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The Older Adult with Cough Assistant Professor, Department of Internal  Medicine Chair, Division of Infectious Disease  Nova Southeastern University College of Osteopathic Medicine © 2007
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  Lecture Outline: 8) Acute bronchitis 9) Seasonal influenza with the threat of pandemic influenza and influenza vaccines 10) Pneumococcal vaccines
“ Squaring” of the Population Source: U.S. Bureau  of Census (1996).
 
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↓  HIV  ↓ PI
30.4% of Deaths in Children < 5 The 10 leading causes of death as a % of all    deaths in the United States
1.4% of Deaths in Children  < 5  The 10 leading causes of death as a % of all  deaths in the United States
 
Chronic Obstructive Pulmonary Disease (COPD) COPD includes emphysema – an anatomically defined condition – characterized by destruction and enlargement of alveoli. COPD also includes chronic bronchitis – a clinically defined disease – manifested by cough productive of sputum, occurring on most days for at least 3 months of the year during 2 consecutive years  when other respiratory or cardiac causes for the chronic productive cough are excluded.
Chronic Obstructive Pulmonary Disease (COPD) The major site of increased resistance to airflow in most patients with COPD is in airways  <  2mm in diameter. There must be a chronic obstructive component to the disease for COPD to exist. It is difficult to move air when COPD exists because of obstruction and increased chest wall tension.
Emphysema – Total  Lung Capacity (TLC) & Residual Volume (RV) are elevated.  P   = 2t/r. Copyright ©2005, The Regents of the University of California
NASA P = 2t/r Laplace formula
  Bullous Emphysema © Univ of AL at Birmingham, Dept. of Path.
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COPD Defined by the GOLD criteria:   GOLD   FEV 1 /FVC    FEV 1  (of Predicted) Stage     0  Normal ( >  75%)  Normal ( >  3.8L -  ♂,   >  2.8L -  ♀ )   1 < 70% >  80% 2 < 70% >  50% & < 80% 3 < 70% >  30% & < 50% 4 < 70% < 30%
COPD – Pathogenesis and Manifestations 1) Caused by interaction between host factors and environmental pollutants – cigarette smoke. 2) Mucociliary dysfunction leads to a continuous sheet of bronchial mucous rather than discreet deposits as in normals. This favors bacterial overgrowth. 3) Airflow obstruction reduces the effectiveness of cough adding to the retention of mucous and  further cough.
 
COPD – Pathogenesis and Manifestations 4) PaO 2  usually remains near normal until the FEV 1  is reduced to ~ 50% of normal (GOLD 3). 5) PaCO 2  usually is not elevated until the FEV 1  is reduced to ~ 25% of normal (GOLD 4). 6) Ventilation/perfusion (V/Q) abnormalities account for the hypoxia, so supplemental O 2  is effective treatment for the hypoxia. Shunting is minimal. Failure of the PaO 2  to improve with supplemental O 2  in a patient with COPD suggests an additional shunting process.
COPD – Pathogenesis and Manifestations 7) Cough, sputum production, and exertional dyspnea are the most common symptoms. 8) The prevalence of cough is related to the severity of airway obstruction. Sixteen percent of  patients with mild airway obstruction but 49% of patients with severe airway obstruction had cough.
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  NCI Clubbing is not a feature of COPD alone.  If clubbing is found, search for lung cancer.
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Self-reported COPD and  PFT abnormalities. At age  >  75,  the rate of  PFT abnormality  is 4 times the rate of self-reported COPD. GOLD 2, 3, or 4 GOLD 1
Women report COPD much  more frequently  than men.
Whites report COPD more often  than Blacks
Was COPD more prevalent previously in Blacks than in Whites, but more recently less prevalent in Blacks?
Blacks use the ER for COPD at a higher rate than Whites.  (Rates are  higher  in older  age groups.)
Blacks are now hospitalized for COPD at a higher  rate than Whites. ? Do Blacks have less access to primary care and does this cause their COPD to get worse?
Since 1990,  hospitalizations  for COPD have  increased  overall.  The largest  increases occurred in persons aged  65-74  yrs (62%) and aged  > 75 yrs (52%).
Death  rate in women due to  COPD  rose ~ 3x from 1980-2000.
The trend of increasing COPD  mortality among women probably  reflects the increase in smoking by  women since the 1940s, in the United  States.  The natural history of COPD among smokers is that smoking behaviors start during youth, lung function decline becomes apparent when smokers reach age 40-50 years. Hospitalizations begin when smokers reach age 50-70, and deaths occur when they reach age 60-80.  NPS
COPD prevalence is higher in older people as COPD is related to pack-years.
  COPD Treatment COPD is a chronic disease with exacerbations. Treatment must be considered for the chronic disease in the stable patient and for exacerbations which average 2-3 per year.
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COPD – Treatment of the Chronic Stable Patient 6) Chronic antibiotics are not indicated. 7) Chronic oral steroids are not indicated. 8) Only smoking cessation and  supplemental O 2 , if the  PaO 2   <  55mm Hg or if  there is pulmonary artery  hypertension or right heart  failure, benefit the natural history of COPD.  The other treatments only benefit symptoms  or reduce exacerbations.  Copyright ©2005, The Regents    of the University of California
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COPD – Treatment of the Acute Exacerbation 5) Non-invasive positive pressure ventilation (NIPPV) in respiratory failure – defined as PaCO 2  > 45mmHg – reduced mortality, length of stay, complications of therapy, and the need for intubation.
