Download Lung Disorders

Lung Disorders
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COMMON MANIFESTATIONS OF
LUNG DISEASE
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DYSPNEA
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Brought about by several physiologic processes:
Increased respiratory effort due to:
1) AIRWAY OBSTRUCTION: COPD, asthma.
2) DECREASED PULMONARY COMPLIANCE: interstitial fibrosis, CHF.
3) DECREASED CHEST WALL COMPLIANCE: obesity, pleural disease.
4) WEAKNESS OF RESPIRATORY MUSCLES: neuromuscular weakness, inanition,,
chronic respiratory failure.
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DYSPNEA
ACUTE DYSPNEA
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Short list:
Asthma, infection.
Pulmonary edema.
Pneumothorax.
Pulmonary embolus.
ARDS, panic attack.
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DYSPNEA
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EVALUATION
CBC, renal function, CXR, spirometry, oximetry.
If > 40 or family Hx → EKG.
ABG’s, V/Q Scan, stress testing, echocardiography where appropriate based on
Signs / Sxs.
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DYSPNEA
TREATMENT
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O2 if hypoxemic.
Treat dyspnea-related anxiety w/ “judicious” use of benzodiazepines, Ativan 0.51.0 mg q6-8.
Pulmonary “rehab,” more appropriate breathing techniques, energy-conserving
techniques, etc.
Um, smoking cessation.
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COUGH
CHRONIC COUGH
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Most commonly from COPD.
In the non-smoker:
GERD, post-nasal drip, asthma.
Side-effect of ACE Inhibitors.
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THE EVAL
Postnasal drip: sinus series, Rx as sinusitis.
PFT’s: asthma, COPD.
GERD: barium swallow vs empiric Rx.
CXR: for patients w/ other Sxs, hemoptysis, fever, weight loss, etc
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COUGH
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TREATMENT
Dependent upon the cause.
Elimination of irritant: tobacco, allergen, environmental, occupational.
D/C beta blockers, ACE inhibitors.
Post-nasal drip: antihistamines, decongestants, intranasal steroids.
Chronic sinusitis: prolonged antibiotic Rx, 2-4 weeks.
Asthma: inhaled steroids and bronchodilators. If not better another cause needs to be
considered.
GERD- proton pump inhibitors, H2 blockers may not cut it.
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HEMOPTYSIS
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Coughing up of blood “that originates below the vocal cords.”
Dual circulation:
1) PULMONARY ARTERIES- from the right ventricle under low pressure to the
pulmonary parenchyma.
2) BRONCHIAL ARTERIES- from the aorta under systemic pressure to the airways,
blood vessels, hilum, and visceral pleura.
The bronchial circulation is only 1-2% of total pulmonary flow, but is common
source of hemoptysis.
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HEMOPTYSIS
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CHASING DOWN THE CAUSE ANATOMICALLY
1) FROM THE AIRWAYS: chronic bronchitis, bronchiectasis, bronchogenic
carcinoma.
2) FROM THE PULMONARY VASCULATURE: left v. failure, mitral stenosis, PE, AVM.
3) FROM THE PULMONARY PARENCHYMA: pneumonia, inhalation of crack,
autoimmune disease such as Goodpasture’s Syndrome and Wegener’s
Granulomatosis.
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HEMOPTYSIS
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CLINICAL FINDINGS
In acute bronchitis in an otherwise healthy person, no big work up needed as long
as it resolves w/ the illness.
Hemoptysis is frequently a sign of serious disease.
Identify the patient at risk for pathology.
CXR, CBC w/ platelets, renal function, UA.
Flexible bronchoscopy.
Chest CT.
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HEMOPTYSIS
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TREATMENT
Mild hemoptysis- identify the cause.
Massive hemoptysis- secure the airway, intubation, suction, ventilation.
Bronchoscopic control sometimes possible.
Selective arterial embolization.
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UPPER AIRWAY OBSTRUCTION
ACUTE
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Can be life-threatening.
CAUSES: Foreign body, laryngospasm, laryngeal edema from burns, angioedema,
trauma to the pharynx/larynx, infections (retropharyngeal abscess, etc), acute
allergic laryngitis.
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ASTHMA
 Chronic, inflammatory disorder of the airways.
 Reversible airway hyper-responsiveness, airway edema,
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bronchoconstriction, mucous production.
5% of the population, 5000 deaths annually.
Prevalence, # hospitalizations, and deaths all increased over the last 20
years.
See text for histopathology, underlying inflammatory changes, mast cells,
etc.
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ASTHMA
 Genetic predisposition, atopy.
 Most common trigger is inhaled allergens.
 Other triggers: exercise, URI’s, rhinitis, sinusitis, postnasal drip, GERD,
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changes in weather, stress.
Also: tobacco smoke, ozone, SO2, NO2.
Some cases due to use of aspirin, NSAID’s, tartrazine dyes.
Catamenial.
“Cardiac asthma.”
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Asthma
Allergens
O “Seasonal pollens
O Year round allergens – dust mites,
moulds, pets, and insect parts
