1. MUDr. Nina Benáková Dermatovenerologická klinika 1. LF UK Praha
Diseases of the veins
MUDr. Nina Benáková
Dermatovenerologická klinika
1. LF UK Praha

2. Importance medical, social, pharmacoeconomic epidemiology, demography
interdisciplinary collaboration, teamwork
Centers for wound healing:
Leg ulcers
Diabetic foot
Decubites
Varices
Chronic venous incompetence

3. deep + superficial venous system + perforators

4. Physiologic blood stream from surface to profundity and proximal

5. venous valves – direction, inhibition of reflux

6. 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

7. 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

9. 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 < 2 mm
reticular 2-4 mm
stem > 4 mm

10. Posttrombotic
syndroma
→ incompetence
of perforators
and superficial veins
→ secondary
varices

11. starburst varices
stem varices

12. Complications of varicouse veins
bleeding
trombophlebitis
in 1/3 cases + deep thrombosis
phlebothrombosis trias of symptoms
in 50% inappparent Diff. dg.
phlebitis migrans recidivans - symptom

13. Therapy of varicous veins
Prophylaxis “regime measures“
therapy of phlebotrombosis – trombolysis
Compression bandages - correct application!
Pharmacotherapy: venotonics, rheologics, oedema-protectives, anticoagulation agents – supportive
Sclerotisation
Surgical therapy

14. 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%

15. 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

16. Classification of CVI varices, reversible edema
varices, permanent edema + trophic changes
varices, edema+ trophic changes + ulcus
(scar)
Trophical changes:
hyperpigmentations
hypodermitis → dermosclerosis
stasis dermatitis → eczema
verrucous hyperplasia
white atrophy
CVI ≠ varices

17. CVI grade II
Stasis dermatitis =
Dermatitis varicosa
corona phlebectatica

18. white atrophy
papillomatosis
= verrucous hyperplasia

19. hemosiderin
hyperpigmentations

22. arterial ulcer
diabetic
gangrene

23. kalosities
neuro - trophic
ulcer
diabetic ulcerations

24. Dif. dg. algorithm ETIO Local Shape Puls Perception / pain ♀ maleol
VENOUS ♀
maleol
medial
bisar +
leg down
ARTERIAL ♂
frontal
leg
round
cutted
0 ,
elevation
METABOLIC
NEUROPAT
acral
necrosis
permanent

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

26. Contact iritative or allergic dermatitis ?

27. erysipelas cellulitis,
dermatolymfangiodermatitis
spinocellular cancer

28. Therapy of leg ulcers Complex I biological – psychological – social
Complex II - medical
therapy of al patient´s disease
and general health status
prophylaxis: regime measures, pressotherapy
causal therapy + skin symptoms:

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

30. Ulcer description Wound assessment nekrotic black granulating red
infection fibrin
yelow
epitelisating
pink

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

34. Modern dressing - overview
Hydrocoloids
Alginates
Hydropolymers
Polyuretan foams
Polyacrylates
exudate absorption, antisepsis
Hydrogels
Silicon foams
Polyuretan films
wet dressing.
antisepsis

36. 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

37. to be continued …

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

39. papillomatosis
= verrucous hyperplasia

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

41. Erysipelas in lymphedema

44. 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