Wound care clinicians usually equate intermittent claudication (IC) specifically to peripheral arterial disease (PAD). However, claudication as a symptomatology is not always specific to PAD, but is terminological to other processes, including the venous system (venous claudication) and the neurospinal axis (neurogenic claudication).1 The differentiator is the anatomical location, whether the symptoms of pain are exacerbated by exercise and relieved by rest.2 The purpose of this editorial is to discuss the clinical implications of claudication as a symptom; the use of diagnostic tools will not be addressed.
The clinical signs and symptoms of PAD include the “rubor of dependency,” the “pallor of elevation,” a history of claudication, and calf pain while walking up an incline.
Although obstruction and claudication in the arterial system are caused by a blockage in the arterial system (inflow), venous obstruction is a blockage of the venous system (outflow), and the most common etiology is postthrombotic syndrome.3 In contradistinction to PAD claudication, venous claudication has a distinct causality and clinical characteristics. “Intermittent Claudication on a Venous Basis” was published as an index case,4 in the Journal of the American Medical Association on April 1, 1961. In this instance, a 32-year-old pregnant woman was diagnosed with IC in a leg following an iliofemoral phlebitis for which she had an anticoagulation. The patient manifested little or no chronic edema and no ulceration. Unfortunately, she did manifest claudication of the thigh, with pain, after walking 1 block or uphill at a more rapid pace, subsiding at rest. Her venous examination was normal. There was no rubor of dependence, and her distal pulses and neurologic examination were normal. She underwent a sympathetic block without results. Her symptoms were consistent with an occluded iliac vein. And the distribution of the symptoms was consistent venous claudication.4
The commonly recognized symptoms and signs of the postthrombotic syndrome include pain with prolonged standing, edema, hyperpigmentation, and ulceration. In terms of claudication, patients also develop severe thigh pain with strenuous exercise in contrast to leg/calf pain in PAD. There remains a paucity of literature on venous claudication, and the pathophysiology is not well elucidated. A more extensive examination of venous claudication by Cockett et al5 described thigh pain that developed within 5 minutes of a “stepping” test.5 The authors asserted that venous claudication and pain occurred only in chronic obstructions involving the proximal ileofemoral venous segments. They also concluded that venous claudication did not occur in patients with either valvular incompetence or postthrombotic occlusion of the peripheral deep veins. Furthermore, they suggested that the obstructions and symptoms might be relieved by graft bypassing the obstructed area.5
The spine consists of 3 articulations, also called the “3-joint complex” (vertebral body–disc–vertebral body joint and 2 facet joints).6 The central spinal canal accommodates and protects the spinal cord and the bilateral neuroforamen, which serve as a conduit to the emanating spinal nerve roots. Any loss of disc height or 2-level degeneration of the disc is characterized by low disc height and disc bulging, resulting in venous compression and spinal or neurogenic claudication. Blood is pumped into the compartment, but venous outlet blood can no longer drain. The accruing metabolic waste products lead to a type of compartment syndrome. The pressure is relieved when you bend forward or sit down. In contradistinction to the claudication of PAD, the pain of neurogenic claudication is relieved by walking up an incline with the spine flexed forward. The continuum of spinal stenosis starts with congestion/stasis and progresses to obstruction of the veins/arteries and structural changes. Only at the final stage does neurocompression occur. “Neurogenic claudication” was first described by Henk Verbiest, who established the relationship between lumbar spondylosis and neurogenic signs and symptoms in the legs. As a result of his work, most clinicians now classify neurogenic claudication as spinal stenosis.2
From a mechanistic view, claudication and pain are a result of compromise to the nerves, arteries, veins, and lymphatics. The compromise can be via external compression from a compartment syndrome, tumor, hemorrhage, or bony growth into the spinal canal or from any neurovascular external compression. From a vascular point of view, claudication may result from intraluminal compromise to an artery (blockage) or vein (thrombus).
Claudication and pain should be evaluated in the context of the patients’ narrative, history, and physical examination. It is important for the wound care clinician to develop a differential diagnosis of the causative factors related to claudication and to consider that a patient may manifest claudication at multiple points in the nerves, arteries, veins, and lymphatics.
1. Rajamanickam A, Krishnan P. History and physical examination in diagnosis of peripheral artery disease. Interv Cardiol Clin 2014; 3: 461–7.
2. Meru AV, Mittra S, Thyagarajan B, Chugh A. Intermittent claudication: an overview. Atherosclerosis 2006; 187: 221–37.
3. Delis KT, Bountouroglou D, Mansfield AO. Venous claudication in iliofemoral thrombosis: long-term effects on venous hemodynamics, clinical status, and quality of life. Ann Surg 2004; 239: 118–26.
4. Weiss MM. Intermittent claudication on a venous basis: case report. JAMA 1961; 175: 1178–80.
5. Cockett FB, Thomas ML, Negus D. Iliac vein compression. Its relation to iliofemoral thrombosis and the post-thrombotic syndrome. Br Med J 1967; 2: 14–9.
6. Rauschning W. New perspectives in spinal anatomy. Spine (Phila, Pa 1976) 2016; 41(Suppl 7): S4–5.