O Foods – fish, egg, peanuts, nuts, cow’s
milk, and soy
O Additives – sulphites
O Work related agents – latex, flour
Irritants
O Respiratory infections – viral colds, bronchitis,
and sinusitis
O Drugs – aspirin, NSAIDs, betablockers
O Tobacco smoke
O Outdoor factors – haze and smog, weather
changes, exhaust fumes
from vehicles
O Indoor factors — paint, detergents,
deodorants, chemicals and perfumes
O GERD
O Temperature change – night-time
O Exercise in cold dry conditions
O Work-related factors – chemicals, dusts,
gases, and metals
O Emotional factors – laughing, crying, yelling
and distress
O Hormonal factors – premenstrual syndrome
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Clinical consequences of airway
remodeling in asthma
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ASTHMA
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SIGNS / SYMPTOMS
Wheezing, difficulty breathing, chest tightness, cough.
Extreme variability in symptoms from one patient to the next.
Worse at night, bronchoconstriction max between 3-4 AM.
COEXISTING CONDITIONDS: nasal polyps, eczema, atopic dermatitis, other
allergic skin disorders.
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ASTHMA
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SIGNS / SYMPTOMS
Wheezing may be absent when bronchoconstriction is extreme, as not
enough air is flowing to produce wheezing. This portends respiratory
failure.
Here we find globally diminished breath sounds and prolonged expiration.
PFT’s
FEV1, FVC, (FEV1 / FVC).
Peak expiratory flow meters for home monitoring.
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ASTHMA
COMPLICATIONS
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Exhaustion.
Dehydration, airway infection.
Cor pulmonale.
Pneumothorax.
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ASTHMA
LONG-TERM TREATMENT
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GOALS:
1) Minimize chronic Sxs that impair normal activity.
2) Prevent recurrences.
3) Minimize need for ER / hospitalizations.
4) Maintain near-normal pulmonary function.
Daily anti-inflammatory therapy w/ inhaled corticosteroids.
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ASTHMA
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LONG-TERM TREATMENT
Therapy dictated by algorithms set forth by the Expert Panel Report 2 from
the NAEPP, step-wise fashion (“stair-step”).
Amount of medication and dosing based on severity of Sxs.
Begin therapy at a higher level of intensity then back down.
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ASTHMA
PHARMACOLOGIC AGENTS
 2 CATEGORIES:
 1) Those that promote long-term control- address airway inflammation.
 2) Those that offer quick relief- bronchodilators
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ASTHMA
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PHARMACOLOGIC AGENTS
LONG-TERM CONTROL MEDICATIONS.
QUICK RELIEF MEDICATIONS.
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ASTHMA
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PHARMACOLOGIC AGENTS
LONG-TERM CONTROL MEDICATIONS.
ANTI-INFLAMMATORY AGENTS
LONG-ACTING BRONCHODILATORS
LEUKOTRIENE MODIFIERS
DESENSITIZATION
MISCELLANEOUS
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ASTHMA
PHARMACOLOGIC AGENTS – LONG-TERM
 LONG-ACTING BRONCHODILATORS
 1) MEDIATOR INHIBITORS- cromolyn sodium, nedocromil. Modulate mast
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cell and eosinophil function.
2) BETA ADRENERGIC AGENTS- inhaled, long-acting. Onset of action is
delayed, not for acute bronchoconstriction, exacerbations. Combined w/
inhaled corticosteroids.
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ASTHMA
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PHARMACOLOGIC AGENTS – LONG-TERM
LONG-ACTING BRONCHODILATORS
3) PHOSPHODIESTERASE INHIBITORS- Theophylline.
Mild bronchodilator.
Control of nocturnal symptoms.
Used in patients w/ moderate to severe persistent asthma along w/
inhaled steroids and beta blockers.
See text re serum concentrations, effects of other meds.
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ASTHMA
PHARMACOLOGIC AGENTS – LONG-TERM
 LEUKOTRIENE MODIFIERS
 Singulair (montelukast), Zileuton.
 Leukotrienes- think of them as a delayed-onset histamine →
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vasodilatation, increased capillary permeability, mucous production, and
bronchoconstriction.
Can minimize need for “rescue” treatment in acute exacerbations;
alternatives to inhaled steroids.
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ASTHMA
PHARMACOLOGIC AGENTS – LONG-TERM
 DESENSITIZATION
 Immunotherapy, “allergy shots.”
 When response to meds for long-term control is not optimal, ie you’ve
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tried everything else without adequate control. This is the top rung of the
outpatient “stair step.”
MISCELLANEOUS
Oral sustained-release beta2 agonists.
Omalizumab- a recombinant antibody that binds IgE.
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ASTHMA
QUICK-RELIEF MEDICATIONS
 1) BETA-ADRENERGIC AGENTS
 2) SYSTEMIC CORTICOSTEROIDS.
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ASTHMA
QUICK-RELIEF MEDICATIONS
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1) BETA-ADRENERGIC AGENTS
Short-acting, inhaled bronchodilators.
For exacerbations only. (“rescue”)
β-1 vs β-2.
Albuterol, terbutaline, bitolterol, pirbuerol.
If need is often for these, long-term control efforts need to be ramped up.
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ASTHMA
