Oxygen alert card should be given to all patients with a previous episode of hypercapnic re spiratory failure. This alerts ambulance crews and medical staff to the potential risk of h ypercapnia with high- \202 ow oxygen and documents usual resting baseline SaO2. However, t he ambulance staff protocols are suf \201 ciently rigid that they are not allowed to overr ide them. In some areas, letters from the patient \200\231s consultant and head of the ambu - lance service must be with the patient. Patient details Carry the card with you at all times Sticky label If you need to call the ambulance service or attend the hospital accident and emergency dep artment, show this card to the GP, paramedics, doctor or emergency department staff looking after you, as it provides them with essential information regarding your personal oxygen n eeds. Introduction If you have a sudden worsening of your lung disease (usually due to a chest in fection) it is essential that you do not receive too much or too little oxygen, either can be dangerous. Too much oxygen can cause a rise in the level of carbon dioxide in your blood and this can make you drowsy and slow your breathing. Too little oxygen can also be danger ous. Latest blood gas recordings: Date: ____/____/_______ On: Air, or % oxygen ____% pH:____ pCO 2_____pO2_____ Oxygen saturation: _______ % Purpose of this card The purpose of this oxygen alert card is to make sure that the doctors or ambulance staff involved in your care are made aware of your special needs regarding ox ygen therapy. The card recommends the appropriate amount of oxygen therapy for you based on your previous blood gas tests. You should receive enough Oxygen to achieve a %O2 saturation of no higher than 92%, but hig her than 86%, if possible. This is usually done with either a 24% or 28% venturi mask. Sign ed Name Designation Fig. 58.1 Oxygen alert card. CHAPTER 58 Oxygen therapy 706 Home oxygen therapy Home oxygen is delivered with essentially three different aims. First, to reduce the long-term complications of chronic hypoxia such as cor pulmo- nale, usually c alled long-term oxygen therapy or LTOT. This requires \211 15 h a day to be successful. Ho me oxygen can also be supplied for the relief of breathlessness, usually called \200\230sh ort \200\231 burst oxygen therapy or SBOT. If SBOT is used for many hours a day, it is some times incorrectly called LTOT, particularly by the oxygen supply companies. Oxygen can also be supplied to ambulant patients so that they can leave the house and travel (ambulatory o xygen). Long-term oxygen therapy (LTOT) Background and indications Two landmark trials of LTOT in t he 1980s: the British MRC Working Party trial and the American Nocturnal Oxygen Therapy Tri al (NOTT). The MRC trial compared COPD patients receiving oxygen for 15 h/day with controls receiving no oxygen. The NOTT trial compared continuous daily oxygen (average 17.7 h/day) with overni ght oxygen (average 12 h). The patients in the MRC trial were on average hypercapnic (mean PaCO2 7.3 kPa), whereas those in the NOTT trial were on average normocapnic (mean PaCO2 5.7 kPa). The main outcome in both trials was improved survival in those patients receiving ox ygen for at least 15 h/day, though this improved survival was not seen in the MRC trial unt il after a year of oxygen therapy. The NOTT trial showed a reduced exercise pulmonary artery pressure (PAP) after 6 months of continuous or nocturnal oxygen therapy. The 8-year survival was related to the fall in mean PAP during the \201 rst 6 months of continuous oxygen use. The MRC trial failed to show a fall in mean PAP with LTOT, but the mean annual increase in PAP (3 mmHg) in patients in the control arm was not seen in the oxygen treated group. The reason for the improved survival with LTOT is not clear, and is unlikely to relate to the small changes in pulmonary haemodynamics seen. COPD is the disease for which LTOT is most commonly prescribed, and the disease in which th e original studies were completed. Subsequent oxygen studies have shown improved exercise e ndurance in COPD patients breathing supplemental oxygen, with improved walking distance and ability to perform daily activities. FEV1 is the strongest predictor of survival in COPD; LTOT does not in \202 uence the decline in FEV1. Additional bene \201 ts of LTOT include: \200 \200 \200 Reduction of secondary polycythaemia Improved sleep quality, by reducing hypoxia-associated brain arousals Reduced cardiac arrthymias, and potentially reducing the risk of noc- turna l sudden death Reduced sympathetic out \202 ow leading to improved renal function, with in creased salt and water excretion, and reduced peripheral oedema HOME OXYGEN THERAPY 707 Indications for LTOT in COPD patients Criteria for prescription of LTOT in the UK are based on the clinical parameters