Skin disease

17 Skin disease


Skin disease is common. Surveys in Europe suggest that approximately 1 in 7–10 of all visits to a primary care physician is for a skin problem. Consultations for skin disease are becoming more common as the absolute incidence of many diseases (e.g. skin cancer, atopic dermatitis) has increased. In addition, the therapeutic options for diseases previously viewed as untreatable have increased and awareness of these therapies is spreading as patients take a greater interest in their health.


A glossary of dermatological words is shown in Box 17.1.



17.1 TERMS USED TO DESCRIBE SKIN LESIONS image











































































Primary lesions
Macule A small flat area of altered colour, e.g. freckle
Papule A discrete raised lesion, which may be coloured; called a nodule if >1 cm
Plaque A raised area of skin with a flat top, typically several cm across; often scaly
Vesicle, bulla A small (∼several mm)/larger (∼several cm) blister, respectively
Pustule A focal visible accumulation of pus in the skin; usually yellow or green
Abscess A localised collection of pus in a cavity, >1 cm in diameter
Weal An evanescent dermal collection of fluid; the fluid is diffuse, unlike in a blister
Papilloma A projecting nipple-like mass, e.g. skin tag
Petechiae, purpura, ecchymosis Petechiae are flat, pinhead-sized macules of extravascular blood in the dermis; larger ones (purpura) may be palpable; deeper bleeding causes an ecchymosis
Burrow A linear or curvilinear papule, caused by a burrowing scabies mite
Comedone A plug of keratin and sebum in a dilated pilosebaceous orifice
Telangiectasia Visible dilatation of small cutaneous blood vessels
Secondary lesions (which evolve from primary lesions)
Scale A flake arising from the stratum corneum, e.g. psoriasis
Crust Exudate of blood or serous fluid, e.g. eczema or tissue fluid
Ulcer An area from which the epidermis and the upper part of the dermis have been lost
Excoriation Damage resulting from scratching; usually a linear ulcer or erosion
Erosion An area of skin denuded by complete or partial loss of the epidermis
Fissure A deep, slit-shaped ulcer, e.g. irritant dermatitis of the hands
Sinus A cavity or channel that permits the escape of pus or fluid
Scar Permanent fibrous tissue resulting from healing
Atrophy Loss of substance due to diminution of the epidermis, dermis or subcutaneous fat
Stria A streak-like, atrophic, pink/purple/white lesion in the connective tissue


PRESENTING PROBLEMS



THE CHANGING MOLE


The challenge when assessing any pigmented lesion is distinguishing between common benign lesions such as seborrhoeic keratoses and melanocytic naevi, and the more serious diagnosis of melanoma. The history and examination may help to make this distinction, but where doubt exists, a biopsy should be taken. If the lesion does not appear malignant, it may be helpful to photograph it with a millimetre scale and review the patient for change in 6 mths.




History



• Change in size, shape or colour of lesion: over what time period?

• Symptoms arising from the lesion: bleeding, tenderness, excessive itch.

• Occupation: jobs involving outdoor work suggest a high lifetime actinic exposure.

• Family history of melanoma.

• Has the patient ever lived abroad in a sunny climate?

• Skin type: pale/tending to burn easily or darker-skinned/tanning readily?


CLINICAL EXAMINATION IN SKIN DISEASE



image




Examination



• Use both the naked eye and a magnifying glass or a dermatoscope.

• Examine other pigmented lesions on the patient’s body; a good degree of homogeneity between individual lesions in size and colour is reassuring.

• Use the ABCDE rule (p. 729) to help determine the likelihood of melanoma.


ITCH (PRURITUS)


Pruritus is defined as an unpleasant sensation that provokes the desire to scratch, characteristic of many skin diseases and some medical conditions. The biological mechanisms governing itch are poorly understood.




History


Assessment of the itchy patient is one of the most difficult clinical problems in dermatology. Helpful hints from the history include:


Time course: Acute (as in urticaria, infestations) or chronic (eczema)?


Localisation: E.g. extensor surfaces of wrists are classically affected in lichen planus, limb flexures in childhood eczema.


Exacerbating factors: Most causes of itch are increased by heating and reduced by cooling. In cholinergic urticaria, exercise or heat dramatically induces itching.


Involvement of other family members: E.g. a scabietic infestation affecting more than one family member.


