Mild and moderate atopic dermatitis (eczema) – a journey from flare to care ACG

Overview

This ACE Clinical Guideline (ACG) provides guidance on diagnosis, severity assessment and management of mild and moderate atopic dermatitis (AD), including topical and non-pharmacological interventions in adults and children. The ACG also covers proactive therapy, systematic assessment of treatment response, and principles of management of secondary bacterial infection. Supplementary materials are available, including a drug table on topical anti-inflammatories and a photo repository.

ACG recommendations

1. Diagnose AD through history taking and clinical examination, focusing on key features such as skin itchiness, dryness, personal or family history of atopic diseases, disease chronicity, lesion morphology and distribution.

2. Assess AD severity based on extent, frequency and intensity of clinical manifestations, and patient- or caregiver-reported impact on quality of life.

3. Review potential triggers for AD and advise on how to minimise exposure.

4. For patients with mild or moderate AD, advise liberal moisturiser use as baseline therapy, and 

   • Prescribe topical corticosteroids (TCS) as first-line anti-inflammatory treatment for active lesions.  

   • If a non-steroidal alternative is required or preferred, consider topical calcineurin inhibitors (as second- line) or topical phosphodiesterase 4 inhibitors (as third-line). 

5. For patients with recurring AD flares (e.g. 2-3 flares/month), prescribe proactive therapy of topical anti-inflammatory treatments to areas of skin prone to flare recurrences.

6. For patients with inadequate treatment response, assess and address possible factors before modifying treatment.

7. Do not routinely give oral corticosteroids for AD, except as a short course for: 

   • Rescue therapy for acute, severe flares, or  

   • Bridging therapy to systemic treatment.

8. For secondary infection of AD, continue patient’s topical anti-inflammatory treatments alongside appropriate antimicrobial agents.

9. Avoid triple combination products of TCS, antibiotics and antifungals in AD patients with suspected or clinically evident bacterial infection.

Download the ACG and references in PDF

Mild and moderate atopic dermatitis (eczema) – a journey from flare to care (Feb 2026) [PDF]

Mild and moderate atopic dermatitis references (Feb 2026) [PDF] 

EtR Framework

The Evidence-to-Recommendation (EtR) framework is a document that outlines the underpinning evidence and rationale for the recommendations in our ACGs. Download the major depressive disorder EtR framework below to learn more about factors that have informed the strength of the ACG recommendations, including certainty of evidence, clinical benefit/risk balance, local resource implications, feasibility considerations, patient preferences and values.

Mild and moderate atopic dermatitis EtR framework with summary of findings

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Introduction

Atopic dermatitis (AD) is a common chronic inflammatory skin condition characterised by dry skin with recurrent episodes of itching and inflammation. It arises from a complex interplay of genetic predisposition, immune dysfunction and environmental factors, leading to impaired skin barrier function and heightened inflammatory responses.¹ The clinical course of AD typically alternates between remission and relapses with symptoms ranging from mild dryness and irritation to severe itch, inflammation and lichenification. In Singapore, AD affects approximately 13.1% of people with higher rates in children (20.6%) than adults (11.1%).² A substantial proportion of children with AD will continue to have the condition throughout their lives.

This ACE Clinical Guideline (ACG) provides evidence-based recommendations for managing mild and moderate AD to prevent disease progression to more severe cases that require specialist intervention (Figure 1). With appropriate therapeutic interventions and comprehensive care routines, many patients can achieve disease control and maintain healthy, flare-free skin. The focus of this ACG is primary care settings where there are numerous opportunities to provide impactful counselling and early interventions that can significantly improve patient outcomes and quality of life.

Click here for larger version of the image

Supplementary guide, Drug table, Photo repository

Diagnosis and severity assessment

Recommendation 1: Diagnose AD through history taking and clinical examination, focusing on key features such as skin itchiness, dryness, personal or family history of atopic diseases, disease chronicity, lesion morphology and distribution.

AD is a clinical diagnosis and it relies on recognising key clinical features through careful history taking and physical examination.

History taking should focus on the two most prominent symptoms: skin itch (present in 94% of patients) and dryness (73% of patients). Explore personal or family history of atopic diseases (e.g. asthma, allergic rhinitis and allergic conjunctivitis) which are present in 53% of people with AD.^5,6 Identifying individual triggers is important during history taking, as these can vary significantly between patients and may include environmental factors, allergens, stress, or specific irritants (refer to Recommendation 3). Clinicians can establish chronicity by checking age of onset, frequency and duration of previous episodes (if any), their specific characteristics and triggers, followed by examining skin for any signs of long-term inflammation (see ‘chronic lesions’ below).

