History and Examination of the Arterial System
Sanjay Rajagopalan
Rekha Durairaj
The goal of a vascular history and examination is to arrive at a diagnosis and to structure appropriate investigations. This may often involve a detailed evaluation of the patient to look for systemic manifestation of vascular disease. A superficial approach devoid of detail and accuracy may often result in therapeutic decisions being delayed.
VASCULAR HISTORY
Patients with arterial disease often present with characteristic symptoms and signs that may enable one to arrive at a diagnosis even prior to the physical examination. This section will deal with elements of a vascular history that may facilitate this process.
Demographics
Atherosclerotic peripheral arterial disease typically presents after the age of 40, whereas Buerger’s disease and certain forms of large vessel vasculitis (Takayasu’s arteritis) often presents between 20 and 40 years. Temporal arteritis and atherosclerotic aneurysms present typically after the age of 65 years. A strong female predilection may be seen in some vasculitic disorders such as primary Raynaud’s syndrome, lupus vasculitis, and Takayasu’s arteritis.
History of Presenting Illness
The type of symptoms and duration, mode of onset, aggravating and relieving factors (effects of elevation, exercise, rest, dependency, temperature, pressure, etc.) should be noted.
Type and Duration of Symptoms
The nature of symptoms may provide a clue to the diagnosis. Historical differentiation of large-vessel from small-vessel disease is possible in both the upper and lower extremities. The most common problems suggesting upper extremity large arterial insufficiency are pain, coldness, ulcers, and gangrene. Small-vessel vasospastic diseases such as Raynaud’s syndrome present as characteristic cold sensitivity, with or without a classic triphasic response (sequential development of digital pallor, cyanosis, and rubor following cold exposure and warming). Although the symptom of Raynaud’s suggests vasospasm of the small arteries of the hand, it may sometimes represent a manifestation of a more proximal etiology (e.g., emboli from the axillary or subclavian artery) that exaggerates the physiologic cold
responsiveness of the digital vascular bed. The presence of tissue necrosis in the upper extremity almost always suggests fixed obstructive disease, even if the patient has Raynaud’s symptoms. A critical historical clue in differentiating upper extremity vasospasm from fixed arterial obstruction is whether the symptoms are constant or intermittent. Thus, fixed cyanosis and ulceration in the finger(s) in a patient with otherwise typical worsening of symptoms on cold exposure is almost always because of fixed disease. Symptoms caused by vasospasm alone are intermittent, and the extremity is asymptomatic and normal in appearance between attacks. Upper extremity large artery involvement is frequently asymptomatic with chronic stenosis of presenting as muscle fatigue or arm claudication, only after physiologic compensatory mechanisms including collateral support have been exhausted. Thoracic outlet syndrome may present as recurrent bouts of pain or numbness with activity, typically involving a dermatomal pattern.
responsiveness of the digital vascular bed. The presence of tissue necrosis in the upper extremity almost always suggests fixed obstructive disease, even if the patient has Raynaud’s symptoms. A critical historical clue in differentiating upper extremity vasospasm from fixed arterial obstruction is whether the symptoms are constant or intermittent. Thus, fixed cyanosis and ulceration in the finger(s) in a patient with otherwise typical worsening of symptoms on cold exposure is almost always because of fixed disease. Symptoms caused by vasospasm alone are intermittent, and the extremity is asymptomatic and normal in appearance between attacks. Upper extremity large artery involvement is frequently asymptomatic with chronic stenosis of presenting as muscle fatigue or arm claudication, only after physiologic compensatory mechanisms including collateral support have been exhausted. Thoracic outlet syndrome may present as recurrent bouts of pain or numbness with activity, typically involving a dermatomal pattern.
Chronic arterial stenoses of the lower extremity is most often asymptomatic (see claudication) with atypical symptoms being relatively common. As lower extremity arterial disease progresses, the patient may experience pain at rest or may present with tissue necrosis and/or gangrene (chronic critical limb ischemia). With atherosclerotic peripheral arterial disease, disease progression is gradual occurring slowly over several years, with many patients reporting no change in their symptoms for years. Abrupt deterioration of symptoms should raise the question of superimposed thrombosis or embolism.
Intermittent claudication (derived from “claudicatio,” Latin for limp) is classically described as cramping pain or weakness occurring with exercise and relieved by rest. Atypical manifestations are more common than classic claudication and may include a variety of symptoms including weakness. Symptoms in claudication are caused by inadequacy of the blood supply to contracting muscles and are therefore localized to muscle groups, including those of the buttocks, thigh, and the calf. Calf symptoms typically predominate in most patients irrespective of the level of disease, perhaps because the calf is metabolically more active than other muscle groups when walking. Aortoiliac disease may present as aching discomfort in the hips and thighs along with a sensation of weakness that may mimic spinal stenosis.
