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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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Case 6
Chief Complaint
Shortness of breath for several months
History and Physical Examination
A 66-year-old retired construction worker comes to the office for evaluation of increasing
shortness of breath over the past 5 months. He describes a dry, nonproductive cough that
began about 1 month before the onset of his shortness of breath. He has been in excellent
physical condition, walking 2 miles daily for many years. Recently, however, he has been
unable to walk 3 blocks without stopping to rest. He is a former smoker of 2 packs per
day for 20 years. He quit 3 months ago because of his difficulty breathing.
Upon examination the patient is well-developed, well-nourished, and in no acute distress.
His T is 36.7 C (98.0 F), BP 140/85 mm Hg, pulse 86/min, and respirations 22/min.
Physical examination shows bibasilar coarse crackles on chest auscultation but is
otherwise clear. Examination of the extremities shows clubbing. The remainder of the
physical examination is unremarkable.
Differential Diagnosis
Interstitial lung disease1.
Occupational etiologies:
Organic source: hypersensitivity pneumonitis—
Non-organic source: asbestosis, silicosis, berylliosis, coal worker’s—
211
Initial Management
Setting: outpatient
Initial Diagnostic
Plan
Results
Reticular marking predominantly in the mid- to lower lung with calcified
pleural plaques mainly on the diaphragm
Right axis deviation; normal sinus rhythm; prominent P waves in lead II; no
ST changes
Low FEV1, low FVC, normal FEV1/FVC, decreased total lung capacity
and residual volume with a decrease in DLCO
Normal ejection fraction, elevated right ventricle systolic pressure with
tricuspid regurgitation
Assessment
pneumoconiosis
Non-occupational etiologies: idiopathic pulmonary fibrosis
Bronchogenic carcinoma (squamous cell carcinoma and small cell carcinoma)
2.
COPD / emphysema
3.
Congestive heart failure
4.
Chest x-ray (PA
& lateral)
Electrocardiogram
Pulmonary
function tests
Echocardiogram
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This is likely an interstitial lung disease for an inorganic occupational etiology or obstructive
lung disease given the patient’s extensive smoking history or a combination of both. The
presence of a dry cough for many months in association with dyspnea on exertion and clubbing
can suggest a pulmonary process as the etiology of this patient’s problem; however, none of
these physical findings are pathognomonic. The radiographic finding of calcified pleural
plaques is classic for asbestos exposure.
Further Diagnostic
Plan
Results
Gram stain negative, culture negative, cell differential predominantly
macrophages, biopsy of the right lower lobe shows diffuse
inflammatory changes with areas of fibrosis; asbestos fibers were noted
CCS NOTE
Echocardiography should be ordered in cases with unexplained dyspnea to exclude
ventricular dysfunction. It will also help in the evaluation of pulmonary hypertension
secondary to hypoxia.
Treatment Plan
Bronchoscopy with
bronchoalveolar
lavage and
transbronchial biopsy
Close observation and follow-up PFTs and chest imaging in the future; consider a 6 min
walk test to evaluate for desaturations
1.
No specific medication or treatment exists at this time; in smokers, encourage cessation2.
213
Discussion
Asbestosis is a common environmental cause of interstitial lung disease. It is produced by
mineral silicate fibers that lodge in the lung and are phagocytosed by pulmonary macrophages,
which are damaged and release lysosomal enzymes. This results in an inflammatory process
that eventually leads to fibrosis.
Construction workers are commonly exposed to large amounts of asbestos. Other industries
associated with asbestos exposure include automobile repair, insulation, textiles, mining,
milling, and shipbuilding.
The disease often develops many years after exposure. There may be a dose-response
relationship between the amount of exposure and the biologic agent. In addition, the fitness of
the exposed individual is important. Because poorly conditioned persons ventilate more, they
are more likely to have a higher exposure and subsequent disease.
