1
Foundations of Clinical
Dermatology
Chapter 1 :: Fundamentals of Clinical Dermatology:
Morphology and Special Clinical
Considerations
:: Erin H. Amerson, Susan Burgin,
& Kanade Shinkai
AT-A-GLANCE
■ Skin diseases have characteristic morphology and
distribution.
■ Morphologic characteristics and reaction
patterns of the skin suggest disease
pathophysiology, helping focus the differential
diagnosis.
■ The history is indispensable in elucidating
complex diagnoses.
■ Knowledge and appropriate use of dermatologic
terminology is essential.
■ The comprehensive mucocutaneous examination,
including hair and nails, should always be
performed.
THE ART AND SCIENCE
OF DERMATOLOGIC
DIAGNOSIS
The diagnosis and treatment of cutaneous diseases
requires the physician’s ability to recognize the pri-
mary lesions and reaction patterns of the skin, and to
put these visual clues into context with the patient’s
history and overall health. In this chapter, we discuss a
fundamental approach to the patient presenting with a
skin problem. We introduce the technical vocabulary of
dermatologic description, also known as morphology.
Accurately identifying morphology is an essential step
Kang_CH001_p0001-0017.indd 1
PA RT
in generating a differential diagnosis. Use of standard
dermatologic terminology is also critical for effective
clinical documentation, research, and communication
with other health care providers.
The process of examining and describing skin lesions
requires perception of subtle details: appreciation of a
specific hue of erythema, a shape or distribution, or the
presence of characteristic findings on nails or mucous
membranes often hold the key to the correct diagno-
sis. Repeated patient encounters help to train the eye
to recognize such patterns. With time and experience,
the physician can associate clinical skin findings with
histopathologic features, enabling a rich understand-
ing of the pathophysiology of skin disease, as well as
clinical-pathologic correlation.
APPROACH TO THE
PATIENT
HISTORY
Dermatology is a visual specialty, and some skin con-
ditions may be diagnosed at a glance. History may be
crucial in complex cases, such as the patient with rash
and fever, or the patient with generalized pruritus.
There is therapeutic value in receiving a patient’s nar-
rative thread, as they feel heard, and they may reveal
information relevant to treatment choice or invite
opportunities for education and reassurance. In prac-
tice, many dermatologists take a brief history, perform
a physical examination, then undertake more detailed
05/12/18 4:47 pm
 1 questioning based on the differential diagnosis that the
examination suggests.
In taking a history from a patient presenting with a
new skin complaint, the physician’s primary goal is to
establish a diagnosis, with a secondary goal of evaluat-
ing the patient as a candidate for therapy. In patients
whose diagnosis is already established, the physician’s
goals are to reevaluate the original diagnosis, monitor
disease progress and complications, and modify treat-
ment accordingly.
Table 1-1 presents an approach to obtaining the
history in a patient presenting with a skin problem.
The physician may choose to customize the history
depending on whether the chief complaint is a growth
Part 1
or an eruption, a nail or hair disorder, or another con-
dition, and whether it is a new problem or a followup
visit for an ongoing condition.
::
Foundations of Clinical Dermatology
PHYSICAL EXAMINATION
SCOPE OF THE COMPLETE
CUTANEOUS EXAMINATION
The complete cutaneous examination includes
inspection of the entire skin surface, including often-
overlooked areas such as the scalp, eyelids, ears,
genitals, buttocks, perineum, and interdigital spaces;
the hair; the nails; and the mucous membranes of the
eyes, nose, mouth, genitals, and anus. Patients pre-
senting with a highly focused complaint, such as a
single wart or acne, may not require a comprehensive
skin examination in routine clinical practice. There are
many advantages to performing a complete cutaneous
examination, including identification of potentially
harmful lesions, such as skin cancers, providing reas-
surance for benign skin findings, locating additional
diagnostic clues (Wickham’s striae on the buccal
mucosa in lichen planus, for instance), opportunities
for patient education (eg, lentigines are a sign of sun
damage and suggest the need for improved sun pro-
tection), and an opportunity to convey the physician’s
concern about the patient’s skin health through a thor-
ough examination. A thorough evaluation increases
the possibility of making a diagnosis at the bedside
and mitigates the risk of overlooking another diagno-
sis. A guide to performing the physical examination
of the patient presenting with a skin problem is pre-
sented in Table 1-2.
IDEAL CONDITIONS FOR THE
COMPLETE SKIN EXAMINATION
A complete skin examination is most effective when
performed under ideal conditions. Excellent lighting,
preferably bright, natural light, is paramount; with-
out good lighting, subtle but important details may
2 be missed. The patient should be fully undressed,
and gowned with additional draping, if desired.
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TABLE 1-1
History Taking in Dermatologic Diagnosis
Chief Complaint and History of the Present Illness
■ Duration: When the condition was first noted and dates of
recurrences or remissions
■ Timing: Constant, intermittent, worst at night, worst in winter
■ Evolution: How the condition has changed or progressed
over time
■ Location: Where lesions were first noted, and how they have
spread, if applicable
■ Symptoms: Pruritus, pain, bleeding, nonhealing, change of preex-
isting skin lesions, associated with fever or other systemic signs
■ Severity: Ask patient to rate severity of pain or pruritus on a
10-point scale to follow severity over time
■ Ameliorating and Exacerbating Factors: Sun exposure, heat, cold,
trauma, exposures (such as chemicals, medications, cosmetics,
perfumes, plants, or metals), relation to menses or pregnancy
■ Preceding illness, new medications, new topical products, or
exposures
■ Therapies tried, including nonprescription or home remedies, and
response to therapy
■ Prior similar problems, prior diagnosis, results of biopsies or other
studies performed
Medical History
■ A history of all chronic illnesses, particularly those that may mani-
fest in the skin, (diabetes, renal and hepatic disease, infection with
HIV or other viruses, polycystic ovarian syndrome, lupus, thyroid
disease) and those that are associated with skin disease (asthma,
allergies)
■ History of surgical procedures, including organ transplantation
■ Immunosuppression: iatrogenic, infectious, or inherited
■ Pregnancies
■ Psychiatric disease
■ History of blistering sunburns, exposure to arsenic or ionizing
radiation
■ Medication History: A detailed history, including prescriptions,
nonprescription medications, vitamins, dietary supplements,
herbal remedies, with particular attention to those medications
started recently
■ Allergies: To medications, foods, environmental antigens, and