©  Univ. of AL Birmingham, Dept. of Path Bronchitis with green pus in right mainstem    bronchus. “It looks bacterial.”
  Rationale for the use of Antibiotics in      Exacerbations of Chronic Bronchitis New strain of H. influenza, S. pneumoniae,  or M. catarrhalis in sputum was associated  with exacerbation of chronic bronchitis as defined by increase in dyspnea, cough, sputum volume or sputum purulence.* This supported bacterial infection as a possible cause of exacerbation of chronic bronchitis. *New Strains of Bacteria and Exacerbations of Chronic Obstructive Pulmonary Disease,  Sanjay Sethi, et al, NEJM Volume 347:465-471 August 15, 2002 Number 7
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Causes of (UACS) 1) Allergic Rhinitis – e) Skin test positivity is not proof of cause. f) Treatment is avoidance of the allergen and nasal steroids, nasal antihistamines, oral    non-sedating antihistamines or leukotriene    inhibitors, or oral antihistamine   decongestants (A/D).
Causes of (UACS) 2) (Perennial) Non-allergic Rhinitis –  a) Vasomotor Rhinitis (VR)  b) Non-allergic rhinitis with eosinophilia      (NARES) VR – Sudden, thin, watery nasal discharge due to odor, temperature change, eating, ETOH
2) (Perennial) Non-allergic Rhinitis – NARES – Symptoms as VR & nasal and ocular    pruritus, excessive lacrimation, eosinophils in nasal secretions;   negative methacholine challenge &   skin test – It is not allergy and not    asthma.
2) (Perennial) Non-allergic Rhinitis – Treatment –ipratropium, Anti-cholinergic A/D   Non-sedating anti-histamines without an  anti-cholinergic effect are not likely to be useful.
  Causes of UACS 3) Postinfectious  a) History of URI – 17% coughing at the end of week 5. b) Older sedating A/D with anticholinergic    effect are effective.  c) Cough of URI or post-URI is not histamine   mediated so that newer non-sedating anti-   histamines without an anti-cholinergic effect are not effective.
4) “Bacterial” (Acute) Sinusitis a) May have cough as the only symptom. b) Sinus pressure and pain may not be found. c) Sinus x-rays may help – Classic findings of    bacterial sinusitis are mucosal thickening and air –fluid level.  d) Sinusitis < 3 weeks in duration is usually    viral.
4) “Bacterial” (Acute) Sinusitis e) First generation A/D for first week or two –    no antibiotics. f) Acute sinusitis in third week or longer –    Antibiotic for H. influenza, pneumococcus,    Moraxella catarrhalis, intranasal steroids,    first generation A/D.
Left Frontal Sinusitis  ↑↑  Left Maxillary Sinusitis ↑↑
  Causes of UACS  5) Allergic Fungal Sinusitis a) Immuno-competent atopic patient with chronic sinusitis and nasal drainage    or purulent  sputum,  refractory to  antibiotics. University of California,  San Diego School of Medicine   NIH USDA
5) Allergic Fungal Sinusitis b) Skin test positive for dematiaceous   (pigmented) fungus, fusarium, or   aspergillus. c) “Allergic mucin” (degenerating eosinophils,    cellular debris, and sparse hyphae) the   consistency of peanut butter fills the sinuses.  d)  No  invasion of sub-mucosa, bone, or blood vessels.
5) Allergic Fungal Sinusitis e) IgE mediated. f) Surgery (endoscopy) is required to remove the “allergic mucin” and polyps and establish sinus aeration and drainage. g) Short term oral steroids and long term intra-nasal steroids after surgery. h) Anti-fungals may be indicated as a trial    before surgery.
Causes of UACS 6) Rhinitis medicamentosa a) Seen with topical  α  agonists used for nasal congestion. (oxymetazoline – Afrin) b) Effect of the drug lessens with repeated use (tachyphylaxis) and rebound nasal congestion occurs. c) Can be seen with cocaine. d) Diagnosis by history. e) Treatment is to stop the drug.
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    Chronic Cough Due to Asthma 1) About 25% of adult chronic cough in non-smokers is due to asthma.  2) Cough variant asthma requires a methacholine inhalational challenge (MIC) as spirometry and physical signs of bronchoconstriction are absent. 3) A negative MIC test excludes asthma, a  positive test ( >  20% fall in FEV 1 ) must be confirmed by response to asthma treatment – inhaled bronchodilators and corticosteroids.
Chronic Cough Due to Asthma 4) Leukotriene receptor antagonists – montelukast (Singulair) and zafirlukast (Accolate) are very effective in treating cough due to asthma.
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Non-Asthmatic Eosinophilic Bronchitis (NAEB) 2) Pathology:  In asthma the mast cells are in the bronchial smooth muscle; in NAEB the mast cells are in the bronchial epithelium. 3) Treatment: Inhaled corticosteroids 4) Prognosis: Of patients with NAEB followed for > 1 year,  9% developed asthma and 16% developed COPD.