General health of the patient: A review of systems may uncover a medical cause of pruritus such as a malignancy, liver disease or anaemia.



Examination


The most important distinction is whether the itch is due to a primary skin condition or secondary to an underlying medical cause.


Generalised pruritus associated with skin disease: Eczema, urticaria, xeroderma (dry skin, often occurring in the elderly), scabies.


Local pruritus associated with skin disease: Lichen planus, psoriasis, dermatitis herpetiformis.


Pruritus with no evidence of skin disease: In the absence of clues pointing to a primary skin disease, detailed physical examination and investigations, including a careful search for lymphadenopathy, may be required. Investigations should include:


• FBC.

• Iron status.

• U&Es.

• LFTs.

• TFTs.

• Possibly a CXR.

Examples of systemic diseases causing itch include:


• Renal failure,

• Liver failure,

• Anaemia,

• Hyper- or hypothyroidism,

• Malignancy.


Management


Management of the underlying primary skin condition or medical condition may alleviate the itch. For those who experience ongoing symptoms in spite of specific management, application of cooling emollients such as 1% menthol in aqueous cream may help. Alternatively, phototherapy with UVB may afford some relief. Although frequently the subject of ridicule, significant itch may incapacitate, cause embarrassment, disrupt sleep and ruin the patient’s self-image. It is easily underestimated and trivialised as a symptom.



THE SCALY RASH (PAPULOSQUAMOUS ERUPTIONS)


A common presenting complaint in general practice is an eruptive scaly rash sometimes associated with itching. Causes are summarised in Box 17.2.



17.2 CLINICAL FEATURES OF COMMON SCALY RASHES image




image



History


How long has the rash been present? Atopic eczema often starts in infancy or early childhood, pityriasis rosea and psoriasis between the ages of 15 and 40. Drug eruptions are acute in onset and a temporal relationship between starting the medicine and the onset of the rash should be sought.


Where on the body did it start? Localisation or distribution of the rash (see Box 17.2) may give clues to aetiology. The ‘herald patch’ of pityriasis rosea is a solitary erythematous lesion on the trunk, which enlarges rapidly.


Is it itchy? Atopic eczema is extremely itchy, psoriasis and pityriasis rosea less so. Drug eruptions and tinea corporis are usually pruritic.


Was there a preceding illness or systemic symptoms? Guttate psoriasis is often preceded by a β-haemolytic streptococcal sore throat. A small percentage of people with pityriasis rosea have a prodromal illness with malaise, headache and arthralgia.



Examination


The distribution of the rash can be very useful in discriminating between the various causes of a scaly rash. Morphological features noted on assessment with a magnifying lens may help to narrow down the diagnosis (see Box 17.2).



ERYTHRODERMA


Eczema, psoriasis, drug eruptions and lichen planus rarely progress to erythroderma, defined as erythema with or without scaling involving >90% of the body surface. It is associated with systemic symptoms due to excessive heat loss through extensively involved skin, and haemodynamic upset characterised by hypotension and tachycardia as a response to a large increase in insensible losses. Causes include:


• Severe eczema.

• Severe psoriasis.

• Cutaneous T-cell lymphoma (Sézary’s syndrome).

• Pityriasis rubra pilaris (a variant of psoriasis).


URTICARIA (NETTLE RASH, HIVES)


Urticaria refers to an area of focal dermal oedema secondary to a transient increase in capillary permeability, largely mediated by mast cell degranulation. The principal mediator released is histamine, which explains the efficacy of H1-blocking drugs in the management of this condition. On certain body sites such as the lips or hands the oedema spreads and is traditionally referred to as angioedema. By definition the swelling lasts <24 hrs. Urticarial vasculitis has a similar clinical presentation but lesions last >24 hrs.


Most cases are idiopathic but physical, drug-induced, infection-related and autoimmune forms exist (Box 17.3).