Morphology and distribution of AD lesions

The morphology of AD varies with disease chronicity:

• Acute lesions: typically present as erythema in lighter skin tones, and may appear violaceous, grey or brown in darker skin tones.¹ Lesions may manifest as papules, vesiculopapules and plaques, often accompanied by exudates or crusting.⁷

• Chronic lesions (developed from persistent scratching): may present as lichenified plaques or prurigo nodules.⁷ After lesions have healed, patients may present with post inflammatory hyper- or hypopigmentation.^6,8

The distribution of lesions typically follows an age-related and symmetrical pattern (Figure 2), though there may be some overlap between age groups:

• Infants and young toddlers (under 2 years): scalp and face, commonly spreading to trunk and extremities (often extensor involvement).^6,7

• Children (2–12 years): neck and flexural areas, with higher prevalence in periorbital and auricular areas, and the ventral aspects of wrists (less cheeks, chin or forehead involvement than infants).^5-7

• Adolescents (13–17 years) and adults: predominantly flexural areas in addition to face, neck and distal extremities. Distribution may be less typical and appear in localised areas like nipples, hands, or feet.^5,6

It is important to note that, AD may present differently in Asian patients compared to non-Asians, including more psoriasiform variants (presenting with clearer demarcation, more prominent scaling and lichenification).^8–10 They also show increased prevalence of prurigo nodularis and follicular prominence¹¹, with greater involvement of truncal, extensor, scalp and auricular areas.⁵

Several conditions can mimic AD and require careful differentiation, including irritant and allergic contact dermatitis, psoriasis, seborrheic dermatitis, scabies or dermatophyte infections.¹

Photo repository on common presentation of AD in different skin tones

Supplementary guide on validated diagnostic criteria, severity assessment tools and mitigation strategies for common AD triggers

Diagnostic criteria

The clinical manifestations of AD can vary widely due to factors such as patient age, disease severity and chronicity, making it difficult to adopt a single set of diagnostic criteria as gold standard in routine clinical practice. Among the most validated and widely cited are the United Kingdom Working Party (UKWP)^12–14 and Hanifin and Rajka¹⁵ criteria, though both have limitations as detailed in Supplementary guide and should be used in conjunction with comprehensive assessment. Given some practical utility of the UKWP criteria in primary settings, this guideline has developed the I-FACED acronym (Figure 3) to support recall and facilitate application in clinical practice.

Recommendation 2: Assess AD severity based on extent, frequency and intensity of clinical manifestations, and patient- or caregiver-reported impact on quality of life.

AD severity can be classified using criteria adapted from NICE guidelines¹⁶ (Table 1) and comprehensively assessed using a practical checklist derived from validated scoring tools such as EASI, SCORAD and DLQI (Figure 4). Although these tools allow detailed assessment, time constraints and patient burden may limit their routine use. Therefore, they are positioned as optional tools (Supplementary guide) that may be used for detailed assessment when necessary.

Once severity is assessed, the goals of treatment are to control flares and to maintain remission (Figure 5).

Use clear and empathetic communication when explaining the disease course and management. Setting realistic expectations helps build trust and encourages adherence to treatment plans which improves quality of life for both patients and their caregivers.

Click here to access patient education leaflets on AD: Adults, caregivers of young children, common questions on AD

Avoidance of triggers

Recommendation 3: Review potential triggers for AD and advise on how to minimise exposure.

Provide tailored counselling to address factors that may trigger or worsen AD. Complete elimination may be feasible for some triggers (e.g. contact allergy), but impractical for others like dust or pollutants, which can typically be minimised rather than avoided entirely. Suspected food allergies require careful evaluation before dietary modifications, to avoid nutritional deficiencies from unnecessary food elimination. Common triggers are outlined below (Figure 7). Refer to Supplementary guide for mitigation strategies.

Pharmacotherapy for mild and moderate AD

Recommendation 4: For patients with mild or moderate AD, advise liberal moisturiser use as baseline therapy, and; 1) Prescribe topical corticosteroids as first-line anti-inflammatory treatment for active lesions 2) If a non-steroidal alternative is required or preferred, consider topical calcineurin inhibitors (as second- line) or topical phosphodiesterase 4 inhibitors (as third-line).

