Home | | Clinical Dermatology | Venous hypertension, the gravitational syndrome and venous leg ulceration

Chapter: Clinical Dermatology: Disorders of blood vessels and lymphatics

| Study Material, Lecturing Notes, Assignment, Reference, Wiki description explanation, brief detail |

Venous hypertension, the gravitational syndrome and venous leg ulceration

Ulcers of the lower leg, secondary to venous hyperten-sion, have an estimated prevalence of around 1%, are more common in women than in men, and account for some 85% of all leg ulcers seen in the UK and USA.

Venous hypertension, the gravitational syndrome and venous leg ulceration

Ulcers of the lower leg, secondary to venous hyperten-sion, have an estimated prevalence of around 1%, are more common in women than in men, and account for some 85% of all leg ulcers seen in the UK and USA.


Satisfactory venous drainage of the leg requires three sets of veins: deep veins surrounded by muscles; superficial veins; and the veins connecting these togetherathe perforating or communicating veins (Fig. 11.6). When the leg muscles contract, blood in the deep veins is squeezed back, against gravity, to the heart (the calf muscle pump); reflux is prevented by valves. When the muscles relax, with the help of gravity, blood from the superficial veins passes into the deep veins via the communicating vessels. If the valves in the deep and communicating veins are incompetent, the calf muscle pump now pushes blood into the super-ficial veins, where the pressure remains high (‘venous hypertension’) instead of dropping during exercise. This persisting venous hypertension enlarges the cap-illary bed; white cells accumulate here and are then activated (by hypoxic endothelial cells), releasing oxygen free radicals and other toxic products which cause local tissue destruction and ulceration. The increased venous pressure also forces fibrinogen and α2-macroglobulin out through the capillary walls; thesemacromolecules trap growth and repair factors so that minor traumatic wounds cannot be repaired and an ulcer develops. Patients with these changes develop lipodermatosclerosis  and have a high serum fibrinogen and reduced blood fibrinolytic activity. Figure 11.7 shows the factors causing venous ulceration.

Clinical features

Venous hypertension is heralded by a feeling of heavi-ness in the legs and by pitting oedema. Other signs include:

1  red or bluish discoloration;

2 loss of hair;

3 brown pigmentation (mainly haemosiderin fromthe breakdown of extravasated red blood cells) and scattered petechiae;

4 atrophie blanche (ivory white scarring withdilatated capillary loops; Fig. 11.8); and

5 induration, caused by fibrosis and oedema of thedermis and subcutisasometimes called ‘lipoder-matosclerosis’.

Ulceration is most common near the medial malleo-lus (Fig. 11.9). In contrast to arterial ulcers, which are usually deep and round, with a punched out appearance, venous ulcers are often large but shallow, with prominent granulation tissue in their bases. Incompetent perforating branches (blowouts) between the superficial and deep veins are best felt with the patient standing. Under favourable conditions the exudative phase gives way to a granulating and healing phase, signalled by a blurring of the ulcer mar-gin, ingrowth of skin from it, and the appearance of scattered small grey epithelial islands over the base. Prolonged ulceration, with lipodermatosclerosis, gives the leg the look of an inverted champagne bottle.


Bacterial superinfection is inevitable in a longstanding ulcer, but needs systemic antibiotics only if there is pyrexia, a purulent discharge, rapid extension or an increase in pain, cellulitis, lymphangitis or septicaemia.

Eczema  is common around venous ulcers. Allergic contact dermatitis  is a common com-plication and should be suspected if the rash worsens, itches or fails to improve with local treatment. Lanolin, parabens (a preservative) and neomycin are the most common culprits.

Malignant change can occur. If an ulcer has a hyper-plastic base or a rolled edge, biopsy may be needed to rule out a squamous cell carcinoma (Fig. 11.10).

Differential diagnosis

The main causes of leg ulceration are given in Table 11.7. The most important differences between venous and other leg ulcers are the following.

Atherosclerotic. These ulcers are more common onthe toes, dorsum of foot, heel, calf and shin, and are unrelated to perforating veins. Their edges are often sharply defined, their outline may be polycyclic and the ulcers may be deep and gangrenous. Islands of intact skin are characteristically seen within the ulcer. Claudication may be present and peripheral pulses absent.

Vasculitic. These ulcers start as painful palpable pur-puric lesions, turning into small punched-out ulcers.

The involvement of larger vessels is heralded by painful nodules that may ulcerate. The intractable deep sharply demarcated ulcers of rheumatoid arthritis are caused by an underlying vasculitis (Fig. 11.11).

Thrombotic ulcers. Skin infarction (Fig. 11.12), lead-ing to ulceration, may be caused by embolism or by the increased coagulability of polycythaemia or cryoglobulinaemia.

Infective ulcers. Infection is now a rare cause of legulcers in the UK but ulcers caused by tuberculosis, leprosy, atypical mycobacteria, diphtheria and deep fungal infections, such as sporotrichosis or chro-moblastomycosis, are still seen in the tropics.