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Gastroesophageal Reflux Disease (GERD) 4) Definitive diagnosis requires complete or near  disappearance of cough with anti-reflux therapy. 5) Failure of cough to disappear with  anti-reflux therapy does not exclude GERD as the cause of cough because therapy may not have been sufficiently intense. 6) PPI therapy may be effective when H 2  blockers  have failed.
Mycobacterium avium complex (MAC) Lung  Infection CDC
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Mycobacterium avium (MAC) Lung Infection 4) Aerosolized water may be the vehicle of transmission and it is suggested that the  change from baths to showers  may be part of the cause of the increase in  incidence. 5) MAC is common in fresh and salt  water in the  southeast US. USPTO NASA
Mycobacterium avium (MAC) Lung Infection 6) MAC is one reason that we  don’t use BCG in the US. 7) In Northern climes people  had either strong or no  reaction to PPD and the  prevalence of + PPD correlated with TB prevalence. 8) In warmer climes many people had smaller  reactions to PPD and the prevalence of these reactions did not correlate with TB prevalence.  CDC
Mycobacterium avium (MAC) Lung Infection 9) The smaller reactions were due to MAC infections that were usually asymptomatic but  conferred partial immunity to TB. 10) The group given BCG had as its “control group” people who were partially immunized against TB “naturally” since much of the testing of BCG was done in the southeast US. 11) The difference in TB incidence between the BCG and “control” patients was therefore reduced.
Mycobacterium avium (MAC) Lung Infection 12) There may be partial  reciprocal immunity  between TB and MAC. BCG may reduce MAC. 13) MAC lung infection  in women without  underlying lung disease is associated  with fibronodular  bronchiectasis not cavities and favors the lingula and right middle lobe. © Slice of Life & Suzanne S. Stensaas Diffuse Bronchiectasis
Mycobacterium avium (MAC) Lung Infection 14) Repeated recovery of MAC from sputum is an indication for treatment to prevent progression. 15) Chronic cough with sputum may continue during a long period of insidious progression. 16) Hemoptysis is rare and constitutional symptoms occur only with advanced disease.  17) MAC may cause HP – no  gender or age predominance –  restrictive lung disease . NASA
Bronchiectasis
© University of Alabama at Birmingham,  Dept of Pathology Bronchiectasis
Mycobacterium avium (MAC) Lung Infection 18) Formerly MAC pulmonary disease was found in men with  underlying  emphysema  and occurred  as upper lobe cavitary  disease.
Mycobacterium avium (MAC) Lung Infection 19) High resolution CT is more sensitive than plain  CXR as a screening test. 20) Repeated positive cultures are needed for  diagnosis as MAC live in environmental water. 21) Treatment – Rifabutin or rifampin +   Clarithromycin or azithromycin +   Ethambutol +   Streptomycin (for 2 months)   Total treatment 18-24 months NIAID    Macrophage
Mycobacterium avium (MAC) Lung Infection 22) Treatment continues for a year after sputum becomes negative. 23) Patients with bronchiectasis grow new strains of MAC indicating a susceptibility to reinfection after cure. A single strain of MAC persists in patients with cavitary lung disease.  24) Sensitivity testing of MAC to individual drugs is not useful in predicting efficacy of therapy, suggesting that synergy among drugs is important for effectiveness.
Mycobacterium avium (MAC) Lung Infection 25) MAC lung disease in women without underlying lung disease may be due alterations in IFN- γ  (interferon –gamma) and TNF- α (tumor necrosis factor-alpha) responses to MAC infection. 26) Both IFN- γ  and TNF- α  increase the concentration of anti-mycobacterial drugs in macrophages, where the organisms are found.
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  Acute Bronchitis 3) In acute bronchitis there is no parenchymal lung infection either by physical examination or chest x-ray. 4) Pulse < 100, Respirations < 24, Temperature  < 100.4 °F, and absence of any physical findings consistent with consolidation make pneumonia sufficiently unlikely that no CXR is needed.  5) Treatment: Two-thirds of patients with acute  bronchitis are prescribed antibiotics.  Antibiotics are  not  indicated.
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Cough Treatment – In the body of the article 4) Opiates – At effective doses cause physical dependence,  depression, respiratory depression, and constipation. 5) Dextromethorphan – Effectiveness similar to codeine. 6) Benzonatate (Tessalon) – Effective in some opioid resistant cough.
Avian Influenza – Pandemic Influenza As of July 7, 2006
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  Influenza Viruses 4) Currently H1N1 and H3N2 circulate in humans. 5) There are many “bird flu” viruses. The one that is of concern as a possible cause of pandemic flu is H5N1. 6) It is the novel hemaglutinin that causes the threat of epidemic/pandemic. 7) Asian outbreaks of H5N1 caused culling of 120,000,000 birds with an expected reduction of Asian GDP of $10 to $15 billion.
