatment \200 Immediate treatment with oxygen, intravenous loop diur etic, and nitrates given iv or sublingually (if adequate BP), opiate, and antiemetic Address cause (eg acute MI, arrhythmia) \200 Stop any exacerbating medications (NSAIDs, B -blockers) \200 Consider thromboprophylaxis (eg low molecular weight heparin) \200 Con sider ventilatory support (begin with non-invasive positive pressure ventilation which can be done in a non \200\223ITU setting and does not present problems of weaning) After improvement is seen begin to plan ongoing treatment \200\224 write up regular loop d iuretic and usually ACE on the drug chart and make plans for further assessment Monitor electrolytes, BP, and weight Prognosis Patients with acute heart failure look extremely unwell yet can often make appare ntly \200\230miraculous \200\231 recoveries as the precipitant is dealed with. Remember th at it is the pre-morbid state and the nature of the acute injury, never age alone, that sho uld determine how aggressively to manage the acute condition. Rapid AF and heart failure \200 A common combination in older patients \200 It is rarel y clear which came \201 rst \200 Treat both simultaneously \200 Digoxin may slow AF i n this situation without depressing the myocardium (may occur with amiodarone). Load 1mg of digoxin over 24hr in divided doses \200\224 eg 500 micrograms iv or po repeated at 12hr, followed by the maintenance dose Always look for a precipitant \200\224 sepsis, MI, PE, etc. 292 CHAPTER 10 Cardiovascular Chronic heart failure 2Begin by reviewing basis for diagnosis as it means a poor prognosis and a commitment to a large number of medications. A multidisciplinary approach is preferable, involving the patient in monitoring where possible (eg daily weighing). Best done by those with an interest, and with facilities for ongoing follow-up, eg DHs (par ticularly suited to the frailer elderly), heart failure clinics, by heart failure specialis t nurses or GPs with special interest. Lifestyle Address cardiovascular risk actors, reduce alcohol intake, increase aerobic exerc ise (ideally as part of a rehabilitation program). Medication Large evidence base for a large number of drugs (see Box 10.3 ). It may be tempt ing to limit the number of drugs in older patients, justi \201 ed by concerns about side e ffects, but if the diagnosis is secure then all classes should be at least attempted. It is probably better to prescribe a low dose of an ACE with a B -blocker, rather than a maximum dose of ACE when the BP may be insuf \201 cient to introduce the B -blocker. Treating cause \200 AF should be slowed and anticoagulation started (cardioversion unlikely to succeed once LV dysfunction) Hypertension should be treated until disease progression drops cardiac output and hence BP Valvular disease should be assessed for surgical correction where appropriate (especially aortic valve disease \200\224 discuss with patient early after ons et of heart failure) Treat anemia and thyroid disease Vaccination Offer in \202 uenza vaccination annually and pneumococcal vaccination (once on ly). Monitoring Should include: \200 Clinical assessment of symptoms and functional capacity ( how far can they walk without stopping etc.) Blood pressure, including postural measurements \200 Fluid status (weigh regularly. Estim ate dry weight, record it and use this to titrate future management. Examine for JVP, oedema, and lung crepitations) Cardiac rhythm (clinical and by ECG) \200 Cognitive state (commonly impaired in heart fai lure due to vascular disease and low BP) Nutritional state (malnutrition common in heart failure. Ask about appetite, assess muscle bulk, check albumin \200\224 consider build-up drinks or dietician input) CHRONIC HEART FAILURE 293 Medication review (are they on all appropriate drugs at maximum tolerated doses?) Side effects (especially ask about postural symptoms, check UC + E) \200 Psychological an d social review, done by an MDT (how are they and carers coping with problems of chronic di sease? Do they need any social support?) Box 10.3 Medication for chronic heart failure \200 Loop diuretics \200\224 (eg furosemid e) Use to control symptoms. Begin with 40mg (20mg in very elderly) and titrate upwards (gui ded by symptoms and examination \201 ndings). Monitor renal function and electrolytes ACE inhibitors \200\224 