This document discusses chronic venous disease, including its pathophysiology, risk factors, stages, and management options. It describes how chronic venous disease is a progressive inflammatory condition caused by damaged valves in the veins. The pathophysiology involves leukocyte activation and damage to the venous walls and valves from increased hydrostatic pressure. Management options discussed include lifestyle modifications, compression therapy, sclerotherapy, endovascular ablation procedures, surgery, and drug therapies. The document focuses on understanding the disease process and providing an overview of diagnostic and treatment approaches.
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CHRONIC VENOUS DISEASE: From pathogenesis to clinicals
1. Dr Shahzad Alam Shah
Laparoscopic and Endoscopic Surgeon
Fatima Jinnah Medical University/ SGRHL Lahore
Pakistan
Chronic Venous Disease
From Pathophysiology To Clinical Practice
A Progressive
Inflammatory Disease
2. • Understanding the Pathogenesis
• Diagnostic Implications
• Why there are diversified treatment options?
• And what are these options?
Chronic Venous Disease;
Objectives
3. Risk or Predisposing Factors
• Hereditary
• Prolonged Standing
• Obesity
• History of DVT, DM,
• Number of Pregnancies
https://medlineplus.gov/ency/article/000203.htm
4. Current challenges for the management of
Chronic Venous Disease.
Disease awareness low
Continue to ignore at initial stages.
Culture to wear the full dress
Late Presentations
Delay in diagnosis and treatment
8. Pathophysiological process of chronic venous disease:
Leukocyte Activation
Adapted from Danziger N. J Mal Vasc.
2007;32:1-7 and Bergan JJ et al. N Engl J Med.
2006;355:488-498.
17. Treatment options
• SURGERY
– Ligation of Incompetent Saphenopopliteal and
Saphenofemoral Junctions
– LSV Stripping
– Phelebectomies
– Perforator Ligation
• ENDOSCOPIC
– Subfascial Endoscopic Perforator Surgery
18. MPFF acts at the heart of venous inflammation
in the venous valves and walls
Adapted from Shoab SS et al. Endothelial activation response to oral Micronized Flavonoid therapy in patients with chronic venous disease – a
prospective study. Eur J Vasc Endovasc Surg. 1999;17:313-318.
Leucocyte
Venous wall
endothelium
CD11b/CD18
VLA-4
VCAM-1 E-selectin ICAM-1
L-selectin
MPFF
19. Venotonic and Anti-Inflammatory Action of Drugs
• MPFF improves venous tone by modulating noradrenergic
signaling and reducing norepinephrine metabolism
• MPFF also protects against inflammation-related valve damage
by inhibiting the leukocyte-endothelium interaction,
decreasing capillary permeability, improving capillary
resistance, and increasing lymphatic ...
20. MPFF inhibits the expression of adhesion molecules on
the surface of leukocytes
MPFF exerts anti-inflammatory effects by
inhibiting the expression of adhesion
molecules on the surface of leukocytes,
thereby limiting leukocyte rolling,
adhesion, and subsequently, infiltration
into the venous valves and walls.
Shoab SS, Porter JB, Scurr JH, Coleridge-Smith PD. Effect of oral micronized
purified flavonoid fraction treatment on leukocyte adhesion
molecule expression in patients with chronic venous disease: a pilot study. J Vasc
Surg. 2000;31(3):456-461.
MPFF significantly reduces edema
Blume J, Langenbahn H, De Champvallins M.
Quantification of oedema using the volometer technique:
therapeutic application of Daflon 500 mg in chronic venous
insufficiency. Phlebology. 1992;7:37-40.
MPFF increased venous tone
Barbe R, Amiel M. Pharmacodynamic properties and
therapeutic efficacy of Daflon 500 mg.
Phlebology.1992;7(suppl 2):41-44.
MPFF significantly reduces pain,
heaviness, and cramps.
Tsukanov YT, Tsukanov AY, Nikolaychuk A. Great
saphenous vein transitory reflux in patients with symptoms
related to chronic venous disorders, but without visible signs
(C0s), and its correction with MPFF treatment.
Phlebolymphology. 2015;22(1):18-24.
it should be emphasized that all CVeD clinical pictures are connected to each other because they have a common pathophysiological biomolecular mechanism(s), in which the crucial events of hemodynamic alterations pave the way for a self-sustained vicious cycle of subsequent inflammatory and proteolytic cascades [1,3]