Presentation on theme: "Palliative Care of Respiratory Symptoms"— Presentation transcript:
1Palliative Care of Respiratory Symptoms James S. Botts, MD, FACPSouthwest Area Medical DirectorVistaCare
2Outline of Topics…Identification of the Patient with Endstage Pulmonary DiseaseDyspneaCoughPulmonary InfectionsHemoptysisPulmonary Hypertension and Cor pulmonalePrimary Pulmonary HypertensionPulmonary FibrosisPulmonary EmboliStridorNeuromuscular Disorders & Restrictive Pulmonary DiseaseBronchiectasis and Cystic Fibrosisα-1 Antitrypsin DeficiencyList of LinksSlide two is the outline of the presentation. As noted in the first column, I will begin with a brief description of the vagaries of identifying the patient who has end stage respiratory disease and a prognosis of less than six months.Next in the first column are listed the symptoms we will be covering which are found in many patients with end stage respiratory disease.The second column is a listing of several pulmonary disorders that deserve special mention in terms of palliative care.
3Identification of Endstage Pulmonary Disease No single event or parameter signals end stagePersistent dyspnea despite optimal medical treatmentDyspnea impairing efforts to leave homeIncreasing number of hospital admissionsLimited improvement after hospitalizationIncreasing number of physician visitsOnset of fear, anxiety or panic attacksExpression of concerns about dyingNo reference to oxygen saturation or other parameter of pulmonary functionIt is difficult to accurately identify those with a prognosis of six months or lessSlide three attempts to identify factors associated with end stage pulmonary disease and a prognosis of less than six months. As you can see there is no single clinical event or laboratory study that can be held as a reliable indicator of a prognosis of less than six months. In particular, oxygen saturations and pulmonary function studies cannot be used as a lone indication of the six months or less prognosis.1. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 903
4Identification of Endstage Pulmonary Disease Using CMS LCD pulmonary guidelines50% of patients qualifying for pulmonary disease will live six months or less (n = 94)*Pulse rate > 100 has the best correlation with a prognosis of six months or less in patients with endstage pulmonary disease65.38% of patients meeting the CMS LCD guidelines for pulmonary disease with a pulse rate > 100 will live less than six months (n = 29)** Hospice Eligibility Evaluation Database (HEED) ; J.S. Botts
5Palliative Care of Dyspnea Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
6Palliative Care of Dyspnea Definition of Dyspnea (American Thoracic Society)“A subjective experience of breathing discomfort consisting of qualitatively distinct sensations that vary in intensity. Physiologic, psychologic and environmental factors all may play a role. The severity varies widely among patients.”(2)Slide 5 is the American Thoracic Society’s definition of dyspnea. As we all know, dyspnea is a subjective experience, however, the definition also includes reference to “qualitatively distinct sensations that very in intensity”.Assuming you are connected to the internet , double clicking the link at the bottom of the screen will take you to a full text consensus statement article on the mechanisms, assessment, and management of dyspnea by the American Thoracic Society.Throughout the remainder of the presentation, you will notice links at the bottom of some of the slides. Most will take you to the Pub MED site where an abstract of the article will appear. The links are all underlined. Those references not underlined will, of course, not link to anything.2. American Journal of Respiratory and Critical Care Medicine - Jan 1999ARS-1
7Palliative Care of Dyspnea Correlation of the complaint with the pathology of the underlying disease.Little correlation in generalSome correlation of the following:“I am drowning.” – Pulmonary edema with CHF“I can’t get enough air in.” – Interstitial disease or pulmonary emboli.(2,3)“Tight”, “Constricted” – a sensation used by those with airways obstruction such as asthma and cystic fibrosis but not COPDSlide 6 describes the qualitative language patients use when describing their dyspnea. In reality, there are only a few descriptions that may sometimes identify the cause of the dyspnea. Note that the “tight”, “constricted” description is one that we all have heard from patients with angina as a source of their complaint.2. Chest. 2005;127:3. Excerpt: Chest. 2005;127:
8The Language of Dyspnea Other studies in the literature have attempted to judge whether or not there are diagnostic clues in the language patients choose to describe their dyspnea or the discomfort they associate with breathing. Mahler et al5 have explored the language that patients with seven different disease states (e.g., asthma, congestive heart failure, interstitial lung disease) use to describe their dyspnea. These authors presented their subjects with a list of 15 descriptors. The investigators then asked each patient to walk along a hospital corridor until he felt an intensity of dyspnea equal to a grade of 3, or moderate, on the Borg scale. Patients were then asked to select those descriptors that best characterized their discomfort after the walk. Of interest, only patients with diagnoses associated with airway obstruction (egg, asthma and cystic fibrosis but not COPD) chose terms that imply tightness, such as "tight" or "constricted," to describe their discomfort. Other terms, such as "work" or "inhalation" were not specific for any diagnostic category. This may make sense from the point of view of the pathophysiology in that asthma and cystic fibrosis, unlike any of the other diagnostic categories, are associated with edema, inflammation, and muscular constriction of the larger airways. The feeling of tightness may be a feeling generated by the stimulation of airway afferents, a physiologic event shared by, and specific to, these two disease entities. A criticism of the work of Mahler et al is, however, that their subjects were asked to choose their words from a list of descriptors that were given to them. In this author’s experience, when patients with asthma are asked to describe their dyspnea using their own words, very few will volunteer a descriptor similar to those given by Mahler et al. Invariably, however, the few patients who do volunteer the word "tight" will have asthma, and the few who volunteer "I can’t breathe in" will have interstitial lung disease or pulmonary emboli. It appears, then, that there is some link between the pathophysiology of a disease and the words that patients choose to describe their discomfort. The fact that very few subjects will use these words, however, should send us another message: that is, it is not reasonable to expect all people, even if they speak the same language, to link the same word or descriptor to a given sensation.Chest. 2005;127: << Back
9Aorta and Carotid Arteries Adapted From: Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 898MotorCortexSensoryCortexDyspneaPeripheralChemoreceptorsAorta and Carotid ArteriesEmotionsPersonalityCentralChemoreceptorsMedullaCorollaryDischargeSense levels of oxygen,carbon dioxide and pHof the blood.MidbrainRespiratoryCenterSense levels of oxygen,carbon dioxide and pH of the blood.Slide 8 depicts the pathophysiology of dyspnea. As you can see, the Midbrain respiratory center receives input from chemoreceptors and mechanoreceptors and in turn sends messages to the sensory cortex and the respiratory muscles of breathing. The sensory cortex also receives messages resulting from emotions. The sensory cortex messages the motor cortex that then stimulates contraction of the muscles of breathing. The sensory cortex is also responsible for producing the sensation of dyspnea.MechanoreceptorsLungs and Chest WallSense stretching of structures in lungs and chest wallRespiratoryMuscles ofBreathingPathophysiology of Dyspnea
10Palliative Care of Dyspnea Assessment of Dyspnea Five etiologic categoriesCardiacPulmonaryNeuromuscularPsychiatric / Social / SpiritualAny combination of the aboveSlide 9 lists the factors that may be responsible for the sensation of dyspnea. Of greatest importance is that dyspnea is often, just as pain is, multifactorial. Just treating the underlying system may not be enough to effect maximal relief.
11Palliative Care of Dyspnea Assessment of Dyspnea History and Physical ExaminationFrequently identifies the specific system responsible for the dyspneaIndicated diagnostic testing followsSlide 10 emphasizes the importance of the history and physical examination which can frequently identify a specific system that is responsible for the dyspnea. Our hospice patients often will not want to have the usual diagnostic testing required to confirm the cause of the dyspnea, making the history and physical even more important in the diagnostic process.
12Palliative Care of Dyspnea Assessment of Dyspnea - Testing Pulmonary TestingABGChest X-rayPulmonary FunctionsBronchial ChallengeHigh resolution CTLung scanPETDiaphragmatic FluoroscopyCardiac TestingEKGEchocardiographyCoronary angiographyMyocardial perfusion scanOtherSleep studiesEsophageal pH monitoringLaryngoscopySlide 11 details some of the diagnostic tests that may be done to support the impressions of a good history and physical examination. As you can see, many of these tests are not practical to conduct on a terminal patient. Often old records can supply results of some of these tests.Often hospice and palliative care patients choose not to be tested, placingmore reliance on the history and physical examination.
