History

Fact Explanation
Erythematous and edematous skin lesions with or without thickening Inflammatory reaction of the skin caused by allergens/ irritants in a genetically susceptible individual [1].
Pruritus Occurs due to the inflammatory reaction caused by the cytokines, leading to an itch-scratch cycle which further worsens the skin lesion [2]. Pruritus can be precipitated by certain environmental / psychological factors [3].
Family history of atopic eczema, allergic rhinitis, allergic conjunctivitis & asthma, and a personal history of atopy (asthma, allergic rhinitis, allergic conjunctivitis) Associated with atopic eczema as there is a genetic predisposition [2].
Chronic or relapsing dermatitis, with relapses occurring following exposure to known allergens/ irritants. Seen due to genetic susceptibility and persistent exposure to allergens / irritants.
References
  1. WELLER, Richard, John HUNTER, John SAVIN, Mark DAHL. Clinical Dermatology. Fourth Edition. Singapore: Blackwell Publishing, 2008.
  2. WOLFF, Klaus. Richard Allen JOHNSON. Fitzpatrick’s Color atlas and synopsis of clinical dermatology. 6th edition. Singapore: McGraw-Hill, 2009.
  3. MALLORY, Susan Bayliss. Illustrated Manual of Pediatric Dermatology: Diagnosis and Management. 1st ed. United Kingdom: Taylor & Francis, 2005.

Examination

Fact Explanation
Skin lesions: Crusty, oozing vesicular eruptions in the acute stage; erythematous, scaly papules in the sub-acute stage; lichenified lesions with fissures in the chronic stage. Pityriasis alba (dry, depigmented, fine scaly patches) in the minor form of atopic eczema [1]. Site of the skin lesions: Children up to 2 years - cheeks and extensor surfaces sparing the diaper area. Older children- flexural surfaces [2]. Damage to the epidermis by allergens / irritants in a genetically susceptible individual activates cytokines causing an inflammatory reaction in the skin, leading to edema and erythema [3]. Edema caused by the inflammation progresses to form vesicular lesions which rupture and cause oozing [3]. Repeated scratching due to prutitus leads to thickening and lichenification [1].
White dermatographism (blanching of the skin when stroked, instead of turning red which is the normal reaction) Due to the tendency of vasoconstriction in the atopic skin [2].
Xerosis (dry skin) Due to reduced water content in the stratum corneum, and reduced secretion of sebum and sweat [2].
Secondarily infected skin lesions with pustules and oozing erosions Bacterial colonization is due to underlying inflammation of the atopic skin [4]. Note: Staphylococcus aureus is found in over 90% of the atopic skin lesions [4]. It worsens inflammation and pruritus [5].
References
  1. BERKE, Rebecca, Arshdeep SINGH, Mark GURALNICK. Atopic Dermatitis: An Overview. American family physician [Online]. American Academy of Family Physicians. July 01 2012, 86 (1), 35-42 [viewed 08 March 2014].
  2. MALLORY, Susan Bayliss. Illustrated Manual of Pediatric Dermatology: Diagnosis and Management. 1st ed. United Kingdom: Taylor & Francis, 2005.
  3. WELLER, Richard, John HUNTER, John SAVIN, Mark DAHL. Clinical Dermatology. Fourth Edition. Singapore: Blackwell Publishing, 2008.
  4. LEUNG, Donald Y.M., Thomas BIEBER. Atopic dermatitis. The Lancet [Online]. Elsevier. 11 January 2003, 361(9352), 151-60 [viewed 09 March 2014]. Available from: doi:10.1016/S0140-6736(03)12193-9.
  5. ALLEN, Herbert B., Nachiket D. VAZE, Catherine CHOI, Tesfu HAILU et al. The Presence and Impact of Biofilm-Producing Staphylococci in Atopic Dermatitis. Journal of American Dermatology [Online]. Journal of American Dermatology. 22 January 2014, [viewed 09 March 2014]. Available from: doi:10.1001/jamadermatol.2013.8627.

