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 Note: consider also smoking cessation, increasing physical activity, and for stroke \200 \223endarterectomy and AF prophylaxis. 3 0 9 This page intentionally left blank 311 Chapter 11 Chest medicine The ageing lung 312 Respiratory infections 314 In \202 uenza 316 HOW TO Treat in \202 uenza-like illness in older people 317 Pneumonia 318 Pneumonia: treatment 320 HOW TO Manage the patient with pneumonia who fails to respond to treatment 322 Vaccinating against pneumonia and in \202 uenza 324 Pulmonary \201 brosis 325 Rib fractu res 326 Pleural effusions 328 HOW TO Aspirate a sample of pleural \202 uid 329 Pulmonary embolism 330 Aspiration pneumonia/pneumonitis 332 Chronic cough 333 Lung cancers 334 Tuberculosis: presentation 336 Tuberculosis: investigation 338 HOW TO Perform and interpret a tuberculin skin test 339 Tuberculosis: treatment 340 Asthma and COPD: assessment 342 Asthma and COPD: drug treatment 344 HOW TO Improve drug delivery in asthma or COPD 345 Asthma and COPD: non-drug treatment 346 Oxygen therapy 348 Asbestos-related disease 350 312 CHAPTER 11 Chest medicine The ageing lung Most of the functional impairment of the lungs that is seen in older people is due to disease, often smoking-related. Intrinsic ageing leads only to mild functional d eterioration. The respiratory system has a capacity well in excess of that required for nor mal activity, so intrinsic ageing: \200 Does not lead to symptoms in the non-smoker witho ut respiratory disease In those with respiratory disease (eg emphysema) will cause progressively worsening symptoms with age even if the disease itself remains stable In acute disease, eg pneumonia, may cause earlier decompensation or a more severe presentation Speci \201 c respiratory changes Seen in healthy older people are similar to those seen in mild chronic obstructive pulmonary disease, and include: \200 Decreased elastic recoil c ausing small airways to collapse at low lung volumes and increased residual volume Increased chest wall stiffness, due to: Degenerative change in intercostal, intervertebral and costovertebral joints Osteoporosis and kyphoscoliosis \200 Weaker respiratory muscles that may have lower endur ance \200 Reduced gas exchange and increased ventilation-perfusion (V/Q) mismatch, due to collapse of peripheral airways while perfusion remains intact Impaired chemoreceptor function, leading to lessened ventilatory response to decreased P a O 2 or increased P a CO 2 Impaired microbial defense mechanisms. Less effective mucociliary clearance and less sensitive cough re \202 ex Observed consequences of these changes These include: \200 Increased susceptibility to in fection (underventilation of and inability to clear sputum from dependent lung zones) Lower maximum minute ventilation (weaker musculature acting against a stiffer chest) An approximately linear fall in PaO2 with age (70.3 % /year). Since alveolar oxygen tension remains stable, the alveolar-arterial (A-a) oxygen gradient rises Reduced exercise capacity. However, oxygen consumption and cardiac output decline in propor tion to lung function, so the lungs are rarely the limiting factor in exercise performance THE AGEING LUNG 313 Breathlessness in older people is often multifactorial \200 Chronic breathlessness in an individual may be the result of, eg, decreased \201 tness, obesity, an inef \201 cient gait (osteoarthritis or stroke), kypho sis, previous lung damage (eg apical \201 brosis due to tuberculosis (TB)) and intrinsic ageing. In this example, note that only one of the factors is speci \201 c to the lung In the acutely breathless patient, pathologies commonly coexist, eg infection, fast AF, and heart failure. The classic treatment triad of digoxin, furosemide, and amoxicillin is not a sign of diagnostic indecision but is often entirely appropriate treatment 314 CHAPTER 11 Chest medicine Respiratory infections Cough with or without sputum, shortness of breath, fever or chest pa in is a very common presentation in older patients. It is very important to try to distingu ish which part of the airway is primarily affected because this implies completely differen t pathogens, prognoses, and treatment strate- gies. Try to avoid aggregating all such patie nts together using the impre- cise term \200\230chest infection \200\231. Upper respiratory tract infections These are caused by viruses, eg rhinovirus, respiratory syncytial virus, in \202 uenza, and parain \202 uenza. Symptoms include nasal discharge a nd con- gestion, fever, and sore throat. These may extend to the lower tract and then inclu de cough, wheeze, sputum production, or worsening of existing cardiopulmonary disease. With increasing age: Upper respiratory tract infection becomes less frequent, but more severe The risk of complications increases. These include: Lower tract infection such as bronchitis or pneumonia, which may be bacterial or viral Bronchospasm \200 Extrapulmonary manifestations such as falls, immobility, and delirium Postinfection weakness, fatigue, and anorexia is more severe and prolonged, maybe lasting several weeks Frequency of hospital admission and death increases substantially Acute bronchitis Occurs with in \202 ammation of the bronchial tree with little or no invo lve- ment of lung parenchyma (which is pneumonia). Is commoner in those with chronic airway s disease (see b \200\230Asthma and COPD: assessment \200\231, p.342). Compared with pneumonia, bronchitis: Has fewer systemic features and a better prognosis \200 Has no chest symptoms and signs, eg pleuritic pain or crepitations, but may have prominent cough and wheeze CXR not routinely indicated \200 Can be managed less aggressively, with more reliance on supportive treatment and bronchodilators than antibiotics. Often viral in origin, if an ant ibacterial is thought appropriate, give amoxicillin to cover Streptococcus pneumoniae (eryt hromycin or clarithromycin if penicillin sensitive) This page intentionally left blank 316 CHAPTER 11 Chest medicine In \202 uenza This is the most serious viral respiratory tract infection, and is often a s evere, systemic illness with pulmonary bacterial superinfection ( Staphylococcus aureus, Ha emophilus in \202 uenzae, Strep. pneumoniae ). It occurs most commonly in December-Februar y. Antigenic shifts result in periodic pandemics (large-scale epidemics). Presentation is similar in young and old, ie rapid onset of fever (rigors, chills), myalgia , headache, and fatigue with variable degrees of prostration. Compared with less threatenin g viruses such as rhinovirus: \200 Nausea, vomiting, diarrhea, high fever, rigors and ocu lar symptoms (eg photophobia) are more common Rhinorrhoea is less common include myocarditis and meningoencephalitis. Mild meningism is common, and if combined with other sinister features (eg altered conscious level) is an indication for CSF sampling. Less common serious complications Diagnosis is usually based on combining clinical assessment with epidemiological data, part icularly current in \202 uenza incidence. Some other viruses can cause an identical clinic al syndrome, and serological test results are not immediately available. Thus an initial as sessment cannot produce an absolutely con \201 dent microbiological diagnosis. The syndrom e may therefore most precisely be labeled \200\230in \202 uenza-like illness \200\231. Positive virological diagnosis in the context of increased community incidence or a care ho me outbreak is helpful by prompting vigorous attempts to reduce transmission of infection. Reducing viral transmission Mass outbreaks of respiratory viral infection are common in car e homes and hospitals. They can occur at any time of year but are commonest from autumn to spring, Viruses are spread by aerosol or hand-to-hand contact (sometimes indirect, via fomi tes such as cutlery or drinking vessels). During an outbreak \200 Reduce transfers of healthy patients into, or symptomatic patient s out of, the affected area Reduce staff movement across work areas (especially applicable to short-term staff who may work in many clinical areas in a short time) \200 Care for sympt omatic patients in single rooms, or in ward bays with similarly infected patients Exclude visitors with respiratory or viral symptoms from the ward \200 Ensure that care s taff have been immunized against in \202 uenza \200 Ensure that scrupulous hand-washing procedures are followed \200 Consider using face masks for staff caring for symptomatic p atients INFLUENZA 317 HOW TO Treat in \202 uenza-like illness in older people The following guidance is ge neric, and should be tailored to the patient, their illness, and their care environment. If the highest quality care cannot be provided, then a prompt step-up of care should be arran ged. This may include hospital admission. \200 Do not underestimate the disease. Mortalit y and morbidity