Contact Dermatitis
Clinical Snapshot
Contact dermatitis is an inflammatory skin reaction that develops after the skin comes into direct contact with an external substance, and contact dermatitis (irritant and allergic combined) accounts for 90-95% of all occupational skin disease.[1] Two genuinely different mechanisms produce it, and telling them apart changes the whole management plan. Irritant contact dermatitis (ICD) — roughly 80% of all contact dermatitis — is a non-immune, direct toxic effect: a chemical or physical agent damages the epidermis and breaks down its barrier function, with severity tracking the dose and duration of exposure rather than any individual susceptibility beyond an already-compromised barrier.[2] Allergic contact dermatitis (ACD) — the remaining 20% — is a delayed Type IV (T-cell-mediated) hypersensitivity reaction that only develops in a patient already sensitized to a specific allergen, most classically nickel, fragrances, and preservatives, and — for the single best-known example — the urushiol oil of poison ivy, oak, and sumac.[3][1]
Nickel is the single most common contact allergen worldwide and in patch-test clinics, positive in roughly 14-15% of patients tested for suspected allergic contact dermatitis, with a pronounced female predominance tied to jewelry and body-piercing exposure; population prevalence of nickel allergy runs approximately 8-19% in adults.[3][4] Fragrance mix, preservatives (balsam of Peru, formaldehyde-releasing agents), and topical antibiotics — notably neomycin — round out the next most frequent allergens.[3] Poison ivy, oak, and sumac exposure produces a reaction in more than 70% of exposed adults and remains the most common single cause of allergic contact dermatitis in North America.[3] In the workplace, wet work, detergents, and solvent exposure make irritant contact dermatitis by far the dominant occupational skin problem, disproportionately affecting healthcare workers, hairdressers, food-service and hospitality workers, cleaners, and construction and metal workers.[2][1] This chapter covers subtype recognition, when patch testing is genuinely needed, matching topical corticosteroid potency and formulation to body site and severity, when widespread or facial/genital disease needs a properly dosed oral corticosteroid course, and the red flags that move a patient beyond routine self-care.
Recognize the Condition
Irritant vs. allergic — how they actually look and feel different
The 2 mechanisms of contact dermatitis
Irritant contact dermatitis
Burning, stinging, or pain — not itch — is typically the dominant early symptom.[3] The skin shows erythema, dryness, scaling, and fissuring, developing either from a single strong chemical exposure or, more commonly, from cumulative milder exposure repeated many times a day — the classic case is dermatitis of the dorsal hands and finger web spaces in someone doing frequent handwashing or wet work.[2] Borders are typically well-demarcated and confined to the actual area of contact, without spread beyond it.[3]
Allergic contact dermatitis
Pruritus is the dominant and often intense symptom, not pain.[3] Acute lesions show erythema, edema, and often vesicles or bullae, sometimes weeping; repeated or chronic exposure instead produces lichenification, scaling, and fissuring.[3] Borders often follow the shape of the contactant, with distinct angles, lines, or streaks — a rectangular patch under a watch band, a band of dermatitis under a nickel-containing belt buckle or jean snap, or linear streaks where a poison ivy leaf brushed the skin — a pattern irritant dermatitis rarely produces.[3] Onset is delayed 24-72 hours after re-exposure in an already-sensitized patient (10-14 days for the first, sensitizing exposure) — this delay is exactly why patients so often fail to connect the rash to its actual cause.[3][1] The reaction can also spread beyond the area of direct contact through hand transfer (touching the allergen, then touching another body part) or, less commonly, a distant "id" (autoeczematization) reaction.[3]
Common Canadian-relevant allergens
Nickel remains the single most frequently identified allergen — found in inexpensive jewelry, watch backs, belt buckles, jean snaps and zippers, eyeglass frames, and some electronics and tools; an inexpensive spot test on a suspect item is a genuinely useful confirmatory step.[3][4] Fragrances (cosmetics, soaps, laundry products) and preservatives (formaldehyde-releasing preservatives, methylisothiazolinone, balsam of Peru) are the next most common non-occupational allergens.[3] Workplace-specific allergens tracked by Canadian occupational health authorities include chromates (cement, leather tanning), rubber accelerators and latex (medical and industrial gloves), epoxy resins (construction, manufacturing), and formaldehyde and other preservatives (healthcare, cosmetology, cleaning).[1]
