Introduction

The skin is the largest organ in the human body. Forming a major interface between man and his environment, it covers an area of approximately 2 m and weighs about 4 kg. The structure of human skin is complex ( Figs 20.1 and 20.2 ), consisting of four distinct layers and tissue components with many important functions ( Box 20.1 ). Reactions may occur in any of the components of human skin and their clinical manifestations reflect, among other factors, the skin level in which they occur, and sometimes they act as a ‘window’ of systemic changes elsewhere in the body, e.g. medical conditions discussed later in the chapter, such as those associated with pruritus (see Box 20.9 ), systemic causes of erythema nodosum (see Box 20.10 ) or paraneoplastic skin conditions ( Box 20.2 ).

Figure 20.1, The anatomy of the full thickness of the skin in section .

Figure 20.2, The anatomy of the epidermis.

Box 20.1
Functions of the human skin

  • Protection: physical, chemical, infection—immune and innate

  • Physiological: homoeostasis of electrolytes, water and protein

  • Thermoregulation

  • Sensation: specialized nerve endings—pain, touch and temperature

  • Lubrication and waterproofing: sebum

  • Immunological reactions: Langerhans’ cells, lymphocytes, macrophages

  • Wound healing

  • Ultraviolet-induced vitamin D synthesis

  • Body odour: apocrine glands

  • Psychosocial: cosmetic

Box 20.2
Paraneoplastic skin disorders

Dermatosis Associated tumour
Dermatomyositis Lung, gastrointestinal (GI) tract, genitourinary tract
Acanthosis nigricans GI tract, lung, liver
Paget’s disease of the nipple/extra-mammary Paget’s disease of the perineum Adenocarcinoma
Erythroderma Haematological
Tylosis-thickening of palms and soles Oesophageal carcinoma
Ichthyosis Lymphoma
Erythema gyratum repens Lung, breast
Necrolytic migratory erythema Glucagonoma

The accurate diagnosis of most skin lesions requires an adequate history, careful examination of the patient and, occasionally, laboratory investigation, but dermatology is predominantly a visual specialty.

History

Detailed information should be sought concerning the present skin condition. This should include the site of onset, mode of spread and duration of the disorder. Any personal history or family history of skin disease, including skin cancer and atopy (an allergic skin reaction becoming apparent more or less immediately on contact), is important. Previous medical conditions should be noted and a full drug history obtained, including the use of over-the-counter and other preparations. The social and occupational history and, in some circumstances, details of recent travel, environmental exposure, especially sunshine and artificial ultraviolet light, and sexual activity are often important ( Box 20.3 ).

Box 20.3
Approach to dermatological patient history

  • Time course of skin eruption

  • Distribution of lesions including initially

  • Symptoms: pruritus

  • Family history: atopy and psoriasis

  • Drug/allergy history

  • Past medical history

  • Contacts: family and partners

  • Provocating factors: sunlight and foods

  • Previous and current treatments

Examination

The whole skin, including hair, nails and assessable mucosae, should be fully inspected (preferably in natural light), but the patient’s modesty should be protected. Sometimes a magnifying lens or dermatoscope is useful.

Colour and pigmentation

Before inspecting any rash or lesion, note the colour of the skin. Normal skin colour varies, depending on lifestyle and light exposure as well as constitutional and ethnic factors.

Pallor can have many causes. It may be:

  • Temporary, owing to shock, haemorrhage or intense emotion

  • Persistent, owing to anaemia or peripheral vasoconstriction

Vasoconstriction is seen in patients with severe atopy—an inherited susceptibility to asthma, eczema and hay fever. Pallor is a feature of anaemia, but not all pale persons are anaemic; conjunctival and mucosal colour is a better indication of anaemia than skin colour. A pale skin resulting from diminished pigment occurs with hypopituitarism and hypogonadism.

Normal skin contains varying amounts of brown melanin pigment. Brown pigmentation owing to deposited haemosiderin is always pathological. Albinism is an inherited generalized absence of pigment in the skin; a localized form is known as piebaldism. Patches of white and darkly pigmented skin (vitiligo) ( Fig. 20.3 ) are owing to a local and complete absence of melanocytes. Several autoimmune endocrine disorders are associated with vitiligo.

Figure 20.3, Vitiligo, a disorder of cutaneous pigmentation that is often autoimmune in origin and associated with other autoimmune disorders.

Abnormal redness of the skin (erythema) is seen after overheating, extreme exertion and sunburn and in febrile, exanthematous and inflammatory skin diseases. Flushing is a striking redness, usually of the face and neck, which may be transient or persistent. Local redness may be caused by telangiectasia, especially on the face. Cyanosis is a blue or purple-blue tint caused by the presence of excessive reduced haemoglobin, either locally, as in impaired peripheral circulation, or generally, when oxygenation of the blood is defective. The skin colour in methaemoglobinaemia is more leaden than in ordinary cyanosis; it is caused by drugs, such as dapsone, and certain poisons.

