Diseases of the Veins
Transcript of Diseases of the Veins
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