of patients showing improved survival in the two LTOT trials. \200 PaO2 <7.3 kPa (55 mmHg) breathing air (i.e. a saturation on air \211 88%), in a stab le clinical state. Borderline results may need reassessment after 3 months, particularly if oximetry SaO2 <92% PaO2 7.3 \200\2238 kPa (56 \200\22359 mmHg, SaO2 89 \200\22390%) if pul monary hyperten- sion (i.e. symptoms and signs of cor pulmonale), polycythaemia, or addi- t ional nocturnal hypoxaemia (SaO2 \211 90% for at least 30% of the night). There is no evid ence that treating solely nocturnal hypoxaemia leads to improved survival Clinical stabilit y is the absence of an exacerbation for the previous 4 weeks. This is usually assessed twic e, several weeks apart, to ensure stability and ideally at least 6 weeks following an exace rbation LTOT is usually prescribed for those with FEV1 <1.5 L or <40% pre- dicted. If the F EV1 is higher in the presence of hypoxia/hypercapnia, it suggests an additional cause for t he ventilatory failure, such as addi- tional obstructive sleep apnoea; further investigatio ns may be indicated Medical management of the disease must be optimized prior to the prescr iption of LTOT PaCO2 does not in \202 uence the prescription of LTOT for COPD. There is a small risk of precipitating worsening hypercapnia with LTOT in those who are already hyperc apnic, particularly if the patient has OSA or is experiencing an exacerbation Blood gasses should be checked on LTOT to ensure the absence of worsening hypercapnia, if symptoms such as headache and confusion suggest that this has occurred, and to ensure a satisfactory incr ease in PaO2. Aim for PaO2 values of 8 \200\2239 kPa (60 \200\22365 mmHg, SaO2 90 \200\2239 2%) Patients should have stopped smoking: the bene \201 t of LTOT in continued smokers is limited, and there is an increased risk of \201 re. However, most studies suggest that ar ound 18% of patients on LTOT continue to smoke; they should be warned of the risks. Indications for LTOT in non-COPD patients There is very limited evidence to support the use of true LTOT in these patient groups and no data showing improved survival; the prescripti on thresholds are therefore not evidence-based. Ensure optimal medical man- agement \201 rst. LTOT is a term best reserved when one is trying to ward off complications of hypoxia, but is often confused with prolonged use of oxygen for palliative purposes; even guidelines confuse the two. Consider in: \200 \200 \200 Interstitial lung disease if PaO2 <8 kPa (SaO2 90%) Cystic \201 brosis if PaO2 <8 kPa (Sa O2 90%) Pulmonary hypertension with PaO2 <8 kPa, in the absence of paren- chymal lung disea se Neuromuscular or skeletal disorders causing ventilatory failure. Consider either oxygen alone (very rarely appropriate), or in combina- tion with NIV (usually via a specialist cen ter) Chronic heart failure if PaO2 <7.5 kPa. Guidelines also include the following, but this is not really LTOT, but pro- longed SBOT. \200 Palliative care \200\224for the dyspnoea of lung malignancy, or other causes of disabling d yspnoea due to terminal disease. CHAPTER 58 Oxygen therapy 708 Indications for SBOT \200 Short-burst oxygen therapy usually refers to intermittent supplemental oxygen to relieve dy spnoea, for periods of 10 \200\22320 min, but the periods may become much longer. Often the resting PaO2/SaO2 may be normal. Some would argue there is a large placebo effect due to t he cooling effect of the oxygen on the face; a similar effect may be achieved by using a fa n. Traditionally used in the following situations, although very little data exist to suppo rt its use in COPD, interstitial lung disease, heart failure, etc.: Pre-oxygenation before exercise Recovery from exercise SOB at rest Palliative care Overnight to reduce sleep disru ption of Cheyne \200\223Stokes breathing in heart failure. \200 \200 \200 \200 Should only be prescribed if clear proven bene \201 t, preferably with objective improveme nt in hypoxia and symptoms. It is expensive to prescribe, based on a daily rate and hours p rescribed, irrespective of actual usage. It is best provided by using one or more oxygen cy linders placed strategically round the house. Use of an O2 concentrator becomes more econom ical above a certain h/day usage. To supply a cylinder to stay in the wardrobe \200\230jus t in case \200\231 is now a very expensive placebo. Indications for ambulatory oxygen Ambulatory oxygen is oxygen delivered by portable equipme nt, and may be suitable for: \200 \200 Patients on LTOT who are mobile Those with exercise desaturation, and who show an improveme nt in exercise capacity or dyspnoea with oxygen; titrate oxygen to limit the exercise desat uration, aiming for SaO2 >90%. This indication is poorly researched and de \201 ned. Ideally clear bene \201 t should be demonstrated, and guidelines recommend