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100
90
75
Saturation
(mL/100 mL
50
50
2
2
26 40 60 140 50
pCO2 (mm Hg)
pO2 (mm Hg)
Clinical Pearl
Bohr Effect is a shift in the O 2 -Hb curve to the right due to an increase in
H+ , pCO 2 , temperature, or 2,3-diphosphoglycerate. This shift facilitates O 2
unloading in peripheral capillaries.
Due to the sigmoid shape of the O 2 -hb curve, an O 2 saturation of <90%
corresponds to a very low pO 2 of < 60 mm Hg.
Nonpleuritic Pleuritic
Pulmonary Pulmonary
Table 3. Differential Diagnosis of neoplastic pneumothorax
Hemoptysis pneumonia hemothorax
PE PE
Airway disease Cardiac pneumonia
acute or chronic bronchitis MI bronchiectasis
bronchiectasis ischemia neoplasm
bronchogenic CA myocarditis/pericarditis TB
bronchial carcinoid tumour Esophageal empyema
spasm Cardiac
Parenchymal disease esophagitis pericarditis
TB ulceration Dressler’s syndrome
lung abscess achalasia GI
pneumonia neoplasm pancreatitis
miscellaneous Mediastinal MSK
Goodpasture’s syndrome Iymphoma costochondritis
idiopathic pulmonary hemosiderosis thymoma fractured rib
Subdiaphragmatic myositis
Vascular disease PUD herpes zoster
PE gastritis
elevated pulmonary venous pressure biliary colic
LV pancreatic
mitral stenosis
F Vascular
vascular malformation dissecting aortic aneurysm
MSK
Miscellaneous costochondritis
impaired coagulation skin
pulmonary endometriosis breast
ribs
Reproduced with permission SE Weinberger, Principles of Pulmonary Medicine , 2nd edition, 1992
Clinical Pearl
Central cyanosis is not detectable until the SaO 2 is < 85%.
It is also marked in polycythemia and less readily detectable in anemia.
Pulmonary Cardiac
CF Cyanotic congenital heart disease
Pulmonary fibrosis Infective endocarditis
Chronic pus in the lung
(bronchiectasis, abscess, Mediastinal
infections, etc.) Esophageal CA
Lung CA (primary or mets) Thymoma
Mesothelioma Achalasia
A-V fistula
Other
Gastrointestinal Graves’ disease
IBD Thalassemia
Chronic infections Other malignancies
Laxative abuse Primary hypertrophic osteoarthropathy
Polyposis
Malignant tumours
Cirrhosis
HCC
FLOW RATE
(L/sec)
LUNG VOLUME
(L)
Figure 4. Expiratory Flow Volume Curves
Obstructive Lung Disease
characterized by obstructed airflow, decreased flow rates (most marked during expiration),
air trapping (increased RV/TLC), and hyperinflation (increased FRC, TLC)
DDx includes asthma, COPD, CF, bronchiectasis
Restrictive Lung Disease
characterized by decreased lung compliance and lung volumes
DDx includes interstitial lung, neuromuscular, or chest wall disease
Obstructive Restrictive
Flow FEV1 9 9 or N
Rates FVC 9 9
(i.e. Lung FEV1 /FV 9 8 or N
Mechanics) C =MMFR
FEF25-75 9 8 or N
TLC 8 or N 9
Lung FRC 8 or N 9
Volumes VC 9 or N 9
R 88 9
RV/TL
V 8 N
C
Diffusing Dco 9 or N 9 or N
Capacity
FEV1 /FVC > 80% predicted FEV1 /FVC < 80% predicted FEV1 /FVC normal
Non Obstructive Defect Airflow Obstruction
Normal Low
CHRONIC EMPHYSEMA
BRONCHITIS
Decreased Decreased
TLC and FRC TLC and FRC
+ increased RV + normal RV
Clinical Pearl
Dco decreases with: 1) decreased surface area, 2) decreased hemoglobin,
3) interstitial lung disease, and 4) pulmonary vascular disease.
