Dermatosis to physical stimuli

Miliariaresult of plugging or rupture of sweat ducts.It occurs in hot humid climates, at any age and is common

in over-clothed infants in hot nurseries. The physical signs depend on where the ducts are

blocked.1. Miliaria crystallina presents as tiny clear noninflamed

vesicles that look like dew. This is the most superficial type.

2. Miliaria rubra (prickly heat) Tiny erythematous and very itchy papules.

3. Miliaria profunda These consist of larger erythematous papules or pustules. This is the deepest type.

4. Miliaria Pustulosa

TreatmentThe best treatment is to move to a cooler climate

or into air conditioning. Clothing that prevents the evaporation of sweat

(e.g. nylon shirts) should be avoided; cotton is best.

Salicylic acid 2% in isopropyl alcohol applied daily to prone areas for prevention.

Topical steroids reduce irritation but should only be used briefly

Calamine lotion cools and soothes

Erythema ab igneIts reticulate pigmented erythema, with

variable scaling, is caused by damage from long-term exposure to local heat – usually from an open fire, hot water bottle or heating pad.

The condition has become less common with the advent of central heating.

Perniosis (chilblains)In this common, sometimes familial conditionInflamed purple–pink swellings appear on the

fingers, toes and, rarely, ears which are painful, and itchy or burning on rewarming. Occasionally they ulcerate

They arrive with winter and are induced by cold.

Caused by a combination of arteriolar and venular constriction, the latter predominating on rewarming with exudation of fluid into the tissues.

TreatmentWarm housing and clothing help. Oral calcium channel blocker nifedipine may

be useful The blood pressure should be monitored at the

start of treatment and at return visits. Nicotinamide (500 mg three times daily) alone

or in addition to calcium-channel blockersSympathectomy may be advised in severe

cases.

Raynaud’s phenomenonThis is a paroxysmal pallor of the digits provokedone or more fingers becomes white. On rewarming, a painful cyanosis appears and the

area turns red before the hands return to their normal colour.

In severe disease the fingers lose pulp substance, ulcerate or become gangrenous

Raynaud’s disease, often familial, is the name given when no cause can be found

some patients with what seems to be Raynaud’s disease will later develop a connective tissue disease, usually scleroderma.

Treatment The main treatment is to protect the vulnerable digits

from cold. Smoking should be abandoned. Calcium-channel blockers (e.g. nifedipine 10–30 mg

three times daily) are the most effective agents although they work best in patients with primary Raynaud’s disease.

Patients should be warned about dizziness caused by postural hypotension

Diltiazem (30–60 mg three times daily) is less effective than nifedipine but has fewer side-effects.

The systemic vasodilator inositol nicotinate may helpA combination of low-dose acetylsalicylic acid and the

antiplatelet drug dipyridamole is also worth trying.

SunburnCauseUVB penetrates the epidermis and superficial dermis,

stimulating the production and release of prostaglandins, leukotrienes, histamine, interleukin 1 (IL-1) and tumour necrosis factor a (TNF-a).

These cause pain and stimulate the production of the inducible nitric oxide synthase (iNOS) enzyme. This generates high concentrations of nitric oxide which cause the characteristic dermal vasodilatation and redness.

Presentation and courseSkin exposed to too much UVB becomes red (redness is

maximal after 1 day) several hours, painful and may blister.

settles over the next 2–3 days, leaving sheet-like desquamation, diffuse pigmentation (a ‘tan’) and, sometimes, discrete lentigines.

Differential diagnosisPhototoxic reactions TreatmentSymptomaticBaths may be cooling and oily shake lotions (e.g. oily

calamine lotion), oil in-water lotions or creams are comforting.

Potent topical corticosteroids help if used early and briefly.

Oral aspirin (a prostaglandin synthesis inhibitor) relieves the pain.

Sprays containing benzocaine also relieve pain, but occasionally sensitize.

PhototoxicityA drug that absorb UVR to cause a non

immunological reaction. Most blamed drugs window glass, protective

against sunburn, does not protect against most phototoxic drug reactions.