13Palliative Care of Dyspnea Assessment of Dyspnea Reporting Intensity of DyspneaVerbal numerical scales (0-10)VAS (Visual Analog Scale)Modified Borg Dyspnea ScaleSlide 12 lists the common methods of assessing the severity of dyspnea. As you can see, the first two, the verbal numerical scale and VAS are similar to those used to assess pain. In the academic literature, the Modified Borg Dyspnea Scale seems to be used most frequently. Double clicking the link at the bottom of the screen will display the Modified Borg Dyspnea Scale.Link to Modified Borg Dyspnea Scale
14Palliative Care of Dyspnea Assessment of Dyspnea Modified Borg Dyspnea ScaleIntensity of Sensation RatingNothing at all 0Very, very, slightVery SlightSlightModerate 3Somewhat severe 4SevereVery SevereVery, Very Severe 9MaximalDerek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 899<< BACK
15Palliative Care of Dyspnea Assessment of Dyspnea Common Physiological Measurements of Respiratory DiseaseSpirometryFEV1 is a POOR predictor of dyspnea and improvements in dyspnea after bronchodilators do not match improvements of FEV1(4,5)Oxygen saturation – with its limitations(6)NOT a good predictor of the subjective feeling of dyspneaSlide 15 reviews the common physiologic measurements that we do on pulmonary patients. The importance of this slide is to emphasize the fact that these physiologic measurements do not give us quantitative information about dyspnea. All patients with dyspnea do not have abnormal oxygen saturations. Likewise, all patients with oxygen saturations < 89% do not have resting dyspnea.4. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 8995. Lareau, S.C. et al. (1999).Dyspnea in patients with chronic obstructive pulmonary disease: doesdyspnea worsen longitudinally in the presence of declining lung function? Heart & Lung6. eMedicine - Pulmonary Function Testing : Article by Raed A Dweik, MD, FACP, FCCP, FRCPC
16Palliative Care of Dyspnea Treatment – Non-Pharmacologic Influenza and pneumonia vaccinesCold facial stimulation (i.e. fan)(6)Nutrition(7)Weight gain for malnourished COPD (“pink puffer”)Weight reduction is accompanied by respiratory muscle weakness. Non-fluid weight gain will help correct thisWeight gain is difficult to achieve – poor response to nutritional supplementsWeight loss for hypercapnic COPD (“blue bloater”)Slide 16 addresses non-pharmacologic treatments for dyspnea. Prevention of influenza or pneumonia, of course, will relieve dyspnea associated with those illnesses. Facial cooling from a fan seems to help, and it is postulated that there are in fact signals that make it to the sensory cortex that help reduce the sensation of dyspnea. Weight reduction in the “pink puffer” can lead to weakening of the respiratory muscles. Attempts to make the pink puffer gain weight usually fail, though proper nutrition should be part of the care plan. Weight loss is a good thing for the blue bloater, reducing the tissue that has to be supplied with oxygen, and in turn reducing cardiopulmonary work.6. Am Rev Respir Dis Jul;136(1):58-617. Am Rev Respir Dis Aug;142(2):283-8.
17Palliative Care of Dyspnea Treatment – Non-Pharmacologic Controlled coughDeep breath followed by coughingFor clearing secretionsForced expiration – incentive spirometryGood for prevention and treatment of atelectasisFollow with controlled cough to clear secretionsEmotional, spiritual and social counsellingThese issues are important just as they are in the control of painAddressing these factors may improve the sensation of dyspneaSlide 17 displays additional non-pharmacologic means of treating dyspnea. I suspect that most of those here today are like I am and tend to forget the importance of these non-pharmacologic measures. Again note that emotional, spiritual and social counselling can be of benefit to the patient with dyspnea just as they are with the treatment of pain.8. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 904
18Palliative Care of Dyspnea Treatment – Non-Pharmacologic Exercise(8)Exercise is the best way to strengthen the respiratory musclesMethodsWalking; stair climbing;Upper extremity and shoulder girdle strengtheningThese are accessory muscles of breathingPulmonary rehabilitationInspiratory resistance breathingNo better than general reconditioning exercise alone in COPD patientsSlide 18 describes the options for getting your patient to exercise and thus strengthen respiratory muscles. While many of our patients are home bound and not candidates for a formal pulmonary rehabilitation program, just the act of getting out of bed on a regular basis may help some patients with dyspnea. Inspiratory resistance breathing does not require the patient ambulating or leaving the home and I suspect it is another simple measure that might help strengthen the respiratory muscles. Likewise, strengthening of upper extremity and shoulder girdle musculature can be conducted at home.8. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 904
19Palliative Care of Dyspnea Treatment – Non-Pharmacologic Controlled Breathing(8)Purse lipped breathingImproves alveolar ventilation and gas exchangeSlow expirationUseful in overcoming associated panic attacksBending forward positionImproves diaphragmatic function through increasing intraabdominal pressureHelps relieve dyspneaSlide 19 details controlled breathing maneuvers that can lessen dyspnea. Again, I suspect that many of us do not emphasize these simple non-pharmacologic methods of reducing dyspnea. Certainly we need to make sure our nurses educate our pulmonary patients as to these maneuvers.8. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 904
20Palliative Care of Dyspnea Treatment – Non-Pharmacologic BiPAP (Bilevel Positive Airways Pressure)Reduces time in ICUReduces need for intubationReduces mortality in COPD exacerbationsImproves quality of life in ALS patients (64)Value of BiPAP in a skilled care setting to “rest” the respiratory muscles is uncertainSlide 20 discusses the advantages of using BiPAP when indicated. While BiPAP may be used at home, most of the time it is a substitute for intubation and a ventilator in a patient with an exacerbation of COPD. Its use in the exacerbation of COPD will certainly reduce the sensation of dyspnea as well as time spent in the ICU, and the need for intubation and use of a ventilator. There are many articles on the use of BiPAP in the treatment of ALS and how it improves the quality of life including a reduction in dyspnea.8. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 90464. Neurology Jul 22;61(2):171-7
21Palliative Care of Dyspnea Treatment – Non-Pharmacologic Summary…Immediate treatmentCold facial stimulation with a fanControlled coughForced expirationPursed lip breathingSlow expirationBend forward postureNon-immediate treatmentVaccinations – influenza & pneumococcalNutritional assessment and treatmentAddressing emotional, social and spiritual issuesExercise – walking; stair climbing; shoulder girdle strengthening
22Palliative Care of Dyspnea Treatment – Pharmacologic BronchodilatorsAntiinflammatoriesOxygenAnxiolyticsMucolyticsAntidepressantsAntibioticsSlide 21 begins the discussion of pharmacologic treatment of dyspnea. As we all know, the end stage pulmonary patient winds up with multiple medications, plus medications to treat the effect of medications. Oxygen is almost always being used as well. Of course, the medication most physicians fail to use for dyspnea in end stage pulmonary patients is also, besides oxygen, the oldest of the listed medications, that of morphine sulfate.ARS-2
23Palliative Care of Dyspnea Treatment – Pharmacologic - Bronchodilators β2 agonists – in COPDDo not necessarily improve FEV1 or FVCDo improve dyspneaAnticholinergicsImprove FEV1Reduce dyspneaPhosphodiesterase InhibitorsTheophyllineLeukotriene AntagonistsSlide 22 lists the classes of bronchodilators. Note in this slide that the FEV-1 is improved with the use of anticholinergics, but not with beta-2 agonists. Both, however, improve the sensation of dyspnea. As we will see on a subsequent slide, there are new selective phosphodiesterase inhibitors in Phase III trials.
