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| Gary M. White & Neil H. Cox |
| Diseases of the Skin |
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Fundamental Dermatology and Terminology |
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TERMINOLOGY OF SKIN LESIONS
Examination of the skin is described in Chapter 2. However, in order to usefully record the features identified on examination, it is important to understand some of the clinicopathological correlates of the abnormalities that may be found, and to know the terminology for the shapes and patterns of skin lesions.
Lesion morphology and surface features
This section describes the fundamental types of skin lesions (known as the primary lesions) that may occur in various disease states. Many of these can be qualfied further by various descriptions of their shape, color, surface changes, and arrangement overall. For example, in a typical case of lichen planus the papules (primary lesion) could be further described as grouped, purplish, flat-topped, and slightly scaly.
Primary skin lesions
Macules and patches
These are flat, discrete areas of altered color (Figure. 1.2). In some instances, such as lentigo (increase in number of basal melanocytes), there may be fine surface scaling as a secondary phenomenon (presumably due to disturbance of the basal keratinocytes by the increased melanocyte density). Authors vary in the size cut-off between a macule (smaller) and a patch, with definitions ranging between 1- and 2-cm size limits. As such definitions are arbitrary and of no particular biological significance, it is more helpful to record the actual size.
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| Figure. 1.2 Vitiligo: a macular lesion with color change but no palpable component. (From Lawrence CM, Cox NH. Physical Signs in Dermatology, 2nd edn. London: Mosby, 2002.) |
Plaques
These are elevated lesions, predominantly flat-topped but palpable (Figure. 1.3). There is more potential for variable surface features (e.g. smooth, scaly, and crusted) than in a macule; surface features are discussed in more detail later in this chapter.
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| Figure. 1.3 Plaques, in this case due to subacute cutaneous lupus erythematosus. These could be further described as having annular accentuation, scaling, and some central atrophy. (Courtesy of Dr. G. Dawn.) |
Papules and nodules
These are raised and essentially dome-shaped lesions (Figs 1.4and 1.5). As with macules and patches, there are variable size cut-offs between papules (which are smaller) and nodules (which are larger). The arbitrary cut-off (either 0.5cm or 1cm in different publications) ignores the possibility of lesions of mixed sizes or of growth from a papule to a nodule. The term maculopapular is applied to eruptions that have mixed features of macules and papules or plaques; although this pattern is frequent in drug eruptions and viral exanthems, it is a rather overused term that often does not accurately describe the predominant component of the eruption.
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| Figure. 1.4 Papules, in this case due to a condition called Gianotti–Crosti syndrome. There are multiple small dome-shaped lesions with some central umbilication. (From Lawrence CM, Cox NH. Physical Signs in Dermatology, 2nd edn. London: Mosby, 2002.) |
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| Figure. 1.5 An example of a nodule, in this case a keloid on the earlobe secondary to ear piercing. (From Lawrence CM, Cox NH. Physical Signs in Dermatology, 2nd edn. London: Mosby, 2002.) |
Blisters (vesicles and bullae)
Blisters can be divided into smaller (0.5- or 1-cm cut-off) vesicles and larger bullae (Figs 1.6and 1.7). Again, this is somewhat arbitrary; in practice most vesicular eruptions (e.g. those of pompholyx eczema, Fig.1.7 ) actually consist of lesions of 1–4mm, whereas most conditions that would usually be described as bullous have at least some lesions of over 1cm. Blisters should be documented as unilocular (e.g. in friction blister and bullous pemphigoid) or multilocular (e.g. in pompholyx eczema).
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| Figure. 1.6 Blister: this is a unilocular blister with clear fluid content in a patient with toxic epidermal necrolysis (see also Chs 16 and 18). Intact blisters are relatively uncommon in this condition. |
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| Figure. 1.7 Multiple small vesicles in this case from pompholyx. |
Pustules
These are similar to blisters but contain pus, which is usually yellow but may be greenish in older pustules (Figure. 1.8). Older pustules usually dry to form brownish scabs.
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| Figure. 1.8 Pustules: multiple yellow pustules on the palm of the hand, in this case due to acute palmoplantar pustulosis. This should be compared with the more common chronic palmoplantar pustulosis (discussed in the context of psoriasis, Ch.7 ), in which the pustules are more variable in size and in stages of evolution. |
Telangiectasia and other vascular lesions
Vascular changes such as telangiectasia (discrete visible vessels) should be distinguished from erythema (increased redness due to increased blood flow rather than due to a fixed structural vascular abnormality) and purpura (small spots of extravasated blood), whether as components of a rash or a discrete localized lesion. Blood that is within vessels can generally be compressed out of the skin by pressure, hence causing blanching, whereas this cannot be achieved with extravasated blood. There are occasional instances where intravascular blood cannot be compressed out using simple clinical techniques (see Diascopy, Ch.2).