should be started early in all with a diagnosis of systolic heart failure unless valvular cause, or renal artery stenosis suspected. Again beg in low (eg ramipril 2.5mg) and titrate upwards monitoring renal function and postural sympt oms B-blockers \200\224 should be started in all stable patients with LV systolic dysfunction after diuretics and ACE inhibitors regardless of whether there are continuing symptoms (imp roves prognosis). Use B -blocker licensed for heart failure, eg carvedilol 3.125mg, bisopro lol 2.5mg, and titrate upwards Spironolactone \200\224 use for continuing symptoms despite loop and ACE. Dose 25mg. Watch potassium levels as ACE and spironolactone will raise this Digoxin \200\224 use in AF, and where there are continuing symptoms despite maximal other therapy in sinus rhythm Thiazide diuretics \200\224 can be added to loop diuretics in end-stage heart failure, eg bendro \202 umethiazide 2.5mg, or metolazone 5mg (monitor electrolytes closely; may be use d on alternate days if causes excess diuresis) Warfarin \200\224 use in AF, or where echo has shown intracardiac thrombus ARBs \200\224 (eg candesartan) useful where ACE intolerant, this class has bene \201 ts in heart failure but its equivalence to ACE inhibition is debated Aspirin/statins \200\224 use for risk factor modi \201 cation where cause is IHD Further reading NICE . Chronic heart failure ( 2010 ) online: M www.nice.org.uk/cg108 . 294 CHAPTER 10 Cardiovascular Dilemmas in heart failure Terminal care \200 Chronic heart failure is a grim diagnosis wi th a poor outlook (only 25 % will survive 3 years \200\224 worse than many cancers) Consider broaching this with all patients in clinic (ideally in a stable phase of the illness) to allow future plans to be made and resuscitation issues discussed. Monitoring of any cognitive impairment allows the timing of this conversation to be careful ly judged As the disease progresses ensure appropriate palliative care measures are taken with carefu l review of symptoms and patient/family anxieties Consider hospice care if available \200 Opiates (eg morphine sulfate solution 2.5 \200 \22310mg) can be given to help relieve the distress of dyspnoea and allow sleep \200 Continuous oxygen therapy may ease discomfort \200 Intermittent iv boluses of furosemide in DH can keep people out of hospital Further reading Stewart S , McMurray JJV . ( 2002 ). Palliative care for heart failure . BM J 325 : 915 \200\223 16 . DILEMMAS IN HEART FAILURE 295 HOW TO Manage the heart failure see-saw One of the commonest dilemmas is balancing drugs in a patient with both heart failure and c hronic renal failure. Aggressive diuretic use will improve the heart failure but lead to thirst, malaise, hyponat raemia, uraemia, postural hypotension, and ultimately anuria. Hydrating to improve renal function will lead to worsening pulmo- nary oedema. Each patient will need a carefully planned balance, accepting moderate elevations in urea a nd/or a bit of oedema, which enables the patient to exist in the greatest comfort. This bal ance will take time and skill to achieve. The following will help: Make all changes slowly and wait for impact \200\224 large dose changes increase oscillation between wet and dry states If a patient is still losing weight on a treatment regimen, they are likely to continue to do so \200\224 do not discharge after an acute event until steady st ate is reached, otherwise they will bounce back into hospital with dehydration and renal fa ilure Get to know the ideal weight, and use this to guide therapy \200 Involve patients and car ers wherever possible \200 Admit and stabilize in hospital \200 Get to know the patient \200\224 continuity of care is very helpful, and community heart failure nurses may play a key role in this 296 CHAPTER 10 Cardiovascular Diastolic heart failure \200 Clinical syndrome of heart failure with preserved LVEF seen on echocardiography ( > 50 % ), where there is no major valvular disease \200 Accounts for a round a third of clinically diagnosed heart failure, and is more common in older patients, especially women, hypertensive patients, and those with LVH Not a benign condition \200\224 ambulatory patients do better than those with systolic hea rt failure, but the mortality is equivalent in older patients or hospitalized. Fourfold inc rease in mortality when