  Influenza Viruses 8) Co-infection of a mammal by a human and an avian influenza virus, and re-assortment of the RNA of the two viruses, was previously thought required for efficient transmission to and replication in a human of the avian virus. 9) Mutation of a single locus  in the avian virus can also  result in efficient human  to human transmission of  the avian influenza virus. Not Required USDA
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Influenza with the Threat of Avian Influenza   Prevention and Treatment 4) Health-care workers involved in the care of patients with documented or suspected avian influenza should be vaccinated with the most recent seasonal human influenza vaccine.  This reduces the likelihood of co-infection with human and avian strains, where genetic rearrangement could lead to the emergence of a potential pandemic strain.
Influenza with the Threat of Avian Influenza   Prevention and Treatment 5) Amantadine and rimantidine should not be used in 2006-07 for prevention or treatment of influenza A until susceptibility of the virus is demonstrated. 6) There is an inactivated seasonal influenza vaccine and an attenuated virus vaccine. 7) The inactivated vaccine is for use in ages 6 months to 9 years, pregnant patients, and age  > 50.
Influenza with the Threat of Avian Influenza   Prevention and Treatment 8) The attenuated influenza vaccine is for use in otherwise healthy patients aged 5 - 49.
What if Pandemic Avian Influenza Occurs?
Health and Human Services (HHS)  Strategic Pandemic Influenza Plan  
HHS Pandemic Influenza Plan – The Threat 1) Containment attempts would require stringent infection- control measures such as  bans on large public gatherings , isolation of symptomatic individuals, prophylaxis of the entire community with antiviral drugs, and various forms of movement restrictions—possibly even including  a quarantine. 2) In the extreme, until a vaccine against the pandemic virus became available in sufficient quantity to have a significant impact on protecting public health, thousands of communities could be countering  influenza simultaneously with  little or no assistance from   adjacent communities, the state,   or the federal government.
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Pandemic Influenza Effect  in the United States Characteristic  Moderate (1958/68-like)  Severe (1918-like) Illness 90 million (30%) 90 million (30%) Outpatient  45 million (50%) 45 million (50%) Medical care Hospitalization 865,000 9,900,000 ICU care 128,750 1,485,000 Mechanical      64,875        742,500 Ventilation  Deaths 209,000 1,903,000
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Planning to Support Healthcare Facilities State health authorities should consider promoting the establishment of local pandemic influenza task forces to: 1) Encourage coordination among state and federal healthcare facilities, such as Veterans Administration hospitals, Indian Health Service facilities, and Department of Defense hospitals.  2) Conduct contingency planning with private sector groups that support hospital functions including medical supply companies, medical gas companies, food and linen companies, internet service providers, and public utilities (water, electricity, gas, telephone, sanitation).
Planning to Support Healthcare Facilities State health authorities should consider promoting the establishment of local pandemic influenza task forces to: 3) Conduct contingency planning with local law enforcement agencies who can help maintain order if a hospital is overwhelmed.  4) Identify alternative sites for patient care and quarantine.  5) Identify community-based organizations that can provide psychological and social support to healthcare workers, public health field workers, and other emergency responders.
Since there are currently insufficient stocks of  anti-viral drugs effective against H5N1 or a  vaccine for H5N1 influenza virus, the current  pandemic mitigation plans use  non-pharmaceutical  interventions.
Interim Pre-pandemic Planning Guidance: Community Strategy for Pandemic Influenza Mitigation in the United States – Early, Targeted, Layered Use of Nonpharmaceutical Interventions CDC – February 2007  http://www.pandemicflu.gov/plan/community/community_mitigation.pdf
  Pandemic Severity Index Case Fatality  Category Projected Ratio   Deaths in US >  2.0% 5 > 1,800,000 >  1.0- < 2.0% 4 900,000 – 1,800,000 >  0.5- < 1.0% 3 450,000 – 900,000 >  0.1- < 0.5%  2 90,000 – 450,000 < 0.1% 1 < 90,000
Mitigation   Pandemic Severity Index  Strategy   2&3 4&5 Isolation of Ill   Recommend Recommend Quarantine Consider Recommend  Household Close School & <  4 weeks <  12 weeks Child Distancing ↓↓  Work & Consider Recommend  Adult Distancing
From Bird to Person Peter D. Zimmerman, Wall Street Journal February 7, 2007 “ Meanwhile, as of the World Health Organization’s compilation on Feb.3, there had been a total of 271 laboratory-confirmed cases of the virus in humans, and of that number a staggering 165, or  61%  died, making it one of the most lethal pathogens in history.”
NOAA Mitigation of pandemic influenza with a case fatality ratio of 61% > 5%.
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  Pneumococcal Vaccines 4) PPV, and polysaccharide antigens in general, are not immunogenic in children less than 2 years of age. 5) PCV is immunogenic is children less than 2 years of age and elicits a T cell dependent response that induces immunologic memory. 6) PCV but not PPV reduces nasopharyngeal carriage of Pneumococcus and thereby may induce “herd” immunity.

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Cough In The Elderly

  • 1. The Older Adult with Cough Assistant Professor, Department of Internal Medicine Chair, Division of Infectious Disease Nova Southeastern University College of Osteopathic Medicine © 2007
  • 2.
  • 3. Lecture Outline: 8) Acute bronchitis 9) Seasonal influenza with the threat of pandemic influenza and influenza vaccines 10) Pneumococcal vaccines
  • 4. “ Squaring” of the Population Source: U.S. Bureau of Census (1996).