Differential Diagnoses

Fact Explanation
Contact dermatitis Causes erythematous vesicular skin lesions. May also cause blistering and necrosis. There is usually a recent history of contact with a chemical or other allergen, and the skin lesions involve the contact area which is most commonly the hand [1].
Psoriasis Can cause pruritus. Skin lesions are well defined silvery-scaly erythematous papules seen on the scalp and joints. There can be associated nail changes (pitting / subungual hyperkeratosis / oncholysis / yellow spots under the nail plate), and a family history of psoriasis [1].
Seborrheic dermatitis Another common skin lesion seen in infants. Consist of orange-red scaly macules / papules distributed on the scalp, face, trunk and skin creases. A distinguishing feature from atopic eczema is that it involves the diaper area. When the scalp is involved, it is called the 'cradle cap' [1].
Scabies Causes generalized itching. There are associated itchy social contacts. Skin lesions include burrows & papules, erythematous crusty plaques and eczematous dermatitis at the heavily mite-infested sites [1].
Nummular eczema Causes severe itching. Skin lesions are scaly, oozing, coin shaped erythematous plaques, consisting of vesicles and papules. It is distributed on the legs, hands and trunk. [1].
Dermatophytosis Causes itching. Skin lesions are sharply demarcated, annular, large, erythematous plaques with a clear center and an active margin, located on moist areas of the skin [1].
Immunologic disorders Wiskott-Aldrich syndrome, X-linked agammaglobulinemia, hyper-IgE syndrome, selective IgA deficiency and Langerhans cell histiocytosis are some rare but important differentials to consider [1].
Lichen simplex chronicus Causes chronic pruritus. Skin lesions are caused by repeated rubbing over a long period. Skin lesions are thickened plaques with papules & follicles, with accentuation of the skin markings [1].
References
  1. WOLFF, Klaus. Richard Allen JOHNSON. Fitzpatrick’s Color atlas and synopsis of clinical dermatology. 6th edition. Singapore: McGraw-Hill, 2009.

Investigations - for Diagnosis

Fact Explanation
Full blood count May show eosinophilia. Note: Atopic eczema is a clinical diagnosis. Investigations may support the diagnosis when the clinical diagnosis is uncertain [1].
Serum Immunoglobulin E May show increased levels [1].
Allergy testing [prick test/ radioallergosorbent test (RAST)] Some of the patients may have food/ inhalant allergies that will support the clinical diagnosis [1].
Histology of skin lesions May show acanthosis with intraepidermal and intracellular edema (spongiosis), and a dermal infiltrate of lymphocytes, monocytes, mast cells and eosinophils [2].
References
  1. MALLORY, Susan Bayliss. Illustrated Manual of Pediatric Dermatology: Diagnosis and Management. 1st ed. United Kingdom: Taylor & Francis, 2005.
  2. WOLFF, Klaus. Richard Allen JOHNSON. Fitzpatrick’s Color atlas and synopsis of clinical dermatology. 6th edition. Singapore: McGraw-Hill, 2009.

Investigations - Followup

Fact Explanation
Bacterial culture from skin lesions Helps to identify staphylococcal infection as over 90% of lesions are infected with staphylococcal aureus [1].
Viral culture of skin lesions and antigen testing for Herpes simplex virus Helps to exclude Herpes simplex infection in crusted lesions, as patients are more prone to infection with Herpes Simplex virus [2].
References
  1. LEUNG, Donald Y.M., Thomas BIEBER. Atopic dermatitis. The Lancet [Online]. Elsevier. 11 January 2003, 361(9352), 151-60 [viewed 09 March 2014]. Available from: doi:10.1016/S0140-6736(03)12193-9.
  2. WOLFF, Klaus. Richard Allen JOHNSON. Fitzpatrick’s Color atlas and synopsis of clinical dermatology. 6th edition. Singapore: McGraw-Hill, 2009.

Management - General Measures

Fact Explanation
Educating the patient about the illness Educating the patient / care-giver on the triggers of eczema will help to prevent relapses by avoiding those causative factors [1]. Educating the patient / care-giver to avoid scratching / rubbing of skin lesions helps to accelerate the healing process [2].
Skin care: Avoidance of irritants; Hydration; Wet dressings. Important as xerosis predisposes to dermatitis. Irritants such as soap / detergent / chemicals / abrasive clothing can worsen the xerosis [1]. Hydration of the skin by oilated baths and emollients such as hydrated petroleum prevent xerosis [2]. Wet dressings can be applied to severely affected lesions to prevent persistent scratching that retards the healing process [1].
Systemic anti-pruritic medication Use of anti-histamines for pruiritis can benefit only some patients as many factors contribute towards the pruritus [1]. Use of Hydroxyzine and diphenhydramine at bed-time is beneficial as the pruritus is worse at night and because of their sedative effect [1]. Note: Use of topical anti-histamines can worsen the condition by inducing sensitization [1].
Stress management Emotional stresses can precipitate itching and relapse, so counselling should be considered in such patients [1].
References
  1. LEUNG, Donald Y.M., Thomas BIEBER. Atopic dermatitis. The Lancet [Online]. Elsevier. 11 January 2003, 361(9352), 151-60 [viewed 09 March 2014]. Available from: doi:10.1016/S0140-6736(03)12193-9.
  2. WOLFF, Klaus. Richard Allen JOHNSON. Fitzpatrick’s Color atlas and synopsis of clinical dermatology. 6th edition. Singapore: McGraw-Hill, 2009.