Risk Factors
- Irritant contact dermatitis: frequent handwashing and wet work (healthcare, food service, cleaning, hairdressing, bartending), exposure to soaps, detergents, solvents, cutting oils, acids, and alkalis, low ambient humidity or cold weather (worsens barrier function), occlusive gloves worn for prolonged periods, and a personal history of atopic dermatitis, since an already-impaired skin barrier lowers the threshold for irritant damage.[2]
- Allergic contact dermatitis: requires prior sensitization to a specific allergen — most often nickel, fragrances, preservatives, rubber chemicals, or urushiol (poison ivy/oak/sumac); the initial sensitizing exposure itself causes no visible reaction, only later re-exposure does.[3][1]
- Female sex correlates specifically with nickel allergy, largely reflecting jewelry and ear/body-piercing exposure.[4]
- Occupational exposure: contact dermatitis (combined irritant and allergic) accounts for 90-95% of occupational skin disease; workers at highest risk include healthcare workers, hairdressers and beauticians, cleaners, construction workers, metalworkers and mechanics, agricultural workers, and food-service and hospitality workers.[2][1]
- Topical medicament exposure — neomycin (a highly sensitizing topical antibiotic) and, less commonly, the topical corticosteroid molecule itself — can each independently cause allergic contact dermatitis, sometimes from a product applied to treat a different dermatitis in the first place.[3]
- Outdoor or occupational exposure to poison ivy, oak, or sumac — landscaping, forestry, utility line work, firefighting, and agriculture carry particular risk.
Red Flags & Refer
Most contact dermatitis is appropriate for standard topical management, but escalate assessment and treatment for any of the following:
- Signs of secondary bacterial infection — increasing pain rather than the expected itch, spreading warmth and erythema beyond the original lesion, purulent drainage, or fever — need evaluation and treatment for infection, not simply a stronger topical corticosteroid; see the Bacterial Skin Infections chapter.
- Widespread involvement, generally described as more than about 20% of the body surface area, needs oral rather than only topical corticosteroid therapy.[3]
- Facial, periorbital, or genital involvement, especially with swelling — these sites are both functionally and cosmetically sensitive (eyelid swelling can threaten vision; genital swelling is intensely uncomfortable) and need prompt, more aggressive treatment; significant or progressing facial swelling also needs urgent assessment to exclude angioedema or an evolving airway threat.
- Classic, more extensive poison ivy/oak/sumac (rhus) dermatitis — this specific allergen is well known to need a full 2-3 week corticosteroid taper rather than a short course, since prematurely stopping therapy risks a severe rebound flare.[3]
- No improvement, or worsening, despite an adequate and adherent trial of appropriately potency-matched topical therapy — reconsider the diagnosis and pursue patch testing rather than simply switching to a stronger topical agent.
- Suspected occupational contact dermatitis persisting despite treatment — this needs a workplace exposure assessment and, often, occupational medicine or dermatology referral for patch testing and formal workplace accommodation, not an indefinitely repeated prescription.[2][1]
- Diagnostic uncertainty, or a symmetric/bilateral distribution that does not match any plausible contact pattern, suggesting an alternative diagnosis such as atopic dermatitis, psoriasis, or a fungal or bacterial process.
Assessment & Diagnosis
History
- Ask specifically and systematically about exposures — new personal-care products, jewelry, occupational chemicals, hobbies, recent outdoor activity, and any new topical medication — rather than only a general "have you touched anything new."
- Establish the timeline relative to exposure: irritant reactions can appear within hours of a single strong exposure or build gradually with repeated milder exposure, while allergic reactions in an already-sensitized patient typically appear 24-72 hours after re-exposure, often long enough that patients no longer connect the two.[3]
- Ask about occupation and specific job tasks, including glove use and hand-hygiene frequency.
