Venous Ulcers.pptx

9,345 views 35 slides Nov 15, 2022
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About This Presentation

Lecture notes for medical students


Slide Content

Tips on using my ppt. You can freely download, edit, modify and put your name etc. Don’t be concerned about number of slides. Half the slides are blanks except for the title. First show the blank slides (eg. Aetiology ) > Ask students what they already know about ethology of today's topic. > Then show next slide which enumerates aetiologies. At the end rerun the show – show blank> ask questions > show next slide. This will be an ACTIVE LEARNING SESSION x three revisions. Good for self study also. See notes for bibliography.

An ulcer is a defect with loss of epidermis and atleast part of the dermis

Causes of lower limb ulceration

Causes of lower limb ulceration Venous insufficiency (45 -60%) Arterial insufficiency (10 -20%) Diabetes (15 -25%) Vasculitis Haematological dissease Infections Trauma Drugs/therapy:- hydroxy urea Skin conditions:- pyoderma gangrenosum , necrobiosis lipoidica malignancies Genetic :- prolidase deficiency, klinefelter`s syndrome

Venous Return

Venous Return With 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 In all patients with venous disease there is failure of these one way valves Worsened by impairment of leg muscle function or ankle joint range of motion

Causes of venous ulcer

Risk Factors

Maternal history of venous insufficiency History of DVT, DM, chronic heart failure or recent edema Obesity Severe trauma to the leg Vigorous exercise Number of pregnancies Risk Factors

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

Pathogenesis

Pathogenesis White cell trapping : Endothelium is damaged by increased venous pressure and leukocyte activation. Proteolytic enzymes and free radicals are released, escape through the leaky vessel walls, and damage the surrounding tissue, leading to injury and ulceration.  Impaired lymphatic function

A non-healing open wound Often near the ankle With or without visible varicose veins

Signs and symptoms

Signs and symptoms Usually preceded by patchy erythema or discoloration of an intense bluish red colour (capillary congestion) Ulcer is typically painless. Patients develop typical ischemic pain on elevation of the ulcerated leg, which is oedematous . Associated with arterial disease can ( 1/3 of cases). Ulcer is covered with yellowish exudate over granulation tissue Non-healing ulcer resembles severe paronychia being boggy, undermined and congested from oedema . Base is white and fibrous

Clinical Features

Clinical Features Non healing ulcer in Gaiter area Shallow ulcers Moist granulating base Irregular border. The base oozes venous blood when manipulated. The tissue surrounding these ulcers may exhibit signs of stasis dermatitis. Patients often report mild pain that is relieved by elevation. Signs of venous hypertension are present- varicose veins, varicose eczema or oedema An oedematous leg not responding to diuretics is a strong clue to the diagnosis

Clinical Features Patients often report mild pain that is relieved by elevation. Signs of venous hypertension are present- varicose veins, varicose eczema or oedema An oedematous leg not responding to diuretics is a strong clue to the diagnosis

Imaging Studies

Imaging Studies Duplex ultrasonography saphenofemoral junction incompetence, incompetent perforating veins, anatomic variants. Venography via computed tomography (CT) scanning or magnetic resonance imaging (MRI ) Catheter-directed venography is typically reserved for direct evaluation of anatomic variations such as May- Thurner syndrome, in which the left common iliac vein is compressed by the right common iliac artery.

Treatment

Treatment Modify activity to promote blood flow Apply compression therapy Provide local wound andskin care Treat and control infection inflammation Improve nutrition

Poor circulation decreases delivery of oxygen and nutrients, prevents removal of metabolic waste products such as carbon dioxide, and ultimately delays healing. Blood Flow: The key to Wound Healing

First Step: Assess for PAD (Peripheral Arterial Disease) Check pedal pulses before compression Use Doppler to check ABPI >0.8 (ankle/brachial press. index) If ABI is <0.5 NOcompression needs referral to vascular surgeon

Mechanical therapy

Compression bandaging Reduces venous pressure Improves calf muscle pump function Opposing gravitational venous reflux Improving lymph drainage Stimulates fibrinolytic activity TYPES: Non-elastic wraps (short stretch) Elastic wraps (long stretch) Stockings Graduated multilayer compression bandaging regimens capable of sustaining pressure for 1 week should be 1 st line Should exert pressure of 30 to 40 mmHg at ankle for effective compression

Surgical treatment

Surgical treatment Ligation and stripping of saphenous veins Endovenous Ablation/ endovenous laser ablation (EVLA) Compressive sclerotherapy Complete extirpation of the communicating veins `feeding` the ulcer

IV- deep vein bypass V – valvuloplasty VI- brachial valve transplant Shave therapy: Excision of ulcer followed by meshed split skin graft. Heals 88% of ulcers Skin grafting Punch grafting Split skin grafts Mesh grafts

Advanced Cases: Surgical Treatment

Advanced Cases: Surgical Treatment S ubfascial endoscopic perforator surgery (SEPS) Improves healing rates, and reoccurence

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 Metal frame used to assist Pt should purchase in pairs of two, replace every 6 months

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