  • 5.  
  • 6.
  • 7. ↓ HIV ↓ PI
  • 8. 30.4% of Deaths in Children < 5 The 10 leading causes of death as a % of all deaths in the United States
  • 9. 1.4% of Deaths in Children < 5 The 10 leading causes of death as a % of all deaths in the United States
  • 10.  
  • 11. Chronic Obstructive Pulmonary Disease (COPD) COPD includes emphysema – an anatomically defined condition – characterized by destruction and enlargement of alveoli. COPD also includes chronic bronchitis – a clinically defined disease – manifested by cough productive of sputum, occurring on most days for at least 3 months of the year during 2 consecutive years when other respiratory or cardiac causes for the chronic productive cough are excluded.
  • 12. Chronic Obstructive Pulmonary Disease (COPD) The major site of increased resistance to airflow in most patients with COPD is in airways < 2mm in diameter. There must be a chronic obstructive component to the disease for COPD to exist. It is difficult to move air when COPD exists because of obstruction and increased chest wall tension.
  • 13. Emphysema – Total Lung Capacity (TLC) & Residual Volume (RV) are elevated. P = 2t/r. Copyright ©2005, The Regents of the University of California
  • 14. NASA P = 2t/r Laplace formula
  • 15. Bullous Emphysema © Univ of AL at Birmingham, Dept. of Path.
  • 16.
  • 17. COPD Defined by the GOLD criteria: GOLD FEV 1 /FVC FEV 1 (of Predicted) Stage 0 Normal ( > 75%) Normal ( > 3.8L - ♂, > 2.8L - ♀ ) 1 < 70% > 80% 2 < 70% > 50% & < 80% 3 < 70% > 30% & < 50% 4 < 70% < 30%
  • 18. COPD – Pathogenesis and Manifestations 1) Caused by interaction between host factors and environmental pollutants – cigarette smoke. 2) Mucociliary dysfunction leads to a continuous sheet of bronchial mucous rather than discreet deposits as in normals. This favors bacterial overgrowth. 3) Airflow obstruction reduces the effectiveness of cough adding to the retention of mucous and further cough.
  • 19.  
  • 20. COPD – Pathogenesis and Manifestations 4) PaO 2 usually remains near normal until the FEV 1 is reduced to ~ 50% of normal (GOLD 3). 5) PaCO 2 usually is not elevated until the FEV 1 is reduced to ~ 25% of normal (GOLD 4). 6) Ventilation/perfusion (V/Q) abnormalities account for the hypoxia, so supplemental O 2 is effective treatment for the hypoxia. Shunting is minimal. Failure of the PaO 2 to improve with supplemental O 2 in a patient with COPD suggests an additional shunting process.
  • 21. COPD – Pathogenesis and Manifestations 7) Cough, sputum production, and exertional dyspnea are the most common symptoms. 8) The prevalence of cough is related to the severity of airway obstruction. Sixteen percent of patients with mild airway obstruction but 49% of patients with severe airway obstruction had cough.
  • 22.
  • 23. NCI Clubbing is not a feature of COPD alone. If clubbing is found, search for lung cancer.
  • 24.
  • 25.
  • 26. Self-reported COPD and PFT abnormalities. At age > 75, the rate of PFT abnormality is 4 times the rate of self-reported COPD. GOLD 2, 3, or 4 GOLD 1
  • 27. Women report COPD much more frequently than men.
  • 28. Whites report COPD more often than Blacks
  • 29. Was COPD more prevalent previously in Blacks than in Whites, but more recently less prevalent in Blacks?
  • 30. Blacks use the ER for COPD at a higher rate than Whites. (Rates are higher in older age groups.)
  • 31. Blacks are now hospitalized for COPD at a higher rate than Whites. ? Do Blacks have less access to primary care and does this cause their COPD to get worse?
  • 32. Since 1990, hospitalizations for COPD have increased overall. The largest increases occurred in persons aged 65-74 yrs (62%) and aged > 75 yrs (52%).
  • 33. Death rate in women due to COPD rose ~ 3x from 1980-2000.
  • 34. The trend of increasing COPD mortality among women probably reflects the increase in smoking by women since the 1940s, in the United States. The natural history of COPD among smokers is that smoking behaviors start during youth, lung function decline becomes apparent when smokers reach age 40-50 years. Hospitalizations begin when smokers reach age 50-70, and deaths occur when they reach age 60-80. NPS
  • 35. COPD prevalence is higher in older people as COPD is related to pack-years.
  • 36. COPD Treatment COPD is a chronic disease with exacerbations. Treatment must be considered for the chronic disease in the stable patient and for exacerbations which average 2-3 per year.
  • 37.
  • 38. COPD – Treatment of the Chronic Stable Patient 6) Chronic antibiotics are not indicated. 7) Chronic oral steroids are not indicated. 8) Only smoking cessation and supplemental O 2 , if the PaO 2 < 55mm Hg or if there is pulmonary artery hypertension or right heart failure, benefit the natural history of COPD. The other treatments only benefit symptoms or reduce exacerbations. Copyright ©2005, The Regents of the University of California
  • 39.
  • 40.
