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306 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
Cogwheel breathing
Asthmatic breathing
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FIG. 8-32 Distinguishing Features of Breath Sounds. In the diagrams, the vertical component indicates rising
and falling pitch, the thickness of the lines indicates loudness, and the horizontal distance represents duration. Inspiration is
longer in vesicular breathing, expiration in bronchial breathing. Bronchovesicular breathing is a mixture of
the two. Normally vesicular breathing is heard over most of the lungs, except that bronchovesicular breathing occurs over the
thoracic portion of the trachea, anteriorly and posteriorly. Bronchial breathing does not occur in the normal lung. In cogwheel
breathing, the inspiratory sound is interrupted with multiple breaks. Asthmatic breathing is characterized by a much
prolonged and higher-pitched expiratory sound than is found in bronchial breathing. Asthmatic breathing is usually, but not
always, accompanied by wheezes.
It is intermediate between vesicular and bronchial breathing. Inspiration and
expiration are of roughly equal duration (Fig. 8-32), though expiration can
be a bit longer. It is normal over the manubrium and the upper interscapular
region. Compression or consolidation of the lung causes breath sounds to
become bronchial.
Bronchial breathing (tubular breathing). In contrast to vesicular breathing,
bronchial breath sounds have a shorter inspiratory than expiratory phase
(Fig. 8-32) and are usually louder. Bronchial breathing does not occur in the
normal lung.
Tracheal breathing. Tracheal breathing is normal in the suprasternal notch
and over the sixth and seventh cervical spines. It is more harsh and hollow
than bronchial breathing.
Wheezes.
Wheezes arise from turbulent airow and vibrating partially
obstructed small airways. Wheezes are heard predominantly during expi-
ration. They occur when airways are narrowed by bronchospasm, edema,
collapse, or by intraluminal secretions, neoplasm, or foreign body. They are
diffuse in asthma and bronchitis, usually accompanying prolonged expiration. An isolated wheeze may signal bronchial obstruction by a tumor or
foreign body. Wheezing is neither sensitive nor specic for detecting airow
obstruction.
Asthmatic or obstructive breathing. In asthma, expiration is several times
longer than in bronchial breathing, and the pitch is much higher. Expiration
is active, not passive, and may require signicant effort. Frequently, but not
always, asthma is accompanied by wheezes audible without the stethoscope.
(Fig. 8-32). Emphysema produces a similar breath sound prole, but wheezing is absent, and the sounds are less intense.
Crackles (rales). Crackles result from the opening and closing of alveoli and
small airways during the respiratory cycle. In pulmonary edema ne crackles are produced by air bubbling through small uid-lled distal airways.
Chest, Trachea, and Respiratory Signs 307
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Inspiratory crackles resemble the sound of hairs being rubbed together. They
are heard in the bases with interstitial lung disease, brosing alveolitis, atelectasis, pneumonia, bronchiectasis, and pulmonary edema, and often in the
apices with tuberculosis.
Rhonchus. Rhonchi are low-pitched gurgling sounds produced by liquid
within the larger airways. They clear or change signicantly after an effective
cough.
Amphoric breath sounds. These are produced by an open pneumothorax or
a large empty supercial cavity communicating with a bronchus. Amphoric
breath sounds resemble blowing air over the mouth of a large bottle.
Auscultating Voice Sounds: In normal lungs whispered words are faint
and the syllables indistinct, except over the main bronchi. Consolidation,
atelectasis, and brosis improve sound transmission resulting in louder
and more distinct words. Because of their pitch and loudness, whispered
and spoken voice sounds are more useful than breath sounds in detecting
pulmonary consolidation, infarction, and atelectasis. Spoken voice sounds
are not as useful as whispered sounds since they are too loud for subtle
discrimination.
Whispered pectoriloquy. Consolidated lung transmits whispered syllables
distinctly, even when the pathologic process is too small to produce bronchial
breathing. This is particularly valuable in detecting early pneumonia, infarction, and atelectasis.
