Pulmonary Board Review

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  • PNDS: sinusitis, allergic rhinitis, perennial nonallergic rhinitis, postinefectious rhinitis, vasomotor rhinitis, environmental irritants
    Rx: first generation antihistamine with decongestant +/- intranasal coritcosteroids, avoidance of allergens, cromolyn sodium
    Cough variant asthma: up to 57% with asthma; often with normal PFTs thus methacholine challenge. Treatment: inhaled corticosteroid for at least 6-8 weeks to see benefit
    GERD
  • Fletcher and Peto found that over a lifetime, FEV1 falls gradually. However, clinically significant airflow obstruction may never develop in many smokers. In those susceptible to COPD, smoking can cause permanent obstructive changes to air passages. The researchers found that if a susceptible smoker quits smoking, rates of FEV1 loss will revert to normal, but lung function is reduced. It is possible to prevent severe or fatal COPD by screening lung function in middle-aged smokers, who could be urged to stop smoking.
    Main point: Decline in FEV1 is accelerated in COPD. Quitting smoking has a profound effect on the rate of decline of FEV1.
  • Pnalobular emphysema
    <1% COPD pts, sx begin pts < 40,
  • Non-granulomatous interstitial pneumonitis
    B. Poorly circumscribed collection of macrophages and multinucleate giant cells. Evolving granuloma.
    C. Later phase of granuloma formation. Lesion becoming more compact and circumscribed
    D. Fully mature non-necrotizing granuloma.
  • Lungs are affected in more than 90% of patients with dyspnea, np cough, and CP occurring in 1/3 to ½ of pts
    Radiographic stages
    Stage 4- fibrosis with hilar retraction, honeycomb changs, and large bullae and cysts
    Surprsingly, on exam lungs are usually clear
  • Anterolateral or posterolat surface of parietal pleua
    Gray white in color
    Central tendon when diaphgram involved
  • Light’s criteria superior to any of the above in identifying exduates. Howver, less accurate in identifying transudates, Albumin graidnet can be utilized.
  • Pulmonary Board Review

    1. 1. Pulmonary Board Review
    2. 2. 1. Evaluation of symptoms: cough and dyspnea 2. PFTs 3. Asthma 4. COPD 5. Interstitial lung diseases 6. Pneumoconioses 7. Pleural disease
    3. 3. Cough  31 year old woman with hypertension presents with cough for 6 weeks non- productive incessant and disrupting sleep. She has lifelong allergies and does endorse some increase rhinorhea recently. She was also started on ramipril for hypertension 3 months ago.  What should you do?
    4. 4. Respiratory symptoms: cough  Cough  Chronic cough = duration > 3 weeks  Most common etiologies  Postnasal drip syndrome  Asthma  GERD  Others:  Chronic bronchitis  Bronchiectasis  ACE inhibitor  Post-infectious  Eosinophilic bronchitis  Endobronchial lesion
    5. 5. Respiratory symptoms: dyspnea  Chronic dyspnea: lasting > 1 month  2/3 of patients with one of the following  COPD  Asthma  ILD  Cardiomyopathy  Others: neuromuscular disease, hyperventilation syndrome, GERD, pulmonary vascular disease  Work-up:  History, PFTs, chest Xray  Cardiopulmonary exercise testing
    6. 6. PFTs: Spirometry  Approach  Is it a good test? First look to see how good the test is: reproducible, adequate exahalation time (at least 6 seconds), technician comments regarding patient effort and compliance  Is there obstruction? FEV1/FVC < 70% indicates obstructive disease. Severity of obstruction as follows:  I: Mild FEV1/FVC < 70%; FEV1 ³ 80% predicted With or without chronic symptoms (cough, sputum)  II: Moderate FEV1/FVC < 70%; 50% £ FEV1 < 80% predicted With or without chronic symptoms (cough, sputum, dyspnea) - III: Severe FEV1/FVC < 70%; 30% £ FEV1 < 50% predicted With or without chronic symptoms (cough, sputum, dyspnea)  IV: Very Severe FEV1/FVC < 70%; FEV1 < 30% predicted  Is there restriction? FVC < 80% predicted indicated possible restrictive disease  Is there airway reactivity? Response to bronchodilator testing: > 12% or > 200mL