QUICK-RELIEF MEDICATIONS
 2) SYSTEMIC CORTICOSTEROIDS
 For moderate to severe exacerbations, lack of response to inhaled short-
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acting β2 therapy.
Sometimes necessary for the long-term control of patients w/ severe
asthma.
PO vs. IV.
Adrenal suppression.
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ASTHMA
 ASSESSMENT, MONITORING, PREVENTION.
 Periodic clinical assessments and self-assessments (peak flow meters) are
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the primary methods of monitoring asthma
Written action plan for self-monitoring, changes to therapy, and treatment
of exacerbations.
Asthmatics should receive vaccinations for influenza and pneumococcal
pneumonia.
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COPD
 Airflow obstruction due to emphysema and chronic bronchitis. Most have
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features of both.
Usually progressive, has variable amounts of airway inflammation, some
of which may be reversible.
COPD and asthma combined = the 4th leading cause of death in the U.S.
Death rate is increasing, esp in elderly men.
Almost all due to smoking.
Other causes:
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COPD
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SIGNS & SYMPTOMS
Present in the 5th and 6th decades of life.
Excessive cough, shortness of breath, and sputum production.
Symptoms often present 10 years or more.
Progressively worsening dyspnea: w/ exertion → w/ mild exertion → at
rest.
Late stages → complicated by pneumonia, pulmonary hypertension, cor
pulmonale, chronic respiratory failure.
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COPD
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SIGNS & SYMPTOMS
See text for comparison of “pink puffer” (emphysema) vs “blue bloater”
(chronic bronchitis).
Thin, uncomfortable, quiet chest- emphysema.
Obese, noisy chest, rhonchi, wheezes- chronic bronchitis.
In reality, most patients have features of both.
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COPD
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IMAGING
Plain X-rays not sensitive enough for a Dx, but show:
Hyperinflation, flattening of the diaphragm.
Bullae- when present in the right clinical setting → diagnostic of
emphysema.
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COPD
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COMPLICATIONS
Spontaneous pneumothorax.
Pulmonary hypertension, cor pulmonale.
Acute bronchitis, pneumonia, pulmonary thromboembolism, LV failure can
worsen otherwise stable COPD.
Hemoptysis- can be from chronic bronchitis but bronchogenic carcinoma
needs to be considered.
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COPD
TREATMENT
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AMBULATORY PATIENTS
1) Smoking cessation.
2) Oxygen therapy.
3) Bronchodilators.
4) Corticosteroids.
5) Antibiotics.
6) Other measures.
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COPD
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TREATMENT
1) SMOKING CESSATION
Requires an active, multidimensional program, not simply telling patients
to quit (5%).
Nicotine gum + behavior modification = 22% sustained abstinence at 5
years.
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COPD
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TREATMENT
2) OXYGEN THERAPY
For patients w/ resting hypoxemia.
The only therapy (“drug”) that has been shown to improve the natural
history of COPD in patients w/ resting hypoxemia.
Correlated w/ prolonged survival, reduced hospitalizations, better quality
of life.
Esp likely to benefit- the hypoxemic patient w/ pulmonary hypertension,
cor pulmonale, erythrocytosis, impaired cognitive function, exercise
intolerance, nocturnal restlessness, morning headache.
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COPD
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TREATMENT
3) BRONCHODILATORS
The most important pharmacologic agents in the management of COPD.
Symptomatic improvement only. Do not alter the progressive
deterioration in lung function.
Ipratropium bromide- an anticholinergic.
Albuterol, metaproterelol- short-acting β2 agonists.
Salmetrol, Formoterol- long-acting β2 agonists.
Oral theophylline- 3rd line agent.
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COPD
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TREATMENT
4) CORTICOSTEROIDS
Only useful in acute exacerbations.
More useful when the predominant component is chronic bronchitis
rather than emphysema.
See text for details.
Inhaled steroids have no effect on the characteristic decline in lung
function in COPD.
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COPD
TREATMENT
5) ANTIBIOTICS
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For:
1) To treat an acute exacerbation.
2) To treat acute bronchitis.
3) To prevent acute exacerbations (prophylaxis).
Evidence supports use in only the 1st two.
Trimethoprim-sulfamethoxazole (Septra).
Amoxicillin-clavulanate (Biaxin).
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COPD
TREATMENT
6) OTHER MEASURES
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See text.
Graded exercise, hydration to promote clearing of secretions.
Expectorants, mucolytics, not helpful.
Cough suppressants to be avoided.
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PNEUMONIA
 Lower respiratory tract infection.
 We will look at community-acquired pneumonia.
 See text for Hospital-acquired pneumonia, anaerobic pneumonia, and
