Venous ulcer

Venous ulcer

1. Venous Ulcer Pranjal Rokaya Resident General Surgery KIST MCTH Moderator Dr Rajat Pradhan 4th January, 2023

2. Outline Ulcer: Introduction The venous system of lower limb Lower limb venous disorders Pathophysiology Risk factors 6. Classification 7. Clinical features 8. Venous ulcer 9. Comparison of ulcers 10. Manag e ment of venous ulcer

3. Ulcer Break in the continuity of covering epithelium(skin or mucous membrane) following molecular death of surface epithelium or its traumatic removal. Classification Clinically 1. Spreading Ulcer 2. Healing Ulcer 3. Callous/Chronic ulcer Pathologically Nonspecific Ulcers Traumatic Arterial Venous Neurogenic (trophic) A/w malnutrition 2. Specific ulcers 3. Malignant ulcers

4. Venous system of lower limb Venous drainage of foot Deep venous system

5. Saphenous vein axis: Superficial system Perforator system

6. Lower extremity venous disorders A large spectrum of morphological and functional abnormalities. Can be congenital or acquired. May or may not be symptomatic. Ranges from minimal dilatation of veins to massive varicosities and ulceration.

7. Venous pathophysiology Venous hypertension

8. Risk factors Advancing age Family history of venous disease Ligamentous laxity Prolonged standing Increased BMI Smoking Lower extremity trauma Prior venous thrombosis Pregnancy High estrogen states Some hereditary conditions

9. Classification: CEAP system C : Clinical E : Etiological A : Anatomic P : Pathophysiology

10. Clinical Etiological C0 No visible or palpable sign of venous disease Ep Primary C1 Telangiectasia, reticular veins Es Secondary C2 Varicose veins Ec Congenital C3 Edema En No cause identified C4 Changes in skin and subcutaneous tissue C5 Healed C6 Active venous ulcer S With symptoms A Without symptoms

11. Anatomical Pathophysiology As Superficial veins Pr Reflux Ad Deep veins Po Obstruction Ap Perforator veins Pr,o Reflux and obstruction An No venous anatomic location identified Pn No venous pathology identifiable

12. Clinical features: Symptoms Limb discomfort including leg heaviness or aching. Throbbing or burning pain: Worse on standing/ sitting with feet dependent for a prolonged period. Itching. Limb swelling. Skin changes

13. Clinical signs by CEAP category Co 20% of patients with clinical symptoms have no visible signs.

14. C1: Telangiectasia / reticular veins Most frequently encountered sign. Telangiectasia: Confluence of dilated intradermal venules/ capillaries less than 1 mm in diameter. Reticular veins: Dilated, bluish subdermal veins, 1-3 mm in diameter .

15. C2: Varicose veins Subcutaneous, dilated, tortuous veins more than 3 mm in diameter. Often a/w superficial axial venous reflux.

16. C3: Edema Dependent ankle edema may progress to include the calf region. In the early stage, present only at end of the day. Clues: Edema limited to lower extremity, often unilateral, a/w ot he r signs. Typically subsides with recumbency. (d/d from lymphatic obstruction). CVP normal. Nonresponsive to diuretics; may develop signs of hypoperfusion

17. C4a: Skin pigmentation/ dermatitis Initially prominent at medial ankle but later encroach upon foot and lower leg. Pigmentation due to hemosiderin deposition. Venous reflux predisposes to stasis dermatitis Presents as eczematous rash.

18. C4b: Lipodermatosclerosis Fibrosing panniculitis of subcutaneous tissue. Characterized by firm are of induration, initially located at medial ankle. In late stage, entire legs can be circumferentially involved. Fibrosis may be extensive enough to strangle lower leg. Prone to repeated bouts of cellulitis.

19. C4c: Corona phlebectatita Crown of numerous small, intradermal veins on medial or lateral aspect of ankle or foot. Indicator of venous hypertension due to saphenous or perforator venous insufficiency.

