Venous Ulceration - Assessment and Treatment

Venous Ulceration - Assessment and Treatment

48 Journal of Tissue Viability 1993 Vol. 3 No 2 VENOUS ULCERATION -ASSESSMENT AND TREATMENT AIDEEN WALSH\ JANET HEDGES 2, NICOLA STUBBING2, BRIAN GW...

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Journal of Tissue Viability 1993 Vol. 3 No 2

VENOUS ULCERATION -ASSESSMENT AND TREATMENT AIDEEN WALSH\ JANET HEDGES 2, NICOLA STUBBING2, BRIAN GWYNN3 1

Registrar in Surgery, 2 Clinical Nurse Specialists, 3 Consultant Surgeon, Department of Surgery, Stafford District General Hospital, Stafford

INTRODUCTION Venous ulceration is a common condition with an incidence of 1.5-1.8/1000 population 1.2 rising up to 20/1000 in women over 80 years- an important point when dealing with an ever aging population. Most patients are treated in the community and present a considerable workload to district nursing services both in terms of time and cost- a figure of £200 million per year cost to the NHS quoted in 1988 3 may be overly conservative.

AETIOLOGICAL ASSESSMENT While venous disease is undoubtedly the commonest cause of lower limb ulceration, many other conditions may predispose to, or cause ulcers and should be considered (Table 1). The classic teaching that venous ulcers always appear over the area of the medial malleolus in the presence of varicosities is frequently untrue and more detailed patient assessment is mandatory. A full history should be taken detailing the length of time the ulcer has been present, the presence and nature of any pain and other features of venous insufficiency including oedema and an eczematous type rash. It is also important to enquire about any previous deep venous thrombosis or surgery to the leg as well as general medical conditions such as diabetes mellitus, rheumatoid arthritis or congestive cardiac failure. It is vital that arterial insufficiency is sought as a cause for ulceration and a history of claudication or foot pain should be enquired about. The Lothian and Forth Valley study 1 showed an incidence of arterial insufficiency of 21% - not surprisingly more common in their elderly patients. Examination of the ulcer should include assessing its site and size as well as specific features of venous disease such as haemosiderin pigmentation of the skin, lipodermatosclerosis and eczema. Primary skin tumours or malignant change in a chronic ulcer (Marjolin 's Ulcer) should be excluded by biopsy. Assessment ofthe arterial supply is undertaken by palpation of pedal pulses and measurement of the ankle-brachial pressure index (ABPI) using Doppler to measure pressure in all three ankle arteries. Where the ABPI (ankle brachial pressure index), calculated by dividing the ankle pressure by the brachial pressure is >0.8, significant arterial disease is unlikely. Portable Doppler ultrasound can also be used for detecting venous reflux by searching for a refluxing signal along the superficial or deep veins. Using a tourniquet to selectively occlude the superficial veins it is then possible to determine whether any reflux is deep or superficial - and if the latter to which system - long or short saphenous - it is related. Specific refluxing perforating veins can also be mapped with a Doppler probe. For such venous assessment a 4 MHz probe is more useful than the higher frequency probes usually employed to measure ABPI. More intensive investigation with Duplex ultrasound, venography,

ambulatory venous pressure monitoring or ascending or descending venography can be helpful in complex orrefractory ulcers, but is rarely necessary for most venous ulcers.

TYPES/CAUSES OF LEG ULCERS VASCULAR Venous Arterial Lymphatic VASCULITIC Collagen diseases e.g. Rheumatoid arthritis, polyarteritis nodosa, scleroderma, systemic lupus erythematosus Allergy METABOLIC Diabetes mellitus Gout Nutritional deficiency Uraemia HAEMATOLOGICAL Polycythaemia rubra vera Sickle cell anaemia Thalassaemia Hereditary spherocytosis Leukaemia INFECTIVE Bacterial Fungal Syphilitic Amoebic Secondary infection of other conditions MALIGNANCY Squamous cell carcinoma Ba-sal cell carcinoma Malignant melanoma Lymphoma MISCELLANEOUS Trauma Burns Frost bite Radiation Insect bites Drug allergy and/or extravasation Table 1

