Vascular and Lymphatic Disorders

Venous ulcers

These are confined to the lower limbs and many are postthrombotic. The increased hydrostatic pressure in the veins resulting from incompetent valves is reflected by increased capillary blood pressure. Leakage of plasma under pressure gives rise to perivascular fibrin deposition which may lead to a decrease in oxygen supply, but direct skin oxygen measurements do not support this view.

There is a fall in oxygenation when an ulcerated limb is exercised, so that ambulant patients experience sustained hypoxia of the skin. Nutrition of the skin is then affected and leads to ischaemia and eventual ulceration. Ulcers around the ankle are often accompanied by:

• Hyperpigmentation following extravasation of red cells and haemosiderin deposition
• Dermatitis and excoriation due to pruritus
• White atrophy (atrophie blanche) caused by hyalinization of skin vessels producing scars in the overlying skin
• Secondary infection with possible cellulitis or thrombophlebitis The differential diagnosis of leg ulcers is shown in Table 20.5.

Some cutaneous markers of malignant disease.
Some cutaneous markers of malignant disease.

Arterial ulcers

Ulcers occurring in skin away from the ankle region are more commonly associated with arterial disease. They may accompany venous hypertension in the legs, especially in the elderly. Cold, atrophic skin with loss of hair, impalpable peripheral pulses with a history of claudication may suggest the diagnosis. The ulcers usually have a punched-out appearance and are often very painful. Doppler studies may help to determine the degree of arterial insufficiency in an affected limb.

Venous insufficiency
Arterial insufficiency

Post cellulitis
Desert sore
Buruli ulcer
Swimming pool granuloma
Superficial or deep fungal

Diabetes mellitus

Sickle cell disease

Kaposi’s sarcoma
Basal-cell carcinoma

Rheumatoid, systemic lupus erythematosus
Pyoderma gangrenosum
Trauma or artefact

Causesof leg ulceration.


GENERAL MA AGEMENT consists of reducing leg venous hypertension. This can be helped by wearing support bandages when standing or by elevation of the limbs when sitting or lying. Exercise should be encouraged and, if the patient is obese, weight reduction recommended.

DERMATITIS should be treated with bland non-steroidal applications such as zinc and salicylic acid paste . Impregnated bandages containing zinc and applied moist can dry out and stiffen to provide occlusion and support.

ULCERS should be cleaned with normal saline or a wealc potassium permanganate solution. A non-adhesive absorbent dressing should be applied with an elasticated bandage up to the knees. These dressings may be viscous materials, alginates, semi-permeable films, hydrogels or hydrocolloids. These are expensive but covering the wound with a permeable membrane will diminish pain and encourage re-epithelialization.

Clean granulating ulcers should have non-adherent dressings applied and left undisturbed for increasing periods as the ulcer heals. A debriding agent (e.g. hydrophilic polysaccharide beads) or surgery may be necessary to remove dead tissue. Pinch grafting may also be necessary. The grafts are removed from the thigh and dotted over the ulcers and left undisturbed for 10 days.

INFECTION. Local antibiotics should be avoided ifpossible. Ps. aeruginosa infection accompanies nonpermeable occlusive dressings. Systemic antibiotics may be required for cellulitis.

FOLLOW-UP care and preventative measures are most important and elastic stockings may always be

VARICOSE VEINS. Treatment may be necessary.

Pressure sores (decubitus ulcers)

These occur in the elderly, immobile, unconscious or paralysed patients. They are due to skin ischaemia from sustained pressure over a bony point. Normal individuals feel the pain of continued pressure and even during sleep, movement talces place to change position continually.

1 The majority of pressure sores occur in hospital: (a) 70% in first 2 weeks of hospitalization
(b) 70% are in orthopaedic patients especially those on traction
2 20-30% occur in the community
3 80% of patients with deep ulcers involving the subcutaneous tissue die in the first 4 months

Altered sensation of the skin increases the risk of ulceration and patients with diseases that affect the circulation and tissue nutrition also are predisposed, e.g. rheumatoid

Pyoderma gangrenosum
Pyoderma gangrenosum

Multiple myeloma
Other paraproteinaemias. especially IgA
Arthropathy (rheumatoid and spondylarthropathies)
Inflammatory bowel disease
Acute leukaemia
Polycythaemia vera
NB No cause is found in 50% of cases

Conditions associated with pyoderma gangrenosum


Lesions most commonly arise as inflammatory pustules or papules that appear on the trunk and limbs. They may rapidly enlarge over several days to produce large necrotic ulcers with a crescentic or polycyclic outline and sloughy base, which undermines a raised purplish prominent rim.

Other patients may have a more slowly progressive indolent ulcer.

Less frequently, but especially in association with acute myelogenous leukaemia, ulceration may be superficial and arise as necrotic bullae.


Rapidly progressive and painful lesions are accompanied by systemic symptoms and require doses of prednisolone 80-100 mg. Azathioprine may be used in combination or alone. The underlying condition should be treated. Tetracyclines, colchicine and clofazimine have been shown to be of benefit in a few patients. Indolent ulcers may respond to topical therapy and intralesional steroid injections.

Antiphospholipid antibody syndromes

Antiphospholipid antibodies including the lupus anticoagulant (LA) and anticardiolipin (ACL) are associated with thrombosis, central nervous disease and spontaneous abortion with or without SLE.


• Livedo reticularis, livedo reticularis with cerebrovascular accidents (Sneddon’s syndrome)
• Thrombophlebitis
• Cutaneous gangrene and necrosis of digits
• Skin ulcerations
• Lesions resembling vasculitis, nodules, macules
• Cutaneous necrosis/infarction
• Subungual splinter haemorrhages

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