Respiratory Acidosis
Acute 10 1
Chronic 10 3
Respiratory Alkalosis
Acute 10 2
Chronic 10 5
Metabolic Acidosis 1 1
Metabolic Alkalosis 3 10
4. If there is metabolic acidosis, what is the anion gap and osmolar gap? (see Nephrology Chapter)
• anion gap = [Na + ]–([C1– ]+[ HCO3– ]); normal = 10-15 mmol/L
• osmolar gap = measured osmolarity – calculated osmolarity
= measured – (2[Na + ] + glucose + urea); normal = 10
Differential Diagnosis of Respiratory Acidosis
characterized by increased PaCO 2 secondary to hypoventilation
respiratory centre depression
• drugs (anesthesia, sedatives)
• trauma
• increased ICP
• post-encephalitis
• stroke
• sleep-disordered breathing (sleep apnea, obesity)
• supplemental O 2 in chronic CO2 retainers (i.e. COPD)
neuromuscular disorders
• myasthenia gravis
• Guillain-Barré syndrome
• poliomyelitis
• muscular dystrophies
• myopathies
• chest wall disease (obesity, kyphoscoliosis)
airway obstruction (asthma, foreign body)
parenchymal disease
• COPD
• pulmonary edema
• pneumothorax
• pneumonia
• pneumoconiosis
• ARDS
mechanical hypoventilation
Differential Diagnosis of Respiratory Alkalosis
characterized by decreased PaCO 2 secondary to hyperventilation
hypoxemia
• pulmonary disease (pneumonia, edema, PE, interstitial fibrosis)
• anemia
• heart failure
• high altitude
respiratory centre stimulation
• CNS disorders
• hepatic failure
• gram-negative sepsis
• drugs (ASA, progesterone, theophylline, catecholamines, psychotropics)
• pregnancy
• anxiety
• pain
mechanical hyperventilation
PaO2 < 95 mm Hg
increased A-a gradient (> 15 mm Hg) normal A-a gradient (< 10-15 mm Hg)
• decreased diffusion capacity
• interstitial lung disease
• emphysema increased PaCO 2 normal PaCO2
• hypoventilation • low FiO 2
(e.g. high altitude)
give 100% O2
Clinical Pearl
asthma triad: asthma, ASA/NSAID sensitivity, nasal polyps.
triggers
• URTIs
• allergens (pet dander, house dusts, molds)
• irritants (cigarette smoke, air pollution)
• drugs (NSAIDs, ß-blockers)
• preservatives (sulphites, MSG)
• non-specific (emotion/anxiety, cold air, exercise, GERD)
• often no identifiable trigger
Pathophysiology
acute asthma: airway obstruction ––> V/Q mismatch ––> hypoxemia
––> 8ventilation ––> 9 PaCO2/8 pH AND fatigue ––> 9 ventilation 8 PaCO2/9 pH
Symptoms
SOB, wheezing, cough (especially nocturnal), chest tightness
R10 – Respirology MCCQE 2006 Review Notes
DISEASES OF AIRWAY OBSTRUCTION
. . . CONT.
Signs
tachypnea
wheezing
respiratory distress
• nasal flare, accessory muscle use, tracheal tug, intercostal muscle indrawing,
pulsus paradoxus, inability to speak (indicates severe asthma)
Red flags
• fatigue, cyanosis, silent chest, diminished respiratory effort, decreased LOC
Profile of Patients at Risk for Severe Asthma
previous non-fatal episodes
• loss of consciousness during asthma attack
• frequent ER visits
• prior intubation
• ICU admission
ominous symptoms and signs
• night-time symptoms
• limited activities of daily living
• use of ß2-agonist > 3 times per day
• FEV 1 or PEF < 60%
Clinical Pearl
The best predictor of a potential life-threatening attack
is an excess consumption of short-acting ß 2 -agonists.