There is no definitive therapy for asbestosis. This disorder, characterized by progressive
dyspnea and cough in association with interstitial fibrosis, is only one of many potential
pulmonary complications of asbestos exposure. Radiographic abnormalities, including pleural
plaques and rounded atelectasis, are attributed to asbestos exposure.
Patients can demonstrate clinical evidence of progressive pulmonary failure with associated
right heart dysfunction.
High resolution CT may aid in the diagnosis.
Chest x-ray reveals the formation of pleural plaques, which are not associated with
pulmonary compromise.
As the disease progresses, linear opacities may appear in the lower lung lobes.
Patients may develop honeycomb lung consistent with severe compromise and end-stage
disease.
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Patients with a history of asbestos exposure are also at increased risk for the development of
bronchogenic carcinoma. This risk increases dramatically with concomitant asbestos exposure
and cigarette smoking (to 70× when compared to the risk of the normal population). Finally,
there is a strong association between asbestos and mesothelioma, although the risk is less than
that of developing bronchogenic carcinoma.
Final Diagnosis
Interstitial lung disease due to asbestosis
215
Case 7
Chief Complaint
“I’m breathing worse.”
History and Physical Examination
A 65-year-old white man comes to the office with worsening dyspnea on exertion over the
last year. He was recently treated for an episode of infectious bronchitis characterized by
fever and a productive cough. He now has a persistent mild nonproductive cough. He
notes a 10-lb weight loss over the last year and has increasingly restricted his activities
because of respiratory compromise. He has a history of smoking 2 packs per day for 50
years but denies alcohol intake.
His T is 37.0 C (98.6 F), BP 150/80 mm Hg, pulse 90/min, and respirations 28/min. He is
thin and frail, using accessory muscles of respiration at rest. He is sitting in a tripod
position. Examination shows no sinus tenderness, decreased breath sounds with scattered
rhonchi, increased antero-posterior diameter, and hyper-resonance to percussion. His
cardiac impulse is visible in the sub-xiphoid area; there is a regular rhythm, distant heart
sounds, and an increased S2. His abdomen is soft, nontender, with no
hepatosplenomegaly. Examination of the extremities shows no cyanosis and no edema.
Differential Diagnosis
Emphysema
1.
Asthma exacerbation
2.
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Initial Diagnostic Plan Results
Flat diaphragm, narrow cardiac silhouette, apical bullae; no
infiltrates are noted
7.35/60/74/32/94% in room air (consistent with a chronic
respiratory acidosis with renal compensation based on the
normal pH with an elevated PaCO2 and elevated HCO3-)
CLINICAL PEARL
In patients presenting with acute exacerbation of COPD, the PFT will be unreliable.
The first test to do is chest x-ray.
Congestive heart failure (CHF)3.
Coronary syndrome, angina4.
Post-obstructive pneumonia for a primary lung tumor5.
Interstitial lung disease6.
PFTs with bronchodilator
response
Decreased FEV1, decreased FVC, decreased FEV1/FVC,
decreased FEF
25-75%
; decreased DLCO, Increased TLC,
increased RV and increased FRC.
Flow volume loop shows an obstructive contour on the
expiratory portion of the loop. There was minimal
bronchodilator response.
Chest x-ray: PA and lateral
ABG (not diagnostic but
helpful in the acute setting,
especially if baseline ABG is
known)
217
In patients without a documented diagnosis of COPD and mild to moderate symptoms,
the first test to do is the PFT, to confirm diagnosis and assess prognosis.
Assessment
Emphysema should be considered first because of physical findings, CXR imaging and most
importantly the PFTs are consistent with obstructive lung disease. This is not a clinical picture
consistent with asthma, even though poorly controlled asthma can result in an obstructive
process; it is less likely given the age of the patient and significant smoking history.