Examination — distribution is the single most useful diagnostic clue
Look specifically for a distribution matching a plausible external contactant: a sharply demarcated patch confined to the actual area of contact (irritant), or a geometric pattern with distinct angles, lines, or streaks reflecting the shape of the allergen itself — a rectangular mark under a watch, a band under a waistband snap, or linear streaks from a brushing plant leaf (allergic).[3] A presentation that is instead symmetric and bilateral without any plausible external contact pattern should raise suspicion for an alternative diagnosis.
Differential diagnosis
| Condition | Features that point away from contact dermatitis |
|---|---|
| Atopic dermatitis | Symmetric, bilateral flexural distribution; personal or family history of atopy; chronic, relapsing course without a clear single trigger. |
| Psoriasis | Well-demarcated, thicker plaques with a silvery scale, often on extensor surfaces and the scalp; look for nail pitting or a family history. |
| Tinea corporis/manuum | Annular, centrally clearing lesions with an active scaling border; confirm with KOH microscopy if uncertain. |
| Scabies | Intense nocturnal pruritus, burrows, and involvement of finger web spaces, wrists, and genitals rather than a single contact-pattern site. |
| Cellulitis | Warmth, spreading margin, systemic symptoms (fever), and pain out of proportion to a simple dermatitis; needs urgent treatment, not a corticosteroid. |
| Seborrheic dermatitis | Greasy scale in the scalp, eyebrows, nasolabial folds, and central chest; chronic and relapsing, not tied to a specific exposure. |
Patch testing
Patch testing is the gold-standard confirmatory test for allergic contact dermatitis and should be pursued whenever the trigger is unclear, the reaction is recurrent or persistent despite reasonable avoidance efforts, or the case is occupational.[3] A standardized screening series (for example, a thin-film rapid-use series screening roughly 29-35 of the most common allergens) is applied to the back and left in place for 48 hours, then read at 48 hours and again at 72-96 hours — the delayed second reading matters, since some true-positive reactions are not yet apparent at the first reading and some irritant false-positives fade by the second.[3] Overall sensitivity and specificity for a standard screening series run around 70-80%; a screening panel does not include every possible allergen, so an occupational exposure or a persistent case with a negative screening panel may need a dermatologist's expanded, customized series.[3] Patch testing is expensive and time-consuming and requires the patient to keep the test area dry and avoid activities that would dislodge the patches, so reserve it for genuine diagnostic uncertainty rather than ordering it routinely for a classic, resolving presentation.[3]
Treatment Targets
- Correctly differentiate irritant from allergic contact dermatitis, since the underlying mechanism shapes both counselling and, in more severe cases, treatment intensity.
- Identify and eliminate the causative agent — treatment without identifying and removing the trigger predictably fails or simply recurs.
- Restore the skin's barrier function and control acute inflammation.
- Relieve pruritus (allergic contact dermatitis) or burning/discomfort (irritant contact dermatitis).
- Prevent secondary bacterial infection of excoriated or fissured skin.
- Match topical corticosteroid potency and formulation to the affected body site and severity, minimizing local and systemic side effects.
- Recognize and appropriately escalate widespread, facial, genital, or classic rhus (poison ivy/oak/sumac) dermatitis to a full, correctly tapered oral corticosteroid course rather than under-treating with topical therapy alone.
- Counsel on trigger avoidance and protective measures to prevent recurrence — the single most effective long-term intervention for either type.