laborious assess- ment, but facilities to do this o ften do not exist. It is up to the specialist prescriber to decide whether to order through the oxygen supply company, and then up to the supply company to decide on the best way to deliver. A 2-month assessment is usually required, to determine the likely number of hours of use. A reasonable initial prescription might be for 1 \200\223 2 h/day. Ideally usage sh ould be regularly reviewed and withdrawn if of no bene \201 t, or not being used. It is us ually provided via portable cylinders, although liquid oxygen is a more convenient option, providing 6 h use per recharge. This page intentionally left blank CHAPTER 58 Oxygen therapy 710 Practical issues \200 Home O2 should not be supplied to patients who still smoke, due to added \201 re risk, an d probable reduced ef \201 cacy by the increased HbCO LTOT is best provided by an oxygen c oncentrator, set at 1 \200\2234 L/min depending on PaO2 or SaO2. Some concentrators can del iver 8 L/min. Concentrators contain a molecular sieve containing zeolite, which traps gas m olecules depending on size and polarity. Can produce up to 96% oxygen, depending on \202 ow (the argon is also concentrated, to 4%) Patients can use nasal prongs or a \201 xed co ncentration mask (uncon- trolled or controlled oxygen, e.g. 24% and 28%) depending on physi - ological requirements and their preference. A back-up cylinder should be prescribed in ca se of power cuts Oxygen humidi \201 cation is possible, but dif \201 cult to arrange and rarely necessary. Only works well above 4 L/min, and tube lengths <1.5 m LTOT should be use d for \211 15 h/day in patients with COPD, although survival improves when used for longer ; therefore use should not be restricted to 15 h/day Patient education in the use of LTOT a nd machine maintenance are important. Specialist respiratory nurses may be involved with th is If using SBOT at >3 oxygen cylinders/week, an oxygen concentrator is more economical (th e oxygen supply company decides on this). How to organize home oxygen \200 The UK-wide integrated oxygen service (2005) ensured that provision of all modalities of do miciliary O2 is from one contractor in each area. Prescription should, in theory, come from respiratory specialists only (doctors, specialist nurses). Local arrangements are de \201 ned by primary case trusts (PCTs); in some areas almost anyone is de \201 ned as a \200 \230respi- ratory specialist \200\231, able to prescribe O2, with consequential escalation of O2 costs The prescriber completes and signs a Home Oxygen Order Form (HOOF), providing t he oxygen supplier with the patient \200\231s details and an exact prescription of the oxyg en required The HOOF is used for the prescription of LTOT, short burst, and ambulatory oxyg en; includes details of the oxygen \202 ow rate, % oxygen, and delivery device/mask requi red The oxygen supplier will invoice the PCT (Local Health Board in Wales); it is vital tha t this information is completed otherwise the HOOF will be returned A Home Oxygen Consent F orm (HOCF) form must be signed by the patient, consenting for the disclosure of relevant me dical information, address, telephone number to the oxygen supplier and \201 re brigade T he HOOF and HOCF are faxed to the oxygen supplier, with copies to the PCT, GP, and clinical lead for home oxygen services An LTOT prescription does not automatically include provisio n for oxygen outside the home; a separate form must be completed The response time for the delivery of LTOT, short-burst oxygen, and standard ambulatory supply is 3 days. Follow-up is needed to ensure: \200 Compliance; withdraw if not using despite support and explanation. Home visit within 4 week s by specialist nurse recommended PRACTICAL ISSUES 711 Con \201 rm the ongoing requirement for LTOT. Some patients improve and no longer need LTO T. Arterial blood gas tensions at 3 months, and then yearly monitoring (may be performed by specialist nurses) Cancelation with the O2 company as soon as a patients dies Inform O2 co mpany of any changes in \202 ow rates/%O2 Inform O2 company of any changes in patient add ress etc. Inform O2 company of admission to hospital for more than a week (reduces cost). \200 \200 \200 Emergency supply is a separate category and should only be pre- scribed when the patient ha s no O2 at home. The supplier is required to deliver this within 4 h of receipt of the orde r. It should not be ordered for more than 3 days. Portable oxygen options \200 DD \200\224460 L. Lightweight and easily portable. Lasts 3 h 50 min at 2 L/min F size \200 \2241360 L. Lasts approximately 11.5 h at 2 L/min PD \200\224300 L. Much smaller, but heavi er than DD. Lasts 2.5 h at 2 L/min E size \200\224600 L. Lightweight and portable. Lasts 5 h at 2 L/min. (Not available on the NHS.) Liquid oxygen Use O2 