Bronchophony. Spoken syllables are normally heard indistinctly. With lung
consolidation syllables are distinct and sound close to the ear.
Egophony. This is a form of bronchophony in which the spoken “Eee” is
changed to “Ay,” with a peculiar nasal or bleating quality. This arises from
compressed lung below a pleural effusion, and occasionally with lung
consolidation.
Auscultating Abnormal Sounds
Rubs (pleural friction rub). See page 301.
Continuous murmur. The continuous murmur of a pulmonary arteriovenous
stula increases in intensity with inspiration. In patients with coarctation of
the aorta, continuous murmurs may be heard below the left scapula and over
the intercostal and internal mammary arteries from the collateral circulation.
Systolic crunching sounds. See Esophageal Rupture, page 355.
Interpretating Pulmonary and Pleural Signs: The ndings of thoracic
inspection, palpation, percussion, and auscultation must be synthesized to
suggest a pathophysiologic process or diagnosis. The signs of altered lung
density are the starting point for differential diagnosis. It is useful to draw a
chest diagram like those in Figures 8-33 and 8-34 to depict your ndings and
generate hypotheses.
308 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
Small pleural
Pleural
Consolidation and
Atelectasis and
+O
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Tracheal deviation
Fremitus
Percussion
Breath sounds
Whisper sounds
Voice sounds
Rales
effusion
V or O
Dull
V
V
V
O
thickening
O or
V
Dull
V
V
V
O
bronchial plug
OO
O
Dull
V or O
V or O
V or O
O
FIG. 8-33 Thoracic Disorders with Dullness and Diminished Vibration.
←, direction of deviation.
Tracheal deviation
Fremitus
Percussion
Breath sounds
Whisper sounds
Voice sounds
Rales
Small
consolidation
N or
Slight dullness
Bronchovescular
N, O, or
N, O, or
+ or O+
Thick-walled
cavity
O
N or
Slight dullness
Bronchovescular
or amorphicor bronchial
Pectoriloquy
FIG. 8-34 Thoracic Disorders with Dullness and Accentuated Vibration.
∧ increased; →, direction of deviation.
Massive
consolidation
OO
Dull or flat
Bronchial
°
, absent; N, normal; +, present;
bronchial plug
O
Dull
O
O
O
O
, absent; ∨, diminished;
°
Large pleural
effusion
O
(a) Hyperresonant
(b) Flat
O or loud
bronchial
O or
O or
Dullness and diminished vibrations
Pleural effusion and pleural thickening. Unless the uid is trapped by loculations in the non-dependent regions of the chest, dullness occurs in the lowermost chest (Fig. 8-33, left). Because the costophrenic sulcus is higher in front,
the dull region is a transverse band broadest posteriorly and laterally. The
superior border of dullness can be difcult to percuss accurately because the
uid layer forms an upward-pointing wedge. Shifting dullness is not usually
demonstrable. Since air is absent, there is no succussion splash. With a small
amount of uid respiratory excursions are normal. In pleurisy an antecedent
Chest, Trachea, and Respiratory Signs 309
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friction rub disappears when an effusion forms. Pleural uid dampens vibrations from the bronchotracheal air column, so vocal fremitus, breath sounds,
and whispered and spoken voice transmit poorly. Small pleural effusions do
not shift the mediastinum. Any longstanding pleural effusion may organize
producing pleural brosis with the same distribution of dullness as the effusion. The thicker the pleura, the more it obstructs sound transmission and the
denser the percussion note. Extensive brosis pulls the trachea to the affected
side. Neoplasms, asbestosis, and mesothelioma also cause pleural thickening.