increases exponentially with age and frailty Give excellent supportive and symptomatic care. Its effectiveness should not be underestimated \200 Fluids. Reduced intake and increased losses (fever) lea d to volume depletion and end organ dysfunction. Encourage frequent oral \202 uid and sus pend any diuretic treatment. Consider early initiation of s/c or iv \202 uids if a viciou s spiral of dehydration and poor intake seems likely to ensue Nutrition. Encourage high-calorie, high-protein drinks or solids. If the illness is especia lly severe, prolonged, or complicated, or if the patient is especially frail or malnourishe d, consider a period of NG feeding. Involve a dietician early Paracetamol. If fever, discomfort, or pain occur \200 Maintain mobility. Bed rest may sen tence the patient to death or dependency. Carers may need clear, \201 rm advice about this Identify and treat complications promptly Carers may need information about important warning signs and the need to seek prompt medical advice Perform regular observations of BP, pulse, and temperature where possible Common serious complications include delirium, secondary bacterial infection, bronchospasm, pressure sores, and circulatory collapse Antiviral agents (the neuraminidase inhibitors zanamivir and oseltamivir) can reduce both the severity and duration of in \202 uenza \200 They are in dicated in patients > 65 years who have an in \202 uenza- like illness during a period of high community incidence, provided they present early (<48h r) They are well tolerated, reduce symptom severity and duration and they may reduce mortality Zanamivir is inhaled, oseltamivir is taken orally Further reading NICE . Amantadine, oseltamivir and zanamivir for the treatment of in \202 uenza ( 2009 ). Online: M www.nice.org.uk/ta168 . 318 CHAPTER 11 Chest medicine Pneumonia Pneumonia \200 This is a syndrome of acute respiratory infection with shadowing on CXR May be primarily lobar, bronchial or mixed pattern \200 Symptoms may be mild and are ofte n non-organ speci \201 c eg fever, malaise Common presenting scenarios include cough (often unproductive), delirium, reduced conscious level, lethargy, anorexia, falls, immobility and dizziness. Rar ely patients can present with shock, coma and adult respiratory distress syndrome (ARDS) Chest pain, dyspnoea and high fever are less common than in younger people. Signs may be minimal: \200 The patient may be well or unwell. Assess severity usi ng the CURB criteria (see b \200\230Characteristics of severe pneumonia: the CURB-65 score \200\231, p.320) Fever is often absent, but vasodilatation is common \200 Tachypnoea is a sensitive sign, as is at least moderate hypoxaemia ( (cid:100) 95 % on air) on oximetry \200 Tests often guide management Chest radiograph often reveals minimal infective in \201 ltrate. Associated problems can include malignancy, effusion, or heart failure Blood cultures should be sent, but sputum culture is rarely useful unless TB is suspected White cell count may be raised, normal, or even depressed \200 CRP is often normal early in the illness. A very high CRP suggests pneumococcal disease or severe sepsis of any cause U,C + E guide \202 uid management. Renal impairment is a sign of poor prognosis Arterial blood gas (ABG) sampling is not usually necessary, unless oxygen saturations are <90 % ; oximetry is much better tolerated and usually suf \201 cien t to guide oxygen therapy Organisms (see Table 11.1 ) Often no causative organism is identi \201 ed \200 Pneumococcus is a common pathogen in all settings, including hospital Viral pneumonia, especially in \202 uenza, is under-recognized, and is the second most com mon cause of community-acquired pneumonia Legionella and Mycoplasma pneumonias are uncommon. Mycoplasma is much more frequent during epidemics, occurring every 3 years or so Unusual organisms are more common in frail patients, in higher dependency environments and in those who have recently received courses of antibiotics. The se organisms include Gram negatives (which colonize the oropharynx) and anaerobes (a result of aspiration of gut contents). MRSA pneumonia and septicaemia is an increasing problem an d may be contracted in the community, ie not just a hospital problem PNEUMONIA 319 Table 11.1 Pneumonia pathogens in various care settings; in approximate order of frequency Community-acquired Care home Hospital Strep. pneumoniae ( > 30 % of cases) Strep. pneumoniae ( > 30 % of cases) Gram-negative aerobic bacilli, eg Klebsiella , Pseudomonas aeruginosa Anaerobes, eg Bacteroides , Clostridium . Especially in those at risk of aspiration, eg imm obility, swallowing dif \201 culty, prolonged recumbency or impaired conscious level Viral, eg in \202 uenza, parain \202 uenza, respiratory syncytial virus Viral, eg in \202 uenza, parain \202 uenza, respiratory syncytial virus Haemophilus in \202 uenzae Staph. aureus Gram-negative aerobic bacilli, eg Klebsiella , P. aeruginosa H. in \202 uenzae Strep. pneumoniae and H. in \202 uenzae . NB These may be the most common pathogens \200 \224 in non-acute settings, eg rehabilitation wards \200\224 in the well, less frail patie nt Gram-negative aerobic bacilli, eg Klebsiella , P. aeruginosa Legionella pneumophila . Mycoplasma pneumoniae if epidemic Anaerobes eg Bacteroides , Clostridium . Especially in those at risk of aspiration, eg immo bility, swallowing dif \201 culty, prolonged recumbency or impaired conscious level Viral, eg in \202 uenza, parain \202 uenza, respiratory syncytial virus Other, eg TB Other, eg TB Following in \202 uenza, think of secondary bacterial infection, especially with Strep. pn eumoniae (most common), H. in \202 uenzae or Staph. aureus Following in \202 uenza, think of secondary bacterial infection, especially with Strep. pn eumoniae (most common), H. in \202 uenzae or Staph. aureus 320 CHAPTER 11 Chest medicine Pneumonia: treatment Treatment is much more than antimicrobials alone: \200 Assess and op timize \202 uid volume status; give oral, s/c, or iv \202 uid as appropriate. Concurren t heart failure is common, but volume depletion more so If there is subjective dyspnoea or moderate/severe hypoxaemia, then supplement oxygen , titrating the inspired oxygen concentration upwards to achieve art erial oxygen saturations > 90 % (see b \200\230Oxygen therapy \200\231, p.348). For lesser degrees of hypoxaemia, it is not necessary to subject patients to claustrophobic, uncomfor table oxygen masks: simply monitoring saturations may be suf \201 cient \200 Exercise ca ution in COPD: observe the patient closely, both clinically and with serial ABG sampling Avoid the use of nasal specs acutely: if ventilatory drive is poor, inspired oxygen concentrations are very uncontrolled Encourage mobility . If immobile, sit upright in bed, and sit out in a chair \200 Request physiotherapy if there is a poor cough, or lobar/lung collapse \200 Use saline nebulizer s to loosen secretions which are dif \201 cult to expectorate and bronchodilator nebulizers when wheeze suggests associated bronchoconstricti on Minimize risk of thromboembolism unless contraindicated through prophylactic heparin, early mobilization, and compression stockings \200 Assess pressure sore risk and act accordingly ( see b \200\230Pressure sores \200\231, p.502) If dyspnoea, anxiety or pain is very distressing, consider opiates . Side effects include respiratory depression, sedation and delirium, so begin with small doses an d assess effect Anticipate possible deterioration, and judge in advance the appropriate levels of intervent ion. Would renal dialysis, ventilation and/or cardiop- ulmonary resuscitation be effective and appropriate? (See b \200\230Diagnosing dying and estimating when treatment is without hope \200\231, p.666) \200 Keep the family informed. Where possible, enlist their help, e g in encouraging eating and drinking Characteristics of severe pneumonia: the CURB-65 score Five key criteria (acronym \200\230 CURB-65 \200\231) determine prognosis: \200 C onfusion (AMTS (cid:100) 8) \200 U rea (s erum urea > 7mmol/L) \200 R espiratory rate ( (cid:116) 30/min) \200 B lood pressure (< 90 systolic and/or (cid:100) 60mmHg diastolic) \200 65 years of age or more The score has a six point scale (0 \200\2235 adverse prognostic features): \200 0 or 1: Low risk of de ath (0 \200\2233 % ). Possibility of home treatment (but consider other factors, eg functional status, hypoxaemia 2: Intermediate risk of death (13 % ). Hospital treatment is indicated \200 3, 4, or 5: S evere pneumonia, with high risk of death (score 3: mortality 17 % , 4: 41 % , 5: 57 % ). Consider intensive care admission. A \201 ve-point scale using only four criteria (CRB-65; urea excluded) can be applied out side hospital and also discriminates effectively between good and poor prognoses (eg mortal ity score 1: 5 % , score 3: 33 % ). PNEUMONIA: TREATMENT 321 Antimicrobials