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SIGNS OF RESPIRATORY DISEASE / General Examination 27
Further Reading
Atkinson S and Fox SB (2004) Vascular endothelial growth factor
(VEGF)-A and platelet-derived growth factor (PDGF) play a
central role in the pathogenesis of digital clubbing. Pathology
203(2): 721–728.
Augarten A, Goldman R, Laufer J, et al. (2002) Reversal of digital
clubbing after lung transplantation in cystic fibrosis patients: a
clue to the pathogenesis of clubbing. Pediatric Pulmonology 34:
378–380.
Brouwers AA, Vermeij-Keers C, van Zoelen EJ, and Gooren LJ
(2004) Clubbed fingers: the claws we lost? Medical Hypotheses
62: 321–324.
Dickinson CJ (1993) The aetiology of clubbing and hypertrophic
osteoarthropathy. European Journal of Clinical Investigation
23: 330–338.
Hippocrates (1849) The Book of Prognostics. In: Adams F (translator) The Genuine Works of Hippocrates. London: Sydenham
Society.
John B, Subhash H, and Thomas K (2004) Journal of the New
Zealand Medical Association, 117: 1192.
Martinez-Lavin M (1997) Hypertrophic osteoarthropathy. Current Opinion in Rheumatology 9(1): 83–86.
Martinez-Lavin M, Matucci-Cerinic M, Jajic I, and Pineda C
(1993) Hypertrophic osteoarthropathy: consensus on its definition, classification, assessment and diagnostic criteria. Journal of
Rheumatology 20(8): 1386–1387.
Menard H (2004) Hypertrophic osteoarthropathy.
Pineda C, Fonseca C, and Martinez-Lavin M (1990) The spectrum
of soft tissue and skeletal abnormalities of hypertrophic osteoarthropathy. Journal of Rheumatology 17: 626–632.
General Examination
T E King Jr, San Francisco General Hospital, San
Francisco, CA, USA
A C Zamora, Hospital Universitario ‘Dr Jose E
Gonzalez’, Monterrey Nuevo Leon, Mexico
& 2006 Elsevier Ltd. All rights reserved.
Abstract
This article describes the initial evaluation of a patient with new
onset respiratory problem. A thorough medical history and
physical examination are the keys in making a specific diagnosis
or narrowing the differential diagnosis of most respiratory disorders. The common signs and symptoms of respiratory problems include dyspnea, cough, hemoptysis, wheezing, chest pain,
and snoring.
Introduction
Patients with respiratory problems commonly present for medical attention because of the development of dyspnea, cough, hemoptysis, wheezing, chest
pain, or snoring. Occasionally, patients are asymptomatic and abnormalities are detected on routine
health screening examination or through the evaluation of another unrelated medical condition. This
article describes the initial evaluation of a patient
with new onset respiratory problem. We will focus
on the interpretation of common presenting symptoms and physical findings. A thorough medical
history and physical examination are the keys in
making a specific diagnosis or narrowing the differential diagnosis.
Medical History
The past medical history is important in defining
and characterizing the patient’s illness. It is important to determine whether or not there are previous
or concurrent nonrespiratory illnesses that could be a
factor in causing or worsening the present clinical
problem. Particular attention needs to be placed on
the identification of occupational and environmental
exposures, smoking history, medication history,
and family history. It is critical that the clinician
obtain and review any prior chest-imaging studies.
Often this process uncovers risk factors for specific
respiratory disorders, identifies the recurrence of a
dormant condition, or uncovers a previously undiagnosed condition.
The family history is occasionally helpful since
familial associations or genetic transmission of
lung diseases have been identified (e.g., asthma,
COPD, cystic fibrosis, a-1 antiprotease deficiency,
sarcoidosis). Life style, habits, and travel history are
important areas to explore. For example, a history of
travel to an endemic area for a particular disease
(e.g., tuberculosis) might identify this as the cause of
the patient’s illness. Finally, the family history might
identify illnesses related to common exposures.
A strict chronological listing of the patient’s entire
lifelong employment must be sought, including specific duties and known exposures to dusts, gases, and
chemicals. The degree of exposure, duration, latency
of exposure, and the use of protective devices should
be elicited. Review of the environment (home
and work, including that of spouse, children, and
friends), especially relating to pets, air conditioners,
humidifiers, hot tubs, evaporative cooling systems
(e.g., swamp coolers), etc., is valuable as well. Symptoms may diminish or disappear after the patient
leaves the exposure for several days; similarly, symptoms reappear on returning to the exposure. Obtaining the occupational and environmental history can
be quite difficult. Consequently, questionnaires are
commonly given to patients that allow them to review their employment record, military service, hobbies, pets, or other potential exposures.
