pulmonary board review 2009. what we’re going to speed through 1. evaluation of symptoms: cough...
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Pulmonary Board Review
2009
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What we’re going to speed through1. Evaluation of symptoms: cough and dyspnea2. PFTs3. Asthma4. COPD5. Interstitial lung diseases6. Pneumoconioses7. Pleural disease8. Sleep9. Pulmonary embolism10. Mechanical ventilation
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Respiratory symptoms: cough Cough
Chronic cough = duration > 3 weeks First: Make sure the patient is not on an ACE inhibitor Most common etiologies
Postnasal drip syndrome Asthma GERD
Others: Chronic bronchitis Bronchiectasis ACE inhibitor Post-infectious Eosinophilic bronchitis Endobronchial lesion
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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
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PFTs: Spirometry Approach
Is it a good test? reproducible, adequate exhalation 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 > 80% predicted
II: Moderate FEV1 < 50-80% predicted III: Severe FEV1 < 30- 50% predicted
IV: Very Severe FEV1 < 30% predicted Is there restriction? FVC < 80% predicted indicates possible restrictive
disease Is there airway reactivity? Response to bronchodilator testing: > 12% or >
200mL
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Lung volumes
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Lung Volumes
0
20
40
60
80
100
120
nl COPD rest n-m obese
RV
FRC
TLC
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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: Fibrotic lung diseases Interstitial edema/alveolar edema
Anemia
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PFTs: flow volume loops Useful in looking for
central airway obstruction
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Flow volume volumes
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Asthma 22 millions pts per year in U.S.
Overall increasing disease prevalence Decreasing number of asthma deaths Significant racial disparities in disease burden
Puerto Ricans African Americans
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Asthma categories of severity 2007 NAEPP report
Intermittent Mild persistent Moderate persistent Severe persistent
Treatment recommendations based upon severity
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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
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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
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Moderate persistent asthma Daily symptoms or > 1 nocturnal awakening per week or Moderate limitation in ADLs or FEV1 60-80%
Rx: step 3 in asthma treatment protocol Low dose inhaled corticosteroids + LABA Medium dose inhaled corticosteroid
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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
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Asthma syndromes Cough variant asthma Aspirin-induced asthma or triad asthma Exercise induced asthma Occupational asthma Allergic bronchopulmonary aspergillosis
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Occupational asthma 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)
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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
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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
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Adapted from Fletcher et al. BMJ. 1977;1:1645-1648.
FE
VF
EV
11 (%
) R
elat
ive
to A
ge
25 (
%)
Rel
ativ
e to
Ag
e 25
Death
Disability
Age (years)5050 7575252500
Symptoms
00
2020
6060
100100
8080
4040
Healthy
COPD
Rehabilitationat 45 (mild COPD)
Exercise Performance Over Time
Rehabilitationat 65 (severe COPD)
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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
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COPD Treatment:
Smoking cessation Oxygen therapy Medical therapy Pulmonary rehabilitation LVRS
Transplantation
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*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 a Pathway 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 bronchodilator A short-acting bronchodilator can be used for rescue. Low-dose methylxanthines can be prescribed if the response to inhaled bronchodilator therapy is can 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.Cooper et al. Cooper et al. BMJBMJ. 2005;330;640-644. (B). 2005;330;640-644. (B)
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 COPDNonpharmacologic Nonpharmacologic
TherapyTherapy
Smoking cessationSmoking cessationAvoidance of exposureAvoidance of exposure
Smoking cessationSmoking cessationAvoidance 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 oxygenLung volume reduction surgeryLung volume reduction surgery
Lung transplantationLung transplantation
Supplemental oxygenSupplemental oxygenLung 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)
ClinicalClinicalstagestage
At riskAt risk
IntermittentIntermittentsymptomssymptoms
PersistentPersistentsymptomssymptoms‡‡
FrequentFrequentexacerbationsexacerbations¶¶
Respiratory failureRespiratory failure
††
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Interstitial lung diseases orDiffuse 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) Others
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
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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
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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
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Figure 3-24
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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
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Diagnosis PFTs Bronchoscopy
BAL limited utility Looks for eosinophilia (> 10%) Lymphocytosis Mast cells
Biopsy limited utility Helps if high pre-test probability of sarcoidosis, HP, LIP,
lymphangitic carcinomatosis Dismal if you are thinking UIP or NSIP
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IPF Older age, M > F Histopath: UIP
Fibroblastic foci Temporally heterogeneous 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
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NSIP Path: temporally uniform with interstital
inflammation Rad: ground glass with areas of fibrosis
Often also seen with CTD such as scleroderma
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DIP/RBILD Path:
Pigmented macrophages Peribronchiolar inflammation
Rad: Patchy ground glass Intralobular septal thickening Mosaic pattern
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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”
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Subacute HP
Mostly mid to upper lung zones
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Chronic HP
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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
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Y. Rosen, M.D. Atlas of Granulomatous Diseases
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Sarcoidosis: Four stages
