Lower Respiratory Disease

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Lower Respiratory Disease

• Joyce Crook, FNP
• 8800

2
Lower Respiratory Disease

• Patients with diseases of the respiratory system
  generally present because of symptoms
• Dyspnea
• Cough
• Hemoptysis
• Chest pain
• Or due to an abnormal CXR or CT scan

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Lower Respiratory Disease

• Acute Disease is usually infectious
• Pneumonia
• Acute Bronchitis
• TB
• Chronic Disease has 2 Primary Forms
• Obstructive diseases-expiratory flow rate is
  impaired
• Restrictive Diseases-lung volumes are reduced

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Lower Respiratory Disease

• Obstructive Diseases
• Asthma (Usually Reversible)
• COPD-Chronic Bronchitis Emphysema
• Bronchiectasis
• Cystic Fibrosis
• Obliterative Bronchiolitis (BOOP, COP)
• Restrictive Diseases
• Interstitial Lung Disease
• Musculoskeletal disorders
• Tumors
• Lung resection

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COPD

• COPD is defined as
• Disease state characterized by airflow limitation
  that is not fully reversible, and is usually
  progressive. It is most commonly caused by
  chronic bronchitis and emphysema.
• COPD causes physical impairment, debility,
  reduced quality of life and death.
• Affects gt 16 million persons in US
• gt120,000 deaths/year in US
• COPD is 4th leading cause of death in the world
• Projected to be the 3rd by 2020
• Cigarette smoking is the single major risk factor
• Underdiagnosed, only 15-20 of smokers are ever
  diagnosed, although the majority develop airflow
  obstruction.

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COPD

• Risk factors
• Cigarette smoking. Primary cause in 80-90
• Intensity expressed as pack-years (packs/day
  multiplied by of years)
• Age (most have been smoking gt20 years)
• Gender no longer a factor
• Increased airway hyperresponsiveness
• Occupational exposures
• Air pollution
• Alpha1-antitrypsin phenotypes (Younger than 45
  years with significant COPD, smoking or
  nonsmoking)

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COPD

• Important to recognize and diagnose early because
  appropriate management can
• Prevent and decrease symptoms
• Reduce frequency and severity of exacerbations
• Improve health status
• Improve exercise capacity
• Prolong survival

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COPD

• Chronic Bronchitis
• defined as chronic productive cough for a
  minimum of 3 months in each of two successive
  years.
• characterized by excessive mucus secretion

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COPD

• Emphysema
• defined as permanent change of gas-exchanging
  airspaces (respiratory bronchioles, alveolar
  ducts and alveoli) which become obliterated from
  small distinct airspaces into large abnormal
  airspaces.

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COPD

• Pathophysiology
• Airflow Obstruction - Persistent reduction in
  forced expiratory flow rate (FEV1). Reduced ratio
  of FEV1/FVC
• Hyperinflation - Increased residual volume (air
  trapping) with progressive increased total lung
  volume
• Gas Exchange abnormality -Ventilation/Perfusion
  mismatching resulting in hypoxemia

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COPD

• Large Airways Pathology
• Ongoing inflammation of the cells lining the
  bronchial walls
• Mucus gland enlargement and goblet cell
  hyperplasia causes increased cough and mucus
  production
• Squamous metaplasia disrupts mucociliary
  clearance due to loss of cilia and predisposes to
  cancinogenesis
• Smooth muscle hypertrophy and hyperreactivity
• Neutrophil influx and bacterial colonization

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COPD

• Small Airways Pathology
• Narrowing and collapse of the small airways
• Replacement of surfactant secreting cells with
  mucus secreting inflammatory cells
• Loss of elastic recoil (major determinate of
  expiratory flow rate)
• Increased resistance to airflow causing
  obstruction during expiration
• Work of breathing is increased

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COPD

• Lung Parenchyma Pathology
• Macrophages accumulate in respiratory bronchioles
  (5X more than nonsmokers)
• They release elastolytic proteinases that damage
  the elastin matrix
• Ineffective repair of elastin with collagen
  deposits results in destruction of gas-exchanging
  airspaces
• In patients with alpa1 antitrypsin deficiency
  this occurs at a much faster rate and in unusual
  areas of lung tissue
• Loss of surface area for gas exchange causes
  hypoxia and hypercarbia

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COPD

• Finally, End-Stage Cardiovascular Changes occur
  due to long standing hypoxia and/or hypercarbia
• Increased pulmonary arterial resistance
• Development of pulmonary hypertension
• Right Heart failure (cor pulmonale)

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COPD

• 3 Typical ways COPD patients present
• Few complaints, but an extremely sedentary
  lifestyle
• Chronic respiratory symptoms such as dyspnea on
  exertion, cough
• With an acute chest illness reporting increased
  cough, purulent sputum production, wheezing, and
  dyspnea with or without fever

