Transcript Chronic Vascular presentation

Chronic venous insufficiency
Management
Chronic venous insufficiency
* Chronic venous insufficiency (C.V.I.)
encompasses disease of the lower limb
veins in which venous return is impaired
usually over a number of years of reflux,
obstruction or calf muscle pump failure.
---------------------- venous hypertension
and ultimately clinical complications
oedema, eczema, Lipodermatosclerosis
and ulceration.
Aetiology:
A- Changes in macrocirculation:
During exercise in normal individual, effective
contraction of the calf muscles combined with vein
patency and valvular competence aids venous
return and reduces venous pressure around the
lower aspect of the leg from about 90 mmHg to 30
mmHg.
Failure of any of these mechanisms may result in
postamubulatory venous hypertension which is the
underlying haemodynamic abnormality in C.V.I.
Causes of venous hypertension
 Superficial venous reflux (long saphenous or short
saphenous vein reflux)
 Deep vein reflux (Primary or secondary to deep
venous thrombosis) It have reported that reflux in
the superficial system is present in approximately
90% of limbs with C.V.I. whereas reflux in the deep
system is detected in only 30% of limbs and the
prevalence of deep venous reflux in limbs with
reflux in the superficial system, is approximately
20%.
 Deep venous occlusion.
 Perforating vein reflux.
 Abnormal calf pump
(Neurological/musculoskeletal).
 Combination of the above.
B- Changes in microcirculation
1- Fibrin cuff theory:
 widening of the pores between endothelial cells allows
the passage of larger molecules out of the intravascular
compartment into the tissues.
This allows the accumulation of fibrin around the
capillaries of the dermis to form a cuff which acts as a
barrier to oxygen and nutrient diffusion to interstitial
tissues and cutaneous skin cells resulting in
local tissue ischaemia and cell death which produces
ulceration.
2- White cell trapping theory:
 It has been proposed that raised venous pressure reduces
the capillary perfusion pressure which in turn causes
trapping of white cells.
 Venous hypertension results in expression of leukocyte
adhesion molecules that permit adherence of leukocytes to
the capillary endothelial cells.
The trapped cells become activated releasing proteolytic
enzymes and oxygen free radicals which produce
endothelial damage and tissue destruction
and local ischaemia.
3- Growth hormone trapping hypothesis
Suggested that the pericapillary cuffs might
interfere with the diffusion of growth factors
which are essential for skin and tissue
repair. This might well explain why
ulcerated or damaged tissue fail to heal.
4- Cutaneous iron overload:
The rise in hydrostatic pressure within the
capillaries combined with increased permeability
leads to extravasations of red blood cells. As they
degenerate the iron is released from the
haemoglobin and deposited within the dermis and
when the amount exceeds the ferritin binding
capacity, iron becomes available in its bivalent
form that can promote the production of oxygen
free radicals and lipid peroxides which in turn can
lead to tissue destruction.
5- Other possible changes:
Arteriovenous shunting.
Decreased response of dermal fibroblasts to
cytokines and growth factors associated with
normal wound healing.
Capillary microthrombosis.
Decreased number of collecting lymphatic
channels and disruption of lymphatic network.
Overactivation of venoarteriolar reflex resulting
in microvascular vasoconstriction in response to
venous pressure above 25 mmHg. Normally this
reflux is abolished by activation of calf muscle
pump and reduction in venous pressure.
CEAP classification of C.V.I.
C. (Clinical class):
- Class 0: No visible or palpable signs of
venous disease.
- Class I: Telangiectasis or reticular veins.
- Class 2: Varicose veins.
- Class 3: Edema.
- Class 4: Skin changes e.g. venous eczema,
pigmentation and lipodermatosclerosis.
- Class 5: Skin changes with healed ulceration
- Class 6: Skin changes with active ulceration
E. (Etiology):
Congenital.
Primary (undetermined cause).
Secondary:
- Post-thrombotic - Post-traumatic
A. (Anatomic distribution of veins):
Superficial.
