Pathophysiology venous reflux

1. Pathophysiology of
venous reflux
Parach sirisriro
1st Aug 2017

2. Reference

3. • Chiu J.J., and Chien S.: Effects of disturbed flow on vascular endothelium:
pathophysiological basis and clinical perspectives. Physiol Rev 2011; 91: pp. 327-387
• Seshadri Raju, MD, FACS,a Mark Ward Jr, MS,a and Tamekia L. Jones, PhD, :
Quantifying saphenous reflux : Journal of vascular surgery venous and lymphatic
disorder , The American venous forum 2015
• Karthik Gujja, MD, MPH, Jose Wiley, MD*, Prakash Krishnan, MD : Chronic Venous
Insufficiency : clinic review article , Peripheral vascular disease Rev 2014
• Jünger M1, Steins A, Hahn M, Häfner HM. Microcirculatory dysfunction in chronic
venous insufficiency (CVI). Microcirculation. 2000;7(6 Pt 2):S3-12
Reference

4. Outline
• Basic concept of venous anatomy and physiology of venous
blood flow
• Concept of Macrocirculatory Dysfunction
• Concept of Venous Microcirculatory Disturbances and
Dysfunction
• Pathology of venous ulcer

5. Chronic venous insufficiency -DEFINITION
• Medical condition where veins cannot pump enough
deoxy blood back to the heart
• “impaired musculovenous pump”
• Mainly in a)Legs
b)CNS
c)Liver

6. • Chronic venous insufficiency have two component
Venous reflux
Venous obstruction
Chronic venous insufficiency

7. Anatomy of the veins of the lower extremity

8. Venous Systems
of the Extremities
Three components:
• Superfcial vein
• Perforating veins
• Deep vein

9. The superfcial system
• The great saphenous vein,

10. Saphenofemoral junction

11. The small saphenous system
runs along the posterolateral
aspect of the calf to join the
popliteal vein behind the knee
Called “Saphenopopliteal
junction”
The superfcial system

12. The deep system
• located in the fascial muscle
compartments,
• follow the same course as the
arteries, and for the most part,
have the same names

13. Deep veins
 Act as reservoir
Accounts for venous return
antigravity backflow to the
right heart
Tissue drainage and
thermoregulation.

14. Perforators
• Perforating veins connect the deep
system with the superficial system
• They pass through the deep fascia
• Guarded by valves-unidirectional
flow from superficial to deep veins
VN20-03-B 10/04

15. Types of
perforators
Perforators of the foot
(venae perforantes pedis)
Perforators of the ankle
(venae perforantes tarsalis)
Perforators of the leg
(venae perforantes cruris)
Perforators of the knee
(venae perforantes genus)
Perforators of the thigh
(venae perforantes femoris)
Perforators of the gluteal muscles
(venae perforantes glutealis)

16. Physiology of
venous blood flow

17. NORMAL VENOUS HEMODYNAMICS
• Two important functions
—return of blood to the heart from the
capillary bed
— maintenance of cardiovascular
hemostasis through changes in
capacitance.

18. NORMAL VENOUS
HEMODYNAMICS

19. Normal venous flow in the Leg

20. Venous Valves
Prevent retrograde flow.
Lower extremities : The
highest concentration
Most commonly bicuspid
and can form sinusoidal
dilatations

21. .
Foot and calf muscles act to squeeze
blood out of deep veins.
One way valve allow only upward and
inward flow.
During muscle relaxation blood is
drawn inward through perforating
veins

22. Risk factors
Age
Pregnancy
The menstrual cycle
Genetics
Obesity and overweight
Posture

23. Pathophysiology of venous reflux

24. ANY RISK FACTOR INCREASED VENOUS PRESSURE
DILATION OF VEIN WALLS
STRECHING OF VALVES-VALVULAR INCOMPETENCE
REVERSAL OF BLOOD FLOW
FAILURE OF MUSCLES TO PUMP BLOOD
VEINS DISTEND,ELONGATE,TORTOUS,POUCHED,INELASTIC
AND FRIABLE

26. Macrocirculatory Dysfunction

27. Venous pressure is increased and return of blood is
impaired
These mechanisms induce venous hypertension,
particularly with standing or ambulation
Macrocirculatory Dysfunction

