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376 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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FIG. 8-53 Signs of Arterial Insufficiency. A. Poor wound healing. B. Nail dystrophy. C. Digital
gangrene.
Raynaud phenomenon occurs more frequently in patients with migraine
(26%) than in those without (6%). There is also an increased prevalence of
chest pain and migraine in patients with Raynaud disease. DDX: Always
inspect the nailbed capillaries (Chapter 6, page 107); abnormal capillaries
are highly suggestive of scleroderma. The sequence of pallor, cyanosis, and
redness is diagnostic when induced by cold exposure. Raynaud disease
should not be confused with the vascular changes of complex regional pain
syndromes (Chapter 4, page 75).
Acrocyanosis. Excessive arteriolar constriction is ascribed to increased sym-
pathetic tone, although humoral factors may contribute. This is a benign
painless condition in which the skin of the hands and feet is persistently cold,
cyanotic, and moist. It is most common in young women. The skin is uniformly cyanotic, which worsens on cold exposure. Elevation and sleep abolish the cyanosis.
Digital gangrene. Gangrene of the nger and toe tips is caused by any disease
or condition impairing peripheral perfusion. Causes include scleroderma,
pneumatic hammer disease, atherosclerosis, thromboangiitis obliterans, cold
agglutination disease, cryoglobulinemia, atheroemboli, sepsis, meningococcemia, vasopressor medications, antiphospholipid syndrome, warfarin skin
necrosis (protein C deciency), ergotism, and chronic renal failure.
Ergotism. Ergots induce intense constriction of peripheral blood vessels;
some individuals are particularly sensitive. Ergot may be taken as a drug or
eaten with dietary grain contaminated by a fungus. The rst symptom is often burning extremity pain (St. Anthony re) with loss of pulses in the hands
and/or feet. Headache, weakness, nausea, vomiting, visual disturbances, and
angina pectoris may occur. Cold skin and mottled cyanosis of the extremities
follows. Finally, symmetrical gangrene involves the ngers and toes, sometimes extending proximally.
Cavernous hemangiomas. Congenital cavernous hemangiomas occur anywhere in the body. The limb is circumferentially enlarged and dilated, purplish, blood-lled, readily compressible sinuses raise the skin surface. This
is distinguished from varicosities by a distribution not congruent with the
Chest, Cardiovascular, and Respiratory Syndromes 377
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large limb veins. With leg involvement standing may pool enough blood to
cause orthostatic hypotension. Massive cavernous hemangiomas trap platelets producing thrombocytopenia, purpura, and bleeding (Kasabach–Merritt
syndrome).
Aneurysms in the arms and neck. The subclavian, axillary, and brachial
arteries are most commonly affected; the carotids are rarely involved. Trauma
to the vessel wall is the most common cause; rarely, the vessels are involved
by mycotic, necrotizing, or atherosclerotic aneurysms. The aneurysms are
easily palpated.
Aneurysms in the legs. The most common sites are the femoral artery in the
Scarpa triangle and the popliteal artery in its fossa. Atherosclerosis is the most
common cause. The aneurysms are readily palpable.
Disorders of the Major Extremity Veins
Deep vein thrombosis. See Pulmonary Embolism, page 343. Intraluminal
thrombus forms, usually in association with a lower extremity vein valve,
with or without an inciting event. The thrombus can propagate proximally
or distally and partially or completely occlude ow. Bland thrombus without
inammation appears more likely to dislodge. Leg veins are the most common
identied source of PE. Hip and knee surgery have particularly a high incidence of associated DVT.
therapy intended to prevent pulmonary embolus and diminish valve damage
predisposing to future thrombosis and venous stasis. The history and physical exam separate patients into low-, intermediate-, and high-risk categories
(Table 8-4). All patients in whom DVT is suspected should undergo further
testing. Diagnostic algorithms constantly change, so consult current protocols.