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COPD

• Subjective
• Three most common symptoms-cough, sputum
  production, and exertional dyspnea
• Most have symptoms for months or years without
  seeking medical attention
• Frequent colds
• Persistent morning cough
• Fatigue
• Dyspnea on exertion-walking, climbing stairs,
  activities involving significant arm work at or
  above shoulder level are particularly difficult
• Activities that allow the patient to brace the
  arms are better tolerated-shopping carts,
  treadmill
• Wheezing
• History of cigarette smoking or alternate
  inhalation exposure

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COPD

• Objective
• Mild to Moderate COPD exam may be normal
• As severity increases
• Distant breath sounds not improved with deep
  breathing
• Hyperinflation
• Prolonged expiratory time
• End expiratory wheezes
• Crackles in the bases
• Distant heart sounds
• AP diameter of the chest increased
• Use of accessory muscles
• Feet and ankle edema
• Clubbing of nailbeds

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COPD

• End-stage COPD Signs
• Often adopts positions which relieve dyspnea such
  as leaning forward with arms outstretched and
  weight on palms
• Using neck and shoulder girdle respiratory
  muscles (accessory muscles)
• Expiration through pursed lips
• Cyanosis
• Enlarged liver due to right heart failure
• Neck vein distention during expiration
• Changes in mental status
• Increased peripheral edema

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COPD

• Diagnostic Testing
• Pulmonary Function Tests
• CXR
• CT scan
• Laboratory tests
• EKG
• Pulse Oximetry

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COPD

• Pulmonary Function Testing
• FVC-Forced Vital Capacity
• Total volume exhaled with one breath
• Normal gt81 of predicted
• FEV1-Forced Expiratory Volume in 1 sec
• Most useful parameter to measure obstruction
• Normal gt 80 of predicted
• FEV1/FVC Ratio
• Normal gt69

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COPD

• Mild Obstruction
• FEV1/FVC 69-62
• Moderate Obstruction
• FEV1/FVC 62-54
• Severe Obstruction
• FEV1/FVC lt54

• FEV1 gt80 of predicted
• FEV1 50-79 of predicted
• FEV1 lt50 of predicted

Complete PFTs include Bronchodilator
reversibility, Diffusion capacity, Total lung
capacity, etc. Exercise stress testing includes
complete PFTs and evaluation of dyspnea related
to exercise capability.
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COPD

• CXR Findings
• Normal in Early COPD
• Chronic Bronchitis-- may have increased lung
  markings especially in lower lobes
• Emphysema low flat diaphragms, areas of
  hypolucency, small cardiac silhouette

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COPD

• CT Scans
• MRI not used to evaluate lung disease
• Useful to diagnose Emphysema
• Done to evaluate persistent or unusual changes
  noted on CXR
• Often done for screening of long term smokers
• With chronic sputum production, done to rule out
  bronchiectasis

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COPD

• Lab Testing
• CBC - R/O anemia, polycythemia
• CMP evaluate nutritional status, R/O renal and
  liver issues
• Serum alpha1-antitrypsin genotyping done for
  patients lt45yoa with COPD (special lab)
• Sputum cultures Not done routinely. Can be
  attempted if sputum is purulent, large in amount
  and unresponsive to antibiotics.
• ABGs more frequently done in hospital setting,
  done with any neuro change to evaluate for
  hypercarbia

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COPD

• EKG
• To obtain baseline data, if not already done
• To evaluate for Right Ventricular Hypertrophy
• Atrial Arrhythmias common

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COPD

• Pulse Oximetry
• Done at every visit to screen for hypoxemia
• Exercise oximetry -- can be hypoxic with activity
  and normal at rest.
• 6 min walk

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COPD

• Differential Diagnosis
• Acute Bronchitis
• Asthma
• Acute Viral Infection
• Chronic Sinusitis
• Bronchiectasis
• Lung Cancer
• Congestive Heart Failure
• Tuberculosis
• Sleep Apnea
• Interstitial Lung Disease
• Gastroesophageal Reflux Disease

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COPD

• Goals of Treatment
• Relieve symptoms
• Prevent disease progression
• Improve exercise tolerance
• Improve health status
• Prevent and treat complications
• Prevent and treat exacerbations
• Reduce mortality
• Prevent and minimize side effects from treatment

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COPD

• These goals can be achieved by
• Assessing and Monitoring Disease
• Reducing Risk Factors
• Managing Stable COPD
• Managing Exacerbations

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COPD

• Assessing and Monitoring Disease
• Detailed medical history
• Exposure to risk factors (pack/years)
• ? Asthma, allergy, sinusitis, respiratory
  infections
• Family history of chronic respiratory disease
• Pattern of symptom development
• History of exacerbations or previous
  hospitalizations for respiratory problems
• Comorbidities
• heart disease, vascular disease, malignancies,
  osteoporosis, musculoskeletal disorders