contactants
■ Social History: Occupation, hobbies and leisure activities, alcohol
and tobacco use, illicit drug use, sexual history (including high-risk
activities for sexually transmitted diseases), diet, bathing habits,
pets, living conditions (eg, alone, with family, homeless, in an insti-
tution), history of travel or residence in endemic areas for infectious
diseases, cultural or religious practices
■ Family History: Of skin disease, atopy (atopic dermatitis, asthma,
hay fever) or skin cancer
■ Review of Systems: May be focused or comprehensive depending
on the diagnosis (asking about specific symptoms that may accom-
pany a dermatologic condition, such as joint symptoms in psoriasis;
asking a comprehensive ROS in the setting of cutaneous signs of
systemic disease such as palpable purpura)
Underwear, socks, shoes, makeup, and eyeglasses
should be removed. The examining table should be
at a comfortable height, with a head that reclines, an
extendable footrest, and gynecologic stirrups. The
examining room should be at a comfortable tempera-
ture for the lightly dressed patient. It should contain a
sink for hand washing and disinfecting hand foam, as
patients are reassured by seeing their physician wash
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 TABLE 1-2
Physical Examination in Dermatologic Diagnosis
General Impression of the Patient
■ Well or ill
■ Obese, cachectic, or normal weight
■ Skin Color: Degree of pigmentation, pallor (anemia), jaundice
■ Skin Temperature: Warm, cool, or clammy
■ Skin Surface Characteristics: Xerosis (dryness), seborrhea
(excessive oil), turgor, hyper- or hypohidrosis (excessive or
decreased sweating), and texture
■ Degree of Photoaging: Lentigines, actinic purpura, rhytides
Morphology
■ Define the primary lesion
■ Describe their color, texture
■ Describe any secondary changes
■ Describe their shape and configuration
■ Describe the Distribution of Lesions: Localized (isolated), grouped,
regional, generalized, universal, symmetrical, sun-exposed, flexural,
extensor extremities, acral, intertriginous, dermatomal, follicular
Aspects of General Physical Examination That May Be Helpful
■ Vital signs
■ Abdominal examination for hepatosplenomegaly
■ Pulses
■ Lymph node examination (especially in cases of suspected infec-
tion and malignancy)
hands before the examination. If the patient and physi-
cian are of opposite genders, having a chaperone in the
room may be required.
RECOMMENDED TOOLS FOR THE
COMPLETE SKIN EXAMINATION
Although the physician’s eyes and hands are the
only essential tools for examination of the skin, the
following are often useful and highly recommended:
■ A magnifying tool such as a loupe, magnifying
glass, and/or dermatoscope.
■ A bright focused light such as a flashlight or
penlight.
■ Glass slides for diascopy and viral direct fluorescent
antibody (DFA) testing, fungal scrapings and touch
preparations, Tzanck smears, scabies prep.
■ Alcohol pads to remove scale or surface oil.
■ Gauze pads or tissues with water for removing
makeup.
■ Gloves: when any contagious condition is
suspected, when contact with body fluids is
possible, when examining mucous membranes and
genital areas, and when performing any procedure.
■ A ruler for measuring lesions.
■ No. 15 and No. 11 scalpel blades for scraping and
incising lesions, respectively.
■ Diagnostic solutions: potassium hydroxide
solution, oil, Tzanck smear, bacterial, viral, and
fungal culture media.
■ A camera for photographic documentation.
■ A Wood lamp (365 nm) for highlighting subtle
pigmentary changes.
Kang_CH001_p0001-0017.indd 3
TECHNIQUE OF THE 1
DERMATOLOGIC PHYSICAL
EXAMINATION
Consistency in a comprehensive mucocutaneous
examination is essential to ensure that no areas are
overlooked. One approach to the complete skin exami-
nation is presented here. First, observe the patient at
a distance for general impressions (eg, asymmetry
due to a stroke, cachexia, jaundice). Next, examine the
patient in a systematic way, usually from head to toe,
uncovering one area at a time to preserve patient mod-
esty. Move the patient and the illumination as needed
for the best view of each body area. Sometimes side
Chapter 1 :: Fundamentals of Clinical Dermatology
lighting best reveals depth and details of skin lesion
borders. Palpate lesions to determine whether they are
soft, firm, tender, or fluid-filled. A magnifier worn on
the head leaves both hands free for palpation of lesions.
Certain lesions, especially pigmented lesions, are
best examined with a dermatoscope to identify char-
acteristic concerning features. Mucosal sites should
be carefully examined with additional illumination
with a penlight or flashlight. During the examination,
patients may be reassured by the physician’s reporting
of benign lesions as they are encountered.
Special examination techniques for hair and nail dis-
orders are discussed in Chaps. 85 through 91.
After completing the examination, it is important
to document the skin findings, including the type of
lesions and their locations, either descriptively or on
a body map. Specific documentation using photogra-
phy and triangulation based on anatomic landmarks
is particularly important for lesions suspicious for skin
malignancy undergoing biopsy, so that the exact loca-
tion may be found and definitively treated at a later
date.
INTRODUCTION TO
MORPHOLOGY
Joseph Jakob von Plenck’s (1738–1807) and Robert
Willan’s (1757–1812) work in defining basic morpho-
logic terminology laid the foundation for the descrip-
tion and comparison of fundamental lesions, thereby
facilitating characterization and recognition of skin
disease.
The eminent dermatology professors Wolff and John-
son have asserted: to read words, one must recognize
letters; to read the skin, one must recognize the basic
lesions. The “letters,” or elemental building blocks of
morphology, are the primary lesion and secondary
(epidermal) change. The skilled clinician uses macro-
scopic characteristics noted on examination to under-
stand where and what types of microscopic pathologic
changes are present, achieving clinical–pathologic
correlation. For example, flat-topped or planar pap-
ules and plaques tend to be processes affecting the
epidermis and superficial dermis, while dome-shaped 3
or nodular lesions often exhibit deeper infiltration into
05/12/18 4:47 pm
 1 the dermis or subcutis. Scaling or crusting indicates
that the epidermis is affected, while a smooth, intact
surface on a palpable lesion reflects a purely dermal or
subcutaneous process.
The combination of primary morphology and sec-
ondary change (or absence of secondary change) deter-
mine a diagnostic category, also known as the “reaction
pattern.” For example, when the primary lesion is a cir-
cumscribed papule or plaque with scale, it likely falls
into the “papulosquamous” reaction pattern, which
suggests a specific set of diagnostic possibilities. Once
the reaction pattern has been determined, a differential
diagnosis comes into focus. This differential diagnosis
may be further honed by other lesional characteris-
Part 1