Jaundice varies from the subicteric lemon-yellow tints seen in pernicious anaemia and haemolytic jaundice to various shades of yellow, orange or dark olive-green in obstructive jaundice. Jaundice, which stains the conjunctivae, must be distinguished from the rare orange-yellow of carotenaemia, which does not. Slight degrees of jaundice cannot be seen in artificial light.

Increased pigmentation may be racial, owing to sunburn or connected with various diseases. In Addison’s disease, a brown or dark-brown pigmentation affects exposed parts and parts not normally pigmented, such as the axillae and the palmar creases; the lips and mouth may exhibit dark bluish-black areas. Note, however, that mucosal pigmentation is a normal finding in a substantial proportion of black patients.

More or less generalized pigmentation may also be seen in the following:

  • Haemochromatosis, in which the skin has a peculiar greyish-bronze colour with a metallic sheen, owing to excessive melanin and iron pigment

  • Chronic arsenic poisoning, in which the skin is finely dappled affecting covered more than exposed parts

  • Argyria, in which the deposition of silver in the skin produces a diffuse slate-grey hue

  • The cachexia of advanced malignant disease

In pregnancy, there may be pigmentation of the nipples and areolae, of the linea alba and sometimes a mask-like pigmentation of the face (chloasma). Chloasma may also be induced by oral contraceptives containing oestrogen. A similar condition, melasma, may be seen in Asian and Afro-Caribbean males.

Localized pigmentation may be seen in pellagra and in scars of various kinds, particularly those owing to X-irradiation therapy. Venous hypertension in the legs is often associated with chronic purpura, leading to haemosiderin pigmentation. The mixture of punctate and fresh purpura and haemosiderin may produce a golden hue on the lower calves and shins. Pigmentation may also occur with chronic infestation by body lice . Erythema ab igne, a reticular pattern of pigmentation, can be seen in patients who use local heat to relieve chronic pain or on the shins of people who habitually sit too near a fire. Livedo reticularis, a web-like pattern of reddish-blue discolouration mostly involving the legs, occurs in autoimmune vasculitis, especially in systemic lupus erythematosus (SLE) and antiphospholipid syndrome, when it is associated with cerebral infarction. The violet-coloured lesions of lichen planus are slightly raised, flat-topped papules ( Fig. 20.4 ). Psoriasis usually presents as a symmetrical plaque on extensor surfaces ( Fig. 20.5 ). Keloid consists of raised and inflamed, overgrown tender scar tissue ( Fig. 20.6 ). Dermatomyositis often produces swelling and heliotrope-coloured erythema of the eyelids without scaling of the skin.

Figure 20.4, Flat-topped papules of lichen planus.

Figure 20.5, Salmon-pink plaque of psoriasis on elbow covered in characteristic silver scale.

Figure 20.6, Multiple keloid scarring of the back caused by acne vulgaris. There is a genetic predisposition to the formation of keloid in scar tissue.

Skin lesions and eruptions

Skin eruptions and lesions should be examined with special reference to their morphology, distribution and arrangement. The terminology of skin lesions is summarized in Boxes 20.4 and 20.5 . Colour, size, consistency, configuration, margination and surface characteristics should be noted.

Box 20.4
Primary skin lesions: a glossary of dermatological terms

Macule Non-palpable area of altered colour
Papule Palpable elevated small area of skin (<0.5 cm)
Plaque Palpable flat-topped discoid lesion (>2 cm)
Nodule Solid palpable lesion within the skin (>0.5 cm)
Papilloma Pedunculated lesion projecting from the skin
Vesicle Small fluid-filled blister (<0.5 cm)
Bulla Large fluid-filled blister (>0.5 cm)
Pustule Blister containing pus
Wheal Elevated lesion, often white with red margin owing to dermal oedema
Telangiectasia Dilatation of superficial blood vessel
Petechiae Pinhead-sized macules of blood
Purpura Larger petechiae that do not blanch on pressure
Ecchymosis Large extravasation of blood in skin (bruise)
Haematoma Swelling owing to gross bleeding
Poikiloderma Atrophy, reticulate hyperpigmentation and telangiectasia
Erythema Redness of the skin
Burrow Linear or curved elevations of the superficial skin owing to infestation by female scabies mite
Comedo Dark horny keratin and sebaceous plugs within pilosebaceous openings

Box 20.5
Secondary skin lesions that evolve from primary lesions

Scale Loose excess normal and abnormal horny layer
Crust Dried exudate
Excoriation A scratch
Lichenification Thickening of the epidermis with exaggerated skin margin
Fissure Slit in the skin
Erosion Partial loss of epidermis which heals without scarring
Ulcer At least the full thickness of the epidermis is lost. Healing occurs with scarring
Sinus A cavity or channel that allows the escape of fluid or pus
Scar Healing by replacement with fibrous tissue
Keloid scar Excessive scar formation (see Fig. 20.6 )
Atrophy Thinning of the skin owing to shrinkage of epidermis, dermis or subcutaneous fat
Stria Atrophic pink or white linear lesion owing to changes in connective tissue

Morphology of skin lesions

Inspection and palpation

Assessment of morphology requires visual and tactile examination. Do not be afraid to feel the lesions. You will rarely be exposed to any infection risk, with the exception of herpes simplex, herpes zoster, syphilis, hepatitis B and human immunodeficiency virus (HIV) disease. If these infections are suspected, it is wise to wear disposable plastic gloves when examining open or bleeding cutaneous lesions. Begin with palpation of the skin. Pass the hand gently over it, pinching it up between the forefinger and thumb, and note the following points:

  • Is it smooth or rough, thin or thick?

