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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2853_Библиотеки_им_академика_М_И_Перельмана
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116 CHAPTER 6: The Skin and Nails
A. FissureB. Ulcer
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Erosions. Erosions are partial thickness loss of epidermis (Fig. 6-11B) that
ooze and heal without scarring.
or following mechanical or thermal trauma.
Examples: After rupture of vesicles or bullae
Fissures.
Fissures are vertical epidermal cleavages extending into the dermis
(Fig. 6-12A) commonly following trauma to thick dry inelastic skin on the
hands and feet.
Ulcers are excavated lesions with loss of epidermis and papillary
Ulcers.
dermis (Fig. 6-12B).
Examples: Chapped lips, hand eczema.
Examples: Trauma, pressure over bony prominences
(pressure ulcers), pyoderma gangrenosum, burns, stasis ulcers, necrotizing
infections (bacterial, fungal).
Generalized Skin Signs.
Petechiae and purpura. See page 129. Disrupted dermal vessels extravasate
blood into the skin producing nonblanching red macules and patches.
Telangiectasia.
with pressure.
Telangiectasia are dilated small blood vessels that blanch
Examples: Spider angiomas, hereditary hemorrhagic telangi-
ectasia, rosacea, sun and irradiation damage.
Gangrene.
Ischemic skin and subcutaneous tissue necrosis creates a black
eschar. In arterial insufciency, the lesions are atrophic and dry (dry gangrene). Other necrotizing processes may produce an edematous weeping,
lesion, moist gangrene.
Examples: Dry Gangrene: Arterial insufciency, vas-
culitis. Moist Gangrene: Aspergillosis, pyoderma gangrenosum, necrotizing
fasciitis.
Urticaria.
leak leading to dermal and epidermal erythema and edema.
Inammatory mediators produce local capillary dilation and
The lesions are
discrete raised erythematous papules and plaques often intensely pruritic.
Precipitating factors are allergic, mechanical, or physical. Individual lesions
FIG. 6-12 Fissures and Ulcers. A. Fissures are vertical splits extending through the epidermis into the dermis.
B. Ulcers are actual loss of epidermal and dermal tissues that may extend into the subcutaneous tissue and muscle down
to bone.
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are present <24 hours distinguishing urticaria from persistent lesions with
a similar appearance, e.g., erythema multiforme. Urticarial lesions lasting
>24 hours suggest urticarial vasculitis. Chronic urticaria may last for years.
Examples:
cise, dermatographia;
Allergic: Drug eruptions, topical sensitivity; Physical: Cold, exer-
Systemic Diseases: SLE.
Dermatographia.
Dermatographia is urticaria caused by stroking the skin.
Normally, a light scratch produces linear macular blanching limited to the
scratched skin. Urtication produces a bright-red macular line becoming more
purple with time. In more severe responses, a red mottled are develops lateral to the red line and a wheal may develop.
Mastocytosis.
Mast cells inltrate the skin producing brown macules that
urticate when stroked (Darier sign). Mastocytosis may be limited to the skin
(urticaria pigmentosa) or produce systemic disease with hepatosplenomegaly
and signs of systemic histamine release (abdominal pain, diarrhea, peptic ulcer, hypotension, ushing).
Angioedema. Localized interstitial edema in the dermis and subcutaneous
tissues may be caused by IgE-mediated allergy, complement activation, nonimmunologic mast cell activation, or it may be idiopathic. Single or multiple
pruritic nonpitting swellings appear on the face, tongue, larynx, hands, feet,
and/or genitalia that subside with or without treatment. Nausea, vomiting,
and diarrhea are indicative of gastrointestinal involvement. Laryngeal angioedema can cause fatal airway obstruction.
CLINICAL OCCURRENCE: IgE-mediated: Hymenoptera (bee) stings, drugs
(e.g., penicillin and other antibiotics), food allergens (e.g., peanuts, shellsh), foreign proteins used therapeutically, many others; Non-IgE-mediated:
Angiotensin-converting enzyme inhibitors, radiologic contrast agents, cold
exposure; Complement Mediated: Hereditary angioedema (C1-esterase deciency), serum sickness, vasculitis.