Pleural uid.
tion from the pleural and pulmonary vessels (increased venous hydrostatic
pressure, decreased oncotic pressure, capillary leak), increased pleural uid
production (inamed pleura or pleural neoplasm), decreased pleural uid
absorption (lymphatic obstruction, systemic venous hypertension), or bleeding into the pleural space.
sion. The lung eld immediately above the the uid can be hyperresonant
(skodaic resonance) from distended air-lled alveolae above the compressed
region. The distribution of dullness is dependent. With substantial amounts
of uid, the trachea is pushed to the unaffected side (Fig. 8-34). Vocal fremitus
is absent. Occasionally, loud bronchial breathing is heard through the uid
from the compressed lung, the unwary mistaking it for consolidation. Fluid
is distinguished from consolidation by diminished breath sounds and absent
fremitus with uid, and bronchial breath sounds with E-to-A change in consolidation. Massive pleural effusion obscures the lung elds on radiographs
so that no appraisal of the parenchyma is possible. In contrast, when the patient with a hydropneumothorax stands, the uid level falls below much of
the lung, permitting lung visualization (Fig. 8-35) [Case with differential diagnosis: Quing DA, Mark EJ. Case 8-2002–A 56-year-old woman with a persistent left-sided pleural effusion. N Engl J Med. 2002;346:843–850].
CLINICAL OCCURRENCE: Increased Transudation: CHF, hypoalbuminemia
(cirrhosis, nephrotic syndrome), PE, SVC syndrome; Increased Production:
Mesothelioma, metastatic cancer, infections (bacteria, mycobacteria, viral,
parasites, fungi), pulmonary infarction, pancreatitis, mediastinitis, collagenvascular diseases (e.g., RA, systemic lupus erythematosus [SLE], drug-induced
lupus, vasculitis), after heart or lung surgery, uremia, Meigs syndrome, pleuropericarditis peritoneal dialysis;
tion (lymphoma, lymphatic carcinomatosis, irradiation, surgical injury), CHF,
SVC syndrome; Bleeding: Ruptured aortic aneurysm or dissection, trauma,
postoperative.
Fluid accumulates in the pleural space because of transuda-
Pleural uid produces a dull or at note to percus-
Decreased Absorption: Lymphatic obstruc-
Pulmonary consolidation with bronchial plugging. Consolidated lung produces dullness. Bronchial plugs block vibrations from the air column, so vocal fremitus, breath sounds, and whispered and spoken voice are absent (Fig.
8-33, middle right). The trachea is not displaced. Bronchial plugging, usually
transitory in lobar pneumonia, is recognized by the sudden loss of air transmission. Imaging distinguishes between pleural effusion and pulmonary
consolidation. Upper chest dullness on physical exam excludes effusion.
Atelectasis with bronchial plug. The volume of atelectatic lung is diminished.
When a considerable amount of lung is atelectatic, the dense mass is pulled
toward the chest wall by the negative intrapleural pressure shifting the
310 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
A. B. C. D.
Lung parenchyma
exposed for X-ray
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Thin wedge or
fluid gives
indistinct
border
Air
FIG. 8-35 Models Illustrating Pleural Effusion and Pneumothorax. A. Suspend a plastic bag filled
with water, noting its contour. B. Introduce air forming an air-fluid level, the contour changes, and a succussion
splash occurs with shaking. C. An uncomplicated pleural effusion: note the tapering upper wedge, or meniscus, of
fluid. D. Hydropneumothorax: when air is introduced, a fluid level forms and the meniscus largely disappears.
trachea to the affected side. The collapsed lung is dull because its density is
increased. The bronchial plug prevents transmission of air vibration, so vocal
fremitus and breath and voice sounds are absent (Fig. 8-33, right). DDX: Tracheal deviation distinguishes atelectasis from consolidation with bronchial
plug and from pleural effusion. Dullness and decreased breath sounds at the
left scapular tip can be caused by a large pericardial effusion compressing the
LLL (Ewart sign).
examination
Air
Pneumonia with small consolidation. A small, deeply placed consolidation
may produce impaired resonance or dullness, depending on its size and distance from the chest wall. The dense lung efciently transmits airway sounds,
so vocal fremitus is increased and bronchovesicular or bronchial breathing
and crackles may be heard (Fig. 8-34, left). Fever, chills, and productive cough
are accompanied by tachypnea and tachycardia. The consolidation produces
whispered pectoriloquy and bronchophony. Small regions of consolidation
must be distinguished from a small cavity lying near a bronchus. A denitive
diagnosis requires imaging. Pneumonia, granulomatous lung inltrates, neoplasm involving bronchus, rheumatoid arthritis (RA), and sarcoidosis may all
produce these ndings.