    7. 7. PFTs: lung volumes  Total lung capacity < 80%  Restrictive lung disease  Structural restriction of the thoracic cage  Neuromuscular disease  FRC < 80%  Restrictive lung disease  Structural restriction of the thoracic cage  Obesity  Residual volume < 80%  Restrictive lung disease  Structural restriction of the thoracic cage
    8. 8. PFTs: lung volumes  TLC > 120%  Hyperinflation seen with emphysema  FRC > 120%  Air trapping  RV > 120%  Air trapping  Neuromuscular disease
    9. 9. PFTs: DLCO  Decreased in:  Diseases that obliterate the alveolar-capillary interface:  Emphysema  Fibrotic lung disease  Pulmonary vascular diseases  Diseases that increase the thickness of the interface:  Interstitial lung diseases  Interstitial edema/alveolar edema  Anemia
    10. 10. PFTs: flow volume loops  Useful in looking for central airway obstruction
    11. 11. Flow volume volumes
    12. 12. Chest CT scanning  High resolution chest CT  Routine chest CT scanning  Spiral CT scanning
    13. 13. Asthma  All of the following are true of asthma EXCEPT:  Asthma death rates have increased  Normal spirometry does not exclude asthma  Uncontrolled asthma can lead to irreversible airway obstruction  De-escalation of asthma therapy can be considered if there has been good asthma control for 1 month
    14. 14. Asthma categories of severity 2007 NAEPP report  Intermittent  Mild persistent  Moderate persistent  Severe persistent  Treatment recommendations based upon severity
    15. 15.  Intermittent asthma:  Symptoms ≤ 2 days per week  Requirement for rescue albuterol ≤ 2 days per week  Nocturnal awakenings ≤ 2 times per month  No limitations in ADLs  Normal PFTs  RX: Intermittent albuterol
    16. 16.  Mild persistent asthma  Symptoms > 2 days per week or  3-4 nocturnal awakenings a month or  Minor limitation in ADLs AND  Normal PFTs  RX: Step 2 low dose inhaled corticosteroids
    17. 17.  Moderate persistent asthma  Daily symptoms or  > 1 nocturnal awakening per week or  Moderate limitation in ADLs or  Decreased FEV1 but > 60%  Rx: step 3 in asthma treatment protocol  Low dose inhaled corticosteroids + LABA  Medium dose inhaled corticosteroid
    18. 18.  Severe persistent symptoms  Ongoing daily symptoms with significant exercise limitation and frequent nocturnal awakenings  Rx:  Step 4: High dose ICS + LABA  Step 5: High dose ICS + LABA + systemic corticosteroid therapy  AND consider omalizumab
    19. 19. Asthma syndromes  Cough variant asthma  Aspirin-induced asthma or triad asthma  Exercise induced asthma  Occupational asthma  Allergic bronchopulmonary aspergillosis
    20. 20.  5 – 15% of all asthmatics  Over 300 agents have been reported to cause OA  Different prevalence for specific populations  OA may develop in 2.5% for hospital workers exposed to latex  2-40% millers and bakers  20% exposed to acid anhydrides  5% exposed to toluene diisocyanate (TDI)
    21. 21.  OA with a latency period: specific antigens identified, mostly HMW antigens although some LMW antigens as well  IgE mediated: usually HMV antigen with a median latency period of ~ 5 years. Atopy is a risk factor  Non-IgE mediated: usually LMW antigens with a median latency period of 2 years. Atopy is not a risk factor  OA without a latency period:  1) nonspecific irritant-induced asthma or  2) reactive airways dysfunction syndrome
    22. 22. COPD  6th leading cause of death worldwide  Underdiagnosed  GOLD: stages of severity  Based of spirometry  Stage 0: normal spirometry but symptoms present  Stage I: Mild ratio < 70% but FEV1 > 80%  Stage II: Moderate  IIa FEV1 50-80%  IIb FEV1 30-50%  Stage III: Severe
