1 CPD credit: Skin reactions to wound dressings

Careful selection of dressings and topical agents can help to prevent allergic reactions. By Professor Richard White


There is a high incidence of allergic contact dermatitis (ACD) in patients with leg ulcers, who may develop skin reactions to wound dressings and topical agents. Preventing ACD in these patients is a priority, to minimise its impact on their quality of life and on treatment costs.

A range of medical products have been implicated, including  commonly used antimicrobials and antiseptics, and dressing components, such as adhesives. 

Standard treatment of ACD is avoidance or removal of the allergen. Emollients and soap substitutes can aid in repairing the skin barrier. Oral antihistamines are useful for pruritus.

Key words 

Allergic contact dermatitis, dressings, leg ulcers, wound care

1 CPD CREDIT For more dermatology CPD go to mimslearning.co.uk/dermatology

Patients with leg ulcers, in particular venous ulcer, exhibit a high incidence of skin reactions to topically applied agents, such as wound dressings and emollients. 

Many of these reactions are sensitisation or ACD. The impact of such reactions includes delayed healing and a consequent increase in treatment costs, as well as reduced quality of life. 

Preventing such reactions should be of concern when selecting a treatment. It is important to be aware of the potential for ACD, and to identify and avoid the use of those dressings and other topical agents known to provoke such reactions.  


The skin surrounding chronic wounds is generally subject to varying degrees of traumatic insult, such as the application and removal of wound dressings/tapes or cleansing procedures. 

This makes the care of peri-wound skin challenging. In patients with venous leg ulcers, changes in the local circulation, in conjunction with venous hypertension, can lead to the development of conditions such as lipodermatosclerosis, atrophie blanche, hyperpigmentation, dryness and scaling. 

Patients with leg ulcers are particularly liable to develop ACD, owing to frequent contact with a variety of topical chemicals, for example, topical steroids/antibiotics, emulsifiers and adhesives applied over a prolonged period of time. 

In addition, it has been postulated that the immune system may be activated early in venous disease by interleukin-1 and -6. The role of IL-1 in Langerhans cell antigen presentation also has an important function in ACD in venous leg ulcer. 

Venous eczema compromises the barrier function of the skin and permits absorption of allergens, resulting in acute sensitisation. Studies have shown that 50-81% of patients with leg ulcers tested for ACD have venous eczema. 

ACD occurs in 1.4-5.4% of the general population and up to 30% of chronic wound patients.1 This is supported by patch
test data showing that 63% and 52% of patients with leg ulcers had reactions to one or multiple allergens, respectively.2 The incidence of skin sensitisation in Asian patients with venous leg ulcers showed ACD to be 61.4%.3  

A variety of medical products have been implicated, including latex, nickel, lanolin, emulsifying agents, balsam of Peru and fragrances. The antimicriobial compounds used in wound preparations and dressings can also cause sensitisation reactions, for example, neomycin sulfate, chloramphenicol, bacitracin and cetrimide cream. 

Commonly used antiseptics, such as silver nitrate, silver sulfadiazine, iodine and triclosan, all have sensitising potential. In addition, reactions to wound dressings or their components (for example, adhesives) are common.4-7 


Contact urticaria syndrome, a type 1 immediate hypersensitivity reaction (in this case to carboxymethylcellulose in a dressing) has been reported,8,9 as well as ACD from a hydrogel dressing.10 

In one case, a patient with recurrent leg ulcers developed severe eczematous lesions of the skin surrounding an ulcer after the use of a protease-modulating matrix; the sensitising agent was regenerated oxidised cellulose.11

When patch tested, patients reacting to hydrocolloid dressings displayed positive to colophony and to DuoDERM E or DuoDERM CGF. It was concluded that pentaerythritol ester of hydrogenated rosin (used as a tackifying agent) retained the sensitising potential of colophony.12 

In a study looking at frequency of contact sensitivities in patients with chronic wounds, 55.5% exhibited contact sensitisation to at least one substance.13 

The most frequent reactions were to PVP-iodine (20%), balsam of Peru (15.6%), fragrance mix (11.1%), colophony (8.8%) and potassium dichromate (6.7%). 

Sensitisation to the Varihesive hydrocolloid of the dressings (also known as DuoDERM and Granuflex 11.1%), Iruxol N (6.7%) and Comfeel hydrocolloid (2.2%) was identified. 

Patients with recalcitrant ulcers showed a higher number of epicutaneous sensitisations to wound dressings than those with ulcers of shorter duration. It is also noteworthy that hydrocolloid dressings and dressings with acrylate adhesive caused severe allergic reactions not seen with soft silicone dressings. 