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COPD

• Assessing and Monitoring Contd
• Current medications
• Appropriateness of current medical treatments
• Impact on patients life
• Limitation of Activity
• Missed work and economic impact
• Effect on family
• Feelings of depression or anxiety
• Social and family support systems
• Possibility for reducing risk factors
• SMOKING CESSATION

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COPD

• Reduce Risk Factors
• Smoking cessation is the single most effective
  and cost effective intervention to reduce the
  risk of developing COPD and slow its
  progression.
• Counseling to urge a smoker to quit should be
  done for every smoker at every health care visit.
• Pharmacotherapy Assistance should be offered if
  counseling not improving compliance
• Nicotine Replacement
• Wellbutrin SR/Zyban - 150mg BID (see dosing
  instructions)
• Chantix 0.5-1mg BID (see dosing instructions)

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COPD Risk and Smoking Cessation
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COPD

• Manage Stable COPD
• Determine disease severity
• Patients symptoms
• Airflow limitation
• Frequency and severity of exacerbations
• General Health status and Comorbidities
• Respiratory Failure
• Implement treatments according to disease
  severity, patients skills and preferences, and
  availability of medications

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COPD

• Medications
• Bronchodilators
• ß²-agonists
• Short acting Albuterol, Levalbuterol(Xopenex)
• Long acting Formoterol(Foradil),
  Salmeterol(Serevent)
• Anticholinergics
• Short acting Ipratroprium(Atrovent)
• Long acting Tiotropium(Spiriva)
• Combination Albuterol/Ipratroprium(Combivent)
• Methylxanthines (rarely used due to toxicity)
• Given PO or IV
• Aminophylline, Theophylline

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COPD

• Bronchodilators are the therapeutic mainstay for
  COPD patients.
• They have been consistently shown to induce long
  term improvements in symptoms, exercise capacity
  and airflow limitation even when there is no
  spirometric improvement on pulmonary function
  testing.
• All symptomatic patients with COPD should be
  prescribed a short-acting bronchodilator.
• Recommended delivery method is inhalation via
  inhaler (HFA), inhaler devices or nebulizer.
• Nebulizer often provides better delivery system
  for patients with severe disease.
• Short acting meds can be inhaled as often as
  every 4 hours if needed.

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COPD

• Combination albuterol/ipratropium achieves an
  additive degree of bronchodilation than cannot be
  achieved by either medication alone.
• Side effects of albuterol frequently encountered-
  tremor, cough, nervousness, palpitations,
  tachycardia. Side effects may be less with
  levalbuterol(Xopenex).
• Long-acting bronchodilators should be added if
  symptoms are inadequately controlled with
  short-acting therapy.
• We regularly add a scheduled long-acting
  bronchodilator if COPD is moderate or severe.
  Tiotropium (Spiriva) and/or combination
  steroid/long-acting beta agonist.
• Multiple trials (UPLIFT, TORCH) have shown that
  long-acting bronchodilators improve lung
  function, decrease dyspnea and exacerbations.
• There are no generic long-acting
  bronchodilators.these medications are expensive.
  

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COPD

• Steroids
• Inhaled Steroids
• Beclomethasone, Budesonide, Fluticasone
• Combination Inhaled Steroids/Long acting
  Bronchodilator
• More effective in reducing exacerbations,
  improving lung function and health status
• Budesonide/Fomoterol (Symbicort)
• Fluticasone/Salmeterol (Advair)
• Mometasone/Fomoterol (Dulera)
• Oral Steroids
• Given intermittently during exacerbations,
  preferably not on a daily basis
• Prednisone, Methylprednisolone

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COPD

• Vaccines
• Yearly Flu Vaccine
• Can reduce serious illness and death in COPD
  patients by 50
• Pneumococcal Pneumonia Vaccine
• Recommended for all persons 65 yoa and older
• Recommended for anyone younger than 65 yoa who
  smokes or has asthma or any chronic respiratory
  disease
• Protects only from Pneumococcal Pneumonia, not
  all causes of pneumonia

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COPD

• Oxygen
• To maintain SaO2 at least 90
• Preserves vital organ function, increases
  survival, exercise capacity, lung mechanics and
  mental state.
• Must register SaO2 lt89 at rest or with exercise
  to qualify for continuous or intermittent Oxygen
• Pulmonary Rehabilitation
• Patients at all stages benefit from exercise
  training, nutritional counseling and education.
• Minimum length 6 weeks

41
COPD

• Mucoactive Agents
• Thick tenacious secretions can be a major
  problem.
• Little evidence that thinning secretions causes
  clinical improvement, however some patients
  report improvement and these are offered.
• Oral expectorants guaifenesin (Mucinex)
  600-1200mg bid, carbocystine (Availnex)2 tabs
  chewed daily
• Inhaled mucolytic acetylcysteine (Mucomyst)
• Diuretics
• May be necessary with evidence of right heart
  failure
• Loop diureticsfurosemide (Lasix) and potassium
  supplements
• Sodium restricted diet

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COPD

• Follow-Up
• Stable, chronic disease should have follow up
  visits every 3-6 months
• Every visit pulse oximetry
• Annual spirometry
• Annual CXR
• Annual CBC, CMP
• Unstable or very severe disease may need to be
  seen every 1-3 months
• ABG monitoring for hypoxemia and hypercarbia may
  be warranted.