17.3 CAUSES OF URTICARIA image



Acute and chronic urticaria



• Autoimmune due to production of antibodies that cross-link the IgE receptor on mast cells

• Allergens (in foods, inhalants and injections)

• Drugs (see Box 17.9)

• Physical (e.g. heat, cold, pressure, sun, water)

• Contact (e.g. animal saliva, latex)

• Infection (e.g. viral hepatitis, infectious mononucleosis, HIV during seroconversion)

• Other conditions (e.g. SLE, pregnancy, intestinal parasites)

• Idiopathic


Urticarial vasculitis



• Hepatitis B

• SLE

• Idiopathic



Clinical assessment


Two important questions are:


• How long does the individual lesion last? (<24 hrs urticaria, >24 hrs urticarial vasculitis).

• How long has the condition been present? (<6 wks acute, >6 wks chronic urticaria).

A directed history is still the best way to elicit any causes or precipitants of urticaria. A record of possible allergens, including drugs (see Box 17.9), should be determined. A family history must be sought in cases of angioedema, in order to determine the likelihood of a C1 esterase inhibitor deficiency. Dermographism may be elicited on examination.



17.9 DRUG ERUPTIONS AND SOME DRUGS WHICH MAY CAUSE THEM image

































































Reaction pattern Clinical features Examples of drugs commonly responsible
Toxic erythema Erythematous plaques, morbilliform rash Antibiotics, sde, thiazides, pbz, PAS
Urticaria Itchy weals, sometimes with angioedema Salicylates, codeine, antibiotics, dextran, ACEI
Erythema and scaling Scaly, pink/red papules, varying sizes Antibiotics, anticonvulsants, ACEI, gold, penicillamine
Allergic vasculitis Painful palpable purpura with ulcers Sde, pbz, indometacin, phenytoin, o.c.
Erythema multiforme Target-like lesions and bullae on limbs Sde, pbz, barbiturates
Purpura Exclude thrombocytopenia, coagulation defect Thiazides, sde, pbz, sulphonylureas, barbiturates, quinine
Bullous eruptions Sometimes with erythema and purpura Barbiturates, penicillamine, nalidixic acid
Exfoliative dermatitis Universal redness and scaling, shivering Pbz, PAS, isoniazid, gold
Fixed drug eruptions Erythematous, occasionally bullous plaques Tetracyclines, quinine, sde, barbiturates
Acneiform eruptions Rash resembles acne Lithium, o.c., steroids, anti-TB drugs, anticonvulsants
Toxic epidermal necrolysis Rash resembles scalded skin Barbiturates, phenytoin, pbz, penicillin
Hair loss Diffuse Cytotoxics, acitretin, anticoagulants, antithyroid drugs, o.c.
Hypertrichosis   Diazoxide, minoxidil, ciclosporin
Photosensitivity Rash limited to exposed skin Thiazides, tetracyclines, phenothiazines, sde, psoralens

ACEI = ACE inhibitors; sde = sulphonamides; o.c. = oral contraceptives; pbz = phenylbutazone; PAS = para-aminosalicylic acid.



Investigations


These need to be directed at the possible underlying cause, as elicited from the clinical history. Some or all of the following may be appropriate:


• FBC, including eosinophil count in suspected parasitic infection.

• ESR: elevated in vasculitis.

• U&Es, LFTs and TFTs: to detect underlying disorders.

• Total and specific IgE to possible allergens, e.g. shellfish and peanuts.

• Antinuclear factor in chronic urticaria or urticarial vasculitis.

• CH50 as a general guide to complement activation and C3 and C4 levels as evidence of complement consumption via both the classical and the alternative pathways.

• Incisional biopsy: may be required for diagnosis of urticarial vasculitis.


Management



• Non-sedating antihistamines (e.g. loratadine) are the mainstay of management.

• The patient should be advised to avoid medicines known to provoke urticaria, such as NSAIDs and codeine-containing preparations.

• The addition of an H2-blocking drug such as cimetidine may be helpful in cases refractory to H1-blockers alone.

• Those with features of angioedema should carry a kit for self-administration of adrenaline (epinephrine) (p. 23).


BLISTERS


Loss of adhesion between adjacent keratinocytes, between keratinocytes and the basement membrane, or between the basement membrane and the dermis leads to a potential space which, because of negative extracellular pressure, fills with fluid: a blister. There is an artificial distinction made by some between small (vesicles, <0.5 cm) and large blisters (bullae, >0.5 cm). The site of blister formation within the skin therefore depends on the aetiology and underlying pathogenesis. The classification of blistering disorders may be considered as:


• Congenital or genetic.

• Acquired (often infective in origin).