24Palliative Care of Dyspnea Treatment – Pharmacologic - Bronchodilators β2 agonistsIn stable COPDShort acting levalbuterol (Xopenex®) – In stable COPD patients, no advantage over racemic mixture (albuterol) in prn doses(9)Long acting β2 agonists salmeterol (Serevent®), formoterol (Foradil®), arformoterol (Brovana®)Slide 23 addresses beta-2 agonist use in stable COPD. As noted, Xopenex is reported to have no advantage in terms of cardiac side effects over the racemic albuterol. Other references, however, report an advantage over the racemic mixture in cardiac adverse effects when treating asthmatics. Patients with stable COPD should be considered for use of long acting beta-2 agonists in order to reduce episodes of “breakthrough dyspnea” and the need to use the short acting beta-2 agonists.9. Chest Sep;124(3):844-9
25Palliative Care of Dyspnea Treatment – Pharmacologic - Bronchodilators AnticholinergicsShort acting –Ipratropium (Atrovent®)Long actingTiotropium (Spiriva®)Tiotropium (Spiriva®) alone is more effective than long acting β2 agonists alone in COPD patients (10)Tiotropium (Spiriva®) added to a regimen of a long acting β2 agonist and a corticosteroid significantly improved dyspnea, FEV1 and FVC in COPD patients(11)Comparing tiotropium alone to fluticasone/salmeterol/tiotropium therapy showed no difference in rates of COPD exacerbation but the combination therapy did improve lung function, quality of life, and hospitalization rates in patients with moderate to severe COPD.(11a)Slide 24 mentions the anticholinergics. Note that tiotropium or Spiriva alone is more effective than the long acting beta-2 agonists alone in COPD patients. Additionally, if tiotropium is added to a regimen of a long acting beta-2 agonist and a corticosteroid there is significant improvement in dyspnea as well as the FEV-1 and the FVC in COPD patients.10. Thorax May;58(5):11. Respirology Sep;11(5):11a. Annals of Internal Medicine April 17; 146( 8):
26Palliative Care of Dyspnea Treatment – Pharmacologic - Bronchodilators Theophylline(12)A non-selective phosphodiesterase (PDE) inhibitor with antiinflammatory and bronchodilatory effectsImproves dyspneaImproves FEV124 hour sustained release preparation may be given once before bedtime without disturbing sleep (13)Is now used less because of narrow therapeutic range and risks of toxicity. ? Resurgence due to antiinflammatory effects and lower serum levels (<10mg/L).(35a)On the horizon, “Cilomilast and roflumilast are selective PDE4 inhibitors that are currently in pre-registration and phase III clinical trials, respectively, for the treatment of COPD (cilomilast and roflumilast) and for treatment of asthma (roflumilast).”(35)Slide 25 discusses theophylline which has many desirable effects making it an antiinflammatory as well as a bronchodilator. It does improve dyspnea and the FEV-1 and can be given in a once a day preparation. Unfortunately, because of its narrow therapeutic range, toxicity is frequent and costs are generated by the frequent blood levels. With the development of the long acting beta-2 agonists, inhaled steroids, and long acting anticholinergics, the use of theophylline has diminished. In the near future there should be the availability of selective phosphodiesterase 4 inhibitors that should minimize adverse effects of the non-selective theophylline. Cilomilast and roflumilast are both in phase III clinical trials.12. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 90313. Chest, Vol 110,35. Curr Opin Investig Drugs May;7(5):412-735a. American Journal of Respiratory and Critical Care Medicine Vol pp , (2003)
27Palliative Care of Dyspnea Treatment – Pharmacologic - Bronchodilators Leukotriene Receptor AntagonistsZafirlukast (Accolade®)–Has bronchodilation effect in COPD and asthmaThere is no additive effect when added to inhaled steroids (34)May reduce pulmonary hypertension in COPD(35)Montelukast (Singulair®)There is long term benefit in elderly COPD patients with moderate to severe disease(36)Slide 26 references two leukotriene receptor antagonists that we are all familiar with. Note that zafirlukast has bronchodilatory effects in COPD and asthma and may reduce pulmonary hypertension in COPD patients. As discussed in future slides, however, the patients with severe COPD and significant pulmonary hypertension are often difficult to identify without the assistance of some high-tech testing which may not be feasible in our end of life patients. Singular, has long term benefit in elderly COPD patients with moderate to severe disease.34. Pulm Pharmacol Ther. 2000;13(6):301-535. Chin Med J (Engl) Mar;116(3):459-6136. Respir Med Feb;98(2):134-8
28Palliative Care of Dyspnea Treatment – Pharmacologic - Antiinflammatories Corticosteroids in the treatment of COPD / DyspneaShort term oral corticosteroids:Acute exacerbation of COPDLong term inhaled corticosteroids:Reduces all cause mortality in moderate to severe COPD(14)Not a first line drug in mild COPD(15)Long term oral corticosteroids:Only in those not responding to inhaled corticosteroidsSometimes beneficial in hospice patients with malnutritionIdentification of those who will benefit from long term use:Remains controversialOne method:Check FEV1 then give a trial of mg prednisone per day for 14 days, then repeat the FEV1. A ≥ 20% increase indicates the patient will benefit from inhaled steroids(16)Slide 27 outlines the use of corticosteroids in the treatment of COPD and dyspnea. The oral corticosteroids are used in exacerbations of COPD, and if treatment of the exacerbation is successful, then the use of inhaled steroids and the discontinuation of the oral preparations. In severe COPD patients oral steroids may have to be continued at the lowest possible dose to avoid Cushingoid adverse effects.Long term inhaled corticosteroids reduce all cause mortality in patients with moderate to severe COPD. Inhaled steroids are not first line drugs in mild COPD.Identification of those COPD patients who will respond to corticosteroids is problematic and remains controversial. One method is to check the FEV-1 before initiation of steroids and then repeat the FEV-1 in 10 to 14 days. If there is improvement, then the patient will likely benefit from corticosteroids. In our end of life patients this is not always practical and most of them come to us already taking an inhaled corticosteroid. I think most of use would not “rock the boat” in this situation and would continue the inhaled steroids.Often the patient on inhaled corticosteroids feels the medication is not beneficial because they do not have the sense of immediate improvement of dyspnea after inhalation of the steroid. Education as to the rationale and use of inhaled corticosteroids is very important to achieve maximal benefit.14. Thorax Dec;60(12): Epub 2005 Oct 1415. Curr Opin Pulm Med Mar;10(2):113-916. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 903
29Palliative Care of Dyspnea Treatment – Pharmacologic - Antiinflammatories Nebulized IndomethacinMay be of value in reduction of mucus secretions in bronchiectasis and chronic bronchitis(52,53)Inhibits production of a proteolytic enzyme, neutrophil elastaseMay have long term beneficial effect on progression of bronchiectasisDyspnea was improved(52)Slide 28 notes the use of nebulized indomethacin, a non-steroidal antiinflammatory agent which frankly I have no experience in using it with this route of administration. It is apparently useful in the treatment of chronic bronchitis and bronchiectasis. It works by inhibiting the production of a proteolytic enzyme, neutrophil elastase. Indomethacin may reduce the progression of bronchiectasis.52. Am Rev Respir Dis Mar;145(3):548-5253. Eur Respir J Sep;8(9):
30Palliative Care of Dyspnea Treatment – Pharmacologic - Oxygen IndicationsResting O2 saturation ≤ 89% with or without dyspneaThose with dyspnea relieved by O2 despite the resting oxygen saturation.Studies have shown ↑ survival with use of long term oxygen, as well as improvement in health related quality of life measures including dyspnea (17,18)The level of O2 saturation does not correlate with the degree of dyspnea (17)Slide 29 discusses the oldest of all of these drugs, oxygen. Oxygen, as we all know is indicated for use in patients who have resting room air oxygen saturations of < 89%. The reason for this guideline is simple. Patients with saturations < 89% will live longer if they use oxygen. Particularly in our patients it is also indicated if it helps in the reduction of dyspnea, despite the level of oxygen saturation.We have all seen patients who seem to not have dyspnea and yet have low saturations. As the slide notes, there is no correlation of the oxygen saturation with the severity of the dyspnea.17. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 90318. Curr Opin Pulm Med Mar;10(2):120-7
31Palliative Care of Dyspnea Treatment – Pharmacologic - Oxygen Beware!Patients on oxygen with high oxygen saturation and confusion or lethargy may have C02 retentionTreat with discontinuation or reduction in oxygen flow and close observationTitrate to the flow of oxygen that does not cause the confusion or lethargySlide 30 contains a warning that the patient with a comfortable high oxygen saturation who is receiving oxygen but is lethargic or confused may be retaining carbon dioxide and the oxygen should be temporarily discontinued and the patient closely observed. If the patient’s lethargy and confusion improve the oxygen may be restarted but with at a low flow. The message here is to continue to observe the patient until a new flow level provides the patient with an optimal flow of oxygen that does not result in confusion or lethargy. While all of us are aware of this some of the nurses are not and they should be educated as to this potential complication of oxygen administration.