The history of tobacco use is important since some
diseases occur largely among current or former
smokers (e.g., chronic obstructive pulmonary disease
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SIGNS OF RESPIRATORY DISEASE / General Examination
(COPD)) or among never or former smokers (sarcoidosis and hypersensitivity pneumonitis). Active
smoking can lead to complications such as pulmonary hemorrhage in patients with Goodpasture’s
syndrome.
A detailed medication history is needed to exclude
the possibility of drug-induced disease, including
over-the-counter medications, oily nose drops, and
supplements. Importantly, lung disease may occur
weeks to years after the drug has been discontinued.
Gender is important in lymphangioleiomyomatosis
which occurs exclusively in premenopausal women.
Also, interstitial lung disease (ILD) in the connective
tissue diseases is more common in women; the
exception is ILD in rheumatoid arthritis which is
more common in men. Age is helpful given that the
majority of patients with asthma, sarcoidosis, and
connective tissue disease present between the ages
of 20–40 years. Conversely, most patients with idiopathic pulmonary fibrosis are over age 60.
symptoms, the relationship of symptoms to activity,
and any factors that may improve or exacerbate
symptoms. In most cases, the primary problem is
heart, lung, or neuromuscular abnormalities, which
can be identified largely by the history and physical
examination. The quality of breathing discomfort
often provides tips to the underlying diagnosis; the
absence of cigarette smoking is strongly against a
diagnosis of COPD. The occupational history may
lead to a diagnosis of asbestosis or hypersensitivity
pneumonitis. The presence of reproducible events
such as exposure to fumes or cold air is common
with airways hyperreactivity.
When developing a differential diagnosis, it is useful
to distinguish respiratory systems dyspnea from cardiovascular dyspnea. It is not uncommon for a patient
to have more than one problem contributing to the
breathing discomfort. Diagnostic testing commonly
follows to identify the specific nature of the disorder.
Dyspnea is classified into the following categories:
Respiratory Symptoms
1. Acute dyspnea has a short list of causes, most of
which are readily identified: asthma, pulmonary
infection, pulmonary edema, pneumothorax, pulmonary embolus, metabolic acidosis, or acute respiratory distress syndrome (ARDS).
2. Orthopnea (dyspnea on recumbency) and nocturnal dyspnea suggest asthma, gastroesophageal reflux disease (GERD), left ventricular dysfunction,
or obstructive sleep apnea.
3. Platypnea (dyspnea that worsens in the upright
position) is a rare complaint associated with
arteriovenous malformations at the lung bases or
with hepatopulmonary syndrome, resulting in
increased shunting and hypoxemia in the upright
position (orthodeoxia).
4. Episodic dyspnea suggests congestive heart failure,
asthma, acute or chronic bronchitis, or recurrent
pulmonary emboli.
5. Chronic dyspnea is invariably progressive. Symptoms often first appear during exertion; patients
learn to limit their activity to accommodate their
diminished pulmonary reserve until dyspnea occurs
with minimal activity or at rest. The most common
causes of chronic dyspnea are asthma, chronic obstructive lung disease, ILD, and cardiomyopathy,
but deconditioning is often a major contributing
factor in patients with chronic lung disease.
The most common presenting symptoms are progressive breathlessness with exertion, cough (with or
without hemoptysis), wheezing, chest pain, or snoring. These are discussed in detail in other articles so
we will only provide a general overview.
Dyspnea
Dyspnea is the term applied to sensations experienced by individuals who complain of uncomfortable
respiratory sensations (see Signs of Respiratory Disease: Breathing Patterns). Dyspnea has been defined
in several ways, for example, ‘difficult, labored, uncomfortable breathing’, an ‘awareness of respiratory
distress’, ‘the sensation of feeling breathless or experiencing air hunger’, and ‘an uncomfortable sensation of breathing’. The sensation of dyspnea derives
from interactions among multiple physiological and
behavioral responses. It is the result of an imbalance
between ventilatory demand and capacity due to increased work of breathing.
Often, the patient has attributed the insidious onset of breathlessness to aging, deconditioning, obesity, or a recent upper respiratory tract illness. Some
patients deny the presence of dyspnea even when
questioned because they perform a limited amount
of activity and so do not ‘experience’ any significant
discomfort. Occasionally a spouse or friend brings
the problem to their attention. It is important to determine the duration and extent of dyspnea, cough,
and sputum production (if any).