pneumonia in the immunocompromised.
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COMMUNITY-ACQUIRED PNEUMONIA
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Common.
Most deadly infectious disease in the U.S.
4th leading cause of death.
14% mortality if hospitalization is required, < 1% if not.
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COMMUNITY-ACQUIRED PNEUMONIA
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PATHOGENESIS
Begins outside the hospital or within 48 hours after admission in a patient who has
not been in a long-term care facility for 14 or more days before the onset of
symptoms.
Occurs when there is a defect in one or more of the defense mechanisms: cough
reflex, mucociliary clearance of secretions, immune response.
Or when there is a large inoculum or a particularly virulent organism.
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COMMUNITY-ACQUIRED PNEUMONIA
PATHOGENESIS
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THE BACTERIAL BUGS:
Strep pneumoniae- 2/3 of cases.
H. flu, Mycoplasma, Klebsiella, Chlamydia pneumoniae, Staph aureus, Legionella.
THE VIRAL BUGS:
Influenza, respiratory syncytial virus (RSV), adenovirus, parainfluenza virus.
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COMMUNITY-ACQUIRED PNEUMONIA
PATHOGENESIS
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THE SCREWY BUGS:
Chlamydia psittaci (psittacosis), Coxiella burnetti (Q fever), Francisella tularensis
(tularemia aka rabbitt fever), fungi such as Blastomyces, Coccidioides,
Histoplasmosis
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COMMUNITY-ACQUIRED PNEUMONIA
LAB
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Sputum culture, possibly gram stain.
HIV if hospitalization required. See text for other tests on hospitalized patients.
IMAGING
CXR- to confirm Dx, look for other associated pathology- cavitation, pleural
effusion, degree of involvement, etc.
Can take up to 6 weeks for CXR findings to clear.
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COMMUNITY-ACQUIRED PNEUMONIA
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TREATMENT
Empiric antibiotic therapy as the organism obtained at culture does not always
correlate w/ the actual pathogen.
CHOICES:
1) Macrolides; clarithromycin, azithromycin (Zithromax, “Z-Pak”).
2) Doxycycline.
3) Fluoroquinolones- levofloxacin (Levoquin), others.
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COMMUNITY-ACQUIRED PNEUMONIA
TREATMENT
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ALTERNATIVES:
Erythromycin, amoxacillin-clavulanate (Biaxin), 3rd generation cephalosporin such
as cefuroxime, cefprozil.
Duration varies acc to severity, etiologic gent, response to therapy.
Treatment until afebrile at least 72 hours is one guideline.
2 weeks for some bugs- see text.
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COMMUNITY-ACQUIRED PNEUMONIA
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PREVENTION
Polyvalent pneumococcal vaccine- prevents or attenuates the severity of the
illness in most immunocompetent patients.
For patients:
1) 65 years of age.
2) Any chronic illness that increases the risk of community acquired pneumonia
Also vaccinate for influenza (flu shot) to prevent the flu and secondary bacterial
pneumonia.
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TB
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Infection w/ Mycobacterium tuberculosis.
15 million people infected in the US.
REVIEW
Inhalation of droplet nuclei w/ M tuberculosis.
The immune response, the lymphocyte, the macrophage, the granuloma.
Primary / latent TB.
Active TB (Reactivation).
Extra-pulmonary TB.
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TB
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SIGNS / SYMPTOMS – OF LATENT TB
Pg 261- “Primary TB is “USUALLY” clinically and radiographically silent.”
That is, they are asymptomatic, and their CXR is normal.
See Pg 262 for findings in those patients whose CXR is not normal. Notice that
these findings are different than those patients w/ active TB.
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TB
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SIGNS / SYMPTOMS – OF ACTIVE TB
Slowly progressive symptoms: malaise, anorexia, fever, weight loss, night sweats.
Chronic cough.
Dry → productive → blood-tinged sputum.
Patient looks chronically ill and malnourished.
No physical findings on chest eval specific for TB.
Occasionally apical rales.
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TB
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TREATMENT
TREATMENT OF HIV NEGATIVE PATIENTS
See pg 265, and table 9-14.
Combinations of:
INH (isoniazid).
Rifampin.
Ethambutal.
Streptomycin, and
Pyrazinamide.
Depending on susceptibility test results.
6 vs 9 months, daily vs 2-3x per week.
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TB
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TREATMENT
TREATMENT OF HIV POSITIVE PATIENTS
Requires expertise in the treatment of both TB and HIV.
Guidelines per the CDC.
Treatment similar to HIV negative, but:
Longer duration of therapy.
Drug interactions w/ protease inhibitors and reverse transcriptase inhibitors for
HIV.
DOT for all who are HIV+.
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Tuberculosis
Pathogenesis: caused by Mycobacterium tuberculosis infection of the lung
• pathogen is distributed systemically within macrophages and survives intracellularly
• respiratory insufficiency
• estimated 2 billion infected worldwide (WHO)