Panniculitic ulcers. These may appear at odd sites,such as the thighs, buttocks or backs of the calves. The most common types of panniculitis that ulcerate are lupus panniculitis, pancreatic panniculitis and erythema induratum.

Malignant ulcers. Those caused by a squamous cellcarcinoma  are the most common, but both malignant melanomas  and basal cell carcino-mas  can present as flat lesions, which expand, crust and ulcerate. Furthermore, squamous cell carci-noma can arise in any longstanding ulcer, whatever its cause.

Pyoderma gangrenosum. These large andrapidly spreading ulcers may be circular or polycyclic, and have a blue, indurated, undermined or pustular margin. Pyoderma gangrenosum may complicate rheumatoid arthritis, Crohn’s disease, ulcerative co-litis or blood dyscrasias.


Most chronic leg ulcers are venous, but other causes should be considered if the signs are atypical. In patients with venous ulcers, a search for contributory factors, such as obesity, peripheral artery disease, cardiac failure or arthritis, is always worthwhile. Investigations should include the following.

   Urine test for sugar.

   Full blood count to detect anaemia, which will delay healing.

   Swabbing for pathogens (see Bacterial superinfec-tion above).

   Venography, colour flow duplex scanning and the measurement of ambulatory venous pressure help to detect surgically remediable causes of venous incompetence.

   Doppler ultrasound may help to assess arterial cir-culation when atherosclerosis is likely. It seldom helps if the dorsalis pedis or posterior tibial pulses can easily be felt. If the maximal systolic ankle pressure divided by the systolic brachial pressure (‘ankle brachial pres-sure index’) is greater than 0.8, the ulcer is unlikely to be caused by arterial disease.

Cardiac evaluation for congestive failure.

Venous ulcers will not heal if the leg remains swollen and the patient chair-bound. Pressure bandages take priority over other measures but not for atheroscle-rotic ulcers with an already precarious arterial supply. A common error is to use local treatment that is too elaborate. As a last resort, admission to hospital for elevation and intensive treatment may be needed, but the results are not encouraging; patients may stay in the ward for many months only to have their appar-ently well-healed ulcers break down rapidly when they go home.

The list of therapies is extensive. They can be divided into the following categories: physical, local, oral and surgical.

Physical measures

Compression bandages and stockings

Compression bandaging, with the compression gradu-ated so that it is greatest at the ankle and least at the top of the bandage, is vital for most venous ulcers; it reduces oedema and aids venous return. The ban-dages are applied over the ulcer dressing, from the forefoot to just below the knee. Self-adhesive ban-dages (e.g. Secure Forte and Coban) are convenient and have largely replaced elasticated bandages. Bandages stay on for 2–7 days at a time and are left on at night. One four-layer compression bandaging system includes a layer of orthopaedic wool (Velband), a standard crepe, an elasticated bandage (e.g. Elset and Litepress) and an elasticated cohesive bandage (e.g. Secure Forte and Coban): it requires changing only once a week and is very effective. The combined four layers give a 40-mmHg compression at the ankle. Once an ulcer has healed, a graduated compression stocking (e.g. Duomed, Medi Strumpf, or Venosan 2502/2003 (UK) or Jobst or Teds (USA)) from toes to knee (or preferably thigh), should be prescribed, preferably at pressures of at least 35 mmHg. A foam or felt pad may be worn under the stockings to pro-tect vulnerable areas against minor trauma. The stocking should be put on before rising from bed. Care must be taken with all forms of compression to ensure that the arterial supply is satisfactory and not compromised.

Elevation of the affected limb

Preferably above the hips, this aids venous drainage, decreases oedema and raises oxygen tension in the limb. Patients should rest with their bodies horizontal and their legs up for at least 2 h every afternoon. The foot of the bed should be raised by at least 15 cm ; it is not enough just to put a pillow under the feet.


Walking, in moderation, is beneficial, but prolonged standing or sitting with dependent legs is not.


Some physiotherapists are good at persuading venous ulcers to heal. Their secret lies in a combination of the following: leg exercises, elevation, gentle massage, ultrasound treatment to the skin around the ulcers, oedema pumps and graduated compression bandaging.


Many patients are obese and should lose weight.

Local therapy

Remember that many ulcers will heal with no treat-ment at all but, if their blood flow is compromised, they will not heal despite meticulous care.

Local therapy should be chosen to:

   control or absorb the exudates;


   reduce the pain;


   control the odour;


   protect the surrounding skin;


   remove surface debris;


   promote re-epithelialization; and


   make optimal use of nursing time.


There are many preparations to choose from; those we have found most useful are listed in Formulary 1.