The dyspnea history should focus on onset and
timing of symptoms, the patient’s position at onset of
The initial evaluation following the history and
physical examination should include a complete
blood count (to exclude anemia as a contributing
factor to respiratory discomfort), renal function test,
chest radiograph, standard spirometry, and noninvasive oximetry during ambulation at a normal pace
SIGNS OF RESPIRATORY DISEASE / General Examination 29
over 200 meters. The chest radiography may provide evidence of hyperinflation and bullous disease
suggestive of obstructive lung disease, or change in
interstitial markings consistent with inflammation
or interstitial fluid. Abnormalities of heart size may
indicate valvular heart disease or other cardiac dysfunction. Standard spirometry can distinguish patients
with restrictive pulmonary disease from those with
obstructive airway disease. Lung-volume measurements and diffusing capacity are generally reserved
for patients in whom ILD is being considered, in those
who have significant declines in oxygen saturation
with exercise, or in those for whom there is a suspicion
of ventilatory muscle weakness. Echocardiography
is reserved for patients in whom chest radiography
reveals the heart to be enlarged, or in whom the
diagnosis of chronic thromboembolic disease or pulmonary hypertension is being considered. Computed
tomography (CT) of the chest is valuable in two circumstances – when patient has crackles on physical
examination or reduced lung volumes on pulmonary
function test even if the radiography is normal, and for
those who have oxygen desaturation with exercise and
a low diffusing capacity (occult emphysema). Cardiopulmonary exercise testing is recommended if the
etiology of a patient’s dyspnea remains unclear after
the initial evaluation described above. This test allows
to determine if the patient’s dyspnea is more likely due
to cardiovascular or respiratory system abnormalities,
or if it is due to deconditioning.
Cough
Cough by definition is an explosive expiration that
provides a normal protective mechanism for clearing
the tracheobronchial tree of secretions and foreign
material. Cough is often divided into three categories: acute (defined as lasting o3 weeks), subacute
(lasting 3–8 weeks), and chronic (lasting 48 weeks).
Coughing may be initiated either voluntarily or
reflexively. As a defensive reflex, it has both afferent
and efferent pathways. The afferent limb includes
receptors within the sensory distribution of the trigeminal, glossopharyngeal, superior laryngeal, and
vagus nerves. The efferent limb includes the recurrent laryngeal nerve and the spinal nerves. The cough
starts with a deep inspiration followed by glottic
closure, relaxation of the diaphragm, and muscle
contraction against a closed glottis. The resulting
markedly positive intrathoracic pressure causes narrowing of the trachea. Once the glottis opens, the
large pressure differential between the airways and
the atmosphere coupled with tracheal narrowing
produces rapid flow rates through the trachea. The
shearing forces that develop, aid in the elimination of
mucus and foreign materials.
The duration of the cough at the time of presentation helps to determine the likely cause. Acute
cough is most often associated with upper respiratory
tract infections such as common cold, acute bacterial
sinusitis, pertussis, exacerbations of COPD, allergic
rhinitis, and rhinitis due to environmental irritants.
Acute cough can be the presenting manifestation of
pneumonia, left ventricular failure, or asthma especially in elderly patients, because classic signs and
symptoms may be minimal or not present.
Subacute cough often follows an upper respiratory
tract infection and lasts for 3–8 weeks, the most
common conditions are postinfectious cough, bacterial sinusitis, and asthma. Postinfectious cough may
result from postnasal drip or clearing of the throat
due to rhinitis, tracheobronchitis, or both, with or
without transient bronchial hyperresponsiveness.
When cough is subacute and is not associated with
an obvious respiratory infection, then the patient
should be evaluated in the same way as patients with
chronic cough (see below).
The main causes (B95% of cases) of chronic
cough include postnasal drip syndrome from conditions of the nose and sinuses, asthma, gastroesophageal reflux disease, chronic bronchitis due to
cigarette smoking or other irritants, bronchiectasis,
or the use of drugs (especially an angiotensin-converting enzyme (ACE) inhibitor). Other causes of
chronic cough include bronchogenic carcinoma, carcinomatosis, sarcoidosis, left ventricular failure, and
aspiration due to pharyngeal dysfunction.
The patient’s clinical history is often very helpful in
arriving at the cause of the cough (if there are symptoms suggestive of a respiratory infection, if there is a
seasonal cause of wheezing or postnasal drip, if the
patient has heartburn or sensation of regurgitation, if
there is sputum or dry cough, etc.) Focus should be
on the smoking history, environmental exposures,
and medication use (e.g., ACE inhibitors or b blockers). Figure 1 provides an algorithm for diagnosing
chronic cough in immunocompetent adults from a
Consensus Panel Report of the American College of
Chest Physicians.