tics, including shape or color, and the arrangement of

lesions in relationship to one another (configuration)
Figure 1-1 Macule, petechiae.
and on the body (distribution).
It is important for the dermatologist in training to
::

be aware that variation and ambiguity in definitions of

Foundations of Clinical Dermatology

morphologic terms exist among the dermatology com- FLAT (NONPALPABLE)

munity. For example, in dermatology textbooks, a pap-
ule has been described as no greater than 1 cm in size,
no less than 0.5 cm, or ranging from the size of a pin-
head to that of a split pea. In this chapter, the authors
have selected definitions that reduce the subjectivity
inherent in some morphologic frameworks.
PRIMARY LESIONS
Macule: A macule is flat, even with the surface level
of surrounding skin or mucous membranes, and per-
ceptible only as an area of color different from the sur-
rounding skin or mucous membrane. Macules are less
than 1 cm in size (Fig. 1-1).

Patch: A patch, like a macule, is a flat area of skin

PRIMARY MORPHOLOGY or mucous membranes with a different color from
its surrounding. Patches are 1 cm or larger in size
The primary morphology describes 3 lesional charac- (Fig. 1-2).
teristics: size, topography, and the character of con-
tents (Table 1-3). The primary morphology should
be the “noun” which all other “adjectives” (such
RAISED (PALPABLE)
as color, shape, size, texture) describe. A macule or PRIMARY LESIONS
patch is not palpable (a color change only) and raised
or depressed lesions that are palpable are papules or
Papule: A papule is an elevated or depressed lesion
less than 1 cm in size, which may be solid or cystic.
plaques. Erosions and ulcerations may be primary or
Among other characteristics, papules may be fur-
secondary.
ther described by their topography. Some examples
include papules that are sessile, pedunculated, dome-
shaped, flat-topped, filiform, mammillated, acuminate
TABLE 1-3 (conical), or umbilicated (Fig. 1-3).
Primary Morphology
PRIMARY
LESION SIZE TOPOGRAPHY CONTENTS

Macule <1 cm Flat N/A (color change only)

Patch ≥1 cm Flat N/A (color change only)
Papule <1 cm Raised/Depressed Solid
Plaque ≥1 cm Raised/Depressed Solid
Nodule ≥1 cm Raised Solid or fluid
Vesicle <1 cm Raised Fluid (serum, blood,
lymph)
Bulla ≥1 cm Raised Fluid (serum, blood,
lymph)
Pustule <1 cm Raised Fluid (pus)
Erosion Any Depressed N/A
4 Ulceration Any Depressed N/A
Figure 1-2 Patch, fixed drug eruption.

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Figure 1-3 Papule, lichen nitidus.
Plaque: A plaque is a solid plateau-like elevation
or depression that has a diameter of 1 cm or larger
(Fig. 1-4).
Nodule: A nodule is a palpable lesion greater than
1 cm with a domed, spherical or ovoid shape. They
may be solid or cystic. Depending on the anatomic
component(s) primarily involved, nodules are of
5 main types: (1) epidermal, (2) epidermal–dermal,
(3) dermal, (4) dermal–subdermal, and (5) subcutane-
ous. Texture is an important additional feature of nod-
ules: firm, soft, boggy, fluctuant, etc. Similarly, different
surfaces of nodules, such as smooth, keratotic, ulcer-
ated, or fungating, also help direct diagnostic consider-
ations (Fig. 1-5). Tumor, also sometimes included under
the heading of nodule, may be used to describe a more
irregularly shaped mass, benign or malignant.
FLUID-FILLED PRIMARY LESIONS
Vesicle and Bulla: A vesicle is a fluid-filled pap-
ule smaller than 1 cm (Fig. 1-6), whereas a bulla (blister)
measures 1 cm or larger (Fig. 1-7). By definition, the
wall is thin and translucent enough to visualize the
contents, which may be clear, serous, or hemorrhagic.
Figure 1-4 Plaque, psoriasis.
Kang_CH001_p0001-0017.indd 5
1
Chapter 1 :: Fundamentals of Clinical Dermatology
Figure 1-5 Nodule, lymphoma cutis.
Vesicles and bullae arise from cleavage at various
levels of the epidermis (intraepidermal) or the dermal–
epidermal interface (subepidermal), sometimes extend-
ing into the dermis. The tenseness or flaccidity of the
vesicle or bulla may help determine the depth of the
split. However, reliable differentiation requires histo-
pathologic examination of the blister edge.
Pustule: A pustule is a circumscribed, raised papule
in the epidermis or infundibulum containing visible
pus. The purulent exudate, composed of leukocytes
with or without cellular debris, may contain organisms
or may be sterile. The exudate may be white, yellow,
or greenish-yellow in color. Pustules may vary in size
and, in certain situations, may coalesce to form “lakes”
of pus. When associated with hair follicles, pustules
may appear conical and contain a hair in the center
(Fig. 1-8).
Figure 1-6 Vesicle, bullous lupus erythematosus. Note
brown incipient crusts marking the sites of earlier blisters 5
now ruptured.
05/12/18 4:47 pm
 1 TABLE 1-4
Types of Scale
TYPE OF SCALE DESCRIPTION

Craquelé/xerotic Desquamation giving the appearance of dried,

cracked skin. Combination of hyperkeratosis
and fissuring, which appears like the cracked
bed of a dry river.
Cutaneous horn Conical projection of compact stratum corneum.
Exfoliative/ Scales split off from the epidermis in finer scales
desquamative or in sheets.
Follicular Scales appear as keratotic plugs, spines, or
filaments.
Part 1

Gritty Densely adherent scale with a sandpaper

Figure 1-7 Vesicles and bullae, linear IgA disease. texture.
Ichthyosiform Scales are regular, polygonal plates arranged in
::

parallel rows or diamond patterns (fish-like,

Foundations of Clinical Dermatology

tessellated, Fig. 1-9).

SECONDARY CHANGE Keratotic/ Scales appear as thick, compact, adherent layers

(EPIDERMAL OR SURFACE hyperkeratotic of stratum corneum.

CHANGE)
Scale is a macroscopic finding indicating a change in
the epidermis, usually the stratum corneum. Scale
may have many different descriptive characteristics,
for instance, soft, rough, gritty, bran-like, or micaceous
(Table 1-4).
Crust describes dried fluid on the skin’s surface due
to serum, blood, pus, or a combination. When crust
is round or oval, it points to the former presence of a
vesicle, bulla or pustule (as seen in Fig. 1-6). Linear or
angulated crusts are indicative of excoriations. Other
specialized types of crust include eschar, which is dry,
adherent, and dark red-purple, brown, or black in color
and signals skin necrosis (Fig. 1-11), or fibrin, which is
a soft, yellow crust on the surface of some ulcers.
Lichenification is a thickening and accentuation of
the skin lines that results from repeated rubbing or
scratching of the skin. It is found primarily in chronic
eczematous processes or neurogenic processes
(Fig. 1-12).
Lamellar Scales are thin large plates or shields attached in
the middle and looser around the edges.
Pityriasiform Scale is small and branny.
Psoriasiform Scale is silvery and brittle and forms thin plates
(micaceous and in several loose sheets, like mica (micaceous
ostraceous) scale). Large scales may accumulate in heaps,
giving the appearance of an oyster shell
(ostraceous scale, Fig. 1-10).
Seborrheic Scales are thick, waxy or greasy, yellow-to-
brown, flakes.
Shellac-like Scale is shiny with a sheet-like desquamating
edge, like peeling paint
Wickham striae Scale appears as a lacy white pattern overlying
violaceous flat-topped papules.
Atrophy of the epidermis results in a shiny quality
with “cigarette-paper” wrinkling. Atrophy of the der-
mis results in a depressed lesion.
A fissure is a linear loss of continuity of the skin’s
surface or mucosa that results from excessive tension

