What Do Diabetic Leg Ulcers Look Like – Accurate diagnosis and treatment of arterial and venous ulcers using macrocirculatory and microcirculatory functions, noninvasive and invasive testing, and imaging where available.
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Chronic leg ulcers affect about 1 million people in the United States, and that number is likely to increase each year.
The etiology of lower extremity ulcers includes a myriad of systemic disorders and associated risk factors (eg, infection, neuropathy, stress, medications) that clinicians should be aware of before considering treatment.
Although venous leg ulcers are the most common leg ulcers, they account for 70% of all leg ulcers,
Arterial ulcers are commonly associated with large-circulation peripheral artery disease (PAD) and are present in 18% to 29% of people aged ≥60 years.
An estimated 50 to 10 million people in the United States have PAD, many of whom are either underdiagnosed or may present with a “silent” disease until complications such as leg ulcers develop.
Patients with lower extremity ischemic wounds have several risk factors that increase the likelihood of severe tissue loss and major amputation, including increased age, male sex, African-American ancestry, and the presence of peripheral neuropathy and/or infected wounds.
In addition, the TASC II consensus statement states that more than 15% of people with diabetes will develop a foot ulcer (mixed causes) in their lifetime, and that 14% to 24% of these patients will require amputation.
Tissue healing is complex and requires precise environments to develop, independent of local hypoxia, inflammation, neuropathy or stress conditions.
Despite significant advances in research, the exact mechanisms leading to ischemic or venous ulcers have not been fully established.
Figure 1. Different manifestations of arterial ulcers (A, B). In addition to the typical features, chronic muscular dystrophy, extensive tissue necrosis, and local suppurative spread all suggest severe ischemia.
Ischemic ulcers are often described as “spontaneous” lower extremity ulcers (usually in the forefoot and toes) that occur when digital collateral blood flow gradually decreases or truncal occlusion occurs.
Arterial wounds may also present as “minor post-traumatic” wounds (eg, common skin tears, lacerations, blisters, abrasions, etc.), as the local blood flow proves insufficient to increase the oxygen demand necessary for complete healing.
Bed rest, smoking, dyslipidemia, uncontrolled hypertension, obesity, hyperglycemia, uremia, hypoalbuminemia, and hyperhomocysteinemia have been associated with detrimental effects on normal tissue healing.
Other localized, specific conditions, such as peripheral neuropathy, local inflammation, edema, regional infection, or abnormal pressure points, are threats to tissue recovery in addition to preexisting vascular damage.
Coexisting multisegmental arterial disease may lead to more distant local ulcers, especially in patients with inadequate collateral reserve in the foot.
Arterial ulcers usually develop around the distal end of the leg, around the toes, forefoot, or heel (Figure 1), especially in bedridden patients. Some arterial ulcers may mimic venous ulcers by periankle localization (Figure 2), and differential diagnosis and treatment may not always be straightforward.
Ischemic ulcers usually show a characteristic yellowish purulent exudate and necrotic fragments, alternating with islands of gangrenous skin (Figure 1).
When areas of skin necrosis, deep fascia, or tendons were removed, there was no granulation tissue (Figure 3A). The boundary of the ischemic wound is marked by typically disorganized and poorly epithelialized tissue (Figures 1 and 2).
The presence of hypoxia (in addition to parallel systemic factors) and uncontrolled hyperglycemia impairs normal tissue infection control.
Not surprisingly, most wounds resulting from critical limb ischemia (CLI) and almost all neuroischemic diabetic foot ulcers are already colonized at the time of referral.
Extensive skin necrotic changes often mask deep foot abscesses or eventually necrotic areas requiring urgent debridement and vascular referral.
It is important to note that a palpable distal pulse does not formally exclude underlying critical ischemic disease at the microcirculatory level.
In addition to the common atherosclerotic ischemic ulcers, there may be other “artery-associated” ulcers such as hypertensive ulcers, peripheral embolic tissue defects (caused by cholesterol particles 0.01-0.2 mm in diameter) and types of systemic arteritis associated with ulcers, collagen disease or microvascular disease .
Figure 2. Ischemic ulcer on the medial ankle of the leg, resembling a “classic” venous ulcer.
Figure 3. Arterial and venous wounds after local debridement. Arterial ulcer: Note the characteristic hypoxia, minor bleeding, and tissue regression after local debridement (A). Venous ulcers: note specific granulation tissue and correct bleeding after removal of necrotic tissue (B).
The true “tip” between viable and infeasible footing structures may depend on local certainties and the adaptability of specific vessels.