Clean ulcers (Fig. 11.13)

Dressings need be changed only once or twice a week, keeping the ulcer moist. Paraffin tulle dressings, plain or impregnated with 0.5% chlorhexidine, 0.25% silver proteinate in compound calamine cream spread on a non-stick dressing, 1% silver sulphadiazine cream, and simple zinc and castor oil ointment, are all helpful and easy to apply. The area should be cleaned gently with arachis oil, 5% hydrogen peroxide or saline before the next dressing is applied. Sometimes immersing the whole ulcer in a tub of warm water helps to loosen or dissolve adherent crusts. The pro-longed use of antiseptics may be harmful.

Many dressings have absorbent and protective pro-perties. These include Granuflex and DuoDERM Extra Thin (which have the advant-age of sticking to the surrounding skin), Geliperm, Kaltostat and Sorbsan in the UK and Duoderm, Opsite and Tegaderm in the USA. Actisorb (UK) is a useful charcoal dressing that absorbs exudate and minimizes odour. Ointments containing recombinant human platelet growth factor may aid revascularization.

Medicated bandages  based on zinc paste, with ichthammol, or with calamine and clioquinol, are useful when there is much surround-ing eczema, and can be used for all types of ulcers, even infected exuding ones. The bandage is applied in strips from the foot to below the knee. Worsening of eczema under a medicated bandage may signal the development of allergic contact dermatitis to a component of the paste, most often parabens (a pre-servative) or cetostearyl alcohols.

Infected ulcers (Fig. 11.14)

These have to be cleaned and dressed more often than clean ones, sometimes even twice daily. Useful pre-parations include 0.5% silver nitrate, 0.25% sodium hypochlorite, 0.25% acetic acid, potassium perman-ganate (1 in 10 000 dilution) and 5% hydrogen per-oxide, all made up in aqueous solution, and applied as compresses with or without occlusion. Helpful creams and lotions include 1.5% hydrogen peroxide, 20% benzoyl peroxide, 1% silver sulphadiazine, 10% povidone-iodine. The main function of dextran polymer beads, and starch poly-mer beads within cadexomer iodine, is to absorb exudate. Although antibiotic tulles are easy to apply and are well tolerated, they should not be used for long periods as they can induce bacterial resistance and sensitize. Resistance is not such a problem with povidone-iodine, and a readily applied non-adherent dressing impregnated with this antiseptic may be useful. Surrounding eczema is helped by weak or moderate strength local steroids, which must never be put on the ulcer itself. Lassar’s paste, zinc cream or paste bandages  are suitable alternatives.

Oral treatment

The following may be helpful.

Diuretics. Pressure bandaging is more important asthe oedema associated with venous ulceration is largely mechanical. Diuretics will combat the oedema of cardiac failure.

Analgesics. Adequate analgesia is important. Aspirinmay not be well tolerated by the elderly. Paracetamol (not available in the USA), or acetaminophen is often adequate but dihydrocodeine may be required. Ana-lgesia may be needed only when the dressing is changed.

Antibiotics. Ulcers need not be ‘sterilized’ by local orsystemic antibiotics. Short courses of systemic anti-biotics should be reserved for spreading infections (see under Complications above) but are sometimes tried for pain or even odour. Bacteriological guidance is needed and the drugs used include erythromycin and flucloxacillin (streptococcal or staphylococcal cellulitis), metronidazole (Bacteroides infection) and ciprofloxacin (Pseudomonas aeruginosa infection). Bacterial infection may prejudice the outcome of skin grafting.

Ferrous sulphate and folic acid. For anaemia.

Zinc sulphate. May help to promote healing, espe-cially if the plasma zinc level is low.

Oxypentifylline (pentoxyfylline) is fibrinolytic, in-creases the deformability of red and white blood cells, decreases blood viscosity and diminishes platelet adhes-iveness. It may speed the healing of venous ulcers if used with compression bandages.

Stanozolol. This anabolic steroid may not heal anexisting ulcer more quickly, but may prevent ulcera-tion in lipodermatosclerosis and may protect against recurrences. The manufacturer’s advice on contrain-dications, e.g. prostatic cancer and abnormal liver function, and on monitoring treatment must not be overlooked.

Oxerutins. These may help the oedema and symptomsof venous hypertension and are said to reduce leakage from capillaries by acting on the endothelial cells.


Autologous pinch, split-thickness or mesh grafts have a place. Lyophilized pig dermis, and synthetic films similar to skin, may also be tried. Sheets of human epidermis grown in tissue culture can be purchased and placed on granulating wound beds. Even if grafts do not take, they may stimulate wound healing and relieve pain. In general, grafts work best on clean ulcers.

Venous surgery on younger patients with varicose veins may prevent recurrences, if the deep veins are competent. Patients with atherosclerotic ulcers should see a vascular surgeon for assessment. Some blockages are surgically remediable.


Study Material, Lecturing Notes, Assignment, Reference, Wiki description explanation, brief detail

Copyright © 2018-2020 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.