6
Figure 1-8 Pustule, pustular psoriasis. Figure 1-9 Ichthyosiform scale, ichthyosis vulgaris.

Kang_CH001_p0001-0017.indd 6 05/12/18 4:47 pm


Figure 1-10 Ostraceous scale, psoriasis.
or decreased elasticity of the involved tissue. Fissures
frequently occur on the palms and soles where the
thick stratum corneum is least expandable.
OTHER LESIONAL
CHARACTERISTICS
In addition to primary morphology, other features of
lesions can be important in narrowing a differential
diagnosis; sometimes, these other characteristics are
the most important determinants of the differential.
For instance, the most notable feature of a rash or
lesion might be its shape or distribution, which points
the clinician to a specific list of possible diagnoses.
COLOR
Perhaps the most important additional feature of a
lesion other than primary morphology is color. The
experienced dermatologist will notice subtle varia-
tions in hue and saturation of a particular color, and
can ascribe meaning to these variations. The most
Figure 1-11 Eschar overlying stellate purpura, calciphylaxis.
Kang_CH001_p0001-0017.indd 7
1
Chapter 1 :: Fundamentals of Clinical Dermatology
Figure 1-12 Lichenification, lichen simplex chronicus.
common types of color on the skin are variations
in brown (hyperpigmentation) and red (erythema),
which will be discussed in depth below. Other colors
and their histopathologic correlations are described in
Table 1-5.
Brown: Brown color is most often representative
of melanin, either within melanocytes or outside of
melanocytes. Less frequently, a brown hue also may
be caused by deposition of other pigments, cells, or
materials in the dermis (such as deposition of hemo-
siderin, amyloid, or mucin; certain types of inflamma-
tion, including inflammation that is granulomatous,
histiocytic, plasmacytic, or mixed). Mast cells induce
melanin production in the overlying epidermis, often
leading to brown color overlying the focus of mast cells
in the dermis. Melanin in the epidermis, whether con-
tained within or outside of melanocytes, appears tan to
muddy brown; when it is very concentrated, as in some
nevi or melanomas or heavily pigmented seborrheic
keratoses, it may appear brown-black. Melanin in the
dermis, either within melanocytes or extracellular, may
appear brown, gray, or blue. This gray-blue color results
from the “Tyndall effect,” named for the 19th-century
physicist John Tyndall, who described the preferential
transmission of longer wavelengths (blue photospec-
trum) when particles are suspended in a medium
(in this case, melanin or other brown pigment suspended
in the dermis). Differentiation between epidermal and
dermal melanin also can be aided by a Wood lamp, which
accentuates epidermal but not dermal melanin.
Oxidized keratin, (within an infundibular cyst, for
instance) and foreign pigmentation (such as tattoos)
can also exhibit the Tyndall effect when located in the
dermis.
When the epidermis is inflamed or damaged, mela-
nin often drops to into the dermis. Therefore, many
subacute, chronic, or recently resolved epidermal
inflammatory diseases or injuries have a brown or gray-
brown tone. The more constitutive pigment in an indi-
vidual’s skin, the more prominent these changes will be.
Red: Also known as “erythema,” red can have infi- 7
nite hues. Pale red, pink, or purple may result from
05/12/18 4:47 pm
 1 TABLE 1-5
Implications of Color Changes in Altered Skin
COLOR PATHOLOGY DIAGNOSTIC EXAMPLES

White Reduced or absent melanin synthesis Tinea versicolor, vitiligo

Keratin Milium
Calcium deposit Calcinosis cutis
Scar Atrophie blanche
Black Dense melanin Melanoma
Intraepidermal hemorrhage Talon noir
Necrosis Cutaneous anthrax
Oxidized keratin (brown to black) Open comedone
Part 1

Brown Melanin Melanocytic nevus, melasma

Red-brown Hemosiderin (“cayenne pepper”) Pigmented purpuric dermatosis
::

Granulomatous inflammation (“apple jelly”) Sarcoidosis (Fig. 1-15)

Foundations of Clinical Dermatology

Histiocytic inflammation Langerhans cell histiocytosis

Mixed inflammation Granuloma faciale
Plasmacytic inflammation (“copper”- or “ham”-colored) Secondary syphilis
Mast cell inflammation Urticaria pigmentosa
Mucin deposition Pretibial myxedema
Amyloid deposition Lichen amyloidosis
Infiltration with smooth muscle Cutaneous leiomyoma
Subacute or chronic epidermal inflammation Subacute lupus erythematosus
Red Vascular dilation or congestion Erysipelas
Neutrophilic inflammation Sweet syndrome
Vascular neoplasm Cherry angioma
Pink or salmon Acute inflammation with dilation of superficial dermal vessels Eczema, drug eruptions, urticaria, pityriasis rubra
pilaris, psoriasis
Orange Granulomatous inflammation with histiocytes having abundant cytoplasm Juvenile xanthogranuloma
Yellow Pus Folliculitis
Lipid Xanthelasma
Histiocytic inflammation Necrobiosis lipoidica (Fig. 1-16)
Elastolysis Pseudoxanthoma elasticum
Sebaceous glands Sebaceous hyperplasia
Bilirubin Jaundice
Green Deep hemosiderin Ecchymosis
Pyocyanin pigment Pseudomonas infection
Myeloperoxidase Chloroma
Tissue eosinophilia Wells syndrome
Blue/gray Deep dermal melanin Blue nevus
Deep deposition of other pigment Argyria, tattoo
Violet to lilac Acute lymphocytic inflammation with dilation of deep dermal blood vessels Borders of evolving morphea, dermatomyositis,
lichen planus
Plum Vascular neoplasm Kaposi sarcoma
Dense lymphocytic inflammation Lymphoma cutis
Malignant neoplasm Nodular amelanotic melanoma
Hemorrhage Ecchymosis

inflammation leading to hyperemia (subtle vascular to purple hue can result from the either malformed or
dilation). More saturated red to purple can indicate ectopic blood vessels (Fig. 1-13) or extravasated erythro-
8 intense hyperemia or vascular congestion (also called cytes (petechiae or purpura, see “vascular reaction pat-
rubor, as seen in erysipelas); even more saturated red tern” below). Variations in the hue of erythema are vast

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 1

Chapter 1 :: Fundamentals of Clinical Dermatology

Figure 1-13 Purple papules, Kaposi sarcoma.

and provide subtle clues to the type of inflammation

present. True red is often associated with neutrophilic
inflammation (as seen in cellulitis or Sweet syndrome);
red-purple (violaceous erythema, Fig. 1-14) with lym-
phocytic inflammation (lymphoma cutis, connective
tissue disease, interface reactions such as lichen planus).
Granulomatous inflammation may appear red-brown
(sarcoidosis, marked by the classis “apple jelly” color
seen in Fig. 1-15, or a juvenile xanthogranuloma) to Figure 1-15 Apple-jelly sign, sarcoidosis.
orange or yellow (Fig. 1-16, necrobiosis lipoidica). One
major caveat is that the true hue of erythema is easiest
to visualize in acute conditions affecting fair skin. Sub- relation to one another. For example, annular or linear
acute or chronic conditions, particularly with epidermal may be the shape of a single plaque, or a configuration
involvement, will have epidermal alteration causing of discrete papules. Demarcation refers to the edge of
epidermal pigment drop-out into the dermis, making an individual lesion and whether it is sharply defined
lesions appear more brown or gray. Hemorrhage can from or blends into the surrounding skin.
also alter the hue, making lesions appear more purple.
Annular: Ring-shaped; implies that the edge of the
lesion has a color and/or texture change that is more
SHAPE AND CONFIGURATION prominent on the leading edge than the center (as seen
OF LESIONS in granuloma annulare, tinea corporis, erythema annu-
lare centrifugum) (Fig. 1-17).
“Shape” describes an individual macule, patch, pap-
ule, or plaque; “configuration” refers to shapes made Round/Nummular/Discoid: Coin-shaped;
from the arrangement of individual primary lesions in solid circle or oval; usually with uniform morphology