32Palliative Care of Dyspnea Treatment – Pharmacologic - Opioids Meta-analysis concludes that opioids in modest doses are effective in treating dyspnea(28)Dose – as little as 2.5 mg of MS q4h(29)Sustained release morphine reduces dyspnea(27) (Don’t start on the sustained release forms.)Slide 31 gives supporting references to the use of oral morphine sulfate in the treatment of dyspnea in the end of life pulmonary patient. The rule of start low and go slow applies.27. BMJ Sep 6;327(7414):523-828. Thorax Nov;57(11):939-4429. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 904
33Palliative Care of Dyspnea Treatment – Pharmacologic - Opioids No clear evidence that inhaled morphine is effective in the relief of dyspnea(30)Slide 32 on the other hand, casts doubt on the use of inhaled morphine sulfate. The bottom line is to use the oral route if at all possible and the result should be better than inhaled morphine.30. Eur Respir J May;10(5):
34Palliative Care of Dyspnea Treatment – Pharmacologic - Anxiolytics BenzodiazepinesScant literature on the use of benzodiazepines in the treatment of dyspnea but they are commonly used (19, 20)Opioids are first line anxiolytic drugs for dyspnea secondary to advanced disease of any cause(21)Slide 33 emphasizes the fact that morphine sulfate is the first line anxiolytic in the treatment of dyspnea. While benzodiazepines are widely used in the treatment of dyspnea there is not an abundance of supporting literature as to their effectiveness in the treatment of dyspnea. Nevertheless, I am sure all of us will continue to prescribe them.19. Q J Med Winter;49(193):9-2020. Am J Hosp Palliat Care Nov-Dec;15(6):322-3021. Can Fam Physician Dec;49:
35Palliative Care of Dyspnea Treatment – Pharmacologic - Anxiolytics Buspirone (BuSpar®)Conflicting reports of its effect on dyspnea(22,23)Concerns about respiratory depression in COPD patients receiving anxiolytics is unfounded.(24)Anxiolytics can be beneficial in some patients with dyspnea, even those without appreciable anxiety.(24)Slide 34 gives us a bit of good news. Concerns about respiratory depression in COPD patients receiving anxiolytics is unfounded. Again, start low and go slow. While there is conflicting evidence about the beneficial effect of non-opioid anxiolytics, the Oxford Textbook of Palliative Medicine notes that “clinical experience suggests that anxiolytics are beneficial in the treatment of breathlessness”, but lists no references for that opinion. It goes on to say that anxiolytics can be beneficial even in patients without appreciable anxiety, again without references. Despite what the literature says, I think the standard of care is to use anxiolytics in many patients with dyspnea.22. Respiration. 1993;60(4):216-2023. Chest Mar;103(3):800-424. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 904
36Palliative Care of Dyspnea Treatment – Pharmacologic - Mucolytics N-Acetylcysteine (Mucomyst®) by mouth or inhalation will help patients with excessive or viscous mucous clear these secretionsEffect on dyspnea has not been studiedEvidence is conflicting as to its reduction of COPD exacerbations(31,32)Slide 35 begins the discussion on mucolytics. N-Acetylcysteine or Mucomyst is useful in patients with excessive or viscous mucous. The effect of this drug on dyspnea has not been studied in the literature. There is controversy about its ability to reduce COPD exacerbations.31. Lancet Apr 30-May 6;365(9470):32. Eur Respir J May;21(5):795-8
37Palliative Care of Dyspnea Treatment – Pharmacologic - Mucolytics Additional agents that may assist in mucolysis and expectoration of thick sputum:Normal or hypertonic saline nebulizationsInhaled mannitol powder (66)Inhaled atropineCorticosteroidsβ2 agonistsIndomethacinTheophyllineGlycerol guaiacolateOf limited valueSlide 36 lists other mucolytic agents. Of note is the use of mannitol powder. This has been used primarily in the treatment of bronchiectasis. Indomethacin has been discussed as an antiinflammatory agent and reduces secretions by a reduction in inflammation. Glycerol guaiacolate has limited value as a mucolytic, though it is a major component of most OTC expectorants and cough syrups.33. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 90466. Respirology Jan;10(1):46-56
38Palliative Care of Dyspnea Treatment – Pharmacologic - Antidepressants SSRIs; Tricyclics – In depressed patients with endstage lung diseaseBeneficial for anxietyBenefit for dyspnea is not conclusive (25,26)Slide 37 addresses the role of antidepressants in the treatment of dyspnea. Evidence is inconclusive, however, in keeping with our goals in end of life care depression is common and should be treated. One would think that if a patient’s depression improves a good number of symptoms would improve. Depression is accompanied by anxiety and is a target symptom of antidepressants. Many of the COPD patients are anxious, and depression should always be a consideration as well as adverse effects from beta-2 agonists or theophylline.25. Psychosomatics Jan-Feb;39(1):24-9.26. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 904
39Palliative Care of Dyspnea Treatment – Pharmacologic - Antibiotics Treatment of ExacerbationsAntibioticsFluoroquinolones (37,38)Amoxicillin almost as effective and cheaper(39)Short acting β2 agonists → long actingShort acting anticholinergics → long actingOral prednisone → Inhaled corticosteroidSlide 38 discusses the treatment of COPD exacerbations which, of course, are accompanied by worsening of dyspnea. Infection is a common reason for an exacerbation of COPD and should be treated with appropriate antibiotics. Fluoroquinolones and amoxicillin are commonly used and a subsequent slide will provide a guideline about which to use in a COPD patient.In addition to antibiotics, short acting beta-2 agonists and anticholinergics in concert with oral prednisone are the mainstays of drug treatment of acute exacerbations. Transition to long acting beta-2 agonists and long acting anticholinergics as well as inhaled corticosteroids should be utilized once the patient stablizes.37. Clin Microbiol Infect May;12 Suppl 3:42-5438. Chest Mar;125(3):953-6439. American Family Physician Vol. 70/No. 4 (August 15, 2004)
41Palliative Care of Cough Assessment Many patients will not want the usual diagnostic testsA thorough history and physical examination is often our best and only tool for assessing the cause of the coughARS-3
42Palliative Care of Cough Assessment CausesAcute infectionsChronic InfectionsAirways DiseaseCardiovascularParenchymal DiseaseIrritantRecurrent AspirationDrug InducedPleural DiseaseVocal Cord DiseaseExamplesPneumonia; Acute BronchitisChronic bronchitis; BronchiectasisCOPD; AsthmaLV failure; pulmonary edemaInterstitial FibrosisGERD; Foreign bodyStroke; Motor neuron diseaseACE Inhibitors; inhaled drugsPneumothorax; pleural effusionParalysis; nodules on cordsSlide 39 is a listing of the non-malignant causes of cough with examples of each cause in the right hand column.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 899
43Palliative Care of Cough Treatment of the Underlying Cause Acute and chronic infectionsAntibioticsAsthma and COPDBronchodilators and anti-inflammatoriesLeft ventricular failureDiuretics, ACE inhibitors, ± β- blockersRecurrent aspirationPostioning of patient; swallowing evaluation → alter food consistencyDrug induced (ACE inhibitors)Discontinue drugPleural diseaseCorrect pneumothorax; drain pleural effusionVocal cord dysfunctionENT evaluation and treatmentGERDPPIs; metoclopramide; positioning of patientPost-nasal dripDecongestants; antihistaminesSlide 40 outlines the treatment of the more common causes of cough.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 899
44Palliative Care of Cough Treatment – Protussive and Antitussive Protussive TreatmentsMeasures to improve cough effectiveness and secretion clearanceAntitussive TreatmentsMeasures to prevent or eliminate coughSlide 41 divides the treatment of cough into two categories, protussive or measures to improve cough effectiveness and secretions, and antitussive or measures to prevent or eliminate cough.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 899