Early diagnosis can be lifesaving.
tightness or a sense of fullness, aggravated by standing and walking, are
noted. Signs: DVT may be accompanied by cutaneous cyanosis of the dependent foot and lower leg. Pitting edema of the foot, ankle, or leg that does not
resolve overnight and venous engorgement on the feet persisting with the legs
elevated to 45 degrees, suggest venous obstruction. Leg pain following the
course of the thrombosed vein may be induced by sneezing or coughing, the
pain disappearing when the vein is compressed proximal to the obstruction
(Louvel sign). Palpation may detect tender vein segments. Homan Sign: With
the knee in exion, forcefully dorsiex the ankle; calf or popliteal pain occurs
in ~35% of DVT patients. Homan sign is neither sensitive nor specic for DVT.
Timely diagnosis facilitates initiation of appropriate
Symptoms: Though often asymptomatic,
Thrombophlebitis. As the name implies, thrombosis is accompanied by inammation of the vein. Inammation may either precede or follow clot
formation. In addition to the signs and symptoms of thrombosis, pain and
inammation are prominent. When acute, the veins are painful and tender,
and the overlying skin is red and hot. Adjacent muscles may cramp. Fever
and leukocytosis are common. Acute femoral vein thrombophlebitis presents
with excruciating pain, massive leg edema, and pallor from arterial spasm
(phlegmasia alba dolens). The signs can suggest arterial embolism, but the pallor
is less intense, there is more cyanosis, the femoral vein is tender, anesthesia is
absent, and arterial pulses can usually be demonstrated by ultrasound. When
the entire venous drainage of an extremity is obstructed, there is extreme
378 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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TABLE 8-4Wells Criteria for Deep Venous Thrombosis Risk Stratification.
Clinical Feature Score
Current cancer or within the last 6 mo 1
Paralysis, significant limb weakness or immobilization of one or both legs 1
Bedridden for >3 d or surgery within 4 wk 1
Localized tenderness along the deep veins 1
Entire leg swollen 1
Calf circumference >3 cm compared to the asymptomatic leg, 10 cm below the tibial
tuberosity
Pitting edema greater in the symptomatic leg 1
Collateral (nonvaricose) superficial veins in the symptomatic leg 1
Alternative diagnosis as likely or more likely the DVT 2
Summary pretest risk estimation score observed prevalence of DVT:
Low
Moderate
High
Adapted from Wells PS, Anderson DR, et al. Value of assessment of pretest probability of deep-vein
thrombosis in clinical management. Lancet. 1997;350:1795–1798.
0 or less
1–2
3 or more
3%
17%
75%
1
pain, massive edema, and deep cyanosis of the entire limb (phlegmasia cerulea
dolens). Arterial and venous imaging are indicated.
CLINICAL OCCURRENCE: Congenital: DVT at an early age, at unusual sites
(e.g. upper extremity, mesenteric vessels), a history of recurrent thromboses
or emboli, a family history of DVT, or DVT with minimal trauma or minor
surgery suggest congenital thrombophilia. Identied etiologies include activated protein C resistance, factor V Leiden mutation, proteins C and S deciency, dysbrinogenemia, homocystinuria, antithrombin III deciency, and
sickle cell disease. Acquired: Antiphospholipid syndrome (lupus-like anticoagulant, anticardiolipin antibodies), heparin-induced thrombocytopenia and
thrombosis (HITT syndrome), leg fractures, limb surgery, trauma, prolonged
inactivity (bed rest, international air travel, automobile travel), infection, cancer (especially mucin-producing adenocarcinomas), hyperhomocysteinemia,
estrogen-containing medications, pregnancy, obesity, venous stasis and insufciency, diabetes mellitus, polycythemia vera, idiopathic thrombocythemia,
and paroxysmal nocturnal hemoglobinuria. Recurrent deep venous thrombosis may precede the diagnosis of cancer.
Post-phlebitic syndrome. Following proximal leg vein DVT, up to 50% of patients develop this syndrome. Pain and tenderness are slight, and the skin
is normal or cool. The leg is swollen, initially with edema, but, if untreated,
progresses to nonpitting brosis of the subcutaneous tissues and skin. Varicose veins may or may not be prominent. Venous stasis dermatitis is common.
Severe cases can be disabling.