Dullness with accentuated vibration
Pneumonia with lobar consolidation. The dense lung causes dullness or
atness on percussion. Consolidated lung in contact with a bronchus efciently transmits vibrations so vocal fremitus is pronounced, there is bronchial breathing, and whispered and spoken voice produce pectoriloquy and
bronchophony (Fig. 8-34, middle right). Crackles are frequently present. Lung
volume is unchanged, so the trachea is midline. These nding are classically
found in lobar pneumonia, but occasionally in lung neoplasms and pulmonary infarction. DDX: Consolidation can be confused with a thick-walled cavity, the distinction being made by imaging. Massive pleural effusion gives
dullness and transmits loud bronchial breath sounds above the effusion, but
the trachea is usually displaced to the unaffected side.
Chest, Trachea, and Respiratory Signs 311
Tr
Tension
Hydropneumothorax
Pulmonary
Closed
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emphysema
acheal deviation O
Fremitus
Percussion
Breath sounds
Whisper sounds
Voice sounds
Hyperresonant Resonant or hyper Hyperresonant
V or O
V or O
Rales
V or O
+ or O
V
pneumothorax
O
O
V or O
V or O
V or O
O
Coin sound
FIG. 8-36 Thoracic Disorders with Resonance Impaired Vibration.
direction of deviation.
pneumothorax
O
V or O
V or O
V or O
O
Coin sound Coin sound
, absent ; ∨, diminished; +, present; →,
°
(a) Hyperresonant
(b) Flat
O
O
O
O
Succussion splash
Shifting dullness
Thick-walled cavity. Dullness, increased vocal fremitus, bronchovesicular
breathing, and pectoriloquy indicate consolidation (Fig. 8-34, middle left).
Amphoric breathing or cracked-pot resonance is rarely heard, but even these
signs can occur in consolidation without cavity.
Resonance and hyperresonance
Pulmonary emphysema. Loss of interstitial elasticity and interalveolar septa
leads to air trapping increasing lung volume. The air trapping holds the chest
in the inspiratory position producing a barrel chest. The diaphragm is attened, so the costal margins move out sluggishly or converge during inspiration (Fig. 8-36, left). The lungs are hyperresonant throughout because of their
low density. Air pockets transmit vibrations poorly so vocal fremitus, breath
sounds, heart sounds, and whispered and spoken voice are diminished or absent. When the breath sounds are audible, they are faint and harsh, distinctively
lacking the rustling quality of vesicular breathing; this may antedate recognizable X-ray evidence of emphysema. The expiratory phase of respiration usually
exceeds the inspiratory phase in proportion to the patient’s degree of airow
obstruction. The elevated clavicles and attened diaphragm in severe emphysema with air trapping cause the thyroid cartilage to be low in a shortened neck
and it descends <4 cm toward the suprasternal notch with full inspiration. The
thyroid is often in a retrosternal position and not palpable. Crackles are not
consistently heard in homogenous emphysema and when present suggest concurrent bronchitis, pneumonia or interstitial lung disease. Similarly, concurrent
wheezing suggests an acute exacerbation of chronic obstructive pulmonary
disease or overlap syndrome with asthma and bronchial hyperactivity.
Closed pneumothorax. When the air leak between lung and parietal pleura
is intermittent or self-limited, a closed pneumothorax forms. If the enclosed
312 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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air volume is small, the lung remains partially inated, and the mediastinum
is not displaced (Fig. 8-36, middle left). An open pneumothorax with pleural adhesions preventing lung collapse and tracheal displacement presents
similarly. Vocal fremitus, breath sounds, and whispered and spoken voice
are usually diminished or inaudible. The chest is resonant or hyperresonant.