Moisturisers as baseline therapy

Moisturisers are the cornerstone of AD management and recommended for all patients with AD, regardless of disease severity. They are generally well-tolerated, safe and provide multiple benefits such as preventing skin dryness and restoring skin barrier, thereby reducing AD signs and symptoms and decreasing flare frequency.¹⁷

Topical anti-inflammatory treatment for active

AD lesions For active AD lesions or flares, prescribe a suitable topical anti-inflammatory in addition to moisturisers. Topical corticosteroids (TCS) remain the first-line treatment due to their strong and well-established efficacy. The choice of TCS (vehicle and potency), should be tailored to the anatomic site and clinical severity (Table 2), balancing therapeutic benefit with potential local side effects (skin atrophy, striae, telangiectasia).⁶ Risks of local side effects increases with higher potency TCS, application to thin-skinned areas, occlusion, or long-term continuous use.

Topical calcineurin inhibitors (TCIs) (e.g. pimecrolimus and tacrolimus) are alternatives if non-TCS options are preferred. The topical anti-inflammatory potency of TCIs is broadly comparable to low- and moderate-potency TCS20,²¹ (see drug table for more details). TCIs are generally well tolerated except for a transient burning or stinging sensation upon application. Despite FDA black box warnings based on high doses of systemic calcineurin inhibitors in animal studies, long-term studies have found no evidence for increased cancer risk in humans.^22,23

Topical phosphodiesterase-4 inhibitors (PDE4i), such as crisaborole, are a newer class of non-TCS anti-inflammatory therapy. They work by down-regulating inflammatory cytokine production and reducing skin inflammation, and are effective in reducing AD signs and symptoms compared to placebo.²⁴ Recent head-to-head trials showed moderate potency TCS had greater efficacy in reducing AD signs and symptoms compared to crisaborole,²⁵ while differences between crisaborole and TCIs were not statistically significant^25–29 (see drug table and Evidence-to-Recommendation summary of findings). Given the limited evidence on PDE4i efficacy versus TCS and TCIs; similar tolerability issues and cost concerns; and it being less accessible in primary care settings, consider PDE4i when conventional treatments (TCS or TCIs) are unsuitable or not tolerated. Topical PDE4i are generally well tolerated except for a transient burning or stinging sensation.

Drug table of topical anti inflammatories

*Individual medications in the TCIs class are listed according to age limit

Click here to access HealthHub content for patient education leaflets on application technique on:

• Moisturisers

• TCS

• TCI

  • Tacrolimus 

  • Pimecrolimus 

While disease severity, patient age and anatomical site (Table 3) are useful for guiding treatment selection, clinicians should also consider other patient factors, treatment history, cost and availability. Clinicians may refer to the comparative efficacy drug table in conjunction with these recommendations to inform treatment decisions.

Mod, moderate; PDE4i, topical phosphodiesterase 4 inhibitor which is currently only crisaborole 2% ointment; Pim, pimecrolimus 1% cream; Tac 0.03, tacrolimus 0.03% ointment; Tac 0.1, tacrolimus 0.1% ointment; TCS, topical corticosteroids

^a Thin skin areas include the periorbital region, face, scalp, neck, flexures, and groin.

^b Minimum approved ages for pimecrolimus 1% cream is ≥ 3months; tacrolimus 0.03% ointment is ≥2 years; 0.1% ointment is ≥16 years; crisaborole 2% ointment: ≥3 months. Individual medications in the TCIs class are listed alphabetically, not in order of preference.

^c While severe AD may initially require the higher potency TCS, the concurrent use of systemic therapies or phototherapy may permit the stepping down to lower potencies as adjunctive therapy, under specialist advice.

While topical anti-inflammatories are the main treatment options for AD, other adjunctive therapies exist, although the evidence supporting their effectiveness is generally limited.

Recommendation 5: For patients with recurring AD flares (e.g. 2–3 flares/month), prescribe proactive therapy of topical anti-inflammatory treatments to areas of skin prone to flare recurrences.

Proactive therapy is a prevention-focused strategy that reduces flare frequency and maintains long-term control by continuing intermittent topical anti-inflammatory treatment on recurrently relapsing skin areas, even after initial AD flare has been controlled. Studies of patients with moderate-severe AD and recurring flares showed that proactive therapy significantly reduced relapse risk with generally low risk of adverse effects, compared to reactive treatment (Figure 8).^28,37,42 Based on expert experience, patients with recurring AD flares (2–3 flares per month) affecting the same specific locations, regardless of overall disease severity, will likely benefit from proactive therapy.

For patients with moderate or severe AD refractory to topical treatment, phototherapy and systemic options including oral conventional immunosuppressants, oral JAK inhibitors, and monoclonal antibodies have been shown to improve AD severity (no treatment hierarchy implied).^{45, 46} Patients requiring such therapies should be referred to specialists treating severe AD, such as dermatologists, allergists or relevant specialists.

Recommendation 6: For patients with inadequate treatment response, assess and address possible factors before modifying treatment.

