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Diseases of the veins

MUDr. Nina Benkov Dermatovenerologick klinika 1. LF UK Praha

Importance
medical, social, pharmacoeconomic epidemiology, demography interdisciplinary collaboration, teamwork Centers for wound healing:
Leg ulcers Diabetic foot Decubites

Varices Chronic venous incompetence

deep + superficial venous system + perforators

Physiologic blood stream from surface to profundity and proximal

venous valves direction, inhibition of reflux

Clinical examination
History and physical examination = fundamental
NO: circumstances of origin and duration OA: internal diseases, risk factors FA, GA, SA+PA RA: venous diseases

aspection- standing: edema, colour, trophic changes, varices palpation- lying: temperature, edema, pain subjective complains, alleviation manoeuvres history+ clinical picture determination of etiology knowledge of patgogenesis, diagnostic examinations and therapeutic possibilities adequate therapy

Functional and scanning examinations


Supportive, confirmative
Historical turnstile tests Trendelenburgs a Perthess test Modern instrumental dopplerimetry and duplex dopplerimetry plethysmography: PPG, LRR Scanning phlebography, scintigraphy CT, MR

Varicous veins
dilatation, elongation, meander like shape epidemiology - race, sex, age, genetics population < 40 yrs. 30%, > 70 yrs. 10x classification - ethiology
primary secondary

classification - lumen
star burst reticular stem < 2 mm 2-4 mm > 4 mm

Posttrombotic syndroma

incompetence of perforators and superficial veins secondary varices

starburst varices

stem varices

Complications of varicouse veins


bleeding trombophlebitis
in 1/3 cases + deep thrombosis

phlebothrombosis
in 50% inappparent

trias of symptoms Diff. dg.

phlebitis migrans recidivans - symptom

Therapy of varicous veins


Prophylaxis
regime measures therapy of phlebotrombosis trombolysis

Compression bandages - correct application!


Pharmacotherapy:
venotonics, rheologics, oedemaprotectives, anticoagulation agents

supportive

Sclerotisation Surgical therapy

Chronical venous incompetence


Functional defect of venous segment
ethio: PTS obstruction 75% / varices 25% valve incompetence venous hypertension

CVI =

trophic and inflammatory skin changes


5%, 2-3x , ulcera 1,5% > 60 yrs. 4%

epidemiology progressive character

Pathogenesis of CVI
valves incompetence hypertension
capillary dilatation permeability
fluid, proteins, fibrinogen

blood flow
adhesion + migration leukocytes enzymes, ROS, MMP, cytokines

edema, hypoxia, malnutrition

chronic inflammation

trophical changes destruction of vessels and subcutaneous tissue


changes in macrocirculation stasis, reflux, hypertension varices changes in microcirculation capillaries, lymphatics, interstitium

Classification of CVI
I. II. III. varices, reversible edema varices, permanent edema + trophic changes varices, edema+ trophic changes + ulcus CVI varices (scar)

Trophical changes:

hyperpigmentations hypodermitis dermosclerosis stasis dermatitis eczema verrucous hyperplasia white atrophy

CVI grade II Stasis dermatitis = Dermatitis varicosa

corona phlebectatica

papillomatosis = verrucous hyperplasia

white atrophy

hemosiderin hyperpigmentations

arterial ulcer

diabetic gangrene

kalosities

neuro - trophic ulcer

diabetic ulcerations

Dif. dg. algorithm


ETIO
VENOUS

Local Shape

ARTERIAL

METABOLIC NEUROPAT

Puls Perception / pain maleol bisar + + medial leg down frontal round 0, + leg cutted elevation acral round necrosis permanent

Complications of CVI
Contact allergic eczema Contact irritative dermatitis Microbial eczema 80 % Erysipelas Spinocellular cancer ulcus Marjolin

Contact iritative or allergic dermatitis ?

erysipelas cellulitis, dermatolymfangiodermatitis

spinocellular cancer

Therapy of leg ulcers


Complex I biological psychological social Complex II - medical
therapy of al patients disease and general health status prophylaxis: regime measures, pressotherapy causal therapy + skin symptoms:

Topical therapy of leg ulcer


correlates with phases of wound healing Chronic wound = no spontaneous healing > 6 weeks despite therapy 1. cleanance necrosis, fibrin, detritus 2. reduction of inflammation and infection microbial film, exudation, inflammation 3. granulation and epitelisation + care of surrounding skin, compression

Ulcer description
Wound assessment

nekrotic black granulating red infection fibrin yelow epitelisating pink

Wound dressing
1. Classical : dressing gauze + ointment
2. Modern : wet wound healing = special materials:
humidity, exchange of gases and vapours, inpermeable for microorganisms, antiseptic

Modern dressing - overview


Hydrocoloids Alginates Hydropolymers Polyuretan foams Polyacrylates Hydrogels Silicon foams Polyuretan films

exudate absorption, antisepsis

wet dressing. antisepsis

Insufficient healing
General factors: age, immunity, internal diseases, abusus; non - compliance Local factors: intensity and extent of vessel disease, ulcer localisation and size, infection. If impossible to eliminate/ reduce the cause = not healable ensure acceptable QoL

to be continued

Lymphedema
chronic solid edema = consequence of lymfatic system dysfunction lymphostasis + high proteins edema chronic inflammation + fibrosis solid complications: erysipelas, lymfangiosarcoma examination: sonography, lymphangioscintigraphy

papillomatosis = verrucous hyperplasia

Classification
Ethiology primary vessel dysplasia secondary non-/inflammatory obstruction Phases of edema: I. latent II. reversible III. ireversible IV. elephantiasis nostras

Erysipelas in lymphedema

Therapy of lymphedema
Symptomatic, prevent progresssion must be started early Decongestion
manual lymphodrainage Instrumental compressive bandages therapeutic exercices

Skin care, infection prophylaxis Systemic Surgical lymfovenous shunts, lymfo-liposuction, ablative

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