compared with controls without heart failure 2Important to recognize and treat, and not to discontinue heart failure treatment on basis of normal LV function alone. Pathology Thick-walled LV with a small cavity. Slow to relax and allow \201 lling in dias - tole, causing increased diastolic pressures (hence pulmonary pressures and so dyspnoea) a nd a low cardiac output (hence fatigue). Diagnosis \200 Clinical suspicion (history as for systolic heart failure) and examination \201 ndings (elevated JVP, pulmonary oedema, hypertension, murmur in the aortic area, 4t h heart sound), are key CXR will show pulmonary congestion, and the ECG evidence of hypertension Echocardiography shows preserved LV function and in skilled hands may show evidence of abnormal diastolic relaxation (Doppler studies show a reduced ratio of early (E) to late or atrial (A) ventricular \201 lling velocities \200\224 E:A <0.5 is suggestive of diastolic dysfunction). However, these changes are very common in older patie nts (E:A often <1) and it is unclear as yet whether asymptomatic diastolic dysfunction warr ants treatment. Thus treatment is based on symptoms, not echo results \200 BNP (see Box 1 0.2 ) may be useful in cases where there are multiple possible aetiologies of dyspnoea as a negative result makes heart failure unlikely, helping to limit polypharmacy Management \200 Prevention \200\224 by BP control at population level \200 Relieve pre cipitants \200\224 treat arrhythmias, anemia, thyroid disease, ischaemia, malnutrition Acute symptoms \200\224 control BP with oral agents as priority. Use diuretics cautiously as can drop cardiac output still further Chronic disease management \200\224 less evidence than for systolic heart failure. Control of BP is key. Diastolic relaxation agents (eg B -blockade) not proven but rate control with these especially where there is dual indication, eg AF or IHD. Diuretics improve symptoms but ensure you don \200\231t dehydrate patients as these patients are vuln erable to reductions in preload. ACE inhibitors and ARBs are likely to help. Improve exerci se tolerance with physical activity This page intentionally left blank 298 CHAPTER 10 Cardiovascular Valvular heart disease The majority of valvular heart lesions in the UK are degenerative (e g senile calci \201 cation is the main cause of aortic stenosis) so valve defects are very common in older patients. The following must be remembered: \200 Listen to the heart of all elderly people \200\224many valve lesions are detected incidentally Think of valvular disease when a patient presents with dyspnoea, heart failure, angina, palpitations, syncope or dizziness. Examine them carefully (see Tabl e 10.5 ). When a murmur is heard, echocardiography should be requested in order to document the valve lesion and formulate a management plan \200 Following a revie w of evidence by NICE in 2008 antibiotic prophylaxis is no longer recommended dental for invasive procedures 2Remember endocarditis if a murmur is heard in the context of an unex- plained fever. Surgical treatment \200 Once the valve lesion is known, decide whether valve replacement is indicated yet (see Table 10.5 ). In many lesions (eg mitral valve disease and aortic reg urgitation) the progression of symptoms alerts to the need for pre-emptive surgery. In aort ic stenosis however, a prompt response to the development of early symptoms is required, an d so the approach is different Consider whether or not the patient is a surgical \200\230candidate \200\231. Remember tha t many lesions are amenable to percutaneous interventions which are feasible in much fraile r patients Bioprosthetic (pig) valves can be used in older patients, which have a shorter life span th an metal valves, but obviate the need for warfarin \200 If surgery is not yet indicated, then ensure there is some sort of call- back/surveillance system in place \200\224 whether repeat echocardiography, or clinic revi ew, or simply ensuring that the patient knows what symptoms should trigger medical review Talking to patients about potential surgery \200 Always ask the patient what they think \200\224 often there will be strong views that come as a surprise to the physician. Many older people are terri \201 ed at the prospect, others are keen to proceed and others will not want to decide \200\224 \200 \230whatever you think, doctor \200\231 Make it clear that obtaining a surgical opinion is not committing the patient to surgery, indeed the surgeon may feel that the risks outweigh the bene \201 ts, but that it is an important \201 rst step Having a frank and useful discussion about risks and bene \201 ts is often dif \201 cult, but should always be attempted before referral is made \200 Ensure you have enough time and take it slowly, giving plenty of opportunity for questions. They may wish to go away and think about it, perhaps returning w ith a family member \200\224 encourage this and do not force a decision Table 10.5 Common valve lesions Valve lesion Symptoms Complications Treatment Who to consider for surgery? Symptoms despite medical management If pliable valve, may be candidate for balloon valvulop lasty Rate control of AF (digoxin and/or B -blocker) Anticoagulation for AF Diuretics if heart fa ilure Antibiotic prophylaxis for invasive procedures AF Systemic emboli Pulmonary hypertension Pulmonary oedema Pressure effects from large LA E ndocarditis Mitral stenosis Dyspnoea Fatigue Palpitations Chest pain Haemoptysis Deteriorating symptoms \200\224 aim to replace valve before extensive LV damage Condition progresses slowly, so not if asymptomatic Rate control of AF Anticoagulation if AF Diuretics if HF Antibiotic prophylaxis for invasiv e procedures Pulmonary oedema AF Endocarditis Mitral regurgitation Dyspnoea Fatigue Palpitations Consider surgical referral If not suitable, then treat angina and heart failure symptomatic ally Avoid ACE inhibitors Antibiotic prophylaxis for invasive procedures Angina Pulmonary oedema Syncope Sudden death Endocarditis Aortic stenosis Angina Dyspnoea Heart failure Dizziness Syncope Sudden death Once symptomatic prognosis poor (2 \200\2233 years), so refer for valve replacement early a fter symptom onset Asymptomatic patient with deteriorating ECG should also be referred Valv uloplasty may be an option for frail patients. V A L V U L A R H E A R T Aortic sclerosis None None None Not applicable Worsening symptoms, worsening cardiomegaly, ECG deterioration Aim to replace valve before e xtensive LV damage Pulmonary oedema Endocarditis Diuretics if heart failure Antibiotic prophylaxis for invasive procedures Aortic regurgitation Dyspnoea Palpitations Heart failure D I S E A S E 2 9 9 300 CHAPTER 10 Cardiovascular Peripheral oedema Swollen ankles are extremely common in older patients. As with all geri- atric medicine, a careful assessment, diagnosis, and appropriate treatment should be carrie d out. 2Swollen ankles do not always indicate heart failure \200\224 Starting a diuretic m ust not be an immediate reaction as this treats only one of several causes and may cause ha rm. Causes \200 Often, mild ankle swelling occurs in an otherwise \201 t person \200\224 t his tends to be worse on prolonged standing and in the heat (sometimes referred to as \200\230 dependant oedema \200\231) It is likely that there is some minor venous disease causing the oedema, but it is essentially benign \200 Peripheral venous disease \200\224 chronic oe dema due to damage to deep veins causing venous hypertension, increased capillary pressure and \201 brinogen leakage. Usually bilateral, but one side is often worse than the other ( see b \200\230Chronic venous insuf \201 ciency \200\231, p.592) Heart failure \200\224 usually bilateral. Look for associated signs, eg raised JVP, cardiac enlargement, pulmonary crepitations, etc. Super \201 cial thrombophlebitis \200\224 acute oedema with a red, hot, very tender venous cord with surrounding oedema DVT \200\224 acute onset painful swollen calf with pitting oedema of ankle. Review thrombotic risk factors 2Always consider DVT with new onset unilateral swelling. \200 Drug side effect \200\224 commonly calcium channel blockers (especially amlodipine) and NSAIDs Low serum albumin \200\224 nephrotic syndrome, gastrointestinal loss, malnutrition, chronic disease, acute sepsis etc Lymphatic obstruction \200\224 consider obstructing pelvic tumors. If oedema is severe, perform rectal and groin examination Traumatic \200\224 after forcefully dorsi \202 exing the foot (usually when walking), lea ding to rupture of the plantar tendon or injury to gastrocnemius. This oedema tends to be u nilateral, tender, above the ankle and with associated bruising to the calf. Treat