Investigations
O2 saturation
ABGs
• decreased PaO 2 during attack (V/Q mismatch)
• decreased PaCO 2 in mild asthma due to hyperventilation
• normal or increased PaCO 2 ominous as patient is no longer able to hyperventilate
(worsened airway obstruction or respiratory muscle fatigue)
PFTs (may not be possible during severe attack)
• spirometry: increase in FEV 1 > 12% with B2 -agonist, or > 20% with
10-14 days of steroids, or > 20% spontaneous variability
• peak expiratory flows: > 20% PEF diurnal variability (not as reliable, but can be done at home)
• provocation testing: decrease in FEV 1 > 20% with methacholine challenge
Treatment
3 components of treatment
• environmental control: address relevant triggers
• patient education: features of the disease, goals of treatment, self-monitoring
• pharmacological therapy:
• “relievers”provide short-term relief (short-acting ß2-agonist, anticholinergic)
• “controllers”provide long-term prevention (inhaled/oral corticosteroids, anti-allergic agent,
long-acting ß2-agonist, methylxanthine, leukotriene antagonists (LRA))
Category Drug
medication plan
• mild asthma (infrequent symptoms, normal PEFs)
• inhaled short-acting ß2-agonist PRN
• low-dose inhaled steroid
• moderate asthma (short-acting ß 2 -agonist needed > 3x/wk, or abnormal lung function)
• add high-dose inhaled steroid (and discontinue low-dose inhaled steroid)
• +/– add additional therapy (LRA, anti-allergic agent, long-acting ß 2 -agonist, theophylline,
anticholinergic)
• severe asthma (frequent symptoms, PEFs < 60% of predicted value,
unable to perform daily activities)
• add oral steroid (and discontinue high-dose inhaled steroid)
• continue with bronchodilators
Clinical Pearl
Remember to step-down therapy to lowest doses which
control symptoms/signs of bronchoconstriction.
management of life-threatening episode
• supportive therapy: sit up, O 2 by mask, cardiac monitoring, oximetry, IV fluids
• continuous ß 2 -agonist and anticholinergics given by wet nebulizer or
meter dose inhaler (+/– epinephrine IM/IV if unresponsive)
• methylprednisolone 125 mg IV in ER, 1-2 mg/kg/day in divided doses
• intubation if decreasing LOC, exhaustion, cyanosis, acidemia, silent chest
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
characterized by progressive development of airflow limitation that is irreversible/minimally reversible
includes chronic bronchitis and emphysema; usually coexist to variable degrees in most patients
five pathophysiological processes associated with COPD
1. Inflammatory narrowing of respiratory and membranous bronchioles
2. Proteolytic digestion of connective tissue framework of the lung
resulting in decreased parenchymal tethering of airways
3. Loss of alveolar surface area and capillary bed
4. Lung hyperinflation caused by loss of lung elastic recoil
5. Increased pulmonary vascular resistance caused by vasoconstriction
and loss of capillary bed
Risk Factors
smoking is the most important risk factor.