Chest, Cardiovascular, and Respiratory Syndromes 379
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Supercial thrombophlebitis. Supercial vein thrombosis and inammation occurs either alone or extends from the deep veins. Patients complain
of tender red subcutaneous nodules or cords, often with a history of recent
trauma. Supercial thrombophlebitis can mask coincident deep vein disease, so underlying DVT should be investigated. Supercial thrombophlebitis rarely causes life-threatening pulmonary embolus.
and other skin and soft-tissue infections can be confused with supercial
thrombophlebitis, but the rm palpable venous cords are diagnostic.
Migratory supercial thrombophlebitis. Successive episodes of thrombophlebitis involve different veins in widely separated parts of the body. In a single
episode, a segment of vein becomes tender, reddened, and indurated. Involution begins in a few days and the adjacent tissues become successively blue and
yellow, often resolving with some skin pigmentation. Arm and leg veins are
most commonly involved, but the subcutaneous veins of the abdomen and thorax may be affected. Although the lesions do not cause serious discomfort, this
complex should prompt a search for an underlying disease. Migratory supercial thrombophlebitis is associated with antiphospholipid syndrome, thromboangiitis obliterans, Behçet syndrome, pancreatic carcinoma, and thrombophilic
hematologic disorders, especially paroxysmal nocturnal hemoglobinuria.
Venous stasis. Vein occlusion and incompetent valves impair ow resulting
in stasis changes. Occlusion is caused by external compression or luminal
plugging by brosis, thrombus, or intravascular neoplasm. The pumping
action of voluntary muscles is inhibited by bed rest and immobilization and
dilated vessels exacerbate stasis. Dilated supercial veins drain poorly into
smaller communicating veins. Deep vein dilatation causes their valves to
become incompetent. Decreased capillary ow produces poor skin nutrition,
chronic inammation, and brosis. Signs of venous stasis are pitting edema,
stasis pigmentation (hemosiderin), erythema, brosis, decreased skin elasticity, and ulceration (see Stasis Dermatitis, Chapter 6, page 135).
DDX: Lymphangitis
Varicose veins. Varicose veins are grossly dilated subcutaneous veins, often
lling by retrograde ow from the deep veins because of incompetent valves
in the perforating and deep veins. They are most common in legs (Fig. 8-54).
Primary varicosities develop spontaneously; secondary varicosities result
from proximal obstruction, e.g., pregnancy, trauma, and thrombophlebitis.
When varicose veins are seen only in one extremity, extrinsic compression
and an arteriovenous stula should be considered. An AVM produces pulsation in the dilated veins.
Axillary vein thrombosis. This usually follows trauma or intensive arm use
in hyperabduction, such as throwing. The entire arm swells and aches. The
tissues are rm without pitting edema. The supercial veins at the superior
thoracic aperture may be dilated. Poor collateral circulation results in cutaneous cyanosis. Axillary vein thrombosis is less likely to lead to lethal pulmonary emboli than deep venous thrombosis in the legs, but it does occur.
When chronic, it must be distinguished from lymphedema. Both conditions
produce solid, nonpitting swelling, but venous obstruction causes some cyanosis of the skin; the skin is pallid in lymphedema. Lymphedema of the arm
was common after radical mastectomy.
DDX:
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FIG. 8-54 Large Superficial Veins of the Legs. The great saphenous vein begins on the medial aspect of the
foot, courses backward under the medial malleolus, up the medial aspect of the calf, behind the medial epicondyle, and then
obliquely across the anterior thigh to the femoral vein as it enters the femoral canal beneath the inguinal ligament. The small
saphenous vein begins on the lateral side of the foot, curves backward beneath the lateral malleolus, and then upward on
the posterior surface of the calf to enter the popliteal fossa and join with the popliteal vein. The middle figure diagrams the
communications between the superficial veins (heavy solid lines) and the deep veins (broken lines)
and the communicating vessels (dotted lines).