45Palliative Care of Cough Treatment – Protussive Treatments Measures to make cough more effective(40)Adequate hydration – po fluids; steam inhalations; saline nebulizationsPhysiotherapy – only in select patients with COPD and bronchiectasis (41)Forced exhalationsAirways vibrationsPostural drainageAssisted cough techniquesSlide 42 begins the listing of protussive treatments and includes adequate hydration and physiotherapy. Physiotherapy measures are only effective in select patients with COPD and bronchiectasis in an effort to mobilize excessive sputum.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 89941. Chron Respir Dis. 2006;3(2):83-91
46Palliative Care of Cough Treatment – Protussive Treatments Measures to make cough more effective(40)Pharyngeal suctioningMini-tracheostomyFor thick, excessive, infected sputumSteroidsAntibioticsInhaled mannitol powder or hypertonic saline (42,43)Slide 43 continues the listing of protussive measures. Again the goal here is to clear secretions from the lung and bronchial airways.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 89942. Cochrane Database Syst Rev Jul 20;(3):CD00150643. J Aerosol Med Fall;15(3):331-41
47Palliative Care of Cough Treatment – Protussive Treatments Increase of secretion clearance (40,44)Liquification of secretionsN-acetylcysteineRecombinant human DNAseArginine – not as effective as N-acetylcysteineUridine-5'-triphosphate – useful for getting sputum samples from mild chronic bronchitics (67)Bronchodilatorsβ2 – agonists (albuterol)Slide 44 refers to several agents that may be utilized to liquify secretions making them easier to expectorate. Arginine is not widely used and is not as effective as Mucomyst. Uridine-5’-triphosphate is useful for obtaining sputum specimens in patients with mild chronic bronchitis. The beta-2 agonists will cause bronchodilation and thus improve sputum yield.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 90044. Expert Opin Pharmacother Feb;5(2):369-7767. Chest Dec;122(6):2021-9
48Palliative Care of Cough Treatment – Antitussive Treatments Used when cough is not reversibleUsed primarily for dry non-productive coughOpioidsOral local anestheticsNebulized local anestheticsOther antitussive agentsAntimuscarinicsSlide 45 lists the antitussive agents which are used primarily for non-reversible non-productive coughs.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 900
49Antitussive Treatment of Cough Slide 46 is in ACP Medicine and is an algorithm for the treatment of cough. The dosages of medication are listed as well.ACP Medicine 2006ARS-4
50Palliative Care of Cough Treatment – Antitussive Treatments OpioidsMorphine is the strongest antitussive (47)Useful especially in the terminal patientCodeine is used widelyIn its OTC form codeine has no more antitussive effect than the demulcent vehicle (47)Dextromethorphan – an opioid derivativeNo analgesic effect in antitussive dosesAs effective as codeine for cough suppressionSlide 47 outlines the opioids used for antitussive purposes. As you can see, our old friend morphine sulfate is the most potent of the opioid antitussives. Codeine is also effective, however, in its OTC mixture it has no more antitussive effect than the demulcent vehicle. Dextromethorphan is an opioid derivative without analgesic effect in doses used to suppress cough. It is as effective as codeine for cough suppression.45. Chest Jan;129(1 Suppl):284S-286S46. Pulm Pharmacol Ther. 2004;17(6):459-6247. Thorax May;59(5):438-4045. Chest Jan;129(1 Suppl):284S-286S46. Pulm Pharmacol Ther. 2004;17(6):459-6247. Thorax May;59(5):438-40
51Palliative Care of Cough Treatment – Antitussive Treatments Oral Local AnestheticsBenzonatate (Tessalon Perles ®)Peripheral acting / opiates largely central actingOften effective in opiate resistant cough (47)Levodropropizine – not available in USAWidely used in EuropePeripheral acting and useful in cancer related cough (47)Slide 48 includes two oral local anesthetics, only one of which is available in the USA. Tessalon Perles are peripheral acting whereas opiates are centrally acting. In patients who are not responding to opiates, you should consider the Tessalon Perles. The greatest benefit to having levodropropizine would be a welcome addition to the USA as it apparently is quite beneficial in treatment of cough related to lung cancer.45. Chest Jan;129(1 Suppl):284S-286S46. Pulm Pharmacol Ther. 2004;17(6):459-6247. Thorax May;59(5):438-40
52Palliative Care of Cough Treatment – Antitussive Treatments Nebulized Local AnestheticsRisk is aspiration 2-4 hours after a treatmentPatient should not eat or drink for 1 hour after RxNebulized lidocaine is effective in reduction of cough (48, 49) (5mg/kg in normal saline)Bupivacaine and Lidocaine have been associated with bronchoconstriction in patients with reactive airways. Consider giving with salmeterol (50)Slide 49 mentions nebulized local anesthetics. The principal risks of using these medications are the potential to aspirate and the occasional patient with asthma that has resultant bronchospasm. Some experts advise administration of salmeterol with bupivacaine or lidocaine to reduce the risk of bronchoconstriction. In order to reduce the risk of aspiration, the patient should be instructed not to eat or drink for at least two hours after a treatment.48. Am J Emerg Med May;19(3):206-749. Emerg Med J Jun;22(6):429-3250. Canadian Family Physician. May 2002
53Palliative Care of Cough Treatment – Antitussive Treatments Other Antitussive AgentsIf cause is bronchospasm, inflammation, or tumor…Theophyllineβ2 –agonistsAnti-inflammatoriesSteroidsSodium cromoglycateSlide 50 points out the importance of treating the underlying cause of the cough. Sometimes with terminal patients we are not able to identify the cause of the cough and an appropriate shotgun approach may be necessary.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
54Palliative Care of Cough Treatment – Antitussive Treatments Other Antitussive AgentsOTC Marketed as Antitussive but Not Proven EffectivePseudoephedrineDexbrompheniramineGuaifenesinSlide 51 shows three medications that are often found in OTC preparations, however, none have been shown to be effective as marketed.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
55Palliative Care of Cough Treatment – Antitussive Treatments AntimuscarinicsIpratropium bromideGood in chronic bronchitisReduces secretions without reduction in mucus viscosityHyoscine .2-.4mg sc prn or Glycopyrronium bromide mg IM prnGood for the death rattle and associated coughMay cause ataxia and hallucinations in the elderlySlide 53 identifies two antimuscarinics used in the treatment of a loose cough. Ipratropium bromide is able to reduce secretions without reduction in the viscosity of the sputum, making it a good choice for chronic bronchitis. Hyoscine or glycopyrronium bromide are useful in treatment of the death rattle, though may cause ataxia, confusion and hallucinations in the elderly patient.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
56Palliative Care of Cough Treatment – Antitussive Treatments Antimuscarinics (68)Ophthalmic Atropine 1% dropsGive sublingually or poScopolamine Patch ®Hyoscine in a patchNot effective for about 12 hoursSlide 53 includes two other methods of controlling the death rattle. While the Scopolamine Patch is convenient it does not become fully effective for about 12 hours after application, which is often times several hours after death. Ophthalmic atropine drops have a rapid onset and may be given sublingually.68. AAHPC Fast Fact and Concept #109: Death rattle and oral secretions
57Palliative Care of Respiratory Infections Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
58Palliative Care of Respiratory Infections Treatment – Establishing Goals Above all - goals must be discussed and formulated with the patient and familyThe patient or POA may ultimately decide against antibiotic therapyIf antibiotics are not chosen as a treatment, symptomatic treatment of fever, dyspnea and cough should be the planIn Slide 54 pulmonary infections are addressed. Of most importance are having good conversations with the patient and/or the POA about the goals of treatment. Especially this is true with patients with recurrent aspiration and a very poor quality of life or the COPD patient who is having multiple exacerbations. Should antibiotics not be chosen, there is still lots to do in treating the symptoms of infection.
