Dr Stephen Hayes reviews key recommendations from the British Association of Dermatologists/Primary Care Dermatology Society guideline on atopic eczema
  • Eczema has a significant impact on quality of life
  • Eczema is always itchy
  • It is important to differentiate between eczema and scabies
  • The three management principles of eczema are:
  • avoidance of anything that makes eczema worse
  • use of bland emollients
  • control of inflammation
  • Patient education is central to management of eczema
  • Patients and their family should be educated and reassured on the use of steroids
  • Immunomodulatory agents are a possible treatment option, particularly in cases of eczema where steroid use is problematic.

This paper is a personal review and discussion of the atopic eczema guideline, which the British Association of Dermatologists (BAD) and Primary Care Dermatology Society (PCDS) have collaborated in and produced.1 As a GP with special interest (GPwSI) in Dermatology for over a decade, I believe that this guideline cuts though the waffle and highlights the key clinical issues. I commend it as a practical consensus-based guide for GPs primarily, but also paediatricians, elderly care doctors, occupational physicians, and others; all of these healthcare professionals will certainly see patients with eczema in their regular caseload as the disease is so common and has so many faces. I will not comment on every paragraph of this effective summary, which should be studied in full.

Is the BAD/PCDS guideline evidence based? Yes and no. Evidence-based medicine (i.e. based on the results of large randomised trials like the classic Scandinavian Simvastatin Survival Study [4S]2) is the ideal but is sometimes impossible to achieve. Eczema treatment outcomes are more difficult to research than, for example, post-myocardial infarction (MI) mortality, as assessed in the 4S study. That study had one easily measurable variable (cholesterol lowered by simvastatin), a single and easily measurable endpoint (cardiac death), and a large amount of funding. Eczema attracts less funding, has ambiguous endpoints, and too many variables to enable that kind of trial. The BAD/PCDS guideline is, therefore, more about expert consensus opinion than randomised controlled trials.

Importance of atopic eczema

Eczema (or dermatitis, which is the same disease, or rather, part of the same disease spectrum) is one of the most prevalent skin diseases in the UK; it is responsible for a significant number of consultations, and reduced patient quality of life. I tell students and those less experienced in this clinical area that if a patient phones to say, ‘I have an itchy rash,’ then if the doctor, without any further information or seeing the patient, replies, ‘It’s probably eczema,’ they will be right more often than not.

Atopic eczema is the dominant and classical form; the principles of its management are transferable to other forms of eczema, such as discoid, asteatotic, contact irritant, contact allergic, and non-specific/spongiotic. These other forms of eczema are not discussed in depth here.

Impact of eczema

Although very rarely fatal, atopic eczema can significantly impact on quality of life. In the case of childhood eczema, the quality of the parents’ life is also affected. In the UK, eczema affects up to 15% of children under the age of 7 years.3 At the more severe end of the spectrum, eczema causes a considerable amount of time off work and significantly reduces quality of life. The average case of chronic eczema, in my experience, causes far more inconvenience, loss of sleep, disrupted routine, and morbidity than basal cell cancer, a condition usually cured with one simple intervention. Eczema care is often suboptimal.4

Pathophysiology of eczema

The hereditary nature of atopic eczema has been appreciated for decades, but more recently, the importance of filaggrin has come to light. Mutations in filaggrin production are found in 50% of patients with severe eczema.5 Filaggrin molecules form a ‘protein glue’ that helps epidermal cells to stick together in the stratum granulosum and stratum corneum and form a barrier. Recent discoveries have refined our understanding of the importance of this barrier function within the epidermis.6,7

Far from being biologically inert, the stratum corneum has an active homeostatic function, regulating epidermal water content, and immunological defences. It is also a barrier for keeping out pathogenic microbes, irritants, and allergens, as well as acting as an intracellular ‘mortar’ to hold the keratinocyte ‘bricks’ together.8 The breakdown products of filaggrin form a hygroscopic, natural moisturiser called natural moisturising factor (NMF).8 Understanding this barrier function and how it is impaired in atopic eczema informs our approach to treating the patient. Mutations in filaggrin cannot be reversed, but understanding how they enable eczema—by degrading the water regulation and protective barrier function of the epidermis—helps us to appreciate the value of emollients in ‘filling the cracks’. The BAD/PCDS guidance takes this new knowledge into account.1

Diagnosis of atopic eczema

Firstly, eczema is always itchy; other diagnostic features listed in the guidance include:1

  • onset under the age of 2 years
  • flexures affected
  • family or personal history of co-existing hay fever or asthma
  • tendency towards dry skin.