  • Is it dry or moist?

  • Is there any visible sweating, either general or local?

The elasticity of the skin should be investigated. If a fold of healthy skin is pinched up, it immediately flattens itself out again when released. Sometimes, however, it only does so very slowly, remaining creased for a considerable time. This is found frequently in healthy old people, but may be an important sign of dehydration, for example after severe vomiting and diarrhoea, or in uncontrolled diabetes mellitus.

Subcutaneous oedema

When oedema is present, firm pressure on the skin with a finger produces a shallow pit that persists for some time. In some cases, especially when the oedema is very long standing, pitting is not found. The best place to look for slight degrees of oedema in cardiac disease is behind the malleoli at the ankles in patients who are ambulant and over the sacrum in those who are confined to bed. The finger pressure should be maintained for 20–30 seconds or slight degrees of oedema will be overlooked. Pitting is minimal or absent in oedema owing to lymphatic obstruction, where the skin is usually thickened and tough.

Subcutaneous emphysema

Air trapped under the skin gives rise to a characteristic crackling sensation on palpation. It starts in, and is usually confined to, the neighbourhood of the air passages. On rare occasions, it may result from the clostridial infection of soft tissues after injury (gas gangrene).

Distribution of skin lesions

Consider the distribution of an eruption by looking at the whole skin surface:

  • Is it symmetrical or asymmetrical ? Symmetry often implies an internal causation, whereas asymmetry may imply external factors.

  • Is the eruption centrifugal (radiating from the centre) or centripetal (radiating to the centre)? Certain common diseases, such as chickenpox and pityriasis rosea, are characteristically centripetal, whereas erythema multiforme and erythema nodosum are centrifugal. Smallpox, now eradicated, was also centrifugal.

  • A disease may exhibit a flexor or an extensor bias in its distribution: atopic eczema in childhood is characteristically flexor, whereas psoriasis in adults tends to be extensor.

  • Are only exposed areas affected, implicating sunlight or some other external causative factor?

  • If sunlight is suspected, are areas normally in shadow involved?

  • Are the genitalia involved?

  • Localized distributions may point immediately to an external contact as the cause, for example contact dermatitis from nickel earrings, lipstick dermatitis, etc.

Swelling of the eyelids is an important sign. Without redness and scaling, bilateral periorbital oedema may indicate acute nephritis, nephrosis or trichinosis. If there is irritation, contact dermatitis is the probable diagnosis. Dermatomyositis often produces swelling and heliotrope-coloured erythema of the eyelids without scaling of the skin. In Hansen’s disease (leprosy), the skin lesions may be depigmented or reddened, with a slightly raised edge; they are also anaesthetic to pinprick testing ( Fig. 20.7 ) and mainly located in skin that is normally cooler than core body temperature.

Figure 20.7, Hansen’s disease.

Configuration of skin lesions

Once the morphology of individual lesions and their distribution has been established, it is useful to describe their configuration on the skin ( Box 20.6 ).

Box 20.6
Configuration of individual lesions

  • Nummular/discoid

  • Round or coin-like

  • Annular

  • Ring-like

  • Circinate

  • Circular

  • Arcuate

  • Curved

  • Gyrate/serpiginous

  • Wave-like

  • Linear

  • In a line

  • Grouped

  • Clustered

  • Reticulate

  • Net-like

The hair

Hair colour and texture are racial characteristics that are genetically determined. The yellow-brown Mongol race has black straight hair, negroid people have black curly hair and Caucasians have fair, brown, red or black hair. Secondary sexual hair begins to appear at puberty and has characteristic male and female patterns. Androgenic male pattern baldness is genetically determined, but requires adequate levels of circulating androgens for its expression. It occurs in women only in old age.

Growth of hair

Unlike other epithelial mitotic activity that is continuous throughout life, the growth of hair is cyclic ( Fig. 20.8 ), the hair follicle going through alternating phases of growth (anagen) and rest (telogen) . Anagen in the scalp lasts 3–5 years; telogen is much shorter, about 3 months. Catagen is the conversion stage from active to resting and it usually lasts a few days. The duration of the anagen phase determines the length to which hair in different body areas can grow. On the scalp, there are on average about 100 000 hairs. The normal scalp may shed as many as 100 hairs every day as a normal consequence of growth cycling. These proportions can be estimated by looking at plucked hairs (trichogram); the ‘root’ of a telogen hair is non-pigmented and visible as a white, club-like swelling. Normally 85% of scalp hairs are in anagen and 15% in telogen.

Figure 20.8, Hair follicle growth stages.

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