Physical examination is necessary to find a nonpulmonary cause of cough such as heart failure or
AIDS. Auscultation of the chest is useful to find
stridor (upper airway disease), rhonchi, or expiratory
wheezing (lower airway disease), inspiratory crackles
(ILD, pneumonia, or pulmonary edema). In a patient
without asthma, sputum studies with greater than
3% eosinophils on staining suggest the possibility of
eosinophilic bronchitis. Sometimes other tests are
needed, for example, bronchoprovocation with methacholine to demonstrate hyperreactivity and confirm asthma; high resolution computed tomography
30
SIGNS OF RESPIRATORY DISEASE / General Examination
Cough gone
Chronic cough
Stop ACEI
Hx
PE
ACEI
Cough
persists
Chest radiograph
Normal
Abnormal
Avoid irritant
Cough gone
Order according to
likely clinical possibility
Abnormality
may not be
related to
cough
Sputum cytology, HRCT scan,
modified BaE, bronchoscopy, cardiac
studies
Cough
persists
Treat accordingly
Evaluate for three most common conditions
singly in the following order, or in
combination:
1. PNDS
Cough gone
2. Asthma
Cough
persists
Cough gone
3. GERD
Consider
postinfectious
cough
Cough
persists
Evaluate for uncommon
conditions
Sputum tests, HRCT scan,
modified BaE, bronchoscopy, cardiac
studies
Cough gone
Cough
persists
Reconsider adequacy of treatment
regimens before considering habit
or psychogenic cough
Figure 1 Guidelines for evaluating chronic cough in immunocompetent adults. ACEI, angiotensin-converting enzyme inhibitor; BaE,
barium esophagography; GERD, gastroesophageal reflux disease; HRCT, high-resolution computed tomography; HX, history; PE,
physical examination; PNDS, postnasal drip syndrome. Reproduced from Irwin RS, Boulet LP, Cloutier MM, et al. (1998) A consensus
panel report of the American College of Chest Physicians. Managing cough as a defense mechanism and as a symptom. Chest
114(2 supplement Managing): 133S–181S, with permission.
(HRCT) to confirm the presence of ILD, COPD, or
bronchiectasis; and 24 h monitoring of esophageal
pH to help identify silent gastroesophageal reflux
disease.
Hemoptysis
The word ‘hemoptysis’ comes from the Greek
‘haima’ for ‘blood’ and ‘ptysis’ for ‘a spitting’ together meaning, ‘a spitting of blood’. The source
SIGNS OF RESPIRATORY DISEASE / General Examination 31
of the blood originates below the vocal cords. It is
classified as massive when more than 200–600 ml
in 24 h, or when the patient is hemodynamically significant or it threatens ventilation.
The history should include questions regarding
smoking habits, past respiratory infections (e.g.,
pneumonia or tuberculosis), bronchiectasis, history
of deep venous thrombosis, bleeding disorders, anticoagulant therapy, and recent weight loss (Table 1).
Physical examination should include careful inspection of the upper airway. Certain findings may be
helpful in suggesting a diagnosis: a saddle nose deformity with rhinitis and septal perforation are signs
of Wegener’s granulomatosis; oral or genital aphthous ulcerations, uveitis, or cutaneous nodules may
be the clinical presentations in patients with Behc¸et’s
disease; clubbing may be a sign of lung carcinoma
or bronchiectasis. In the examination of the lungs, a
pleural friction rub may suggest pulmonary embolism. Cardiac examination may demonstrate findings
of cor pulmonale or mitral stenosis.
Chest imaging studies may help to identify lung
parenchymal pathologies. HRCT can demonstrate
lesions that may not be visible in chest radiograph,
such as bronchiectasis or a small bronchial carcinoma. When performed with contrast material, CT
may detect pulmonary embolism, thoracic aneurysm,
or arteriovenous malformation.
Fiberoptic bronchoscopy is commonly performed,
both for anatomic localization of the bleeding site
and to exclude neoplasm. Flexible bronchoscopy can
be performed at bedside, does not require general
anesthesia, and is usually quicker than the rigid
bronchoscopy. It also allows easy access to the upper
lobes. The disadvantages are a limited suctioning
capability and an inability to localize bleeding when
the hemorrhage rate is rapid. The diagnosis yield increases when patients undergo bronchoscopy within
48 h of a bleeding episode. In general, bronchoscopy
should be performed in patients who smoke, in those
who are older than 40 years, and those who have
bleeding that persists (even intermittently) for more
than 2 weeks. Some authors have found bronchogenic carcinoma in as many as 15–20% of bronchoscopies in patients with normal chest radiography.
Except for life-threatening situations, CT should be
performed before bronchoscopy.
