vasc disenglindian
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Chronic Venous
Insufficiency
Chronic Venous Insufficiency
Has been recognized since ancient times
By Greek physicians (Hyppocrates 460-377 B.C.) By Roman physicians (centuries later)
These disease entities continue to defy understanding.
Chronic Venous Insufficiency (CVI) of the Legs
Common and progressive disorder found in many parts of the world a condition with ambulatory venous hypertension affects approximately 5% to 15% of the adult
population. One percent develop venous ulcers CVI consumes 1-2% of the healthcare budget of the
European countries
Chronic Venous Insufficiency has a major impact on health economics :
in Germany leg ulcers caused >1.2 million hospitalisation days, for a cost of 1.5 billion EURO
In France CVI amounted to 2.25 billion EURO in UK costs associated with leg ulcers went up to
230-400 millions Sterling Pounds
CVI The term CVI is used to describe signs and symptoms
of chronic venous hypertension in the lower limbs
This condition is generally considered as the pathophysiological trigger of skin changes, the most serious of which is ulceration
CVI The clinical hallmark of CVI is distal venous hypertension,
which follows the development of valvular incompetence, reflux, and/or venous obstruction.
At the cellular level there is abnormal metabolism of the connective tissue matrix of the vein wall with a marked increase in fibrouse tissue and abnormal deposition of collagen in both the vein wall and the skin.
CVI-classificationsWidmer’s Classification
It is based exclusively on objective signs
3 stages: 1. Corona phlebectatica paraplantaris, edema 2. Trophic lesions (lipodermatosclerosis, atrophie
blanche, dermatitis). 3. Active or healed leg ulcer
CVI-classifications
CEAP ClassificationC: Clinical
E: Etiology
A: Anatomy
P: Pathophysiology
CEAP classificationThe clinical part (C) is based on objective clinical signs of
chronic venous disease according to 7 classes:
0 = No visible or palpable signs of venous disease
1 = Telangiectasia or reticular veins
2 = Varicose veins
3 = Edema
4 = Skin changes (pigmentation, venous eczema, lipodermatosclerosis)
5 = Skin changes as defined above with healed ulcer
6 = Skin changes as defined above with active ulceration
Subjective Symptoms and Objective Signs
Pain - weak or absent
Heavy legs
Cramps at night
Paresthesias or burning sensation
Localized itch without skin changes
Edema
Skin Changes at CVIGravitational dermatitis
Hyperpigmentation
Lipodermatosclerosis
Their presence mirrors microcirculatory disorders
LipodermatosclerosisThere is a proliferation of the dermal capillaries and fibrosis on subcutaneous tissue
It is a combination of: induration pigmentation inflammation
VENOUS LEG ULCERS
Large scale studies suggest that about 1% of the population develop a chronic leg ulcer at some point in their live. Most of the ulcers have chronic venous origin. Venous disease is identified as the most common predisposing risk factor.
VENOUS LEG ULCERS
Venous ulcers are approximately 80% of all leg ulcerations and they are also known to have the highest recurring rates.
Venous ulcers are not generally as painful, do not lead to amputation, do not require surgical intervention as often as ulcers caused by arterial insufficiency.
VENOUS LEG ULCERS
However, their chronic course, unpredictable behavior, morbidity, the associated economic burden have to led to a renewed interest in the development of new approaches to improve the speed of healing, the quality of live and work productivity.
Venous UlcerDefinition:
An ulcer in the lower leg due to CVI
Clinical Findings:
The sites of predilection is the inner aspect of the distal third of the leg
Shape - rounded, elongated or very large like a cuff (so-called gaiter ulcer)
Venous Ulcer
Clinical Findings:base - flat, covered with fibrous plough
margins - sharp or rolled border
CLINICAL CHARACTERISTIC
Venous ulcers are usually located over the medial malleolus where the long saphenous vein is more superficial and the pressure is greatest.
CLINICAL CHARACTERISTIC
Trauma or infection may localize ulcers more proximal or laterally. Ulcers above the mid calf or on the foot commonly suggest another cause.
CLINICAL CHARACTERISTIC
Venous ulcers are shallow, they generally have borders with irregular margins that are either flat or with a slight steep elevation. The ulcer bed is covered initially by yellow fibrinous slough.
Healing is very slow, often from months to years.