minor risk factors include:
• environmental factors: air pollution, occupational exposure, IV drug abuse or talcosis
• treatable factors: low BMI, 〈 -1-antitrypsin deficiency, bronchial hyperactivity
• demographic factors: age, family history, male sex, history of
childhood respiratory infections and socioeconomic status
Emphysema
pathologic definition: dilatation and destruction of air spaces distal to the
terminal bronchiole without obvious fibrosis
decreased elastic recoil of lung parenchyma causes decreased expiratory
driving pressure, airway collapse, and air trapping
2 types
• centriacinar (respiratory bronchioles predominantly affected)
• typical form seen in smokers
• primarily affects upper lung zones
• panacinar (respiratory bronchioles, alveolar ducts, and alveolar sacs affected)
• responsible for less than 1% of emphysema cases
• primarily affects lower lobes
• think of 〈 -1-antitrypsin deficiency (normal (MM), heterozygote (MZ), homozygote (ZZ))
• ZZ can develop emphysema in their thirties, especially smokers
clinical presentation (see table 11)
investigations (see table 12)
Chronic Bronchitis
clinical diagnosis
definition: chronic cough and sputum production on most days for at least
3 consecutive months in 2 successive years
obstruction due to narrowing of the airway lumen by mucosal thickening and excess mucus
usually due to smoking but air pollution increasingly important
exacerbations due to respiratory tract infections (typically viral), air
pollution, bronchospasm, mucus plugging, and CHF
some have features of asthma and chronic bronchitis (asthmatic bronchitis)
Treatment of COPD
Non Pharmacological
patient education: enables patients to take control of their disease and improves compliance
smoking cessation: decreases rate of decline of FEV 1 , reduce cough and sputum
eliminate respiratory irritants/allergens (occupational/environmental)
exercise rehabilitation to improve physical endurance
nutrition: poor nutrition is associated with increased mortality
intermittent mechanical ventilation to relieve dyspnea and rest respiratory muscles
CPAP is used as an adjunct to weaning patients from mechanical ventilation
and minimize dyspnea during exercise
Pharmacological Treatment
vaccination with pneumovax and yearly H. influenza
bronchodilators: mainstay of current drug therapy increase airflow and reduce dyspnea
• anticholinergics eg. ipratropium bromide
• inhaled, injected or taken orally
• more effective than ß2-agonists with fewer side effects.
• slow onset of action take daily rather than on a PRN basis.
• inhaled ß2-agonist eg. salbutamol and albuterol, salmeterol
• inhaled, injected or taken orally
• rapid onset of action
• significant side effects such as hypokalemia when used at high doses
Etiology
obstruction
• tumours
• foreign bodies
• thick mucus
post-infection (results in dilatation of bronchial walls)
• TB
• measles
• pertussis
• pneumonia
• allergic bronchopulmonary aspergillosis
impaired defences (leads to interference of drainage, chronic infections, and inflammation)
• hypogammaglobulinemia
• CF
• defective leukocyte function
• ciliary dysfunction (Kartagener's syndrome: bronchiectasis, sinusitis, situs inversus)
Clinical Presentation
chronic cough
purulent sputum (but 10-20% have a dry cough)
hemoptysis (can be massive)
recurrent pneumonia
clubbing
local crackles (inspiratory and expiratory)
wheezes
Diagnosis
PFTs
• often demonstrate obstructive pattern but may be normal
CXR(Colour Atlas R2)
• nonspecific: increased markings, linear atelectasis
• specific: "tram tracking" - parallel narrow lines radiating from hilum
high-resolution thoracic CT (diagnostic)
• “signet ring” : dilated bronchi with thickened walls, diameter bronchus > diameter of
accompanying vessel
Treatment
vaccination: influenza and Pneumovax
antibiotics (oral, IV, inhaled)
bronchodilators
steroids
postural drainage/physiotherapy
surgical excision: for localized disease refractory to medical treatment
CYSTIC FIBROSIS (CF)- see Pediatrics Chapter
C1 transport dysfunction: thick secretions from exocrine glands
–
(lung, pancreas, skin, gonads) and blockage of secretory ducts
results in severe lung disease, pancreatic insufficiency and azoospermia
presents in childhood with recurrent lung infections that become persistent and chronic
(see Pediatrics Chapter)
chronic lung infections
• S. Aureus: early
• P. aeruginosa : most common
• B. cepacia: worse prognosis but less common
• aspergillosis
Investigations
