Clinical Vascular Examination

Chronic Arterial Insufficiency

The natural history of arteriosclerosis in the lower extremity can be viewed as a progression of symptoms that reflect the degree of vessel occlusion and presence of collateral circulation. Symptoms classically begin with an intermittent and reproducible pain termed claudication, a derivation of the Latin word for “limp.” Intermittent claudication is characteristically brought on by a given degree of exercise and relieved after a few minutes of rest. These symptoms reflect the demand for an increase in blood flow that cannot be met due to atherosclerotic narrowing in one or more arterial segments. The compression of stenotic arteries by exercising muscle, and lack of compensatory vasodilation in diseased segments may also contribute to limited extremity perfusion. This pain is often described as aching, cramping, weakness, or fatigue, and may present in the buttocks, thighs, calves, or foot. This diagnosis must be considered with any exertional limitation of the lower extremity muscles or any history of walking impairment that gets better shortly after rest. Among patients with claudication, 25% will experience worsening symptoms, 5% will eventually require revascularization, and only 1%–2% will come to major amputation.

The specific distribution of claudication reported by the patient is an important focus of the history. Symptoms typically occur in the muscle groups immediately distal to the region of stenosis. The exact site(s) of discomfort or pain should be recorded along with the relationship of this pain to rest or degree of exertion. Narrowing of the aortoiliac vessels classically presents with the constellation of buttock pain, impotence, and lower extremity muscle atrophy, known as Leriche syndrome . Similarly, occlusion of the femoral, popliteal, or proximal tibial arteries will present with exertional calf pain. The presence of intermittent claudication has been found by multiple studies to be reliable symptom used in the diagnosis of peripheral arterial disease. A recent meta-analysis found that the presence of claudication increased the likelihood of arterial disease being present by more than threefold, whereas its absence lowers the likelihood by half that moderate to severe disease is present.

Chronic arterial insufficiency can progress to critical limb ischemia, characterized by rest pain, gangrene, or tissue loss. Rest pain represents progression of ischemia and is usually localized to the lower leg or foot, made worse by elevation (upright) and relieved by the dependent (recumbent) position. This pain may start as a dull, aching sensation in the toes, which progresses to a severe burning pain at night when the patient is lying supine. Patients may describe hanging a foot or limb over the bed or sleeping in a chair to obtain relief. The pain may intensify with cold exposure and be relieved somewhat with application of heat, although strong analgesics are usually needed to manage the discomfort. Skin ulceration and gangrene occur when the minimal nutritional and metabolic requirements of the extremity are not met by adequate blood flow. Usually, multiple levels of arterial disease (iliac, femoral, tibial) are present for this critical ischemia to occur. The pain associated with this process may intensify initially, then diminish or disappear as the tissue necrosis involves the peripheral sensory nerves.

The degree of chronic arterial insufficiency can be categorized by the Fontaine classification ( Table 3.1 ) system based on clinical symptom severity and degree of tissue loss assessed on history and physical exam. Asymptomatic patients are stage I; and patients with claudication are further stratified into those with mild claudication (stage IIA) and those with moderate-severe claudication (stage IIB). It is important to note that progression to chronic limb ischemia in patients with chronic arterial insufficiency is the same whether or not they experience symptoms, because symptomology often depends on patients’ activity levels. Fortunately, only a small proportion of patients (1%–3%) experiencing intermittent claudication will ultimately require major amputation within 5 years.

Patients with ischemic rest pain are classified as stage III and those with ulcers or gangrene are deemed stage IV. The presence of these severe indicators of occlusive disease portends a poor prognosis with 1-year mortality and major amputation rates of up to 25%.