Venous UlcerComplications:
superinfection contact allergy squamous cell carcinoma (Marjolin
ulcer) on the basis of a long standing ulcer
Venous UlcerDifferential Diagnosis
75-90% of all ulcers are of venous origin
It should always be born in mind that lower leg ulcers can have great many causes
Venous UlcerDifferential Diagnosis
Arterial leg ulcers: Arteriosclerosis Diabetic angiopathy Polyarteritis nodosa Cutaneous polyarteritis nodosa Ulcus cruris hypertonicum Martorell
Venous UlcerDifferential DiagnosisCrural leg ulcer in some dermatoses: Sclerodermia progressiva Lupus erythematosus profundus Necrobiosis lipoidica Fasciitis necroticans
Venous UlcerDifferential DiagnosisNeoplastic leg ulcers: Basal cell carcinoma Squamous cell carcinoma Malignant melanoma
Arterial UlcersClinic
Are frequently pretibial or involve toes: They are painful at night The edges are sharply defined Exudation is minimal The slough is black with bare tendons or bones beneath There is no pigmentation in the surrounding skin
Cutaneous polyarteritis nodosa
A benign disease, limited to the skin It may be accompanied by myalgias,
but without severe systemic manifestations
The prognosis is generally favorable
Cutaneous polyarteritis nodosa
The disease primarily affects the legs and feet,
also the lower arms and other regions of the body
The clinical signs include: painful subcutaneous nodules which may
ulcerate focal livedo reticularis
Periarteriitis nodosa cutanea benigna
Diseases of the Microcirculation
Ulcus hypertonicum Martorellan example of microcirculatory
disorder leading to leg ulcerextremely rare condition
Ulcus Cruris Hypertonicum (Martorell 1945)
Synonyms
Martorell Syndrome, hypertensive ischemic ulcer.
Clinical Findings The lesions usually occur in women between 40 and 60 years
of age With a long history of hypertension and raised diastolic blood
pressure Without evidence of arterial occlusive disease or CVI or
diabetes
Ulcus Cruris HypertonicumClinical Findings
the ulcer appears bilaterally on the outher side of the leg, between the mid and lower third
flat with a necrotic base and livid reticulate edge severe pain no tendency to heal
Ulcus Hypertonicum Martorell
Ulcus Cruris Hypertonicum
Treatment The first priority is the treatment of the
hypertension Alleviation of pain with non-steroidal
antiinflammatory and vasodilating drugs. Local treatment follows the general guidelines
for the treatment of leg ulcers
Treatment of CVI
1. Graduated compression bandaging
- elastic compression bandages
- compression stockings
Treatment of CVIThe primary aims of graduated compression management
( from the toes to the knee) are:
-to reduce the pressure on the superficial venous system
-to aid venous return of blood to the heart
-to discourage oedema by reducing the pressure difference between the capillaries and the tissues
Treatment of CVI
2. Local treatment- cleansing of the ulcer base (proteolytic
enzyme preparations, mechanically)
- stimulation of wound granulation and epithelialization
Local Treatment
Venous ulcer
Ulcer cleaning Granulation Epithelialization
ULCER CLEANING
The ulcer cleaning is usually done by the use of normal saline or Ringer solution.
The use of irritants like chlorhexidine, iodine, hydrogen peroxide and topical antibiotics should be avoided.
DEBRIDEMENT
The removal of dead tissue speeds ulcer healing. The main options are:
Enzymatic treatment Mechanical debridement (curette,
scissors)
NEXT LINE TREATMENT
Promotion of healthy granulation tissue Stimulation of epithelialization
Treatment of CVI3. Systemic treatment
venotonic drugs - a number of rutosides are widely used (Venoruton, Detralex=Daflon, Endotelon)
vasoactive agents - pentoxifylline: improves red cell deformability, prevents inappropriate white cell activation, enhances fibrinolysis
POOR PROGNOSTIC INDICATORS
For venous ulcer healing are: large size long duration history of venous ligation ABI of less than 0.8 presence of fibrin on more than 50% of the ulcer
surface
ADVERSE LOCAL CONDITIONS
Other local conditions that can delay healing are: Ulcer infection Contact dermatitis/eczema Excess exudate Dehydration Excessive use of topical antiseptics or antibiotics
FAILURE to HEAL
If the ulcer fails to heal, the diagnosis has to be reevaluated and the following additional investigations should be done:
Biopsy Autoimmune screen Blood sugar level X-ray
RECURRENCE after TREATMENT
“Once an ulcer patient always a potential ulcer patient”
Recurrence rates of venous ulcers after treatment are high. Once the patient’s ulcer is healed, careful skin care, continuous vigilance and strict use of compression therapy must be emphasized.