• Autoimmune.



Clinical assessment


Genetic causes of blistering: These often present at birth or shortly after. They include epidermolysis bullosa, bullous ichthyosis and incontinentia pigmenti. Infection is a more common cause of blistering at birth, including herpes simplex acquired through vertical transmission, and impetigo.


Acquired forms of blistering: These are common in childhood and adulthood (Box 17.4), and may be infectious in origin (e.g. staphylococcal scalded skin syndrome), drug-related, metabolic (e.g. porphyria), or part of another primary skin complex such as acute eczema or pompholyx. Toxic epidermal necrolysis may be life-threatening, can occur at any age and is often due to drugs. Loss of skin compromises fluid balance and thermoregulation and leads to severe pain and risk of infection. Intensive care is often required.



17.4 CAUSES OF ACQUIRED BLISTERS image




image

Autoimmune blistering diseases (Box 17.5): These are more common in later life, with the exception of dermatitis herpetiformis and pemphigus gestationis which occur in younger patients. Diagnosis is based on clinical features and immunopathology of biopsies. Rarely, some of these conditions may be related to an underlying malignancy (e.g. paraneoplastic pemphigus, epidermolysis bullosa acquisita associated with lymphoma, multiple myeloma or inflammatory bowel disease). Patients with a suspected diagnosis of dermatitis herpetiformis should be investigated for coeliac disease.



17.5 CLINICAL FEATURES OF SOME IMMUNE-MEDIATED BLISTERING SKIN CONDITIONS image




image

image

Fig. 17.1 Bullous pemphigoid. Large tense and unilocular blisters clustered in and around the axilla.



LEG ULCERS


Ulceration of the skin is the complete loss of the epidermis and part of the dermis. There are numerous aetiologies, summarised in Box 17.6, but when present on the lower limb, ulceration is usually due to arterial or venous insufficiency. The site of the ulceration gives clues as to its aetiology (Fig. 17.2).



17.6 MAIN CAUSES OF LEG ULCERATION image

























Venous hypertension
Arterial disease Atherosclerosis, vasculitis, Buerger’s disease
Small-vessel disease Diabetes mellitus, vasculitis
Abnormalities of blood Sickle-cell disease, cryoglobulinaemia, spherocytosis, immune complex disease
Neuropathy Diabetes mellitus, leprosy, syphilis
Tumour Squamous cell carcinoma, basal cell carcinoma, malignant melanoma, Kaposi’s sarcoma
Trauma Injury, artefact

image

Fig. 17.2 Causes of lower leg ulceration.




Clinical assessment



• The ulcer should be swabbed to exclude infection.

• Arterial sufficiency should be assessed with Doppler USS.

• Venous sufficiency may be assessed with venography to highlight any surgically remediable venous disease.

• Urinalysis to detect glycosuria ± a fasting glucose level should be taken to rule out diabetes.


LEG ULCERATION DUE TO VENOUS DISEASE



Clinical assessment


This is a common clinical problem in middle to old age. Clinical signs include:


• Varicose veins.

• Haemosiderin deposition.

• Oedema.

• Lipodermatosclerosis: firm induration of the skin of the leg, with a shiny appearance, producing the ‘inverted champagne bottle’ sign.

• Ulceration, typically on the medial malleolus.

• Malignant transformation of a chronic ulcer into squamous cell carcinoma is termed ‘Marjolin’s ulcer’.


Management



• General management: dietary advice for the obese and encouragement to take gentle exercise.

• Oedema: should be reduced with the use compression bandages (once arterial sufficiency is confirmed; ratio of ankle : brachial systolic pressure >0.8), elevation of the legs when sitting, and the judicious use of diuretics.

• Antiseptic soaks, e.g. potassium permanganate.

• Non-adhesive absorbent dressings (alginates, charcoals, hydrogels or hydrocolloids) for highly exudative ulcers.

• Silver-containing dressings for infected wounds ± antibiotics, as guided by swabs.

• Management of surrounding venous eczema with topical steroid.

• Vein surgery: may help some younger patients with persistent venous ulcers.