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COPD

• Patient Education
• Teach patient to immediately consult health care
  provider when signs and symptoms of respiratory
  infection or respiratory distress develop.
• Avoid extremes of temperature, air pollution,
  humidity.
• Avoid crowds esp in flu and cold season.
• Adherence to medication regime is important to
  maintain function.
• Physical exercise is beneficial to deter
  functional decline.
• High altitude and air travel can pose problems
  for borderline hypoxemic patients.
• Annual flu shots.
• QUIT SMOKING.

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COPD

• Exacerbation
• An event in the natural course of the disease
  characterized by a change in the patients
  baseline dyspnea, cough and/or sputum that is
  beyond normal day-to-day variations, is acute in
  onset, and may warrant intervention.
• The most common cause (80) of exacerbation is
  infection.
• Most patients with COPD have airways colonized
  with one or all of the following bacteria
• Streptococcus pneumoniae
• Haemophilus influenzae
• Moraxella catarrhalis

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COPD

• Management of exacerbations
• Diagnosis
• Made from acute increase in symptoms-cough,
  dyspnea, sputum volume/change in character.
• Sputum purulence (yellow, green, brown) an
  important indicator.
• Constitutional symptoms, decrease in spirometry,
  tachypnea are variably present.
• CXR usually unchanged
• Sputum cultures are unreliable and should not be
  performed regularly.

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COPD

• Management of exacerbations
• Antibiotic Therapy
• Antibiotics improve clinical outcomes for
  moderate to severe exacerbations
• Empiric antibiotics should be effective against
  the three most common pathogens (S. pneumoniae,
  H. influenza, M. catarrhalis) ie
• Levaquin (levofloxin)
• Avelox (moxifloxin)
• Doxycycline
• Bactrim (trimethoprim-sulfamethoxazole)
• Augmentin (amoxicillin-clavulanate)
• Zithromax (azithromycin)
• Biaxin (clarithromycin)
• Cefzil (cefprozil)
• Omnicef (cefdinir)

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COPD

• Fluoroquinolones (Levaquin, Avelox) associated
  with higher rate of success and lower rate of
  recurrenceBut they are expensive.
• Other factors to consider when choosing
  antibiotics
• Allergies
• Age
• Renal status
• Cardiac disease
• Other medications- esp Coumadin

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COPD

• Steroids
• Prednisone (most common) 10-15 day taper
• 40mgX3d, 30mgX3d, 20mgX3d, 10mgX3d
• 30mgX5d, 20mgX5d, 10mgX5d
• Bronchodilators
• Increase frequency of short-acting
  bronchodilators until symptoms improve.
• Preferably ß²-agonists anticholinergics
  (albuterol/ipratropium)
• Home or Hospital?

49
COPD

• Indications for Hospital Admission
• Marked intensity of symptoms
• Failure of outpatient treatment
• Significant comorbidities
• Onset of new physical signs ie cyanosis,
  peripheral edema
• Severe background COPD
• Newly occurring arrhythmias
• Diagnostic uncertainty
• Older age
• Insufficient home support

50
COPD

• Oh, One last thing
• QUIT SMOKING !

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Community-Acquired Pneumonia

• Community-Acquired Pneumonia (CAP)
• Defined by IDSA as Acute infection of the lung
  parenchyma associated with at least two symptoms
  of acute infection (cough, fever, dyspnea) and
  accompanied by the presence of an acute
  infiltrate on CXR or by auscultatory findings
  (altered breath sounds, localized crackles)
  consistent with pneumonia in a patient not
  hospitalized or in a long-term care facility for
  14 days prior to onset of symptoms.

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Community-Acquired Pneumonia

• Overall rate 8-15/1000 persons per year
• Most common in the young (lt5yoa) and
• elderly (gt60yoa)
• Occurring more in winter
• Mengtwomen
• gtSmokers, alcoholics, young adults in close
  settings (college students, military recruits)
• Fifth leading cause of death in persons gt65yoa
• Eighth most common cause of death in US
• Timely diagnosis and appropriate management is
  critical because of morbidity associated with
  bacterial pneumonia
• Causes 10 million outpatient visits/year
• More than 1 million hospitalizations/year

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Community-Acquired Pneumonia

• Pathophysiology
• Tissue typically becomes consolidated as alveoli
  fill with exudate
• Gas exchange may be impaired as blood is shunted
  around nonfunctional aveoli
• There may be consolidation of a lobe or the
  infection may show patchy distribution.
• Viral and Mycoplasma infections are characterized
  by infiltrate in interstitial spaces and no
  consolidation.
• Fungal or tubercular infections produce patchy
  granulomas.