28. • Valve failure
Primary :
preexisting weakness in the vessel wall or
valve leaflets
Secondary :
direct injury, superfcial phlebitis, or
excessive venous distention resulting from
hormonal effects or high pressure
Macrocirculatory Dysfunction

29. Macrocirculatory Dysfunction

30. Valve failure of the deep veins
Blood volume is pumped out of the extremity,
Refill occurs rapidly by both arterial inflow and
pathologic retrograde venous flow.
Venous pressure remains elevated
Macrocirculatory Dysfunction
Karthik Gujja, MD, MPH, Jose Wiley, MD*, Prakash Krishnan, MD : Chronic Venous Insufficiency :
clinic review article , Peripheral vascular disease Rev 2014

31. Dysfunction or incompetence of the valves
in the superfcial venous system
Retrograde flow of blood and the
development
of increased hydrostatic pressure.
Macrocirculatory Dysfunction
Karthik Gujja, MD, MPH, Jose Wiley, MD*, Prakash Krishnan, MD : Chronic Venous Insufficiency :
clinic review article , Peripheral vascular disease Rev 2014

32. • Failure of valves located at junctions of
the deep and superfcial systems
• At the saphenofemoral and
saphenopopliteal junctions, allows high
pressure to enter the superfcial veins.
Macrocirculatory Dysfunction
Karthik Gujja, MD, MPH, Jose Wiley, MD*, Prakash Krishnan, MD : Chronic Venous Insufficiency :
clinic review article , Peripheral vascular disease Rev 2014

33. Macrocirculatory
Dysfunction
Karthik Gujja, MD, MPH, Jose Wiley, MD*, Prakash Krishnan, MD : Chronic Venous Insufficiency :
clinic review article , Peripheral vascular disease Rev 2014

34. Macrocirculatory
Dysfunction
Karthik Gujja, MD, MPH, Jose Wiley, MD*, Prakash Krishnan, MD : Chronic Venous Insufficiency :
clinic review article , Peripheral vascular disease Rev 2014

35. Venous Microcirculatory Disturbances
and Dysfunction

36. High venous pressure the capillary bed
Chronic damage and microcirculatory dysfunction.
Venous Microcirculatory Disturbances
and Dysfunction
Jünger M1, Steins A, Hahn M, Häfner HM. Microcirculatory dysfunction in chronic
venous insufficiency (CVI). Microcirculation. 2000;7(6 Pt 2):S3-12
“glomerulus-like” capillaries

37. Venous Microcirculatory Disturbances
and Dysfunction
Capillaries of patients with CVI increased pericapillary edema
The accumulation of fluid, macromolecules, & extravasated red blood cells
Fragmentation and destruction of
microlymphatics and dysfunction of local nerve fibers
Jünger M1, Steins A, Hahn M, Häfner HM. Microcirculatory dysfunction in chronic
venous insufficiency (CVI). Microcirculation. 2000;7(6 Pt 2):S3-12

38. Pathology of venous ulcer

39. Fibrin Cuff theory
•
Associated with restriction of
oxygen diffusion across the vessel
wall leading to edema and
dermatosclerotic skin changes.

40. Fibrin cuff theory
valvular incompetence venous stasis
ambulatory venous hypertension
Defective micro circulation Excessive RBC lysis eczema
Excessive release of hemosiderin and fibrin
Pigmentation,dermatitis and lipodermatosclerosis
capillary endothelial damage lack of exchange of nutrients
Anoxia
ULCER

41. Water Hammer Effect
• This theory is the most widespread pathogenesis of CVI.
• It contends that reflux is mainly transmitted to the
superficial veins through perforators.
• Studies by Raju and Fredericks have shown that this effect
explains and correlates with most venous ulceration cases.

42. WBC TRAPPING THEORY
• Raised venous pressure reduced capillary perfusion trapping of WBC
• Venous hypertension expression of leucocyte adhesion molecules
Adhesion of WBC to capillary endothelial cells
release of proteolytic enzymes and free radicals
Endothelial damage, tissue destruction, local ischemia

43. Summary
• Chronic venous insufficiency have two component
Venous reflux and Venous obstruction
• Normal Flow : Superficial veins drain into the deep veins From the
foot up to the heart Superficial vein disease always starts with
abnormal valves and interruption to normal flow called venous
reflux

44. Thank You