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Wounds and Ulcers: Back to the Old Nomenclature

Article  in  Wounds: a compendium of clinical research and practice · December 2010

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COMMENTARY

AT
Wounds and Ulcers: Back to the Old
Nomenclature

Michel H. Hermans, MD

WOUNDS 2010;22(11):289–293
From Hermans Consulting, Inc.,
Newtown, Pennsylvania
Address correspondence to:
Michel H. Hermans, MD
Hermans Consulting, Inc.
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3 Lotus Place
Newtown PA 18940
Phone: 215-579-9745
Email: hermansconsulting@com-
cast.net
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Abstract: Currently, most skin lesions are called wounds and primarily
are divided into acute and chronic, the difference being the time peri-
od 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 vio-
lence (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 differ-
ences 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.

he traditional, non-medical definition of a wound according to many

T 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 grad-
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ual occurrence and/or chronic nature, and an internal factor in their defini-
tions 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 injur-
ing 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
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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
Vol. 22, No. 11 November 2010 289

Hermans
in appearance, demographics, anatomical locations,
physiology and pathology, as well as the required med-
ical interventions, possible medical options and out-
comes 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.
Etiology
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)
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and whether by physical contact or, for example, certain
types of radiation (a thermal injury).
According to the “traditional” medical and encyclope-
dia 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 prin-
ciples lie behind the development of diabetic foot ulcers
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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.
Physiology
T
Healing is a complex process but, in principle, all
lesions go through similar steps: hemostasis, inflamma-
tion, proliferation and remodeling, again with similar cel-
lular and humoral contributions. Certain lesions more or
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less skip some of the sequential steps by themselves: sur-
gical, sutured incisions do not develop a visible granulat-
ing 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 care-
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ful regulation, since they are naturally aggressive and cor-
rosive. 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
290 WOUNDS www.woundsresearch.com
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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 dif-
ferent types of cells,7,8 and when tissue is injured, they
begin to break down several components of the dam-
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aged extracellular matrix, which is a necessary step prior
to the influx of “rebuilding” cells and humoral com-
pounds. 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 inhi-
bition of angiogenesis and continuous breakdown of the
extracellular matrix.12 Many compounds, such as metallo-
proteinases (MMPs) are not active in resting, non-dam-
aged 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 chron-
ic than in acute lesions. In contrast, MMP-10 is not detect-
ed 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 trau-
ma.14,15 Tarnuzzer et al15 showed major differences in the
levels of epithelial growth factor, tumor necrosis factor-a
(TNF-a), 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 modu-
lation of cytokine and chymokine expression by skin,
involving, among others, interleukin-1, -6, and -8, TNF-a,
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 relat-
ed 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 pro-
duced 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 (prevent-
ing) wound healing24: the presence of a biofilm, more
than that of planktonic bacteria, may very well con-
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tribute 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 loca-
tions. For example, pressure ulcers most commonly are
located on the buttocks, sacrum, hip, heels, scapulae, and
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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 approxi-
mately 20% TBSA.
The differences in size and location have implications
for the amount of dressings, dressing techniques and
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dressing time involved. Complex dressing techniques,
such as the application of compression bandages, are
generally not required in trauma care but major skin trau-
ma requires daily or sometimes twice daily dressing
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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 necro-
sis, may lead to the absorption of massive amounts of tox-
ins, potentially leading to life threatening systemic
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effects.29,30
Periwound Skin
Skin surrounding a trauma, at least initially, does not
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show the typical aspects of long lasting (hyper) inflam-
matory influences; normal, but not excessive signs of
inflammation are present. Even a non-infected, full-thick-
ness 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 sur-
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rounding, for example, a venous leg ulcer, is often
indurated, with signs of lipodermatosclerosis and hyper-
pigmentation 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 inflamma-
tory 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 trau-
ma cannot be prevented, but ulceration or its reoccur-
rence can. Proper foot inspection and foot care,32 includ-
ing reconstructive surgery for Charcot’s foot,33 reduces
the incidence and recurrence of diabetic foot ulcers.
Similarly, pressure ulcer prevention, by taking appropri-
ate measures is often successful and the use of compres-
sion is known to prevent (recurrence of) venous ulcera-
tion.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 rapid-
ly leads to acute and very serious morbidity and the
injury itself, as well as some of its accompanying syn-
dromes, such as systemic inflammatory response syn-
drome (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, res-
piratory 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 sutur-
ing, the use of flaps, etc.). Ulcers, even deep ones, usual-
ly are treated with a variety of dressings, heal by second-
ary 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
Vol. 22, No. 11 November 2010 291

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and aggressive excision than traditional ulcer debride-
ment with curette, scissors, and/or enzymes.
The prevention or treatment of hypertrophic scars,
keloid, and contracture formation is an important out-
come in trauma care. Significant scar formation is usually
not a major problem, particularly for patients with dia-
betic 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
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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, some-
times 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
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elderly patient with diabetes or severe venous hyperten-
sion: the underlying etiologies turn a wound with good
healing potential into an ulcer with poor healing ten-
dencies. 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 strong-
ly favors many or all other aspects of one of these two
categories. For example, infectious lesions such as necro-
tizing fasciitis are neither caused by an underlying etiol-
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ogy nor the consequence of an external force; still, clini-
cal behavior (rapid and serious systemic morbidity, lead-
ing to death without intervention) and treatment
approach is similar to that of a major skin trauma. Toxic
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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
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a very high incidence in the second example.
Conclusion
The old nomenclature, where categories of skin
292 WOUNDS www.woundsresearch.com
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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 bet-
ter related to appearance, demographics, outcomes, and,
most importantly, therapeutic possibilities and require-
ments than the age of the lesion per se
se..
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