Frequently, pneumothorax cannot be distinguished from a normal or emphysematous chest by percussion alone. Asymmetric breath sounds suggest
pneumothorax on the quieter side. The trachea may deviate toward the affected side during inspiration (pendular deviation).
Open pneumothorax. In open pneumothorax there is continuous and
open air leak between lung and pleural cavity so the pneumothorax is
at atmospheric pressure. The affected lung completely collapses and the
mediastinum may be drawn toward the unaffected side by elastic recoil
of the unaffected normal lung. Overlying the pneumothorax, the chest
wall is hyperresonant or tympanitic. Fremitus and breath and voice
sounds are absent. The patient is usually severely dyspneic and may be
cyanotic.
Tension pneumothorax. A one-way tissue valve permitting air entry into
the pleural space during inspiration prevents its expulsion during expiration, the intrapleural pressure rapidly increasing. The affected lung
is collapsed and the increasing intrapleural pressure causes extreme
tracheal deviation, compression of the unaffected lung, and decreased
venous return to the heart (Fig. 8-36, middle right). Decreased respiratory excursion, a distended tympanic hemithorax, and tracheal
away from the affected side are diagnostic of tension pneumothorax.
There is deep cyanosis, severe dyspnea, and shock; release of air from
the pleural cavity is lifesaving.
deviation
Hydropneumothorax. Upper thoracic hyperresonance or tympany with inferior dullness suggests hydropneumothorax or massive pleural effusion
(Fig. 8-36, right). In either case, the trachea can be displaced to the unaffected side. In hydropneumothorax, the hyperresonant region does not
transmit fremitus, breath sounds, or voice sounds. The lung above a simple
hydrothorax transmits well. With hydropneumothorax, percussion easily identies the uid level; the level is vague in simple effusion. Shifting
dullness is readily demonstrated by percussion with hydropneumothorax.
The air-lled cavity carries bell tympany, and a succession splash may be
demonstrated.
Sounds suggesting hydropneumothorax. Fluid moves silently in a cavity devoid of air. When the cavity contains both air and uid, body movements
cause a succussion splash, audible to patient and examiner. Grasp the patient’s
shoulders shaking the thorax while listening with and without a stethoscope.
An abdominal succussion splash is present in the normal and dilated stomach.
A thoracic succussion splash suggests hydropneumothorax, but a uid-lled
stomach herniating into the thorax through a diaphragmatic hernia can also
produce the splash. Occasionally, a falling-drop sound is heard, resembling a
drop of water hitting a uid surface. A metallic tinkle may be heard when air
bubbles emerge through a small bronchopleural stula below the uid level;
when the stula is larger, the air may gurgle, a lung-stula sound.
Cardiovascular Signs 313
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Sputum Signs
Bloody sputum—hemoptysis. Priority is to identify the likely anatomic site
of hemorrhage. Blood-streaked sputum is most commonly caused by inammation in the nose, nasopharynx, gums, larynx, or bronchi. If occurring only
after severe paroxysms of coughing, it is attributed minor airway trauma.
Pink sputum, from blood mixing with respiratory secretions in the alveoli or
bronchioles, is characteristic of pneumonia and pulmonary edema. Massive
bleeding occurs with erosion of a bronchial artery by cavitary tuberculosis,
aspergilloma, lung abscess, bronchiectasis, embolism with infarction, bronchogenic carcinoma, or a broncholith. Alveolar hemorrhage, from pulmonary
vasculitis or blunt chest trauma, may not produce bloody sputum until the
degree of hemorrhage and anemia is severe. Frankly bloody hemoptysis in
the setting of trauma, recent cardiac or thoracic surgery, tracheostomy or
aneurysm may be associated with life-threatening arterial-bronchial or arterial-tracheal stula.