    23. 23. Adapted from Fletcher et al. BMJ. 1977;1:1645-1648. FEVFEV11(%)RelativetoAge25(%)RelativetoAge25 Death Disability Age (years) 5050 7575252500 Symptoms 00 2020 6060 100100 8080 4040 Healthy COPD Rehabilitation at 45 (mild COPD) Exercise Performance Over Time Rehabilitation at 65 (severe COPD)
    24. 24. COPD risk factors  Tobacco:  15-20% 1ppd smokers develop COPD  25% 2ppf smokers develop COPD  Genetic factors: Alpha1-antitrypsin deficiency  Gender: Males more at risk than females  Bronchial hyperresponsiveness  Atopy and asthma  Childhood illnesses  Prematurity
    25. 25. COPD  Treatment:  Smoking cessation  Oxygen therapy  Medical therapy  Pulmonary rehabilitation  LVRS  Transplantation
    26. 26. *Four-step algorithm for the implementation of inhaled treatment;*Four-step algorithm for the implementation of inhaled treatment; †† Pathway on left is recommended; pathway on right side is aPathway on left is recommended; pathway on right side is a valid alternative;valid alternative; ‡‡ Defined as need for rescue medication on more than 2 occasions per week;Defined as need for rescue medication on more than 2 occasions per week; §§ A short-acting bronchodilatorA short-acting bronchodilator can be used for rescue. Low-dose methylxanthines can be prescribed if the response to inhaled bronchodilator therapy iscan be used for rescue. Low-dose methylxanthines can be prescribed if the response to inhaled bronchodilator therapy is insufficient;insufficient; ¶¶ Defined as 2 or more exacerbations per year.Defined as 2 or more exacerbations per year. Inhaled TherapyInhaled Therapy 0000 IIII IIIIIIII Salmeterol or formoterol +Salmeterol or formoterol + ipratropium, salbutamol,ipratropium, salbutamol, or combinationor combination Salmeterol or formoterol +Salmeterol or formoterol + ipratropium, salbutamol,ipratropium, salbutamol, or combinationor combination *Tiotropium +*Tiotropium + albuterolalbuterol *Tiotropium +*Tiotropium + albuterolalbuterol IIIIIIIIIIII Salmeterol or Formoterol +Salmeterol or Formoterol + Tiotropium§Tiotropium§ Salmeterol or Formoterol +Salmeterol or Formoterol + Tiotropium§Tiotropium§ *Tiotropium +*Tiotropium + salmeterol or formoterol§salmeterol or formoterol§ *Tiotropium +*Tiotropium + salmeterol or formoterol§salmeterol or formoterol§ IVIVIVIV *Tiotropium + salmeterol or formoterol*Tiotropium + salmeterol or formoterol + inhaled corticosteroid+ inhaled corticosteroid§§ *Tiotropium + salmeterol or formoterol*Tiotropium + salmeterol or formoterol + inhaled corticosteroid+ inhaled corticosteroid§§ Clinical Algorithm for the Treatment of COPDClinical Algorithm for the Treatment of COPD NonpharmacologicNonpharmacologic TherapyTherapy Smoking cessationSmoking cessation Avoidance of exposureAvoidance of exposure Smoking cessationSmoking cessation Avoidance of exposureAvoidance of exposure VaccinationVaccination (influenza, pneumococcal)(influenza, pneumococcal) VaccinationVaccination (influenza, pneumococcal)(influenza, pneumococcal) Pulmonary rehabilitationPulmonary rehabilitation (Exercise prescription)(Exercise prescription) Pulmonary rehabilitationPulmonary rehabilitation (Exercise prescription)(Exercise prescription) Supplemental oxygenSupplemental oxygen Lung volume reduction surgeryLung volume reduction surgery Lung transplantationLung transplantation Supplemental oxygenSupplemental oxygen Lung volume reduction surgeryLung volume reduction surgery Lung transplantationLung transplantation *Short-acting bronchodilator as needed*Short-acting bronchodilator as needed (for example, ipratropium, salbutamol, or combination)(for example, ipratropium, salbutamol, or combination) *Short-acting bronchodilator as needed*Short-acting bronchodilator as needed (for example, ipratropium, salbutamol, or combination)(for example, ipratropium, salbutamol, or combination) GOLD StageGOLD Stage (approximate)(approximate) ClinicalClinical stagestage At riskAt risk IntermittentIntermittent symptomssymptoms PersistentPersistent symptomssymptoms‡‡ FrequentFrequent exacerbationsexacerbations¶¶ Respiratory failureRespiratory failure ††