59Palliative Care of Respiratory Infections Treatment – Antibiotic Selection COPD with FEV1 < 50% (Most hospice patients with end stage lung disease) exacerbations should be treated with a quinoloneCOPD with FEV1 > 50% use ampicillin, tetracycline or trimethoprim/sulfaSlide 55 provides guidelines as to the selection of antibiotics in exacerbations of COPD. Of course, often times we don’t have access to results of our patient’s PFTs. While an FEV-1 is not required for eligibility, the Medicare guidelines suggest an FEV-1 of < 30% after bronchodilator. On this basis the patient receiving the hospice benefit with terminal lung disease probably has an FEV-1 of < 50% and should, therefore, receive the quinolone51. ACP Medicine Chapter 14:Respiratory Medicine: III Chronic Obstructive Disease of the Lung
60Palliative Care of Respiratory Infections Treatment – Antibiotic Selection Bronchiectasis and Cystic FibrosisCoverage of anaerobic bacteria and pseudomonas are importantAntibiotics should be given in high doses, sometimes rotated and for 3-4 week coursesCiprofloxacinMetronidazoleAugmentinIn slide 56 the special antibiotic needs of bronchiectasis and cystic fibrosis patients are discussed. Because of the frequency of pseudomonas infections, ciprofloxacin, metronidazole and Augmentin are recommended with 3-4 week courses and rotation of antibiotics from one episode of infection to another.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
61Palliative Care of Respiratory Infections Treatment – Antibiotic Selection Bronchiectasis and Cystic FibrosisNebulized antibioticsGentamicin (300 mg bid)Tobramycin (300 mg bid)Slide 57 points out that there is a role for nebulized aminoglycosides in patients with bronchiectasis or cystic fibrosis.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
62Palliative Care of Hemoptysis Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
63Palliative Treatment of Hemoptysis Assessment Majority of cases are mild to moderate<20% are massive (> 500 cc per day)Most common causesInfection ~ 80%TBAbscessesBronchiectasisMalignancy ~ 20%Hemoptysis, another frightening complication of advanced lung disease, is covered in slide 60. Most often hemoptysis is not massive, defined as > 500 cc per day. Of the non-malignant causes of hemoptysis the most frequent are cavitary TB, abscesses, and bronchiectasis. Malignancy accounts for about 20 % of the patients with hemoptysis.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
64Palliative Treatment of Hemoptysis Assessment History and Physical ExaminationExamination of the sputumPresence of food particlesHematemesisT/E fistulaPurulent sputumInfectionLaboratory and X-Ray StudiesChest x-rayCT with contrastBronchial artery or pulmonary artery arteriogramSlide 61 addresses the evaluation of hemoptysis. Often times the only information we have is from a good history and physical examination. If food particles are seen in the bloody sputum, one must think of hematemesis or a T/E fistula. Of course, purulent bloody sputum points to an infectious cause. Ideally a chest x-ray, CT with contrast, and bronchial and pulmonary arteriography, and bronchoscopy should be done to identify the cause. In our hospice patients these studies are often not practical to accomplish.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
65Palliative Treatment of Hemoptysis Treatment - Anticipatory Anticipation - If resuscitation is or is not the goalEducation of patient, family and caregiversGoals must be establishedDark colored towelsMorphineAnxiolyticsLorazepamDiazepamMidazolamSlide 62 discusses the management of massive hemoptysis. The most important thing we can do for patients at risk of hemoptysis, is to anticipate massive hemoptysis. This includes the patient, family and caregiver having unified goals, and coaching those living with the patient as to what to do if massive hemoptysis occurs. If possible there should be quick access to morphine and anxiolytics in an emergency pack.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
66Palliative Treatment of Hemoptysis Treatment of Massive Hemoptysis If resuscitation is the goal…Patent airway + oxygenIntubation and ventilation if neededPositionLateral decubitusHead downBleeding lung downDetermine the site of bleedingAvoid excessive manipulationCough suppression (codeine mg po q6h)Assuming the patient wants aggressive treatment slide 64 lists the steps to take when massive hemoptysis occurs. Once a patent airway is maintained and oxygen administered, the patient should be placed in the lateral decubitus position with the bleeding side dependent. Then the site of the bleeding should be determined as previously described. Excessive manipulation should be avoided and a cough suppressant can be given if indicated.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
67Palliative Treatment of Hemoptysis Treatment of Massive Hemoptysis – Goal Resuscitation If resuscitation is the goal…(continued)Immediate bronchoscopyIf source identified, lavage with iced saline and adrenalin (10cc of 1:10,000 dilution)Topical thrombinBalloon catheter tamponadeVasopressinBronchial stent placementIf source not foundCT with contrastBronchial or pulmonary angiographySlide 64 discusses the treatment of massive hemoptysis assuming that aggressive treatment has been chosen by the patient. Since many of our patients are at home, this often will be difficult to execute. Immediate bronchoscopy should be done to identify the source of bleeding and to stop the bleeding using a variety of techniques. If the source is not discovered and the patient is still alive, CT with contrast should be done and if the site is still in question, bronchial arterial and / or pulmonary angiography should follow.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
68Palliative Treatment of Hemoptysis Treatment of Massive Hemoptysis – Goal Resuscitation If resuscitation is the goal…(continued)Bronchial arterial embolizationSuccessful in % of casesEspecially good in those with dilated bronchial arteries (bronchiectasis)ComplicationsRebleeding - commonAnterior spinal artery infarction and paraplegia – 5%Ischemic necrosis of the bronchusArterial dissectionSurgical resection of the bleeding tissueBronchial arterial embolization is discussed on slide 65. It is successful in stopping the massive hemoptysis in 70 to 100% of patients. Bronchiectasis is often associated with dilated bronchial arteries and bronchial artery arteriograms followed by embolization can be very useful. Dreaded complications include not only rebleeding, but also thrombosis of the anterior spinal artery with resultant paraplegia in 5% of patients, ischemic necrosis of the bronchus and arterial dissection. If not successful, the next step is surgical resection of the bleeding tissue.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 901
69Palliative Care of Pulmonary Hypertension and Cor Pulmonale Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
70Palliative Care of Pulmonary Hypertension and Cor Pulmonale Clinical ManifestationsDependent edemaRight ventricular hypertrophyRight ventricular dilatationThe manifestations of pulmonary hypertension and cor pulmonale are listed in slide 68. These we are all familiar with.ARS-5
71Palliative Care of Pulmonary Hypertension and Cor Pulmonale Etiology and Pathophysiology Most chronic pulmonary diseases can ultimately cause pulmonary hypertension and cor pulmonalePathophysiology (56)COPD – severe pulmonary hypertension only in a small percentage of COPD patientsHypoxia → constriction of pulmonary arterial vasculature – However…Poor correlation between arterial p02 and pulmonary artery pressure in COPDChronic inflammationRepeated hyperinflation of the lungsCigarette smokingPulmonary Emboli and Pulmonary FibrosisObstruction of the pulmonary vasculaturePrimary Pulmonary HypertensionEtiology unknownSlide 66 begins the discussion about pulmonary hypertension and cor pulmonale. Of course most chronic pulmonary diseases are capable of causing pulmonary hypertension and cor pulmonale, however, in COPD patients severe pulmonary hypertension occurs only in a small percentage of patients. In addition to the hypoxic pulmonary arterial vasoconstriction, chronic inflammation, cigarette smoking and repeated hyperinflation of the lungs contribute to production of pulmonary arterial hypertension. Interestingly, there is a poor correlation between the arterial oxygen tension and pulmonary artery pressure in COPD patients.Obstruction of the pulmonary vasculature as in pulmonary emboli and pulmonary fibrosis can result in pulmonary hypertension.Of course, the poorly understood entity of primary pulmonary hypertension causes cor pulmonale.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 90956. The Proceedings of the American Thoracic Society 2:20-22 (2005)
72Pathophysiology of Edema in COPD Palliative Care of Pulmonary Hypertension and Cor Pulmonale PathophysiologyPathophysiology of Edema in COPDExercise →↑ right ventricular end diastolic pressure →↑ stretching of the right atrium →↑ sympathetic tone →↑ renin angiotensin aldosterone production →↑ renal distal tubular retention of water and sodium →↑ edema (56)C02 retention →↑ renal proximal tubular sodium retention →↑ edemaSlide 67 displays the cascade of pathophysiologic events leading to pulmonary hypertension in COPD patients. The two major triggers are exercise and CO2 retention. Do not conclude from this slide that COPD patients should not exercise. The thing to take away from this slide is that the renin, angiotensin, aldosterone sequence plays a major role in the development of edema and ultimately pulmonary hypertension in COPD patients.56. The Proceedings of the American Thoracic Society 2:20-22 (2005)
73Palliative Care of Pulmonary Hypertension and Cor Pulmonale Treatment Treat the underlying pulmonary diseaseOxygenLong term oxygen therapy in COPDOnly produces a small decrease in pulmonary artery pressureIn acute exacerbations of COPDDelivered with BiPAP , reduces pulmonary artery pressureSlide 69 outlines the treatment of pulmonary hypertension and cor pulmonale. First, treat the underlying cause. In COPD long term treatment with oxygen when indicated will help, and prevention and appropriate treatment of COPD exacerbations will help in treating cor pulmonale.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 909