Ulcers and other breaks in the skin
Breaks in the skin may be divided into the following.
| | Ulcers—the term can be applied to any skin break but is generally taken to imply a defect extending into the dermis (Figure. 1.9); |
| | Erosions—these are superficial, involving the epidermis only. |
| | Fissures—a specific morphology of skin break resembling a small slit. |
Excoriations are a type of erosion or ulcer caused by scratching, the term describing the process by which the break has occurred rather than being used as a term for a specific primary lesion.
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| Figure. 1.9 Ulcers: defects through the epidermis reveal underlying dermis or fat. This ulceration of penis was probably due to Behçet disease, although the patient did not fulfill criteria for the diagnosis, as he had no oral ulcers (see Ch.14 ). |
Weals
These are due to dermal edema. Patients often confuse weals and blisters, so a history of ‘blisters' may be misleading. Gentle pressure on a blister will alter its shape, which generally returns to the previous shape very quickly unless the fluid content is highly proteinaceous, and firm pressure may cause the blister to spread or to break. By contrast, gentle pressure on a weal has no effect (except blanching if it is erythematous), while firm pressure may compress fluid out of it to leave an indentation that slowly refills. However, the simplest distinction is that blisters can be punctured and then leak fluid.
Surface morphology and secondary changes
It is useful to note certain surface features of papules, nodules, and plaques.
Overall shape
Papules and nodules can be further characterized as dome-shaped, flat-topped, umbilicated, etc.
Surface changes
A particularly important issue is distinction between disorders with and without an epidermal component, implied by scaling and crusting (Fig.1.10 ). Thus, for example, annular lesions of ringworm (scaly) and granuloma annulare (no scaling) can readily be distinguished.
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| Figure. 1.10 Examples of scaling. ( a ) In psoriasis, shown here on the scalp, scaling is typically well formed and has a silvery color. Compare with the different quality and pattern of the marginal scaling in ( b ) erythrokeratoderma variabilis. (Panel b from Lawrence CM, Cox NH . Physical Signs in Dermatology, 2nd edn. London : Mosby, 2002.) |
Useful terms are as follows:
| | Smooth—this may be like the normal skin surface or smoother. |
| | Scaly—scaling is due to flakes of keratin, which can be felt, and rubbed or scraped off the skin. It can be qualifed as fine (e.g. in pityriasis versicolor) or coarse (e.g. in psoriasis), and as loose or adherent. Disorders with scaly papules and plaques are termed papulosquamous. |
| | Hyperkeratotic—this implies a formed mass of keratin rather than the flakiness of scaling; for example, the cutaneous horn of keratoacanthoma or the diffuse hard keratin of keratodermas. |
| | Crusted—crust is due to dried blood or exudate, often mixed with keratin but not due to keratin alone. Hardened surface blood is known as an eschar, or colloquially as a scab (the latter term is also applied to dried pus or proteinaceous exudates). |
Texture changes
Alterations in any skin component may cause thinning (atrophy) or thickening. Epidermal atrophy causes a fine wrinkling appearance of the skin (except over the surface of a nodule, where it may produce abnormally smooth and tight-looking skin due to the tension that is being exerted). It is often combined with dermal atrophy (Figs 1.11 and 1.12 ). Dermal atrophy may lead to a herniation of the underlying fat (a process termed anetoderma). Fat atrophy in the absence of dermal atrophy causes a deep indentation of the skin.
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| Figure. 1.11 Atrophy of the skin, in this case in striae distensae. This occurs due to stretching of the skin (e.g. on abdomen or thighs in pregnancy or when the skin is damaged by excessive use of topical corticosteroids). The skin appears thinned, and dermal vasculature is readily visible in the line of the applied tension that has stretched the skin. |
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| Figure. 1.12 Lichen sclerosus et atrophicus. In this condition, there is epidermal atrophy together with a homogenization and edema of the upper dermal collagen. This produces a typically white color and a thinned appearance of the skin. In this patient, the two lines of lesions represent a Koebner response. |
Thickening of the skin includes epidermal thickening (e.g. lichenification due to rubbing), dermal thickening (e.g. sclerosis due to increased collagen in scleroderma, and peau d'orange appearance due to dermal mucin), and fat hypertrophy ( Fig.1.13 ).
