VENOUS ULCER

CURRENT PERSPECTIVE
Dr. Jitendra Kumar Jha

Break in skin, present for more than

6 wks, between the malleoli and tibial tuberosity, that is presumed to be wholly or partly due to venous disease.

 Most disabling manifestation of CVI Ambulatory venous hypertension is the hallmark of CVI and is due to venous obstruction, venous reflux or a combination of both

Pathophysiology of CVI
Etiology
- congenital - primary - secondary

Risk factors
- obesity - tobacco use - multiparity - hormone therapy - obstruction within a proximal segment - DVT

Reflux disease
Venous thrombosis Recanalization
venous valve destruction venous insufficiency

 Reflux may also be idiopathic (30%) Incidence increases when popliteal or proximal vein undergo thrombosis Highest incidence of skin changes in chronic obstruction with reflux Limited movement of ankle joint in patients with CVI

Microcirculation
obstruction and reflux dilated and tortuous capillaries High microvascular flow poor venous drainage and venous hypertension transmural pressure in postcapillary vessels skin nutrition and transcutaneous pO ulceration

Coleridge Smith hypothesis

Venous hypertension Reduced capillary perfusion and flow rate WBC to be trapped Release toxic O metabolite and proteolytic enzyme Capillary damage and ischaemia

Clinical evaluation
CEAP CLASSIFICATION
C - clinical sign (A asymptomatic and
S - symptomatic)

Class 0 No visible or palpable sign of venous ds Class 1 - Telengiectasia or reticular veins Class 2 - Vericose vein Class 3 - Oedema Class 4 - Skin changes Class 5 - Healed ulceration Class 6 - active ulceration

E - Etiology
Ec - Congenital Ep - Primary Es - Secondary

A - Anatomical
As - Superficial Ad - Deep Ap - Perforating vein

P - Pathophysiology Pr - Reflux Po - obstruction Pr,o - both

Investigations
Phlebography - Ascending Phlebography
gold standard investigation when duplex scanning is equivocal

- Descending Phlebography
role restricted to cases where venous reconstruction is considered or in recurrent varicose vein

Duplex Scanning - Investigation of choice - 4-7 Mhz multifrequency transducer - Cephalic flow of blood is shown as blue - Reflux shown as red and lasts more than 0.5 secs - Disadvantage Operator dependent Difficult in obese and in edematous pts

Liquid crystal thermography - Reflux seen as hot spot Varicography Ambulatory venous pressure (AVP) - Best method to access ambulatory hypertension - Normal AVP is kept at 30 torr by action of calf muscles. - Venous ulcer unlikely at AVP less than 40 torr.

 Photoplethysmography
Ambulatory strain gauge plethysmography Air plethesmography

Foot volumetry
Capillaroscopy Skin biopsy

Treatment
Goals
- To achieve healing of ulcer - To prevent recurrence - To ensure pt compliance - To provide for return to normal lifestyle

Compression Therapy
- Elastic wraps - Gradient compression stocking
to be effective, the pressure exerted must be above 40mm Hg at the level of ankle - UNNA type paste boot - Polyurethane Foam dressing

OREGON PROTOCOL
Proposed by Mayberry et al Bed rest at home or hospital Application of compression stocking all the time to reduce edema Mean healing time of 5.3 mons Healing rate of 93% Recurrence rate of 16%

Topical therapy
Recombitant human granulocyte macrophage colony stimulating factor Agents which promote healing
Silver sulphadiazine Sulfhydryl compounds Tissue plasminogen activator Sulodexide Amikacin gel Human recombitant epidermal growth factor

 Free radical scavengers

Allopurinol Dimethyl sulfoxide

Pentoxifylline - adjuvant to compression therapy Aspirin - promotes ulcer healing by antithrombotic property (Ibboton et al)

 Semipermeable polyamide mesh placed over graft allows absorption of exudates and shortens mean time for healing (Mahajan et al) Cryopreserved cultured epidermal allograft achieve more rapid healing and greater reduction in ulcer size than hydrocolloid dressing (Teepe et al) DuoDERM - moisture retentive hydrocolloid dressing with fibrinolytic properties in vivo and in vitro

Surgical options
Daily dressing and debridement split skin graft Shave therapy Microvascular free flap

 Treatment of SVI - Flush ligation at saphenofemoral junction - Stripping of saphenous vein with stab avulsion of varicosities - Stab avulsion alone
Saphenous vein ligation alone is inferior to ligation and stripping

 Treatment of Perforator Incompetence

- Classic Lintons operation - Felder or Rob procedure
subfascial ligation without resection of fascia using a posterior midline incision

- Dodd procedure
Posteromedial incision

- Modified Rob procedure

posterior stocking seam approach with Y shaped incision on either side of Achilles tendon

- Subfascial endoscopic perforator surgery SEPS

 Treatment of Deep venous disease

- Direct valve repair
- Vein valve transposition - Vein valve transplantation - Venous by-pass

Conclusion
Ulceration is the most disabling manifestation of CVI Patient education about leg care and compliance is important Compression therapy with appropriate surgery in selected cases

Thank You