diseases of the veins
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Diseases of the veins
MUDr. Nina Benáková
Dermatovenerologická klinika
1. LF UK Praha
Importance
medical, social, pharmacoeconomic• epidemiology, demography• interdisciplinary collaboration, teamwork• Centers for wound healing:
Leg ulcersDiabetic footDecubites
VaricesChronic 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→ determination of etiology knowledge of patgogenesis, diagnostic examinations and
therapeutic possibilities → adequate therapy→ adequate therapy
Functional and scanning examinations
Supportive, confirmative• Historical – turnstile tests
Trendelenburg´s a Perthes´s 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 - ethiologyprimarysecondary
• classification - lumenstar burst < 2 mm reticular 2-4 mmstem > 4 mm
Posttromboticsyndroma
→ incompetence of perforators
and superficial veins
→ secondaryvarices
stem varicesstarburst varices
Complications of varicouse veins
• bleeding
• trombophlebitisin 1/3 cases + deep thrombosis
• phlebothrombosis trias of symptoms
in 50% inappparent Diff. dg.
• phlebitis migrans recidivans - symptom
Therapy of varicous veins
• ProphylaxisProphylaxis “regime measures“
• therapy of phlebotrombosis – trombolysis
• Compression bandages Compression bandages - correct application!
• Pharmacotherapy: venotonics, rheologics, oedema-protectives,
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
• epidemiology ≈ 5%, ♀ 2-3x ↑, ulcera ≈ 1,5%• progressive character > 60 yrs. 4%
Pathogenesis of CVI
changes in macrocirculation → stasis, reflux, hypertension → variceschanges in microcirculation→ capillaries, lymphatics, interstitium
valves incompetence → hypertension
capillary dilatation↑permeability
fluid, proteins, fibrinogen
↓blood flow adhesion + migration leukocytesenzymes, ROS, MMP, cytokines
chronic inflammationedema, hypoxia, malnutrition
trophical changesdestruction of vessels and subcutaneous tissue
Classification of CVI
I. varices, reversible edema
II. varices, permanent edema + trophic changes
III. varices, edema+ trophic changes + ulcus
(scar)
Trophical changes:
• hyperpigmentations• hypodermitis → dermosclerosis• stasis dermatitis → eczema• verrucous hyperplasia• white atrophy
CVI ≠ varices
CVI grade IIStasis dermatitis =Dermatitis varicosa
corona phlebectatica
papillomatosis = verrucous hyperplasia
white atrophy
hemosiderin hyperpigmentations
arterial ulcer diabeticgangrene
diabetic ulcerations
kalosities
neuro - trophic ulcer
Dif. dg. algorithm
ETIO Local Shape Puls Perception
/ painVENOUSVENOUS
♀maleol
medial
bisar + +
leg downARTERIALARTERIAL
♂frontal
leg
round
cutted
0 ,
±
+
elevationMETABOLICMETABOLIC
NEUROPATNEUROPATacral 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 patient´s disease
and general health statusprophylaxis: 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, detritus2. reduction of inflammation and infection
microbial film, exudation, inflammation3. granulation and epitelisation
+ care of surrounding skin, compression
nekrotic
black
infection fibrin
yelow
epitelisating
pink
granulating
red
Ulcer description
Wound assessment
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
exudate absorption, antisepsis
• Hydrogels• Silicon foams• Polyuretan films
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 progresssionmust 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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