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| Figure. 1.13 In this case, mixed fat hypertrophy and atrophy (note the normal skin color because the abnormality is deep to the skin). |
These processes, and the predominant level of the skin that is affected, can usually be identified from the physical signs, both palpable and visible (e.g. increased skin markings in lichenification, more visible vessels due to atrophy).
Shapes and patterns, symmetry
These processes, and the predominant level of the skin that is affected, can usually be identifid from the physical signs, both palpable and visible (e.g. increased skin markings in lichenification, and more visible vessels due to atrophy).
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| Figure. 1.14 Annular lesion: a complete circle. In this case due to erythema migrans of Lyme disease. Parts of a circle are termed arcuate or arciform. |
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| Figure. 1.15 Classic target lesions, comprising multiple concentric circles, typically (as in this case) seen in erythema multiforme triggered by herpes simplex virus infection. |
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| Figure. 1.16 This net-like or chicken wire pattern is termed livedo (see also Ch.14 ). A uniformly sized faint livedo pattern is common over fatty areas of skin, especially in babies and young women, and is a physiologic phenomenon reflecting areas of slower flow of deoxygenated blood (known as cutis marmorata). |
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| Figure. 1.17 Skin color may be rather subjective, but the hand on the left in this picture is clearly more yellow than the normal control. This patient had carotenemia, which may occur as a metabolic defect or in hypothyroidism, but is commonly dietary due to excessive carotene intake. |
Shapes of individual lesions
Examples of lesional shapes, and conditions with which they are associated, are listed in Table 1.1 ; some specific common examples are addressed in more detail in Tables 1.2 - 1.4 .
Table 1.1 MAIN SHAPES OF SKIN LESIONS |
| Shape | Description | Example(s) |
|---|---|---|
| Discoid (nummular) | A filled circle | Discoid eczema |
| Petaloid | Discoid lesions that have merged together | Seborrheic dermatitis on the trunk |
| Arcuate | Incomplete circles | Urticaria |
| Annular | Open circles with different central skin compared with | Tinea corporis, granuloma annulare (see also Table 1.2) |
| Polycyclic | Circles that have merged together | Psoriasis |
| Livedo | Chicken wire criss-cross pattern | Erythema ab igne, vasculitis |
| Reticulate | A finer lace-like pattern | Oral lichen planus |
| Target | Multiple concentric rings | Erythema multiforme |
| Stellate | Star-shaped | Lesions of meningococcal septicemia |
| Digitate | Finger-shaped | Parapsoriasis |
| Linear | Straight line | Koebner reaction to a scratch in lichen planus (see Tables 1.3 and 1.4) |
| Serpiginous | Snake-like | Cutaneous larva migrans |
Table 1.2 EXAMPLES OF LESIONS OR GROUPINGS OF LESIONS THAT PRODUCE ANNULAR MORPHOLOGY |
| Scale | Typically annular | Often Include annular components |
|---|---|---|
| Present | Ringworm Erythema annulare centrifugum |
Psoriasis Seborrheic eczema Pityriasis rosea (herald patch) Impetigo Subacute cutaneous lupus erythematosus Mycosis fungoides |
| Absent | Granuloma annulare Jessner lymphocytic infiltrate ‘Annular erythemas’ Erythema annularis telangiectoides Serum sickness |
Urticaria Erythema multiforme Lichen planus Sarcoidosis |
(After Lawrence CM, Cox NH. Physical Signs in Dermatology, 2nd edn. London: Mosby, 2002.)