with res t and NSAIDs Other \200\224 eg hypothyroidism, osteoarthritis of the knee, ruptured Baker \200\231s cyst, poststroke paralysis Assessment \200 History \200\224 How acute was the onset? Is it unilateral or bilateral? Is it painful, red and hot? What are the associated physical symptoms \200\224 importantl y dyspnoea (may indicate PE or heart failure)? Examination \200\224 Look for physical signs. Always listen to the heart and lungs and look for sacral oedema when ankle swelling is found. Consider rectal/groin ex amination Investigations \200\224 Be guided by your clinical suspicion. Consider ECG (unlikely to be normal in heart failure), urea and electrolytes, albumin, FBC, TFTs 2D-dimer in elderly patients with swollen ankles is rarely helpful. While a negative result effectively rules out DVT, many elderly patients will have an elevated d-dimer \200\224 o nly use the test if you would proceed to ultra- sound scanning in the event of a positive r esult. PERIPHERAL OEDEMA 301 Treatment All patients with ankle swelling should have a careful assessment for disease, wi th treatment dependant on cause: \200 Stop drugs if they are responsible (consider replac ing with alternatives) \200 If heart failure, then full assessment and treatment is requi red \200 For chronic venous disease use leg elevation and compression bandaging or stockings (see b \200\230Chronic venous insuf \201 ciency \200\231, p.592) With severe lymphoedema, massage and pneumatic boots can be useful. Consider referral to specialist lymphoedema clinics If low albumin, treat cause and increase dietary intake If no disease is found then managem ent is pragmatic. Patients may \201 nd the ankle swelling unsightly, have dif \201 culty \201 tting on their shoes or even com- plain of an aching pain. Support hosiery may help . Many patients may be happy to tolerate the minor inconvenience once they have been assure d that there is no serious pathology. It may then be appropriate to start a low dose of thiazide or loop diuretic (eg bendro \202 umethiazide 2.5mg) but this will necessitate occasional monitoring of electrolytes and clinical review to ensure the bene \201 ts of treatment still outweigh the risks. Ankle swelling and nocturnal polyuria \200 During the day, a large amount of \202 uid c an collect in the interstitial space in the ankles At night, when the legs are elevated, this \202 uid is partly returned to the circulating volume and can cause a diuresis \200\224 hence nocturnal polyuria \200 Paradoxically, t reating such a patient with diuretics to limit the swelling may ultimately help with the polyuria 302 CHAPTER 10 Cardiovascular Preventing venous thromboembolism in an older person Venous thromboembolism (VTE), which in corporates DVT and PE is a major cause of morbidity and mortality in hospitalized patients on both medical and surgical wards. The UK Department of Health has recently introduced nat ional initiatives to reduce rates. Recognition \200 Older patients present atypically so diagnosis is often delayed \200 T hey less frequently complain of pain and decreased ability to walk, and their legs more com monly have asymmetrical swelling due to other conditions, eg chronic venous insuf \201 cie ncy, arterial or joint disease, etc. Prophylaxis \200 Most hospitals now use a standardized risk assessment score/tool for all patients Age > 60 is known to be a risk factor for VTE, as is reduced mobility compared to normal so almost all older patients will qualify for prophylactic treatment unless risks of treatmen t (bleeding risk) outweigh bene \201 ts Contraindications are sometimes absolute (eg immediately after stroke, haematemesis) but mo re commonly are relative (eg extensive bruising after a fall) and the geriatrician must wei gh risks and bene \201 ts on a case by case basis Aspirin is no longer considered effective VTE prophylaxis but patients on aspirin for other reasons are at higher risk of some bleeding complications (especially gastrointestinal) when low molecular weight heparin is given Review \200 Reassessment is required every few days or when there is a material change in the patient condition Patients who move into rehabilitation settings often regain mobility and it is unclear from the evidence when prophylactic low molecular weight is no longer required. Options include stopping at: \200 