Rigid bronchoscopy is less frequently used but has
been found to be safe and well tolerated under local
anesthesia and conscious sedation, when performed
by experienced hands. It offers better suctioning capability, continuous airway control, and a larger lumen for introducing packing materials and clearing
clots and debris from the airways of patients with
active bleeding. Its disadvantages include a reduced
Table 1 Common causes of hemoptysis
Cardiac
Mitral stenosis
Tricuspid endocarditis
Drugs/toxins
Anticoagulants
Aspirin
Crack cocaine
Hematologic
Coagulopathy
Platelet dysfunction
Thrombocytopenia
Infection
Fungal
Lung abscess
Mycetoma
Necrotizing pneumonia
Tuberculosis
Iatrogenic
Bronchoscopic
Lung biopsy
Swan-Ganz catheter use
Neoplastic
Bronchial adenoma
Lung cancer
Metastasic disease
Pulmonary
Bronchitis
Bronchiectasis
Pulmonary embolism
Cryptogenic
Foreign body
Cryptogenic hemoptysis
Systemic
Goodpasture’s syndrome
Idiopathic pulmonary hemosiderosis
Systemic lupus
Systemic vasculitides
Traumatic
Aortic aneurysm
Chest trauma
Fat embolism
Ruptured bronchus
Vascular
Aortic aneurysm
Arteriovenous malformation
Pulmonary hypertension
range of visibility of upper lobe and the need for
general anesthesia.
Chest Pain
The evaluation of acute chest pain should begin with
a clinical history that focuses on the characteristics of
the pain, the time of onset, and the duration of
symptoms, and an examination that emphasizes vital
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SIGNS OF RESPIRATORY DISEASE / General Examination
signs and cardiovascular status. An electrocardiogram should be obtained within 5 min after presentation, followed by a chest X-ray.
The goal of the initial evaluation of the patient is
to rule out coronary artery disease (CHD) and conditions that are life-threatening. Common causes
of chest pain include muscle or skeletal chest pain,
costochondritis, gastroesophageal reflux, and stable
angina pectoris. Unstable angina was an uncommon
cause in a recent large prospective study. Nonetheless, cardiac pain must be ruled out quickly.
Quality of the pain. The patient with ischemia often denies feeling chest ‘pain’. The sensation is commonly described as squeezing, tightness, pressure,
constriction, strangling, burning, heartburn, fullness
in the chest, to band-like sensation, knot in the center
of the chest, lump in the throat, ache, heavy weight
on chest (elephant sitting on chest), like a bra too
tight, and toothache (when there is radiation to the
lower jaw). Some patients cannot qualify the nature
of the discomfort but will place fist in the center of
the chest (the ‘Levine sign’). Patients with a history of
CHD tend to have the same quality of chest pain
with recurrent ischemic episodes.
Location of the pain. Unlike the muscular or pleuritic pain that can be located, ischemia is more diffuse and thus difficult to locate.
Radiation. The radiation of the pain to right
arm (2.9 likelihood ratio) or even toward both arms
(7.1 likelihood ratio) is a predictor of acute myocardial infarction. Pain associated with acute cholecystitis radiates to the right shoulder. The pain of
aortic dissection radiates toward the back and that of
pericarditis toward one or both trapezes.
Onset of the pain. The pain due to pneumothorax,
aortic dissection, or acute pulmonary embolism is
sudden; ischemic pain is gradual and increases with
time, and pain of the musculoskeletal type has a very
vague beginning.
Provocation. If the chest pain increases when eating, we suspect a gastrointestinal cause or myocardial ischemia. Myocardial ischemia also increases by
exercise, cold, and emotional stress. The pain that
increases with the change of position suggests a
musculoskeletal source. Pleuritic type of pain increases with deep breathing and when lying down.
Other useful findings. Vital signs can be helpful,
for example, a marked difference in blood pressure
between the two arms suggests the presence of aortic
dissection. Hyperestesia combined with a skin rash
indicates herpes zoster. Chest auscultation for pleural
or pericardial rub, signifies heart murmur, crackles,
wheezes or signs of consolidation are useful in suggesting possible cause of the chest pain, for example,
pericarditis, valvular heart disease, ILD, asthma, or
pneumonia respectively. Also, careful examination of
the abdomen is important, with attention to the right
superior quadrant and epigastrium.
Wheezing
A wheeze is a continuous musical sound that lasts
longer than 250 msec. Wheezing occurs during inspiration or expiration and originates from airways
of any size; conversely, stridor is an inspiratory
wheezing that is loudest over the central airways.
The whistling sound (wheezing) occurs when a patient attempts to exhale through bronchial passages
that are constricted or excreting excess mucus due to
irritation, infection, or allergy.
The more common symptoms are tightening in
the chest and dyspnea. In evaluating patients with
wheezing, it is important to be aware that ‘‘All that
wheezes is not asthma; all that wheezes is obstruction.’’ Using the history, physical examination, lung
function studies, and knowledge of the spectrum of
differential diagnostic possibilities, especially those
that have been shown to be the most common is how
we can make the diagnosis (see Table 2).
Snoring
Snoring is an inspiratory sound produced by vibration of the soft tissues of the upper airway during
sleep. Snoring is a common symptom in the general
population. However, snoring may indicate a more
serious medical problem, such as obstructive sleep
apnea (OSA) or the upper airway resistance syndrome (UARS). Some patients appear asymptomatic
unless the clinician makes a systematic effort to elicit
symptoms. Consequently, it is important to recognize
whether clinical features suggest an underlying sleeprelated breathing disorder and if some form of objective testing is indicated. The physiology, clinical
significance, and evaluation of snoring is discussed
elsewhere in this text.