Refer to local guidelines, re \202 ecting pathogen sensitivities, and drug costs. Community or care home settings \200 Amoxicillin orally is usually effective (vs. Strep. pneumoniae and H. in \202 uenzae ). Erythromycin or clarithromycin if penicillin-allergic Add clarithromycin (or erythromycin which has more gastric side effects) if there are features of atypical pneumonia, there is a Mycoplasma epidemic, or the patient may have had in \202 uenza Co-amoxiclav orally has added activity against some Gram-negatives and Staph. aureus , and may be more effective in the frail patient or where aspiration is likely Cipro \202 oxacin alone should be used rarely \200\224 it has Gram negative activity, but is less effective against Strep. pneumoniae , an important pathogen in most s ettings. If an antimicrobial is sought that will cover both chest and urinary sepsis, a bet ter choice may be co-amoxiclav or trimethoprim iv antibiotics are only necessary if the patient is very unwell (CURB-65 score of 3 or above) or unable to swallow. Co-administration of cefuroxime and erythromycin is a good choice in the unwell patient, treating all likely pathogens effectively. If you suspect MRSA pneumonia, add vancomycin. Convert to oral therapy and change broad to narrowe r spectrum drugs when the patient \200\231s condition improves and/or culture results are k nown to minimize complications, eg CDAD (see b \200\230 Clostridium dif \201 cile -associ ated diarrhea \200\231, p.614). Often, only 48hr or less of broad spectrum, iv therapy is n eeded Hospital-acquired infection This presents a dif \201 cult dilemma. Hospitalized patients, especially those who are more frail and have spent longer in hospital, are prone to Gram- n egative and anaerobic pulmonary infections. However, they are also sus- ceptible to the adv erse effects (especially diarrhea) of broad spectrum antimicrobials. A hierarchical approach is sensible, considering likely pathogens and illness severity; \200 In the less frail patient who remains well, begin amoxicillin alon e, co-amoxiclav or a combination of amoxicillin and cipro \202 oxacin (all po). Broaden the s pectrum only if the patient deteriorates or culture results suggest that the likely pathoge n is insensitive If a patient is at high risk of Gram-negative infection (frail, dependency, prolonged stay, invasive procedures, aspiration risk), begin with iv cefuroxime (or equivalent). Narrow th e antimicrobial spectrum when the patient \200\231s condition improves and/or a pathogen is identi \201 ed \200 If the patient has received multiple courses of treatment, seek microbiology advice In all cases take blood cultures, and monitor the patient carefully Further reading British Thoracic Society guidelines online: M www.brit.thoracic.org.uk . 322 CHAPTER 11 Chest medicine HOW TO Manage the patient with pneumonia who fails to respond to treatment Is the dia gnosis correct? \200 Consider other chest pathology such as heart failure, pulmonary embo lism, pleural effusion, empyema, cancer or cryptogenic organizing pneumonia. Extrathoracic pathology mimicking pneumonia includes acidosis (tachypnoea), and biliary or pancreatic pat hology Review the history, examination and investigations \200 Consider admission to hospital an d further tests Is there a complication? For example effusion, empyema, heart failure, sile nt myocardial infarction or pulmonary embolism Is the antibiotic being taken regularly and in adequate dose? \200 Is concordance a probl em? Could a friend or relative help prompt tablet-taking, or would a dosette box help? Syrups may be swallowed more easily than tablets. An experienced nurse can help where there are swallowing dif \201 culties If swallowing remains ineffective, or drug absorption in doubt (eg vomiting) then consider iv therapy Is the organism resistant? \200 Take more blood cultures \200 Consider a change in anti microbial, taking into account likely pathogens and their known sensitivities Consider atypical infection; send urine for Legionella antigen test, especially if the pati ent is immunocompromised or if a patient appears disproportionately unwell. Remember MRSA p neumonia especially in those known to be previously colonized Could other elements of care be more effective? For example: \202 uid balance, oxygenatio n, nutrition, posture, and chest physiotherapy. Is this an end-of-life situation? \200 Is treatment to extend life now inappropriate, the failure to