Dry skin—xerosis and anhydrosis.
function leads to excessive drying.
Loss of sebaceous and/or sweat gland
The skin is dry, often cracked, and leathery.
Lacking normal oils, xerotic skin is more permeable to water. Aging results in
progressively more xerotic skin. Causes of dry skin include ichthyosis, anticholinergic drugs, denervation in peripheral neuropathies such as diabetes,
and removal of skin oils by frequent bathing with soap.
Decreased skin turgor—extracellular uid decit. Loss of extracellular uid
increases viscosity of interstitial uid. Not to be confused with decreased cuta-
neous elastic tissue. Check the lying, sitting, and standing BP and pulse for
postural changes; check skin turgor and look for longitudinal furrowing of the
tongue. Loss of total body water (dehydration) does not change skin turgor.
Decreased skin elasticity. Destruction or disruption of the dermal elastic
bers results in decreased elasticity. Decreased elasticity is evident as wrin-
kling and redundancy of the skin. It is a normal consequence of aging accelerated by sun exposure (solar elastosis), stretching (pregnancy, obesity), and
glucocorticoid excess (Cushing syndrome and iatorogenic). Pseudoxanthoma
elasticum is an uncommon cause.
118 CHAPTER 6: The Skin and Nails
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Scars. Epidermal injuries heal without scar but may alter pigmentation.
Injury to dermal elastic and collagen bers results in scarring. Deeper injury
to the subcutaneous fat and muscle results in visible depressions or masses.
All cutaneous scars are initially raised and red, fading over months to years
to a pallid hue as the vascularity diminishes. Sutured wounds healing without infection or tension produce thin scars with minimal bridging brosis.
Wounds healing by secondary intention leave wide inelastic scars. The pattern of scarring reects the mechanism (sharp trauma, burn, excessive tension, scarication, etc.) and etiology.
Surgical and traumatic scars.
ma. Without a history, the cause may only be inferred by its size, pattern, location, and contour (smooth or jagged). Suture marks indicate surgical repair
but not the depth of incision or injury. Full thickness burns heal with deep,
irregular, broad, inelastic scars.
Hypertrophic scars and keloids. In some individuals, cutaneous injury vari-
ably produces persistent raised, red, hypertrophic scars. Scars extending beyond the boundary of the inciting wounds are called keloids. Keloids may
progressively thicken over time. Keloids are more prevalent in dark-skinned
persons and after complicated wounds. They can occur after minor injury
anywhere on the body.
Striae. Stretching normal skin ruptures elastic bers in the reticular dermis.
In adrenal hypercorticism, the epidermis itself becomes fragile and easily
tears under normal tension. Striae are permanent. Multiple 1–6 cm scars run
axially under the epidermis in regions under chronic tension. When recent,
they are pink or blue; older striae are white. Although most common on the
abdomen, they are also found on the shoulders, thighs, and breasts. Striae are
different from traumatic and therapeutic scarring. Precipitating conditions
include abdominal distention (pregnancy, obesity, ascites, tumors), subcutaneous edema, Cushing syndrome (usually fresh-appearing purple striae).
Crepitus. Gas in subcutaneous tissues or muscle produces a peculiar sensation when pressure is applied caused by bubbles sliding under the ngers,
often accompanied by a crackling sound. Bubbles feel like small nontender
uctuant nodules moving freely with palpation. DDX: Subcutaneous crepitus
is pathognomonic of subcutaneous emphysema or gas gangrene. In subcutaneous emphysema, the bubbles contain air that entered the tissues through
operative wounds or trauma, e.g., fractured rib piercing the lung. Infection
with some anaerobic and microaerophilic organisms produces gas by fermentation. Severe local infection and systemic toxicity distinguish it from subcutaneous emphysema.
Identify each scar relating it to surgery or trau-
Changes in Skin Color.