    27. 27. Interstitial lung diseases or Diffuse parenchymal lung disease  DPLD of known cause:  Drugs  Connective tissue disease  Occupational lung disease  Granulomatous disease  Sarcoidosis  Hypersensitivity pneumonitis  Idiopathic interstitial pneumonia (IIP)  Idiopathic pulmonary fibrosis (i.e., usual interstitial pneumonia)  Non-specific interstitial pneumonia  Desquamative interstitial pneumonia  Respiratory bronchiolitis interstitial lung disease  Cryptogenic organizing pneumonia  Acute interstitial pneumonia (Hamman Rich syndrome)  Lymphocytic interstitial pneumonia  Misc  Lymphangioleiomyomatosis  Histiocyotsis X  Pulmonary alveolar proteinosis
    28. 28. DPLD  Chest Xray can be normal in  10-15% patients with diffuse lung disease  30% patients with bronchiectasis  60% patients with emphysema  High resolution chest CT  Sensitivity of 90% and specificity approaching 100%  Can provide a confident diagnosis in ~50% cases; ~93% of these cases are ultimately proven correct  Findings usually seen in DPLD  Ground glass opacity  Findings consistent with fibrosis  Interlobular and intralobular septal thickening  Honeycombing
    29. 29. HRCT : ground glass opacity  Nonspecific term referring to presence of a hazy increase in lung opacity without obscuration of underlying vessels.  Results from volume averaging of morphologic abnormalities too small to be clearly resolved by HRCT: minimal thickening of the intralobular septa, alveolar interstitium, presence of cells or fluid partially filling alveolar spaces  Often indicative of ongoing, active, potentially treatable disease  Crazy paving: ground glass superimposed on reticular pattern  Initially described with PAP  DDX: pulmonary edema, ARDS, pulmonary hemorrhage, AIP, PCP, viral infection, BOOP, eosinophilic pneumonia, BAC, etc
    30. 30. HRCT findings: linear and reticular opacities  Intralobular interstitial thickening  “fine reticular pattern” with lines of opacity separated by a few mmm  Fine lacy or netlike appearance  When seen in fibrosis, often seen in conjunction with dilated bronchioles (“bronchiolectasis”)  DDX:  IPF  Chronic hypersensitivity pneumonitis  Pneumoconioses  ILD: NSIP, DIP  Lymphangitis carcinomatosis  Pulmonary edema  Pulmonary hemorrhage  Pneumonia  Alveolar proteinosis
    31. 31. HRCT findings: linear and reticular opacities  Intralobular interstitial thickening  “fine reticular pattern” with lines of opacity separated by a few mmm  Fine lacy or netlike appearance  When seen in fibrosis, often seen in conjunction with dilated bronchioles (“bronchiolectasis”)  DDX:  IPF  Chronic hypersensitivity pneumonitis  Pneumoconioses  ILD: NSIP, DIP  Lymphangitis carcinomatosis  Pulmonary edema  Pulmonary hemorrhage  Pneumonia  Alveolar proteinosis
    32. 32. Figure 3-24
    33. 33. Honeycombing, DDX  IPF and other causes of UIP: common finding typically basal and subpleural  Asbestosis: common finding in advanced disease in the basal subpleural regions  Chronic hypersensitivity pneumonitis: peripheral, patchy, diffuse with midlung predominance being common  Sarcoidosis: upper lobe predominant  NSIP and other ILDs: uncommon
    34. 34. DPLD  General approach:  Timeline  Smoking history  Occupational history  Environmental and toxin exposures  Drug history  Extrapulmonary symptoms and manifestations  Sarcoidosis  CTD  Testing  PFTs  HRCT  CTD serologies  Assess for exertional hypoxemia
    35. 35.  Exercise limitation and exertional hypoxemia
