Flashcards in Venous Insufficiency and Ulceration Deck (23):
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)
-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
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?
1. 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?
C: clinical (i.e. severity of AFx)
A: anatomic classification
P: pathophysiologic classification
What are the major types of leg ulcers?
2. Neuropathic (DM, EtOH, spinal cord lesions)
3. Stasis / venous
CFx ischaemic leg ulcers?
-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
Signs of chronic arterial insufficiency?
-Atrophic nails / skin
-slow capillary return
CFx neuropathic ulcers?
-Hx diabetes / other causes of neuropathy
Signs of neuropathy (a/w neuropathic ulcers)?
-2 point discrimination diminished
-Vibratory perception decreased
Location of neuropathic ulcers?
-Plantar surface of MTPs
-Dorsum of IP joints
-Base of 5th MT
-MM or LM
-Callused posterior rim of heel pad
CFx venous ulcers?
-Hx venous insufficiency (VVs, thrombophlebitis, DVT)
-Previous venous surgery
Appearance venous ulcers?
-Large, irregular area
-Location: over gaiter area (common = medial malleolus)
-Moist, granulating base
-Surrounded by zone of inflammation and stasis dermatitis
Ix in ulcer workup?
-BSL + HbA1C
-Xray/bone scan / MRI
-Duplex (art / venous)