Abstract:   Currently, most skin lesions are called wounds and primarily are divided into acute and chronic, the difference being the time period during which they have been in existence and/or their tendency to heal properly or not. Etiology is not taken into account when applying the definitions of chronic versus acute. The traditional definition of wounds and ulcers was based primarily on etiology, where a wound (now called an acute or surgical wound) was said to be caused by violence (eg, an outside force such as a bullet, a surgical incision) and an ulcer, presently called a chronic “wound,” was defined as being caused by some kind of internal etiology (eg, venous hypertension with its secondary consequences to skin integrity). Based on the differences in etiology and physiology, morbidity and mortality, therapeutic options and requirements, and other aspects of different types of skin lesions, this author proposes to reinstitute the “old” nomenclature.   The traditional, non-medical 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 by an external agent.”1–3 The same encyclopedias mention inflammation, a gradual occurrence and/or chronic nature, and an internal factor in their definitions of an ulcer.   However, in the medical community virtually all skin lesions now are called wounds (diabetic, venous, pressure, surgical, fungating carcinoma, traumatic, etc.). Generally, the term wound is not used in relation to the injuring mechanism anymore. Whether the primary tissue breakdown is internal or caused by an external force is not taken into account either, nor are other physiological aspects. A chronic wound is defined as one that has been in existence for more than 3 weeks or that has failed to proceed through an orderly and timely process to produce anatomic and functional integrity or proceed through the repair process without establishing a sustained and functional result.4   If an ulcer is defined as a gradual disturbance of tissues by an underlying (and thus internal) etiology/pathology and a wound (as in trauma) as an acute disturbance of tissues by an external force, the observed differences in appearance, demographics, anatomical locations, physiology and pathology, as well as the required medical interventions, possible medical options and outcomes become a great deal more logical. For the purposes of this commentary, a chronic lesion will be referred to as an “ulcer,” while the term “wound” will refer to trauma.


  Trauma is derived from the Greek word meaning “wound.” As mentioned, trauma is caused by an external force, whether accidental or by choice (an operation) and whether by physical contact or, for example, certain types of radiation (a thermal injury). According to the “traditional” medical and encyclopedia definition, an ulcer is caused by an internal etiology. A venous leg ulcer is the consequence of venous stasis, which leads to physiological and anatomical changes: the skin lesions are secondary to these changes. Similar principles lie behind the development of diabetic foot ulcers and pressure ulcers. Along the same lines, a radiation “burn,” as opposed to a thermal injury, is not really a burn and, thus not a wound but an ulcer: ionizing radiation to treat malignancies is very powerful, and depending on the type of radiation, penetrates deep into the tissue. Often direct primary damage is caused to the vascular structures,5 which leads to secondary tissue damage, including skin breakdown.


  Healing is a complex process but, in principle, all lesions go through similar steps: hemostasis, inflammation, proliferation and remodeling, again with similar cellular and humoral contributions. Certain lesions more or less skip some of the sequential steps by themselves: surgical, sutured incisions do not develop a visible granulating surface. In other lesions, such as full thickness burns, surgical intervention (excision and grafting) is used to avoid the regular healing sequence (granulation) and to speed up closure.   Reactive oxygen species (ROS), proteinases and many other soluble mediators (secreted by neutrophils which rapidly invade a skin lesion in very large numbers) and cells are crucial for dealing with necrosis, debris and microbial invasion. The humoral compounds need careful regulation, since they are naturally aggressive and corrosive. Normally, for every up-regulating mechanism, a down-regulating, counter-acting mechanism exists in the body. When this balance is not adequate, a situation of prolonged and persistent inflammation may occur. For example, in a venous leg ulcer persistent PMNs increase ROS production,6 thus inducing a vicious cycle.   Metalloproteinases (MMPs) are produced by many different types of cells,7,8 and when tissue is injured, they begin to break down several components of the damaged extracellular matrix, which is a necessary step prior to the influx of “rebuilding” cells and humoral compounds. MMP activity is counterbalanced by tissue inhibitors of metalloproteinases (TIMPs).9,10 In an ulcer (as well as during the development of a hypertrophic scar)11 the balance between MMP activity (over expressed) and TIMP activity (relatively under expressed) is disturbed.8 One of the consequences of all these imbalances in MMPs and TIMPs in an ulcer is inhibition of angiogenesis and continuous breakdown of the extracellular matrix.12 Many compounds, such as metalloproteinases (MMPs) are not active in resting, non-damaged tissue.13   The physiological difference between a wound and a trauma is illustrated by the number of stromal cells expressing MMP-1 and MMP-3, which is greater in chronic than in acute lesions. In contrast, MMP-10 is not detected in the dermis of ulcers.8 TIMP-1 expression near the basement membrane is positive in acute, but not in chronic, lesions.8   Cytokine profiles in ulcers differ from those in trauma.14,15 Tarnuzzer et al15 showed major differences in the levels of epithelial growth factor, tumor necrosis factor-a (TNF-α), transforming growth factor-β (TGF-β) and insulin-like growth factor 1 (IGF-1), in fluid obtained from a healing mastectomy incision, compared to fluid obtained from ulcers. They and others16 also confirmed the significant differences in protease levels.   The imbalance in “destroying and rebuilding” forces, as well as the disruption in signaling pathways,17 confirm the chronically inflamed status of an ulcer,18 which indeed is caused by an underlying etiology/pathology.   Studies indicate that ionizing radiation induces modulation of cytokine and chymokine expression by skin, involving, among others, interleukin-1, -6, and -8, TNF-α, TGF-β,19,20 and the expression of some of the cytokines is dose dependent.19,20 Indeed, instead of radiation burns these injuries should be called radiation ulcers or, even better, cutaneous radiation syndrome since, clinically, this type of lesion behaves like an ulcer, not like a wound.   None of the events mentioned above is primarily related to time, either; for example, the imbalance of MMPs and TIMPs in ulcers can be identified very early on, not only after 3 weeks have passed, as the definition of a “chronic wound” indicates.