The timing and intensity of the primary CLI threat, the type of initial arterial pathology, the residual arterial trunk and branches, and the timeliness of debridement and revascularization play a critical role in any arterial wound evaluation.
The degree of local infection and the number of collaterals lost to inflammation and pyogenic thrombus formation determine the degree of tissue loss.
Interventional therapists often encounter patients with PAD who have more than one factor detrimental to wound healing while interfering with physiologic healing.
“True” arterial ulcers are relatively rare in routine clinical practice. Informed physicians should always suspect other concomitant pathological conditions, such as venous insufficiency or neurological effects, especially in diabetic patients.
Figure 4. Venous ulcer. Clear progression of scarring (D) with chronic inflammation between the inflammatory (A) and exudative phase (B) to the granulation phase (C) and ulcer recurrence.
Venous ulcers are seen in patients with a history of long-standing chronic venous disease (Figure 4). In this setting, orthostatic blood pressure increases in the deep venous limb system, exacerbating venous hypertension.
This primary pathologic condition progresses from the perforating veins to the superficial venous system, resulting in persistent venous blood pooling and abnormal oxygen saturation.
With venous valvular insufficiency, the normal unidirectional flow (from the superficial to the deep system) no longer exists and valvular insufficiency results in bidirectional flow.
Obstruction of venous blood drainage results in chronic venous and capillary congestion, local inflammation and edema, leading to progressive skin and subcutaneous tissue changes (lipoderm sclerosis).
Unlike arterial ulcers, where ulceration and necrosis are usually associated with specific measurable thresholds (below 30–40 mm Hg, assessed by SPP or TcPO
), and for venous ulcers there is no clear degree of blood pooling and abnormal local tissue desaturation that constantly marks ulcer development. Approximately 50% to 60% of patients with venous ulcers have incompetent superficial and perforating veins.
Approximately 25% of venous ulcers with proven venous pathology are associated with concomitant ischemic arterial disease (Figure 5).
If a mixed arteriovenous ulcer is diagnosed (Figure 5), classical compression therapy should be modified accordingly or omitted.
Modern recommendations for assessing venous ulcers suggest that both legs need to be examined in the supine and upright positions.
Other venous features include bone edema, varicose veins, localized hemosiderosis, ankle abduction, areas of localized seborrheic sclerosis or “white atrophy,” and scar tissue from previous wounds (Fig. 7).
Ulcers vary in size and location, but are usually located on the inside of the bone and around the medial malleolus (Figures 4 and 7).
These wound beds often contain a high fibrin exudate. Most venous ulcers are infected on examination and may then contain purulent debris.
Eczema skin changes and venous dermatitis may also occur in the surrounding skin area (Figure 4D and Figure 7B).
Figure 6. More complex tissue defect in diabetic patients with mixed arteriovenous and neuropathic ulcers. Initial presentation of CLI (A) and clinical evolution at 7 weeks due to multidisciplinary team approach (B).
Venous ulcers and major clinical disability. Prolonged or underestimated vein disease can lead to irreversible skin and tissue deformities, which affects the patient’s quality of life.
Recurrent ulcers with malignant scarring associated with loss of subcutaneous fat and fibrotic skin changes can result in an “inverted champagne bottle” appearance of the leg.
Practical points. Any distal leg or foot ulcer should first be suspected of associated ischemic disease unless careful clinical and noninvasive diagnostic testing proves otherwise.
If ignored, venous ulcers are not as harmless or harmful as previously thought (however, they can lead to serious complications such as malignancy, osteomyelitis, sepsis, gait disturbances, etc.). In the case of concomitant venous disease or related complications, they require aggressive screening and treatment.
Conditions other than a primary arterial, venous, or mixed arteriovenous etiology should be excluded for proper evaluation of a leg ulcer. Although rare, ulcers can also result from venous malformations (for example, Klippel-Trénaunay or Parkes-Weber syndrome)
Several diagnostic methods can help clinicians better identify etiologies or parallel risk factors for lower extremity ulcers.
Figure 8. Bone scintigraphy SPECT with 99mTcsestamibi tracer showing the blood supply to the calf and foot muscles. Three-dimensional images with spatial resolution showing normal (left limb, A) and ischemic (right limb, B) perfusion in the distal foot.
Accessory artery testing is recommended for PAD if the initial clinical diagnosis is equivocal or if the wound does not show a clear trend toward tissue recovery. TASC II standard
Recognize the concomitant threat of ischemia when ankle pressure falls below 50 mmHg or toe systolic pressure falls below 30 to 40 mmHg (Table 1).
Likewise, an ankle-brachial index (ABI) value below 0.5 (remember that ABI can be normal or high due to calcification of the arterial wall),
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