Management - Specific Treatments

Fact Explanation
Anti-inflammatory agents: Topical glucocorticoids Effective in controlling acute exacerbation [1]. Side effects rely on the potency of the medication and the length of use [1], and include skin atrophy, stunting, osteoporosis and suppression of pituitary adrenal axis [2]. Important: Ultra-high potency glucocorticoids should be used for a very short period on lichenified lesions only, and should not be used on the face or other sensitive areas [1]
Non-steroidal anti-inflammatory agents: Topical calcineurin inhibitors (Tacrolimus/ pimecrolimus) Effective in treating sub-acute atopic eczema and minor flares [2]. They suppress inflammation and itching. Side effects are less, with the most common being local burning sensation. However, there should be caution against the long term use of this medication as its effect on skin cancer and viral skin infections is yet to be researched [1].
Coal tar preparations Less effective than glucocorticoids. Used in the chronic stage [1]. Caution: Can induce folliculitis and photosensitivity and there is a theoretical risk of cancer [1].
Topical/ systemic antibiotics Used in secondarily infected skin lesions. Topical preparations (mupirocin/ fusudic acid) can be used for localized lesions whereas systemic antibiotics (macrolides/ cloxacillin/ 1st generation cephalosporins) are used for extensive super-infection [1].
Antiviral treatment Used in cutaneous herpes simplex infection as it can cause life-threatening dissemination in atopic eczema [1]. Note: Patients with atopic eczema are more prone to viral infections such as herpes simplex, molluscum contagiosum and warts [3]
Phototherapy Narrow band ultraviolet B is an effective adjunctive method in treating moderate to severe atopic eczema [4]. Photochemotherapy with PUVA (psoralen & ultraviolet A) can be used in severe atopic eczema [1]. Side effects include skin erythema & pain, pruritus, pigmentation, premature skin aging and risk of skin malignancy [1].
Systemic immuno-modulatory agents Cyclosporin can be tried for severe refractoty patients [3]. It effectively reduces the eczema and itching [5]. Caution: Treatment should not exceed 3-6 months, due to its side effects profile that includes hypertension and reduced renal function [2]. Methotrexate and azathioprine can also be used with caution [1]. Efalizumab (T cell modulator) has shown a promising effect but needs further research [6].
References
  1. LEUNG, Donald Y.M., Thomas BIEBER. Atopic dermatitis. The Lancet [Online]. Elsevier. 11 January 2003, 361(9352), 151-60 [viewed 09 March 2014]. Available from: doi:10.1016/S0140-6736(03)12193-9.
  2. WOLFF, Klaus. Richard Allen JOHNSON. Fitzpatrick’s Color atlas and synopsis of clinical dermatology. 6th edition. Singapore: McGraw-Hill, 2009.
  3. MALLORY, Susan Bayliss. Illustrated Manual of Pediatric Dermatology: Diagnosis and Management. 1st ed. United Kingdom: Taylor & Francis, 2005.
  4. REYNOLDS, Nick J., Vera FRANKLIN, Janine C. GRAY, Brian L. DIFFEY, Peter M. FARR. Narrow-band ultraviolet B and broad-band ultraviolet A phototherapy in adult atopic eczema: a randomised controlled trial. The Lancet [Online]. Elsevier. 23 June 2001,357 (9273), 2012-16 [viewed 09 March 2014]. Available from: doi:10.1016/S0140-6736(00)05114-X.
  5. WAHLGREN, C.F., A. SCHEYNIUS, O. HAGERMARK. Antipruritic effect of oral cyclosporin A in atopic dermatitis. Acta Dermato Venereologica [Online]. Acta Dermato Venereologica. 70 (4), 323-329 [viewed 09 March 2014]. Available from: doi: 10.2340/0001555570323329.
  6. WEINBERG, Jeffrey M., Elaine C. SIEGFRIED. Successful Treatment of Severe Atopic Dermatitis in a Child and an Adult With the T-Cell Modulator Efalizumab. Archives of dermatology [Online]. Archives of dermatology . 2006,142(5),555-558 [viewed 09 March 2014]. Available from: doi:10.1001/archderm.142.5.555.