Dermatology

Published on 03/03/2015 by admin

Filed under Internal Medicine

Last modified 03/03/2015

Print this page

This article have been viewed 1253 times

17 Dermatology

A swollen red leg

Case history

The A&E officer asks you to come and see a 50-year-old man who is unwell and has a red, swollen leg. He thinks he needs anticoagulation for a possible DVT.

On arrival you check if this was of sudden onset or a chronically swollen leg. You ask if there is a past history of DVT or whether there are any risk factors, such as a long car journey, air travel, immobility or a family history of clotting disorders. You also ask about any recent illness, e.g. heart failure, blood disorder.

What should you do next?

You do a full medical examination.

On examination the patient weighs 102 kg and has a temperature of 38°C. The leg is indeed red, swollen, hot and tender below the knee. You note a small ulcer on the medial side of the leg above the ankle. Dorsalis pedis pulse is palpable.

What is your diagnosis?

Cellulitis, probably due to streptococci gaining entry via the venous ulcer.

How do you treat?

Penicillin V plus flucloxacillin 500 mg × 4 daily, having ascertained that he is not allergic to penicillin. Oral therapy should be for 10–14 days. When the cellulitis is very severe, parenteral benzylpenicillin 1.2 g × 4 daily and flucloxacillin 1 g × 4 daily, i.e. 3 days’ intravenous therapy should be given initially, followed by 10 days’ oral therapy.

Progress.

The patient’s leg improved with antibiotics and he was discharged after 3 days. He was given compression stockings for his venous hypertension. He was referred to a dietitian for advice on weight reduction.

Further reading

Kilburn SA, Featherstone P, Higgins B, Brindle R. Interventions for cellulitis and erysipelas. Cochrane Database Syst Rev. 6, 2010. CD004299

Leg ulceration

Take a full history of associated diseases (diabetes mellitus, rheumatoid arthritis, past history of deep vein thrombosis, varicose veins, heart disease, hypertension, vasculitis, sickle cell, scleroderma).

Causes and signs

Investigations

• General: FBC, U&Es, LFTs, autoantibodies (vasculitis), blood sugar, vitamin B₁₂, T Pallidum enzyme immunoassay (neuropathic ulcer)

• Venous: Doppler ultrasound – always perform before compression bandaging

• Arterial: Doppler ultrasound, digital substraction angiography

Management

• Venous ulcers: elevation, exercise, compression dressings. Antibiotics if infected (always check Doppler pressures before considering compression as many ulcers have mixed venous and arterial aetiology). Adequate analgesia.

• Arterial ulcers: investigate arterial supply, dressings with NO compression. Adequate analgesia.

• Vasculitic ulcers: vasculitic screen, e.g. ANCA, ANA, rheumatoid factor.

• Neuropathic ulcers: keep ulcer clean and remove pressure or trauma from affected area.

Note: Operating on varicose veins rarely helps venous insufficiency problems – ‘re-plumbing’ of the veins is not possible.

Contact your hospital’s tissue viability nurse for assistance with dressings and compression bandaging and for arranging longer-term community nursing follow-up.

Information

Compression bandages

• Four-layer bandaging provides high levels of graduated compression with pressure decreasing up the leg

• 80% of ulcers can be healed within 6 months

Erythema nodosum

Erythema nodosum (EN) is a hypersensitivity reaction to various antigens (e.g. drugs, infectious agents and unknown antigens), producing an inflammation in the dermis and subcutaneous layer (panniculitis).

It presents with painful, tender, dusky blue red nodules, usually on the shins and lower limbs (Fig 17.1).

Figure 17.1 Erythema nodosum.

Case history

An unmarried 16-year-old Asian girl presents to an inner city A&E with her mother. She has painful red lumps on her shins and arthralgia. Walking has become painful. She is otherwise well, with no relevant previous medical history.

On examination she has tender, red/purple lumps on her shins. No other signs. A clinical picture was of erythema nodosum.

Initial treatment

• Aspirin 600 mg as required (unless the identified cause of the EN).

• Bed rest if severe.

• Tubigrip support bandages.

• If severe symptoms and/or cutaneous ulceration, use dapsone (up to 100 mg daily)/steroids (30 mg daily decreasing course).

Note: monitor for haemolytic anaemia and avoid dapsone if G6PD deficient.

Urticaria and angio-oedema

Urticaria or hives is characterised by short-lived dermal swelling (weals) anywhere on the body (Fig. 17.2). These usually itch and, except in some subtypes, resolve without bruising within 24 h (often within 10–20 min). They can form bizarre serpiginous or annular-shaped lesions. The latter show central clearing, not central necrosis as seen in erythema multiforme.

Figure 17.2 Urticaria.

Angio-oedema is a deeper form of swelling affecting the dermis and subcutis, usually affecting the mucous membranes, e.g. eyes, lips, tongue, genitals, and much less commonly the larynx and gastrointestinal tract. It is generally not itchy but can be painful and disappears within 72 h. It may occur in isolation or with urticaria (45% cases).

The incidence of urticaria/angio-oedema is about 15% in a person’s lifetime and both conditions are more common in atopics.

Case history

A 22-year-old woman presents in A&E with a 6-hour history of a florid raised red rash all over the body. It is very itchy and distressing and has caused swelling around her eyes and her right hand. Previous medical history was of atopic eczema as a child and mild hay fever.