Perforator.
Deep.
P. (Pathophysiologic mechanism):
Reflux.
Obstruction.
Reflux and obstruction.
Chronic venous insufficiency
CLINICAL STUDY
History of :
• D.V.T.
•Peripheral arterial disease
•Medical problems:- diabetes
Examination for
•varicose veins
•Skin change:- oedema-pigmentation-ulcer{above medial malleolus}
•Peripheral pulses record
•Full neurological examination:- sensory deficitreduced movement
OBESITY/VENOUS ULCER IS ASSOCIATED IN (40%) OF PATIENT
Chronic venous insufficiency
INVESTIGATION
Non-invasive
Duplex scanning
Phlebography
Descending
Ascending
Treatment
Conservative treatment:
1- Elevation of the legs at rest helps to reduce oedema,
decrease exudates from ulcers and accelerate regression of
skin changes.
2- Graduated elastic compression which is highest at the
ankle and decreases proximally
3- Dressings:
The commonest topical ulcer dressings include hydrocolloids (e.g.
dermasorb), Hydrogels (e.g. Geliperm), Alginates (e.g. Kaltostat),
synthetic foams (e.g. lyofoam), capillary and osmotic absorbants
(e.g. debrisan) and polyurethane sheets (e.g. opsite).
4- Systemic medications to promote
healing:
Zinc:
Improves ulcer healing in patients with low
serum zinc level.
Stanozolol (Stromba)
This fibrinolytic enhancing agent has been used
in the treatment of preulcerative
Pentoxyfylline (Trental
lipodermatosclerosis
Oxyrutosides (Paroven)
It reduces capillary permeability and white blood cell migration
and improve tissue oxygenation.
Free radical scavengers
Using either allopurinol or dimethyl sulfoxide
Others:
Prostaglandin E l. Diuretics. Aspirin.
Surgical Treatment
I) Superficial venous surgery.
II) Perforating vein surgery.
III) Deep venous reconstruction .
A- Venous incompetence
1- Valvuloplasty:
* Internal valvuloplasty involving suturing the edge of the valve cusp
close to the vein wall in order to tighten it.
* External valvuloplasty involving suturing of valve cusps at the line
of insertion into the vein wall in order to tighten floppy edges without vein
opening.
2- Valve transposition:
* Involves dividing the incompetent vein e.g. superficial femoral and
reinserting it end to side or end to end into a neighboring vein e.g. profunda
femoris or long saphenous vein.
3- Valve transplantation:
* Involves removing a segment of brachial or axillary vein
containing one or more competent valves and reinserting it into the
popliteal or femoral vein.
4- External support of vein wall by a Dacron cuff:
* To support an incompetent valve thereby making it competent.
5- Reducing the venous diameter in the region of an incompetent valve:
* By removing a triangle of vein wall above the valve.
B- Venous outflow obstruction
Following deep venous thrombosis there may be failure in recanalization
leaving a functional venous outflow obstruction.
1- Femorofemoral cross-over graft for iliac obstruction:
The long saphenous vein on the unaffected is sutured to a suitable vein
in the groin on the affected side which may be the common femoral,
the superficial femoral or even the long saphenous vein.
2- Saphenopopliteal bypass:
In patients with outflow obstruction due to stenosed or occluded deep
thigh veins using the long saphenous vein as a bypass channel. The long
saphenous vein is divided below the knee and is sutured end to side to
the popliteal vein or one of the tibial veins
IV) Skin grafting:
It is done after treatment of underlying venous abnormality and
preparation of the ulcer removing all the slough and necrotic tissue .
It will reduce the healing time.
1- Split skin mesh grafts.
2- Pinch grafts.
3- Full-thickness skin grafts.
V) Flaps:
When a patient has had repeated ulcers which have irreparably
damaged the skin and subcutaneous tissues which are scarred and
avascular.
* Cross - leg fasciocutaneous flaps.
* Vascularized free fasciocutaneous flaps.