Physical Examination
Examination of the patient with pulmonary disease
includes inspection, palpation, percussion, and auscultation of the chest.
Inspection. This includes the respiratory rate and
rhythm, breathing pattern, as well as the depth and
symmetry of lung expansion. Respiratory rate normal
values are 12–14 breaths per min. Tachypnea is an
increased rate of breathing. During normal breathing,
the primary muscle of respiration is the diaphragm,
but when the patient uses the intercostals and sternocleidomastoid muscles (accessory muscles), it indicates labored breathing. The chest normally expands
SIGNS OF RESPIRATORY DISEASE / General Examination 33
Table 2 Causes of wheezing based on anatomic site of obstruction
Extrathoracic upper airway obstruction
Intrathoracic upper airway obstruction
Lower airway obstruction
Postnasal drip syndrome
Vocal cord dysfunction
Hypertrophied tonsils
Epiglottitis
Laryngeal edema
Laryngostenosis
Postextubation granuloma
Retropharyngeal abscess
Neoplasms
Anaphylaxis
Malignancy
Obesity
Klebsiella rhinoscleroma
Mobile supraglottic soft tissue
Relapsing polychondritis
Laryngocele
Abnormal arytenoid movement
Vocal cord hematoma
Bilateral vocal cord paralysis
Cricoarytenoid arthritis
Wegener’s granulomatosis
Tracheal stenosis
Foreign body aspiration
Benign airway tumors
Malignancies
Intrathoracic goiter
Tracheobronchomegaly
Acquired tracheomalacia
Herpetic tracheobronchitis
Right sided aortic arch
Asthma
COPD
Pulmonary edema
Aspiration
Pulmonary embolism
Bronchiolitis
Cystic fibrosis
Carcinoid syndrome
Bronchiectasis
Lymphangitic carcinomatosis
Parasitic infections
Reproduced with permission from Irwin RS, Diagnosis of wheezing illnesses other than asthma in adults. In: UpToDate, Rose (ed.)
UpToDate, Wellesley, MA, 2005. Copyright & 2005 UpToDate, Inc. For more information visit http://www.uptodate.com.
Table 3 Extrapulmonary physical findings associated with lung diseases
Physical findings
Associated conditions
Fever
Infections, eosinophilic pneumonia, drug reactions, cryptogenic organizing pneumonia, hypersensitivity
pneumonitis, sarcoidosis, lymphoma, lymphangitic carcinoma
Skin changes
Erythema nodosum
Maculopapular rash
Heliotrope rash
Telangiectasia
Raynaud phenomenon
Cutaneous vasculitis
Subcutaneous nodules
Calcinosis
Café-au-lait spots
Eye changes
Uveitis
Scleritis
Keratoconjunctivitis
sicca
Albinism
Salivary gland
enlargement
Peripheral
lymphadenopathy
Myositis; muscle
weakness
Arthritis
Sarcoidosis, connective tissue disease, Behc¸et syndrome, histoplasmosis, coccioioidomycosis
Drug-induced diasease, amyloidosis, lipoidosis connective tissue disease, Gaucher disease
Dermatomyositis
Scleroderma
Connective tissue disease (scleroderma)
Systemic vasculitides, connective tissue disease
Von Recklinghausen disease, rheumatoid arthritis
Dermatomyositis, scleroderma
Neurofibromatosis
Sarcoidosis, Behc¸et syndrome, ankylosing spondilitis
Systemic vasculitis, systemic lupus erythematosus, scleroderma, sarcoidosis
Lymphocytic interstitial pneumonia, Sjögren syndrome
Hermansky–Pudlak syndrome
Sarcoidosis, Lymphocytic interstitial pneumonia, Sjögren syndrome
Sarcoidosis, lymphangitic carcinomatosis, Lymphocytic interstitial pneumonia, Sjögren syndrome
Connective tissue disease, sarcoidosis, drugs
Connective tissue disease, vasculitis, sarcoidosis, Goodpasture syndrome
Reproduced from Schwarz MI, King TE Jr, and Raghu G (2003) Approach to the evaluation and diagnosis of interstitial lung disease.
In: Schwarz MI and King TE (eds.) Interstitial Lung Diseases, 4th edn., p. 8. Hamilton, ON: BC Decker, with permission from
BC Decker.
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SIGNS OF RESPIRATORY DISEASE / General Examination
simultaneously. Asymmetric expansion of the chest is
usually due to an asymmetric process affecting the
lungs, and suggests unilateral pleural or parenchyma
problem. Visible abnormalities of the thoracic cage
include kyphoscoliosis which can alter compliance of
the thorax and cause dyspnea.
