Venous Insufficiency and Ulceration Flashcards
What is chronic venous insufficiency?
Chronic elevation of deep venous pressure (venous HTN) and blood pooling in lower extremities.
Aetiology of chronic venous insufficiency?
- Calf muscle pump dysfunction and valvular incompetence (phlebitis, varicosities or DVT)
- Venous obstruction
- AV fistulas, venous malformations
What are the clinical features of chronic venous insufficiency?
- Pain, LL oedema (relieved with elevation)
- Pruritus, haemosiderin deposits
- Stasis dermatitis, subcutaneous fibrosis
- Ulceration: shallow, above medial malleolus, weeping, painless, irregular outline
- Signs of DVT/varicose veins / thrombophlebitis
Ix in chronic venous insufficiency?
- ambulatory venous pressure measurement
- Doppler U/S
- photoplethysmography
Conservative Mx chronic venous insufficiency?
- Compression stockings, elevation, avoid prolonged standing
- Ulcers: zinc oxide wraps, split thickness skin grafts, ABx, debridement
Surgical Mx chronic venous insufficiency?
- Surgical ligation of perforators in ulcer region, greater saphenous stripping
- venous bypass if short segment obstruction
Pathophysiology of venous chronic venous disease?
- Blood flow superficial -> deep through unidirectional valves
- Exercise: calf muscle pump + vein patency + competent valves decrease venous pressure 90>30mmHg.
- Failure of any of these results in chronic venous insufficiency
What are the two theories of venous hypertension causing venous ulceration?
- White cell trapping hypothesis
2. Fibrin cuff hypothesis
What is the white cell trapping hypothesis of venous ulceration?
- WBCs larger, less bendy than RBCs
- When perfusion pressure decreased by venous hypertension, WBC plug capillaries -> RBCs congest behind
- WBCs activated –> adhere to endothelium –> release of proteolytic enzymes and ROS
- Endothelial and tissue damage
What is the fibrin cuff hypothesis of venous disease causing venous ulceration?
- increased venous pressure transmitted to capillaries==> capillary elongation and increased endothelial permeability
- fibrinogen deposited into tissues ==> fibrin
- accumulation of fibrin barrier to oxygen ==> tissue hypoxia ==> ulceration
How is severity of venous disease classified?
CEAP C: clinical (i.e. severity of AFx) E: etiology A: anatomic classification P: pathophysiologic classification
What are the major types of leg ulcers?
- Ischaemic
- Neuropathic (DM, EtOH, spinal cord lesions)
- Stasis / venous
CFx ischaemic leg ulcers?
- Painful ulcer
- Hx claudication
- CV RFx
- previous peripheral vascular surgery
Location of ischaemic leg ulcers?
-Distal periphery: dorsum of foot / pretibia
Appearance of ischaemic leg ulcer?
- Puched out edges
- Ulcer base: poorly developed grey granulation tissue
- Surrounding skin pale / mottled with no sigs of inflammation
- Little bleeding with debridement
