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Your wound is not my wound

Michel H.E. Hermans, M.D.

Hermans Consulting Inc.


Crucial to the definition of a wound, according to many encyclopedias* is a break in the continuity of any bodily tissue due to violence, where violence is understood to encompass any action of external agency, including, for example, surgery. In contrast, all these encyclopedias mention inflammation, a chronic nature and an internal factor in their definition of an ulcer. Interestingly enough, in the medical community virtually all skin lesions are now called wounds (diabetic, venous, pressure, surgical, fungating carcinoma etc.). They largely are divided in chronic wounds and acute wounds: a chronic wound is often defined as one that has been in existence for more than 3 weeks while an acute wound is younger. Surgical wounds are often mentioned as a separate category while, according to the definition below, they are simply an example of a trauma. If an ulcer is defined as a gradual disturbance of tissues by an underlying (and, thus, internal) etiology/pathology and a wound (trauma) as an acute disturbance of tissues by an external force, the required differences in medical approach and treatment options, appearance, demographics, anatomical locations, physiology and pathology are more logical

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Wounds (traumata) usually are treated to heal by primary intention: they are closed with sutures (cuts, surgical incisions), grafts (burns), or flaps (deep defects) or, in the case of superficial partial thickness burns, heal with support of dressings before granulation tissue develops. Surgical wound bed preparation is usually more rigorous: aggressive excision is more common than traditional debridement (with curette, scissors, enzymes). The use of modern dressings in burn care is not as common[11], while in ulcer care modern, non-surgical therapies are more frequently used (personal observation). Ulcers, even deep ones, usually are treated with a variety of dressings and heal by secondary intention. Ulcers also have a much poorer tendency to heal unless the underlying etiology is treated (i.e. off loading in diabetic foot ulcers[12] , compression or vein stripping in venous leg ulcers[13]). Skin grafting for ulcers is not very successful[14] when compared to wounds, while infection in grafted wounds is not as common as in grafted ulcers[15]. Pinch grafting generates even poorer results in ulcers and is not used in trauma care [16].


Ulcers can be changed into acute wounds by treating, and sometimes removing the underlying etiology (i.e. compression/saphenous vein ablation in venous leg ulcers). This, in itself may lead to significant changes in wound bed properties and healing tendencies[17]. Alternatively, the ulcer may be extensively debrided or excised into healthy tissue and may be closed primarily, with sutures (rare), a graft or flap. Conversion of a wound into an ulcer is not uncommon: a typical example would be a pretibial laceration in an elderly patient with diabetes or severe venous hypertension: the underlying etiologies turn a wound with good healing potential into an ulcer with poor healing tendencies. A Marjolin's ulcer (carcinomatous degeneration) of a (burn) scar is an example of a late term conversion.


Healing is a very complex process but, in principle, all wounds go through similar steps with similar cellular and humoral contributions. Reactive oxygen species (ROS), proteinases and many other soluble mediators and cells are crucial for dealing with necrosis, debris and microbial invasion. These compounds need careful regulation, since, by nature, they are aggressive and corrosive. "Normally", for every up-regulating mechanism, a down-regulating, counter acting mechanism exist. When regulation is not adequate, a situation of prolonged and persistent inflammation may occur: for example, in an ulcer, PMN's increase ROS production[1], thus inducing a vicious circle. An important category of "cleaning" compounds, normally not active in resting, non-damaged tissue, consists of the metalloproteinases (MMP's). MMP's can be produced by many different types of cells: they break down several components of the damaged extracellular matrix, which is a necessary step, prior to the influx of "healing" cells and compounds such as cytokines. MMP activity is counterbalanced by Tissue Inhibitors of Metalloproteinases (TIMP's). In an ulcer (as well as during the buildup of a hypertrophic scar) the balance between MMP activity (over expressed) and TIMP activity (relatively under expressed) is disturbed[2]: one of the consequences in an ulcer is inhibition of angiogenesis and continuous breakdown of the extracellular matrix[3]. Cytokine profiles in ulcers differ from those in acute wounds (trauma)[4, 5], and, in fact, they may be inadequate in ulcers, which is assumed to contribute to the poor healing tendencies by disrupting optimal signaling pathways[6]. These phenomena (and many others) confirm the chronically inflamed status of an ulcer[7] which, indeed, is caused by an underlying etiology/pathology.


The preferred outcomes of treatment are often different. While, of course, healing is the overall outcome, large trauma may be immediately life threatening: thus, the immediate and primary outcome in such a case is survival and prevention or treatment of shock, respiratory failure etc. Generally, ulcers are rarely acutely life threatening. Outcomes, in addition to healing, would be prevention of recurrence (i.e. through treatment of venous hypertension, surgical repair of a Charcot's foot). In burn care, after reepithelialization, prevention or treatment of hypertrophic scars, keloid and contracture formation is an important outcome as well. In contrast, because of the typical demography of patients with, especially, diabetic foot ulcers and venous leg ulcers, as well as their typical location, these sequelae are rare in these types of lesions.


Classification of skin lesions based on etiology, as opposed to age of the lesion, is more logical since the etiology/pathology based definition is more related to appearance, demographics, therapy (topical and/or systemic), outcomes etc. than the age of the lesion per se. There should be a bigger overlap in techniques used for ulcer care vs. trauma care. Many wounds could benefit from the expertise on modern dressings, built up in ulcer care, while many ulcers could benefit from a more surgical approach.