Palpation. The trachea at the suprasternal notch,
detects shift in the mediastinum. The symmetry of lung
expansion can be assessed, confirming the findings
observed by inspection. Vibration produced by spoken
sounds is transmitted to the chest wall and is assessed
by the presence or absence and symmetry of tactile
fremitus, especially on the posterior chest wall. Transmission of vibration is decreased or absent if pleural
liquid is interposed between the lung and chest wall; in
contrast, transmitted vibration may increase over an
area of underlying pulmonary consolidation.
Percussion. Assess the resonance or dullness of the
tissue underlying. The normal sound of underlying aircontaining lung is resonant. Dull areas correspond to
lung consolidation or pleural effusion and hyperresonant areas suggest emphysema or pneumothorax.
Auscultation. We listen for both the quality and
intensity of the breath sounds and the presence of
abnormal or adventitious sounds. Normal lung
sounds heard over the periphery of the lung are
called vesicular breath sounds, in which inspiration is
louder and longer that expiration. Normal sounds
heard over the suprasternal notch are called tracheal
or bronchial lung sounds and have a hollow quality
that tends to be louder on expiration.
The breath sounds are diminished in intensity or
absent if there is an endobronchial obstruction, or
when there is fluid in the pleural space. When sound
transmission is improved and has a more pronounced
expiratory phase, a consolidated lung is present.
Listening through the consolidated lung, the spoken
sound (bronchophony) or the whispered sound
(pectoriloquia) is part of the routine evaluation as
is the presence of egophony, which is the sound of a
spoken E that becomes more like an A.
Adventitious sounds can be continuous or discontinuous. Continuous ones are divided into wheezes
and rhonchi. Wheezes that are more prominent during expiration than inspiration, reflect the oscillation
of airway walls that occurs when there is airflow
limitation, as may be produced by bronchospasm,
airway edema or collapse, or intraluminal obstruction
by neoplasm or secretions. Rhonchi originate in the
large airways when excessive secretions and abnormal airway collapsibility cause repetitive rupture of
fluid films and frequently clear after cough.
Discontinuous sounds are called crackles which
are typically inspiratory, are produced by the sound
created when alveoli and small airways open and
close with respiration. Fine crackles are heard in
ILD or filling alveoli liquid as pulmonary edema.
Coarse crackles result from air bubbling through
fluid and are heard in pneumonia and late pulmonary
edema.
Appearance
Normal
Clubbed
(a)
Nail-fold angles
C
D
Normal
B A
B
Clubbed
A
C
D
(b)
Phalangeal depth ratio
Normal
DPD IPD
Clubbed
DPD IPD
(c)
Schamroth sign
Normal
Clubbed
(d)
Figure 2 Appearance on inspection for clubbing: (a) normal finger viewed from above and in profile, and the changes occurring in
established clubbing, viewed from above and in profile. (b) The
finger on the left demonstrates normal profile (ABC) and normal
hyponychial (ABD) nail-fold angles of 1691 and 1831, respectively.
The clubbed finger on the right shows increased profile and hyponychial nail-fold angles of 1911 and 2031, respectively. (c) Distal
phalangeal finger depth (DPD)/interphalangeal finger depth (IPD)
represents the phalangeal depth ratio. In normal fingers, the IPD is
greater than the DPD. In clubbing, this relationship is reversed. (d)
Schamroth sign: in the absence of clubbing, opposition of the index
fingers nail-to-nail creates a diamond-shaped window (arrowhead). In clubbed fingers, the loss of the profile angle due to the
increase in tissue at the nail bed causes obliteration of this space
(arrowhead). Reproduced from Myers KA and Farquhar DR (2001)
The rational clinical examination. Does this patient have clubbing?
Journal of the American Medical Association 286: 341–347, with
permission. Copyright & (2001) American Medical Association.
All rights reserved.
SIGNS OF RESPIRATORY DISEASE / Lung Sounds 35
Extrapulmonary Signs of Pulmonary Disease
Table 3 lists the extrapulmonary physical findings
associated with lung diseases.
Digital clubbing There are structural changes at the
base of the nails that include softening of the nail bed
and loss of the normal 1501 angle between the nail
and the cuticle (Figure 2). The distal part of the finger
is enlarged in comparison with the proximal part. It
may be a normal variant but more commonly is a
sign of underlying pulmonary disease such as lung
cancer, ILD, and chronic infections in the thorax
such as bronchiectasias, lung abscess, and empyema.
It is not commonly seen in COPD; if present, a complicating lung carcinoma may be present.
Cor pulmonale In the mid or late stages of pulmonary diseases, findings of pulmonary hypertension
(e.g., augmented P2, right-sided lift, and S3 gallop)
and cor pulmonale may become evident. These can
be primary manifestations of a connective tissue disorder (e.g., progressive systemic sclerosis) though.