74Palliative Care of Pulmonary Hypertension and Cor Pulmonale Treatment β2 – agonistsReduce pulmonary artery pressureIncrease right ventricular ejection fractionDiuretics – the primary treatment of edemaEdema is secondary to –Hypoxic renal dysfunctionExcessive release of pituitary hormonesNot caused by right heart failureCaution: hypochloremic alkalosis → ↓ ventilation and C02 retentionCalcium Channel BlockersOnly short term effect on pulmonary hypertensionMay produce ventilation-perfusion mismatch and worsen oxygen saturationMay produce systemic hypotensionAs shown in slide 70, beta-2 agonists reduce pulmonary arterial pressure and stimulate right ventricular contractile force. Edema in cor pulmonale is more a consequence of the renin, angiotensin, aldosterone production than the increased pressures of right ventricular heart failure. So we are seeing lots of COPD patients with edema and mild pulmonary hypertension, but not severe pulmonary arterial hypertension.There were great expectations for calcium channel blockers in the treatment of pulmonary hypertension, but the effects are short lived and long term use may even be somewhat detrimental in that V/Q miss-matching may occur resulting in a reduction of arterial oxygen levels, and, of course systemic hypotension may result as well.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 909
75Palliative Care of Pulmonary Hypertension and Cor Pulmonale Treatment ACE InhibitorsCause systemic hypotensionNo improvement in pulmonary vascular resistance, gas exchange or ventilatory parametersFor completeness, in slide 71, ACE inhibitors are of no value in treating pulmonary hypertension.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 909
76Palliative Care of Primary Pulmonary Hypertension Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
77Palliative Care of Primary Pulmonary Hypertension Treatment Endothelin antagonistsBosentan (Tracleer®) (57) –Oral endothelin receptor blockerMild improvement in dyspnea36 meter increase in 6 minute walking distanceApproved for use in pulmonary arterial hypertensionMay be used in patients with COPD and severe pulmonary hypertension, but these patients are difficult to identify in an end of life setting. Clinical trials are ongoing.(58)Caution – Numerous drug interactionsSlide 72 addresses use of the endothelin antagonist bosentan or Tracleer. The good news is that it is an oral medication and improves dyspnea in patients with pulmonary hypertension. The bad news is that the bulk of our patients are COPD patients without severe pulmonary hypertension. COPD patients with severe pulmonary hypertension are not easily identified. Only about 10 % of COPD patients have significant pulmonary hypertension. Bosentan has numerous drug interactions so before prescribing, be sure there will be no drug interactions. Before considering this drug in COPD it is best to have objective evidence of pulmonary hypertension such as pulmonary artery pressures and evidence of right ventricular hypertrophy.57. U.S. Pharmacist Vol. No: 30:05 Posted: 5/16/0558. Curr Opin Pulm Med Mar;9(2):139-43
78Palliative Care of Primary Pulmonary Hypertension Treatment Prostacyclin AnalogsEpoprostenol (Flolan®) and Treprostinil (Remodulin®)Improves exercise toleranceMust be given as a continuous infusionIloprost (Ventavis®)InhaledBeraprost – Not available in USAImprovement in symptomsThe prostacyclin analogs are mentioned in slide 73. Epoprostenol and treprostinil both have to be given as a continuous infusion but both improve exercise tolerance. Iloprost is inhaled making it a more practical drug to use in the treatment of primary pulmonary hypertension.57. U.S. Pharmacist Vol. No: 30:05 Posted: 5/16/05
79Palliative Care of Primary Pulmonary Hypertension Treatment Phosphodiesterase V InhibitorsSildenafil (Viagra®)Improves exercise toleranceOther phosphodiesterase V inhibitors are being evaluatedTadalafil (Cialis®) – only once daily dosingAnticoagulantsWarfarin –To prevent microthrombi formation in pulmonary circulationTo prevent thrombophlebitis in the lower extremitiesKeep INR atReduces progression of the disease and those symptoms that will worsen with progression of the diseaseSlide 74 mentions the phosphodiesterase V inhibitors, specifically Viagra and Cialis both of which improve exercise tolerance in primary pulmonary hypertension.Patients with primary pulmonary hypertension are at high risk of thrombophlebitis and thromboembolism. INR should be kept in the 1.5 – 2.0 range. Warfarin reduces progression of the disease and the symptoms of primary pulmonary hypertension.57. U.S. Pharmacist Vol. No: 30:05 Posted: 5/16/05
80Palliative Care of Pulmonary Fibrosis Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
81Palliative Care of Pulmonary Fibrosis Treatment Pneumoconioses – Most Common CauseIdiopathic Pulmonary FibrosisTreatment with interferon gamma-1bConflicting evidence of effectiveness (59,60)Metaanalysis suggests it does prolong life ( 61)In general pulmonary fibrosis patients do not retain CO2High flows of oxygen may be usedPulmonary fibrosis is mentioned in slide 75. Pneumoconioses is the leading cause. For idiopathic pulmonary fibrosis interferon gamma-1b has been used but with conflicting evidence of effectiveness and no prolongation of life.The important thing to take away from this slide is that in general patients with pulmonary fibrosis are not CO2 retainers and high flows of oxygen may be used to help their dyspnea.59. Mayo Clin Proc Sep;78(9):1082-760. Ann Pharmacother Oct;39(10): Epub 2005 Sep 1361. Chest Jul;128(1):203-6
82Palliative Care of Pulmonary Emboli Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
83Palliative Care of Pulmonary Emboli Most deaths from PE are a result of inadequate prophylaxisWhich end of life patients should receive prophylaxis?End stage cardiopulmonary patientsCancer patients with prothrombotic tumorsMinimal data on prophylactic treatment VTE in end of life outpatientsSlide 79 addresses a difficult issue in many of our hospice patients, that of prophylactic anticoagulation. As noted most deaths from pulmonary emboli are a result of inadequate prophylaxis. End stage cardiopulmonary patients, immobile patients, and patients with prothrombotic tumors are all candidates for anticoagulants and many are at high risk of bleeding from such therapy.
84Palliative Care of Pulmonary Emboli Current VTE ProphylaxisHydrationNot crossing legsTraditional stockings probably not effectiveEncouraging mobilityDrug therapyLow molecular weight heparin is preferredNo prothrombin time neededOnce daily injectionWarfarinINR should be 2-3Difficult to regulate in the end of life patient because of other drug therapies and fluctuating liver functionsSlide 80 lists the measures to prevent venous thromboembolism. Noteworthy is that traditional stockings are probably not effective and that low molecular weight heparin is preferred over warfarin since laboratory monitoring is not needed. Warfarin is difficult to regulate in the end of life patient because of other drug therapies and in some patients fluctuating liver functions.
85Palliative Care of Pulmonary Emboli On the horizon…XimelagatranOral medicationAs effective as low dose warfarin with enoxaparinNot yet approved because of potential hepatotoxicity and ↑ incidence of coronary eventsIdraparinuxOnce weekly injectionIn phase III trialsSlide 82 flashes some hope for two new anticoagulants for prevention of venous thromboembolism and pulmonary emboli. Ximelgatran is an oral medication which is effective, but not yet approved by the FDA because of potential hepatotoxicity and coronary events.Another attractive prospect on the horizon is Idaparinux, a once a week injection not requiring laboratory monitoring.62. Semin Vasc Med Aug;5(3):276-84
86Palliative Care of Stridor Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
87Palliative Treatment of Stridor CausesInfection – epiglottitis, diphtheriaTumorAspirated objectsThick sputumBlood clotsForeign bodiesDislodged tumor particlesCrohn's Disease – rare – resistant to dexamethasone (54)Diffuse Idiopathic Skeletal Hyperostosis (DISH) Forestier’s Disease – from large cervical spine osteophytes compressing the trachea (55)Achalasia – megaesophagus compression of trachea (56)Myasthenia gravis – presenting with exertional stridor (57)Psychogenic stridor (58)Drug hypersensitivity – amphotericin (60)Stridor is presented in slide 58. Some unusual causes of stridor are listed. While this presentation does not include malignant pulmonary disease, neoplasm or aspiration are probably the most common causes of in our hospice patients.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 90254. Chest Aug;130(2):579-8155. J Laryngol Otol Jan;113(1):65-756. Eur J Gastroenterol Hepatol Nov;9(11):1125-857. Thorax Jan;51(1):108-959. Gen Hosp Psychiatry May;16(3):213-2360. Ann Allergy Asthma Immunol Nov;91(5):460-6
88Palliative Treatment of Stridor Treatment – Non-pharmacologic and Pharmacologic Postural manipulationHeimlich maneuver – for acute onset stridorPhysiotherapyBronchoscopy or laryngoscopyTracheostomyStentsMedicationsDexamethasone 16 mg po qd for edema or inflammationOxygen / Helium 4:1 MixtureInfliximab – for Crohn’s Disease (54)Slide 59 outlines the treatment of stridor. We must not forget the Heimlich maneuver may be appropriate in our hospice patients who are so prone to dysphagia and recurrent aspiration resulting in stridor. In those patients in whom a quick fix is not possible endoscopy and tracheostomy can be offered. Medical treatments include an oxygen helium mixture and administration of dexamethasone. Crohn’s disease as a cause is very unusual, but I thought interesting, and apparently resistant to corticosteroids but responsive to infliximab.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 90254. Chest Aug;130(2):579-81
89Palliative Care of Neuromuscular and Restrictive Pulmonary Disorders Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
90Palliative Care of Neuromuscular Disorders and Restrictive Pulmonary Disease Hypercapnia and sleep disorders are very common in neuromuscular disordersMS and ALS – bulbar disorders result in dysphagia and frequent aspiration and pneumoniaLong term anticoagulation is often prescribed for thromboembolic prophylaxisGlossopharyngeal breathing is a good technique to improve ventilation in patients with high cervical injuriesSlide 76 touches on neuromuscular and restrictive pulmonary diseases. Hypercapnia and sleep disorders are common in ALS and MS. Thromboembolic prophylaxis are important in these patients. Glossopharyngeal breathing can improve ventilation in patients with high cervical injuries.