Premorbid mobility level \200 Steady state \200 Discharge Heparin injections should usually be stopped for patients receiving pallia- tive care. PREVENTING VTE IN AN OLDER PERSON 303 Options for thromboprophylaxis (Table 10.6 ) Table 10.6 Thromboprophylaxis options for older patients Prophylactic treatment Risks/disadvantages in older patients Notes Earlier mobilization may increase falls risk and increase nursing time General measures, eg promote mobilization, avoid dehydration Incorrectly applied stockings (wrinkles) can worsen venous return Contraindicated in arterial disease, neuropathies, skin fragility/breaks and heart failure Graduated anti-embolism stockings Proven to be no help in patients with stroke Not always well tolerated Older patients need help to put on and maintain correct position so increased nursing time A reduced dose should be used in patients with eGFR <30mL/min/1.73m 2 Low molecular weight heparin Bleeding risks more common in older patients include risk of falls, low platelets and antic oagulant treatment Inferior vena cava \201 lter Only in very high risk (eg PE despite warfarin) who need additional or alternative prophyla xis to full warfarinization Oral direct thrombin inhibitors are now available (eg dabigatran) which have an anticoagula nt effect without need for intensive monitoring. The number of licensed indications are gro wing and it is likely to play a major role in VTE prevention and treatment in the near futu re. Further reading NICE . Venous thromboembolism; reducing the risk ( 2010 ) online: M www.nic e.org.uk/cg92 . Cayley WE Jr . ( 2007 ). Clinical review: Preventing DVT in hospital inpati ents . BMJ 335 : 147 . 304 CHAPTER 10 Cardiovascular Peripheral vascular disease Peripheral vascular disease is common in older patients \200 \224 causing symp- toms in 10 % of those over 70 years. Symptoms \200 Only a third of older patients will have the classic symptoms of intermittent claudication and often decreasing activity levels will mask developing disease . It may be dif \201 cult to distinguish the pain from that of osteoarthritis Claudication pain may progress to ischaemic rest pain (night-time pain, often relieved by h anging foot over bed), then to ulceration \200\224 due to trauma with poor healing (small, punctate, painful ulcers at pressure points, eg toes, lateral malleolus, metatarsal heads) and possibly gangrene Around 80 % of patients with claudication remain stable or improve; only 20 % deteriorate, and 6 % require amputation (ongoing smokers and diabetics are most at risk) Examination \200 Loss of pulses (best discriminator is an abnormality of the posterior tibial pulse) \200 Possibly bruits \200 Coolness to touch \200 Slow capillary re \201 ll (over 2sec) \200 Shiny hairless skin with atrophic nails and poor wound healing Peripheral vascular disease as a marker of other vascular disease \200 5-year mortality i n peripheral vascular disease is 30 % , mostly due to cardiovascular disease It is easy to detect peripheral vascular disease non-invasively by measuring the ankle \200\223brachial pressure index (ABPI) ( see b \200\230HOW TO Me asure ABPI \200\231, p.305) The impact of broad vascular risk management on subsequent vascular disease burden has yet to be quanti \201 ed, but is likely to be substantial 2If a patient complains of leg pains , screen for peripheral vascular disease and if detected initiate full vascular secondary p revention. Management Although very common, many elderly people will modify their lifestyle to reduce symptoms. It is important to actively seek out symptoms. Adopt the following treatment approach: Modify risk factors \200 Advise increasing exercise (NOT decreasing) \200 Commence anti platelet agent \200\224 commonly aspirin; clopidogrel may have slightly more ef \201 cacy Consider other drugs \200\224 phosphodiesterase inhibitors (eg cilostazol) have antiplatel et activity and act as vasodilators. The herbal remedy Ginkgo biloba probably has no impact , but does no harm PERIPHERAL VASCULAR DISEASE 305 Do not necessarily stop B -blockers (traditionally thought to worsen claudication). The evi dence for this is weak and B -blockers have a major role in modifying cardiac risk Refer for revascularization when appropriate. Percutaneous revascularisation is relatively low risk and should be considered for lifestyle-limiting