  • 41. COPD – Treatment of the Acute Exacerbation 5) Non-invasive positive pressure ventilation (NIPPV) in respiratory failure – defined as PaCO 2 > 45mmHg – reduced mortality, length of stay, complications of therapy, and the need for intubation.
  • 42. © Univ. of AL Birmingham, Dept. of Path Bronchitis with green pus in right mainstem bronchus. “It looks bacterial.”
  • 43. Rationale for the use of Antibiotics in Exacerbations of Chronic Bronchitis New strain of H. influenza, S. pneumoniae, or M. catarrhalis in sputum was associated with exacerbation of chronic bronchitis as defined by increase in dyspnea, cough, sputum volume or sputum purulence.* This supported bacterial infection as a possible cause of exacerbation of chronic bronchitis. *New Strains of Bacteria and Exacerbations of Chronic Obstructive Pulmonary Disease, Sanjay Sethi, et al, NEJM Volume 347:465-471 August 15, 2002 Number 7
  • 44.
  • 45.
  • 46.
  • 47. Causes of (UACS) 1) Allergic Rhinitis – e) Skin test positivity is not proof of cause. f) Treatment is avoidance of the allergen and nasal steroids, nasal antihistamines, oral non-sedating antihistamines or leukotriene inhibitors, or oral antihistamine decongestants (A/D).
  • 48. Causes of (UACS) 2) (Perennial) Non-allergic Rhinitis – a) Vasomotor Rhinitis (VR) b) Non-allergic rhinitis with eosinophilia (NARES) VR – Sudden, thin, watery nasal discharge due to odor, temperature change, eating, ETOH
  • 49. 2) (Perennial) Non-allergic Rhinitis – NARES – Symptoms as VR & nasal and ocular pruritus, excessive lacrimation, eosinophils in nasal secretions; negative methacholine challenge & skin test – It is not allergy and not asthma.
  • 50. 2) (Perennial) Non-allergic Rhinitis – Treatment –ipratropium, Anti-cholinergic A/D Non-sedating anti-histamines without an anti-cholinergic effect are not likely to be useful.
  • 51. Causes of UACS 3) Postinfectious a) History of URI – 17% coughing at the end of week 5. b) Older sedating A/D with anticholinergic effect are effective. c) Cough of URI or post-URI is not histamine mediated so that newer non-sedating anti- histamines without an anti-cholinergic effect are not effective.
  • 52. 4) “Bacterial” (Acute) Sinusitis a) May have cough as the only symptom. b) Sinus pressure and pain may not be found. c) Sinus x-rays may help – Classic findings of bacterial sinusitis are mucosal thickening and air –fluid level. d) Sinusitis < 3 weeks in duration is usually viral.
  • 53. 4) “Bacterial” (Acute) Sinusitis e) First generation A/D for first week or two – no antibiotics. f) Acute sinusitis in third week or longer – Antibiotic for H. influenza, pneumococcus, Moraxella catarrhalis, intranasal steroids, first generation A/D.
  • 54. Left Frontal Sinusitis ↑↑ Left Maxillary Sinusitis ↑↑
  • 55. Causes of UACS 5) Allergic Fungal Sinusitis a) Immuno-competent atopic patient with chronic sinusitis and nasal drainage or purulent sputum, refractory to antibiotics. University of California, San Diego School of Medicine NIH USDA
  • 56. 5) Allergic Fungal Sinusitis b) Skin test positive for dematiaceous (pigmented) fungus, fusarium, or aspergillus. c) “Allergic mucin” (degenerating eosinophils, cellular debris, and sparse hyphae) the consistency of peanut butter fills the sinuses. d) No invasion of sub-mucosa, bone, or blood vessels.
  • 57. 5) Allergic Fungal Sinusitis e) IgE mediated. f) Surgery (endoscopy) is required to remove the “allergic mucin” and polyps and establish sinus aeration and drainage. g) Short term oral steroids and long term intra-nasal steroids after surgery. h) Anti-fungals may be indicated as a trial before surgery.
  • 58. Causes of UACS 6) Rhinitis medicamentosa a) Seen with topical α agonists used for nasal congestion. (oxymetazoline – Afrin) b) Effect of the drug lessens with repeated use (tachyphylaxis) and rebound nasal congestion occurs. c) Can be seen with cocaine. d) Diagnosis by history. e) Treatment is to stop the drug.
  • 59.
  • 60. Chronic Cough Due to Asthma 1) About 25% of adult chronic cough in non-smokers is due to asthma. 2) Cough variant asthma requires a methacholine inhalational challenge (MIC) as spirometry and physical signs of bronchoconstriction are absent. 3) A negative MIC test excludes asthma, a positive test ( > 20% fall in FEV 1 ) must be confirmed by response to asthma treatment – inhaled bronchodilators and corticosteroids.
  • 61. Chronic Cough Due to Asthma 4) Leukotriene receptor antagonists – montelukast (Singulair) and zafirlukast (Accolate) are very effective in treating cough due to asthma.
  • 62.
  • 63.