LEG ULCERATION DUE TO ARTERIAL DISEASE


Deep, painful and punched-out ulcers on the lower leg, especially if they occur on the shin and foot and are preceded by a history of intermittent claudication, are likely to be due to arterial disease. Risk factors include smoking, hypertension, diabetes mellitus and hyperlipidaemia. The foot is cyanotic and cold, and the skin surrounding the ulcer is atrophic and hairless. The peripheral arterial pulses are absent or reduced. Doppler studies are required, and if arterial insufficiency is confirmed, compression bandaging should be prohibited and advice sought from a vascular surgeon.



LEG ULCERATION DUE TO VASCULITIS


These ulcers start as painful, palpable, purpuric lesions and turn into small, punched-out ulcers. The involvement of larger vessels is heralded by painful nodules which evolve into intractable, deep, sharply demarcated ulcers. Management includes treatment of the underlying disorder as well as immunosuppression with, for example, systemic corticosteroids or cyclophosphamide.



LEG ULCERATION DUE TO NEUROPATHY


The most common cause of a neuropathic ulcer is diabetes. The ulcers occur over weight-bearing areas such as the heel. Microangiopathy also contributes to ulceration in diabetes. This is discussed in detail on page 414.



TOO LITTLE OR TOO MUCH HAIR



ALOPECIA


The term means nothing more than loss of hair and is a sign rather than a diagnosis. There are many causes and patterns, but an important distinction is whether the alopecia is scarring or non-scarring. The causes of alopecia are summarised in Box 17.7; the most common are discussed here.



17.7 CLASSIFICATION OF ALOPECIA image


















Localised Diffuse
Non-scarring
Tinea capitis, alopecia areata, androgenetic alopecia, traumatic (trichotillomania, traction, cosmetic), syphilis Androgenetic alopecia, telogen effluvium, metabolic, hypo- or hyperthyroidism, hypopituitarism, diabetes mellitus, HIV disease, nutritional deficiency, liver disease, post-partum, alopecia areata, syphilis
Scarring
Developmental defects, discoid lupus erythematosus, herpes zoster, pseudopelade, tinea capitis/kerion, idiopathic Discoid lupus erythematosus, radiotherapy, folliculitis decalvans, lichen planus pilaris

Tinea capitis: Fungal scalp infection is increasingly common in the UK. Any patient developing an area of hair loss and scaling in the scalp should have the area scraped and affected hairs plucked for mycological examination.


• Endothrix (within the hair shaft) infections, e.g. Trichophyton tonsurans, cause relatively uninflamed patchy baldness with breakage of the hairs at the skin surface (‘black dot’). There is no fluorescence under Wood’s light.

• Ectothrix (outside the hair shaft) species of fungi, such as Microsporum audouinii, show minimal inflammation, although M. canis infections (from dogs and cats) are more inflamed and can be identified by green fluorescence with Wood’s light.

Kerions are boggy, highly inflamed areas of tinea capitis and are usually caused by zoophilic fungi (from animals, e.g. cattle ringworm, T. verrucosum). Treatment is systemic, with oral terbinafine, griseofulvin or itraconazole. Topical therapy with an antifungal shampoo is recommended as an adjunct and arachis oil is used to remove crusting.


Alopecia areata: This non-scarring condition appears as sharply defined, non-inflamed bald patches, usually on the scalp. During the active stage of hair loss pathognomonic ‘exclamation mark’ hairs are seen (broken-off hairs 3–4 mm long, which taper off towards the scalp). The condition may affect the eyebrows, eyelashes and beard. The hair usually regrows spontaneously in small bald patches, but the outlook is less good with larger patches and when the alopecia appears early in life or is associated with atopy. Alopecia totalis describes complete loss of scalp hair and alopecia universalis complete loss of all hair. There is an association of alopecia areata with autoimmune disorders, atopy and Down’s syndrome.


Androgenetic alopecia: Male-pattern baldness is physiological in men >20 yrs old, although rarely it may be extensive and develop at an alarming pace in the late teens. It also occurs in females, most obviously after the menopause. The distribution is of bitemporal recession and then crown involvement.



Investigations



• Laboratory tests, including an FBC, ESR, U&Es, LFTs and TFTs, an autoantibody profile and, in cases where lupus or lichen planus is suspected, a biopsy should allow a diagnosis to be reached in most cases.

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  2. Diabetes mellitus
  3. Infectious diseases
  4. Cardiovascular disease

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Apr 3, 2017 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Skin disease

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