respond a sign that the diagnosis is of \200\230dying \200\231 ( see b \200\230Diagnosing dying and estimating when is treatment without hope \200\231, p.666)? If the patient canno t tell you their wishes, determine their likely views by discussing with family and friends , a decision informed by your judgment of where in their life trajectory your patient sits In determining prognosis consider comorbidity \200\224 is this an abrupt, potentially reve rsible illness in an otherwise \201 t person, or a further lurch downhill for a patient w ith multiorgan failure.Not for nothing is pneumonia referred to as \200\230the old man \200\231s friend \200\231, sometimes bringing to a brisk and welcome end a period of irrevo cable decline and suffering This page intentionally left blank 324 CHAPTER 11 Chest medicine Vaccinating against pneumonia and in \202 uenza Vaccine delivery \200 Both vaccines shou ld be offered simultaneously in October or early November to all aged > 65 years, especially: \200 The frail \200 Care home residents \200 The immunosuppressed \200 Those with comorbidity, eg heart failure, COPD Reliable delivery of these vaccinations depends upon effective information management systems in general practice, and substantial efforts by patients, ca rers, district nurses, and GP nurses A common reason to have missed immunization is to have been a long-term inpatient (eg undergoing rehabilitation) during the autumn immunization period. H ospitals should ensure that these inpatients are immunized Vaccinating healthcare workers, especially those working in long-term care settings, reduce s the spread of infection and therefore death due to in \202 uenza among patients Pneumococcal vaccine \200 Pneumovax II, a multivalent pneumococcal polysaccharide vacc ine, is effective against 65 % of serotypes Immunity remains for at least \201 ve years, perhaps for life \200 Bacteraemia is reduc ed by at least 50 % . The effect on incidence of pneumonia itself is less clear In \202 uenza vaccine \200 The trivalent vaccine is prepared from currently prevalent se rotypes \200 Immunity develops in <2 weeks, and it is therefore useful during epidemics Immunity remains for up to 8 months \200 The risk of pneumonia, hospitalization, or death due to in \202 uenza is reduced by over half Postexposure antiviral prophylaxis \200 Pharmacological prophylaxis of in \202 uenza is currently recommended when an unimmunized, high-risk group adult (eg care home resident) ha s had close contact with a person with in \202 uenza-like illness during a period when \202 u is prevalent (NICE 2008) Treatment with neuraminidase inhibitors must be initiated within 24hr (for oseltamivir) or 24hr (for zanamivir) ( see b \200\230Upper respiratory tract infections \200\231, p.314) Consider why immunization was not performed. Is it too late to administer this year (this contact may not have \200\230 \202 u, but the next one might)? If not, then optimize the chances of immunization next year PULMONARY FIBROSIS 325 Pulmonary \201 brosis This common problem is much underdiagnosed in older people due to a combination of under-investigation and overlap of clinical signs with common pathologies s uch as heart failure. Consider when breathlessness coexists with profuse \201 ne chest crepitations, with or wi thout clubbing. On CXR, there may be bilateral pulmonary shadowing consistent with pulmonar y oedema, but with little supporting evidence (eg normal heart size, absent Kerley B lines) . Causes \200 Idiopathic. The most common type in older people, known as usual interstitial pneumonia Connective tissue disease, eg rheumatoid arthritis (most common), systemic lupus erythemato sus, sarcoidosis. Lung involvement is sometimes the \201 rst manifestation of the multisy stem disease Drugs, eg amiodarone, nitrofurantoin rarely \200 Occupational exposure, eg asbestos, sili ca \200 If localized, consider TB, bronchiectasis, and radiotherapy Tests \200 The diagnosis is usually con \201 rmed by high-resolution CT scanning, which can also help distinguish subgroups likely to respond to immunosuppressive treatment Respiratory function tests may be useful (a restrictive picture with decreased transfer fac tor is usual) but typically adds little in the frail older person Refer to a respiratory physician to con \201 rm diagnosis and guidance on management Prognosis This is very variable \200\224 about a third are clinically stable, a third impr ove and a