Table 1.3 EXAMPLES OF LESIONS OR GROUPINGS OF LESIONS THAT PRODUCE LINEAR MORPHOLOGY |
| Deternimant of patterns | Example(s) |
|---|---|
| Blood vessels Lymphatics Dermatome Nerve trunks Developmental and Blaschko lines Skin stretching Infestation |
Thrombophlebitis, Mondor disease (linear thrombophlebitis on the trunk) Eczema related to varicose veins Tem poral arteritis Lymphangitis Sporotrichosis, fish tank granulomas Herpes zoster, zosteriform nevus, zosteriform Darier disease, zosteriform metastases Leprosy (thickened cutaneous nerves) Pigmentary demarcation line, linea nigra Epidermal nevi, incontinentia pigmenti, hypomelanosis of Ito, linear psoriasis, linear lichen planus, lichen striatus Striae due to growth spurt (on lower back) Larva migrans (wavy, not straight, lines) |
| External injury Plants Allergens Chemical Thermal Physical Other determinants |
Phytophotodermatitis Elastoplast, nail varnish (neck), necklace, waistbands, etc. Caustics (e.g. phenol) Burns To normal skin Keloid scar, bruising, dermatitis artefacta, amniotic constriction bands To abnormal skin Purpura (cryoglobulinemia, amyloid, vasculitis) Blisters (epidermolysis bullosa, porphyrias) Inoculation Warts, mol luscum contagiosum Koebner phenomenon Psoriasis, lichen planus, others (Table 1.4) Other Scar sarcoid Linear scleroderma (limb, central forehead) Senear-endash Caro ridge (on hands in psoriasis) Dermatomyositis (linear pattern on dorsum of fingers; Gottron sign) Interstitial granulomatous dermatitis (rope sign) |
(After Lawrence CM, Cox NH. Physical Signs in Dermatology, 2nd edn. London: Mosby, 2002.)
Table 1.4 DISORDERS THAT MAY SHOW THE KOEBNER REACTIONa |
| Commonly | Less Commonly |
|---|---|
| Psoriasis Pityriasis rubra pilaris Lichen planus Lichen nitidus Vitiligo Lichen sclerosus |
Small vessel vasculitis Erythema multiforme Elastosis perforans serpiginosa Necrobiosis lipoidica Eruptive xanthomas Scleromyxedema Pemphigus |
aViral warts are often stated to exhibit the Koebner phenomenon, but this is
incorrect: viral warts in the line of a skin injury are due to direct inoculation of
virus. Similarly, vasculitis in scratch marks or pressure areas may occur
immediately after the insult, and is probably due to local hydrostatic pressure
changes and trauma causing vascular leakage, rather than actually provoking
the vasculitic process.
Arrangements of multiple lesions
Useful terms to describe arrangements of multiple lesions include grouped (agminated), scattered or disseminated, and confluent. Other terms may be based on anatomic factors (e.g. dermatomal lesions of herpes zoster) or probable causes (e.g. photosensitivity distribution). See also Tables 1.2 and 1.3.
Blaschko lines warrant specific mention: they are developmental lines that have a swirled pattern on the trunk (more linear on the limbs), and this pattern can therefore often identify an eruption as having a congenital or genetic basis.
Koebner reaction
This specific pattern of eruption (also known as the isomorphic response) is usefully described here. A number of dermatoses have the ability to create lesions in areas of minor injury (Fig.1.12, Table 1.4 ); these include frank cuts, but often the triggering insult may not overtly breach the skin. Such lesions are often linear, as scratches are a common trigger, but other shapes are seen in burns, for example. A similar process that occurs at skin puncture sites, especially if autologous blood or saline are injected, occurs in pyoderma gangrenosum and Behçet disease, and is known as pathergy.
Note that viral warts are often stated to exhibit the Koebner phenomenon, but this is incorrect: viral warts in the line of a skin injury are due to direct inoculation of virus. Sarcoidosis often occurs in scars, but affects old scars rather than new minor injuries.
Symmetry
Degree of symmetry is also a useful feature of skin eruptions. In general, markedly symmetric eruptions are endogenous in causation, although there are inevitably some exceptions (e.g. contact allergy to footwear is usually symmetric). Conversely, asymmetric eruptions often have external causes. Fungal infections of the skin are an important example, exemplified by unilateral palmar involvement, a situation that should routinely prompt inspection of the feet for tinea pedis. Asymmetric hand eruption also occurs in cooks, hairdressers, and others who hold a tool in the dominant hand while handling wet or irritant materials with the non-dominant hand.
Color
Skin color involves contributions from several pigments.
| | melanins (red, brown, or black; these usually provide the dominant pigment in normal skin) |
| | blood (red, purple, or blue) |
| | carotenoids (yellow; Fig.1.17 ) and . |
| | dermal fibrous tissue (white). |
A wide range of skin colors occur in different physiologic and pathologic states. The subtleties of color may not be appreciated without experience. For example, patches of vitiligo (loss of melanin) and of nevus anemicus (loss of red color due to vasoconstriction) are both often termed ‘depigmented' by non-specialists, but the vitiligo is white or pale pink, whereas nevus anemicus is usually a pale yellowish brown color (i.e. hypopigmented rather than depigmented). Some shades of color are quite characteristic (e.g. the yellow-orange color of xanthomas), and others are sufficiently useful that they narrow the list of likely diagnoses (e.g. purplish or violaceous coloring of lichen planus or dermatomyositis). Thus an accurate description of shades of red or other color changes can be diagnostically useful (Table 1.5).