Journal of Tissue Viability 1993 Vol. 3 No 2 49 PATHOPHYSIOLOGY - THE RATIONALE FOR COMPRESSION Venous ulcers are the result of failure of epithelial repair and regeneration in poorly nourished skin. Inadequate cellular nutrition arises as a result of impaired diffusion of metabolites and nutrients to and from the local capillaries, this being caused by proteins (principally fibrin) laid down in the tissues having previously been forced out of the capillary bed by high pressure at the venous end. Visual evidence of this is apparent by the haemosiderin deposition seen in so many affected limbs as a result of haemoglobin breakdown. Such abnormalities in the microcirculation impair healing and also predispose to secondary infection which further aggravates the condition.

Treatment is primarily aimed at abolishing infection and counteracting the venous hypertension such that the tissues have an opportunity to heal. Even with optimal treatment healing may be delayed due to the increased diffusion distance from capillary to cell, compounded by possible impairment of fibrinolysis seen in the skin of these patients. The easiest way to counteract venous hypertension is to elevate the limb - but in most cases the prolonged period of bed rest this would entail to heal an ulcer is inappropriate. Complications such as deep venous thrombosis, pressure sores and respiratory tract infections must be borne in mind and the economics of prolonged inpatient care are an important consideration in the present health service environment. To counteract the forces across the capillary wall an external pressure of 40 mmHg at the ankle is required which, when combined with calf muscle pump activity in an ambulant patient, is usually sufficient to promote an environment conducive to ulcer healing. A problem evident for many years has been the failure of bandaging to achieve and maintain such compression. Even when elastic bandages managed to achieve pressures of25 mmHg at the ankle this force has been measured to disappear after 24 hours 4 • However, in 1988 Blair et al4 at Charing Cross Hospital were able to show that a multi layer bandaging system reliably achieved graduated compression of 40 mmHg at the ankle reducing to 17 mmHg at the knee - and maintain this for up to one week. Furthermore there is good evidence from that same unit that sophisticated and frequently expensive dressing materials do not influence healing and a simple, inexpensive dry dressing against the ulcer is as good as anything else 5 • In the absence of cellulitis in the limb systemic antibiotics are not indicated and the ulcer should be simply washed with physiological saline solution to remove debris and commensal bacteria. Gentle mechanical debridement of slough and debris is often possible and may aid healing. Topical antibiotics and other lotions are of little proven benefit and frequently lead to local sensitivity reactions and the emergence of resistant bacteria. The four layer bandage system comprises a non-adherent dry dressing to the ulcer followed by orthopaedic wool (Velband, Johnson & Johnson, Soffban, Smith & Nephew) wrapped around the leg from toe to knee. An average leg requires one roll. The aim is to protect bony prominences and produce a more cylindrical shape for the next layers. The wool also serves to soak up any ulcer exudate. The next layer is a simple cotton

crepe bandage which also soaks exudate over the following week and at application holds the wool neatly in position. The third layer which compresses at about 20 mmHg is a firm elastic bandage. This is usually Elset (Seton) which is applied at half stretch in a figure of eight manner but Thuane may be better in larger legs. Layer four is Coban (3M) - an elastic cohesive bandage which adds to the compression, holds the bandage together and improves the cosmetic appearance. Modifications to this regime may be necessary with larger diameter legs requiring heavier bandages e.g. Thuane, and smaller legs needing more wool. In these cases it should be remembered that ankles which are very oedematous at the start of treatment must be re-measured after the first week as the need for added compression may have disappeared. When one is applying such powerful compression, it is vital to be assured of a good arterial supply to the limb and all patients should have an ABPI assessment prior to treatment - an index less than 0.8 represents a contra-indication to four layer compression. Correct application of the bandages is another factor and the technique should only be used after appropriate tuition. COMPRESSION TREATMENT IN THE COMMUNITY We have been involved in the setting up of a community based scheme to treat venous ulcers in Mid Staffordshire Health District. The first step to the success of this programme was the appointment of a community based Nurse Specialist, in our case a District Sister of some years standing, who was well aware of the extent of the problem, who received tuition in Doppler pressure measurement and bandaging technique and who showed enthusiasm for the regime of treatment. The first venous ulcer clinic was started in the hospital out-patients department and was placed alongside a Consultant Vascular Surgeon's Clinic. This ulcer clinic was staffed and run, however, entirely by district nurses. Since this first clinic, three more weekly clinics have been established in the community, this time in local health centres. Over the next five years it is expected that a network of clinics geographically equidistant from each other will be established throughout the district. At these clinics the Nurse Specialist teaches and supervises her colleagues in the techniques of diagnosis and treatment and experiences are shared. New patients are assessed as described above with venous Doppler assessment and ABPI measurement. We have found that patients themselves tend to find these clinics an enjoyable social event, the majority being elderly and they frequently look forward to what may be their one outing of the week. Transport to and from the clinics is arranged by a valuable network of volunteer drivers available within our district. Where patients are immobile, assessment and treatment is undertaken in their own homes.

