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Choosing the right dressing for optimal wound healing

Sylvie Hampton
BSc (Hons) DpSN RGN
Independent Tissue Viability Consultant

The art of wound healing is developed through experience, and science must be found in education. Bryant wrote: "Nursing interventions can either enhance or delay wound healing; thus nurses must be knowledgeable regarding the wound-healing process and the implications for wound management."(1) It is the responsibility of the practitioner to learn and understand the processes that lead to healing and to use that knowledge and skill when selecting a dressing.
However, not all nurses have followed developments in wound care, and the overwhelming variety of dressing choices can add to confusion. Research has found a gap between theory and practice with a lack of sound indepth knowledge among nurses.(2) Practice is often based on tradition. Nurses frequently have problems selecting appropriate care because of the resistance of colleagues to change.(3) The advent of clinical governance dictates that patient care is based on clinical evidence, so professionals can no longer select wound dressings by personal ­preference, nor let the relationship between suppliers and  purchasers influence the purchase of dressings.(4)
This article investigates the application of dressings in different phases of wound healing and in pressure ulcers, and provides a basic description of healing and suggestions for dressing choice.

The acute wound

Phase 1
The acute wound is caused by accidental or planned (surgery) trauma. Immediately the clotting cascade stimulates the release of histamine from mast cells, which results in vasodilation and increased capillary permeability. This phase of inflammation occurs in response to injury of vascularised tissues; its purpose is to deliver defensive materials (blood cells and fluid) to the site of injury. The inflammatory phase will lead first to vasoconstriction to prevent blood loss, and then vasodilation to facilitate the delivery of oxygen and defence materials to the wound.(5) Macrophages and polymorphonuclear leucocytes are "workhorses" and in the first 24 hours are attracted to the injured site where they lyse clots and debris, destroy and remove bacteria, and allow fluid-filled cavities to form into which fibroblasts and endothelial cells can grow. Macrophages continue to play an important part in wound healing, producing a number of growth factors that have an important role.
An acute wound needs protection from the external environment to prevent pathogenic bacteria entering the vulnerable wound surface. The dressing should provide an ideal environment (Table 1). The best dressing for most acute wounds is a hydrocolloid or film dressing.


Phase 2
The next stage is the destructive phase, which can last up to seven days, when polymorphs and macrophages cause phagocytosis - destruction of bacteria and removal of dead cells. Macrophages stimulate the release of fibro­blasts and a factor that stimulates angiogenesis (production of new blood vessels) within the wound. During this phase there is likely to be excessive exudate and possibly malodour. The colour of the exudate and the peculiarities of the malodour depend on the type of bacteria.
At this stage the wound may become chronic. Research has shown that chronic wound exudate can delay healing by inhibiting the growth of fibroblasts.(6) The presence of microbial antigens perpetuates the inflammatory process, so that the mechanism which should promote wound repair becomes detrimental and leads to further tissue damage.(7) The cycle of wound healing is interrupted, inflammation subsides, macrophages decrease in number and growth factors decline, leading to a reduction or halt in the healing process. The dressing requirements are different in this phase (Table 2).






Phases 3 and 4

These two stages of wound healing require little ­assistance from dressings. Phase 3 involves proliferation, when a collagen matrix is laid down and ­angiogenesis is rapid and apparent as red loops in the base of the wound. The healing status of the wound can be interrupted by inappropriate selection of ­dressings that cause trauma to the wound bed, or by the introduction of pathogenic bacteria.

Necrotic wounds
Up to this point necrosis has not been addressed as the wound is often acute (generally owing to sustained ­pressure), but cannot always act as an acute wound because the cause of the ulcer remains a problem. Necrotic tissue must be removed for the wound to heal. Before application of any dressing the pressure must be removed by the provision of an air mattress. Once on the mattress there are several dressing choices (Table 3).



Necrotic 'dry' gangrene toes (Figure 6) should be left dry. Any attempt to moisten them could lead to clinical infection. When left to mummify, they will eventually demarcate quite naturally. 'Wet' gangrene should be well protected and surgical opinion sought.


Clinical infection and colonisation
Dressings are pointless in a wound that is clinically infected. Clinical infection is defined by cellulitis, pyrexia, the patient feeling unwell, an increased ­malodour and possibly increased pain. Systemic anti-biotics should be considered. Dressing selection is almost immaterial unless the infection is corrected.
Colonisation is where the wound contains exudate with a colony of bacteria. The bacteria are likely to proliferate, causing malodour and an increased exudate production, but are unlikely to affect the clinical status of the host as they sit on the wound bed, not in the tissues.

Dressing selection can be easily achieved if the rule of providing an optimum wound-healing environment is obeyed. To become skilled in wound healing, the ­practitioner requires an understanding of the wound-healing process that is supported by experience. Selection should be based on a sound rationale.



  1. Bryant R. Acute and chronic wounds: nursing management. Missouri: Mosby; 1992.
  2. O'Connor H. Bridging the gap? Nursing Times 1993;89(Suppl. 32):2-5.
  3. Flanagan M. Variables influencing nurses' selection of wound dressings.J Wound Care 1992;1(1):33-43.
  4. Rainey J. It's all in the sales pitch. Nursing Times 1996;92(Suppl. 39):71-3.
  5. Majno G, Joris I. Cells, tissues and disease: principles of general pathology. Oxford: Blackwell Science; 1996.
  6. Phillips TJ, Al-Amoudi HO, Leverkus M, Park HY. Effect of chronic wound fluid on fibroblasts. J Wound Care 1998;7(10):527-32.
  7. Thompson P. The microbiology of wounds. J Wound Care 1998;7(9):477-8.
  8. Lock P. The effects of temperature on mitotic activities at the edge of experimental wounds. Proceedings of Symposium on Wound Healing, Finland. Kent: Lock Laboratories Research; 1979.
  9. Winter GD. Formation of the scab and rate of epithelialisation of ­superficial wounds in the skin of a young domestic pig. Nature 1962;193:293-9.

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