University of Medicine and Pharmacy [623599]

University of Medicine and Pharmacy
“Iuliu Hațieganu”
Cluj-Napoca
Faculty of Medicine

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Contents
General Part
1. Definition (-)
2. Classification (-)
2.1 Venous Ulcers (-)
2.2 Arterial Ulcers (-)
3. Epidemiology (-)
4. Aetiopathogenesis (-)
5. Paraclinical investigations (-)
5.1. Inflammatory tests (-)
5.2. Glycemia (-)
5.3. Eco Doopler (-)
5.4. Hypertension (-)
6. Differential Diagnosis (-)
6.1. Vasculitis (-)
6.2. Tumors (-)
6.3. Infections (-)
7. Treatment (-)

1. Introduction
Wound healing was considered a m ysterious process for centuries, with wound
management being based on the preference of the practioner rather than on
the scientific principles (1)
In an era when most of the wounds became infected and in which there was
not a clear definition and distiction between chronic wounds, acute wounds
and ulcers Hippocrates (460 –370 b.c.e.), worked frequently with wounds both
at his home ‘office’ and while traveling (2).
There are many elements that impair the process of healing and alter or
postpone the no rmal sequence of wound healing. Wound healing is a highly
regulated, complex process that is very important for maintaining th e barrier
function of the skin (3). It is also know that repair is an exceptionaly complex
process that includes hundreds, posibly thousands of ‘linked’ and overlapping
processes (1)
As for the term, Dorland’ s Medical Dictionary defines ‘wound’ as « the
disruption in the countinuity of a body structure » . The clinical word ‘wound’ as
its commonly found in books, dictionaries and accepted in the terminology,
relates mostly to acute mechanical trauma such as a gunshot wound, a stab
wound, or an acute inju ry (4).
However w ounds and more particulary chronic wounds represent an unmet
need for patients and a provocation for healthcare pro viders. In the USA alone
it is roughly c alculated that 7 million patient s are affected per year , which
costs the US healthcare system more than 25 bilion annually (5).
With the number of patients growing some 6.5 million yearly due to the rise in
frequency of diabetes and other chronic diseases that might influence wound
healing. (han chronic wounds) Thus the process of the healing of a superficial
woun d needs many factors to work in concert , and in order to address viable
obstacles to wound healing , varying from hypoxi a to infection, wound
dressings and treatments ha ve also proggresed considerably (2).

2. Definition
2.1 Acute Wounds
Acute wounds in most cases are surgical or traumatic in origin. Their
occurrance happends promptly and in the majority of individuals move quickly
and predictably through the repair procedure and result in durable closure
(1).These wounds are formed usually due to some form of trauma that could
be either penetrating or blunt (animal bites, gunshots, surgical incisions) (6).
Cutaneous wound can also be named a break in the continuity of the skin,
which will result in the disruption of the function and anatomic stracture (7).The
procces of cutaneous healing itself can be extremerly complicated , dependent
on an complex interplay among a number of high ly regulated factors working in
coherance to restore impaired skin in the directi on of r epaired barrier function
(2).
Tissue damage resulting from a wound stimulates a coordinated physiological
response which provide haemostasis and begins the procedures of
proliferation ,inflammation and remodelling, although acute wounds, including
surgical incisions,normally pass throu gh these phases relatively rapidly (6)

2.2 Chronic Wounds
The meaning of a chronic wound is not clearly defined in the literature.C hronic
wounds develop when there is a di sturbance in the standard healing process ,
they fail to heal within a normal interval of time when simila r wounds would
have otherwise been already cured (8).
Although there is no clear cut definition that points to the chronicity of a wound
most phycisians would agree that a wound that fails to heal within the timeline
of 3 to 4 month s may be deemed as chronic.The estimated time for healing is
not random but rather depends on factors suc h as the cause, the size of the
wound and the patients gen eral clinical st atus (4).
Chronic wounds all have unique origins.SImilaritie s in pathogenesis have
made it realistic to devide them into various groups such as venous leg ulcers ,

diabetic fo ot ulcers and pressure ulcers (9).There are countless other factors
that could also slow down wound healing .Such are chronic dsieases, vasc ular
insufficien cy, diabetes , malnutrition, ageing, and local factors like pressure
infection and oedema.The aetiology of chronic wounds is varying , holding back
the efforts of resear chers to find a single therapeutic agent as the ‘elixir’ of
healing (10).
Furthermore chronic wounds are a burden to both the patient and the health
care system (3) t here are over 4 million Americans affect ed with these types of
wounds with an annual treatment cost of 9 billion. A great percentage of these
wounds occur in the gr owing eld erly community .This becomes a burden for the
society due to increasing health care cost s and the loss of productivity wound s
(8).
Despite th e distictions in etiology , at the molecular level chronic wounds share
certain common features including excessive levels of proinfl ammatory
cytokines, proteases , ROS and sensescent cells as well as the existance of
persistent infection and shortage in stem cells that are frequentl y dissfunctional
(11).
As a matter of fact chronic wounds do not lack key substrates known to be
involved in healing.Instead proinflammatory cytokines proteinases , cellular
adhesion molecules, growth factors and growth factor receptors seem to be
boosted in wounds which support the inflammation hypothesis (12).