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Community-Acquired Pneumonia

• Common Causes
• Majority of cases associated with relatively few
  agents
• Streptococcus pneumoniae (Most common)
• Mycoplasma pneumoniae (walking pneumonia )
• Haemophilus influenzae (Second most common)
• Chlamydophila pneumoniae
• Respiratory viruses-influenza types A B,
  adenovirus,respiratory syncytial virus and
  parainfluenza
• Legionella (More common in smokers, alcoholics,
  elderly)
• Staphylococcus aureus (Elderly, other chronic
  diseases)

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Community-Acquired Pneumonia

• Commonly Classified as Typical or Atypical
• Typical-(S. pneumoniae, H. influenzae, Klebsiella
  pneumoniae)
• Dyspnea, productive cough, fever, chest pain
• Adventious breath sounds, dullness to percussion,
  egophony
• CXR-consolidated lobar pneumonia
• Atypical-(M. pneumoniae, influenza viruses,
  C.pneumoniae, Legionella)
• Fever, nonproductive cough, severe headache,
  malaise, myalgia, sore throat, runny nose
• Often normal lung exam
• CXR-patchy interstitial infiltrates
• More common in young adults

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Community-Acquired Pneumonia

• Diagnostic tests
• CXR (AP/Lat)
• Useful to determine pathogen
• Identifies possible complications such as pleural
  effusions
• Possibly normal early in process or patients
  unable to mount inflammatory response (AIDS,
  chemo patients)
• Things that can mimic pneumonia on
  CXRAtelectasis, Pleural Effusion, Pulmonary
  Embolism, Pulmonary Edema, Bronchogenic Cancer
• Good clinical judgment essential

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Community-Acquired Pneumonia

• Pulse Oximetry
• May help identify pneumonia in patients without
  obvious signs
• CBC with differential, BMP
• Helpful to determine if patient should be
  hospitalized especially if gt65yoa or coexisting
  illnesses
• Sputum culture with gram stain
• Not routinely recommended
• Attempted if no response to empiric antibiotic or
  fungi suspected
• Most reliable sample obtained from bronchoscopy
• Blood cultures
• Only severe CAP
• Urinary antigen tests (Legionella, Strep)
• No response to empiric antibiotics
• International travel past 2 weeks

58
Community-Acquired Pneumonia

• Differential Diagnosis
• Acute Bronchitis
• Chronic pulmonary disease (Asthma, COPD)
• Atelectasis
• Lung abscess
• Pulmonary embolus
• Congestive Heart Failure
• Neoplasm
• Sarcoidosis
• Bio-terrorism (anthrax, pneumonic plague, etc)

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Community-Acquired Pneumonia

• MANAGEMENT
• 1st Essential Decision Home or Hospital
• 20 Require hospitalization
• Inpatient care 25X more costly than outpatient
  care
• Majority without comorbidities can be treated at
  home
• Various scoring criteria available but clinical
  judgment should always supersede prognostic
  scores.
• Risk factors for Mortality or complications from
  CAP
• Age gt65
• Coexisting disease-COPD, Diabetes, CRF, CHF,
  Liver disease, Aspiration, Post-splenectomy,
  Alcoholism, Malnutrition, CVA, Immunocompromised
  for any reason.
• Abnormal physical findings-Resp rategt30, SBPlt90,
  Tgt101, confusion
• Abnormal lab-BUNgt50, Nalt130, Hgblt9, ABG pHlt7.35
  or PaO²lt60

60
Community-Acquired Pneumonia

• EMPIRIC ANTIBIOTIC THERAPY
• (2007 IDSA/ATS CAP Management Guidelines)
• Previously Healthy Pt with No Risk Factors
• Macrolide-azithromycin, clarithromycin,
  erythromycin
• Doxycycline (only if allergic to macrolide)
• Patient with Comorbidities (Excludes HIV)
• Respiratory Fluoroquinolone (levofloxin,
  moxifloxacin, gemifloxin)
• ß-lactam (cefdinir, cefotaxime, ceftriaxone,
  amoxicillin/clavulanate)
• Plus Macrolide or doxycycline
• Hospitalized patients-nonICU
• Respiratory Fluoroquinolone (levofloxin,
  moxifloxacin, gemifloxin)
• ß-lactam (cefdinir, cefotaxime, ceftriaxone,
  amoxicillin/clavulanate)
• Plus Macrolide or doxycycline
• Hopsitalized patients-ICU
• IV ß-lactam Plus IV Fluoroquinolone or Macrolide

61
Community-Acquired Pneumonia

• Treat for a minimum of 5 days
• Common treatment 7-10 days
• Before treatment discontinued, patient should be
• Afebrile X 48-72 hours
• Be clinically stable.
• Have no signs of
• Tachypnea
• Tachycardia
• Hypotension
• Mental status changes