• yearly mortality = 2 million
• incidence in NA is rising
Multi Drug Therapy
Isoniazid
- most effective agent against Mycobacterium tuberculosis
- able to penetrate macrophages (active intra- and extracellularly)
- inhibits mycolic acid synthesis (component of mycobacterial cell wall)
Rifampin
- often given in combination with isoniazid (transcription inhibitor)
- combination cures 95-98% of TB caused by susceptible strains within 9 mo.
• Others
pyrazinamide, ethambutol, streptomycin
- given in combination with isoniazid plus rifampicin
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Tubrculosis
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Drug toxicity:Isoniazid- Dermatitis/ Polyneuritis/ Hepatitis
Rifampin- Red coloration of sweat, urine/ Hepatitis/ Flu like syndrome
Ethambutol- Optic neuritis- Color blindness
Pyrizinamide- Arthralgias/ Hepatitis
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PLEURAL EFFUSION
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An abnormal accumulation of fluid in the pleural space.
Systemic disease: CHF, cirrhosis, nephrotic syndrome, sarcoidosis, connective
tissue disease, etc.
Infection: TB, fungi, rickettsiae.
Neoplasia: lung cancer, lymphoma, breast cancer.
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PLEURAL EFFUSION
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BOTTOM LINE: all new accumulations of fluid in the pleural space should be
evaluated by thoracentesis to determine composition of fluid, presence of
malignant cells, infection.
SIGNS / SYMPTOMS
Dyspnea, cough, pleuritic chest pain.
Large effusions more symptomatic than smaller ones, symptoms more common in
patients w/ existing cardiopulmonary disease.
Dullness to percussion, shifting dullness.
Diminished breath sounds.
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PLEURAL EFFUSION
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See text re evaluation of the fluid, transudate vs exudate, etc., cytologic exam,
culture.
See text re imaging.
See text re treatment: the bottom line is that treatment is aimed at the underlying
etiology of the effusion.
See text re local measures (thoracentesis, pleurodesis) that can be used for relief
of effusions causing significant symptoms.
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PNEUMOTHORAX
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CLASSIFICATION:
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SPONTANEOUS VS TRAUMATIC.
IF IT’S NOT TRAUMATIC, IT’S SPONTANEOUS
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PRIMARY- in the absence of pulmonary disease.
SECONDARY- due to / is a complication of preexisting pulmonary disease (COPD,
asthma).
ALSO IATROGENIC (an acupuncture needle).
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PNEUMOTHORAX
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PRIMARY:
Most commonly in tall, thin men between ages 10-30.
Rupture of a bleb.
Family Hx, smokers.
SECONDARY:
COPD, asthma, cystic fibrosis, TB, menstruation (catamenial pneumothorax),
interstitial lung disease (sarcoid), Pneumocystis infection.
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PNEUMOTHORAX
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TENSION PNEUMOTHORAX
A one-way valve effect from chest wall trauma, allowing air into the pleural space
with each breath, but it is not self-limiting as in rupture of a bleb.
Is a medical/surgical emergency requiring placement of a chest tube.
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PNEUMOTHORAX
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SIGNS / SYMPTOMS
CHEST PAIN- mild to severe, on the affected side.
DYSPNEA- 100%.
Sxs begin at rest.
Respiratory compromise from the pneumo can be life-threatening in patients w/
underlying COPD or asthma.
For small pneumo’s (<15%) → only mild tachycardia.
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PNEUMOTHORAX
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SIGNS / SYMPTOMS
For larger pneumo’s → decreased/absent breath sounds over the area of the
pneumo, decreased tactile fremitus, decreased movement of the chest.
W/ a tension pneumo → marked tachycardia, hypotension, and possibly shift of
the mediastinum/trachea away from the affected side.
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PNEUMOTHORAX
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IMAGING
CXR- Detection of a visceral pleural line.
Best taken on expiration when the lung is least expanded, allowing better
visualization in a smaller pneumo.
Pleural effeusion may be present.
Tension pneumo- contralateral shift of the trachea and mediastinum.
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PNEUMOTHORAX
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DIFFERENTIAL Dx
Can mimic PE, MI, pneumonia.
TREATMENT
Depends on severity.
<15%- observation, resolution.
>15%- evacuation by a chest tube, or a 16 gauge intravenous catheter (angiocath)
in a pinch like Mark Wahlburg in that Movie w/ George Clooney.
Risk of recurrence in smokers is 50%.
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PNEUMOTHORAX
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TREATMENT
Surgery occasionally needed- thoracotomy, thoracoscopy- for recurrences, for
bilateral pneumothoraces, and for failure of resolution w/ a chest tube.
Surgery- resection of blebs; pleurodesis- installation of a substance (usually talc or
doxycycline) that in effect is an irritant and results in fusion of the visceral and
parietal pleurae thereby obliterating the pleural space.
73
PNEUMOTHORAX