Presentation and courseTenderness and redness occur only in areas

exposed both to sufficient drug and to sufficient UVR

The signs and symptoms are those of sunburn. The skin may later develop a deep tan.

Differential diagnosisPhotoallergic reactions Investigationsphotopatch testing TreatmentThis is the same as for sunburn. Drugs should be stopped if further exposure

to ultraviolet light is likely.

PhotoallergyDrugs, topical or systemic, and chemicals on

the skin can interact with UVR and cause immunological reactions.

CauseUVR converts an immunologically inactive form

of a drug into an antigenic molecule inducing an immunological reaction, analogous to allergic contact dermatitis, is induced if the antigen remains in the skin or is formed there on subsequent exposure to the drug and UVR. Many of the same drugs that cause phototoxic reactions can also cause photoallergic ones.

Presentationsimilar to phototoxicity, but the reaction usually

becomes eczematous, appears later and lasts longer. The eruption will be on exposed areas such as the

hands, the V of the neck, the nose, the chin and the forehead. There is also a tendency to spare the upper lip under the nose, the eyelids and the submental region

Often, the eruption does not occur on the first exposure to ultraviolet, but only after a second or further exposures. A lag phase of one or more weeks is needed to induce an immune response.

CourseThey tend to resolve when either the drug or the exposure to UVR

is stopped, but this may take several weeks. ComplicationsSome drugs, such as the sulphonamides, can cause chronic actinic

dermatitis.InvestigationsPhotopatch testing can confirm the diagnosis. The chemical is

applied for 24 h and the skin is then irradiated with UVA. An acute photoallergic contact dermatitis is then elicited.

A control patch, not irradiated, rules out ordinary allergic contact dermatitis. 

TreatmentThe drug should be stopped and the patient protected from further

ultraviolet exposurePotent topical corticosteroids or a short course of a systemic

corticosteroid will hasten resolution and provide symptomatic relief.

Polymorphic light eruptionThis is the most frequent cause of a so-called ‘sun allergy’.Cause It is speculated that UVR causes a natural body chemical to

change into an allergen. Mechanisms are similar to those in drug photoallergy. Some people seem genetically predisposed, because other family

members may also be affected. PresentationSmall itchy red papules, papulovesicles or eczematous plaques

arise from 2 h to 5 days, most commonly at 24 h, after exposure to UVR.

The eruption is itchy and usually confined to sun-exposed areas, remembering that some UVR passes through thin clothing.

Not all exposed skin develops disease so there are papules and plaques rather than generalized redness.

Treatmentsunscreens Protective clothing, such as wide-brimmed hats, long-

sleeved shirts and long trousersIn some patients, a 4-week course of psoralen with UVA

(PUVA) in the late spring can create enough tan to confer protection for the rest of the season.

Moderately potent topical steroids usually improve the eruption.

A tapering course of systemic steroids for severe or early spring outbreaks.

Hydroxychloroquine may be effective when used over the sunny season.

Callosities and cornsBoth are responses to pressure. A callosity is a more diffuse type of thickening of the

keratin layer, which seems to be a protective response to widely applied repeated friction or pressure.

often occupational (e.g. they are seen on the hands of manual workers).

Usually painless, they need no therapy.

Corns have a central core of hard keratin, which can hurt

if forced inwards. appear where there is high local pressure, often

between bony prominences and shoesFavourite areas include the under surface of the toe

joints, and the soles under prominent metatarsals.‘Soft corns’ arise in the third or fourth toe clefts when

the toes are squeezed together by tight shoes; such corns are often macerated and may present as eroded nodules, causing diagnostic confusion.

The main differential is from hyperkeratotic warts, but these will show tiny bleeding points when pared down, whereas a corn has only its hard compacted avascular core surrounded by a more diffuse thickening of opalescent keratin.

TreatmentThe right treatment for corns is to eliminate the

pressure that caused them, but patients may be slow to accept this. While regular paring reduces the symptoms temporarily

well-fitting shoes are essentialCorns under the metatarsals can be helped by soft

spongy soles, but sometimes need orthopaedic surgery to alter weight bearing.

Special care is needed with corns on ischaemic or diabetic feet, which are at greater risk of infection and ulceration.

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