9
Figure 1-14 Violaceous Gottron papules, dermatomyositis. Figure 1-16 Yellow, necrobiosis lipoidica diabeticorum.

Kang_CH001_p0001-0017.indd 9 05/12/18 4:47 pm

 1Part 1
Figure 1-17 Annular lesion, granuloma annulare.
::
Foundations of Clinical Dermatology
from the edges to the center (nummular eczema,
plaque-type psoriasis, discoid lupus) (Fig. 1-18).
Arcuate: Arc-shaped; often a result of incomplete
formation of an annular lesion (urticaria, subacute
cutaneous lupus erythematosus).
Linear: Resembling a straight line; often implies
an external contactant or Koebner phenomenon has
occurred in response to scratching; may apply to a
single lesion (such as a scabies burrow, poison ivy der-
matitis, or bleomycin pigmentation) or to the arrange-
ment of multiple lesions (as seen in lichen nitidus or
lichen planus).
Geographic: A shape similar to a land mass; edges
are reminiscent of a coastline
Reticular or Retiform: Net-like or lacy in
appearance, with somewhat regularly spaced rings or
crossing lines with sparing of intervening skin (as seen
in livedo reticularis, cutis marmorata) (Fig. 1-19).
10
Figure 1-18 Nummular lesion, nummular dermatitis.
Kang_CH001_p0001-0017.indd 10
Figure 1-19 Reticular eruption, livedo racemosa.
Stellate: Having multiple angulated edges, resem-
bling a star (Fig. 1-11).
Serpiginous: Serpentine or snake-like (cutaneous
larva migrans, for instance, in which the larva migrates
this way and that through the skin in a wandering pat-
tern) (Fig. 1-20).
Targetoid: Target-like, with a center darker than
the periphery. Typical targets (eg, erythema multi-
forme) have 3 zones: a dark red-purple or dusky cen-
ter, encircled by a paler pink zone, followed by a rim
of darker erythema. Atypical targets have just 2 zones,
a dark or dusky center with a paler pink rim. Note
that both have a center darker in comparison to the
outer zone; if the center is paler than the outer zone, it
should be termed “annular” (Fig. 1-21).
Whorled: Like marble cake, with 2 distinct col-
ors interspersed in a wavy pattern; usually seen in
mosaic disorders in which cells of differing genotypes
are interspersed (as seen in incontinentia pigmenti,
hypomelanosis of Ito, linear and whorled nevoid
hypermelanosis).
Figure 1-20 Serpiginous erythema, jellyfish sting.
05/12/18 4:47 pm

Figure 1-21 Atypical targetoid lesions, Stevens-Johnson
syndrome due to medication.
Grouped/Herpetiform: Lesions clustered
together (a classic example is herpes simplex virus
reactivation noted as grouped vesicles on an erythem-
atous base; also seen with certain arthropod bites).
Scattered: Sparse lesions that are irregularly
distributed.
Polycyclic: Formed from coalescing circles, rings,
or incomplete rings (as seen in urticaria, subacute cuta-
neous lupus erythematosus) (Fig. 1-22).
Figure 1-22 Polycyclic eruption, pityriasis rosea.
Kang_CH001_p0001-0017.indd 11
DISTRIBUTIONS OF MULTIPLE 1
LESIONS
Dermatomal/Zosteriform: Unilateral and lying
in the distribution of a single spinal afferent nerve root;
the classic example is herpes zoster (Chap. 165).
Blaschkoid: Following lines of skin cell migration
during embryogenesis; generally longitudinally ori-
ented on the limbs and circumferential on the trunk,
but curvilinear rather than perfectly linear; described
by Alfred Blaschko and implies a mosaic disorder
(such as incontinentia pigmenti, inflammatory linear
verrucous epidermal nevus).
Chapter 1 :: Fundamentals of Clinical Dermatology
Lymphangitic and Sporotrichoid: Lying
along the distribution of a lymph vessel; implies an
infectious agent that is spreading centrally from an
acral site. Lymphangitic lesions are usually a red
streak along a limb due to a staphylococcal or strepto-
coccal cellulitis. When individual papules or nodules
lie along the distribution of a lymphatic network, this
pattern is termed “sporotrichoid” and suggests a par-
ticular infectious differential.
Sun Exposed/Photodistributed: Occurring
in areas usually not covered by clothing, namely the
face, dorsal hands, and a triangular area correspond-
ing to the opening of a V-neck shirt on the upper
chest (examples include photodermatitis, subacute
cutaneous lupus erythematosus, polymorphous light
eruption, squamous cell carcinoma). Photo-accentuated
means the sun-exposed skin has a more dense distribu-
tion of lesions compared to non-sun-exposed skin.
Sun Protected: Occurring in areas usually cov-
ered by one or more layers of clothing; usually a der-
matosis that is improved by sun exposure (such as
parapsoriasis, mycosis fungoides).
Acral: Occurring in distal locations, such as on the
hands, feet, wrists, ankles, ears, or penis.
Truncal: Occurring on the trunk or central body.
Extensor: Occurring over the dorsal extremities,
overlying the extensor muscles, knees, or elbows
(psoriasis is a classic example).
Flexor: Overlying the flexor muscles of the extremi-
ties, the antecubital and popliteal fossae (childhood
atopic dermatitis, for instance).
Intertriginous: Occurring in the skin folds, where
2 skin surfaces are in contact, namely the axillae, ingui-
nal folds, inner thighs, inframammary skin, and under
an abdominal pannus; often related to moisture and
heat generated in these areas.
Seborrheic: Favoring the hair-bearing locations
of the skin, including scalp, eyebrows, beard, central
chest, axillae, genitals. Also often favors the nasolabial
and postauricular creases.
11
Follicular: Papules centered around hair follicles.
05/12/18 4:47 pm
 1 TABLE 1-6
A Selection of Cutaneous Diagnostic Signsa
CUTANEOUS SIGN DESCRIPTION SIGNIFICANCE