When evaluating inadequate treatment response, defined as a lack of satisfactory improvement in AD signs, symptoms or impact on quality of life after 2 weeks, clinicians should systematically consider different factors (see below) before modifying treatment.

Most patients with mild and moderate AD can be effectively managed in primary care.

Consider specialist referral for the following situations:

• Uncertain diagnosis (including suspected allergic contact dermatitis with unidentifiable allergen requiring patch testing)

• Unsatisfactory response to topical treatments in primary care such as:

  • Flare persisting for more than 2 to 4 weeks after appropriate treatment

  • Flares still occurring frequently after 3–6 months of proactive therapy

  • Significant adverse effects or poor tolerance to topical treatment(s)

• Extensive (e.g. >10%) body surface area affected

• Significant impact on quality of life (including social or psychological problems)

• Severe complications such as skin infections requiring intravenous antibiotics and antivirals (e.g. severe cellulitis, eczema herpeticum), and erythrodermic flare – refer to emergency department

Recommendation 7: Do not routinely give oral corticosteroids for AD, except as a short course for; 1) Rescue therapy for acute, severe flares, or 2) Bridging therapy to systemic treatment

Oral corticosteroids (OCS) are not recommended for routine use in the mild and moderate management of AD. Although they provide rapid symptom relief, benefits are short-lived, and disease activity typically rebounds after discontinuation.^1,19,51 Long-term or repeated use carries significant risks such as infection, hypertension, glucose intolerance, weight gain, gastritis, reduced bone mineral density, and adrenal suppression.⁵² Reliance may also delay the initiation of more appropriate and effective long-term treatment.

OCS is strongly discouraged in children due to the additional risk of growth retardation.^52,5

Short courses of OCS may be considered for rescue therapy during acute, severe flares - defined as episodes with widespread inflammation, persistent itching and significant impairment of quality of life (following NICE severity definition) - or as bridging therapy while initiating slower-acting systemic treatments.^51,54 When prescribed, clinicians must communicate temporary benefits and risks through shared decision-making, emphasising adherence to prescribed duration and need for effective long-term alternatives.

OCS, oral corticosteroids; OD, once daily

Management of AD with secondary bacterial infection

Patients with AD are predisposed to skin infections due to multiple factors such as skin barrier. skin barrier disruption, inflammation, bacterial colonisation and dysbiosis of skin flora.⁵⁵ Scratching also disrupts the skin barrier and may allow entry of pathogens. It may be challenging to distinguish between an AD flare and infected AD as both can present with erythema, weeping, and worsening skin symptoms.⁵⁶

Bacterial infection in AD is mostly commonly caused by Staphylococcus aureus (S. aureus), followed by Streptococcus pyogenes (S. pyogenes).⁵⁶ Skin swabs are not necessary in most cases, as bacterial colonisation is common in AD patients regardless of infection status,⁵⁷ and routine swabbing of AD patients with suspected infection could lead to inappropriate antibiotic prescribing.⁵⁶ If infection worsens, consider a skin swab to check for other causative organisms or resistant strains.^19,56

Recommendation 8: For secondary infection of AD, continue patient’s topical anti-inflammatory treatments alongside appropriate antimicrobial agents.

For this ACG’s management of secondary bacterial infection of AD, antimicrobial agents refer to either antiseptics or antibiotics.

In general, the patient’s anti-inflammatory treatments (TCS or TCI) should be continued alongside appropriate antimicrobial agents during episodes of infected AD, including severe viral infections such as eczema herpeticum.^19,56 Both TCS and TCIs have been shown to reduce S. aureus colonisation, increase microbial diversity, and reduce scratching by managing the underlying inflammation.⁵⁵ Evidence of effectiveness for antimicrobial agents (antibiotics or antiseptics) in combination with topical anti-inflammatories in infected AD remains limited. For topical antibiotics, studies show significant reduction in S. aureus isolation rates, but only modest improvements over TCS alone in overall disease signs and symptoms.⁵⁸

Clinicians should weigh the need for antimicrobial treatment against the risk of contributing to antimicrobial resistance. AD flares can clinically mimic skin infection,⁵⁶ making it difficult to distinguish between inflammatory f lares and actual bacterial infections. As such, infections may be incorrectly diagnosed when none is present, resulting in unnecessary antimicrobial prescribing. Clinicians must carefully assess whether an infection is truly present before prescribing antimicrobials.

When the decision to treat as a secondary AD infection has been reached:

• Topical antiseptics may be used to reduce microbial load, although resistance may develop with prolonged use. Evidence supporting their use in infected AD is limited and derived from a few small trials.^{17, 21, 58} Staphylococcus resistance to antiseptics is emerging (to triclosan, and to a lesser extent to chlorhexidine and octenidine, whilst povidone-iodine has limited evidence of antimicrobial resistance).^59,60 Nevertheless, antiseptic resistance is less common than antibiotic resistance.