conserver devices (reduce O2 wastage during expiration). \200 \200 \200 Table 58.1 Oxygen supplier 24 h contact details Supplier Region Telephone Fax Air products plc North West, Yorkshire and Humberside, East Midlands, West Midlands, London North Wales 0800 373580 0800 214709 Air Liquide North East SW London, Thames Valley, Hants & Isle of Wight SE London, Kent, Surrey & Sussex South West 0808 2020999 0500 823773 0191 4974340 0800 7814610 Eastem England BOC Medical 0800 136603 0800 1699989 Further information http://www.primarycarecontracting.nhs.uk/uploads/HOS/june_2007/appendix _10.pdf http://www.lunguk.org/oxygen-suppliers.asp NICE COPD Guidelines. http://guidance.nice.org.uk/CG12/niceguidance/pdf/English/download.ds px Guidelines for emergency oxygen use in adult patients. BTS website \200\224in preparation Venturi principle. http://www. \202 exicare.com/content/education/education_oxygen_ \201 xedmask.htm Oxygen alert cards and controlled oxygen: preventing emergency admissions at risk Gooptu et al. Emerg Med J.2006; 23: 636-638 http://www.dh.gov.uk/en/Policyandguidance/Medicinespharmacyandindustry/Prescriptions/ Homeo xygenservice/index.htm. DOH website http://www.homeoxygen.nhs.uk/lookup.php This page intentionally left blank 713 Chapter 59 Palliative care Lung cancer and mesothelioma 714 Other symptoms 718 Non-malignant respiratory disease 720 CHAPTER 59 Palliative care 714 Palliative care is de \201 ned by the World Health Organization as an approach that improv es the quality of life of patients and their families facing the problems associated with l ife-threatening illness, through the prevention and relief of suffering by means of early i denti \201 cation, impeccable assess- ment, and treatment of pain and other problems, phys ical, psychosocial and spiritual. Palliative care is moving away from being involved just a t the end of life, especially in developing countries when curative possibilities are less readily available and palliative treatments may be the only option. In the UK, patients may be under palliative care teams intermittently for symptom control, respite care, etc., and may not see the service again for months or years. Within chest medicine, palliative care is most commonly considered for patients with lung c ancer and mesothelioma; many other patients with progressive end-stage respiratory disease (such as COPD, CF, and \201 brotic lung disease) also bene \201 t from speci \201 c pal liative interventions. These two areas are discussed separately below, although there is mu ch overlap in the management. Lung cancer and mesothelioma \200 \200 \200 \200 Involve the specialist palliative care team early Treat symptoms promptly Recognize problem s are often mixed, complex and multiple Recognize that delirium, dyspnoea, and decreased mo bility often herald the terminal phase of cancer. Pain \200 \200 Aim to determine cause, type, and site Start with simple analgesia and increase according t o the WHO anal- gesic ladder, moving from non-opioid analgesia through weak opioids to stro ng opioids. Reassess repeatedly and regularly If moving to morphine from weak opioid, 5 \200\22310 mg should be adequate. 10 \200\22320 mg or more required to replace a strong opi oid (60 mg codeine qds is equivalent to 5 mg morphine 4-hourly. If pain was not previously controlled, start at 10 mg morphine 4-hourly). If \201 rst dose of morphine no more effec tive than previous analgesia, increase next dose by 50% Prescribe analgesia as required for breakthrough pain (see box) Give drugs a chance to work at appropriate doses, particularly if they have not had strong opioids before. Allows assessment of analgesic effect and side -effects. Usually increase every 3rd day if required Once pain is reasonably controlled, mo rphine dose can be converted to slow release morphine by dividing total amount by two and g iving that dose as modi \201 ed release morphine 12-hourly. The breakthrough dose is one-s ixth of the total 24-h dose (e.g. 15 mg slow release morphine bd, then 5 mg (immediate rele ase morphine sulfate) for breakthrough pain) \200 LUNG CANCER AND MESOTHELIOMA 715 Treat drug side-effects, e.g. constipation, nausea. Prescribe prophylactic laxatives with m orphine. Warn people they may feel more drowsy if starting morphine or having dose increase , but this usually settles within a few days Patients with renal failure are more likely to develop opioid toxicity (drowsiness, confusion, myoclonus) as they have dif \201 culty ex creting morphine metabolites. They may need alternatives to morphine (e.g. methadone, alfen tanil, fentanyl) if their pain is not controlled on low- dose morphine The addition of an a nti-in \202 ammatory drug can be effective for bone pain and for liver capsule pain if the re are hepatic metastases Consider radiotherapy for localized pain in the