Bloody gelatinous (Currant-Jelly) sputum. Copious tenacious, bloody sputum is prominent in pneumonia caused by Klebsiella pneumoniae or Streptococ-
cus pneumoniae.
Rusty sputum. In pneumococcal pneumonia, minor frank hemoptysis may
precede purulent sputum containing degraded blood.
Frothy sputum—pulmonary edema. Alveoli ooded with transudated uid,
yield thin blood tinged sputum containing air bubbles suggesting pulmonary
edema of any cause.
Purulent sputum.
kocytes, enter the airways and alveoli in response to lower airway infection.
The exudate may be yellow, green, or dirty gray. Scant purulent sputum is
typical of acute bronchitis, resolving pneumonia, and a small tuberculous cavity or lung abscess. Copious purulent sputum occurs with lung abscess, bronchiectasis, or bronchopleural stula communicating with an empyema. Fetid
sputum characterizes anaerobic infection and/or lung abscess. Lung abscesses
with minimal connection to the airways do not produce much sputum.
Stringy mucoid sputum. In asthma there is increased mucous production
and mucous plugging or small, and sometimes large, airways.
Broncholiths. Sputum broncholiths originate in calcied lymph nodes eroding a bronchus or from calcareous granulomas in silicosis, tuberculosis, or histoplasmosis. They may suggest the source of pulmonary hemorrhage [Harris
NL, McNeely WF, et al. Case 14-2002. Case records of the Massachusetts
General Hospital. N Engl J Med. 2002;346:1475–1482].
Inammatory cells, predominately polymorphonuclear leu-
CARDIOVASCULAR SIGNS
Interpretation of physical signs from inspection, palpation, and precordial
percussion assumes normal anatomic relations of the heart and chest wall.
With thoracic deformity, e.g., kyphoscoliosis and pectus excavatum, caution
is advised.
314 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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Inspection
Dyspnea (shortness of breath). See page 294.
Pallor. See Chapter 6, page 127.
Cyanosis. See Chapter 6, page 127.
Palpation
Edema. Extracellular uid partitions between the vascular and interstitial
compartments by a net equilibrium between hydrostatic and oncotic pressures. Normally, intravascular uid ows into the extravascular interstitial
space in the precapillary arterioles and capillaries since hydrostatic pressure
(intravascular > interstitial) is only partially offset by the opposing oncotic
pressure (intravascular > interstitial). In the postcapillary venules, lower
intravascular hydrostatic pressure is more than compensated by intravascular oncotic pressure, resulting in interstitial saline owing back into the
intravascular space. Concomitantly, interstitial uid, proteins, and cells are
returned to the blood from the interstitial space and via lymphatics. Altering one or more of these forces upsets this equilibrium. Increasing venous
pressure in CHF produces dependent edema; venous occlusion can result in
localized edema. Obstructed lymphatics lead to lymphedema. Low plasma
albumin (the plasma protein contributing most to oncotic pressure) lowers
the plasma oncotic pressure, permitting edema to form that may rst appear
where tissue pressure is low, e.g., the periorbital tissue. Increased capillary
permeability causes edema that is not dependent. Tissue inammation, triggered by bacterial, chemical, thermal, or mechanical means, increases capillary permeability creating localized edema.
Excessive interstitial uid accumulation, either localized or generalized,
is edema. Extensive generalized edema is anasarca. In adults, ~4.5 kg (10 lb) of
uid must accumulate before pitting edema is detectable. Edema is demonstrated by gently pressing a thumb into the skin against a bony surface, e.g.,
the anterior tibia, dorsum of the foot, or sacrum. When the thumb is withdrawn, an indentation persists.
The distribution of edema is important diagnostically. Responding to grav-
ity, dependent edema rst appears in the feet and ankles, or over the posterior
calves or sacrum in supine patients. As the dependent uid volume increases,
a uid level may be detected, which seldom rises above heart level. Anasarca
is recognized at a glance when it obliterates supercial landmarks. Chronic
edema leads to brosis of the subcutaneous tissues and skin so they no longer
pit on pressure, brawny edema. Symmetric edema affecting both legs suggests
a problem in the pelvis or more proximally, whereas edema limited to the
arms and head suggests SVC obstruction.