Choose Initial Treatment
Step 1 — match topical corticosteroid potency to body site and severity
For localized mild-to-moderate disease of either type, once the trigger has been identified and avoidance counselled (see Non-Pharmacologic Management), a topical corticosteroid selected by potency and body site is first-line.[3][5] Canadian topical corticosteroid potency is conventionally graded into 7 groups (Group 1 = ultra-high potency, Group 7 = lowest potency); the practical rule is to use the lowest potency that will control the condition.[5]
Face, eyelids, groin, axillae, and other skin-fold/flexural sites a low-potency agent (Group 6-7, e.g., hydrocortisone 1-2.5%) — these sites absorb topical corticosteroid disproportionately well, so a higher-potency agent here meaningfully raises the risk of atrophy, striae, and telangiectasia.[5][3]
Trunk and extremities, moderate disease a mid-potency agent (Group 3-5, e.g., triamcinolone acetonide 0.1%) applied twice daily.[5]
Thicker or more resistant plaques on the trunk/limbs a high-potency agent (Group 2, e.g., betamethasone dipropionate 0.05%) — reserve for genuinely resistant disease rather than a routine first choice.[5]
Palms, soles, or severe localized disease an ultra-high-potency agent (Group 1, e.g., clobetasol propionate 0.05%) — limit to a maximum of about 50 g/week and no more than 2 weeks of continuous use given the higher atrophy risk and rare HPA-axis suppression, and avoid occlusive dressings at this potency.[5]
Ointments are generally preferred for dry, fissured, or lichenified skin given their occlusive, more potent delivery; lotions are the least occlusive formulation and are most useful for acute, oozing, or flexural involvement — a genuinely good fit for acute contact dermatitis specifically.[5] "Apply sparingly" means just enough to cover the affected area, not so little that the patient under-doses out of an exaggerated fear of the medication — assess for simple nonadherence before concluding a first topical agent has actually failed.[5]
Step 2 — pruritus control
An oral antihistamine can improve comfort and sleep, but the itch of allergic contact dermatitis is a T-cell-mediated, not histamine-mediated, process — antihistamines are an adjunct for symptom relief, not a substitute for identifying the trigger and using an appropriately potent topical corticosteroid.[3] A non-sedating agent (cetirizine, loratadine, fexofenadine) during the day and a sedating agent (diphenhydramine, hydroxyzine) at bedtime specifically when itching is disrupting sleep are both reasonable choices.
Step 3 — when to use oral (systemic) corticosteroid therapy
Widespread disease (more than about 20% of body surface area), significant facial or genital involvement, or a classic, extensive rhus (poison ivy/oak/sumac) reaction a short course of oral prednisone: 0.5-1 mg/kg/day for 5-7 days, then reduce the dose by about half for a further 5-7 days.[3] For severe rhus dermatitis specifically, taper more gradually over 2-3 weeks rather than stopping abruptly — a shorter course risks a genuine rebound flare that can be worse than the original reaction.[3] Do not use a standard prepackaged oral corticosteroid "dose pack" (for example, a 6-day methylprednisolone pack) for this indication — the dose and duration are both too low, and stopping this abruptly is a well-recognized cause of rebound dermatitis.[3]
Step 4 — treat secondary bacterial infection if present
A macerated, weeping, or frankly infected area — especially where fissuring or excoriation has broken the skin barrier — needs an appropriate oral or topical antibiotic directed at the bacterial component, in addition to continued dermatitis management; see the Bacterial Skin Infections chapter for specific antibiotic selection.
Occupational contact dermatitis
Beyond acute treatment, occupational contact dermatitis needs workplace-level counselling: substitution of the causative product where feasible, engineering controls, correct glove selection (cotton liners under occlusive gloves for wet work; nitrile rather than latex gloves if a rubber-accelerator or latex allergy is suspected), and, for cases that persist despite these measures, referral for formal workplace assessment and, where appropriate, a workers' compensation claim.[2][1]
Non-Pharmacologic Treatment
- Identify and avoid the causative agent — the single most effective intervention for either type, and the only one that reliably prevents recurrence.
- For known or suspected wet-work/detergent irritant exposure: minimize handwashing frequency to what is genuinely necessary, use lukewarm rather than hot water, pat rather than rub dry, and apply a fragrance-free emollient immediately after each washing or wet exposure to help restore the barrier.[2]
- Wear appropriate gloves for wet work or chemical handling — cotton liners under occlusive rubber or vinyl gloves reduce sweat-related irritation with prolonged wear; choose nitrile rather than latex gloves if a rubber-accelerator or latex allergy is a concern.[2][1]
- Apply cool compresses or a cool soak — for example, an aluminum acetate (Burow's solution) soak — to acute, oozing, or vesicular lesions; this is soothing, astringent, and helps dry weeping skin.