  • 64. Non-Asthmatic Eosinophilic Bronchitis (NAEB) 2) Pathology: In asthma the mast cells are in the bronchial smooth muscle; in NAEB the mast cells are in the bronchial epithelium. 3) Treatment: Inhaled corticosteroids 4) Prognosis: Of patients with NAEB followed for > 1 year, 9% developed asthma and 16% developed COPD.
  • 65.
  • 66. Gastroesophageal Reflux Disease (GERD) 4) Definitive diagnosis requires complete or near disappearance of cough with anti-reflux therapy. 5) Failure of cough to disappear with anti-reflux therapy does not exclude GERD as the cause of cough because therapy may not have been sufficiently intense. 6) PPI therapy may be effective when H 2 blockers have failed.
  • 67. Mycobacterium avium complex (MAC) Lung Infection CDC
  • 68.
  • 69. Mycobacterium avium (MAC) Lung Infection 4) Aerosolized water may be the vehicle of transmission and it is suggested that the change from baths to showers may be part of the cause of the increase in incidence. 5) MAC is common in fresh and salt water in the southeast US. USPTO NASA
  • 70. Mycobacterium avium (MAC) Lung Infection 6) MAC is one reason that we don’t use BCG in the US. 7) In Northern climes people had either strong or no reaction to PPD and the prevalence of + PPD correlated with TB prevalence. 8) In warmer climes many people had smaller reactions to PPD and the prevalence of these reactions did not correlate with TB prevalence. CDC
  • 71. Mycobacterium avium (MAC) Lung Infection 9) The smaller reactions were due to MAC infections that were usually asymptomatic but conferred partial immunity to TB. 10) The group given BCG had as its “control group” people who were partially immunized against TB “naturally” since much of the testing of BCG was done in the southeast US. 11) The difference in TB incidence between the BCG and “control” patients was therefore reduced.
  • 72. Mycobacterium avium (MAC) Lung Infection 12) There may be partial reciprocal immunity between TB and MAC. BCG may reduce MAC. 13) MAC lung infection in women without underlying lung disease is associated with fibronodular bronchiectasis not cavities and favors the lingula and right middle lobe. © Slice of Life & Suzanne S. Stensaas Diffuse Bronchiectasis
  • 73. Mycobacterium avium (MAC) Lung Infection 14) Repeated recovery of MAC from sputum is an indication for treatment to prevent progression. 15) Chronic cough with sputum may continue during a long period of insidious progression. 16) Hemoptysis is rare and constitutional symptoms occur only with advanced disease. 17) MAC may cause HP – no gender or age predominance – restrictive lung disease . NASA
  • 75. © University of Alabama at Birmingham, Dept of Pathology Bronchiectasis
  • 76. Mycobacterium avium (MAC) Lung Infection 18) Formerly MAC pulmonary disease was found in men with underlying emphysema and occurred as upper lobe cavitary disease.
  • 77. Mycobacterium avium (MAC) Lung Infection 19) High resolution CT is more sensitive than plain CXR as a screening test. 20) Repeated positive cultures are needed for diagnosis as MAC live in environmental water. 21) Treatment – Rifabutin or rifampin + Clarithromycin or azithromycin + Ethambutol + Streptomycin (for 2 months) Total treatment 18-24 months NIAID  Macrophage
  • 78. Mycobacterium avium (MAC) Lung Infection 22) Treatment continues for a year after sputum becomes negative. 23) Patients with bronchiectasis grow new strains of MAC indicating a susceptibility to reinfection after cure. A single strain of MAC persists in patients with cavitary lung disease. 24) Sensitivity testing of MAC to individual drugs is not useful in predicting efficacy of therapy, suggesting that synergy among drugs is important for effectiveness.
  • 79. Mycobacterium avium (MAC) Lung Infection 25) MAC lung disease in women without underlying lung disease may be due alterations in IFN- γ (interferon –gamma) and TNF- α (tumor necrosis factor-alpha) responses to MAC infection. 26) Both IFN- γ and TNF- α increase the concentration of anti-mycobacterial drugs in macrophages, where the organisms are found.
  • 80.
  • 81. Acute Bronchitis 3) In acute bronchitis there is no parenchymal lung infection either by physical examination or chest x-ray. 4) Pulse < 100, Respirations < 24, Temperature < 100.4 °F, and absence of any physical findings consistent with consolidation make pneumonia sufficiently unlikely that no CXR is needed. 5) Treatment: Two-thirds of patients with acute bronchitis are prescribed antibiotics. Antibiotics are not indicated.
  • 82.
  • 83. Cough Treatment – In the body of the article 4) Opiates – At effective doses cause physical dependence, depression, respiratory depression, and constipation. 5) Dextromethorphan – Effectiveness similar to codeine. 6) Benzonatate (Tessalon) – Effective in some opioid resistant cough.
  • 84. Avian Influenza – Pandemic Influenza As of July 7, 2006
  • 85.
  • 86. Influenza Viruses 4) Currently H1N1 and H3N2 circulate in humans. 5) There are many “bird flu” viruses. The one that is of concern as a possible cause of pandemic flu is H5N1. 6) It is the novel hemaglutinin that causes the threat of epidemic/pandemic. 7) Asian outbreaks of H5N1 caused culling of 120,000,000 birds with an expected reduction of Asian GDP of $10 to $15 billion.