I would also add:

  • the physical signs of excoriation (i.e. fingernail-induced scratch mark damage)
  • lichenification (i.e. increased emphasis of skin creases due to chronic rubbing)
  • vesicles—a sign often missed unless looked for with a lens and light, but when present, are a strong confirmation of an eczema diagnosis.

The guidance mentions the importance of differentiating between eczema and scabies, and the need to suspect scabies when the rash is of recent origin.1 I see many patients with eczema who have been repeatedly treated for scabies. Less often, I see patients with scabies who have been misdiagnosed with eczema. Both mistakes can easily happen. The hands of the patient should be examined for signs of burrows as these are indicative of scabies.

It is a widespread myth that eczema is often due to a food allergy, but as the guideline acknowledges, this is rarely the case. There will generally be a clear history in individuals in whom foods, such as egg, shellfish, cow’s milk, is causative.9

Treatment principles

Three principles of management can be applied, with limited modification, to the range of conditions termed as eczema or dermatitis (these words are Greek and Latin for inflamed skin). These principles are based on the pathology and clinical features of the condition and are as follows:10

  • A—avoid anything that makes eczema worse. Above all this means detergents (e.g. soap, shampoo, bubble bath) because they degrade the skin barrier by solubilising skin lipids. All soaps will do this, whether they contain additives or not. Hence, the need for non-detergent skin cleansers, such as emulsifying ointment or dual purpose emollients
  • B—bland emollients. The clinician needs to become familiar with a range of oilier and creamier alternatives. On finding the one that suits the patient best, large amounts of emollient should be prescribed and regular use encouraged.1 The use of antimicrobial emollients is mentioned and it is logical to try them in cases of recurrent infective episodes
  • C—control inflammation. A decade ago, ‘C’ would have stood for corticosteroids, but calcineurin inhibitors (tacrolimus and pimecrolimus) are now available, which have an immunomodulatory function and are regarded as anti-inflammatory. See below for advice on steroids.

Steroid use

The guideline goes into detail about the process of discussing eczema with parents and patients.1 Incorrect health beliefs or assumptions may need to be explored. One of the common, misleading health beliefs in eczema care relates to application of steroids.1113 The potential hazards relating to excessive use of potent, topical steroids are well known, but have been exaggerated. Consequently, patients, and parents of young children, are afraid to use sufficient quantities. Therefore, this phobia needs to be anticipated and negotiated.

The guideline emphasises that emollient use should be more frequent, generous, and of longer duration than steroid use, in a ratio of about 10:1.1 Steroid potency and frequency of use should be tailored to each case and stepped up or down according to response. My personal recommendation is to go in strongly and then step down, because quick relief is what I would wish for myself. It seems reasonable to give a patient, who has extensive inflammation, one or two large tubes of potent or very potent steroid and advise them to use it twice-daily at first, and then reduce the dose according to response, before reviewing the situation in 14 days; this is my clinical approach. This method seems even more appropriate for the elderly, who often present with dreadful, uncontrolled eczema. In this population, every day spent in a distressed state, with an itchy rash, represents a significant proportion of the days remaining to them, so why should we hold back on providing potent steroids? Obviously, milder steroid potencies should be used in children, particularly on the face and the flexures, because of increased absorption by thinner skin and touching folds. Negotiation, explanation, and review are the key to safety and success.

Oral steroids should be avoided. Even in the most extreme cases of inflammatory skin disease, the twice-daily application of a very potent topical steroid for 5 days will be as effective as oral prednisolone, but with fewer risks.


The role of the immunomodulators, tacrolimus and pimecrolimus, are discussed in the BAD/PCDS guideline.1 They have a treatment role, particularly in patients with severe chronic eczema, when long-term steroid use is problematic. It was once hoped that these agents might take over from topical steroids as they do not cause skin thinning. However, side-effects from treatment and costs have not allowed this. The guidance mentions the common side-effect of skin warming or burning, which usually diminishes after a week and doctors should try to guide patients through this. My practise is to warn patients about this side-effect and to advise them to use this treatment on a small test area of skin at first. Perhaps the current BAD/PCDS guidance is too cautious: there were concerns about possible skin cancer following long-term use of immunomodulators when tacrolimus first came out14 (based on extrapolation from systemic use in transplant patients), but after 10 years of experience this does not seem to have become a problem. In my opinion, there is now enough experience of this useful second-line treatment to allow any GP who is sufficiently confident to use it, and not just fully accredited GPwSIs.