SECTION 2
The Breasts
BREAST PHYSIOLOGY
The Female Breast: The breast is a highly complex, specialized skin-related
gland. The mammary glands are undeveloped in children and men. In
women, ovarian estrogen production at puberty initiates development which
reaches maturity in the childbearing years. Luteal progesterone secretion at
onset of ovulation results in alveolar development. Other hormones, including prolactin, adrenocorticotropic hormone, corticosteroids, growth hormone, thyroxine, and androgens, play facultative roles in breast development
and milk production. The mature breast is conical or hemispheric, containing 15–20 subdivided lobes, arranged radially, each with a separate excretory
lactiferous tubule and nipple orice. Considerable fat surrounds the glands,
so discrete lobes are not ordinarily palpable. Vertical brous bands (Cooper
ligaments) pass from the pectoralis fascia through the breast parenchyma to
the skin, suspending the breast on the chest wall. A fascial cleft separates the
deep surface of the breast from the thoracic wall, permitting some mobility.
The adult breast has four major components: stroma, ductal epithe-
lium, glandular acini, and the myoepithelium, each inuenced by a variety
Physical Exam of the Breasts 381
Note axillary tail
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of hormones. The breast glands respond to pituitary and ovarian hormones.
Follicular estrogens stimulate minimal mitotic activity, whereas luteal progesterone provokes signicant cell division increasing breast size. If conception
takes place, estrogens, progesterone, and prolactin stimulate extensive alveolar
and ductal proliferation. With parturition progesterone suppression of prolactin ceases, allowing the epithelium to become actively secretory, releasing milk.
The Male Breast: The undeveloped male breast is easily examined.
Unfortunately, exam is frequently neglected delaying recognition of serious
disease. Men have residual breast anlage that will respond to hormones from
adolescence to old age. Breast development is stimulated by abnormal hormone production, including hyperthyroidism, prolactin-secreting adenomas,
acromegaly, testicular and adrenal tumors, and many drugs in addition to estrogens. Liver disease increases circulating estrogenic hormones so gynecotmastia
is associated with advanced liver disease, particularly alcoholic cirrhosis.
SUPERFICIAL BREASTS ANATOMY
The breast’s roughly circular contact with the pectoral fascia extends from the
second to the sixth or seventh ribs with an axillary tail projecting laterally and
superiorly along the axillary and serratus anterior fascia (Fig. 8-55).
The nipple lies slightly below and lateral to the center of the breast. It has
papillae containing the lactiferous tubule orices and pigmented skin extending onto the surface of the breast as the areola. Nipple and areola color vary
from pink to brown, depending on the individual’s complexion and parity.
Both darken, and the areola enlarges after the second month of pregnancy.
The sebaceous glands of Montgomery (areolar glands) form small elevations
on the areolar surface. Their secretions protect the nipples during nursing.
Areolar stimulation causes the subcutaneous radial and circular muscle bers
to contract producing nipple erection.
PHYSICAL EXAM OF THE BREASTS
The American Cancer Society and others provide guidelines for periodic
breast cancer screening in women by breast exam and mammography. Also,
FIG. 8-55 Quadrants of the Breast. The hemisphere of the breast is divided into quadrants by imaginary vertical
and horizontal lines intersecting at the nipple. The quadrants are named upper medial, upper lateral, lower medial, and lower
lateral. Popularly, these quadrants are also named, respectively, upper inner, upper outer, lower inner, and lower outer. Note
the protrusion of the upper lateral quadrant, called the axillary tail, in which breast tissue extends to the axilla.
382 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
of mass
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regularly examine the male breast since breast cancer, and other conditions
enlarging breast tissue in men, are easily identied on exam. The breasts are
usually inspected and palpated with the patient sitting and supine. If the
patient complains of a breast lump or a possible mass is detected, a more
extensive exam is required. The breasts engorge before menses and during
pregnancy, making the exam more painful and less accurate. The best time for
breast exam is 5–7 days after onset of menses.
Breast Examination: The patient is examined sitting and supine, being cer-
tain to examine the creases under and between the breasts. If the patient has
noted a lump, ask her to point it out. Always palpate the opposite breast
rst. Palpate both breasts in all four quadrants by compressing breast tissue
between the three middle ngers pads and chest wall. Search for warmth,
tenderness, and masses. When a mass is found, note its location, size, mobility, and consistency. Test for xation to the underlying fascia by grasping the
mass between thumb and forenger attempting to move it back-and-forth
transversely, then up-and-down. Repeat this procedure while the pectoralis
muscle is tensed. Gently pinching the overlying skin reveals dimpling indicating that the mass is xed to the skin (Fig. 8-56A). Transilluminate the mass
to determine if it is opaque or translucent (Fig. 8-56B). Finish with regional
lymph nodes palpation (Chapter 5, page 83 and Fig. 5-2).