See also: Chronic Obstructive Pulmonary Disease:
Smoking Cessation. Signs of Respiratory Disease:
Breathing Patterns; Clubbing and Hypertrophic Osteoarthropathy. Sleep Apnea: Overview. Symptoms of
Respiratory Disease: Cough and Other Symptoms;
Dyspnea; Chest Pain.
Further Reading
American Thoracic Society (1999) Dyspnea. Mechanisms, assessment, and management: a consensus statement. American Journal of Respiratory and Critical Care Medicine 159: 321–340.
Braman SS and Corrao WM (1987) Cough: differential diagnosis
and treatment. Clinics in Chest Medicine 8: 177–188.
Cahill BC and Ingbar DH (1994) Massive hemoptysis. Assessment
and management. Clinics in Chest Medicine 15: 147–167.
Fitzgerald RS and Lahiri S (1986) Reflex response to chemoreceptor stimulation. In: Cherniack NS and Widdicombe JG (eds.)
Handbook of Physiology, Section 3: The Respiratory System,
Vol. 2. Control of Breathing, pp. 313–362. Bethesda: American
Physiological Society.
Irwin RS (2005) Diagnosis of wheezing illnesses other than asthma.
In: Rose BD (ed.) UpToDate. Wellesley, MA: UpToDate.
Irwin RS, Boulet LP, Cloutier MM, et al. (1998) Managing cough
as a defense mechanism and as a symptom. A consensus panel
report of the American College of Chest Physicians. Chest 114(2
supplement Managing): 133S–181S.
Irwin RS and Madison JM (2000) The diagnosis and treatment of
cough. New England Journal of Medicine 343: 1715–1721.
Jean-Baptiste E (2000) Clinical assessment and management of
massive hemoptysis. Critical Care Medicine 28(5): 1642–1647.
Lee TH and Goldman L (2000) Evaluation of the patient with acute
chest pain. New England Journal of Medicine 342: 1187–1195.
Luce JM and Luce JA (2001) Perspectives on care at the close of
life. Management of dyspnea in patients with far-advanced lung
disease: ‘‘once I lose it, it’s kind of hard to catch it.’’ Journal of
the American Medical Association 285: 1331–1337.
Manning HL and Schwartzstein RM (1995) Pathophysiology of
dyspnea. New England Journal of Medicine 333: 1547–1553.
Myers KA and Farquhar DR (2001) The rational clinical examination. Does this patient have clubbing? Journal of the American Medical Association 286: 341–347.
O’Neil KM and Lazarus AA (1991) Hemoptysis. Indications for
bronchoscopy. Archives of Internal Medicine 151: 171–174.
Schwarz MI, King TE Jr, and Raghu G (2003) Approach to the
evaluation and diagnosis of interstitial lung disease. In: Schwarz
MI and King TE Jr (eds.) Interstitial Lung Diseases, 4th edn.,
p. 8. Hamilton, ON: BC Decker.
Weinberger SE (2005) Etiology and evaluation of hemoptysis. In:
Rose BD (ed.) UpToDate. Wellesley, MA: UpToDate.
Lung Sounds
D C J Howell, Centre for Respiratory Research,
University College London, London, UK
& 2006 Elsevier Ltd. All rights reserved.
Abstract
Sound has a number of vital characteristics including frequency,
intensity, duration, and quality. These components determine
the plethora of lung sounds that can be heard by the human ear.
Historically, lung sounds were detected by placing the ear on the
chest wall of the patient. However, with the discovery of the
stethoscope, this practice was abandoned. Although much can
be elucidated about underlying chest pathology by listening to a
patient breathing while standing at the end of the bed, auscultation has added much to the clinical examination of patients
with respiratory disease. Lung sounds can broadly be divided
into breath sounds and voice sounds, and can be normal and
abnormal. Abnormal lung sounds can be either abnormally
transmitted by breath or voice, or may be adventitial (accidental). In this article, the range of various normal and abnormal
sounds that the lung produces will be discussed and their pertinence to respiratory disease highlighted.
The Perception of Sound, the
Stethoscope, and Auscultation
Prior to discussing lung sounds in detail, it is prudent
to elaborate on the nature of sound itself. Sounds
consist of audible vibrations, which are created by
alternating regions of compression and rarefaction of
air. Sound has a number of important characteristics
including frequency, intensity, duration, and quality.
The frequency of sound reflects a measurement of
the number of vibrations per unit time, in cycles
per second, and is expressed in hertz (Hz). The large
range of normal and abnormal lung sounds will be
elaborated upon below but as examples, a sound
producing a large amount of vibrations per unit time
will be interpreted on clinical examination as a highpitched wheeze. Conversely, sounds with low vibrations per unit time are heard as low-pitched wheezes.