- Use a mild, fragrance-free cleanser rather than harsh soap on affected skin, and apply a fragrance-free emollient routinely to support barrier repair, even between flares.
- After known poison ivy/oak/sumac exposure, wash the skin as soon as possible and launder any clothing, tools, or gear that contacted the plant — urushiol residue can persist on surfaces, including pet fur, for a long time and cause further reactions on re-contact.[3]
- For confirmed or suspected nickel allergy: choose stainless-steel, titanium, or surgical-grade jewelry, use an inexpensive nickel spot-test kit to screen suspect items, and consider a nickel-binding topical barrier product on unavoidable contact surfaces such as a belt buckle.[3][4]
- Discourage scratching — it both worsens irritant damage and raises the risk of secondary bacterial infection; trimming nails short and using cool compresses for itch control are practical, low-cost adjuncts.
Special Populations
Pregnancy
Low-to-mid potency topical corticosteroids are preferred and considered compatible in pregnancy given minimal systemic absorption at recommended use; reserve high- and ultra-high-potency agents, and large-surface-area or prolonged use of any potency, for genuine need. Non-sedating oral antihistamines (loratadine, cetirizine) are generally preferred if an oral agent is needed. A short course of oral prednisone is reasonable for severe, widespread disease when the benefit outweighs the risk — this decision should be made with the prescriber rather than deferred by default.
Breastfeeding
Topical corticosteroids at any potency are compatible with breastfeeding; if applying near the breast or nipple, wash the area before the next feed. Non-sedating oral antihistamines are preferred over sedating agents. A short oral prednisone course is also compatible with breastfeeding.
Pediatrics
Children have a higher body-surface-area-to-weight ratio and thinner skin than adults, increasing systemic absorption risk from topical corticosteroids — favour the lowest effective potency and the shortest effective course, and avoid ultra-high-potency agents where possible. Dose antihistamines by weight per the current product monograph. Nickel-related allergic contact dermatitis is common in children, most often from snaps, jewelry, and ear piercings.
Older adults
Skin thins with age, increasing both topical corticosteroid absorption and the visible impact of atrophy and purpura — use the lowest effective potency and monitor closely. Avoid sedating 1st-generation antihistamines (diphenhydramine, hydroxyzine) where possible given anticholinergic burden and fall risk; a non-sedating agent is preferred.
Darker skin tones
Postinflammatory hyperpigmentation is common after either type of contact dermatitis and can persist for months after the dermatitis itself resolves — counsel on this expected course so it is not mistaken for treatment failure. Potent topical corticosteroids also carry a real risk of hypopigmentation, which is more visible in darker skin.
Occupational contact dermatitis
Workers in wet-work, healthcare, hairdressing, food-service, construction, and metalworking roles carry the highest occupational risk. Management includes the workplace measures described in Choose Initial Treatment, plus, for cases that persist despite these measures, referral for a formal workplace assessment.[2][1]
Monitoring & Follow-Up
Reassess within 1-2 weeks of starting topical therapy to confirm both improvement and adherence — before concluding a first topical agent has failed, confirm it was actually used as directed and that the causative agent was truly identified and avoided, since continued unrecognized exposure is the single most common reason a technically correct plan appears to fail. Set realistic expectations: irritant contact dermatitis can take several weeks to fully normalize even after the irritant is removed, given how long full barrier repair actually takes, while allergic contact dermatitis pruritus and inflammation typically resolve within about 1-3 weeks of appropriate treatment and trigger avoidance. Counsel that postinflammatory hyperpigmentation, particularly in darker skin, is an expected part of resolution that gradually fades rather than a sign the treatment failed.