Role of infection

The BAD/PCDS guideline mentions that secondary infection can be a cause of treatment failure or eczema exacerbation. The usual culprit is Staphylococcus aureus and signs of infection are discussed in the recommendations. Treatment with oral flucloxacillin for 7 days is required; erythromycin can be used if allergic eczema is diagnosed. The problems associated with widespread resistance to topical fusidic acid are mentioned.1

Other advice

The guidance also includes advice on when to refer patients for specialist help or for patch testing. Simple tips, like keeping nails short and smooth to diminish scratch damage, are also mentioned.1 I was pleased to see that the routine use of antihistamines is discouraged1 and I heartily concur. The use of old-fashioned antihistamines, (e.g. promethazine or chlorpheniramine) as nocturnal sedatives may help, but it is rare to find patients with eczema who gain any benefit from modern, non-sedating antihistaminess.


The BAD/PCDS guideline on atopic eczema is both useful and concise. It should be studied alongside NICE Clinical Guideline 57 on atopic eczema in children.9 This will greatly help practitioners in all disciplines, especially GPs, to better understand and manage this common and often distressing condition.

  • The British Association of Dermatologists and Primary Care Dermatology Society guideline summary is straightforward and commissioners could share this with GP practices to help educate them on the appropriate treatment of eczema
  • Local referral guidelines should sit above this summary guideline and include options for GPwSI services where available
  • Local formularies should list suitable emollients and cost-effective steroid creams, with guidance on the amounts to be prescribed
  • Immunomodulatory treatments should normally be initiated by dermatologists or GPwSIs
  • Tariff prices for dermatology outpatients = £112 (new), £69 (follow up).a
  1. Primary Care Dermatology Society, British Association of Dermatologists. Guidelines for the management of atopic eczema. London: PCDS and BAD, 2009. Available at: www.bad.org.uk/Portals/_Bad/Guidelines/Clinical%20Guidelines/PCDS-BAD%20Eczema%20reviewed%202010.pdf
  2. Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet; 344: 1383–1389.
  3. National Eczema Society website. Atopic. www.eczema.org/atopic (accessed 20 September 2012).
  4. Van Gils R, Van der Valk P, Bruynzeel D et al. Integrated, multidisciplinary care for hand eczema: design of a randomized controlled trial and cost-effectiveness study. BMC Public Health 2009; 9: 438.
  5. World Allergy Organization website. Food allergy and atopic eczema. www.worldallergy.org/educational_programs/world_allergy_forum/orlando2012/lack.php (accessed 20 September 2012).
  6. Sandilands A, Sutherland C, Irvine A, Irwin McLean W. Filaggrin in the frontline: role in skin barrier function and disease. J Cell Sci 2009; 122 (9): 1285–1294.
  7. Mildner M, Jin J, Eckhart L et al. Knockdown of filaggrin impairs diffusion barrier function and increases UV sensitivity in a human skin model. J Invest Dermatol 2010; 130 (9): 2286–2294.
  8. Del Rosso J, Levin J. Skin structure and function: the clinical relevance of maintaining the functional integrity of the stratum corneum in both healthy and disease-affected skin. J Clin Aesthet Dermatol 2011; 4 (9): 22–42.
  9. National Institute for Health and Care Excellence. Atopic eczema in children. Clinical Guideline 57. London: NICE, 2008. Available at: www.nice.org.uk/guidance/CG57 nhs_accreditation
  10. Holden C, English J, Hoare C et al. Advised best practice for the use of emollients in eczema and other dry skin conditions. J Derm Treatment 2002; 13: 103–106.
  11. National Eczema Association Support Community website. Steroid phobia: a major obstacle to effective eczema control. www.inspire.com/groups/national-eczema-association/discussion/steroid-phobia-a-major-obstacle-to-effective-eczema-control (accessed 20 September 2012).
  12. National Eczema Society website. Steroid phobia—a major obstacle in caring for eczema sufferers. www.eczema.org/documents/167 (accessed 20 September 2012).
  13. National Eczema Association website. How often should I be applying topical steroids? www.nationaleczema.org/living-with-eczema/ask-the-doctor/how-often-should-i-be-applying-topical-steroids (accessed 20 September 2012).
  14. National Institute for Health and Care Excellence. Pimecrolimus and tacrolimus for atopic dermatitis (eczema). Technology Appraisal 82. London: NICE, 2004. Available at: www.nice.org.uk/guidance/TA82G