chest related to cancer Pleuritic pain Consider PE, treat any infection. Consider non-steroidal anti-in \202 ammatory drug intercostal nerve block Bone metastases causing local tenderness Star t a strong opioid. If there is no improvement after 3 dose increases, add a non-steroidal a nti-in \202 am- matory drug for a 1-week trial. If single site, consider radiotherapy or i ntercostal nerve block. If multiple sites, consider bisphosphonates (so long as not hypocal caemic), e.g. 90 mg of pamidronate IV every 4 weeks. Neuropathic pain can be treated with s peci \201 c antidepressants (e.g. ami- triptyline 10 \200\22350 mg) or anticonvulsants (e. g. carbamazepine or sodium valproate 200 mg/day, gabapentin) Consider referral to pain clin ic or specialist center for further interven- tion, such as a intercostal nerve block, tran scutaneous electrical nerve stimulation (TENS), cervical cordotomy, or complementary therap ies. \200 Treatment of breakthrough pain \200 If already on non-opioid analgesic: give one extra dose of the regular analgesic If already on a regular oral opioid: give 4-hourly oral dose (= one sixth of total 24 hour dose), e.g . 60 mg/day = 10 mg dose If on transdermal opioid patch: Fentanyl \200\224give 1-hourly dos e e.g. 25 g/h patch, give 25 g SC or sublingually. Buprenorphine \200\224give 6-hourly dose, e.g. 35 g/h patch = 200 g SC or sublingually If already on continuous SC infusion of opioid: Diamorphine \200\224give 4-hourly dose, e.g. 30 mg/24 h = 5 mg dose SC. Fentany l \200\224give 1-hourly dose, e.g. 500 g/24 h = 20 g dose SC Consider increasing regular analgesic dose if the breakthrough pain occurs before the next regular dose. If there is no response to the addi- tional breakthrough pain treatment, repe at after 4 h if non-opioid or 1 h if opioid, with same dose. If still no response, consider changing from non-opioid to weak opioid, or weak opioid to strong opioid. CHAPTER 59 Palliative care 716 Conversions between opiates More potent opioids or routes do not provide greater analgesic ef \201 cacy, but may provide an alternative route to ensure adequate absorption, or if pa tient experiencing side-effects (usually toxicity and confusion) \200 Oral morphine to subcutaneous morphine Conversion factor is 2, e.g. 60 mg/24 h oral morp hine = 30 mg SC morphine Oral morphine to diamorphine infusion Conversion factor is 3, e .g. 60 mg/24 h oral morphine = 20 mg/24 h SC diamorphine Oral morphine to transdermal fenta nyl (patch) Oral morphine in mg/24 h 3 = transdermal fentanyl in g/h, e.g. 75 mg oral m orphine in 24 h = 25 g/h transdermal fentanyl. Use transdermal fentanyl for patients with stable pain. Dyspnoea \200 Consider possible causes (see box opposite). Dyspnoea may be due to the underlying lung dis ease, or due to an additional pathology Dyspnoea is frightening and made worse by anxiety a nd panic Lung cancer and pulmonary metastases are associated with the sensa- tion of shortn ess of breath, often due to stimulation of receptors by malignant in \201 ltration or lymp hangitis carcinomatosis Optimize treatment of any underlying lung disease with bronchodila- tors and steroids if appropriate Treat concurrent chest infection Opioids (e.g. 2.5 \200 \2235 mg morphine sulfate solution 4-hourly) relieve the sensation of dyspnoea without affe cting respiratory function Oxygen cylinders for intermittent short burst/prn use may help s ymptoms Fan blowing cool air onto the face can be helpful Consider the need for tumor debul king by bronchoscopy or an airway stent in a patient with lung cancer experiencing dyspnoea due to bron- chial obstruction or compression with tumor If PE diagnosed, consider treatme nt with low molecular weight heparin as warfarin can cause INR to be variable and dif \201 cult to optimize Subcutaneous opiate infusion may relieve symptoms as death approaches; us e with haloperidol, midazolam or levomepromazine. \200 \200 \200 LUNG CANCER AND MESOTHELIOMA 717 Causes of breathlessness in patients with lung cancer \200 \200 Pneumonia Underlying chronic lung disease (e.g. COPD, UIP) or concomitant cardiac disease L obar collapse Pleural effusion Pneumothorax SVCO Upper airway obstruction Pulmonary emboli Lymphangitis carcinomatosis Chest wall in \201 ltration Phrenic nerve paralysis Pericardia l effusion Respiratory muscle weakness, due to cachexia, paraneoplastic syndromes, steroid myopathy Anemia Depression Anxiety and panic. \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 CHAPTER 59 Palliative care 718 Other symptoms Anxiety \200 \200 \200 Leads to dyspnoea, which in turn worsens anxiety Explain they will not suffocate, symptoms will pass Benzodiazepines (such as short-acting lorazepam 0.5 \200\2231 mg sublingually 8 \200\22312-hourly) are effective for respiratory panic. Acute panic may be helped by midazo lam 2.5 mg IV, increased