Apple-jelly sign A yellowish hue is produced from pressure on the lesion Noted in granulomatous processes (Fig. 1-15)
with a glass slide
Asboe–Hansen sign Lateral extension of a blister with downward pressure Noted in blistering disorders in which the pathology is
above the basement membrane zone
Auspitz sign Pinpoint bleeding at the tops of ruptured capillaries with Not entirely sensitive or specific for psoriasis
forcible removal of outer scales from a psoriatic plaque
Buttonhole sign A flesh-colored, soft papule feels as though it can be Noted in a neurofibroma
pushed through a “buttonhole” into the skin
Carpet tack sign Horny plugs at the undersurface of scale removed from a Noted in lesions of chronic cutaneous lupus
Part 1

lesion
Darier sign Urticarial wheal produced in a lesion after it is firmly Noted in urticaria pigmentosa and rarely with cutaneous
rubbed with a finger or the rounded end of a pen; the lymphoma or histiocytosis
::

wheal, which is strictly confined to the borders of the

Foundations of Clinical Dermatology

lesion, may not appear for several minutes

Dermatographism Firmly stroking unaffected skin produces a wheal along Symptomatic dermatographism represents a physical
the shape of the stroke within seconds to minutes urticaria
Pseudo-Darier sign Transient induration of a lesion or piloerection after Noted in congenital smooth muscle hamartoma
rubbing
Fitzpatrick (dimple) Dimpling of the skin with lateral compression of the Characteristic of dermatofibroma
sign lesion with the thumb and index finger produces
dimpling as a result of tethering of the epidermis to
the dermal lesion
Nikolsky sign Lateral pressure on unblistered skin with resulting shearing Noted in blistering disorders in which the pathology is above
of the epidermis the basement membrane zone; relevant entities include
pemphigus vulgaris and toxic epidermal necrolysis
a
Others are discussed in the chapters on diseases in which the signs occur.

Localized: Confined to a single body location.

TABLE 1-7
Generalized: Widespread. A generalized eruption Papulosquamous Reaction Pattern—Common
consisting of inflammatory (red) lesions is called an Examples
exanthem (rash). A macular exanthem consists of mac-
Psoriasis
ules, a papular exanthem of papules, a vesicular exan-
Lichen planus
them of vesicles, etc.
Pityriasis rosea
Pityriasis rubra pilaris
Bilateral Symmetric: Occurring with mirror- Pityriasis lichenoides chronica
image symmetry on both sides of the body. Syphilis (secondary)
Mycosis fungoides (MF)/parapsoriasis
Universal: Involving the entire cutaneous surface Drug (lichenoid, pityriasis rosea-like)
(as in erythroderma, alopecia universalis). Subacute and discoid lupus, dermatomyositis
Table 1-6 describes some clinically relevant maneuvers Tinea corporis
that point to particular cutaneous or systemic diseases. Tinea versicolor
Seborrheic dermatitis
Nutritional deficiency

REACTION PATTERNS Lichenoid id reaction

Porokeratosis
Superficial basal cell carcinoma
Certain combinations of primary and secondary mor-
Squamous cell carcinoma in situ
phologies point the clinician to a subset of diseases.
Groups of diagnoses that share similar morphologic Toolbox
History
characteristics are termed “reaction patterns,” suggest-
Distribution
ing a particular list of differential diagnosis. Reaction
Examine scalp, nails, mucous membranes
patterns are an especially useful tool when no charac- KOH preparation, fungal culture
teristic shape, configuration, or distribution is apparent. Rapid plasma reagin (RPR)
12 Determining the reaction pattern can also help guide Biopsy for routine histology
workup (Tables 1-7 through 1-15) and initial treatment.

Kang_CH001_p0001-0017.indd 12 05/12/18 4:47 pm

 TABLE 1-8 TABLE 1-9
1
Eczematous Reaction Pattern—Common Vesiculobullous Reaction Pattern—Common
Examples Examples
Same or Similar Histology Pustules
Atopic Psoriasis
Irritant contact Acute generalized exanthematous pustulosis (AGEP)
Allergic contact Sneddon–Wilkinson/IgA pemphigus
Nummular Candida
Dyshidrosis Dishidrotic Herpes Simplex Virus (HSV) or Varicella Zoster Virus (VZV) infections
Xerotic/asteatotic Follicular pustules (acne/rosacea, bacterial folliculitis; Majocchi
Stasis granuloma, pityrosporum folliculitis, eosinophilic folliculitis)
Photoallergic drug eruption Impetigo
Actinic dermatitis/actinic prurigo Miliaria pustulosa
Id or “autoeczematization”

Chapter 1 :: Fundamentals of Clinical Dermatology

Vesicles/Bullae
Eczematous drug eruption Acute eczematous process
Seborrheic dermatitis Allergic contact dermatitis
Lichen simplex chronicus Bullous arthropod
Mimickers-Scraping, Biopsy May Be Helpful HSV/VZV
Scabies Coxsackie
Tinea Bullous tinea
Some blistering disorders (bullous pemphigoid, dermatitis Autoimmune blistering diseases
herpetiformis) Porphyria cutanea tarda, pseudoporphyria
Mycosis fungoides Polymorphous light eruption
Nutritional deficiency Inherited blistering diseases
Polymorphous light eruption Impetigo
Toolbox Miliaria crystallina
History Bullous diabeticorum
Distribution Vesicles/Pustules as Secondary Processes
Examine scalp, nails, mucous membranes Infection (cellulitis, necrotizing fasciitis, deep fungal, atypical
Patch testing mycobacteria, leishmaniasis, scabies, nocardiosis)
Scraping (scabies, KOH) Edema
Biopsy for routine histology, direct immunofluorescence (DIF) Chemical/thermal/Ultraviolet burn
Bacterial culture, HSV culture (if superinfection suspected) Necrosis
Fixed drug eruption, erythema multiforme, Stevens–Johnson
syndrome, Toxic epidermal necrolysis
Neutrophilic dermatoses (leukocytoclastic vasculitis, Sweet syndrome,
pyoderma gangrenosum)
The first step to determining the reaction pattern is Halogenodermas
identifying the primary lesion. In generalized erup- Toolbox
tions, or when mixed morphologies are present, it is History
useful to go to the edge of a larger lesion or group of Distribution
lesions to determine the primary morphology. It is Examine scalp, nails, mucous membranes
important to note that some diseases with variable KOH and/or fungal culture—blister roof, pustule
morphologies may fall into more than one reaction Bacterial culture—blister fluid, pustule
pattern. DFA, Viral culture—blister base
Biopsy for routine histology, DIF, tissue culture (bacterial,
mycobacterial, fungal)

REACTION PATTERNS WITH ECZEMATOUS

SURFACE CHANGE
PAPULOSQUAMOUS
In papulosquamous eruptions, the primary lesion is
a relatively thin or flat-topped papule or plaque with
scale. Crust or lichenification is usually not present.
Histopathologically, these processes involve the epi-
dermis and superficial to mid-dermis. Individual
papules or plaques are typically well demarcated, and
there is often normal skin visible between each discrete
papule or plaque (Table 1-7).
Eczematous eruptions consist of thin erythematous
papules and plaques with epidermal change. On
the surface of an acute eczematous process, there is
enough epidermal spongiosis (edema between kera-
tinocytes) to cause the formation of serous crust-
ing, microvesicles, or sometimes frank bullae. When
microvesicles collapse, they form characteristic tiny
round crusts often admixed with scale and subtle or
overt fissuring. When subacute to chronic, the sur-
face is often dry, scaly, fissured, and/or lichenified
from rubbing or scratching. Compared with papulo- 13
squamous eruptions, eczematous primary lesions are

