Venous ulcer for MBBS

1. VENOUS ULCER
DR. MD. SHERAJUL ISLAM
FCPS (SURGERY), FACS(USA)
ASSISTANT PROFESSOR, SURGERY
SHEIKH SAYERA KHATUN MEDICAL COLLEGE

2. ULCER
An ulcer is a discontinuity of an epithelial surfaces due
to sloughing out of inflammatory necrotic tissues

3. CAUSES OF LOWER LIMB ULCERATION
1. Venous insufficiency (45 -60%)
2. Arterial insufficiency (10 -20%)
3. Diabetes (15 -25%)
4. Vasculitis
5. Haematological disease

4. CAUSES OF LOWER LIMB ULCERATION
6. Infections
7. Trauma
8. Drugs/therapy: Hydroxy urea
9. Skin conditions: Pyoderma gangrenosum
Necrobiosis lipoidica
10. Malignancies
11. Genetic : Prolidase deficiency
Klinefelter's syndrome

5. VENOUS LEG ULCERS

6. VENOUS LEG ULCERS
• Ulcers caused due to venous insufficiency
• Often at lower medial aspect of leg `gaiter region`
• With or without visible varicose veins

7. NORMAL PHYSIOLOGY

8. NORMAL PHYSIOLOGY
• Muscle contraction-- deep veins are compressed-- one way valves in
deep system allow the high pressure flow to move against gravity
• One way valves in perforators close --to prevent pressure injury to the
skin
• There is failure of these one way valves in all patients with venous
disease
• Worsened by impairment of leg muscle function or ankle joint range of
motion

9. INCOMPETENT PERFORATORS AND REFLUX
• Failure of venous valve (REFLUX) and poor calf muscle function
leads to ambulatory venous hypertension and sustained capillary
hypertension
• 60% of venous ulcer patients have isolated superficial vein
insufficiency

10. INCOMPETENT PERFORATORS AND REFLUX

11. PATHOGENESIS
1. Capillary stasis:
Stasis of venous blood in post-thrombotic syndrome gave rise to anoxia and
hence venous ulcers(`Homans` )
2. Fibrin cuff theory:
Venous ulcer could be result of deposition of pericapillary fibrin due to
leakage of fibrinogen through pericapillary spaces (Browse and Bermand)
fibrinogen polymerizes to form fibrin
Oxygen diffusion barrier
Increase in collagen IV in and around capillary

12. PATHOGENESIS
3. White cell trapping:
Leukocytes may become trapped in capillaries in static blood, obstructing
the flow(Coleridge and Smith)
4. Trapping growth factors:
Pericapillary fibrin cuff , α-2 macroglobulin interfere with growth factor
transport (`Felanga and Eaglestein)

13. PATHOGENESIS
5. Multicausal model/ Maastricht model:
Elevated pressures on vascular side of capillaries lead to structural
changes in capillary wall
Inter endothelial space broadens
Collagen IV layer disintegrates
Capillary wall becomes thicker
Water diffusion is affected- oedema
Larger molecules (fibrin ) escape- fibrin cuff formation
α-2 macroglobulin escapes and traps TGF-β

14. CAUSES OF VENOUS ULCER

16. SIGNS AND SYMPTOMS
• Patchy erythema or discoloration of an intense bluish red colour
(capillary congestion)
• Ischemia of the skin leads to necrosis, often following a minor episode
of trauma (scratching, small knocks, dermatitis)
• Ulcer is typically painless
• Patients develop typical ischemic pain on elevation of the ulcerated
leg, which is oedematous

17. SIGNS AND SYMPTOMS
• Associated with arterial disease in1/3rd of cases
• Ulcer is covered with yellowish exudate over granulation tissue
• Healing ulcers have a shallow sloping edge with healthy granulation
tissue in their base and little slough
• Pink lip of epithelium at the edge of ulcer is uniform and supplied by
relatively uncongested capillaries