in incre- ments of 1 mg, given in a controlled environment with ox ygen Amitryptilline or citalopram may be effective longer-term treatments Relaxation exerci ses, diaphragmatic breathing training, and complemen- tary therapies may help some patients . \200 Cough \200 \200 \200 \200 \200 Treat the underlying cause Try simple or codeine linctus Nebulized saline may help expector ation Methadone linctus 1 \200\2232 mg nocte or bd may be of bene \201 t Nebulized local a nesthetic may help, e.g. 5 mL 2% lidocaine 6-hourly or bupivacaine 5 mL 0.25% 6-hourly (avo id in asthmatics, as it causes bronchospasm). Pharyngeal numbness is likely to occur, so av oid \202 uids for 1 \200\2232 h afterwards. Consider radiotherapy if haemoptysis due to l ung cancer. Consider discontinuing antiplatelet drugs or anticoagulants If massive haemopty sis, consider tranexamic acid, plus emergency supply of opioids and benzodiazepines to ensu re pain control and reduction of fear by decreasing awareness. Pleural effusion \200 Drain if symptomatic and pleurodese early if recurrent, although not if prognosis is poor ( less than 3 months) Consider in-dwelling tunneled catheter to drain \202 uid if effusion is symptomatic and pleurodesis has failed due to trapped lung. Poor appetite \200 Common symptom; may be primary due to cachexia \200\223anorexia syn- drome, or secondary du e to mouth problems such as candidiasis, nausea, hypercalcaemia, drugs, or depression May b e improved in the short term (about 6 weeks) by a course of oral steroids, such as predniso lone 20 mg daily Cachexia leads to decreased respiratory muscle strength and increased shor tness of breath Consider nutritional supplements. Brain metastases \200 Steroids relieve the cerebral oedema associated with brain metastases, e.g. dexamethasone 4 mg bd \200\223qds initially and then decrease Avoid steroid dosing in the evening, as slee p is affected Cranial radiotherapy may be considered if there is a good response to steroid s. \200 This page intentionally left blank CHAPTER 59 Palliative care 720 Non-malignant respiratory disease (COPD, CF, \201 brotic lung disease) The main problems associated with severe non-malignant respiratory disease are dyspnoea, hypoxia, immobility, and psychosocial problems, including depression. End-stage COPD patients may have very fre quent exacerba- tions for some years before a \201 nal terminal event. One study has show n those with end-stage COPD are more likely to have depression anxiety than those with t erminal cancer, but they are less likely to receive speci \201 c treatment for their emoti onal problems or any targeted palliative care. It may be appropriate therefore to shift the focus in patients with severe end-stage respiratory disease away from management of acute exacerba- tions towards a more palliative approach to care. Dyspnoea \200 \200 Dyspnoea is frightening and made worse by anxiety and panic Patients may decrease their mob ility to avoid dyspnoea, and subse- quently become more deconditioned. Dyspnoea may be due to the underlying lung disease or an additional pathology (PE, infection, pneumothorax, car diac failure) Sitting upright reduces airway obstruction and optimizes ventilation. Relaxin g and dropping the shoulders can improve ventilation, when anxiety has caused patient to \200\230hunch up \200\231 Calm gentle reassurance can decrease anxiety and reduce dyspnoea Fan blowing cool air onto the face can be helpful Optimize treatment of any underlying lung disease with bronchodila- tors and inhaled steroids Treat concurrent exacerbations with an tibiotics and oral steroids Stop smoking Consider pulmonary rehabilitation, if appropriate Opioids (e.g. 2.5 \200\2235 mg morphine sulfate solution 4-hourly) relieve the sensation of dyspnoea without affecting respiratory function Oxygen cylinders for intermittent short bu rst use may help symptoms. Consider concentrator if multiple cylinders being used \200 \200 \200 \200 \200 Hypoxia \200 \200 \200 SaO2 <92% LTOT may be appropriate (see p 706) Oxygen cylinders for intermittent or ambulato ry use may help symp- toms, but little data to support their use. Anxiety and depression \200 \200 \200 \200 May be due to fear and uncertainty over prognosis Lead to dyspnoea, which in turn worsens a nxiety Explain they will not suffocate; symptoms will pass Benzodiazepines (such as short-a cting lorazepam 0.5 \200\2231 mg sublingually 8 \200\22312-hourly) are effective for respir atory panic Acute panic may be helped by midazolam 2.5 mg IV, increased in steps of 1 mg, g iven in a controlled environment with oxygen NON-MALIGNANT RESPIRATORY DISEASE 721 Depression rates are high in patients with COPD. Consider antidepres- sant treatment and co unseling. Amitriptyline or citalopram may be effective at helping anxiety also Relaxation e xercises, diaphragmatic