Constitutive diffuse brown skin—normal melanin pigmentation. This
is the inherited constitutive skin color. Persons of African descent have the
greatest melanin density. Lesser amounts occur, in order, from South Asians,
Native Americans, Indonesians, Oriental Asians (Chinese and Japanese), to
Western Europeans who have the least. There is also variation within ethnic
groups of related genetic background. For example, natives of India are often
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very dark, and inhabitants of the Mediterranean region are darker than the
Northern Europeans. Individual variation within a family is also large.
Tattoos.
Tattoos are common and may indicate increased risk for blood-borne
disease. Determine where and by whom tattoos were placed and the sterility
and any instrument sharing. Ask about high-risk behaviors, e.g., intravenous
drug use or high-risk sexual behaviors.
Malignant melanoma.
Nevi—moles.
See page 154.
Acquired diffuse brown skin—melanism.
See page 155.
Mechanisms stimulating mela-
nin production include secretion of ACTH and/or MSH and iron deposition
in the skin. Melanism is skin darkening from augmented melanin production
in facultative pigment deposits.
The brown color is diffuse and accentuated in
palmar creases, recent scars, and pressure points at elbow, knee, and knuckles. Pigmentation of the oral mucosa is abnormal in whites. Melanism should
prompt a search for underlying disease.
CLINICAL OCCURRENCE: Congenital: Hemochromatosis, porphyria,
alkaptonuria; Endocrine: Addison disease, Nelson syndrome, Graves disease,
hypothyroidism, pregnancy (melasma—primarily on the face), contraceptive hormones; Infectious: Whipple disease; Inammatory/Immunologic:
Scleroderma; Metabolic/Toxic: Cirrhosis, pernicious anemia, B
acid deciency, drugs (busulfan, arsenicals, dibromomannitol); Neoplastic:
and folic
12
Hormone-secreting neoplasms; Psychosocial: Tanning.
Hemochromatosis.
Blue-gray color.
See Chapter 9, page 457.
Deposition of foreign substances discolors the skin.
Increased concentrations of unsaturated or abnormal hemoglobin in the cutaneous vessels gives cyanosis (page 127) that blanches with pressure. Consider
as etiology use of amiodarone or minocycline; silver deposition of silver
(argyria), gold, or bismuth salts; hemochromatosis, cyanosis, sulfhemoglobinemia, methemoglobinemia, arsenic poisoning.
Silver (Argyria). Silver salts from ingestion or intranasal absorption are de-
posited in the skin producing a blue-gray or slate color accentuated in sun
exposed areas. The mucosa and nail lunulae may be deposition sites. The
pigmentation may appear years after exposure and is typically permanent. It
is easily differentiated from cyanosis by not blanching with pressure.
Arsenic. Arsenic ingestion produces a diffuse gray coloration with superimposed 2–10 mm dark macules, often accompanied by punctate hyperkeratoses of the palms and soles. The skin manifestations appear 1–10 years after
arsenic ingestion.
Alkaptonuria (ochronosis). An inherited deciency of homogentisic acid
oxidase results in accumulation of black homogentisic acid polymers in the
connective tissues and urine. The accumulations give a faint blue-gray color
to the skin, especially over the pinnae, tip of the nose, and sclerae. Blackened
120 CHAPTER 6: The Skin and Nails
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extensor tendons in the hands may be seen through the skin. Often a dark
buttery pattern appears on the face and the axillae genitalia are pigmented.
Exogenous ochronosis (pseudoochronosis) results from prolonged use of topical medications, notably hydroquinone used for bleaching skin. Treated areas
develop the blue-gray appearance of ochronosis.
Acquired diffuse yellow skin.
Yellow discoloration results from pigment
deposition in the skin. The most common causes are jaundice and carotenemia, which are easily distinguished on clinical grounds by their different
distributions and presentations.
Jaundice.
Carotenemia.
See, Chapter 9, page 414.
Fat-soluble carotene concentrates in the stratum corneum
of the palms and soles and is excreted in sebum. The liver converts carotene to vitamin A with the assistance of thyroid hormone. The liver fails to
metabolize carotene in myxedema and diabetes. Carotene deposition appears
as
yellow skin especially on the forehead, nasolabial folds, behind the ears,
and on the palms and soles. Carotenemia results from chronically ingesting
copious quantities of carrots, squash, oranges, peaches, apricots, and leafy
vegetables.
