About physiology of venous return from lowerlimb , pathology behind varicosity and classification of varicose vein disease. ( Reference : Bailey and Love)

2. PROF.S.P.GAYATHRE.M.S
ASSISTANT PROFESSORS:
Dr.G.KARTHIKEYAN,M.S
Dr.R.SYED RAJ,M.S
S4 UNIT

3. PATHOPHYSIOLOGY
OF
VENOUS DISEASES

5. 1.What are the two major veins of hand?
2.Have you ever seen varicose veins of hands?
Ulnar and radial vein
3.Do you know why?

7. To overcome the
effect of GRAVITY
LOWER LIMB has
some special
mechanism

8. PRESSURE GRADIENT

9. HIGH PRESSURE
LOW PRESSURE

10. PERIPHERAL PUMP
Calf ,
Thigh &
Foot pump UNIDIRECTIONAL
NONREFLUXING
VALVES
NEGATIVE
INTRATHORACIC
PRESSURE
VIS-A-TERGO
VENA COMITANTES
SYMPATHETIC
ACTIVITY
FACTORS
RESPONSIBLE
FOR NORMAL
VENOUS
RETURN

11. MOTOR PIPE TANK
SOLEUS MUSCLE VEINS HEART
1.MUSCLE PUMP

12. STRUCTURE

13. DURING MUSCLE RELAXATION, PRESSURE WITHIN CALF
COMPARTMENT FALLS
BLOOD FROM SUPERFICIAL VEINS ENTER DEEP VEINS
SUPERFICIAL VENOUS pressure cont. To fall TILL
THRESHOLD IS REACHED
THRESHOLD IS APPROX. 30mmHg
VENOUS INFLOW NOW KEEPS PACE
WITH EJECTION FROM DEEP VEINS
Patency of veins
Competent valves
RELAXATION PHASE

14. RELAXATION CONTRACTION

15. DURING MUSCLE CONTRACTION, PRESSURE WITHIN
CALF COMPARTMENT RISES TO 200-300mmHg
BLOOD FROM DEEP VEINS ENTER IVC
VALVES OF PERFORATOR VEINS CLOSED
TO PREVENT REFLUX
CONTRACTION PHASE

16. AMBULATORY VENOUS HYPERTENSION
REFLUX OBSTRUCTIVE

17. 2. NON REFLUXING VALVES

18. 3.NEGATIVE INTRATHORACICPRESSURE

19. 4.VIS-A-TERGO
12mmHg 32 mmHg

20. 5.VENAE COMITANTES

21. PATHOGENESIS
ChangesinVeinWall
Smooth Muscle Proliferation
Increased MMP
Collagen deposition
Decreased elastin content

22. Changes in vein wall
over stretching of veins
increase in size of veins but valve leaflets don’t expand
Secondary valvular Incompetence
Backflow( reflux)
Pooling and further dilation of veins
Varicosity – Dilated Tortuous Veins

23. COMPETENT VALVE INCOMPETENT VALVE

25. PRIMARY:
 Congenital weakness in vessel wall
 Congenital absence of valves
 Congenital Valvular incompetence
 Familial (FOX C2 gene)
 Lysosomal enzyme activity(Haardt)
 Chronic inflammatory process(Class II MHC &
Macrophages)
ETIOLOGY

26. SECONDARY :
OBSTRUCTION
TO FLOW:
DESTRUCTION
OF VALVES:
1.Pregnancy
2.Pelvic tumor:
Ovarian ca
Fibroid uterus
3.Ascites
4.Retroperitoneal fibrosis
5.Iliac vein thrombosis
1.Deep vein thrombosis
HIGH PRESSURE
FLOW:
1.AV fistula
KLIPPEL
TRENAUNAY
SYNDROME

27.  Gender
 Age
 Ethnicity
 Body mass
index&height
 Family history
 Pregnancy
 occupation and lifestyle
factor;
 smokers,
 constipation
 occupations which involve
prolonged standing.
 Traffic police
 Bus conductors
 Sports man
 Nurses
 Surgeons
 hair stylists
 Factory workers
OTHER RISK FACTORS

29. • C = CLINICAL CLASSIFICATION
• E = ETIOLOGICAL CLASSIFICATION
• A = ANATOMICAL CLASSIFICATION
• P =PATHO-PHYSIOLOGICAL
CEAP CLASSIFICATION

30. TELANGECTASIA :
<1 mm
Spider veins, thread veins,
hyphen webs
RETICULAR VEINS:
Dilated, subdermal veins
1-3mm in diameter
CLASS 1

31. VARICOSE VEINS:
Varicose veins are defined
as dilated, usually
tortuous, subcutaneous
veins 3 mm in diameter
measured in the upright
position with demonstrable
reflux.
CLASS 2

32. CLASS 3
DEPENDENT PITTING EDEMA:
Result of increase in
volume
of fluid
Elevation/compression
bandaging

33. CLASS 4A
PIGMENTATION:
Brownish Discolouration
Hemosiderin deposition
ECZEMA :
Erythematous dermatitis
Progress to blistering,
weeping or scaling eruption
of the skin

34. CLASS 4B
LIPODERMATOSCLEROSIS:
Localised chronic
inflammation and fibrosis of
skin and subcutaneous
tissue
Severe stage of chronic
venous disease
ATROPHIE BLANCHE:
Localized white atrophic
skin - dilated capillaries and
hyperpigmentation
site

35. CLASS 5
HEALED ULCER:

36. CLASS 6
ACTIVE ULCER:
epidermal defect
gaiter area

38. IDENTIFIED

40. IDENTIFIED

41. SAPHENA VARIX:
Large groin varicosity
Painless lump
standing
recumbent
Cough impulse

42. CORONA PHLEBECTASIA:
Fan shaped patterns of
small intradermal veins
Site
Malleolar or Ankle Flares