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The Palliation of Dyspnea in Far Advanced Lung Cancer Dr. Anna Towers Division of Palliative Care McGill University
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Palliation of dyspnea Work of: Dr. Sam Ahmedzai Professor of Palliative Medicine Sheffield, UK
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Effect of palliative drugs on respiratory muscles and ventilatory activity The benzodiazepine midazolam reduces tidal volume and depresses ventilation by affecting the thoracoabdominal muscles Opioids inhibit rib cage movement
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Effect of opioids on the medullary respiratory centre Opioids reduce the hypercapnic drive in the medullary centre (respiratory depression) (the hypercapnic drive = mathematical relationship between ventilation and pCO2) i.e. opioids render the the medullary centre less sensitive to rising pCO2 levels i.e. opioids render the the medullary centre less sensitive to rising pCO2 levels
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Effect of severe hypercapnea on dyspnea Dyspnea may abate when the CO2 level rises above 75 – this could be due to the compensatory release of natural endorphins Patients with severe hypercapnea are often somnolent (CO2 narcosis), partially due to the above mechanism
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Clinical definition of dyspnea Greek : Dys= bad or difficult Pneo= breathing A SUBJECTIVE sensation of difficulty in breathing, not necessarily related to exertion, that compels the individual to increase his ventilation or decrease his activity (Ahmedzai)
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Effects of dyspnea on the patient Reduction in : quality of life, general function, activities of daily living Although dyspnea is subjective, the effects on function are objectively observable
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Terms often confused with dyspnea Tachypnea (e.g. increased breathing rate caused by fever) Hyperpnea (increased ventilation through metabiolic acidosis e.g. diabetic ketoacidosis) Hyperventilation (Psychologically induced increased respiration)
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Patients’ description of dyspnea “I feel like I am suffocating.” “I am afraid and feel like I am drowning.” “I have a tightness in the chest”
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Prevalence of dyspnea in terminal illness 70% of those in the last 6 weeks of life – all diagnoses (National Hospice Study U.S.A.) 60% of those with lung cancer (St. Christopher’s Hospice, UK)
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Causes of dyspnea in lung cancer Pulmonary Pleural Thoracic cage Cardiac/ pericardial
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Pulmonary causes of dyspnea in lung cancer Airway collapse/ lung collapse Thromboembolism Pneumonia Lymphangitis carcinomatosa Radiation fibrosis Noncancer causes: COPD/asthma
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Pleural causes Pleural effusion Pleural tumour
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Impaired thoracic cage function Respiratory muscle wasting in anorexia/cachexia syndrome, leading to respiratory muscle fatigue Chest wall tumours
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Pericardial causes Pericardial tumour, effusion, tamponade
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Management of dyspnea DIAGNOSE AND TREAT REVERSIBLE CAUSES
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Common reversible causes Pleural effusion Pneumonia Tumour mass or lymphangitis that can be reduced with palliative oncologial treatments Superior vena cava syndrome
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SVC syndrome Superior vena cava syndrome is considered an oncological and palliative EMERGENCY Is usually very responsive to radiotherapy and high-dose corticosteroids Treatment should always be considered unless prognosis is very short
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Treatment of carcinomatous lymphangitis Palliative chemotherapy Radiotherapy Where prognosis is very short: High dose dexamethasone (Start with at least 12 mg per day and titrate down. Stop steroid if there is no response after a 2-week trial.) (Start with at least 12 mg per day and titrate down. Stop steroid if there is no response after a 2-week trial.)
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General drug treatment for dyspnea Inhaled or nebulized bronchodilators Corticosteroids (usually at least 12 mg per day of dexamethasone is required) Respiratory sedatives (opioids, nonopioids)
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Respiratory sedatives Opioids (morphine, hydromorphone, fentanyl, oxycodone, methadone etc) Benzodiazepines
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Palliative approach Aim is to prolong (good quality) life, or to improve quality of life where life cannot be prolonged Discuss treatable causes with patient and/or family and obtain consent to treat Consider the prognosis, adverse effects, social considerations (such as the burden of travel from home etc)
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Palliative oncological treatments for dyspnea Aim for improved quality of life rather than life prolongation Palliative chemotherapy Radiotherapy external beam or brachytherapy Endobronchial laser therapy Endobronchial stent
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Respiratory sedatives Have the effect of suppressing respiratory awareness – with or without an effect on ventilatory drive Non-opioids Opioids
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Respiratory sedatives: non-opioid Benzodiazepines: Lorazepam (Ativan), midazolam) Phenothiazines: (methotrimeprazine (Nozinan)
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Respiratory sedatives: opioid Reduce anxiety Reduce sensitivity to hypercapnea Improve cardiac function Reduce concurrent pain that may be a factor in producing anxiety and sensation of dyspnea
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Respiratory sedatives: opioid Note: codeine does NOT reduce breathlessness Most commonly used opioids to control dyspnea: morphine hydromorphone (Dilaudid) Fentanyl patch oxycodone
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Nebulized opioids Route of delivery being studied Note: nebulized morphine may induce histamine release and bronchospasm in some patients
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How to use opioids in dyspnea management Use prn only if dyspnea is intermittent (aggravated by exertion, anxiety) Have patient control the prn medication Give just enough to relieve dyspnea, aiming, if possible, to avoid sedation If combined with a benzodiazepine, small doses of opioid are usually sufficient
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