Influence of Microorganisms

  A biofilm is a protective polysaccharide matrix produced by bacteria. Most, if not all, ulcers develop a biofilm over time, while biofilm formation in trauma seems to be less common unless they remain open for a prolonged period and, possibly, become an ulcer.21–23 Biofilms are considered to play a major role in (preventing) wound healing24: the presence of a biofilm, more than that of planktonic bacteria, may very well contribute to maintaining the chronic status of an ulcer25 or even to a skin lesion becoming a chronic one.26

Location and Size

  Venous leg ulcers, diabetic foot ulcers, pressure ulcers and ulcers due to tropical diseases27 have typical locations. For example, pressure ulcers most commonly are located on the buttocks, sacrum, hip, heels, scapulae, and occiput.28 In contrast, trauma occurs everywhere on the body.   The relative size of a lesion plays a practical role: 200 cm2 for a venous leg ulcer is considered large whereas that size trauma (eg, burn) in an adult would represent close to 2% of the total body surface area (TBSA). A burn is considered medium size when it would be approximately 20% TBSA.   The differences in size and location have implications for the amount of dressings, dressing techniques and dressing time involved. Complex dressing techniques, such as the application of compression bandages, are generally not required in trauma care but major skin trauma requires daily or sometimes twice daily dressing changes. Size of a lesion also has immediate implications for where and how a patient is treated, since it has an impact on overall morbidity (see below): many ulcers are treated in outpatient clinics whereas large lesions require hospitalization, often in specialized units (eg, burn units, surgical intensive care units).   The size of a lesion also has implications for possible systemic effects; very extensive lesions, particularly when they are accompanied by a large amount of necrosis, may lead to the absorption of massive amounts of toxins, potentially leading to life threatening systemic effects.29,30

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 (lanolin in creams) to which the patient may have been exposed. These periwound skin problems, again, are the result of underlying pathology,31 either the same that caused the primary lesion or secondary to the prolonged inflammatory status of the primary lesion and they contribute to the overall healing problems.

Clinical Relevance

  The differences between an ulcer and a wound have clinical relevance. By definition, the occurrence of trauma cannot be prevented, but ulceration or its reoccurrence can. Proper foot inspection and foot care,32 including reconstructive surgery for Charcot’s foot,33 reduces the incidence and recurrence of diabetic foot ulcers. Similarly, pressure ulcer prevention, by taking appropriate measures is often successful and the use of compression is known to prevent (recurrence of) venous ulceration.34 Thus, primary outcome in ulcer care, in addition to healing, is preventing recurrence.   Acute mortality from ulcers is rare and is therefore not a major clinical concern. In contrast, major trauma rapidly leads to acute and very serious morbidity and the injury itself, as well as some of its accompanying syndromes, such as systemic inflammatory response syndrome (SIRS) or myoglobinuria,35 may lead to rapid death.36 Thus, major trauma requires acute, extensive, and often interventional care, which is expensive, but when compared to ulcer care of relatively short duration and survival, through prevention or treatment of shock, respiratory failure, etc. is, at least initially, often the primary outcome.   The difference in etiology and mechanism of injury also guides the differences in treatment; wounds usually are treated to heal by primary intention (through suturing, the use of flaps, etc.). Ulcers, even deep ones, usually are treated with a variety of dressings, heal by secondary intention and have a much poorer tendency to heal unless the underlying etiology is treated.37,38 Surgical wound bed preparation usually entails more rigorous and aggressive excision than traditional ulcer debridement with curette, scissors, and/or enzymes.   The prevention or treatment of hypertrophic scars, keloid, and contracture formation is an important outcome in trauma care. Significant scar formation is usually not a major problem, particularly for patients with diabetic foot ulcers and venous leg ulcers, because of the characteristic demography of these patients, as well as the location of these types of ulcers.   Ulcers can be changed into acute wounds by treating, and sometimes removing, the underlying etiology (eg, compression/saphenous vein ablation in venous leg ulcers). This in itself may lead to significant changes in wound bed properties and healing tendencies39 since the chronic nature of the ulcer is reversed. In addition, sometimes an ulcer can be treated by extensive (surgical) debridement or excision and primarily closure with a graft or a flap.   Conversion of a wound into an ulcer may also occur. A typical example would be a pretibial laceration40 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 late term conversion.41,42   Some skin lesions fit neither a wound (trauma) nor an ulcer category, but their clinical behavior usually strongly favors many or all other aspects of one of these two categories. For example, infectious lesions such as necrotizing fasciitis are neither caused by an underlying etiology nor the consequence of an external force; still, clinical behavior (rapid and serious systemic morbidity, leading to death without intervention) and treatment approach is similar to that of a major skin trauma. Toxic epidermal necrolysis is caused by an underlying etiology (i.e. drug anaphylaxis) but is not chronic in nature and treatment is quite often performed in surgically oriented institutions, such as burn centers.   Not making the etiology-based distinction between wound and ulcer may lead to serious medical mistakes, such as not excising and grafting a burn that has existed for weeks or grafting a venous leg ulcer without taking care of the venous hypertension that is the underlying etiology. In the first example, unnecessary suffering and serious scar formation will result, while graft failure has a very high incidence in the second example.


  The old nomenclature, where categories of skin lesions are not based on how long they have been in existence but on what has caused them still makes a lot of sense. The etiology/pathology based definition is better related to appearance, demographics, outcomes, and, most importantly, therapeutic possibilities and requirements than the age of the lesion per se.


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