Influence of micro organisms

A biofilm is a protective polysaccharide matrix, produced by bacteria. Most, if not all ulcers develop a biofilm over time, while wounds (traumata) rarely develop a biofilm[8] unless they remain open for a prolonged period and, possibly, become an ulcer. Biofilms are considered to play a major role in (preventing) wound healing[9]: the presence of a biofilm, more than that of planktonic bacteria, may very well contribute to maintaining the chronic status of an ulcer[10].


Venous leg ulcers, diabetic foot ulcers and pressure ulcers have typical locations: for the latter, the buttocks, sacrum, hip, heels, scapulae and occiput are common locations indeed. In contrast, wounds (traumata) occur everywhere in the body. This may cause practical problems since wounds on the back (not uncommon in burns, for example) are more difficult to dress. Relative size plays a practical role as well: a relatively large venous leg ulcer may be 200 cm2, whereas that size trauma (i.e. burn) in an adult would represent about 3% total body surface area (TBSA). A burn is called medium size when it would be about 20% TBSA. This has implications for the amount of dressings, dressing techniques and dressing time involved. On the other hand, complex dressing techniques, such as the application of compression bandages, are generally not required in trauma care.

Periwound skin

Skin surrounding a trauma, at least initially, does not show the typical aspects of long lasting (hyper)inflammatory influences: normal, but not excessive signs of inflammation are present. Even a non-infected, full thickness burn that has not been excised for 3 weeks does not necessarily show signs of hyperinflammation or other serious problems at its edges. In contrast, the skin surrounding, for example, a venous leg ulcer, is often indurated, with signs of lipodermatosclerosis and hyperpigmentation and may show signs of allergic reactions due to the many allergenic compounds (i.e. lanoline in creams) to which the patient may have been exposed.


Trauma (superficial partial thickness burn: PBD 0) No signs of hyperinflammation or periwound inflammation

Ulcer (> 6 months in existence) Hyperinflammation, both in the lesion as well as surrounding it


1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. Wlaschek, M. and K. Scharffetter-Kochanek, Oxidative stress in chronic venous leg ulcers. Wound Repair Regen, 2005. 13(5): p. 452-61. Saarialho-Kere, U.K., et al., Cell-matrix interactions modulate interstitial collagenase expression by human keratinocytes actively involved in wound healing. J Clin Invest, 1993. 92(6): p. 2858-66. Ulrich, D., et al., Effect of chronic wound exudates and MMP-2/-9 inhibitor on angiogenesis in vitro. Plast Reconstr Surg, 2005. 116(2): p. 539-45. Tarnuzzer, R.W. and G.S. Schultz, Biochemical analysis of acute and chronic wound environments. Wound Repair Regen, 1996. 4(3): p. 321-5. Yager, D.R., et al., Wound fluids from human pressure ulcers contain elevated matrix metalloproteinase levels and activity compared to surgical wound fluids. J Invest Dermatol, 1996. 107(5): p. 743-8. Baker, E.A., et al., Temporal and quantitative profiles of growth factors and metalloproteinases in acute wound fluid after mastectomy. Wound Repair Regen, 2008. 16(1): p. 95-101. Loots, M.A., et al., Differences in cellular infiltrate and extracellular matrix of chronic diabetic and venous ulcers versus acute wounds. J Invest Dermatol, 1998. 111(5): p. 850-7. James, G.A., et al., Biofilms in chronic wounds. Wound Repair Regen, 2008. 16(1): p. 37-44. Percival, S.L., P. Bowler, and E.J. Woods, Assessing the effect of an antimicrobial wound dressing on biofilms. Wound Repair Regen, 2008. 16(1): p. 52-7. Bjarnsholt, T., et al., Why chronic wounds will not heal: a novel hypothesis. Wound Repair Regen, 2008. 16(1): p. 2-10. Hermans, M.H., Results of an internet survey on the treatment of partial thickness burns, full thickness burns, and donor sites. J Burn Care Res, 2007. 28(6): p. 835-47. Brem, H., et al., Wound-healing protocols for diabetic foot and pressure ulcers. Surg Technol Int, 2003. 11: p. 85-92. Kunimoto, B., et al., Best practices for the prevention and treatment of venous leg ulcers. Ostomy Wound Manage, 2001. 47(2): p. 34-46, 48-50. Turczynski, R. and E. Tarpila, Treatment of leg ulcers with split skin grafts: early and late results. Scand J Plast Reconstr Surg Hand Surg, 1999. 33(3): p. 301-5. Jewell, L., et al., Rate of healing in skin-grafted burn wounds. Plast Reconstr Surg, 2007. 120(2): p. 451-6. Ahnlide, I. and M. Bjellerup, Efficacy of pinch grafting in leg ulcers of different aetiologies. Acta Derm Venereol, 1997. 77(2): p. 144-5. Borges, E.L., M.H. Caliri, and V.J. Haas, Systematic review of topic treatment for venous ulcers. Rev Lat Am Enfermagem, 2007. 15(6): p. 1163-70.

Encyclopedia Brittanica, Merriam-Webster on line, Wikepedia, Robert (French), van Dale (Netherlands) Conditions such as TEN's do not really fit either the time based or etiology based definition. However, from a physiological point of view, TEN's would fit the acute wound definition, as would many infections with breach/breakdown of the epidermis. The same is true for conditions such as an incised abscess.


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