vasc disenglindian

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.