DDX: Water-soluble bilirubin pigments are more uniformly dis-
tributed including discoloration of sclerae and thin skin.
Erythema. Erythema is skin reddening caused by dilation of the cutaneous vasculature that blanches with pressure, and is often accompanied by
increased skin temperature.
Examples: Local inammatory lesions, local
infection (e.g., cellulitis, lymphangitis), scarlet fever, scarlatiniform drug
eruptions, polycythemia, porphyria, pellagra, lupus erythematosus, rstdegree burns. Transient erythema occurs in blushing and in some cases of
metastatic carcinoid.
Hypopigmentation and depigmentation. Loss of skin pigmentation is patchy
or diffuse, usually with discrete borders. The distribution and pattern are important for identifying a specic etiology.
Examples: Depigmentation: Vitiligo, albi-
nism; Hypopigmentation: Tinea versicolor, scars, stria, and sites of subcutaneous
steroid injection or topical steroid application on ethnically dark skin.
Hyperpigmentation. Increased cutaneous melanin deposition results from
local or systemic factors.
Examples: Addison disease, hemochromatosis,
porphyria, arsenic poisoning, progressive systemic sclerosis (scleroderma),
sun exposure, post-inammatory hyperpigmentation, chronic local irritation
from burning or scratching.
Acanthosis nigricans. Asymptomatic hyperpigmented velvety plaques are
seen on the neck, axillae groin, and other body folds.
CLINICAL OCCURRENCE: Congenital: Hereditary benign; Endocrine:
Diabetes, increased androgens, acromegaly, Cushing syndrome, Addison
disease, insulin resistance syndromes, hypothyroidism; Metabolic/Toxic:
Obesity, drug induced, for example, nicotinic acid, glucocorticoids; Neoplastic:
Paraneoplastic.
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Hair Changes.
Hirsutism and hypertrichosis. Hirsutism is excess terminal hair growth
from androgen-sensitive pilosebaceous units because of excess androgen
secretion or genetically determined increased androgen sensitivity. In hir-
sutism hair grows in a masculine pattern on the face, shoulders, back, chest,
abdomen, thighs, and buttocks. Hirsutism is especially distressing to women.
Distinguishing normal variants from androgen excess can be difcult. Hyper-
trichosis is excess vellus hair growth, evenly covering the body. Less hair than
normal is hypotrichosis.
CLINICAL OCCURRENCE: Hirsutism: androgen-secreting tumors, poly-
cystic ovary, late-onset congenital adrenal hyperplasia, glucocorticoid excess,
prolactinemia, carcinoma, drugs (e.g., certain oral contraceptives, testosterone, anabolic steroids);
Hypertrichosis: congenital, anorexia nervosa, hypo-
thyroidism, dermatomyositis, malnutrition, drugs (minoxidil, phenytoin,
hydrocortisone, cyclosporine, penicillamine, and streptomycin).
Alopecia.
Alopecia is congenital or acquired hair loss. History and hair
loss pattern assist diagnosis. Hormonal hair loss is androgenic alopecia. Local
trauma and traction on hairs or obsessive pulling or twisting hair (trichotil-
lomania) also cause alopecia. The most frequently encountered causes are
androgenic alopecia (male or female pattern baldness), alopecia areata, telogen efuvium, anagen efuvium, hypothyroidism, and drugs.
Alopecia areata. The hair loss is an autoimmune condition. There is complete or patchy loss of hair follicles without other skin changes. It is associated
with other autoimmune disorders.
Telogen efuvium. Physiologic stressors such as pregnancy, illness, or emotional distress shift the growth cycle from anagen to telogen which may last
for a few months. When the growth phase begins again the new shafts extrude the old hairs, resulting in diffuse hair shedding.
Anagen efuvium. Antimetabolites such as chemotherapeutic agents cause
arrest of the growth phase and diffuse hair loss which resolves when the
drugs are withdrawn.
Graying. Loss of hair pigmentation is normal with age. The age of onset
is familial to some extent.