Acute Arterial Insufficiency

The clinical presentation of acute arterial insufficiency and limb ischemia is characterized by the new onset of extremity pain ( Table 3.2 ) with concurrent changes in neurological function. Pain is typically the first symptom to be described and is characteristically elicited by passive flexion or stretch of the extremity. This pain is usually not localized exclusively to the distal foot and is not affected by limb position, which helps differentiate it from the rest pain of chronic arterial insufficiency. Sensory loss is the earliest neurological sign, and may be very subtle at first but progresses quickly to frank paresthesias. When extremity perfusion continues to be compromised, muscle strength and motor control become diminished. This spectrum of clinical symptoms and findings are termed the “6 P’s,” which stand for pain, pallor, poikilothermia, paresthesias, paralysis, and pulselessness ( Fig. 3.1 ).

The onset and pattern of these symptoms is an important clue to the cause of blood flow obstruction. The diagnosis of arterial embolism is suggested by the sudden onset of severe pain in an extremity not previously affected by claudication or other symptoms of occlusive arterial disease. This acute pain may be described as crippling and often may leave the distal extremity weakened. A careful review of the patient’s history will usually reveal the source of emboli or associated risk factors. This includes ventricular thrombi generated weeks to months after a myocardial infarction or during atrial fibrillation with or without adequate anticoagulation. Other origins of emboli include deep venous thrombus with a patent foramen ovale, mechanical heart valves, endocarditis, or aneurysms located in the aorta or infrainguinal arterial system.

Acute arterial thrombosis is the other main cause of acute insufficiency and is frequently superimposed on an already narrow atherosclerotic lesion. The pain associated with thrombosis is usually not as abrupt, typically following a crescendo course. Classically a history of claudication or poor circulation is obtained in these patients. The severity and duration of symptoms often correlate with the presence of collateral circulation in the region of the narrowed vessel, which helps to restore distal perfusion. In the absence of collaterals, the pain of thrombosis may be similar to embolic disease. It is important to assess whether the patient has an antecedent coagulation disorder that may predispose to arterial thrombosis. In comparison, patients with deep vein thrombosis may have complaints related to swelling, erythema, and dull pain in the affected extremity. The presence of palpable pulses and/or signs of adequate perfusion in the affected extremity helps differentiate venous thrombosis from an arterial etiology.

The Rutherford classification for acute limb ischemia ( Table 3.3 ) quantifies the degree of ischemia and provides guidelines for determining when to intervene. Based on clinical assessment of motor and sensory function as well as the presence or absence of Doppler signals, a limb can be classified as viable (class I), marginally threatened (class IIA), immediately threatened (class IIB), or irreversibly damaged (class III). It can be difficult to differentiate between class IIB and class III limb ischemia, especially when patients present early. Although class IIB and class III limbs are typically managed differently—with immediate revascularization indicated for the former and delayed revascularization after angiographic investigation offered for the latter—an important exception is the class III limb that presents very soon after onset due to an embolic occlusion. This subgroup of patients can often achieve functional limb salvage after immediate revascularization. Therefore it is crucial to distinguish between an embolic versus thrombotic occlusion, particularly in patients with class III limbs.

It cannot be stressed enough the importance of early diagnosis and intervention: the earlier that an acutely ischemic limb can be recognized and revascularized, the better the patient’s outcome. However, even with widespread utilization of endovascular revascularization techniques such as thrombolysis, up to 15% of patients with acute limb ischemia will require amputation within 1 year.

Cerebrovascular Disease

Patients presenting with carotid disease usually have had a recent transient ischemic attack, stroke in evolution, or completed stroke with persistent neurological deficits. Transient ischemic attacks may include an account of transient monocular blindness or amaurosis fugax. These brief visual impairments are often described by patients as a “fog,” “shade,” or “curtain falling over the eye.” When neurological deficits are fixed, their distribution should be correlated with a point of occlusion in the cerebrovascular circulation. It is important to document the location and chronology of neurological symptoms in all of these patients. Furthermore, a great number of patients with carotid artery disease will be asymptomatic at presentation, but may be identified by certain clues in the history. A recent report of nonspecific visual changes may be the first clues that a patient has significant carotid stenosis. Other sources of embolic disease must also be ruled out, including a patient history of cardiac arrhythmias or known patent foramen ovale.