    36. 36. IPF  Histopath: UIP  Fibroblastic foci  Temporally hetergeneous  Minimal inflammation  Lots of collagen deposition  Predominantly subpleural and basilar  Similar findings in abestosis, rheumatoid lung disease  Progressive disease with a median survival 2-3 years from diagnosis
    37. 37. NSIP  Path: temporally uniform with interstital inflammation  Rad: ground glass with areas of fibrosis  Often also seen with CTD such as scleroderma
    38. 38. DIP/RBILD  Path:  Pigmented macrophages  Peribronchiolar inflammation  Rad:  Patchy ground glass  Intralobular septal thickening  Mosaic pattern
    39. 39. DPLD: Hypersensitivity pneumonitis  Disease of varying intensity and manifestation caused by the immunologic response to inhaled antigen, usually organic  Hundreds of antigens have been described. Occupations with highest frequency of HP:  Farmers “Farmer’s lung”  Poultry workers “Poultry worker’s lung,” “Bird breeder’s lung,” “Bird fancier’s lung”  Animal workers  Grain processing “Grain handler’s lung”  Textiles  Lumber  Also described with inhalation of contaminated water  “Humidifier lung,” “Air conditioner lung,” “Hot tub lung”
    40. 40. DPLD: Hypersensitivity pneumonitis  Disease of varying intensity and manifestation caused by the immunologic response to inhaled antigen, usually organic  Hundreds of antigens have been described. Occupations with highest frequency of HP:  Farmers “Farmer’s lung”  Poultry workers “Poultry worker’s lung,” “Bird breeder’s lung,” “Bird fancier’s lung”  Animal workers  Grain processing “Grain handler’s lung”  Textiles  Lumber  Also described with inhalation of contaminated water  “Humidifier lung,” “Air conditioner lung,” “Hot tub lung”
    41. 41. Subacute HP Mostly mid to upper lung zones
    42. 42. Chronic HP
    43. 43. HP: Treatment and prognosis  Treatment  Remove the inciting antigen from the environment or remove the patient from the environment  Corticosteroids for severe cases  Prognosis  Acute and subacute disease have excellent outlooks  Chronic can progress to end stage fibrosis
    44. 44. Y. Rosen, M.D. Atlas of Granulomatous Diseases
    45. 45. Sarcoidosis: Four stages
    46. 46. Sarcoidosis in the lungs: Stage I  Only the lymph nodes are enlarged  Pulmonary function is intact  55-90% pts with Stage I sarcoidosis resolve spontaneously
    47. 47. Sarcoidosis: Stage II  Lymph nodes enlarged  Inflammation in the lung  Lung function is impaired  40-70% pts resolve spontaneousl y
    48. 48. Sarcoidosis: Stage III  Lymph nodes are not enlarged  Only 10-20% resolve spontaneously
    49. 49. Sarcoidosis  90% with lung involvement  75% liver  20% skin  20% eyes  25% spleen  10% MSK  5% heart  5%
    50. 50. Pneumoconioses  Silicosis  CWP  Asbestosis  Talcosis  Berylliosis
    51. 51. Silicosis: Exposure  Mining  Quarrying  Tunneling  Stone cutters  Sandblasting  Glass manufacturing  Foundry work  Enameling  Quartz crystal manufacturing  Rubber industry
    52. 52. Silicosis: clinical presentations  Chronic silicosis  Accelerated silicosis  Progressive massive fibrosis  Acute silicosis
    53. 53. Chronic silicosis  Usually 10-30 years after initial exposure.  Can become radiographically apparent even after removal of exposure  Ranges from asymptomatic with normal PFTs to very very symptomatic with restrictive spirometry and low DLCO
    54. 54. Chronic silicosis: CXR findings  Simple silicosis is the earliest finding of chronic silicosis  Nodules usually 1-3 mm
    55. 55. Chronic silicosis: CXR findings  As disease progresses, nodules increase in number and coalesce to form larger lesions
    56. 56. Chronic silicosis: CXR findings  Eggshell calcification
    57. 57. Progressive massive fibrosis (PMF)  Occurs in a minority of pts with chronic silicosis  More likely to occur in pts with accelerated silicosis  PFTs abnormalities: mixed obstructive/restriction, air trapping
    58. 58. PMF: CXR findings  The nodules coalesce into conglomerate masses  Calcified lymph nodes “eggshell calcification”