On examination she had red, raised weals all over her body and periorbital swelling.

Diagnosis.

Urticaria with angio-oedema.

Classification of urticarias

Acute

By definition this lasts < 6 weeks. Few cases have an identifiable allergen. They are IgE mediated. In the most severe form there is an anaphylactic reaction but this is fortunately very rare:

• Acute idiopathic urticaria and angio-oedema: accounts for > 90% of urticaria. A good history (not type 1 allergy testing) should exclude an allergic cause. Viral infections will sometimes set off an acute urticaria.

• Acute allergic: drug reactions, insect bites, foods (e.g. peanuts or seafood), can cause this type of reaction, as well as contact urticaria caused by, e.g. latex, tomatoes. A history of an almost immediate reaction (seconds to minutes) after contact with an allergen should alert one to this form.

Chronic

By definition if urticaria persists > 6 weeks. Only 2–4% cases have an identifiable cause and extensive investigation is not indicated. Some cases are autoimmune and functionally significant IgG (which acts against the high-affinity IgE receptors on mast cells) can be demonstrated in patient’s serum. In a few patients an acute illness (hepatitis, brucellosis), focal sepsis (e.g. dental abscess), dermatophyte or parasitic infections can precipitate a reaction but this is very rare.

Physical

Reproducible wealing occurs in response to a specific physical stimulus, e.g. friction, pressure, cold, heat, water, sun. The diagnosis might be suspected from the patient’s history or site of urticaria i.e. pressure sites in cases of dermographism or delayed pressure urticaria.

Preferred regimes if no contraindications

• Loratidine 10–20 mg daily or cetirizine 10–20 mg daily or fexofenadine 180 mg daily (all non-sedating anti-histamines).

• Sedative anti-histamines, e.g. hydroxyzine 25–50 mg at night.

Refer: to dermatology department if no response to anti-histamines.

Refer: to type 1 allergy clinic (usually different to dermatology) only if allergic urticaria is suspected from history.

Management of severe angio-oedema

• Adrenaline (epinephrine): 1 : 1000 (1 mg/mL) IM. Adult dose 0.5–1.0 mL.

• IV chlorphenamine: 10–20 mg (max. 40 mg/24 h).

• IV hydrocortisone succinate: 100–300 mg.

Home (injectable adrenaline) pens

These should never be prescribed lightly and only after full investigation in an allergy clinic when relevant allergens have been proven and where a genuine anaphylactic reaction has occurred. They are most commonly used in those severely allergic to nuts. Injectable adrenaline pens are not appropriate for isolated severe cutaneous urticaria or angio-oedema.

Patients/parents need to attend an allergy clinic to be instructed in both when and how to use the pens and, indeed, how frequently if the first injection only gives temporary relief (two pens should be prescribed).

Adrenaline (epinephrine) 1 : 1000 (1 mg/mL) is available in pre-loaded injections to deliver a dose of 0.3 or 0.5 mg (adult) or 0.15 mg (paediatric) and injections should be carried out by the patient.

Progress.

This patient was given prednisolone 30 mg daily for 7 days and started on loratidine 20 mg daily. The nature of the complaint was explained to her; no specific antigen was identified. She was seen by her doctor after 4 days and was completely free of symptoms. She continued with loratidine for 1 month.

Hereditary angio-oedema (HAE)

Skin lesions may develop and laryngeal obstruction can occur. Lesions appear as deep swellings with associated enlarging oedematous borders that last up to 2–4 days. Urticaria does not occur as part of HAE. Patients generally suffer from recurrent attacks of painful angio-oedema, which can be precipitated by minor trauma, emotional upset, infections and temperature change. Involvement of the gastrointestinal tract can cause severe acute pain and simulate a surgical emergency. Recurrent abdominal pain occurs often and starts in childhood. HAE is inherited in an autosomal dominant fashion with either a functional or absolute deficiency of C1 esterase inhibitor (C1-INH). 80% of cases give a positive family history (e.g. of sudden death). Acquired forms are seen in SLE or lymphoma.

Remember

Hereditary angio-oedema (HAE)

Patients can develop laryngeal obstruction requiring urgent treatment.

Investigations

Two blood samples need to be sent for both absolute levels and functional assay of C1-INH (discuss with laboratory first). Only do this test in patients with recurrent angio-oedema who do not have urticaria. Refer all such patients to local immunologist/dermatologist depending on local expertise.

Management

Patients are unresponsive to anti-histamines, which can exacerbate the condition, systemic steroids and adrenaline (epinephrine). Refer all patients for management: acute treatment of choice in A&E is intravenous (C1-INH) concentrates. If unavailable, fresh frozen plasma can be used. Most already diagnosed cases/families will know where local supplies of C1-INH are to be found. Icatibant (a bradykinin antagonist) and ecallantide (a kallikrein inhibitor) are also of benefit in acute attacks.

In adults, chronic treatment or ‘prophylaxis’ with attenuated androgens, e.g. stanozolol or danazol, is required if episodes are frequent.

Further reading

Morgan BP. Hereditary angioedema – therapies old and new. N Engl J Med. 2010;363:581–583. (and 513–22, 523–31, 532–41)

Related

Kumar & Clarks Cases in Clinical Medicine