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                             Veins and Lymphatics 2016; volume 5:5988

Compression after trauma
Rolf Jelnes
Wound Clinic, Medical Center, Sygehus
Sønderjylland, Sønderborg, Denmark

Traumatic ulcers are a large entity in wound
care. In our clinic, data from the database1

show that the number of patients is compara-
ble to venous leg ulcers, diabetic foot ulcers
and pressure ulcers (Table 1). In spite of this,
not very much is written about the entity in the
literature.
The traumatic wounds are typically located

on the anterior and lateral aspect of the lower
limb. The causes are different from low energy
trauma (as stumbling up the stairs or a trolley
in the supermarket (Figures 1 and 2) to acci-
dents with a sharp trauma.
After low energy trauma, the patients are

able to continue their daily work until a lesion
appears on the skin. When it increases in size
the patient seeks the General Practitioner who
typically prescribes an antibiotic treatment. If
nothing else is done, apart from moist wound
healing, the time to heal can be as long as
more than 6 months with the well known con-
sequences for the patient and the society in
terms of personal and social costs.
Studies on deep tissue injury have shown

that cell deformity, within minutes, causes cell
damage leading to cell death.2 The subcuta-
neous tissue is the tissue with lowest blood
perfusion, thus making it more susceptible to
ischemia.
A possible mechanism for the development

of the traumatic ulcer could be: i) subcuta-
neous adipose tissue cells die, due to the blunt
trauma; ii) within the cell the osmotically
active proteins are let loose themselves in the
interstitium, drawing water to the area; iii)
edema is created in the ageing skin the
amount of collagen and elastin is reduced3

especially in women after menopause, leading
to reduced forces to counteract the edema
(intrinsic compression).
As an edema has developed, the rationale

for compression, with either bandages or
stockings with high stiffness, seems obvious.
The impressive healing rate of 25% per week
(Table 1) supports this view.

References

1. Hafner J, Nobbe S, Partsch H, et al.
Martorell hypertensive ischemic leg ulcer:
a model of ischemic subcutaneous arteri-
olosclerosis. Arch Dermatol 2010;146:961-
8.

2. Senet P, Beneton N, Debure C, et al.
Hypertensive leg ulcers: epidemiological
characteristics and prognostic factors for
healing in a prospective cohort. Ann
Dermatol Venereol 2012;139:346-9.

3. Senet P, Vicaut E, Beneton N, et al. Topical
treatment of hypertensive leg ulcers with
platelet-derived growth factor-BB: a ran-
domized controlled trial. Arch Dermatol
2011;147:926-30.

4. Vuerstaek JD, Reeder SW, Henquet CJ,
Neumann HA. Arteriolosclerotic ulcer of
Martorell. J Eur Acad Dermatol Venereol
2010;24:867-74.

Correspondence: Rolf Jelnes, Wound Clinic,
Medical Center, Sygehus Sønderjylland, Sydvang
1,�6400 Sønderborg, Denmark.
E-mail: rolf.jelnes@stofanet.dk

This work is licensed under a Creative Commons
Attribution 4.0 License (by-nc 4.0).

©Copyright R.Jelnes, 2016
Licensee PAGEPress, Italy
Veins and Lymphatics 2016; 5:5988
doi:10.4081/vl.2016.5988

Table 1. Distribution of wounds according
to underlying diagnosis.

                         Number               Healing
                       of wounds        rate per week

Traumatic ulcers       558                              25%
Pressure ulcers         503                                 -
Venous leg ulcers     450                              18%
Neuropathic foot      444                                 -
ulceres                            
Neuroischemic         283                                 
foot ulcers                     

Figure 1. Large traumatic ulcer on the pos-
tero-lateral aspect of the calf.

Figure 2. Traumatic ulcer on the anterior
aspect of the calf.

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