sweat chloride test
• increased concentrations of sodium, chloride, and potassium > 60 mmol/L is diagnostic in children
• heterozygotes have normal sweat tests (and no symptoms)
PFTs
• characteristic of obstructive airway disease
• early: only small airways will be affected
• later: characteristics of obstructive disease with airflow limitation, hyperinflation, decreased Dco
ABGs
• hypoxemia, hypercapnia later in disease with eventual respiratory failure and cor pulmonale
CXR
• hyperinflation, increased pulmonary markings, bronchiectasis
Treatment
• chest physio and postural drainage
• bronchodilators (ventolin +/– atrovent)
• inhaled DNase (reduces mucus viscosity)
• antibiotics (e.g. ciprofloxacin)
• lung transplant
Prognosis
median survival age is 31 years for males and 30.5 for females
death usually due to lung disease (pneumonia, respiratory failure, cor pulmonale)
MCCQE 2006 Review Notes Respirology – R15
INTERSTITIAL LUNG DISEASE
Pathophysiology
inflammatory process in the alveolar walls ––> thickening and destruction
of pulmonary vessels and fibrosis of interstitium leading to
• decreased lung compliance
• decreased lung volumes
• impaired diffusion
• hypoxemia without hypercarbia (V/Q mismatch) due to vasoconstriction and fibrosis
• pulmonary HTN and subsequent cor pulmonale secondary to hypoxemia and blood vessel destruction
Causes of interstitial lung disease
65% due to unknown agents
Table 13. Causes of Interstitial Lung Disease
Upper Lung Disease Lower Lung Disease
Clinical Presentation
SOB, especially on exertion with decreasing SaO 2
dry crackles
+/– dry cough
clubbing
features of cor pulmonale
Investigations
CXR(see Colour Atlas R1)
• decreased lung volumes, reticulonodular pattern (nodular (< 3 mm),
Kerley B lines, hilar/mediastinal adenopathy, lytic bone lesions
• DDx: pulmonary fibrosis, pulmonary edema (CHF), PCP, TB (miliary),
sarcoidosis, pneumoconiosis, lymphangitic carcinomatosis
• DDx of cystic lesions: end-stage emphysema, PCP, histiocytosis X, Lymphangiomyomatosis
PFTs
• restrictive pattern (decreased lung volumes and compliance)
• normal FEV 1 /FVC (> 70-80%)
• FEF25-75 may be decreased due to lower lung volumes
• flow rates are actually normal or supernormal when corrected for absolute lung volume
• Dco decreased due to less surface area for gas exchange
ABGs
• hypoxemia and normal or decreased PaCO 2
Clinical Pearl
The CXR can be normal in up to 15% of patients with interstitial lung disease.
Clinical Pearl
Sarcoid is silent on auscultation.
as fibrosis occurs, CXR shows reticulonodular pattern especially in upper zones
common extrapulmonary manifestations
• cardiac
• eye involvement (anterior uveitis)
• skin involvement (skin papules, erythema nodosum)
• peripheral lymphadenopathy
• hepatosplenomegaly
• arthralgia
less common extra-pulmonary manifestations involve bone, heart, CNS and kidney
2 sarcoid syndromes
• Lofgren’s syndrome = erythema nodosum, bilateral hilar lymphadenopathy, fever, and arthralgias
• Heerfordt-Waldenstrom syndrome: fever, parotid enlargment, anterior uveitis, facial nerve palsy
Laboratory Abnormalities
hypercalcemia, hypercalciuria in 10% (hypercalcimia more common)
lymphopenia (decreased T cells)
increased ESR
hypergammaglobulinemia
elevated ACE
Diagnosis
biopsy
• transbronchial or mediastinoscopic biopsy of lymph node for granulomas
• in ~75% of cases transbronchial biopsy shows granulomas in the parenchyma even if the CXR is normal
Staging
radiographic, based on CXR
• Stage 0: no CXR changes
• Stage I: bilateral hilar lymphadenopathy
• Stage II: bilateral hilar lymphadenopathy and diffuse interstitial disease
• Stage III: interstitial disease only (reticulonodular pattern)
• Stage IV: pulmonary fibrosis (honeycombing)
Treatment
85% of stage I resolve spontaneously
50% of stage II resolve spontaneously
steroids for persistent pulmonary infiltrates, PFT abnormalities,
hypercalcemia, or involvement of eye, CNS, kidney, or heart
Prognosis
approximately 10% mortality secondary to progressive fibrosis of lung parenchyma
Langerhans-cell Histiocytosis
aka eosinophilic granuloma, histiocytosis X
clonal proliferation of dendritic cells
cells have X-bodies on EM
typically affects young-middle aged smokers
presentation: dyspnea, cough or both
• spontaneous pneumothorax
Clinical Pearl
The CXR in chronic eosinophilic pneumonia shows a peripheral alveolar
infiltrate referred to as the “photographic negative of pulmonary edema”
(pattern is often migratory).