62
Community-Acquired Pneumonia

• Patient Education
• Supportive Care
• Increase fluids (3L/24hrs)
• Expectorants-Guaifenesin (600-1200mg bid)
• Analgesics/Antipyretics (pain fever control)
• Avoid smoking
• Restrict activity
• Cough suppressant with codeine or hydrocodone
  (only if needed for sleep)

63
Community-Acquired Pneumonia

• Follow-Up
• Contact patient with moderate to severe symptoms
  within 24 hours by phone or office
• With effective antibiotic coverage, improvement
  in clinical symptoms should be seen within 48-72
  hours however antibiotic should not be changed
  within first 72 hours unless there is marked
  clinical deterioration.
• Patients with moderate and severe symptoms who
  are improving, schedule return visit in 3-4 days
  to assess response. Then re-evaluate in 2-4 weeks
  with CXR.
• CXR should be done on all patients gt40yoa and all
  smokers within 3 months.
• Abnormality that does not clear should be
  evaluated for cancer
• Pleural effusion is most common complication. If
  not resolved, must be evaluated for empyema.

64
Community-Acquired Pneumonia

• Follow-Up cont
• Smoking cessation
• Patients may be most receptive to antismoking
  counseling while they are still ill or
  recovering. The follow up visit is an opportune
  time for this discussion.
• Pneumococcal and flu vaccinations, if indicated

65
Community-Acquired Pneumonia

• Prevention
• Yearly flu vaccine recommended for
• Everyone gt50yoa
• Persons at risk for complications of influenza
• Household contacts of high-risk persons
• Health care workers
• Pneumococcal vaccine recommended for
• Everyone 65 yoa or older
• Anyone who smokes or has Asthma
• Underlying chronic medical conditions
• Residents of long-term care facilities
• Vaccinated patients have a lower risk of
  developing respiratory failure, lower risk of
  death from any cause, and reduced hospital stay,
  compared to those not vaccinated.

66
Interstitial Lung Disease

• Interstitial Lung Disease (ILD)
• Involves the parenchyma of the lung
• alveoli
• alveolar epithelium
• capillary endothelium
• the space between these structures
• perivascular tissue
• lymphatic tissues
• More than 200 known individual diseases
• Classified together because of similar clinical,
  radiographic, physiologic and pathologic
  manifestations.
• Most are associated with considerable morbidity
  and mortality

67
Interstitial Lung Disease

• Nonmalignant disorders and are not caused by
  identified infectious agents
• Precise pathway leading from injury to fibrosis
  is not known
• Two major histologic patterns
• Granulomatous pattern
• Alveolitis, Interstitial Inflammation and
  Fibrosis
• Further subdivided into Known and Unknown
  Etiology

68
Interstitial Lung Disease

• ILD with Granuloma Examples
• Sarcoidosis
• Wegeners granulomatosis
• Churg-Strauss
• Hypersensitivity pneumonitis
• Organic dusts-aspergillosis, bird breeders,
  detergent workers, farmers, etc
• Inorganic dusts-silica, talc, coal, aluminum,
  graphite, beryllium, etc
• Infectious agents-viral pneumonia, CMV, miliary
  TB, histoplasmosis,etc
• ILD with Inflammation and Fibrosis Examples
• Idiopathic pulmonary fibrosis
• COP (Cryptogenic organizing pneumonitis) formally
  called BOOP(Bronchiolitis Obliterans)
• Collagen vascular diseases-SLE, RA, Scleroderma,
  CREST syndrome, polymyositis
• Eosinophilic lung syndromes
• Cardiac Failure
• Aspiration pneumonia
• Radiation
• Asbestosis
• Gases-chlorine gas, oxygen, sulfur dioxide
• Drugs-cytoxan, methotrexate, amiodarone,
  hydralazine, hydrochlorothiazide, antibiotics,
  NSAIDS, mineral oil, etc

69
Interstitial Lung Disease

• Pathophysiology
• Pulmonary inflammation develops after lung injury
  characterized by various WBCs into the alveolus
  and alveolar wall.
• The influx of immune cells is accompanied by
  fluid accumulation in the walls and alveolar
  airspace. This immune reaction damages the
  alveoli.
• The alveolar walls become thickened and
  distorted.
• As the disease progresses, the destroyed alveoli
  are eventually replaced with fibrotic connective
  tissue and cystic airspaces.
• The cystic airspaces that result are lined with
  cuboidal or columnar epithelium and do not
  participate in gas exchange.