Patient sitting with arms down. With the disrobed patient sitting, compare
breast size and shape; the left may normally be slightly larger. Look for bulging or attening of the contour, nipple displacement or retraction, skin dimpling, dilated supercial veins, or peau d’orange skin changes (Fig. 8-57A).
Patient sitting with arms raised. With the arms raised overhead, look for a shift in
the relative position of the nipples, and for skin dimpling, or bulging (Fig. 8-57B).
A. Compression to
show dimpling
FIG. 8-56
shortening of the suspensory ligaments of the breast from neoplasm or inflammation. B. Transillumination: the density
of a mass may, on occasion, be ascertained by transillumination of the breast; transparency probably means a cyst full of
fluid; other masses are opaque.
Further Breast Examination. A. Breast compression to accent dimpling: dimpling is a sign of
B. Transillumination
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Patient sitting with hands pressing hips. Pressing the hands downward on
the hips puts tension on the breast ligaments arising from the pectoralis major
fascia which can reveal dimpling. For a mass in the axillary tail, tense the
serratus anterior muscle by having the patient press her hand downward on
your shoulder (Fig. 8-57C).
Patient sitting with trunk bent forward. When the breasts are large and pendulous, having the patient lean forward so the breasts hang free from the
chest wall facilitates inspection and palpation between the ats of both hands
(Fig. 8-57D).
Patient supine. Most breast masses are detected in this position; proper technique is critically important (Fig. 8-57E). The entire breast from the second
to sixth rib and from the sternal border to the midaxillary line is palpated
against the chest wall. The lateral half of the breast is best palpated with the
patient rolled onto the contralateral hip and the medial half with the patient
supine, both with the ipsilateral hand behind the head. Palpate with the three
middle nger pads rotating in small circular motions and moving in vertical
overlapping passes from rostral to caudal and then caudal to rostral in the
next pass. Vary nger pressure from light to medium to deep.
Nipple exam. Inspect the anterior trunk for supernumerary nipples. Look for
ssures, scaling, excoriation, and nipple retraction or deformity.
BREAST SYMPTOMS
Breast Pain: The patient with pain or a lump in the breast often fears can-
cer. Many women will, at some time, experience breast discomfort signicant enough to seek a physician’s advice. Common causes of breast pain
are engorgement during the luteal phase of the menstrual cycle, pregnancy,
hematoma, cysts, mastitis and abscess, galactocele, and nipple disorders
including ssures, inammation, and epithelioma.
Breast Mass: Breast masses arise from cystic changes, benign proliferation
of ductal or acinar tissue, infection, inammation or brosis of the breast
stroma, and neoplastic change in the ductal epithelium (ductal carcinoma)
or the acinar tissues (lobular neoplasia). A breast mass must be accurately
described noting its location (use the nipple as the center of a clock face: state
the o’clock position and the radial distance from the nipple), size, shape,
consistency (hard, rm, uctuant, soft), texture (smooth, irregular), mobility
(mobile, xed to the breast tissue, pectoral fascia or skin), and tenderness.
Thoroughly examine the regional lymph nodes (axillary, infraclavicular, and
supraclavicular) for lymphadenopathy. Masses identied by the patient or
clinician should never be ignored or be assumed to be benign. The patient’s
age and breast cancer risk factors should not deter evaluation of a breast
mass. See page 386 for a discussion of common breast masses.
All masses persisting through one complete menstrual cycle and all masses in
postmenopausal women require evaluation by a clinician experienced in the diagnosis
and management of breast diseases and breast cancer. A normal mammogram or nonvisualization of a palpable mass by ultrasonography does not exclude cancer.