PNEUMOCONIOSES
reaction to inhaled inorganic dusts 0.5-5 mm in size
no effective treatment, therefore key is exposure prevention through the use of protective equipment
Asbestosis
workers at risk: insulation, shipyard, construction, brake linings
usually need > 10-20 years of exposure; may develop with shorter but heavier exposure
CXR
• rounded melectasis
• lower > upper lobe
• early: fibrosis with linear streaking
• later: cysts and honeycombing
• asbestos exposure can also cause pleural thickening (+/– calcification) or pleural effusion
microscopic examination characteristically reveals ferruginous bodies: yellow-brown rod-shaped structures
which represent asbestos fibres coated in macrophages
asbestos exposure also increases risk of bronchogenic CA and malignant mesothelioma
• risk dramatically increased for smokers
clubbing is much more likely in asbestosis than silicosis or coal worker's pneumoconiosis
treatment: prevention of disease progression and development of complications
reduce silica exposure
CXR: may be normal but alveolar infiltrates may be seen if hemorrhage is profuse
treatment
• acutely: corticosteroids; plasmapheresis to remove anti-GBM antibodies
• immunosuppressive therapy (corticosteroids, cyclophosphamide)
to decrease anti-GBM antibody production
• severe/unresponsive cases: bilateral nephrectomy
Systemic Lupus Erythematosus (SLE)
lungs and/or pleura are involved in > 50% of patients
classical findings
• pleural effusion (common)
• pulmonary vasculitis
• diffuse interstitial lung disease (relatively uncommon)
• acute lupus pneumonitis and pulmonary hemorrhage
• diaphragmatic weakness (“shrinking lung syndrome”)
• PE (due to lupus anticoagulant)
Rheumatoid Arthritis (RA)
classical findings
• pulmonary rheumatoid nodules (Caplan’s syndrome CWP and RA)
• pleural effusions
• diffuse interstitial lung disease (rare)
• pulmonary vasculitis
• cryptogenic organizing pneumonia
• bronchiolitis obliterans
Scleroderma
technically not a vasculitis since vessel wall changes are due to fibrosis without actual inflammation
scleroderma most often affects the lungs and can cause severe interstitial fibrosis and/or pulmonary HTN
may also have lung disease secondary to recurrent aspiration if esophageal dysfunction is present
pleural disease uncommon
may have increased incidence of lung cancer
may also cause an isolated PHTN (usually CREST)
Clinical Pearl
Scleroderma is the most common collagen vascular disease to affect the lung.