Edema limited to one extremity suggests a local problem with vascular
channels or local inammation. Edema formation is the same whether it is
generalized or local. To evaluate local edema, the examiner must consider the
local anatomy of the arteries, veins, lymphatics and soft tissues, the presence
of any inammatory or structural disease, and then form hypotheses as to the
likely mechanism and anatomic site of the problem.
Exclusive dependence upon bedside exam can overlook cardiovascular
causes of bilateral leg edema, so consider BNP measurement and/or echocardiography estimating right heart pressures, RV and LV size and function, and
Cardiovascular Signs 315
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tricuspid valve function. The following approach, based upon the anatomic
distribution of edema, is diagnostically useful.
CLINICAL OCCURRENCE: Localized Edema—Inammation: Infection,
angioedema, contact allergy;
Valves:
With or without varicosities; Venous Thrombosis: Postoperative,
immobilization, prolonged air or automobile travel;
Compression:
Injuries:
(insects, snakes, spiders); Congenital: Amniotic bands, arteriovenous stulas,
Milroy disease; Bilateral Edema Above the Diaphragm: SVC obstruction;
Bilateral Edema Below the Diaphragm: CHF with elevated jugular venous
pressure, including pulmonary hypertension from left heart abnormalities,
intrinsic pulmonary disorders, right heart abnormalities, and constrictive
pericarditis; Portal Vein Hypertension or Obstruction: Cirrhosis, portal vein
thrombosis, schistosomiasis;
sion, pregnancy; Loss of venous tone: Drugs (calcium channel blockers, angiotensin-converting enzyme inhibitors, other vasodilators), convalescence, lack
of exercise; Generalized Edema—Hypoalbuminemia: Nephrotic syndrome,
cirrhosis, chronic liver disease, protein losing conditions (e.g., enteropathy,
burns, stulas); Renal Retention of Salt and Water: Corticosteroids, NSAIDs;
Increased Capillary Permeability: Sepsis, systemic inammatory response syn-
drome, interleukin-2, idiopathic capillary leak syndrome.
Idiopathic edema. Recurrent and chronic edema occurs in women in the third
to fth decades without heart, liver, or kidney disease or venous or lymphatic
obstruction. Affective disorders and obesity may coexist. Possible mechanisms include mild persistent precapillary arteriolar dilatation, exaggerated
capillary leak on standing, and inappropriate chronic diuretic administration, often started for minor peripheral edema (diuretic-induced edema). Each
mechanism inappropriately activates renin–aldosterone leading to salt and
water retention.
Malignancies, constricting garments; Chemical or Physical
Burns, irritants and corrosives, frostbite, chilblain, envenomation
Metabolic/Toxic: Gout; Insufciency of Venous
Venous or Lymphatic
IVC obstruction: Thrombosis, extrinsic compres-
Heat-related edema. Pitting ankle edema often occurs in normal adults within 48 h of arriving in the tropics from a temperate climate, or in temperate
zones when weather changes from cool and dry to warm and humid. It spontaneously resolves with acclimatization.
Angioedema. Painless subcutaneous soft-tissue edema begins abruptly and
spreads to involve several centimeters of tissue with diffuse borders. Erythema is not prominent. Angioedema often involves the face, lips, or tongue
and laryngeal involvement is life threatening. Causes include hereditary absence of C1 esterase, allergen exposure, and angiotensin-converting enzyme
inhibitors.
Apical impulse, point of maximal impulse (PMI). Careful examination of
the apical impulse yields useful information about heart size, force of LV contraction, obstruction to LV ejection, and stroke volume.
Increased amplitude. Increased force of LV contraction increases the apical impulse amplitude. Common causes are LV hypertrophy (arterial hypertension,
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