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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
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Sarcoidosis: Stage II Lymph nodes
enlarged Inflammation
in the lung Lung function
is impaired 40-70% pts
resolve spontaneously
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Sarcoidosis: Stage III Lymph nodes are not
enlarged Only 10-20% resolve
spontaneously
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Sarcoidosis 90% with lung
involvement 75% liver 20% skin 20% eyes 25% spleen 10% MSK 5% heart 5%
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Pneumoconioses Silicosis CWP Asbestosis Talcosis Berylliosis
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Silicosis: Exposure Mining Quarrying Tunneling Stone cutters Sandblasting Glass manufacturing Foundry work
Enameling Quartz crystal
manufacturing Rubber industry
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Silicosis: clinical presentations
Chronic silicosis Accelerated silicosis Progressive massive fibrosis Acute silicosis
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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
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Chronic silicosis: CXR findings Simple silicosis is the
earliest finding of chronic silicosis
Nodules usually 1-3 mm
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Chronic silicosis: CXR findings As disease
progresses, nodules increase in number and coalesce to form larger lesions
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Chronic silicosis: CXR findings Eggshell calcification
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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
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PMF: CXR findings The nodules coalesce
into conglomerate masses
Calcified lymph nodes “eggshell calcification”
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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
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Asbestos-related lung diseases Pleural plaques Benign asbestos related pleural effusion Asbestosis Mesothelioma
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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%
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Asbestos: Pleural plaques
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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
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Rounded atelectasis
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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
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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
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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
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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.
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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
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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
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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
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Pleural fluid analysis: Cell count and differential Neutrophils
Typical of acute inflammatory process Eosinophils > 10%
air, blood most common etiologies. Other:
Parapneumonic #1, malignancy, tuberculosis, BAPE, drugs (dantrolene, bromocriptine,
nitrofurantoin), parasites, Churg-Strauss Lymphocytes > 50%
malignancy, tuberculosis or s/p CABG Mesothelial cells:
Uncommon in tuberculous effusions. Major exception: AIDS
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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%
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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
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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%
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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
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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
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Pleural fluid analysis: other ADA level > 50 U/L in pts without empyema or
rheumatoid arthritis 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
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Pleural fluid analysis: lipid studies
Triglycerides > 110 mg/dL diagnostic of chylothorax
Triglycerides 50-110mg/dL equivocal Triglycerides < 50: not a chylothorax
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Pleural fluid analysis: lipid studies
Triglycerides > 110 mg/dL diagnostic of chylothorax
Triglycerides 50-110mg/dL equivocal Triglycerides < 50: not a chylothorax
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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
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ACCP recommendations 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
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Sleep disordered breathing Obstructive sleep apnea
RFs Obesity Facial soft tissue abnormalities Smoking! Nasal congestion DM
Mild AHI 5-15 Sedentary daytime sleepiness Sats > 90% more than 95% of time during sleep
Moderate: AHI 15-30 Daytime sleepiness requiring behavioral changes
Severe: > 30 disabling daytime sleepiness and signs of cardiopulmonary failure Nocturnal sats < 90% more than 20% of the time
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Sleep disordered breathing Outcomes:
3-6x risk of all cause mortality Associated with: HTN, PH, MI, CVA, arrythrmias Treatment is associated with decreased mortality
Treatment: Weight Alcohol and drug avoidance NIPPV for
AHI > 5 and clinical sequelae (sleepiness, mood disorder, cardiovascular disease)
AHI > 15 without symptoms Oral appliances Surgery (UPPP)
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Obesity hypoventilation syndrome Definition
Awake alveolar hypoventilation (pCO2 > 45) Obesity (BMI > 35) No other cause of hypoventilation
Usually seen with OSA Cor pulmonale
Outcomes: High mortality
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Obesity hypoventilation Treatment
OSA present: Trial of CPAP is appropriate Transition to BiPap if volume cycled positive
airway pressure if symptoms persist or persistent daytime hypercapnia
Treatment of acute respiratory failure: BiPAP or VCPAP
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Pulmonary embolism Mortality 30% without apporpriate treatment Mortality decreases to 2-8% with
appropriate diagnosis and treatement Increased risk of death
RV dysfunction Elevated BNP Elevated troponin
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Copyright restrictions may apply.
Writing Group for the Christopher Study Investigators, JAMA 2006;295:172-179.
Clinical Decision Rule*
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Treatment Anticoagulation IVC filter Thrombolysis
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Mechanical ventilation Complications of invasive mechanical
ventilation Recognize PEEP related hypotension Appropriate ventilator management for
ARDS
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Whew!