BREAST SIGNS
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FIG. 8-57 Patient Positions for Breast Examination. T he patient is st ripped to the waist and sits facing t he exam-
iner. A. The patient stands with arms at sides. The examiner looks for elevation of the level of a nipple, dimpling,
bulging, and peau d’orange. B. The patient raises her arms. Dimpling and elevation of the nipple are accentuated
when there is a mass fixed to the pectoral fascia. C. The patient pushes her hands down against her hips. This
flexes and tenses the pectoralis major muscles while the examiner attempts to move the mass to determine fixation to the
underlying fascia. D. Examining large and pendulous breasts. The patient is asked to lean forward, so the breasts
hang free from the chest wall, making; retraction and masses more evident. E. In the supine position. The examiner
presses the breasts against the chest wall with the flat of his hand. The normal lobules are less prominent and significant
masses are more distinctly felt.
Breast Tenderness (Mastodynia): During the luteal phase of the menstrual
cycle and with pregnancy and lactation the breasts undergo glandular proliferation becoming larger, more engorged, and tender. Many women, in
child-bearing years, have tenderness that varies through the menstrual cycle
never resolving completely. The breasts can be rm and lobular but without
distinct masses. Common causes of breast pain are engorgement during the
luteal phase of the menstrual cycle, pregnancy, hematoma, cysts, mastitis and
abscess, galactocele, and nipple disorders including ssures, inammation,
and epithelioma.
Breast Cysts: Cystic change in the breast creates single or multiple tender
uid-lled cysts. The patient has tenderness uctuating through the menstrual cycle. Exam discloses one or more smooth, usually mobile, tender tense
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masses either uctuant or rm. Ultrasonography or needle aspiration conrms the cyst.
Supernumerary Nipples (Polythelia) and Breasts (Polymastia): Extra
nipples occur frequently in both sexes as minor developmental errors;
rarely, they are associated with glandular tissue forming a complete breast.
Supernumerary nipples are smaller than normal and often mistaken for
moles. Close examination may disclose a miniature nipple and areola. Most
occur in the mammary line (milk line) on the thorax and abdomen. They are
found rarely in the axilla or on the shoulder, ank, groin, or thigh where they
must be distinguished from moles.
Inverted Nipples: A common harmless developmental anomaly results in
the nipple having a crater-like depression. Nipple retraction appearing after
maturity suggests underlying neoplasm or inammation.
Nipple Fissures: Breaks in the skin are usually caused by local infection,
possibly in association with an unsuspected abscess.
Duct Fistula: A chronic draining wound close to the nipple and areola may be
a stula from an underlying duct.
Skin or Nipple Retraction: Acquired nipple retraction and skin dimpling are
caused by shortened suspensory ligaments, and/or xation to the underlying
pectoral fascia by tumor or inammation. Skin and nipple retraction and/or
limited breast mobility on the chest wall suggest an underlying mass. Always
examine for regional lymphadenopathy. Retraction can also be the result of
previous mastitis, but that should not be assumed unless the evolution from
acute mastitis to xation and retraction has been personally observed.
Nipple Discharge: Abnormal breast secretions are concerning. Most causes
are benign. Discharges are serous, bloody, or opalescent. Bilateral discharges
usually result from hormonal inuences. A pathologic condition is more likely
if the discharge is unilateral. To detect nipple discharge, gently compress
the nipple and areola between the thumb and forenger. Cytology or breast
biopsy may be necessary. Common causes of breast discharge are intraductal
papilloma, brocystic disease, and sclerosing adenosis. Less common causes
are chronic cystic mastitis, duct ectasia, galactocele, papillary cystadenoma,
keratosis of nipple, fat necrosis, acute mastitis or abscess, tuberculosis, toxoplasmosis, and eczema of the nipple. Malignant lesions include ductal carcinoma, lobular carcinoma, sarcomas, and Paget disease of the nipple. Invasive
breast cancers do not ordinarily cause a discharge.
Nipple Scaling and Excoriation—Paget Disease: An invasive malignancy
extends along the ductal system, lactiferous tubules, and/or supercial lymphatics onto the nipple, areola, and skin, then further extends in the skin.
Patients feel tingling, itching, and burning. The nipple, being reddened, scaling,
and excoriated, appears eczematoid. Complete nipple destruction may occur.
Areolar Gland Abscess: The sebaceous glands of Montgomery become
inamed, forming tender, palpable abscesses in the periphery of the areola.
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