18. VENOUS ULCER AT INNER ASPECT OF LEG

19. A NON HEALING ULCER WITH A THICK FIBROUS BASE WITH NECROTIC
TURGID EDGE

20. SIGNS AND SYMPTOMS
Signs of venous hypertension are present-
LDS
varicose veins
varicose eczema
oedema
An oedematous leg not responding to diuretics is a strong clue to the
diagnosis

21. LDS- LIPODERMATOSLEROSIS

22. COMPLICATIONS:
• 1)Infection- >105 /cm2 tissue
S. aureus
GAB Hemolytic streptococcus
Candida
• 2)Haemorrhage
• 3)Lymphoedema
• 4)Malignant change
• 5)Subcutaneous calcification
• 6)Bone changes

23. DIAGNOSIS
Clinical:
Gaiter area
Signs of venous hypertension
Past history of venous thrombosis
Past history of treatment for varicose veins
Family history of venous disease
Colour Doppler duplex USG: usually, after ulcer heals
Confirm venous reflux, superficial venous incompetence
Confirm deep venous compliance

24. DIAGNOSIS
Plethysmography:
To investigate calf muscle pump function when Colour Duplex is
normal
Skin biopsy: not indicated in venous ulcer
Skin malignancy or vasculitis suspected
Arterial disease must be excluded by
ABPI
Arterial duplex doppler scanning
arteriography

25. MANAGEMENT
Done by the following means:-
• 1. CONSERVATIVE TREATMENT
• 2. SYSTEMIC MEDICATIONS
• 3. SURGICAL OPTIONS
The goals of treatment are:
.To reduce edema
.Improve ulcer healing
. Prevention of recurrence

26. COMPRESSION THERAPY
• Contraindications to compression therapy include
Clinically significant arterial disease
Uncompensated heart failure
• Methods include
1. Inelastic
2. Elastic
3. Intermittent pneumatic compression

27. COMPRESSION THERAPY
• • Compression therapy is the standard of care for venous ulcers and
chronic venous insufficiency
• • Compression therapy reduces edema, improves venous reflux,
enhances healing of ulcers, and reduces pain
• • After an ulcer has healed, lifelong maintenance of compression
therapy reduce the risk of recurrence

28. 1. INELASTIC COMPRESSION :
• Inelastic compression therapy provides high working pressure during
ambulation and muscle contraction, but no resting pressure
• The most common method of inelastic compression therapy is the
Unna boot, a zinc oxide–impregnated, moist bandage that hardens
after application

29. 1. INELASTIC COMPRESSION :
• Disadvantages:
Because of its inelasticity, the Unna boot does not conform to changes
in leg size and may be uncomfortable to wear
The Unna boot may lead to a foul smell from the accumulation of
exudate from the ulcer, requiring frequent reapplications

30. UNNA BOOT

31. 2. ELASTIC COMPRESSION :
• Elastic compression therapy methods conform to changes in leg size
and sustain compression during both rest and activity
• Stockings or bandages can be used; however, elastic wraps are not
recommended because they do not provide enough pressure
• Compression stockings are removed at night and should be replaced
every six months because they lose pressure with regular washing

32. 2. ELASTIC COMPRESSION :
• Elastic bandages are alternatives to compression stockings (multilayer
bandages are more effective than single layer)
• Disadvantages:
Multilayer compression bandages require skilled application in the
physician’s office one or two times per week
Depending on drainage

33. ELASTIC COMPRESSION

35. 3. INTERMITTENT PNEUMATIC COMPRESSION:
• Comprises a pump that delivers air to inflatable and deflatable
sleeves that embrace extremities, providing intermittent compression
• Generally reserved for bedridden patients who cannot tolerate
continuous compression therapy
• Disadvantages : Expensive
Requires immobilization of the patient

36. INTERMITTENT PNEUMATIC COMPRESSION

37. LEG ELEVATION
• Leg elevation requires raising lower extremities above the level of the
heart
• Aim of leg elevation:
Reducing edema
Improving microcirculation and oxygen delivery
Hastening ulcer healing