    59. 59. Coal worker’s pneumoconiosis  AKA, black lung disease or anthrasilicosis  Rate and quantity of dust accumulation most important factor in pathogenesis of CWP  Clinical presentations similar to silicosis: 1. Simple 2. Chronic 3. PMF
    60. 60. Asbestos-related lung diseases  Pleural plaques  Benign asbestos related pleural effusion  Asbestosis  Mesothelioma
    61. 61. Asbestos: Pleural plaques  Usually first identified > 20 years after initial exposure  Occur in 50% persons exposed to asbestos  Parietal pleura adjacent to ribs, particularly along 6th -9th ribs and along diaphragm  Calcifications on CXR in 20% and on chest CT in 50%
    62. 62. Asbestos: Pleural plaques
    63. 63. Benign asbestos pleural effusion  Most common pleuropulmonary manifestation within the first 20 years of exposure… but can present <1 post-exposure to >50 years after first exposure  Typical presentation: acute pleuritic CP, fever, other systemic sx but can be insidious  Can resolve spontaneously  Pleural fluid analysis: exudative, serosanguinous, predominance of eosinophils, cytology with atypical macs, occasionally positive for RF  Rounded atelectasis and/or diffuse pleural thickening may be sequelae
    64. 64. Rounded atelectasis
    65. 65. Asbestos: Mesothelioma  Annual incidence 1:1,000,000/year  Incidence peaking now b/c of inadequate control measures in 60s and 70s  Any level of exposure may be a risk factor  Usually presents 20-40 years after exposure
    66. 66. Asbestosis  Presents > 30 years after initial exposure  Requires long term, heavy exposure  Criteria for diagnosis: 1. History of asbestos exposure 2. Dyspnea 3. Basilar crackles in two or more locations 4. Reduced lung volumes 5. Radiographic abnormalities
    67. 67. Talc related diseases  Talcosilicosis: caused talc mined with a high silica content  Talcoasbestosis: crystalline talc contaminated by asbestos fibers  Talcosis: inhalated of pure talc leading to bronchitis  IV talc injection: from cutting heroin with talc  formation of granulomas within the pulmonary vasculature  pulmonary hypertension
    68. 68. Berylliosis  Think aerospace, automotive, computer, ceramics, and nuclear industries  Clinical manifestations:  Acute disease due to direct irritant effects: rhinitis, pharyngitis, tracheobronchitis, chemical pneumonitis  Chronic disease: Think sarcoidosis except we have an etiology. Dx: finding beryllium somewhere or lymphocyte transformation test.
    69. 69. Diagnostic evaluation of pleural effusion  Thoracentesis  Helpful in 75% cases  Can be therapeutic as well  Routine labs:  LDH, total protein, glucose, pH, gram stain and culture, cytology, cell count and differential  Additional labs that may be helpful  Albumin, cholesterol, triglycerides, amylase, adenosine deaminase, AFB
    70. 70. Pleural fluid analysis: Light’s criteria  Pleural fluid protein/serum protein > 0.5  Pleural fluid LDH / serum LDH > 0.6  Pleural fluid LDH > 2/3 upper limits of normal for serum LDH *Very accurate at identifying exudates (~98%) but less accurate with transudates
    71. 71. Pleural fluid analysis: Other pleural chemistries to help differentiate exudate from transudate  Cholesterol  Absolute pleural fluid cholesterol > 45- 60mg/dL  Pleural fluid albumin gradient < 1.2 g/dL  Bilirubin: pleural fluid bilirubin/serum bilirubin > 0.6  Cholinesterase: pleural fluid/serum > 0.23
    72. 72. Pleural fluid analysis: Cell count and differential  Neutrophils  Present in transudates and exudates  Eosinophils  Significant numbers (>10%): air, blood most common etiologies.  Other etiologies:  Parapneumonic #1,  malignancy, tuberculosis, BAPE, drugs (dantrolene, bromocriptine, nitrofurantoin), parasites, Churg-Strauss  Lymphocytes:  >50% lymphocytes: malignancy, tuberculosis or s/p CABG  Mesothelial cells:  Uncommon in tuberculous effusions. Major exception: AIDS