Examples: Normal aging, premature aging syn-
dromes, pernicious anemia, chloroquine therapy; localized graying occurs in
vitiligo lesions.
Fingernail Signs.
Transverse nail plate furrow—Beau line. An acute illness decreases nail
growth seen as a transverse furrow whose width reects the duration of
As the nail elongates, the furrow becomes visible from beneath the
illness.
mantle, progresses distally, and is nally pared off (Fig. 6-13F).
Transverse white banded nail plates—Mees lines. The transverse white
bands are laid down during a systemic illness or poisoning. With recovery,
normal nail growth resumes, producing a white band moving distally as the
nail plate grows (Fig. 6-13N; Fig. 6-14). The bands probably result from minor
122 CHAPTER 6: The Skin and Nails
DEFORMED NAIL PLATES
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DISCOLORED NAIL PLATES
Diagnosis of Fingernail Lesions I. Many nail lesions are depicted. It is necessary to know whether the
FIG. 6-13
lesion is in the nail plate or in the nail bed. The distinction can usually be made by noting if the abnormal color is changed by
pressure on the nail plate, indicating a lesion of the nail bed. See text for descriptions.
FIG. 6-14Mees Lines. White transverse lines form in the nails at the time of an acute illness. With very severe illness
grooves appear called Beau’s lines.
DISCOLORED NAIL BEDS
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injury, less than Beau lines. Examples: Heavily associated with poisoning
(arsenic, thallium, uoride), but also can be seen with chemotherapy, infectious febrile illnesses, renal insufciency, cardiac failure, myocardial infarction, Hodgkin disease, sickle cell disease, and many others.
Nail pitting.
Occasional nail pits are normal. Large numbers are seen in pso-
riasis, especially psoriatic arthritis. Other skin signs of psoriasis may be subtle or absent. These also can be seen with eczema. Nail pitting in transverse
bands is associated with alopecia areata.
Splinter hemorrhage.
Minor capillary bleeding, conned within ridges
under the nail plate, appear as longitudinal red lines. They are asymptomatic
(Fig. 6-15J).
Examples: Trauma is most common. Consider systemic throm-
botic and embolic illness (e.g., endocarditis, antiphospholipid syndrome,
vasculitis).
SEPARATION OF BED AND PLATE (Onycholysis)
SUBUNGUAL LESIONS
Diagnosis of Fingernail Lesions II. Many nail lesions are depicted. It is necessary to know whether the
FIG. 6-15
lesion is in the nail plate or in the nail bed. The distinction can usually be made by noting if the abnormal color is changed by
pressure on the nail plate, indicating a lesion of the nail bed. See text for descriptions.
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Subungual hematoma. Bleeding into the closed space between the nail bed
and plate is intensely painful. Relief of pressure and pain occurs when this is
drained or bleeding dissects out from under the nail (Fig. 6-15K).
Nail fold inammation—paronychia. Nail fold infection produces pain,
redness, uctuance and purulent drainage. Chronic infection of the nail base
damages the matrix causing permanent nail deformity. Staphylococci are
most common bacterial cause and seen in acute paronychia. Candida infection
is prevalent in hands frequently immersed in warm water or in persons who
bite their cuticles and is the leading infectious cause of chronic paronychia.
The cuticle is rounded, erythematous, thickened, retracted from the plate but
not tender. Several nails can be involved.
Subungual pigmentation—ungual melanoma.
or black longitudinal streak that is larger than 3–4 mm and enlarging may
be the only sign. Melanin can leach into the nail fold, which is known as the
Hutchinson side.
Nail plate dystrophy.
ifest as opacity, furrows, ridges, pits, splits, and fraying (Fig. 6-13J).
Chronic fungal infections (onychomycosis), psoriasis, lesions of nerves supplying the limb, vascular decits, amyloidosis, and collagen diseases.
White nail plates—partial leukonychia.
plates are common and most often indicate minor trauma.
White nail plates—total leukonychia.
nant with varying penetrance the nail plates are completely chalk white
(Fig. 6-13K).