3. Classification
3.1 Venou s ulcers
Venous leg ulcers are open lession s betwwen the knee and the ankle joint (the
gaiter area), and are prone to occur on the lateral and medial aspects of the
leg when venous insufficiency is present.( understanding tge venous ulcer)
(13)
The most common occurance of venous ulcers is over the malleolus and to a
lesser degree over the lateral surface of the ankle (LEG ULCERS DG
NEGUS) (14). Venous ulcers differ in size from just a few centimiters to giant

ulcers which could be cirrcumferential and progress to inv olve the whole of the
gaiter of the lower leg.They are most frequently infected when seen for the f irst
time but the infecit on resp onds fast to daily cleaning, firm compression
bandaging, non -irritant dressings and the correct antibiotic treatment .Antibiotic
treatment though doesnt not immidiately help with the leg ulcer healing.In
contrast the infected ichemic ulcers usually f ail to respond to antibiotic
treatment until the the ichemia is successfully fully treated. A clean venous
ulcer wound has a base formed of healthy pinnk granulations covered
sometimes by a little debris, and the edges contain sloping pink epithelium.The
granulation tissue portrays the surface of capillary loops.Lastly
lipodermatosclerosis (pigmented, indurated skin) which is a result of
pericapillary firbrin and hemosiderin deposition is seen frequently surrounding
a venous ulcer (LEG ULCERS DG NEGUS) as well as eczema purpura and
white atrophy.B lack skin necrosis is an unusual finding though (15) (DIFF DG
OF LEG ULCERS) Venous ulceration can be caused by a po st-thrombotic
syndrome or by varicose veins although a mixed pathology of superficial and
deep venous insufficiency as well as oedema are also usual findings in
patients.
Some known facts about lower limb venous ulceration are that it represents the
most a dvanced stage of chronic venous disorder (16)(L abbade characteristics
clinical) as well as m ost v enous ulcers are often recurrent, occur commonly in
women and elderly people and the open types can persist from weeks to
years . (17)(agale)
There are also other types of leg ulcers known , however the venous ones
account for 40 -85% of all leg ulcers (13). ( understanding the venous)
The most common cause of lower -leg ulcers, accounting for nearly 80% of all
cases is venous insuffieciency and as evidence shows approximately 1% of
the populati on will suffer from leg ulceration at a given point in their lives .
In the United States from the 7 million poeple that suffer from venous
insufficiency almost 1 million will develop venous ulcers (17) (Agale) aetio epidi
Lastly venous ulcers can exist in people from all socioeconomic backgrounds,

however evidence shows that in poeple coming from lower socioeconomic
backgrounds they take longer to heal and appear to have a higher recurrence
rate (13)

3.2 Arterial Ulcers
Arterial ulcers are caused by a deficit in the arterial blood supply of the lower
limb (venous ulcers iriving) or by reduced oxygen supply in the tissue due t o Risk factors for development of venous ulcers (5)

 Age > 55 years
 Male sex
 Presence of reflux in deep and perforator veins, deep
obstruction and combination of reflux and obstruction
 Parental history of ankle ulcers and family history of
venous insufficiency
 History of superficial/ deep vein thrombosis and
pulmunary embolism
 Previous ulcer history
 Sever lipodermatosclerosis
 Skeletal or joint disease in lower extremities
 Higher body mass index
 Physical inactivity

arterial occlusions.( diff dg)
These occlusions of the arteries apart from creating an eventual ulcer will also
result in arterial insufficiency which is known to be the most common form of
ischaemia.The most frequent aetiology is progressive atherosclerosis of the
medium and large sized arteries(j grey), in which case they become stenotic
due to lipid deposition in the arterial vessel walls, as a result of increased
levels of circulating chole sterol or triglycerides and further exasparated by
smoking, uncontrolled hypertension, and diabetes mellitus.(krisner
Other factors that influence the formation of arterial ulceration are
thromboangiitis, vascultis, thalassaemia, pyoderma gangrenos um, and sickle
cell disease but are also commonly seen occuring after unsignificant trauma or
as the consequence of localized pressure. J grey
Additional damage to the arterial system occurs with concurrent hypertension
through destruction of the intimal layer of the artery , and further reduction in
the arterial blood supply causes tissue hypoxia and tissue damage.
Lastly thrombotic and atheroembolic episodes may also be a factor in tissue
destructin and tissue hypoxia .irving