20. C5,C6: Venous ulceration Chronic venous disease common cause of lower extremity ulcers. Commonly have superficial, deep or perforator reflux; alone or in combination. Located low on medial ankle or near the lateral malleolus. Never in forefoot or above the level of knee.

21. Venous leg ulcer: Epidemiology Responsible for 85% of all chronic lower limb ulcers in resource rich countries. Prevalence: 0.1-0.3 % in adults (2-4% in elderly). 15-30% of patients have concomitant arterial occlusive disease

22. Venous ulcer: Pathology Not confirmed : Venous oxygen saturation found higher in ulcerated limbs.

23. Venous ulcer: Pathology

24. Venous ulcer: Morphology Distribution : Medial ankle (gaiter region). Shape : Shallow and flat Margin : Thin and blue of growing epithelium. Edge : Sloping; pale purple in color. Floor : Pale granulation tissue Base : Never penetrates deep fascia Discharge : Seropurulent with an occasional trace of blood.

25. History Complete medical history should be obtained. Diabetes, hypertension, CKD. Smoking history. Occupation history. Past history of DVT. Family history. Increased JVP: Sign of RHF

26. Examination General and systemic examination. Assessment of signs of venous disease. Ulcer : Size, shape, number, position, edge, base, margin, discharge. Pulse examination. Neurological assessment Types of ulcer edges

27. ABI to r/o PAD/mixed ulcer

28. Comparison of major types of leg ulcer Venous Arterial Neuropathic History Prior DVT, stroke Obesity, multiple pregnancies Pain upon prolonged standing Cigarette smoking Diabetes Dyslipidemia Intermittent claudication Diabetes Other causes of peripheral neuropathy Location Gaiter distribution Malleolar regions (M>L) Pressure sites Distal points (toes) Pressure sites Pain Mild to moderate Severe Painless Morphology Irregular borders Shallow Necrotic eschar Punched out Punched out

29. Comparison of major types of leg ulcer Venous Arterial Neuropathic Other findings Varicosities Peripheral edema Stasis dermatitis Weak/absent pulses Prolonged CRT Pallor on leg elevation (45 deg for 1 min) Peripheral neuropathy with decreased sensation. Relevant studies Duplex ultrasonography Ankle-brachial index CT angiography MR angiography

30. Investigations All new patients : CBC, RBS, ESR, CRP; Sickle cell test a. Duplex scan Presence of reflux in the deep and superficial venous system. Extent and distribution of reflux Presence of obstruction in the deep venous system. Presence of thrombus in the superficial system.

31. Investigations b. Venography Ascending : Dye injected into a superficial pedal vein. Descending : Dye into the deep venous system at the groin or popliteal vein. Observation of flow defines regions of thrombus or obstruction. Adjunct to clinical exam and duplex scanning to identify specific valvular incompetence.

32. Management

33. a. General measures Avoidance of prolonged standing. Elevation of feet to at least heart level for 30 mins 3 to 4 times a day. Daily walking and ankle flexion exercises. Skin care : Skin cleansing and use of emollients.

34. Skin care Stasis dermatitis For chronic dryness, petroleum-based emollient. If oozing or vesiculation: Mid potency topical steroid. b. Contact dermatitis Avoid use of topical moisturizers/ antibiotics .

35. b. Compression therapy Keystone of management is to decrease venous HTN. Primary way: Use of compression Four-layer bandaging system Orthopedic Wool Elastic bandage Cotton crepe Cohesive bandage

36. …Bandaging The ideal interface pressure is 35-40 mm Hg. The interval between bandage applications is based on the amount of exudate and speed of healing. Compression in mixed ulcer controversial. For ABPI >0.5, a pressure of 30 mm Hg is safe and effective. For ABPI <0.5, must undergo revascularisation before any compression.

37. Compression stockings Different commercially available stockings with graded pressure

38. c. U lcer care Basic wound care techniques are required. Role of antibiotics Only in those with acute cellulitis or clinically infected ulcer. Routine use in uncomplicated ulcers doesn’t reduce bacterial colonization or improve the healing rate; can cause emergence of resistance.