White proximal nail beds—Terry nails. Associated with cirrhosis, but of
unknown mechanism, the proximal ≥80% of the nail bed is white (Fig. 6-15D)
with a pink distal band.
White proximal nail beds—half-and-half nail (Lindsay nails). Somewhat
similar to Terry nails, the proximal 40% to 80% of the nail bed is white while
the distal portion is red, pink, or brown (Fig. 6-15E). The demarcation is a
sharply curved line parallel to the free edge. Venous congestion deepens
the distal color, while inducing only a slight pink in the proximal bed. Most
patients have advanced kidney disease.
Separation of the nail—onycholysis. The normal line of plate adhesion to bed
is a smooth curve (Fig. 6-15F). In onycholysis, the plate separates more proximally, collecting debris underneath, inaccessible to cleaning (Fig. 6-15G–I).
Examples:
Hyperthyroidism, psoriasis, and fungal infection.
Abnormal nail growth produces dystrophic nails man-
A single nail with a brown
Examples:
Irregular white areas in the nail
Inherited as an autosomal domi-
Yellow nail plates—yellow-nail syndrome. Associated with impaired
lymph drainage, it can antedate lymphedema. The nail plates become yellow
or yellow-green, thicken, and grow slowly with more transverse curvature
(Fig. 6-13M). Absence of the cuticle is characteristic. Ridging and onycholysis
may occur.
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Brittle nail plates—onychorrhexis. Keratin layers delaminating at the cut
edge present a stepped appearance with frayed and torn borders (Fig. 6-13B).
Examples:
Aging, malnutrition, iron deciency, thyrotoxicosis, or calcium
deciency.
Longitudinal brown-banded nail plates (melanonychia).
This is a normal
variant in black-skinned persons. Most commonly more than one nail is
affected (Fig. 6-13L). Similar longitudinal bands occur with some antiretroviral medications. Consider melanoma if a single band affects a single nail.
Discolored nail plates. Drugs, infections, and stains color the nail plates
(Fig. 6-13O). The color is a clue to etiology: blue-green = Pseudomonas infection; brown or black or yellow = fungal infections, uorosis, quinacrine; and
blue-gray = argyria.
White-banded nail beds—Muehrcke lines. Paired, narrow, arcuate pale
bands, parallel to the lunulas, appear in the nail beds (Fig. 6-15A) during
hypoalbuminemia (<2.0 g/dL), resolving with normalization of albumin.
They are not in the nail plates, so do not move distally with nail growth.
Red lunula. Red lunulas (Fig. 6-15B) are associated with heart failure, rheumatoid arthritis, SLE, hepatic cirrhosis, pulmonary disease, carbon monoxide
poisoning, and dermatologic diseases including psoriasis.
Azure lunula—hepatolenticular degeneration (Wilson disease). The lunulas
are light blue (Fig. 6-15C). Examine the corneas for Kayser–Fleischer rings.
Painful red or violet subungual spot—glomus tumor.
Exquisitely painful
sensory glomus body tumors are common in the nail bed, appearing as a
round red or violet spot (Fig. 6-15L) resembling a hemangioma, but the latter
is not tender. This also could represent skin cancers including squamous cell
carcinoma.
Concave nail plate—spoon nails (koilonychia). The nails are concave, saucer nails (Fig. 6-13G) with a thin nail plate.
Examples: Iron deciency; rare in
rheumatic fever, lichen planus, and syphilis.
Nail plate hypertrophy. Piling up of irregular keratin layers thickens the nail
plate (Fig. 6-13I). It may be familial or the result of chronic fungus infection.
Absence of nails. The nails may be congenitally absent, sometimes in association with ichthyosis. A traumatized nail may be shed, matrix damage preventing regrowth.
Malnourished nails. The nails, growing slowly or not at all and thickening
over time, are dry, brittle, and have transverse ridges.
Irregular, short nails—bitten nails. The free edge may be absent from nail
biting (Fig. 6-13A).
Square, round nail plates. In acromegaly and congenital hypothyroidism
disproportionate lateral growth produces nail plates wider than long.
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