VENOUS ULCER

Dr.S.Susrusha
3 B.D.S
rd
 Ulcer
Discontinutity of skin or mucous membrane
which occur due to microscopic death of tissue
*It can occur on skin ,oral cavity, duodenum
intestine,etc
Pathologic classification:
1. Non specific ulcer :
 Arterial ulcer
Venous ulcer
Diabetic ulcer
Traumatic ulcer
 2. Specific ulcer : occurs due specific bacteria
eg: tubercular ulcer ,syphyilic ulcer

3.Malignant ulcer: sqamous cell carcinoma

. Basal cell carcinoma
. Malignant melanoma
VENOUS ULCER
It is non specific pathologic ulcer
Also called gravitational ulcer
 They include varicose ulcers and
thrombotic ulcer
 Precipitating Factors : 1.venous stasis.
2.tissue anoxia
 Varicose veins: Dilated veins as a penalty
for vertically against

1.Superficial venous system

2.Perforators
3.Deep venous system
 Superficial venous system of leg
Tributaries of dorsal venous arch ( permits
reverse flow of blood through its competent
valves)

Ascending to medical malleolus(runs along

medical side of leg)

Ascends in thigh

Ends at the saphenofemoral Junction by

joining femoral vein
2. Perforators : veins
thatjoin superficial veins to
deep veins
3 types :
1. Leg perforators : 3 in
number
2. Knee perforators : just
below the knee(boyds )
3. Thigh perforators :
palm beneath above
knee perforators
 3. Deep venous
system :
Comprises of
FEMORAL
and POPLITEAL veins
. Any damage to the
valvespresent in these 3
types of veins leads to
varicose inturn leads to
venous ulcer
Normal phsiology:

1.Calf Muscle Pump:

alternative contraction
and relaxation of
muscles of leg
2. Competent valves:
* helps for uni
directional flow of
blood .

• When these valves

are
weak or absent
results
In varicose veins
Deep vein
thrombosis :
Thrombosis(solid
mass in blood
stream) which
obstruct the
blood flow to
heart and also
the movement
of valves
Pathophysiology:
Sustained venous pressure

Results in extra vasation of

cells

Release of free radicles

Distruction of tissue leading

to ulceration
2 hypothesis :

Fibrin cuff Hypothesis:

 Capillary proliferation + Inflammation
Chronic inflammatory cells (macrophages)are
responsible for development of venous ulcer.
Perivascular cuff –develops around the capillaries
Fibrin cuffs is made up of connective tissue proteins
 fibrin
Collagen IV
Fibronectin
 White cell trapping hypothesis:
 Hypertension

 Leukocytes are trapped and gets activated

 Release proteolytic enzymes

 Damage the epithelium

 Predisposing factors:
1.Ambulatory venous hypertension
2.Perivascular fibrin cuff resulting in poor diffusion of
oxygen to the tissues
3.White cell trapping
4.Reactive oxygen species are increased and they
generate free radicals and they generate free
radicals leading to tissue damage
5.Inhibition of growth factors leading to poor repair
Other factors:
.Lipodermatosclerosis
. Refers to various skin changes in the lower leg
associated with varicose veins such as:
.Thickening of subcutaneous tissue
.Indurated wood like feel
.pigmentation
 Venous pressure

Capillary leakage

Extravasation of blood and fibrin into

surrounding tissue

Blood Globin + Haem

Haem+ Iron Haemosiderin
pigmentation
Features:
 •situated in medical maleolus area
•long saphenous vein : medial side
• Short saphenous vein :lateral side
Ulcer is oval, small, painless and pigmented
Superficial shallow
Bleeding from ulcer
Dilated veins above the ulcer
Ulcer shows evidence of healing
If infected or cause periositis tibia
 Treatment

Rest with elevated limb

Elastic crepe bandage helps in venous
return
Active exercises
Passive excercises
If infected – antibiotics are prescribed
Continued…..