cl audication that does not respond to medical therapy, where there is a focal stenosis or whe n there is limb-threatening ischaemia in a patient who is not \201 t for surgery. Electiv e surgery is usually reserved for low-risk patients (under 70 years with no diabetes and no distal disease) who are \201 t enough to tolerate the procedure. Age has a signi \201 c ant impact on surgical risk \200\224 relative risk of mortality increases by 1.62 with eac h decade HOW TO Measure ABPI When? \200 To con \201 rm peripheral vascular disease as a cause of claudication \200 To diagnose vascular disease before implementing secondary prevention To diagnose the etiology of (venous) ulcers \200 To ensure compression bandaging is safe Equipment \200 Blood pressure cuff with sphygmomanometer \200 Hand-held Doppler probe M ethod \200 In \202 ate the cuff around the upper arm as usual and use the Doppler probe over the brachial artery to measure the systolic blood pressure Repeat in the other arm and use highest value \200 Next in \202 ate the cuff around the ankle and use the probe to measure the systolic pressure in the dorsalis pedis and posterio r tibial arteries Take the highest of the four ankle readings and divide by the higher of the two arm readings to give the ABPI Interpretation \200 > 1.3 \200\224 non-compressible calci \201 ed vessels; reading has limited value \200 1.0 \200\2231.3 \200\224 normal range \200 <0.9 \200\223angiographi c peripheral vascular disease very likely \200 0.4 \200\2230.9 \200\224 likely to be ass ociated with claudication \200 <0.4 \200\224 advanced ischaemia 306 CHAPTER 10 Cardiovascular Gangrene in peripheral vascular disease The onset of gangrene is relatively common in peopl e with severe periph- eral vascular disease and causes considerable distress. It often pose s management dif \201 culties, as many frail elderly are judged inappropriate for open sur gery. Slowly progressive disease with dry gangrene \200 Cyanotic anesthetic tissue with necrosi s \200 Distal, with clear demarcation \200 Often a low-grade in \202 ammatory response (elevated white cell count and CRP) The patient may feel unwell and anorexic \200 Non-urgent surgical review is appropriate, but the approach is often to allow auto-amputation \200\224 a lengthy and sometimes distre ssing process, for patient and family. This may be managed as an outpatient Surgical amputation may be considered but as there is often inadequate local circulation to allow healing, this may need to be extensive, or combined with bypass (the latter carrying a signi \201 cant operative risk). Sometimes amputation vastly improves the quality of li fe for a bed- bound patient with gangrene. Discussion about possible amputation should be a pproached with tact and sensitivity \200\224 patients are often very against loss of a lim b, even when they have not walked for years. Ensure that the patient and family are aware o f the rationale for treatment, and that there is regular review of analgesia requirements Wet gangrene \200 Moist, swollen, and blistered skin \200\224 usually in people with dia betes 2This is a life-threatening condition and urgent surgical review is required, in all but the most terminal of patients \200 The usual approach to management is to start iv an tibiotics prior to debridement and amputation Acute ischaemia 2This is a limb-threatening condition and demands urgent action \200 Usua lly due to embolization \200 Distal emboli cause so-called \200\230blue toe syndrome \200\231. The main object of treatment is to prevent recurrence as little can be done to sa lvage occluded small vessels. This may include angiography to establish the source, and/or anticoagulation depending on the \201 tness of the patient Proximal emboli cause diffuse acute ischaemia. Revascularization of the limb is nearly alwa ys attempted (unless there is already irreversible ischaemic changes) and the approach can be tailored to the frailty of the patient \200\224 ranging from thrombolysis, percutaneous thromboembolectomy (possible under local anesthesia) to emergency bypass procedures This page intentionally left blank 308 CHAPTER 10 Cardiovascular Vascular secondary prevention (Table 10.7) Atheromatous vascular disease (cardiac, peripher al vascular, and cerebral) accounts for a huge amount of morbidity, mortality, and expendit