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| Figure. 1.18 Black dermographism. Gold rings are a common cause, usually after there has been a solvent or abrasive agent under the ring. In this case, the culprit was a sunscreen containing titanium, which presumably had an abrasive effect. |
Blanching of the skin on pressure is often ascribed great diagnostic importance but is a feature of virtually all dermatoses and of normal skin: any skin with patent blood vessels will be less red when these are occluded. The converse, however, is a useful sign of extravasation of blood, as discussed earlier. The color contribution from blood in the skin is altered by the degree of blood flow, where it is occurring (from superficial or deep vessels), state of blood oxygenation, and abnormal hemoglobins (e.g. methemoglobin and carboxyhemoglobin).
The presence of scaling alters color by introducing air–keratin interfaces that reflect light. This can be exaggerated (notably in psoriasis) by scratching the scaly surface, and can be reduced by applying oil or water. Thus many patients will note that scaly skin lesions look redder when they take a bath or apply topical medications.
Inflammation of the skin disrupts pigmentation. Postinflammatory hyper- or hypopigmentation is a common feature of many dermatoses but causes much diagnostic confusion; hyperpigmentation in particular may take a considerable time to resolve. It is important to understand that when melanin pigment is positioned deep in the dermis, rather than at the usual epidermal level, the different refraction of light gives it a more blue color; this explains the overall grayish brown color of dermal postinflammatory hyperpigmentation, and also the purple color of lichen planus (red from inflammation plus blue-brown from disturbed pigmentation).
External pigments may also stain the skin (Fig.1.18 ) on occasion, dyes leached out of new clothing may cause diagnostic confusion.
Colors that may be diagnostically useful are listed in Table 1.5.
Table 1.5 COLORS THAT MAY BE DIAGOSTICALLY USEFUL |
| Color | Example(s) |
|---|---|
| Black | Melanin (e.g. some nevi, melanoma) Exogenous pigments (e.g. tattoos, pencil or ink) Exogenous chemicals (e.g. silver nitrate, gold salts; Fig. 1.14) |
| Blue-grey | Deeply situated blood(e.g. some angiomas) Deep melanin (e.g. blue nevus) Inflammatory (e.g. orf) Drugs (e.g. phenothiazines, minocycline) |
| Dark brown | Melanin near surface(e.g. melanocytic nevi) Exogenous pigments (e.g. dithranol staining) |
| Pale brown | Melanin near surface(e.g. lentigo, freckles) |
| Muddy brown | Melanin in superficial dermis (e.g. postinflammatory pigmentation) |
| Purple | Vascular lesions (e.g. angiomas) Other disorders where telangiectasia is a prominent feature (e.g. lupus pernio or chronic sarcoidosis, dermatomyositis) |
| Dusky blue | Reduced hemoglobin (e.g. poor arterial supply, cyanosis) Methemoglobinemia |
| Violaceous and lilac | Lichen planus Edge of plaques of morphea Connective tissue disorders (e.g. dermatomyositis) |
| Pink-red | Many exanthemata and common disorders, such as psoriasis |
| Red-brown | Inflammatory (e.g. seborrheic eczema, secondary syphilis) Hemosiderin (e.g. pigmented purpuric dermatoses) |
| Scarlet-red | Lesions with strong arterial supply (e.g. pyogenic granuloma, spider nevus) Altered hemoglobin (e.g. carbon monoxide poisoning) |
| Orange | Hemosiderin (e.g. lichen aureus) Inflammatory (e.g. pityriasis rubra pilaris) |
| Yellow-white or yellow-pink | Xanthomatous disorders |
| Yellow-orange | Carotenemia (ingested carotene, myxedema) |
| Yellow-green | Jaundice |
| Green | Exogenous pigment (e.g. copper salts) |
| White-ivory | Lichen sclerosus et atrophicus, morphea |
| White (or pale pink, depending Albinism, piebaldism on vascularity) |
Albinism, piebaldism Vitiligo, halo nevus White dermographism, steal effect around vascular lesions |
(After Lawrence CM, Cox NH. Physical Signs in Dermatology, 2nd edn. London: Mosby, 2002.)
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White/Cox: Diseases of the Skin, 2ed.(c) 2006, Elsevier Inc. All rights reserved.