Kang_CH001_p0001-0017.indd 13 05/12/18 4:47 pm

 1 TABLE 1-10 TABLE 1-11
Dermal “Plus” Reaction Pattern—Common Macular Reaction Pattern—Common Examples
Examples
Pink
Infections Vascular anomaly or neoplasm (such as nevus simplex)
Mycobacteria: TB and atypical mycobacteria Exanthems (drug, viral)
Fungal: kerion, subcutaneous mycoses, deep fungal mycoses, Macular granuloma annulare, interstitial granulomatous
mycetomas drug eruption
Parasites: leishmaniasis, Chagas, nodular scabies Tinea versicolor (can induce scale)
Bacteria: bartonella, botryomycosis, blastomycosis-like pyoderma, Red
anthrax, gonococcus, syphilitic gumma Red to red-purple
Viral: molluscum, disseminated VZV, verrucous HSV, poxviruses Vascular anomaly or neoplasm (such as telangiectasia,
Neoplasias: Kaposi sarcoma, SCC, BCC, Merkel cell carcinoma, port-wine stain)
amelanotic melanoma, metastases, etc. Petechiae (due to trauma, thrombocytopenia, Rocky Mountain
Inflammatory: Neutrophilic (Sweet syndrome, pyoderma
Part 1

spotted fever, Parvovirus, scurvy)

gangrenosum, halogenodermas), lymphoma (tumor-stage CTCL, Ecchymosis
B-cell lymphomas), sarcoidosis, polyarteritis nodosa, palisaded Red to red-brown
neutrophilic and interstitial granulomatous dermatitis Pigmented purpura
::

Toolbox Telangiectasia macularis eruptive perstans (TMEP)

Foundations of Clinical Dermatology

History Erythema ab igne

Distribution Fixed drug eruption
Examine scalp, nails, mucous membranes, lymph nodes Brown
Culture surface (viral, bacterial, fungal) Melasma
Biopsy for routine histology Lentigo
Biopsy for culture (bacterial, fungal, mycobacterial) Junctional melanocytic nevus
Melanoma
Some birthmarks (Café au lait macule, nevus spilus)
typically ill demarcated, and individual lesions vary Postinflammatory pigmentation
widely in their size and spacing. Because most eczema- Tinea versicolor
Patch-stage KS
tous eruptions share a common histology, the distribu-
Flat warts
tion and history are key in differentiating among them
Diabetic dermopathy
(Table 1-8).
White
Vitiligo
VESICULOBULLOUS Contact leukoderma
Inherited (piebaldism, ash-leaf macule, nevus anemicus)
Sometimes vesicles and bullae are quite obvious; other Postinflammatory pigmentation
times, when all the blisters have ruptured, the clini- Pityriasis alba
cian must recognize their “footprints”—clues to their Hypopigmented MF
recent presence. Because blisters are filled with fluid, Tuberculoid leprosy
Guttate hypomelanosis
when they collapse, they often leave behind round,
Flat warts
oval, arcuate, or geographic erosions or crusts. When
Progressive macular hypomelanosis
small ruptured vesicles are grouped together, as in her- Bier spots
pes simplex, they form crust with “scalloped” edges.
Gray/Blue
Other subtle clues include erosions with “mauserung”
Blue nevus
desquamation, a rumpled rim of epidermis hanging Nevus of Ota
from the erosion’s edge, or milia, which can result from Mongolian spot
healing of deeper blisters (Table 1-9). Lichen planus pigmentosa and related disorders
Some diseases with prominent surface change defy Drug effect (minocycline, amiodarone, hydroxychloroquine)
categorization into papulosquamous, eczematous, or Deposition (ochronosis, silver)
vesculobullous reaction patterns. The astute clinician Tattoo
can recognize an eruption as difficult to characterize Toolbox
and is aware this actually suggests a differential diag- History
nosis in itself. Some examples include scabies, acan- Shape
tholytic diseases (Grover, Darier disease), some drug Distribution
eruptions, some “id” reactions, and some paraneoplas- Examine mucous membranes
Wood lamp
tic conditions.
KOH (for tinea versicolor)
Biopsy for routine histology

DERMAL “PLUS”
These are dermally infiltrated papules, nodules or
14 plaques with surface change: hyperkeratotic scale, crust,
vesicles, pustules, erosion, or ulceration (Table 1-10).

Kang_CH001_p0001-0017.indd 14 05/12/18 4:47 pm

 TABLE 1-12 TABLE 1-13
1
Dermal Reaction Pattern—Common Examples Subcutaneous Reaction Pattern
Inflammatory Inflammatory
Neutrophils (Sweet syndrome, pyoderma gangrenosum, Erythema nodosum
neutrophilic eccrine hidradenitis) Lupus and other connective tissue-related panniculitis
Lymphocytes (tumid lupus, cutaneous lymphoid hyperplasia, Subcutaneous Sweet syndrome, GA, sarcoidosis (Darier-Roussy)
morphea, lichen sclerosus)
Infectious
Histiocytes (xanthomas, xanthogranulomas, granuloma
Erythema induratum
annulare, sarcoidosis, Rosai-Dorfman, Multicentric
Nocardia, actinomyces
Reticulohistiocytosis, palisaded neutrophilic, and interstitial
granulomatous dermatitis) Physical
Mixed (erythema elevatum diutinum, granuloma faciale) Traumatic
Mastocytoma Cold
Plasmacytoma Other

Chapter 1 :: Fundamentals of Clinical Dermatology

Well syndrome Lipodermatosclerosis
Angiolymphoid hyperplasia with eosinophilia Enzyme-mediated (pancreatic, alpha-1 antitrypsin)
Infectious Steroid and other drug injections
Cellulitis, Erysipelas, bartonella (Bacillary angiomatosis, Subcutaneous fat necrosis of the newborn
cat scratch) Panniculitis-like CTCL
Mycobacteria (TB, leprosy, atypical mycobacteria) Toolbox
Subcutaneous and deep fungal infection History
Neoplastic Distribution
Kaposi sarcoma (plaque, tumor-stage) Biopsy for routine histology, tissue culture
Lymphomas (CTCL, B-cell)
Leukemia cutis
Adnexal neoplasms
Vascular neoplasms DERMAL
BCC, SCC, nevus, melanoma, spindle cell neoplasms,
Merkel cell A dermal reaction pattern is a papule or plaque with-
Cutaneous metastases out surface change where the infiltrative process is in
Keloid, hypertrophic scar the dermis (Table 1-12).
Dermatofibroma, Dermatofibrosarcoma protuberans
Depositional
Colloid milium SUBCUTANEOUS
Amyloid
Mucin Subcutaneous reaction pattern is a deeper papule
Gout or plaque, usually without surface change, though
Calcium occasionally they may ulcerate and crust. The infil-
Toolbox trative or inflammatory process is in the subcutis
History (Table 1-13).
Distribution
Examine lymph nodes, mucous membranes
Biopsy for routine histology, tissue culture PURPURIC
Purpura are red or purple macules, patches, papules,
or plaques that result from bleeding into the skin.
Because blood has extravasated, they do not blanch
REACTION PATTERNS when pressure is applied. They may range in color
from true red to red-purple or magenta to red-brown
WITHOUT SURFACE (“cayenne pepper”). Purpuric macules are sometimes
CHANGE called “petechiae”; purpuric patches are sometimes
called “ecchymoses.” Ecchymosis may also overlie a
plaque or nodule from dermal or subdermal hemor-
In the absence of surface change, the epidermis and its
rhage, known as hematoma, and may appear yellow-
melanin are unaltered, often allowing color and topog-
green when a few days old. Purpuric papules, or
raphy to be the defining characteristics. Shape, config-
“palpable purpura,” typically represent inflammation
uration, and distribution are also helpful.
of small vessels associated with hemorrhage, as in leu-
kocytoclastic vasculitis, a coagulopathy affecting small
vessels, as in cryoglobulinemia, or very small emboli.
MACULAR Purpuric plaques represent ischemia, embolism, infarc-
tion, intravascular infection, or inflammation of small-
Macules can derive their color changes from changes medium or medium vessels, that may lead to necrosis 15
in the epidermis or dermis (Table 1-11). of the overlying epidermis. These can manifest as pink