ure. Secondary prevention measures evolve continually as individual clinical trials reach comple tion. Although some interventions are primarily applied to a speci \201 c pathology, most impact on all vascular systems. The cumulative effect of therapies is not yet known, but th e consensus is that they will substantially reduce the burden of future vascular events. Traditionally, older patients have been under-provided with secondary prevention measures, for a number of reasons: \200 There is often polypharmacy, and reluc tance among patients and healthcare professionals to add to this It was thought that secondary prevention bene \201 ts were seen only with long-term (perha ps 5 \200\22310 years) treatment. Unless life expectancy was greater than this, therapy was not begun It may be \200\230shutting the door after the horse has bolted \200\231 \200\224 the dama ge has already been done But consider several contrary points: \200 Recent evidence suggests that some therapies ( statins and ACE inhibitors) act quickly, possibly due to endovascular stabilization Although older patients are under-represented in clinical trials, where older patients have been included (eg the Heart Protection Study) the bene \201 ts have been equal, if not gr eater than in younger patients Do not assume that a disabled person will not bene \201 t from prevention of further event s. In a bed-bound stroke patient who has to be spoon- fed a further stroke that removes swa llowing ability altogether may deprive that person of their only pleasure in life As with much of geriatric medicine, frank discussion with the patient is advised. Many pati ents will have strong views and fall into one of two groups \200\224 the fatalists, who pr efer not to take medication \200\230just in case \200\231, and the \200\230belt-and-brace s \200\231 patients who welcome all possible measures Drug doses are determined by clinical trial evidence \200\224 often a high dose in generally robust patients. Adopt a pragmatic approach in frail patients, with lower doses as these may be effective with fewer side effects Reduce doses of renally cleared medication with low GFR We do not advocate the blind prescr iption of all secondary prevention to all of older patients \200\224 such an approach woul d be clinically inappropriate for some and unlikely to be cost-effective. What we do sugges t is that each patient is considered on a case-to-case basis and, where possible, included in the discussion to reach an individually tailored action plan. Further reading The Heart Protection Study Collaborative Group (HPS) . ( 2002 ). Lancet 360 ( 9326 ): 7 \200\223 22 . Heart Outcome Prevention Evaluation (HOPE) Study . ( 2000 ). N Engl J Med 342 : 145 \200\223 53 . Clopidogrel versus aspirin in patients at risk of ischa emic events (CAPRIE) . ( 1996 ). Lancet 348 : 1329 \200\223 38 . Table 10.7 The main secondary prevention agents Agent Dose Action Outcome Special points Aspirin 75 \200\223300mg od Antiplatelet activity Prevention of all vascular events Use lower doses Beware gastric irritation Consider co-prescription of proton pump inhibitor /H2 antagonist Enteric coated formulations unlikely to be very useful Reportedly, lower gastric side effects. Slightly higher ef \201 cacy than aspirin as monot herapy Clopidogrel 75mg od Antiplatelet activity Mainly as an alternative to aspirin where not tolerated, or as an addition in cardiac and s ome stroke disease. V A S C U L A R Start slowly as commonly causes headache Low bleeding risk Dipyridamole MR 200mg bd Antiplatelet activity Addition to aspirin in cerebrovascular disease NOT for cardiac disease (can exacerbate angi na) S E C O N D A R Y Antihypertensives Various agents Blood pressure reduction Prevention of all vascular events The lower the BP, the greater the bene \201 t, but take care to avoid hypotensive side eff ects Prevention of all vascular events Dose stated is often not tolerated in older patients \200\224 aim as high as tolerated, bu t start with 1.25mg ACE inhibitors eg Ramipril 10mg od Blood pressure reduction and possible endovascular effect P R E V E N T O N Prevention of all vascular events Should be prescribed for vast majority Lower doses may be better tolerated \watch for myalg ia and raised LFTs Statins eg Simvastatin 40mg od Cholesterol lowering and possible endovascular effect I