PROGNOSIS.
After successful treatment, no long-term complications.
30% of patients w/ a spontaneous pneumothorax will experience a recurrence.
Surgery/pleurodesis reduces recurrence.
74
LUNG CANCER




THE SKINNY
AKA BRONCHOGENIC CARCINOMA.
The most common cause of cancer death in men and women. Prostate is the most
common in men, but mortality is higher for lung. Breast is more common in
women, but mortality is higher for lung.
13% of new cancer diagnoses.
28% of all cancer deaths.
75
LUNG CANCER



THE SKINNY
More people die of lung cancer than from colon, breast and prostate combined.
80% of lung cancers are related causally to smoking.
Other factors: environmental (asbestos, radon gas), industrial (bis-chloromethyl
ether), metals (nickel, chromium, arsenic, iron oxide), second-hand cigarette
smoke.
76
LUNG CANCER
SURVIVAL



Mean age at Dx is 60.
40% survive 1 year.
Combined 5 year survival for all stages is 15%, up from 12% from 1974-1976.
77
LUNG CANCER






HISTOLOGIC TYPES
Squamous cell carcinoma- 25-35%- arise from the bronchial epithelium, are
endobronchial.
Adenocarcinoma- 35-40%- arise from mucous glands, appear as a peripheral
nodule/mass.
Large cell carcinoma- 5-10%.
Small cell carcinoma- 15-20%.
For staging, separated into small cell lung cancer (SCLC) and non-small cell lung
cancer (NSCLC).
SCLC spreads earlier, more aggressive and if untreated median survival is 6-18
weeks.
78
LUNG CANCER


CLINICAL FINDINGS
Symptomatic in 75-90% at time of Dx.
Presentation depends on the type and location of the primary tumor, the extent of
local spread, and presence of distant metastases and any paraneoplastic
syndromes.
79
LUNG CANCER






SIGNS / SYMPTOMS
Anorexia, weight loss, asthenia- 55-90%.
New cough or change in a chronic cough- 60%.
Hemoptysis- 6-31%.
Pain- non-specific vs pain from bony metastases- ribs, vertebrae, pelvis- 25-40%.
Brain mets- 10%- headache, N/V, new-onset seizure, altered mental status.
Pleural effusion- 12-33%.
80
LUNG CANCER





SIGNS / SYMPTOMS
Bronchial obstruction- “post-obstructive” pneumonia.
Change in voice- involvement of the recurrent laryngeal nerve.
Superior vena cava syndrome.
Horner’s Syndrome- ptosis, miosis, anhydrosis- from involvement of the
paravertebral sympathetic chain or inferior cervical ganglia.
Liver mets- asthenia, weight loss.
81
LUNG CANCER




PARANEOPLASTIC SYNDROMES
SIADH, ACTH, PTH, COUPLE OTHERS
10-20% of lung cancer patients.
May be the presenting feature leading to the Dx, and may be a bigger source of
morbidity than the malignancy itself.
Symptoms of these syndromes can be addressed and improved w/ treatment even
in cancers “not curable.”
82
LUNG CANCER





LAB
Dx made on the basis of cytology or histology.
Cytology is sensitive but low-yield.
Thoracentesis of a malignant effusion.
Fine-needle aspiration of an abnormal node- supraclavicular, cervical.
Bronchoscopy- see text. Can visualize the bronchi and aspirate, biopsy, wash and
do all kinds of cool sampling of all kinds of stuff not limited to the bronchi. Also
mediastinoscopy, thoracotomy.
83
LUNG CANCER
IMAGING



CXR, CT.
Identify abnormalities in nearly all cases.
Dx still requires cells (cytology) or tissue (histology).
84
LUNG CANCER
STAGING

See text, Table 9-15.


TREATMENT (THE SHORT VERSION)
Curable only w/ surgical resection- Stages I & II.
Other stages (III, IV) - chemo & radiation- but even this only gives an increase in
median survival of from 5 months to 7 months.
85
SARCOIDOSIS




“A systemic disease of unknown etiology characterized in about 90% of patients by
granulomatous inflammation of the lung.”
Can also involve peripheral nerves, heart, liver, kidney, other tissues.
North American blacks (women more than men) and northern European whites.
Onset in 3rd or 4th decade.
86
SARCOIDOSIS





SIGNS / SYMPTOMS
Malaise, fever, dyspnea of insidious onset.
Other Sxs based on other organ system involvement.
Some are asymptomatic and diagnosed only after an abnormal CXR.
Physical findings in the lung often absent- no crackles as you might expect.
Other organ system involvement can lead to: lymphadenopathy,
hepatosplenomegaly, erythema nodosum, parotid gland enlargement.
87
SARCOIDOSIS






LAB
Dx requires biopsy, finding of granuloma formation.
Lab may show:
Leukopenia, elevated sed rate (ESR).
Hypercalcemia, hypercalciuria.
Elevated levels of angiotensin converting enzyme.
PFT’s can show an obstructive defect but more commonly a restrictive defect.
88
SARCOIDOSIS
IMAGING