39. … Ulcer care Systemic antibiotics reserved for patients with: Local heat and tenderness. Increasing erythema of surrounding skin. Lymphangitis (red streaks traversing up the limb. Rapid increase in size of ulcer. Fever.

40. Ulcer care: Debridement Removal of necrotic tissue and fibrinous debris aids in the formation of granulation tissue and enhances re-epithelialization. Regular dressing to control exudate, maintain moisture balance, and control odor and pain. Options include simple nonadhesive dressing, paraffin gauze, hydrogels, hydrocolloids, and silver-impregnated dressings. Few trials support a role of skin grafting for very large ulcers or ulcers present >12 months

41. Ulcer healing and recurrence Continued use of compression bandaging after healing reduces recurrence. Patient offered the strongest compression with which they can comply. Ulcers that persist beyond 6 months or recurrent ulcers should undergo a venous duplex ultrasound to identify segments of venous incompetence amenable to venous ablation.

42. d. Pharmacotherapy Variety of agents that affect venous tone used. Increase tone by a mechanism related to NE pathway. Other actions include reduction of capillary hyperpermeability, improved lymphatic drainage, anti-inflammatory effects, and decreased blood viscosity.

43. …Pharmacotherapy Flavonoids Hydroxyethylrutoside ( HR ) Escin (horse chestnut seed extract: HCE ) Micronized purified flavonoid fraction Meta-analysis of 15 RCTs showed HR has a higher response in pain and swelling control vs placebo. Two meta-analyses: HCE improved symptoms related to chronic venous insufficiency vs placebo

44. ..Pharmacotherapy Aspirin: Insufficient evidence to detect beneficial effect or even harm. Stanazolol: Several RCTs have noted improvement in lipodermatosclerosis areas and possibly faster ulcer healing rates. Pentoxifylline: Metanalaysis of 11 trials: Significantly more effective for complete or partial ulcer healing than placebo (800 mg TDS). Sulodexide, calcium dobesilate: low-quality evidence.

45. e. Surgical therapy Speciality referral in case of: Arterial insufficiency. Nonhealing ulcer. Ulcer recurrence. Suspected contact dermatitis. Resistant or recurrent cellulitis.

46. Surgical therapy

47. i. Ligation and stripping Fully dissect the point of junctional incompetence and remove refluxing axial vein and dilated tributaries. G roin incision made, GSV dissected up to SFJ, GSF tributaries ligated, then SFJ ligated and GSF stripped to around knee.

48. ii. Endothermal ablation Safer, faster recovery, cost effective. Concept: A device inserted into incompetent axial vein p/c. Vein surrounded by LA solution; compresses the vein emptying it of blood. Device produces thermal energy that destroys structure of vein , resulting in permanent occlusion.

49. Endothermal ablation Laser ablation Laser energy at wavelength 1470 nm transmitted to blood itself. Steam bubbles are generated by laser energy, coagulation occurs after energy delivery. Radiofrequency ablation Radiofrequency heat is delivered at a temperature of 120 C. Directly injures vein wall endothelium, resulting in collagen contraction and thrombosis of treated vein.

50. iii. Ultrasound guided sclerotherapy Used for treatment of incompetent perforators and large venous tributaries causes by neovascularisation. Injection of sclerosing agent directly into veins. Most commn agent: Sodium tetradecyl sulphate. Causes cellular death resulting in thrombosis, fibrosis and sclerosis.

51. Prognosis Nearly all venous ulcers can be healed. Even with successful ablation and/or compression; a reulceration rate of 20-30% by five years. Reulceration is greatest in the post-thrombotic leg.

52. Summary Venous leg ulcer a/w profound impairment in quality of life. High chances of recurrence. Treatment a/w high cost to the healthcare system and patient. The mainstay of t/t: reduction in venous hypertension with compression and superficial venous ablation.

53. References Bailey and Love textbook of surgery, 27th edition. Sabiston textbook of Surgery, 11th edition. Swartz textbook of surgery.

54. Thank You.