breathing training, and complemen- tary therapies may help some pat ients Cough \200 \200 Treat the underlying cause Refer to physiotherapy to improve cough ef \201 cacy, particula rly if large volume secretions Consider mucolytics, steroids, antibiotics Try simple or cod eine linctus Nebulized saline may help expectoration Methadone linctus 1 \200\2232 mg nocte or bd may be of bene \201 t Oral local anesthetics, such as benzocaine and lignocaine loz enges may be useful for laryngeal, pharyngeal or tracheal irritation, but associated risk o f aspiration Nebulized local anesthetic may helps, e.g. 5 mL 2% lidocaine 6-hourly or bupiv acaine 5 mL 0.25% 6-hourly (avoid in asthmatics, as it causes bronchospasm). Pharyngeal num bness is likely to occur, so avoid \202 uids for 1 \200\2232 h afterwards. \200 \200 \200 \200 Other problems \200 Malnutrition, thirst \200 Nausea, vomiting, constipation \200 Sle ep disturbance \200 Chest pain \200 Fatigue \200 Oral candidiasis \200 Impact on ca rers and family of patient with chronic respiratory disease Further information British National Formulary \200\224useful information on prescribing in palliative care in its \201 rst section Palliative care formulary www.palliativedrugs.org (free to register) Liverpool Care Pathway \200\224care pathway designed by palliative care team to enable gene ric care workers to deliver optimum hospice type care to a dying patient, whatever their lo cation or diag- nosis. Sample care pathway available online: www.mcphil.org.uk/liverpool_ca re_pathway This page intentionally left blank 723 Chapter 60 Pulmonary rehabilitation Aims and patient selection 724 Program 726 CHAPTER 60 Pulmonary rehabilitation 724 Aims and patient selection Pulmonary rehabilitation is a well-established multidisciplinary program of care for patients with chronic respiratory impairment. The program is individua lly tailored for each patient. Pulmonary rehabilitation is not available yet in every cente r, although it is probably the most cost-effective intervention in COPD. Aims of rehabilitation \200 \200 \200 To reduce disability and handicap in people with chronic lung disease To improve quality of life and restore independence To diminish the health care burden of disease. Early studies measured pulmonary function tests and found there was no improvement after pu lmonary rehabilitation. The \201 rst positive study of pulmonary rehabilitation measured functional status. Meta-analysis of 14 RCTs using a variety of different style programs has con \201 rmed the bene \201 t of rehabilitation, with improvements in functional exercis e. \200 Further UK RCT of patients with severe air \202 ow obstruction showed improvements in exer cise, health status, and health economic advantages Patients who had completed rehabilitati on courses had no fewer hospital admissions for exacerbations than those who had not had re habilitation, but hospital stays were shorter (10 days vs. 21 days) Patients with COPD who have completed rehabilitation courses perform better than controls on walking tests and hav e less subjective dyspnoea Rehabilitation programs containing lower-extremity training are better, when compared with controls, than those using just respiratory muscle training Shor t-term programs achieve overall similar outcome bene \201 ts across the spectrum of patien t disability. A minimum program length of 6 weeks is recommended Decline in exercise tolera nce and health status tends to occur between 6 and 12 months after completion of a course. Sustained improvement with ongoing rehabilitation sessions has yet to be evaluated. Candidates \200 \200 Anyone with chronic lung disease causing functional impairment The majority of candidates w ill have COPD, but also asthma, pulmonary \201 brosis, and bronchiectasis Any stage of a lung disease, when symptoms are affecting a patient \200\231s activity. Ideally receiving o ptimum medical treatment Well-motivated patients seem to bene \201 t most Patients with po or lower limb mobility may bene \201 t from upper limb exercise Oxygen therapy is not a co ntraindication to rehabilitation Stable ischaemic heart disease is not a contraindication t o rehabilitation. \200 \200 Candidates in whom rehabilitation may not be indicated \200 Unstable ischaemic heart disease, severe valvular heart disease, cognitive impairment, loco motor dif \201 culties Poorly motivated people with geographical or transportation problem s making attendance dif \201 cult tend to do less well. This page intentionally left blank CHAPTER 60 Pulmonary rehabilitation 726 Program Programs are usually run on an out-patient basis, but can be done in the community, in the home, or as an in-patient. They are run by a multi- professional team \200\224physi cian, physiotherapist, occupational therapist, dietician, nurse, pharmacist, social