38. DRESSINGS
• Dressings are often used under compression bandages to promote
faster healing and prevent adherence of the bandage to the ulcer

39. • Treament of underlying cause of eczema:
Varicose
Contact allergy
Contact irritant
Emollients , Steroids if inflammed
• Cleansing and debridement:
1. Irrigation of ulcer with warm tap water, sterile saline
2. Debridement improves wound healing

40. SYSTEMIC THERAPY
• Antibiotics:- only used if there is clear evidence of infection
• Pentoxyphylline:-
Fibrinolytic
Reduction in leukocyte adhesion
Dose of 400 to 800mgs TDS
• Oral enteric coated aspirin:- 300mg

41. SYSTEMIC THERAPY
• Flavonoid drugs (e.g. oxerutins)
• Daflon 500
• Stanazolol:
androgenic steroid with fibrinolytic property.
Improves LDS
• Iloprost infusion (vasodilator that inhibits platelet aggregation)
• Sodium dobesilate:- 500 mgs BD

42. TYPES OF DEBRIDEMENT
• I. SHARP DEBRIDEMENT
• II. MECHANICAL DEBRIDEMENT
• III.AUTOLYTIC DEBRIDEMENT
• IV.ENZYMATIC DEBRIEMENT
• V. BIOLOGICAL DEBRIDEMENT

43. DRESSING AND TOPICAL THERAPIES
Should keep ulcer moist not wet
Simple ,low adherent
Left undisturbed as long as possible
`strike through` of exudate to outside of the bandage is indication
for change

44. DRESSING AND TOPICAL THERAPIES
1.Knitted viscose primary dressings + superimposed absorbent pad
(secondary dressing)
2. Hydrocolloid dressing- dry sloughy wounds to reduce pain
3. Absorptive dressing (alginate, foam, hydrofibre) – highly exuding
wound
4. Zinc paste bandage (unna boot)

45. SURGICAL TREATMENT
• Between 50-70 % of ulcers heal at 3 months
80-90% by 12 months
• 50% overall recurrence rate by 5-7 yrs. mostly in post thrombotic limbs
Surgical ligation of saphenous vein and incompetent communicating veins is `no
better than` stanozolol and stockings in preventing ulcer
Various procedures used:
• I. Ligation and stripping of saphenous veins
• II. Compressive
• III. Complete extirpation of the communicating veins `feeding` the ulcer

46. SURGICAL TREATMENT
• IV. Deep vein bypass
• V. Valvuloplasty
• VI. Brachial valve transplant
• Shave therapy:
Excision of ulcer and surrounding LDS followed by meshed split
skin graft
Heals 88% of ulcers

47. SURGICAL TREATMENT
• Skin grafting
Punch grafting
Split skin grafts
Mesh grafts
• Subfascial endoscopic perforator surgery (SEPS)
• •Improves healing rates, and recurrence

48. LIFELONG: COMPRESSION THERAPY
• After healing of ulcer, fit for custom stockings
• Remove and bathe each evening, apply moisturizer
• Each morning put on to prevent edema
• Pt should purchase in pairs of two, replace every 6 months

49. ASSOCIATIONS & COMPLICATION OF VENOUS ULCER
1. General disease
Obesity
Hypertension
Cardiovascular diseases
2. Anaemia, hypoproteinemia
3. Depression
4. Inverted foot, equinus ,calf muscle atrophy
5. Zinc depletion

50. ASSOCIATIONS & COMPLICATION OF VENOUS ULCER
6. Infections:
staph. Aureus
groupA β- haemolytic streptococci
pseudomonas
candida albicans
7. Contact dermatitis
8. haemorrhage

51. ASSOCIATIONS & COMPLICATION OF VENOUS ULCER
• 9. Lymphoedema
• 10.Malignant change
• 11.Sub cutaneous calfication
• 12.Bone changes