  • 87. Influenza Viruses 8) Co-infection of a mammal by a human and an avian influenza virus, and re-assortment of the RNA of the two viruses, was previously thought required for efficient transmission to and replication in a human of the avian virus. 9) Mutation of a single locus in the avian virus can also result in efficient human to human transmission of the avian influenza virus. Not Required USDA
  • 88.
  • 89.
  • 90. Influenza with the Threat of Avian Influenza Prevention and Treatment 4) Health-care workers involved in the care of patients with documented or suspected avian influenza should be vaccinated with the most recent seasonal human influenza vaccine. This reduces the likelihood of co-infection with human and avian strains, where genetic rearrangement could lead to the emergence of a potential pandemic strain.
  • 91. Influenza with the Threat of Avian Influenza Prevention and Treatment 5) Amantadine and rimantidine should not be used in 2006-07 for prevention or treatment of influenza A until susceptibility of the virus is demonstrated. 6) There is an inactivated seasonal influenza vaccine and an attenuated virus vaccine. 7) The inactivated vaccine is for use in ages 6 months to 9 years, pregnant patients, and age > 50.
  • 92. Influenza with the Threat of Avian Influenza Prevention and Treatment 8) The attenuated influenza vaccine is for use in otherwise healthy patients aged 5 - 49.
  • 93. What if Pandemic Avian Influenza Occurs?
  • 94. Health and Human Services (HHS) Strategic Pandemic Influenza Plan  
  • 95. HHS Pandemic Influenza Plan – The Threat 1) Containment attempts would require stringent infection- control measures such as bans on large public gatherings , isolation of symptomatic individuals, prophylaxis of the entire community with antiviral drugs, and various forms of movement restrictions—possibly even including a quarantine. 2) In the extreme, until a vaccine against the pandemic virus became available in sufficient quantity to have a significant impact on protecting public health, thousands of communities could be countering influenza simultaneously with little or no assistance from adjacent communities, the state, or the federal government.
  • 96.
  • 97. Pandemic Influenza Effect in the United States Characteristic Moderate (1958/68-like) Severe (1918-like) Illness 90 million (30%) 90 million (30%) Outpatient 45 million (50%) 45 million (50%) Medical care Hospitalization 865,000 9,900,000 ICU care 128,750 1,485,000 Mechanical   64,875   742,500 Ventilation Deaths 209,000 1,903,000
  • 98.
  • 99.
  • 100. Planning to Support Healthcare Facilities State health authorities should consider promoting the establishment of local pandemic influenza task forces to: 1) Encourage coordination among state and federal healthcare facilities, such as Veterans Administration hospitals, Indian Health Service facilities, and Department of Defense hospitals. 2) Conduct contingency planning with private sector groups that support hospital functions including medical supply companies, medical gas companies, food and linen companies, internet service providers, and public utilities (water, electricity, gas, telephone, sanitation).
  • 101. Planning to Support Healthcare Facilities State health authorities should consider promoting the establishment of local pandemic influenza task forces to: 3) Conduct contingency planning with local law enforcement agencies who can help maintain order if a hospital is overwhelmed. 4) Identify alternative sites for patient care and quarantine. 5) Identify community-based organizations that can provide psychological and social support to healthcare workers, public health field workers, and other emergency responders.
  • 102. Since there are currently insufficient stocks of anti-viral drugs effective against H5N1 or a vaccine for H5N1 influenza virus, the current pandemic mitigation plans use non-pharmaceutical interventions.
  • 103. Interim Pre-pandemic Planning Guidance: Community Strategy for Pandemic Influenza Mitigation in the United States – Early, Targeted, Layered Use of Nonpharmaceutical Interventions CDC – February 2007 http://www.pandemicflu.gov/plan/community/community_mitigation.pdf
  • 104. Pandemic Severity Index Case Fatality Category Projected Ratio Deaths in US > 2.0% 5 > 1,800,000 > 1.0- < 2.0% 4 900,000 – 1,800,000 > 0.5- < 1.0% 3 450,000 – 900,000 > 0.1- < 0.5% 2 90,000 – 450,000 < 0.1% 1 < 90,000
  • 105. Mitigation Pandemic Severity Index Strategy 2&3 4&5 Isolation of Ill Recommend Recommend Quarantine Consider Recommend Household Close School & < 4 weeks < 12 weeks Child Distancing ↓↓ Work & Consider Recommend Adult Distancing
  • 106. From Bird to Person Peter D. Zimmerman, Wall Street Journal February 7, 2007 “ Meanwhile, as of the World Health Organization’s compilation on Feb.3, there had been a total of 271 laboratory-confirmed cases of the virus in humans, and of that number a staggering 165, or 61% died, making it one of the most lethal pathogens in history.”
  • 107. NOAA Mitigation of pandemic influenza with a case fatality ratio of 61% > 5%.
  • 108.
  • 109. Pneumococcal Vaccines 4) PPV, and polysaccharide antigens in general, are not immunogenic in children less than 2 years of age. 5) PCV is immunogenic is children less than 2 years of age and elicits a T cell dependent response that induces immunologic memory. 6) PCV but not PPV reduces nasopharyngeal carriage of Pneumococcus and thereby may induce “herd” immunity.