third deteriorate at rates that vary greatly between individuals. Some can live w ith pulmonary \201 brosis for years without signi \201 cant functional impairment. Treatment \200 Treat or remove any underlying cause, eg drugs \200 A minority respond s lowly (over weeks) to immunosuppression (eg prednisolone and azathioprine). Monitor closely for side effects. In non-responders, ta il off and stop. In responders, reduce dose cautiously. Ensure bone protection with calcium , vitamin D, and bisphosphonates Home oxygen therapy is often useful \200 Give opiates for distressing dyspnoea \200 In those in whom dyspnoea progresses, consider end-of-life issues including treatment limitation, and a change of focus from life-extending measures t o a purely palliative approach 326 CHAPTER 11 Chest medicine Rib fractures Common in older people. \200 Often a result of falls or even minimal bony s tress such as coughing in a person with osteoporosis Consider the possible contribution of alcohol, which causes both falls and osteoporosis Diagnosis Rib fractures should be diagnosed clinically. \200 Point tenderness and crepitu s are often found \200 Pressure over the sternum may provoke the pain in a lateral rib \200 CXR, even with multiple projections, may miss the fracture, but is useful in excludin g early complications such as pneumo- or haemo- thorax Radioisotope bone scans are very sensitive but not speci \201 c (hot spots are often found without clinical fracture) so they are rarely indicated Management Rib fractures heal without speci \201 c treatment. The major problem is pain, w hich commonly leads to voluntary splinting of the injured area. There is hypoventilation an d a failure to clear secretions, and secondary pulmo- nary infection can occur. \200 The patient should be encouraged to breathe deeply and to cough. Supporting the injured area wh en coughing, using a small pillow, minimizes pain. Strapping of the affected area is no lon ger done, as it increases complication rates Regular analgesia should include paracetamol, plus a weak opiate in most cases. A short course of NSAIDs may be helpful Admit to hospital if pain is severe and the patient unable to cough, or if complications (usually infection) have occurred In cases of severe pain (eg multiple fractures), consider strong opiates or intercostal/paravertebral blocks. Involve the local pain team Reassure the patient that the injury itself is not severe, will heal without immobilization and that coughing will prevent complications, not cause further damage. This page intentionally left blank 328 CHAPTER 11 Chest medicine Pleural effusions A frequent (clinical or radiological) \201 nding, sometimes incidental. Common causes are heart failure, post-pneumonia, PE, and malignancy (especially lung prima ry, mesothelioma, leukemia, lymphoma, and meta- static adenocarcinoma (ovary, stomach)). The differential diagnosis is wide, but narrowed when the results of CXR and pleural \202 uid aspiration are known (Table 11.2 ). Table 11.2 Differentiating cause, by protein level Transudate (protein <25g/L) Exudate (protein > 35g/L) Heart failure Malignancy Hepatic cirrhosis Infection, including TB Hypoproteinaemia, Gastrointestinal causes, eg malabsorption, sepsis eg pancreatitis Nephrotic syndrome Multisystem disorders, eg rheumatoid (Exudative causes if low serum protein) (Heart failure after diuresis) Empyemas, malignancy, and TB produce exudates with low pH (<7.2), low glucose (<3.3mmol/L) but high lactate dehydrogenase (LDH) \200 Transudates are usually not due to focal lung p athology, and so usually affect both lungs. Unilateral effusions due to transudates occasio nally do occur, more commonly on the right side Effusions due to heart failure are typically small and bilateral, with cardiomegaly; they can be unilateral, but usually a tiny contralateral effusion is seen, ma nifesting as blunting of the costophrenic angle; if the angle remains sharp, other causes a re more likely A massive unilateral effusion is usually due to malignancy \200 A uniformly bloodstained effusion is usually due to infection, embolism, malignancy or trauma Chronic effusions \200 If bilateral transudates, should be treated as for heart failure \200 If the diagnosis is not clear after CXR and aspiration consider chest physician refer ral and tests including CT, pleural biopsy (CT-guided rather than blind), video-assisted th oracoscopy with biopsy (VATS), and echocardiogram