Variable.
Bilateral hilar adenopathy.
Parenchymal involvement.
Alone or combined.
89
SARCOIDOSIS






TREATMENT
Oral corticosteroids for patients with:
Disabling constitutional symptoms.
Hypercalcemia, CNS or cardiac involvement.
Granulomatous hepatitis.
Progressive pulmonary lesions.
Months to years.
90
SARCOIDOSIS




PROGNOSIS
Prognosis worse for patients w/ pulmonary parenchymal involvement. Best for
patients with hilar adenopathy only.
Can progress to pulmonary fibrosis, cavitation, bronchiectasis.
Death from pulmonary insufficiency in 5%.
See text re cardiac involvement.
91
PULMONARY EMBOLISM
 AKA pulmonary venous thromboembolism
 200, 000 deaths per year in the U.S, although later in the chapter it says

50,000.
3rd leading cause of death in hospitalized patients.
92
PULMONARY EMBOLISM
 REVIEW: risk factors, Virchow’s Triad (venous stasis, hypercoagulability,


endothelial damage)
REVIEW: things that embolize: air, fat, amniotic fluid, foreign bodies,
tumor cells, septic emboli.
The most common thing that embolizes is a thrombus, usually formed in
the deep venous circulation (popliteal v, ileofemoral v), but can arise from
anywhere in the venous circulation or the heart.
93
PULMONARY EMBOLISM
SIGNS / SYMPTOMS





Dx is difficult, for 2 reasons:
1) Sxs depend on the size of the embolus and the patients preexisting
cardiopulmonary status.
2) Common signs and symptoms of a PE are not specific to this disorder.
No Sx or combination of Sxs is specific to PE.
Must maintain a high index of suspicion.
94
PULMONARY EMBOLISM
SIGNS / SYMPTOMS





Dyspnea-75-85%.
Pain on inspiration- 65-75%.
Tachypnea- >50%.
In one study, 97% of patients had one or more of 3 findings: dyspnea, chest pain,
tachypnea.
Physical findings- none are diagnostic, and Sxs alone should be enough to consider
the Dx of PE regardless of physical findings.
95
PULMONARY EMBOLISM




LAB
EKG- abnormal in 70%. Right ventricular strain, right bundle branch block. Done
also to R/O MI, pericarditis. See text.
ABG- acute respiratory alkalosis; arterial pO2 low; BUT ABG’s alone are not
diagnostic.
See text for “d-Dimers” etc.
“Profound hypoxia w/ a normal CXR in the absence of preexisting lung disease is
highly suspicious for PE.”
96
PULMONARY EMBOLISM
IMAGING





1) CXR.
2) LUNG SCANS.
3) CT.
4) VENOUS THROMBOSIS STUDIES.
5) PULMONARY ANGIOGRAPHY.
97
PULMONARY EMBOLISM






IMAGING
1) CXR.
Done to R/O other common lung disorders that may explain the patients
symptoms.
Does not establish the Dx of PE.
In a PE the CXR will show: atelectasis, parenchymal infiltrates, pleural effusion.
Most helpful when normal.
After the CXR, if another Dx is not found, we move to the V/Q scan.
98
PULMONARY EMBOLISM





IMAGING
2) LUNG SCANS
The ventilation-perfusion or V/Q scan.
Actually it’s 2 scans:
1) The ventilation scan- inhalation of radioactive gas and the distribution of that
material is determined via the scan.
2) The perfusion scan- microaggregated albumin tagged w/ a radioisotope is given
IV, they lodge in the pulmonary circulation, and their distribution is measured via
the scan.
99
PULMONARY EMBOLISM
IMAGING




2) LUNG SCANS
A negative scan is one in which ventilation (as measured by the radionuclide scan)
is uniform, and perfusion is uniform as well. They “match.”
In a PE, there is normal ventilation, but the embolus impairs perfusion in the
segment affected by the PE, so there is a “mis-match.”
The result ain’t that simple, though; what we get is a low, intermediate, or high
probability of a PE.
100
PULMONARY EMBOLISM
IMAGING




2) LUNG SCANS
A negative scan is good, a high-probability scan is good.
For the low and intermediate probability scan, the next step may be pulmonary
angiography.
See text for whom we may and may not subject to angiography. Algorithms pg 289.
Look at this. Really.
101
PULMONARY EMBOLISM
IMAGING




3) CT
See your text.
The “Helical” or “Spiral” CT may be on its way to replacing the V/Q scan as the
imaging modality of 1st choice, but we’re not there yet.
Detects the actual thrombus.
102
PULMONARY EMBOLISM





IMAGING
4) TEST FOR VENOUS THROMBOSIS
Since 70% of patients with PE will have DVT, it would follow that if we could
document DVT in a patient w/ suspected PE but a non-diagnostic V/Q scan, we
could proceed w/ anticoagulation therapy and avoid angiography.
Various studies: venous ultrasonography (the procedure of choice), doppler
studies, venography.
Sensitivity not nearly as good as pulmonary angiography.
The d-Dimer test may become the test of choice to make this Dx due ti it’s high
sensitivity.
103
PULMONARY EMBOLISM
IMAGING
 5) ANGIOGRAPHY
 Catheterization of the pulmonary arteries w/ injection of dye.
 The gold standard for diagnosis. ie, has the highest sensitivity and specificity of any


current test.
Is “safe,” but invasive, and not without risk of complications, death.
See text for a few other thoughts re angiography.

