Development of a Clinical Pathway for Atopic Dermatitis Patients: A Case-Based Approach

December 2016 | Volume 15 | Issue 12 | Original Article | 1485 | Copyright © December 2016

Lyn C. Guenther MD FRCPC,a Anneke Andriessen PhD,b Charles W. Lynde MD FRCPC,c John W. P.Toole BSc MD FRCPC,d Gary R. Sibbald MD FRCPC MACP FAAD M.Ed DSc (Hons),e James N. Bergman MD FRCPC,f Marc Bourcier MD FRCPC,g and Ian D.R. Landells MD FRCPCh

aWestern University, London Ontario, Canada; Guenther Dermatology Research Centre, Ontario, Canada bAndriessen Consultants, Malden and UMC St. Radboud, Nijmegen, Netherlands cUniversity of Toronto,Toronto, Ontario, Canada dUniversity of Manitoba, Canada eUniversity of Toronto, Mississauga, Ontario, Canada fUniversity of British Columbia,Vancouver, British Columbia, Canada gMoncton, New Brunswick, NB, Canada hMemorial University of NL; Nexus Clinical Research, St. John’s, NL, Canada

BACKGROUND: Atopic dermatitis (AD) is a common chronic skin condition, associated with significant patient morbidity. There are a myriad of excellent evidenced based guidelines to guide clinicians by an extensive review of all the available treatments. However, while well written and complete these papers may not always allow easy transition to clinical application. OBJECTIVE: The purpose of this paper was to develop a practical case-based approach for the treatment and maintenance of AD, enabling translation of guidelines into clinical care. METHODS: After literature searches, selected AD trials and recent existing guidelines were reviewed. Using a nominal group process for consensus, an expert panel of Canadian dermatologists determined the case features and corresponding treatments. RESULTS: A patient focused clinical pathway with 7 cases was developed. For each case scenario, treatment for mild, moderate, and severe disease was recommended. CONCLUSION: A practical case-based clinical pathway was developed for easy clinical application and optimal patient care. J Drugs Dermatol. 2016;15(12):1485-1494.


Atopic dermatitis (AD) or eczema is a chronic, relapsing, inflammatory skin disease, which affects up to 25% of children and 2-3% of adults.1 Hereditary and environmental factors predict a higher risk for early infantile atopic dermatitis.3 The diagnosis of AD is clinical: chronic, relapsing course, dry irritated skin, pruritus, erythema, scaling, edema, excoriations/erosions, oozing, crusting, and licheni cation in characteristic locations based on age (ie, facial, neck, and exten- sors in infants and children). Flexural involvement may occur at any age; sparing of groin and axillae.4There is often co-existing asthma and hay fever.3 Itch is a predominant feature to the point where AD has often been referred to as the “itch that rashes.”2 There are many triggers that may aggravate AD and different triggers play different roles in individual patients. Examples of triggers that can exacerbate eczema include but are not limited to soaps/detergents/perfumes, rough fabrics, allergens (eg, animal dander, dust mites, mold, pollen, perfume, food), stress, environmental (dryness/ cold), sweating, and secondary infection/bacterial colonization.1 Patient/parent ed- ucation should be directed towards identifying and avoiding eczema triggers. Many patients with eczema suffer more in the winter when the weather is dry and cold, while other suffer more in a warm, humid environment.1,2 AD interferes with quality of life in children and parents of af- fected children more than most other conditions including other skin conditions.5-9 Intense itching frequently leads to sig- ni cant sleep disturbances as well as irritability and reduced performance at school and work. 5-9 Even in remission, AD can have long term behavioral and neurocognitive effects.9 Quality of life may be further reduced due to the social stigma of the visible skin condition.7 The skin of patients with AD has a compromised skin barrier function. Filaggrin null gene mutations and a high total serum IgE level tend to be associated with more severe, chronic disease, but not all patients with AD have a laggrin defect or high