• Topical antibiotics, if indicated, should be used judiciously. When antibiotics are necessary, select narrow spectrum agents with appropriate duration (e.g. 5 to 7 days); widespread, prolonged or indiscriminate antibiotic use escalates antibiotic resistance. Global surveillance data indicate only 80% fusidic acid susceptibility and 98% for mupirocin.⁶¹ For mild impetiginised AD, topical fusidic acid may treat S. aureus and S. pyogenes skin infections, while topical mupirocin should be reserved for confirmed methicillin-resistant S. aureus (MRSA) where infection has worsened.⁵⁶

• Dual combination creams (TCS plus suitable topical antimicrobial) may reduce treatment regimen complexity and support patient adherence.

• Systemic antibiotics are indicated for severe or widespread infected AD, or when patients are systemically unwell.⁵⁶

• If the response to initial treatment course is suboptimal and symptoms persist, reassess the diagnosis and management plan, and consider escalating care, such as a skin swab to guide targeted antibiotic choice, or referral.⁵⁶

Recommendation 9: Avoid triple combination products of TCS, antibiotics and antifungals in AD patients with suspected or clinically evident bacterial infection.

Products containing a combination of TCS, antibiotics and antifungals should be avoided:

Inappropriately high potency TCS: The TCS components in locally available products, such as betamethasone dipropionate 0.05% are typically high-potency formulations. This may be unnecessarily potent for many AD patients, increasing the (avoidable) risk of local side effects such as skin atrophy, especially without proper monitoring.

Limited role of gentamicin: Products containing aminoglycosides like gentamicin, have poor penetration and limited bactericidal activity against S. aureus and S. pyogenes, without synergistic combinations with beta-lactams.^64,65 As such, they are not suitable as a monotherapy for treating common gram-positive skin infections.

Risk of contact dermatitis: Topical aminoglycosides commonly found in these combinations, such as gentamicin and neomycin, have been shown to cause contact dermatitis in some individuals, potentially worsening the existing skin condition.^{64, 65}

Unnecessary antifungal component: Most bacterial infections in AD do not require concurrent antifungal treatment. Their use potentially exposes patients to unnecessary medication, given the limited evidence supporting topical antifungals in AD patients.⁶⁶

ACG supplementary guides

Supplementary guide on atopic dermatitis diagnosis criteria, severity assessment tools and mitigation strategies (Feb 2026) [PDF] 

Drug table on topical anti-inflammatories (Feb 2026) [PDF] 

Atopic dermatitis photo repository (Feb 2026) [PDF] 

Expert group

Chairpersons

Clin Assoc Prof Mark Koh Jean Aan, Dermatology (KKH)

Dr Michael Warren Lim, Family Medicine (NUP)

Members

Clin Assoc Prof Chan Poh Chong, Paediatrics (NUH)

Dr Roland Chu, Dermatology (Loke Skin Clinic)

Dr Goh Tze Chien Kelvin, Family Medicine (Northlink (Woodlands) Clinic)

Ms Helena Hor, Pharmacy (Watson’s Personal Care Stores Pte Ltd)

Ms Huang Xiaoling, Pharmacy (NSC)

Dr Mohana D/O Rajakulendran, Paediatrics (Petite Practice)

Adj Assoc Prof Nisha Su Yien Chandran, Dermatology (NUH)

Dr Suraj Kumar, Family Medicine (Drs Bain & Partners)

Dr Tan Hwee Mian Jane, Family Medicine (SHP)

Ms Wang Yu Yan, Nursing (NSC)

Dr Nelson Wee, Family Medicine (Silver Cross Medical)

Dr Yeap Youwen, Family Medicine (NHGP)

Dr Yew Yik Weng, Dermatology (NSC)

For more information on the Expert Group composition and other details, click here.

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Other related resources

Patient education aid – common questions on atopic dermatitis (Feb 2026) [PDF] 

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Suggested citation:

Ministry of Health, Singapore. 2026. Available from: go.gov.sg/acg-ad Agency for Care Effectiveness (ACE). Mild and moderate atopic dermatitis (eczema) – a journey from flare to care. ACE Clinical Guideline (ACG), Ministry of Health, Singapore. 2026. Available from: go.gov.sg/acg-ad

The Ministry of Health, Singapore disclaims any and all liability to any party for any direct, indirect, implied, punitive or other consequential damages arising directly or indirectly from any use of this ACG, which is provided as is, without warranties.