    73. 73. Pleural fluid analysis: Cell count and differential  Neutrophils  Present in transudates and exudates  Eosinophils  Significant numbers (>10%): air, blood most common etiologies.  Other etiologies:  Parapneumonic #1,  malignancy, tuberculosis, BAPE, drugs (dantrolene, bromocriptine, nitrofurantoin), parasites, Churg-Strauss  Lymphocytes:  >50% lymphocytes: malignancy, tuberculosis or s/p CABG  Mesothelial cells:  Uncommon in tuberculous effusions. Major exception: AIDS
    74. 74. Pleural fluid analysis: cell count  Red blood cells  Blood-tinged fluid typically 5000 to 10000 RBC/mm3  Grossly bloody: 100000 RBC mm3  Trauma  Malignancy  Pulmonary embolism  Infection  Hemothorax: pleural fluid hct to blood hct > 50%
    75. 75. Pleural fluid analysis: Glucose  Glucose < 60mg/dL suggestive of the following disorders  Parapneumonic effusion: the lower the glucose, the more complicated the effusion  Malignant effusion: 15-25% pts with malignant effusion have low pleural glucose levels. The lower the glucose, the higher the tumor burden  Rheumatoid disease: majority of pts with rheumatoid effusion (78%) have pleural glucose < 30mg/dL  Tuberculous effusion  Rare: Paragonimiasis, hemothorax, Churg-Strauss, lupus pleuritis
    76. 76. Pleural fluid analysis: amylase  Elevated levels suggestive of 1 of 3 dx  Pancreatitis: often higher than serum levels **Pseudocyst communication: amylase > 1000U/L  Esophageal rupture  Malignant effusions: amylase level elevated in 10%
    77. 77. Pleural fluid analysis: LDH  Serial LDHs can be helpful:  Increasing levels: worsening process  Decreasing levels: resolving process  LDH isoenzymes:  Mostly LDH-4 and LDH-5  If predominance LDH-1, the increase is due to blood
    78. 78. Pleural fluid analysis: pH  pH < 7.2:  Parapneuymonic effusion  Esophageal rupture  Rheumatoid pleuritis  Tuberculous pleuritis  Malignant pleural disease  Hemothorax  Systemic acidosis  Paragonimiasis  Lupus pleuritis  Urinothorax  Reasons for caution  Often not measured correctly: must be measured using a blood gas machine  Must be collected anaerobically in a heparinized syringe  Lidocaine may falsely lower the pH
    79. 79. Pleural fluid analysis: other  ADA level > 50 U/L in pts without empyema or rheumatoid arhtritic is virtually diagnostic of a tuberculous effsuion  Interferon-gamma level > 3.7 U/mL also quite good at distinguishing tuberculous effusions  RF: Pleural fluid titer > 1:320 strongly suggestive of rheumatoid effusion  ANA: tends to correlate with serum ANA
    80. 80. Pleural fluid analysis: lipid studies  Triglycerides > 110 mg/dL  diagnostic of chylothorax  Triglycerides 50-110mg/dL  equivocal  Triglycerides < 50: not a chylothorax
    81. 81. Pleural fluid analysis: lipid studies  Triglycerides > 110 mg/dL  diagnostic of chylothorax  Triglycerides 50-110mg/dL  equivocal  Triglycerides < 50: not a chylothorax
    82. 82. Parapneumonic effusions and empyemas  Pleural fluid characteristics associated with need for pleural fluid drainage  Pus in the pleural space  Positive gram stain or culture  Glucose < 40  pH < 7.0  LDH > 3 x the ULN  Loculated pleural fluid
    83. 83. ACCP recommedations  Class I: Small < 10mm on decubitus film  No thoracentesis needed  Class II: Typical parapneumonic effusion  More than 10mm on decubitus film  needs sampling  Pleural fluid characteristics:  Glucose > 40  pH > 7.2  LDH < 3x ULN  Treatment: antibiotics alone  Class III: Borderline complicated  pH 7.0 -7.2 or LDH > 3x ULN  Normal glucose  Negative pleural micro  Treatment: Antibiotics plus serial thoracenteses  Class IV through VII: Complicated  pH < 7.0 or glucose < 40 or pleural fluid micro positive  tube thoracostomy
    84. 84. Whew!

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