Common Errors to Avoid
- Using a high- or ultra-high-potency topical corticosteroid on the face, eyelids, or skin folds — these sites absorb medication readily, and this combination meaningfully raises the risk of atrophy, striae, and telangiectasia.
- Prescribing a standard prepackaged oral corticosteroid "dose pack" for widespread or severe rhus (poison ivy/oak/sumac) dermatitis — the dose and duration are both inadequate, and abrupt discontinuation risks a genuine rebound flare.
- Treating the rash without ever identifying or addressing the actual trigger — recurrence is essentially guaranteed if the causative exposure continues.
- Assuming an oral antihistamine alone adequately controls allergic contact dermatitis — the underlying process is T-cell-, not histamine-, mediated, so antihistamines help comfort and sleep but do not substitute for an appropriately potent topical corticosteroid.
- Reaching for a combination topical antibiotic-corticosteroid product, particularly one containing neomycin, as a default — neomycin is highly sensitizing and can itself cause allergic contact dermatitis, sometimes from the very product meant to treat it.[5]
- Missing early secondary bacterial infection and continuing to treat spreading warmth, increasing pain, or purulent drainage as "just a flare."
- Using an occlusive dressing with an ultra-high-potency topical corticosteroid without specific indication — occlusion can increase absorption up to 10-fold and meaningfully raises systemic exposure.[5]
- Overlooking an occupational contributor and not counselling on workplace modification, glove selection, or referral — treating the flare without addressing an ongoing occupational exposure invites recurrence.
- Ordering patch testing routinely for every classic, resolving presentation rather than reserving it for genuine diagnostic uncertainty, recurrence, or an occupational case.
Clinical Decision Algorithm
Drug Tables
How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.
Topical Corticosteroids, by Potency
Use the lowest potency that controls the condition; match potency to body site (low potency for face/eyelids/flexures, higher potency for palms/soles/resistant plaques). Ointments suit dry/fissured/lichenified skin; lotions suit acute, oozing, or flexural disease.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Hydrocortisone 1-2.5%, topical | Dosing: Apply BID-TID | Local burning/stinging; atrophy uncommon at this potency | None clinically significant given minimal systemic absorption | Low potency (Group 6-7). 1st-line agent for the face, eyelids, groin, axillae, and other flexural/skin-fold sites. |
| Desonide, topical 0.05% | Dosing: Apply BID | Local burning/stinging; atrophy and striae uncommon at this potency | None clinically significant given minimal systemic absorption | Low-mid potency. A reasonable alternative to hydrocortisone for sensitive sites, including in young children. |
| Triamcinolone acetonide 0.1%, topical | Dosing: Apply BID | Striae, telangiectasia, atrophy, purpura with prolonged use | None clinically significant given minimal systemic absorption | Mid potency (Group 3-5). Reasonable default for non-facial, non-flexural localized disease on the trunk or limbs. |
| Betamethasone dipropionate 0.05%, topical | Dosing: Apply BID | Striae, telangiectasia, atrophy, purpura; HPA-axis suppression with extensive/prolonged use | None clinically significant at recommended topical doses | High potency (Group 2). Resistant or thicker plaques on the trunk/limbs only — not for the face or skin folds. |
| Clobetasol propionate 0.05%, topical | Dosing: Apply once or twice daily, maximum 2 weeks | Skin atrophy, striae, telangiectasia; systemic absorption possible with extensive-area or occlusive use | None clinically significant with topical use at recommended doses | Ultra-high potency (Group 1). Palms, soles, or severe localized disease; limit to about 50 g/week and 2 weeks continuous use, and avoid occlusion. |
Oral Antihistamines — Pruritus Adjunct
Symptom relief only; the itch of allergic contact dermatitis is T-cell-, not histamine-, mediated, so an antihistamine does not substitute for an appropriately potent topical corticosteroid and trigger avoidance.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Cetirizine | Adults: 10 mg PO once daily | Mild sedation (dose-related), headache, dry mouth | Additive CNS depression with alcohol or other sedatives | Non-sedating; a metabolite of hydroxyzine — avoid in patients with hydroxyzine hypersensitivity. |