worker, and psychologist. A minimum program length of 6 weeks is recommended. Programs should be r egularly audited by the department. \200 Physical training The main component of the program, with aerobic exercise such as walking and cycling 2 \200\2233 times per week, with 2 super- vised/class sessions. May include upp er limb strength exercise with weights. Individually prescribed exercise programs, designed for each patient to work to high intensity. Bene \201 t increases with training intensity . Oxygen supplementation may be required if signi \201 cant desat- uration occurs during e xercise to below 80% Disease education Psychological and social intervention with advice on anxiety and depression, smoking cessation, plus physiotherapy and occupational therapy inp ut Nutritional education to optimize body weight and muscle mass. \200 Pre-rehabilitation assessment \200 \200 \200 Optimize medical treatment Oxygen saturation on exercise ECG may be warranted, especially i f history of cardiac disease. Outcome assessment measures \200 Physical Often with shuttle walk tests (SWT) or 6-min walk test (6MWT) to assess ability an d progress (see box opposite) Health status Disease-speci \201 c questionnaires: \200 Ch ronic Respiratory Questionnaire (CRQ) \200 St George \200\231s Respiratory Questionnaire \200 Generic questionnaires \200 Short Form-36 (SF-36) \200 Hospital Anxiety and Depr ession scores (HADS) are measured, but are insensitive to change during pulmonary rehabilit ation Practical Pulmonary Function Status \200\223Dyspnoea Questionnaire (PFS-DQ) may be us ed to measure performance and satisfaction relating to activities of daily living. program 727 Shuttle walk test (SWT) 10-m course between two points. Walking speed determined by external audio-tape signals ( \200\230beeps \200\231), and the patient should pace their walk to reach each point at a be ep. The patient is required to incrementally increase their speed as the beeps occur more f requently. Test \201 nishes when the patient needs to stop and distance achieved calculat ed. 6-min walk test (6MWT) 30-m course between two points on a hard \202 at surface. Patients do as many 60-m laps as they can around the 2 points in 6 min. They deter- mine their pace and intensity of exercise. They are allowed to rest in the time if they need to. Total dis tance walked in 6 min is counted. Results vary according to mood and encouragement. Future developments \200 Determining which components of rehabilitation are the most valuable to improvements in exe rcise: intensity of exercise program, type of exercise How to optimally maintain the improv ements following a rehabilitation program Performance enhancement using oxygen, steroids, n utrition, creatine, heliox, non-invasive ventilation. Further information Nici L et al. ATS/ERS statement on pulmonary rehabilitation. Am J Respi r Crit Care Med 2006; 173: 1390 \200\223413 Troosters T et al. Pulmonary rehabilitation in COPD. Am J Respir Crit Care Med 2005; 172: 19 \200\22338 Lacasse Y, et al. Pulmonary rehabi litation for COPD (Cochrane Review). CD003793 Salman et al. Rehabilitation for patients with COPD: meta-analysis of RCTs. J Gen Int Med 2 003; 18(3): 213 \200\22321 BTS Statement on Pulmonary Rehabilitation. Thorax 2001; 56: 827 \200\22334 Grif \201 ths TL et al. Results at one year of outpatient multidisciplinary pul monary rehabilitation: a randomized controlled trial. Lancet 2000; 355: 362 \200\22368 Laca sse Y et al. Meta-analysis of pulmonary rehabilitation in COPD. Lancet 1996; 348: 1115 \200 \22319 This page intentionally left blank 729 Chapter 61 Smoking cessation Aims and nicotine replacement therapy 730 Non-nicotine replacement therapy 732 CHAPTER 61 Smoking cessation 730 Aims and nicotine replacement therapy Smoking is the main cause of chronic obstructive pulm onary disease and lung cancer. The NHS spends 1.7 billion per year caring for people with smoking-related conditions. Government targets have been set to reduce the number of smoke rs in the UK and health authorities have been allo- cated funding for smoking cessation ser vices. \200 Approximately 31% of men and 29% of women in the UK smoke and 82% of smokers start as teena gers The incidence of smoking is increasing in developing countries Smoking is also associa ted with bladder, oesophageal, cervical, and renal cancers, as well as cardiovascular and c erebrovascular disease Nicotine exerts its effects on the CNS and is very addictive Peak ni cotine withdrawal time is 2 \200\2233 days 0.4% of smokers manage to stop each year Stoppin g smoking is associated with an average weight gain of 2 kg Government legislation in the U K banned smoking in the workplace and public places from 1st July 2007 and increased the ag e for sale of tobacco from 16 to 18 on 1st October 2007. \200 \200 \200 \200 \200 