The hospital based clinics run concurrently with one of the weekly vascular surgical clinics and this enables close liaison between the community services and the surgical team. Venous ulcer referrals to the vascular service can be managed by the district nurses with ease, and likewise patients with therapeutic problems or complicated ulcers can be seen by a Consultant Vascular Surgeon without the need for further GP referral. This direct contact adds considerably to the confidence which most

50 Journal of Tissue Viability 1993 Vol. 3 No 2 GPs now have in the programme, whereby they are happy to refer patients directly to the Nurse Specialist, confident that should a problem be uncovered or arise, it will be dealt with correctly and promptly. Review of our results over the first eighteen months shows that 206 leg ulcers in 173 patients have been treated. An overall healing rate of 59% - with figures at 12 and 24 weeks of 31% and 50% -the longest taking 50 weeks. These results are disappointing when compared to the 74% twelve week healing rate achieved in the initial Charing Cross study 4 but represent an advance on our experience prior to the programme. However, many of these ulcers were so chronic that in some cases the patient could not ~emember lif~ with
and durable. Replacement on a weekly basis considerably reduces nursing workload when compared to our previous treatm~nts which were haphazard and required dressing changes three times each week. We expect the costs of this treatment to be similarly reduced. The main drawback currently has been the cost of the bandages

used as many of these are not available on FP1 0 tariff. Costs of

the programme have therefore fallen on the Acute Unit or community nursing budget and should perhaps be absorbed by the FHSA or GP Fundholders. The Department of Health no ~O';Jbt m~dful of the long-term savings possible has madekn~wn Its !nten~on to pi~~ all_ the ~dages necessary on the tariff, but ratificati
REFERENCES 1. Callam MJ, Rockley C, Harper D, DaleJ. Chronic ulceration of the leg: extent of the problem and provision of care. Br Med J, 1985; 1: 1855-66. 2. Comw~ll N, Dore CJ, Lewis JD. Leg Ulcers: epidemiology and aetiology. Br J Surg, 1986; 73: 693-6. 3. Editorial. Kings Fund grant to help treat leg ulcers. Br Med ], 1988; 297: 1412. 4. BlairSD, WrightDDI,BackhouseCM,RiddleE McCollum CN. Sustained compression and healing of chr~nic venous ulcers. Br Med J, 1988; 297: 1159-61. 5. BlairS, Backhouse C, Wright D, Riddle E, McCollum CN. Do dressings influence the healing of chronic venous ulcers? Phlebology 1988; 3 (1): 129-34.

21st TISSUE VIABILITY SOCIETY MEETING BRISTOL UNIVERSITY 23 - 24 SEPTEMBER 1993

'Bridging the Gap'

1st Day Implementing Research Findings into Practice 2nd Day Tissue Viability from Hospital to the Community

Call for Papers. Conference Co-ordinators: Dr N Cullum, Dr J Young, Mr W Haughton, Miss J Davies, Mr K Gerbhardt Further details from: The Secretary Tissue Viability Society, Salisbury District Hospital, Salisbury SP2 8BJ. Tel 0722 336262 Ext 4057. Fax 0722 336262