See text for use of MRI. Right now it’s a research tool.
104
PULMONARY EMBOLISM
IMAGING
 5) ANGIOGRAPHY
 When to use: consider: 1) degree of clinical suspicion for PE, 2) results of V/Q scan, and
3) results of venous ultrasound.

See Figure 9-3 for algorithms re how to proceed in establishing the diagnosis.
These algorithms speak to how difficult it can be to establish the Dx while trying to
do so in a non-invasive manner and without subjecting everyone to angiography.
105
PULMONARY EMBOLISM





PREVENTION
Since we know the risk factors and the clinical scenarios in which PE happens, it
gives us the opportunity to target prevention.
It is still underutilized- your text says about 50% of fatal PE’s receive any preventive
therapy.
Anticoagulation- “mini-dose” heparin, various types.
IPC devices, elastic / compression stockings.
Early ambulation post-op.
106
PULMONARY EMBOLISM
TREATMENT



1) ANTICOAGULATION.
2) THROMBOLYTIC THERAPY.
3) OTHER.
107
PULMONARY EMBOLISM
TREATMENT




1) ANTICOAGULATION.
“Secondary therapy” in the sense that it stops further clot formation and allows
for fibrinolysis to lyse the existing clot.
IV heparin acutely followed by 3-6 months of anticoagulation with coumadin /
warfarin.
Reduces the risk of both recurrent venous thrombosis and death from PE by 8090%.
108
PULMONARY EMBOLISM
TREATMENT



1) ANTICOAGULATION.
HEPARIN- binds to and accelerates the activity of anti-thrombin III, which
inactivates thrombin, factor Xa, and factor IXa.
WARFARIN- effects synthesis of the Vitamin K dependent clotting factors. Many
many drug interactions effecting serum levels resulting in under or over
anticoagulation, resulting in hemorrhage which can be fatal (intracanial).
109
PULMONARY EMBOLISM



TREATMENT
1) ANTICOAGULATION.
Duration of treatment w/ warfarin may need to be longer than 6 months, possibly
for life, in patients who have non-reversible risk factors for future clot
development such as The Factor V (Leiden) mutation, Protein S or Protein C
deficiency, or antiphospholipid syndrome, as compared to patients w/ a transient
risk factor such as pelvic or orthopedic surgery.
For these patients, need to juggle the benefits of continued treatment vs. the risk
of hemorrhage.
110
PULMONARY EMBOLISM
TREATMENT





2) THROMBOLYTIC THERAPY
W/ streptokinase, urokinase, and TPA.
No benefit for most patients.
Significant risk of hemorrhage
Reserved for patients at high risk of death in whom a more rapid resolution of the
clot may be lifesaving. These patients are hemodynamically unstable and sick sick
sick.
111
PULMONARY EMBOLISM
TREATMENT



3) OTHER
Placement of an inferior vena cava filter- a “basket”- for patients: a) with
contraindications to anticoagulation, b) who continue to flip emboli despite
anticoagulation, and c) chronic/recurring emboli.
Surgical embolectomy- procedure of last resort in patients who are critically ill and
getting worse. Carries a high mortality rate.
112
PULMONARY EMBOLISM




PROGNOSIS
50,000 or 200,000 deaths per year, depending on which of these numbers you
want to believe. Either way, it’s a bunch.
In most deaths, the PE is not recognized ante mortem or death occurs prior to
initiation of specific therapy.
As such, need to target prevention.
Outlook for the survivors is good, and depends more on the underlying disease
process (Factor V mutation, etc) rather than the clot itself.
113
SLEEP APNEA






See your text. Pg 310.
Central vs obstructive sleep apnea.
Obstructive way more common.
Association w/ obesity. Other causes: nasal polyps, deviated septum,
congenital/traumatic defects.
Association w/: hypertension, cardiac disease, sudden death. Also
fatigue, cognitive defects, etc
Lack of time spent in REM/Stage IV/ Delta wave sleep and its associated
problems.
114
SLEEP APNEA






Diagnosis: the “somnogram.” EEG combined w/ measurements of O2, CO2, O2 sat.
,etc. Documentation of apneic episodes.
TREATMENT
Address the underlying problem.
Weight loss (you can at least try).
CPAP.
Surgical correction if the polyps, septum, etc.
Aggressive treatment is warranted due to the association between cardiovascular
disease, sudden death.
115