70
Interstitial Lung Disease

• Clinical Presentation
• Typical patient presents with insidious onset of
  dyspnea on exertion, often with fatigue and cough
• Dyspnea has no other cause ie asthma, COPD, CHF
  etc
• Other presentations
• Fatigue w/o dyspnea
• Dry cough w/o other respiratory symptoms
• Predominant systemic symptoms ie fever, weight
  loss
• Abnormal CXR w/o symptoms
• Incidental abnormalities of PFTs
• Productive cough w/o dyspnea

71
Interstitial Lung Disease

• Initial Evaluation
• History Careful documentation of past medical
  history may provide the most important clues.
  Particularly the following elements
• Age, Gender, Smoking History, Duration of Illness
• Prior medication use-include OTC petroleum
  products, amino acid supplements
• Family History
• Occupational History-Lifelong work history
  including duties and known exposure to dusts,
  gases and chemicals
• Environmental exposures-Home and work, Spouse and
  children, Pets especially birds, Hobbies, Water
  damage, Cooling systems, Humidifiers, Hot tubs
• Symptoms-Dyspnea, Cough, Hemoptysis, Wheezing,
  Chest pain, Joint pain or swelling, Fatigue,
  Raynauds phenomenon, Dry mouth or eyes, Fever

72
Interstitial Lung Disease

• Physical Exam - Usually not specific
• Crackles- common inflammatory, less granulomatous
  disease
• Inspiratory squeaks- common in bronchiolitis
• Cor pulmonale, Cyanosis, Clubbing- late findings
  of advanced disease
• Laboratory May not be helpful but should
  include
• CBC
• CMP (LDH often elevated but nonspecific)
• ANA, Rheumatoid factor (Connective tissue
  disease-RA, SLE, etc)
• ACE (Sarcoid marker)
• ANCA (Wegeners, vasculitis)
• Sed Rate (often elevated but nonspecific)

73
Interstitial Lung Disease

• CXR May be abnormal but is nonspecific.
  However, may be normal in 10 of patients.
• Complete evaluation for symptomatic patient with
  normal CXR
• Complete evaluation for asymptomatic patient with
  abnormal CXR
• Failure to evaluate may lead to progressive,
  irreversible disease
• CT High Resolution Chest CT (1mm cuts)
• Superior to CXR for early detection and
  confirmation of ILD
• Better assessment of extent and distribution of
  disease
• Coexisting disease identified (adenopathy,
  carcinoma, emphysema)
• May be sufficient to preclude need for biopsy
• Useful to determine areas for biopsy sample

74
Interstitial Lung Disease

• CT Findings
• Pulmonary Opacities usually described as
• Nodules
• Lines (reticular)
• Both (reticulonodular)
• Ground glass or hazy appearance
• Honeycombing-created by the cyst-like spaces of
  advanced disease
• Some ILDs have Unique Findings
• Sarcoidosis- hilar lymphadenopathy
• Wegeners Granulomatosis- lower lobe cavities and
  nodules
• COP- peripheral and lower lung zone ground glass
  opacities
• Idiopathic Pulmonary Fibrosis- patchy,
  predominantly basilar reticular opacities with
  traction bronchiectesis and honeycombing

75
Interstitial Lung Disease

• Echocardiogram
• Pulmonary Hypertension associated with disease
  severity and survival
• Complete Pulmonary Function Testing
• Most forms produce Restrictive Defect
• Reduced total lung capacity (TLC), functional
  residual capacity (FRC), and residual volume (RV)
• FVC and FEV1 decreased due to reduced TLC
• FEV1/FVC normal or increased
• Lung volumes decrease as lung stiffness worsens
  with disease progression
• DLCO (diffusing capacity) commonly
  decreased-nonspecific
• ABG
• Normal pO2 at rest does not rule out significant
  hypoxemia during exercise or sleep

76
Interstitial Lung Disease

• Lung Biopsy
• Indications for
• To provide a specific diagnosis
• To assess disease activity
• To exclude neoplastic and infectious processes
  that mimic ILD
• To identify a more treatable process than
  originally suspected To establish a definitive
  diagnosis and predict prognosis before proceeding
  with therapies which may have serious side
  effects
• Done by
• Fiberoptic bronchoscopy with transbronchial lung
  biopsy
• Video-assisted thoracoscopic lung biopsy (VATS)
• Open lung biopsy
• Relative contraindications
• Serious CV disease
• Honeycombing evidence of end-stage disease on CT
• Severe pulmonary dysfunction or other major
  operative risk especially in the elderly

77
Interstitial Lung Disease

• Differential Diagnosis
• The patient with unexplained dyspnea and fatigue
  should have a complete workup of following
  systems
• Pulmonary
• Cardiac
• Hemotologic
• Renal
• Neuromuscular
• Endocrine
• The possibilities are immense.
• There are over 200 known clinical disorders in
  ILD.

