Point-Counterpoint: Is Ischemia A Direct Risk Factor For Ulceration?

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Point-Counterpoint: Is Ischemia A Direct Risk Factor For Ulceration?
Point-Counterpoint: Is Ischemia A Direct Risk Factor For Ulceration?
Point-Counterpoint: Is Ischemia A Direct Risk Factor For Ulceration?
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Author(s): 
By Peter A. Blume, DPM, Kenneth L. Cornell, DPM, Bauer Sumpio, MD, and John Aruny, MD; and Mardon R. Day, DPM

   Yes, these panelists say ischemia plays a significant role in chronic ulcerations and emphasize the importance of a thorough vascular workup in these patients.

By Peter A. Blume, DPM, Kenneth L. Cornell, DPM, Bauer Sumpio, MD, and
John Aruny, MD

   Clinicians must consider numerous factors when evaluating and treating ulcerations of the foot. Ulceration in the foot most frequently occurs as a result of a combination of neuropathy, ischemia and trauma. Ulcerations that become chronic in nature frequently result in a lower extremity that is at an increased risk of major amputation. With these ulcerations, arterial insufficiency is a key component that one must identify and manage appropriately.

   Atherosclerosis of lower extremity vessels has been identified as a causative factor in lower extremity ischemia. The comorbidities of diabetes mellitus, hypertension, hyperlipidemia and tobacco use are known to accelerate the progression of lower extremity atherosclerosis.1 Patients with lower extremity arterial insufficiency may be asymptomatic or present with intermittent claudication, ischemic rest pain or tissue necrosis (gangrene). Obtaining a detailed patient history, ensuring a proper vascular assessment and pursuing a consultation with a vascular surgeon for further assessment/treatment are essential in order to promote wound healing and prevent lower extremity amputation.

   When patients have a history of diabetes, macrovascular and microvascular alterations contribute to arterial insufficiency. Atherosclerosis affects the larger peripheral arteries of the cerebral, coronary and lower extremity vasculature. It has been noted that the walls of the arteries affected by atherosclerosis exhibit endothelial cell and smooth muscle cell dysfunction. In patients with peripheral arterial disease (PAD), endothelial cells have a reduced ability to proliferate and migrate in the arterial wall. Conversely, vascular smooth muscle cells demonstrate increased migration, adhesion and proliferation that contribute to the development of atherosclerotic lesions in the arterial wall.2 These focal segmental lesions in the arterial wall result in stenosis of the arterial lumen and an increased resistance to normal blood flow in the artery. Inflammation has been established as a risk marker and a risk factor for atherothrombotic disease states, including PAD.

   Researchers have identified elevated C-reactive protein (CRP) levels in patients with PAD and diabetes.3 C-reactive protein has been found to bind to endothelial cell receptors, promoting apoptosis. In addition, CRP stimulates endothelial production of procoagulant tissue factor, leukocyte adhesion molecules and chemotactic substances, and inhibits endothelial cell nitric oxide synthase, which results in abnormalities in the regulation of vascular tone. C-reactive protein increases the local production of compounds, impairing fibrinolysis and lending to thrombus formation on the arterial wall.

   Nitric oxide is a potent stimulus for vasodilatation and inhibits inflammation by altering the leukocyte-vascular cell wall interface. In addition to limiting platelet activation, nitric oxide acts to inhibit vascular smooth muscle cell migration and proliferation. Therefore, disruption of nitric oxide homeostasis has a significant role in the formation of atherosclerotic plaque development.4 The formation of atherosclerotic plaques in the arterial cell wall can initiate the formation of a platelet-fibrin thrombus. If the platelet-fibrin thrombus is firmly attached to the cell wall, it can continue to increase in dimension until the lumen of the artery is completely obstructed. If the platelet-fibrin thrombus is loosely adhered to the arterial cell wall, the thrombus can be sheared loose by turbulent blood flow and travel to arterioles, causing complete occlusion of the vessel.5

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