The clinical presentation of ACD in conjunction with venous leg ulceration is often confusing. The venous disease often presents with fibrotic changes in the skin, such as lipodermatosclerosis. Poorly controlled exudate frequently leads to excoriation of the skin around the ulcer. Infections, such as erysipelas and especially cellulitis, must be excluded. 

Figures 1-3 illustrate typical ACD reactions. The cutaneous eruption shows erythema, swelling, papules and vesicles in the affected area. Lesions can spread well beyond the area exposed to the allergen. 

Figure 1: Reaction to antibacterial dressing, showing vesicles (Image: Professor RIchard White)

Figure 2: Skin stripping after reaction to dressing adhesive (Image: Professor Richard White)

Figure 3: Marked erythema and vesiculation rules out reaction to exudate. Ulcer shows slough and Pseudomonas infection (Image: Professor Richard White)

Patch testing is the gold standard method for the diagnosis of ACD14 and has generally been used to identify components of wound care treatment (for example, emollients, dressings) that might have allergens responsible for skin sensitisation reactions. 

A commercially available ‘leg ulcer series’ of known allergens is available for this investigation. It has been suggested that testing high-risk patients should be a prerequisite for choosing appropriate dressings that will not cause sensitisation reactions. Alternatively, steering away from choosing dressings and treatments that have already been shown to be potential sensitisers (such as hydrocolloid dressings) would appear to be a more logical approach.


Standard treatment of ACD is simply avoidance or removal of the allergen. Appropriate emollients and soap substitutes may then be used to aid in repairing the skin barrier. Oral antihistamines are useful for the treatment of pruritus. 

Moderate ACD responds to topical corticosteroids used in the lowest concentration and potency that produces a beneficial effect. Severe ACD may require treatment with systemic corticosteroids or other immunosuppressive agents, although evidence supporting their use is limited.

The continuing high prevalence of sensitisation to topical agents in leg ulcer patients suggests that currently, not enough is being done to avoid the problem. 

  • Professor Richard White is professor of tissue viability, Institute for Health, University of Worcester

Competing interests: None declared


1. Stone N, Powell S. Do topical medicaments cause more harm than good? Dermatol Pract 2000; 8(3): 20-3.

2. Saap L, Fahim S, Arsenault E et al. Contact sensitivity in patients with leg ulcerations: a North American study. Arch Dermatol 2004; 140(10): 1241–6.

3. Lim KS, Tang MB, Goon AT et al. Contact sensitization in patients with chronic venous leg ulcers in Singapore. Contact Dermatitis 2007; 56: 94–8.

4. Mallon E, Powell SM. Allergic contact dermatitis from Granuflex hydrocolloid dressing. Contact Dermatitis 1994; 30(2): 110-11.

5. Cameron J, Powell S. Contact dermatitis: its importance in leg ulcer patients. Wound Management 1992; 2(3): 12-13.

6. Sasseville D, Tennstedt D, Lachapelle JM. Allergic contact dermatitis from hydrocolloid dressings. Am J Contact Dermat 1997; 8(4): 236-8.

7. Siegel DM. Contact sensitivity and recalcitrant wounds. Ostomy Wound Manage 2000; 46(1A Suppl): 65S-74S.

8. Johnsson M, Fiskerstrand EJ. Contact urticaria syndrome due to carboxymethylcellulose in a hydrocolloid dressing. Contact Dermatitis 1999; 41(6): 344-5. 

9. Pasche-Koo F, Piletta-Zanin P, Politta-Sanchez S et al. Allergic contact dermatitis to carboxymethylcellulose in Comfeel hydrocolloid dressing. Contact Dermatitis 2008; 58(6): 375-6. 

10. Lee JE, Kim SC. Allergic contact dermatitis from a hydrogel dressing (Intrasite Gel) in a patient with scleroderma. Contact Dermatitis 2004: 50: 376–7. 

11. Wounds International. Using Promogran/Promogran Prisma on wounds with elevated protease activity: case studies

12. Suhng EA, Byun JY, Choi YW et al. A case of allergic contact dermatitis due to DuoDERM Extrathin. Ann Dermatol 2011; 23(Suppl 3): S387–9.

13. Waring M, Bielfeldt S, Springmann G et al. An instant tack wound dressing designed to reduce skin stripping. Wounds UK 2012; 8(2): 60-7.

14. Nelson JL, Mowad CM. Allergic contact dermatitis: patch testing beyond the TRUE test. J Clin Aesthet Dermatol 2010; 3(10): 36-41. 

These further action points allow you to earn more credits by increasing the time spent and the impact achieved
Audit your patients who are undergoing active woundcare to determine the incidence of ACD
Produce a protocol for prescribing wound dressings in patients with ACD 
Hold a clinical meeting with prescribers to discuss rational prescribing in patients with ACD
Save notes on this article with your free online CPD organiser 

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