PULMONARY HYPERTENSION
pulmonary artery pressure is > 30 with exercise mean > 25 mm Hg
Primary Pulmonary Hypertension
idiopathic change in arterial walls
commonly complain of dyspnea, fatigue, syncope, chest pain
• disease of young women (20-40 years)
• positive serology (ANA) > 30%
• patients frequently have Raynaud's syndrome
• treatment: vasodilators (i.e. prostacyclin PGI2), long term anticoagulation, transplantation
• prognosis: poor, with 2-3 year mean survival from time of diagnosis
• may be associated with the use of anorexic drugs (e.g. aminorex, fenfluramine)
Secondary Causes of Pulmonary Hypertension
Cardiac Disease (Passive)
increased LAP (e.g. chronic LVF, mitral stenosis)
increased pulmonary vascular flow
• as with a L —> R shunt (ASD, VSD, PDA)
• as right sided pressure increases due to increased flow, pressure
eventually becomes greater than left sided pressure resulting in a
R —> L shunt and cyanosis (irreversible Eisenmenger's complex)
Pulmonary Vasoconstriction (Reactive)
primary response to hypoxia but also to acidosis from hypercapnia (i.e. with chronic lung disease)
note: chronic hypoxia also causes polycythemia which will increase viscosity and increase pulmonary
arterial pressure
Loss of Pulmonary Vessels (Destructive)
loss of vascular bed surface area as with interstitial lung disease/pulmonary fibrosis, emphysema,
scleroderma, pneumonectomy, multiple lobectomies, bronchiectasis, CF
pulmonary arterial pressure may be normal at rest but increased with
exercise due to insufficient recruitment/distention of vessels
STEP 1.
NO
NO IV Heparin
NO
YES NO
STEP 3.
Can the risk be reduced for future PE? alleviate RF, TED stockings, antithrombotic treatment
EMPYEMA
definition: grossly purulent pleural effusion
etiology: contiguous spread from lung infection (most commonly
anaerobes), infection through chest wall (e.g. trauma, surgery)
symptoms: fever, pleuritic chest pain
investigations: pleurocentesis
• PMNs (lymphocytes in TB), +/– visible organisms on Gram stain
treatment
• antibiotics, chest tube drainage (if pH < 7.2), surgical drainage (if loculated)
PNEUMOTHORAX
definition: the presence of gas in the pleural space
pathophysiology: intrapleural pressure positive instead of negative, preventing lung inflation
etiology
• traumatic
• penetrating or nonpenetrating chest injuries
• iatrogenic (CVP line, thoracentesis, mechanical ventilation and 8 alveolar pressure)
• spontaneous (no history of trauma)
• primary (no underlying lung disease)
• spontaneous rupture of apical subpleural bleb of lung
at apex into pleural space
• predominantly healthy young tall males
• secondary (underlying lung disease)
• rupture of subpleural bleb (most common cause is COPD)
• necrosis of lung tissue adjacent to pleural surface
e.g. pneumonia, abscess, PCP, lung CA
symptoms
• can be asymptomatic
• acute onset pleuritic chest pain
• acute onset dyspnea
signs
• shift of trachea to opposite side
• ipsilateral diminished expansion
• decreased tactile/vocal fremitus
• hyperresonant percussion note
• ipsilateral diminished breath sounds
CXR(see Colour Atlas R8)
• small: separation of visceral and parietal pleura seen as fine
crescentic line parallel to chest wall at apex
• large: increased density and decreased volume of lung on side of pneumothorax
• see Diagnostic Medical Imaging Chapter
treatment
• small pneumothoraces resolve spontaneously
• large ones or those complicating underlying lung disease require
placement of a chest tube connected to underwater seal +/– suction
• for repeated episodes: pleurodesis with sclerosing agent or partial pneumectomy/bleb resection
Tension Pneumothorax
emergency! (see Emergency Medicine Chapter)
ASBESTOS-RELATED PLEURAL DISEASE
exudative pleural effusion
pleural thickening or calcification, pleural plaque (Hyalinosis Simplex)
mesothelioma
• primary malignancy of the pleura
• decades after even light asbestos exposure
• smoking is not a risk factor