Kang_CH001_p0001-0017.indd 15 05/12/18 4:47 pm

 1 TABLE 1-14 TABLE 1-15
Purpuric Reaction Pattern—Common Examples Erythemas
Vasculitis Exanthems
Small vessel Viral
Hypersensitivity vasculitis (to drug or infection) Bacterial (toxic shock syndrome, scarlet fever, meningococcus,
Henoch–Schoenlein purpura (IgA vasculitis) mycoplasma)
ANCA+ Drug (morbilliform eruption, drug-induced hypersensitivity
Connective-tissue disease associated syndrome)
Medium vessel Graft-vs-host disease
Polyarteritis nodosa Kawasaki disease
Churg–Strauss Miliaria rubra
Levamisole hypersensitivity Figurate
Macular arteritis Erythema annulare centrifugum
Part 1

Infectious Deep gyrate erythemas

Meningococcemia Erythema migrans
Purpura fulminans Erythema marginatum
Ecthyma gangrenosum
::

Urticaria/Urticaria
Hyperinfection strongyloidiasis Urticaria
Foundations of Clinical Dermatology

Aspergillus, mucor, and other vasculotropic fungi Neutrophilic urticaria

Embolic Papular urticaria
Cholesterol emboli Urticarial vasculitis
Septic emboli (endocarditis and others) Dermal hypersensitivity reaction
Vasculopathy Polymorphous eruption of pregnancy
Calciphylaxis Urticarial bullous pemphigoid
Cryoglobulin, cryofibrinogen Acute hemorrhagic edema of childhood
Antiphospholipid antibody syndrome, livedoid vasculopathy, Targetoid
livedo racemosa Erythema multiforme
Coumadin/heparin necrosis Mycoplasma-induced rash and mucositis
Levamisole hypersensitivity Fixed drug eruption
Other hypercoagulable states Urticarial vasculitis
Other Paraneoplastic pemphigus
Vascular or intravascular neoplasms (Kaposi sarcoma, Rowell-type lupus
angiosarcoma, intravascular lymphoma) Toolbox
Cutis marmorata History
Petechiae (trauma, thrombocytopenia, Rocky Mountain spotted Distribution
fever, Parvovirus, scurvy) Examine mucous membranes
Ecchymoses Biopsy for routine histology, DIF
Toolbox Viral studies
History Other lab workup depending on morphology and history
Distribution
Other lab workup depending on morphology and history
Biopsy for routine histology
■
Biopsy for DIF
Morbilliform erythemas are exanthems that
Biopsy for tissue culture
are typically consist of diffuse symmetric
blanching pink, red, or magenta macules and
papules.
■ Figurate erythemas are annular, arcuate, or
papules (usually medium vessels) or stellate dark polycyclic blanching pink to red plaques. They
purple plaques (Fig. 1-23), and may be accompanied generally do not have surface change, with the
by pink, red, or purple net-like (“retiform”) hyper- exception of erythema annulare centrifugum,
emia (“livedo”). If the overlying epidermis becomes which exhibits prototypical “trailing scale.”
necrotic, bullae, ulcer, and/or eschar may form at the ■ Urticarial erythemas are pink, blanching
surface (Table 1-14). macules, papules, or plaques, often exhibiting a
characteristic “wheal and flare” appearance, with
ERYTHEMAS blanching of the skin surrounding the primary
lesion (Fig. 1-24).
Erythemas are blanching red-pink macules, patches, ■ Targetoid erythemas have at least 2 zones of color,
papules, or plaques, or a combination, usually with- with a darker center compared to the periphery.
out surface change. This reaction pattern may be sub- The center often has a “dusky,” or gray-violet, hue,
divided into morbilliform erythemas, figurate erythemas, owing to epidermal necrosis, or vesiculates as the
16 urticarial erythemas, and targetoid erythemas (Table 1-15). necrotic epidermis detaches.

Kang_CH001_p0001-0017.indd 16 05/12/18 4:47 pm


Figure 1-23 Retiform purpura with ulceration and eschar,
cutaneous polyarteritis nodosa.
CONCLUSION
In the age of digital photography, the basic art and
science of morphology remains paramount in der-
matology to achieve accurate diagnosis and a deeper
understanding of clinical–pathologic correlation.
As Siemens (1891–1969) wrote, “he who studies
skin diseases and fails to study the lesion first will
never learn dermatology.” Careful evaluation of the
skin and systematic identification of primary mor-
phology, secondary changes, and reaction pattern
is essential to the art and science of dermatologic
diagnosis.
Kang_CH001_p0001-0017.indd 17
1
Chapter 1 :: Fundamentals of Clinical Dermatology
Figure 1-24 Urticarial phase, bullous pemphigoid.
ACKNOWLEDGMENTS
The authors are truly grateful for the opportunity to
build upon the work of Amit Garg, Nikki A. Levin,
and Jeffrey D. Bernhard, authors of a previous version
of this chapter. The authors thank Lindy P. Fox and
Ilona J. Frieden for sharing materials and insights that
informed this work.
SUGGESTED READINGS
Burgin S. A Guidebook to Dermatologic Diagnosis. New York,
NY: McGraw-Hill. In press.
duVivier A. Atlas of Clinical Dermatology, 4th ed. Philadelphia,
PA: Saunders; 2012.
Ghatan HEY. Dermatological Differential Diagnosis and Pearls,
2nd ed. Boca Raton, FL: CRC Press; 2002.
Schneiderman P, Grossman ME. A Clinician’s Guide to
Dermatologic Differential Diagnosis. Boca Raton, FL: CRC
Press; 2006.
White GM, Cox NH. Diseases of the Skin: A Color Atlas and Text,
2nd ed. Maryland Heights, MO: Mosby; 2005.
Wolff K, Johnson R, Saavedra A, et al. Fitzpatrick’s Color
Atlas and Synopsis of Clinical Dermatology, 8th ed.
New York, NY: McGraw-Hill; 2017.
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