All patients with leg and foot ulcers require in depth examination of the arterial
blood supply.Upon physical examination palpation of the dorsalis pedis and
posterior tibialis pulses have to be performed and in case the pulses are weak
or nonpalpable furt her examination with Doppler and other measurements
such as the ankle -brachial index should be carried out.In case of unusual
findings in the initial testing further specific and more complex tests may be
required, such as Doppler arterial wave forms and p ulse volume
recordings.krisner
Arterial ulcers usually appear over the toes, heels, and bony prominences of
the foot. They have well demarcated edges and a pale, non granulating,often
necrotic base and appear ‘punched out’. J grey
The sorrounding skin ussually has a shinny texture and may also manifest
trophic changes such as alopecia, dry ,scaly, erythrematous skin and chronic
pigmentation ^iring. On further examination the skin can also be cool to touch,
thin, hairless, and brittle, whilist the toenai ls thicken and turn opaque and may Risk factors for development of arterial ulcers
 Advanced age
 Diabetes
 mellitus
 Smoking
 Hypertension
 Hyperlipidaemia
 Obesity

eventually dissapear .Gangrene of the extremities may eventually be seen j
grey^ .Examination of the arterial system may show a decreased or absent
pulse in the dorsalis pedis, posterior tibial,femoral and popliteal arterie s.Having
said that palpation of the peripheral arteries can often be tough and not always
precise .^irving .Bruites may also appear in the proximal leg arteries considered
a sign of atherosclerosis. ^J gray . In such cases the use of a Doppler probe to
detec t the peripheral pulses is useful and permits the practitioner to listen to
the quality of the sound.The sound of a normal arterial system is triphasic, but
if there is indication of arterial insufficiency, the sound may be biphasic or even
monophasic^ irv ing.
Typically patients with arterial ulcers have a reduced capillary refill time.With
ordinary capillary refill, after co mpressing the dorsum of the foot or the great
toe for a few second s, the colour of the skin should be able to return to normal
in less than two or three seconds. A delay in retu rn of the regular colour is
suggesting vascular compromise. A delay of more than 10 – 15 seconds in
return of colour after raising an ischaemic leg to 45 degrees for 1 minute
(Buerger’s test) is also indicatve for v ascular compromise. j grey^
Another tool useful for determining peripheral vascular disease in the
abesnece of non -compressible vessels deriving from vessel calcification for
istance (diabetes, or tissue oedema) is the ankle brachial index (ABI). G gre^
A cut-off ABI value of ( ≤ 0 – 9 ) has been determined by the Inter -Society
Consensus for the Management of Peripheral Arterial Disease for diagnosing
peripheral vascular disease at rest.In diabetic or elderly patients, imprecise
increased ABI may require fur ther testing, such as toe -brachial index (<6
considered abnormal) or transcutaneous oxygen measurments (<40 mmHg
considered abnormal)krisner*.
Further information on arterial occlusion, stenosis, and areas of diffuse and
continous atheromatous disease can be given by a duplex ultrasou nd, and the
best possible investigation for preoperative planning that allows direct
evaluation of the vascular anatomy of the lower limb is arteriography. J grey

3.3 Diabetic foot ulceration
One of the most significant and harmful complications of diabetes, is the
diabetic foot.It is defined as ulceration of the foot associated with neuropathy
and/or peripheral arterial disease of the lower limb in pati ents suffering from
diabetes.(MANAGEMENT). Diabetic foot problems constitute for more hospital
admission s than any other long term complication of diabetes and account for
nearly 50% of all diabetes -related hospitalized bed days. Diabetic foot ulcers
affect 15% of all diabetic patients and as a consequence a big financial burden
is generated. (j ahmad diabetic foot)
^Foot ulceration in diabetes mellitus is frequently seen , it is disablind and
oftenly leads to leg amputation.(diabetic foot ulcers) ^
About 50% of all lower limb amputations are performed in patients suffering
from diabetes making diabetic lower extremity complications a noteworthy
public health concern in both d eveloping and developed countries .(j ahmad
diabetic foot)
It is roughly estimated that the prevalence of diabetic foot ulceration i n the
diabetic populatio n is 4 -10% with the condition b eing more common in the
older patients and that about 5% of all the patients with diabetes present to the
hospita l with foot ulceration h istory. The majority (60-80%) of foot ulcers will
recover, while 10 -15% of them will remain active and 5 -24% will eventually
lead to limb amputation with a time period of 6 -18 months following the first
evaluation

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