Peripheral arterial disease (arteriosclerosis)
Arterial thrombosis ⁄ macrothromboembolism and microthromboembolism (fibrin, platelets)
Fat embolism (hypercholesterolemia, hyperlipidemia)
Detachment of cholesterol-containing plaques from aorta, aneurysm, or atrium (atrial fibrillation)
Thromboangiitis obliterans (Buerger disease)
Arteriovenous anastomosis (congenital ⁄ traumatic)
Trauma, rupture, infection, vascular procedures
Raynaud phenomenon, scleroderma
Hypertension: ulcus hypertensivum (Martorell ulcer)
Increased blood viscosity (increased fibrinogen level, paraneoplastic, paraproteinemia, leukemia)
Blood transfusion reactions
Small vessel: small vessel-leukocytoclastic vasculitis, microscopic polyangiitis, Wegener granulomatosis, allergic granulomatosis (Churg–Strauss), Henoch–Schonlein purpura, essential cryoglobulinemic vasculitis, erythema induratum Bazin, livedo reticularis, livedo vasculitis, and Sneddon syndrome
Medium-sized: polyarteritis nodosa, Kawasaki disease
Large vessel: giant cell arteritis (polymyalgia rheumatica, Takayasu arteritis)
Sickle cell anemia, other forms of anemia, thalassemia, hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, essential thrombocythemia, thrombotic thrombocytopenic purpura, granulocytopenia, polycythemia, leukemia, monoclonal dysproteinemia (Waldenstrom disease, myeloma), polyclonal dysproteinemia (cryofibrinogenemia, purpura, hyperglobulinemia, cold agglutinins)
Arterial ulceration almost always involves bony high point and is due to pressure necrosis where the relatively mild pressures involved are sufficient to cause ischemia where the arterial perfusion pressure is low.
Arterial ulcers are associated with pain making them very distinct from venous ulcers. Vascular pain is a complex issue leading to sympathetic changes causing skin hyperalgesia, dystrophic skin with shinny appearance.
According to a recent report, chronic kidney disease (CKD), hypertension, and myocardial ischemia may also be associated with increased risk of developing foot ulcers including severe ulcers that necessitate amputation .
11.4 Clinical Features
11.4.1 History and Assessment
The first step toward diagnosis of any leg ulcer is to compile a comprehensive history and assessment of the patient (Table 11.2) . This should include general health status, social and occupational situation, past and current medical history of relevant diseases (such as deep vein thrombosis, diabetes, autoimmune disorders, inflammatory bowel disease, and connective tissue disease), condition of the skin, current vascular status, limb size and shape, and history and status of the ulcer.
Characteristics of different types of ulcers
Associated Vasc Sx
Small, punched out
P.Hx ulcers or surgery or angioplasty or tissue loss
Often large and messy
± atrophie blanche
No arterial Sx unless combined.
Previous Ulcers/DVT/compression Rx etc.
Pressure areas – foot (great and little toe), May be Charcot’s foot
Often based on joint/tendon/bone
Look for deformity of the foot
Acute on chronic inflammation
No vascular Sx unless superimposed PVD
May be normal
Well-perfused skin, no chronic changed unless chronic infection
Ragged in some cases
Bleeding, Should granulate
Inflamed, indurated base
Background of palpable purpuric change
Look for skin/joint/CREST/genital/serosal/constitutional manifestations/deep organ manifestations
The patient should be asked about lower extremity pain, paresthesia, anesthesia, and claudication. It is important to determine the duration of ulceration and whether it is a first episode or recurrent. Pain is a major problem for patients with leg ulcers unless there is a neuropathic component. Lack of pain, therefore, suggests a neuropathic etiology. Patients should also be asked about their mobility.
A typical arterial ulcer is located distally in extremities (toes, heels, and bony prominences of the foot) and usually present with nocturnal rest pain. The ulcer appears “punched out,” with well-demarcated edges and a pale, nongranulating, often necrotic base (Fig. 11.1a), which differentiates it from other types of ulcers (Table 11.3). The surrounding skin may exhibit dusky erythema and may be cool to touch, hairless, thin, and brittle, with a shiny texture. The toe nails thicken and become opaque and may be lost . Gangrene of the extremities may also occur.
(a) Arterial ulcer, (b) vasculitic ulcers, (c) Martorell ulcer
History and assessment of the patient with limb ulcer
History of ulcer development
Past and current medical problems
General health status
Limitations to self-care
Ankle–brachial pressure index
Sensation and pain
Site-venous, arterial, pressure
Vasculitic ulcers tend to have some characteristics similar to ischemic ulcers, including their location, size, and shallow depth. There are several typical differences, however. Vasculitic ulcers frequently have irregular shapes and borders (Fig. 11.1b). Additionally, the floor of the wound tends to be necrotic with significant vascularity. The surrounding skin is usually hyperemic rather than pale. Vasculitis may also feature other cutaneous manifestations, including palpable purpura, petechiae, and persistent urticaria .
A rare condition exists called Martorell ulcer (Fig. 11.1c), seen in patients with prolonged, severe, or suboptimally controlled hypertension . The ulceration is secondary to tissue ischemia caused by increased vascular resistance. The ulcers are usually located at the lower limb, above the ankle region, contain black necrosis and are extremely painful. By definition, the distal arterial pulsations are normal, and the diagnosis is made by histological examination, which shows concentric intima thickening and marked hypertrophy of the media of small-sized and medium-sized arteries, and by exclusion of other conditions that may cause ulceration in this area. The differential diagnosis consists of arteriosclerotic occlusion of small-sized arteries, diabetic angiopathy, vasculitis, thromboembolic occlusion (e.g., in atrial fibrillation), and pyoderma gangrenosum. Treatment consists of reducing hypertension, adequate control of pain, and local wound care .
Examination of the arterial system may show a decreased or absent pulse in the dorsalis pedis and posterior tibial arteries. There may be bruits in the proximal leg arteries, indicating the presence of atherosclerosis.
Clinical course of the ulcer can suggest its etiology. Possible considerations to rule out include diabetes; hypertension; hyperlipidemia; coronary artery disease; alcohol and tobacco use; thyroid, pulmonary, renal, neurologic, and rheumatic diseases; and specifically cutaneous factors including cellulitis, trauma, and recent surgery.
Diagnosis includes blood investigations for risk factor screening and noninvasive and invasive vascular investigations.
11.6 Blood Investigations
Blood investigations such as complete blood count, erythrocyte sedimentation rate, blood sugar, lipid profile, renal function tests, and liver function tests are essential in patients with chronic leg ulcers.
Laboratory screening tests for vasculitis: urine analysis for proteinuria, hematuria, cylindruria, routine and immunohistopathology of skin biopsies, antinuclear antibodies, rheumatoid factor, complement C4, circulating immune complexes, paraproteins, immunoglobulin fractions, antineutrophil cytoplasmic antibodies (ANCA), serological tests, and cultures for underlying infections .