91Non-invasive mechanical ventilation Palliative Care of Neuromuscular Disorders and Restrictive Pulmonary DiseaseNon-invasive mechanical ventilationRocking bedsAbdominal pneumatic beltsNegative pressure ventilatorsNasal CPAPSlide 77 lists the non-invasive methods for mechanical ventilation in patients with neuromuscular disease and hypoventilation. These, of course, can improve the sensation of dyspnea.
92Palliative Care of Bronchiectasis and Cystic Fibrosis Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
93Palliative Care of Bronchiectasis and Pulmonary Fibrosis Nebulized Deoxyribonuclease (DNAse)Hydrolysis of extranuclear DNA that accumulates with neutrophil degradation in infected airwaysUseful in cystic fibrosis and to a lesser extent in bronchiectasisSlide 78 mentions that in bronchiectasis and in cystic fibrosis, the mucous contains large numbers of neutrophils because of the chronically infected bronchi. This results in large amounts of extranuclear DNA and tenacious sputum.The use of nebulized DNAse to hydrolyze intra-airway extranuclear DNA has proven useful in the treatment of bronchiectasis and cystic fibrosis.40. Derek, D. et al. (2004). Oxford Textbook of Palliative Medicine, pp. 908
94Palliative Care of α-1 Antitrypsin Deficiency Welcome every one to October’s First Friday phone call. For those that don’t know me I am Jim Botts, the Southwest Area Medical Director. Today we are to cover Palliative Care of Respiratory Symptoms.Main Menu…
95Palliative Care of α-1 Antitrypsin Deficiency “AAT replacement therapy is for enzyme deficient patients with impaired FEV-1 (35-65% of predicted value), who have quit smoking and are on optimal medical therapy but continue to show a rapid decline in FEV-1 after a period of observation of at least 18 months.”(63)Treatment of lung disease caused by Alpha-1 antitrypsin deficiency is summarized in a quote on slide 83. Not every patient with alpha-1 antitrypsin deficiency needs to receive enzyme therapy.63. Treat Respir Med. 2005;4(1):1-8
97Links - 1 Spiriva Cost Spiriva vs. Serevent Respiratory Sep;11(5):Is a long-acting inhaled bronchodilator the first agent to use in stable chronic obstructive pulmonary disease?Emerging drugs for the treatment of chronic obstructive pulmonary disease.Pharmacologic treatment of chronic obstructive pulmonary disease: past, present, and future.Names of leukotriene related drugsEffect of Intravenous Magnesium Sulfate on Chronic Obstructive Pulmonary DiseaseAddition of anticholinergic solution prolongs bronchodilator effect of beta 2 agonistsComparison of the bronchodilating effect of salmeterol and zafirlukast in combinationRetrospective evaluation of systemic corticosteroids for the management of acute exacerbationsEfficacy and safety of inhaled corticosteroids in patients with COPDRoflumilast for the treatment of chronic obstructive pulmonary diseaseCorticosteroids and Chronic Obstructive Pulmonary DiseaseTheophylline in chronic obstructive pulmonary disease: new horizons.Corticosteroid resistance in chronic obstructive pulmonary disease: inactivation of histone deacetylase.Inhaled corticosteroids and mortality in chronic obstructive pulmonary disease.Inhaled corticosteroids in chronic obstructive pulmonary disease: is there a long-term benefit?Health-related quality of life in individuals with chronic obstructive pulmonary disease.Improving health-related quality of life in chronic obstructive pulmonary disease.
98Links - 2Diazepam in the treatment of dyspnea in the 'Pink Puffer' syndrome.The palliation of dyspnea in terminal disease More research neededAn approach to dyspnea in advanced disease. Opioids are first line drugsBuspirone effect on breathlessness and exercise performance in patients with chronic obstructive pulmonary disease.Effects of buspirone on anxiety levels and exercise tolerance in patients with chronic airflow obstruction and mild anxiety.Sertraline effects on dyspnea in patients with obstructive airways diseaseRandomized, double blind, placebo controlled crossover trial of sustained release morphine for the management of refractory dyspneaA systematic review of the use of opioids in the management of dyspneaDisabling dyspnea in patients with advanced disease: lack of effect of nebulized morphineRoflumilast for the treatment of chronic obstructive pulmonary diseaseEffects of N-acetylcysteine on outcomes in chronic obstructive pulmonary disease (Bronchitis Randomized on NAC Cost-Utility Study, BRONCUS): a randomized placebo-controlled trialN-acetylcysteine reduces the risk of re-hospitalization among patients with chronic obstructive pulmonary diseaseShort-term effects of montelukast in stable patients with moderate to severe COPDTherapeutic responses in asthma and COPD. Bronchodilators Review of effects of PDE4 Inhibitors and LRAsLong-term montelukast therapy in moderate to severe COPD--a preliminary observationCurrent and future pharmacologic therapy of exacerbations in chronic obstructive pulmonary disease and asthma.Should patients with acute exacerbation of chronic bronchitis be treated with antibiotics? Advantages of the use of fluoroquinolones.
99Links - 3Short-term and long-term outcomes of moxifloxacin compared to standard antibiotic treatment in acute exacerbations of chronic bronchitisMoxifloxacin vs. Alternatives for Chronic BronchitisPalliative Home Care for Advanced Lung DiseaseIs there a role for airway clearance techniques in chronic obstructive pulmonary disease?Nebulized hypertonic saline for cystic fibrosisOsmotic stimuli increase clearance of mucus in patients with mucociliary dysfunctionPotential future therapies for the management of cough: ACCP evidence-based clinical practice guidelinesPotential new cough therapies.Current and future drugs for the treatment of chronic coughComparison of lidocaine and bronchodilator inhalation treatments for cough suppression in patients with chronic obstructive pulmonary disease.Lidocaine inhalation for cough suppressionEffect of indomethacin on bronchorrhea in patients with chronic bronchitis, diffuse panbronchiolitis, or bronchiectasisIn vivo study of indomethacin in bronchiectasis: effect on neutrophil function and lung secretionStridor in Crohn disease and the use of infliximab
100Links - 4An unusual case of stridor due to osteophytes of the cervical spine: (Forestier's disease).Myasthenia gravis presenting with stridorAchalasia presenting as acute stridorPsychogenic stridorAmphotericin-induced stridor: a review of stridor, amphotericin preparations, and their immunoregulatory effectsUse of the Dumon Y-stent in the management of malignant disease involving the carina: a retrospective review of 86 patientsThoracic embolotherapy for life-threatening hemoptysis: a pulmonologists perspectiveBronchial and non bronchial systemic artery embolization for life-threatening hemoptysis: a comprehensive reviewPulmonary hypertension and right heart failure in chronic obstructive pulmonary diseaseAdvances in the treatment of secondary pulmonary hypertensionOverview of treprostinil sodium for the treatment of pulmonary arterial hypertensionSildenafil for pulmonary hypertensionOral sildenafil is an effective and specific pulmonary vasodilator in patients with pulmonary arterial hypertension: comparison with inhaled nitric oxideTreatment of Pulmonary HypertensionInterferon gamma-1b as therapy for idiopathic pulmonary fibrosis. An intra-patient analysis.Interferon gamma-1b therapy for advanced idiopathic pulmonary fibrosisInterferon gamma-1b in the treatment of idiopathic pulmonary fibrosisInterferon-gamma1b therapy in idiopathic pulmonary fibrosis: a metaanalysisEmphysema in alpha1-antitrypsin deficiency: does replacement therapy affect outcome?Ximelagatran vs low-molecular-weight heparin and warfarin for the treatment of deep vein thrombosis: a randomized trial.
101Links - 5Is long-term low-molecular-weight heparin acceptable to palliative care patients in the treatment of cancer related venous thromboembolism? A qualitative study.Acceptability of low molecular weight heparin thromboprophylaxis for inpatients receiving palliative care: qualitative study.Treating patients with venous thromboembolism: initial strategies and long-term secondary prevention.Inhaled mannitol for the treatment of mucociliary dysfunction in patients with bronchiectasis: effect on lung function, health status and sputum.Improved sputum expectoration following a single dose of INS316 in patients with chronic bronchitis.