78
Interstitial Lung Disease

• Treatment
• Regardless of etiology, end-stage fibrosis is
  irreversible and untreatable.
• First action is to determine if exposure to
  environmental agents or drugs is the cause and
  remove the exposure.
• Second to determine the correct diagnosis, giving
  the best chance for therapeutic success
• Medications most commonly used--prednisone and
  cytotoxic agentsusually suppress rather than
  cure the process
• Many patients are older adults and the decision
  to treat with immunosuppressive drugs should not
  be taken lightly, toxicity and adverse effects of
  these medications can be substantial
• Supplemental oxygen is the only proven treatment
  that prolongs survival

79
Interstitial Lung Disease

• Corticosteroids
• Current mainstay of therapy
• Trial is reasonable for even advanced disease
• Steroid responsiveness is the best predictor of a
  better prognosis.
• Generally high dose (60-100mg) for 3-6 months
• Sarcoidosis and COP respond more quickly to lower
  doses
• Patients not well controlled or responsive,
  Cytoxan or Immuran is usually added in an attempt
  to slow progression
• Maintain a high index of suspicion for infection
  in patients on immunosuppressive therapy and
  treat aggressively
• Other complications to consider are lung cancer
  and pneumothorax

80
Interstitial Lung Disease

• Follow-Up and Referral
• Reassessment of disease activity generally every
  3 months or more often if needed.
• Responsiveness is defined as decrease in
  symptoms
• Radiographic improvement
• No further decline in clinical, radiographic or
  physiologic parameters
• Pulmonologist Referral
• If no specific cause of dyspnea or cough can be
  found
• If symptoms exceed the physiologic and
  radiographic abnormalities
• If empiric management (bronchodilators,
  diuretics, smoking cessation) resulted in
  atypical or unsatisfactory outcome
• If lung biopsy or other specialized testing is
  needed
• If immunosuppressive therapy contemplated

81
Interstitial Lung Disease

• Conclusion
• Most common ILD is Idiopathic UIP (usual
  interstitial pneumonitis)
• Another common name is Pulmonary Fibrosis
• UIP has a 5 year survival of 20
• ILD associated with Connective Tissue Disorders
  has better survival
• Lung Transplant may be considered
• Maintaining oxygenation with supplemental oxygen
  is necessary to prevent or slow development of
  right heart failure (cor pulmonale) and improve
  functional ability.
• Using oxygen is often resisted by patients and
  teaching is necessary and important to increase
  compliance.

82
Pneumothorax

• Spontaneous Pneumothorax
• Primary spontaneous pneumothorax (PSP) occurs
  without a precipitating event in a person with no
  known lung disease
• Secondary spontaneous pneumothorax (SSP) occurs
  as a complication of underlying lung disease.
  Most common cause is COPD with the rupture of
  blebs.
• Risk factors PSP- MengtWomen, Smoking (7-102
  times higher than non-smokers), Family history,
  Marfan syndrome, thoracic endometriosis,
  homocystinuria.
• SSP-COPD, Pneumocystis jirovecii, cystic
  fibrosis, TB.
• Presentation usually occurs at rest, sudden
  onset of dyspnea and pleuritic chest pain on the
  same side as the pneumothorax. Severity of pain
  related to the volume of air in the pleural space
• Physical findings Decreased chest excursion on
  the affected side, diminished breath sounds,
  hyperresonant percussion, hypoxemia

83
Pneumothorax

• Labored breathing and hemodynamic compromise
  (tachycardia, hypotension) suggests the
  possibility of tension pneumothorax which needs
  emergency decompression.
• Diagnosis made by CXR
• Treatment All patients with SSP should be
  hospitalized.
• Observation-at least 6 hours without progression
  of size
• Oxygen-resorption rate is markedly increased
  using oxygen
• Aspiration (only PSP) can be attempted
• Chest tube with water seal or Heimlich valve,
  with or without suction
• If air leak persists after 3 days with chest
  tube, needs video-assisted thoracoscopic surgery
  (VATS) for bleb resection or pleurodesis
• If discharged after observation or aspiration
  will need F/U CXR 24-48 hours to document
  resolution.

84
Pneumothorax
85
Pneumothorax

• http//radiologymasterclass.co.uk/tutorials/chest/
  chest_pathology/chest_pathology_page4.html
• http//radiologymasterclass.co.uk/gallery/chest/pn
  eumothorax/pneumothorax_a.html

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Lower Respiratory Disease

• References
• Hull, C. (2007). Community-Acquired Pneumonia
  Management Guidelines. Clinician Reviews, 17(9),
  28-34.
• (2009). Multiple articles Data File. Available
  from http/?/?.www.uptodate.com
• Dunphy, L. (2001). Primary Care The Art and
  Science of Advanced Practice Nursing.
  Philadelphia F.A. Davis Company.
• Uphold, C. (2003). Clinical Guidelines in Family
  Practice (4th ed.). Gainsville, FL Barmarrae
  Books, Inc.
• Kasper, D. (Ed.). (2005). Harrison's Principles
  of Internal Medicine (16th ed.). New York
  McGraw-Hill.