signs and symptoms: persistent chest pain, dyspnea, cough,
bloody pleural effusion, weight loss, clubbing
diagnosis:: biopsy (pleuroscopic or open)
treatment: resection (requires careful patient selection); however, rarely
successful (average survival < 1 year)
general investigations
• routine labs: determine prognosis and need for hospitalization
• ABGs: assess adequacy of gas exchange and ventilatory insufficiency
in more severe cases, oxygen saturation is sufficient in most
• sputum culture and Gram stain, blood cultures, pleural fluid
cultures, serology/viral cultures (epidemiology)
• CXR (see Colour Atlas R10)
• shows distribution, extent of infiltrate +/– cavitation
• bronchoscopy +/– washings for severely ill patients unresponsive to
treatment and the immunocompromised
DDx
• acute bronchitis, effusion (can be due to pneumonia), PE, CA,
pulmonary edema, bronchiectasis, hypersensitivity pneumonitis,
BOOP, drug-induced pneumonitis, chronic eosinophilic pneumonia
criteria for hospitalization
• demographic factors: elderly, nursing home residents
• co-existing illness: neoplasm, CHF, cerebrovascular disease, chronic liver/renal disease
• physical examination:: altered mental status, tachypnea, tachycardia, hypotension,
extremes of temperature
• laboratory findings: hyponatremia, acidemia, hyperglycemia, hypoxemia, azotemia,
decreased hematocrit
• radiographic findings: pleural effusion
Clinical Pearl
Ghon Complex: CXR finding of a calcified nodule plus calcified hilar/mediastianal
lymphadenopathy, pathognomonic of previous primary infection by TB.
treatment
• INH and rifampin x 6 months with pyrazinamide x the first 2 months
• multiple drug resistant strains (MDR-TB): INH, rifampin,
pyrazinamide, and ethambutol, then modified with sensitivities
• if untreated, 50% will die within 5 years
• prophylaxis
• INH +/– vitamin B6 for 6-12 months for patients with skin test
conversion within the last two years
• with positive skin test: < 35 years old, abnormal CXR,
immunocompromised or predisposed to TB
• who are close contacts of someone with active TB
• HIV contact of infected person
• rifampin for contacts of INH-resistant TB carriers
• the risk of developing TB in immunocompetent patients after skin test conversion is 1% per year
for the first 5 years and 0.1% per year subsequently (10% lifelong risk)
Features Calcified pattern: central, “popcorn,” Usually not calcified; if calcified, pattern is eccentric or
calcified, pattern is eccentric or speckld; no satellite lesions; cavitation with thick wall may
diffuse, or concentric satellite lesions have pleural effusions, lymphadenopathy
usually no cavitation; If cavitated,
wall is smooth and thin no other
lung pathology
Doubling Time Doubles in < 1 month or > 2 years Doubles in > 1 month < 2 years
observe
cancer calcification no diagnosis
Clinical Pearl
2/3 of primary lung CA is found in the upper lung; 2/3 of metastases
in the lower lung (hematogenous spread secondary to increased
blood flow to the base of the lung).
Investigations
initial diagnosis
• imaging: CXR (see Colour Atlas R7) , CT
• cytology: sputum
• biopsy: bronchoscopy, percutaneous
staging work-up
• blood work: LETs/LFTs, calcium, ALP
• imaging: CXR, CT thorax and abdomen, skeletal survey, bone scan, neuroimaging
• invasive: bronchoscopy, mediastinoscopy, mediastinotomy, thoracotomy
SCLC NSCLC
REFERENCES
Bartlett JG, Dowell SF, Mandell LA et al. Practice Guidelines for the Management of Community-Acquired Pneumonia in Adults. Clin Infect Dis
2000;31:347-82.
Baumann MH. Treatment of spontaneous pneumothorax. Curr Opin Pulm Med . 2000 Jul;6(4):275-80. Review.
File TM. The epidemiology of respiratory tract infections. Semin Respir Infect 2000 Sep;15(3):184-94. Review.
Gotfried M, Freeman C. An update on community-acquired pneumonia in adults. Compr Ther 2000 Winter;26(4):283-93. Review.
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