CHF should also be considered in an elderly patient complaining of dyspnea, but there is no
evidence of increased jugular venous pressure or pulmonary edema on the examination. If CHF
is truly a concern, consider ordering a BNP level or transthoracic echocardiogram. Patients
with COPD and significant hypoxemia can develop pulmonary hypertension and cor pulmonale.
Coronary syndrome would be a consideration if this patient had chest pain or discomfort
and/or history of coronary risk factors. Post-obstructive pneumonia, secondary to a primary
lung tumor can be a strong consideration based upon the significant smoking history.
Bronchogenic tumors such as squamous cell carcinoma and small cell carcinoma would be the
most likely tumors seen in smokers and both can invade the bronchus resulting in a post-
obstructive pneumonia. However, given the absence of radiographic findings this would be
less likely. Interstitial lung diseases associated with smoking may present with shortness of
breath and involve the lung parenchyma, however the PFTs are not consistent with a restrictive
intrinsic process.
Chronic Treatment
Smoking cessation (cognitive behavioral therapy, nicotine replacement and
medications)
1.
Home O2 if the patient has PaO2 ≤55 or saturation <88%, or patient has cor pulmonale
2.
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CCS NOTE
Acutely ill patients in the office should be transferred to the emergency department. The
first dose of medication can be given in the office (such as bronchodilator and steroid)
before the transfer.
Acute Treatment (exacerbation/inpatient)
and PaO2 >55 to 59. Consider 6 minute walk test to evaluate for desaturation on
exertion
Treatment guidelines are based upon severity of disease. Inhaled bronchodilators are
the cornerstone therapy (both long and short acting). In severe COPD studies have
shown a role for inhaled corticosteroids.
3.
Pulmonary rehabilitation4.
Lung volume reduction in specialized group of emphysema patients5.
Referral for lung transplant in some6.
Screening for lung cancer with low dose CT chest in high-risk patients (smokers)7.
Oxygen to maintain O2 saturation at approximately 90%1.
Inhaled bronchodilators: anticholinergic agents (ipratropium bromide) and/or beta-
agonists (e.g., albuterol)
2.
Oral antibiotics if treating for a bacterial pneumonia or bronchitis (e.g., azithromycin
and ceftriaxone or fluoroquinolones)
3.
Sputum culture and Gram stain; send for Legionella urinary antigen if considering
atypical bacteria
4.
Corticosteroids5.
Strongly consider non-invasive positive pressure ventilation (BiPAP) for increased
work of breathing and to hopefully prevent intubation and mechanical ventilation
6.
219
The only treatments that have increased survival in chronic obstructive pulmonary disease are
home O2, smoking cessation and lung transplant.
Pneumococcal vaccine should be given every 5 years and influenza vaccine yearly to all
patients with chronic obstructive pulmonary disease.
Discussion
Emphysema, a major category of COPD, is defined as irreversible dilatation of the distal air
space with associated destruction of the alveolar septae. It is subdivided into pathologic
patterns in which either the respiratory bronchioles alone (centroacinar) or more distal
portions (panacinar) are involved. Cigarette smoking causes the following changes, all
contributing to the generation of emphysematous changes.
Antitrypsin is an enzyme responsible for the inhibition of trypsinase and elastinase in the lung,
and patients deficient in this enzyme experience severe panacinar emphysema. Always
consider alpha-1 antitrypsin deficiency in patients with emphysema involving the base of the
lung and liver abnormalities.
Emphysema is characterized by a loss of airway elastic recoil and caliber resulting in collapse
during forced expiration (referred to as the loss of radial traction). This leads to a prolonged
expiratory phase, an increase in residual capacity, and air trapping with increases in lung
Mechanical ventilation is a clinical decision, not based upon a lab value or
radiographic imaging, and should be discussed with the patient and family if possible
7.
Abnormalities in ciliary movement
Hyperplasia of mucous-secreting glands
Inhibition of the alveolar macrophages
Release of proteolytic enzymes from neutrophils
Inhibition of antiproteolytic enzymes
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