| Loratadine | Adults: 10 mg PO once daily | Headache, fatigue, dry mouth | Clearance decreased in severe hepatic impairment — use a lower initial dose | Non-sedating alternative to cetirizine; also a reasonable choice in pregnancy and breastfeeding. |
| Fexofenadine | Adults: 60 mg PO BID, or 180 mg PO once daily | Headache, nausea | Aluminum- or magnesium-containing antacids and fruit juices can decrease bioavailability | Non-sedating; renal impairment increases the risk of CNS accumulation. |
| Diphenhydramine | Adults: 25-50 mg PO at bedtime PRN | Sedation, anticholinergic effects, next-day grogginess | Additive CNS depression with alcohol/sedatives; may increase levels of some CYP2D6 substrates | Reserve for bedtime use when itching disrupts sleep; use caution in older adults given anticholinergic burden and fall risk. |
| Hydroxyzine | Adults: 25-50 mg PO at bedtime PRN | Sedation, dry mouth, blurred vision, dizziness | Additive CNS depression with alcohol, opioids, or other sedatives | Alternative sedating agent to diphenhydramine; same bedtime-only rationale and older-adult caution. |
Oral Corticosteroid — Widespread or Severe Disease
Reserve for widespread disease (over about 20% body surface area), significant facial/genital involvement, or a classic, extensive rhus (poison ivy/oak/sumac) reaction. Never substitute a prepackaged short "steroid dose pack" — the dose and duration are both inadequate for this indication.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Prednisone, oral | Standard course: 0.5-1 mg/kg/day PO for 5-7 days, then reduce by about half for a further 5-7 days Severe rhus dermatitis: Taper gradually over 2-3 weeks rather than stopping abruptly | Insomnia, mood changes, increased appetite, hyperglycemia; adrenal suppression and rebound dermatitis with an inadequate course | Numerous — review the full interaction profile even for a short course | No plain oral prednisone tablet monograph currently exists in the Pharmasist Drug Database; named as text only. |
Topical Adjuncts (Non-Corticosteroid)
Symptomatic and barrier-supportive measures used alongside, not instead of, an appropriately potent topical corticosteroid when one is indicated.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Calamine lotion | Dosing: Apply to affected areas as needed | Local dryness | None significant | Widely available OTC option with a long safety record for mild pruritus; no Pharmasist Drug Database monograph exists for this product. |
| Aluminum acetate solution (Burow's solution) | Dosing: Dilute per product directions; soak or compress 15-30 minutes, 2-3 times daily | Local dryness with overuse | None significant | Astringent cool-soak solution for acute, oozing, or vesicular lesions; no Pharmasist Drug Database monograph exists for this product. |
Secondary Bacterial Infection
Reserve for genuine signs of secondary infection — spreading warmth/erythema, purulent drainage, or fever — not routine dermatitis; see the Bacterial Skin Infections chapter for full antibiotic selection.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Cephalexin | Adults: 250-500 mg PO QID Children: Weight-based pediatric dosing per the current product monograph | GI upset, hypersensitivity reactions | May increase INR with warfarin | Reasonable oral option for uncomplicated secondary bacterial infection of excoriated or fissured skin. |
References
- Dermatitis, Allergic Contact — Canadian Centre for Occupational Health and Safety, OSH Answers. CCOHS OSH Answers
- Dermatitis, Irritant Contact — Canadian Centre for Occupational Health and Safety, OSH Answers. CCOHS OSH Answers
- Diagnosis and Management of Contact Dermatitis — American Family Physician (Usatine RP, Riojas M). Am Fam Physician 2010;82(3):249-255
- Nickel allergy and allergic contact dermatitis: A clinical review of immunology, epidemiology, exposure, and treatment — Contact Dermatitis (Ahlström MG, Thyssen JP, Wennervaldt M, Menné T, Johansen JD). Contact Dermatitis 2019;81(4):227-241
- Topical Corticosteroids — RxFiles, Community Drug Utilization Program (Regier L, Downey S). RxFiles, May 1998
Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.