The amount of exercise producing pain is generally reproducible, and patients can typically quantify their exercise capacity in terms of walking distance or time. Factors such as time of day, meals, medications, and a host of other factors may influence symptoms in a number of patients. The pain of intermittent claudication is typically relieved by rest, usually within 5 minutes, and may be relieved by slowing the pace of walking. The amount of exercise required to precipitate pain is roughly inversely related to the severity of the narrowing of the vessel, and pain is usually manifested one segment below the area of stenosis (assuming a single focal lesion at these levels). One may approximately deduce the level of involvement by considering the location of symptoms although this is frequently not predictive. Thus in some patients, aortic disease is manifested by buttock pain, iliac disease by thigh muscle pain, and superficial femoral arterial disease (the most commonly affected artery) by calf claudication. However, since multilevel disease is usually the norm in atherosclerosis, the symptoms typically reflect the most distal significant disease or the area with the poorest collateral support.
Upper Extremity Claudication. This is seen in individuals with subclavian artery stenosis. Radiologic subclavian steal may be seen if the stenosis is proximal to the origin of the vertebral artery (Chapter 16).
Differential Diagnosis of Claudication. Table 1.1 lists conditions that may mimic lower extremity claudication (pseudoclaudication) and their characteristics. Nocturnal cramps are by far the commonest nonvascular cause of cramping and are thought to represent an exaggerated neuromuscular response to stretch. Table 1.2 lists causes of true claudication that are nonatherosclerotic.
Rest Pain. Rest pain becomes a prominent feature as blood flow becomes insufficient to supply the basal needs of extremity and its sensory nerve supply. Rest pain is classically defined as severe nocturnal pain or burning that begins in the feet especially over the metatarsal heads, is relieved by dependency, and is aggravated by elevation of the legs above the level of the heart. Rest pain is a sign of very severe ischemia that may be limb threatening if no intervention is undertaken. Metatarsalgia is an occasional differential diagnosis for rest pain. This is usually seen with DJD or rheumatoid arthritis, is aggravated by dependency, and may be relieved on standing.
Neuropathic Pain and Causalgia. Neuropathic pain and causalgia (see Chapter 18, complex regional pain syndrome) are both often described as burning discomfort involving the extremities. The former is commonly seen in conditions such as diabetes that have a propensity to involve the nerves and is often associated with additional deficits in a typical glove-andstocking distribution typically in the lower extremity. Complex regional pain syndrome (previously referred to as reflex sympathetic dystrophy) is a distinct pain syndrome that is an important differential diagnosis for upper extremity pain. It usually occurs in response to an inciting trauma (which may be trivial and may not be recalled by the patient), including medical conditions such as myocardial infarction, deep venous thrombosis, and hip fracture. It is additionally characterized by hyperalgesia, allodynia, and abnormal sudomotor activity that is disproportionate to the inciting injury and occurring beyond the territory of a single nerve.
Erythermalgia (erythromelalgia) is a characteristic condition associated with burning pain discomfort and redness of the extremities (lower more common than upper) that is typically worsened by heat. This may be primary or secondary to conditions such as myeloproliferative disorders, lymphoma, diabetes, hypertension, and drugs such as calcium channel blockers and bromocryptine (Chapter 18).
Mode of Onset of Illness
Acute arterial insufficiency is typified by the five Ps (pain, pallor, paresthesias, paralysis, poikilothermia) (Chapter 7). Abrupt onset of pain with pallor often suggests an embolic phenomenon. Acute arterial thrombosis superimposed on a preexisting atherosclerotic plaque or stenosis is the other major cause of acute limb ischemia. With arterial thrombosis the clinical presentation is not as dramatic as embolism. The patient is, however, aware of a change in clinical status. Table 1.3 enumerates the differences between an embolic and an in situ thrombotic episode. The symptoms may then worsen or may abate depending on the patient’s ability to recruit collateral pathways. A common site of thrombosis in the lower extremity is the superficial femoral artery, although it may occur anywhere from the aorta to the digital arteries. Occasionally thrombosis may be precipitated by a decrease in blood flow velocity because of a low cardiac output state, as may occur with congestive cardiac failure or after myocardial infarction.
TABLE 1.1 DIFFERENTIAL DIAGNOSIS OF INTERMITTENT CLAUDICATION | |||||||||||||||||||||||||||||||||||||||||||||||
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TABLE 1.2 NONATHEROSCLEROTIC CAUSES OF ARTERIAL STENOSIS AND RESULTANT SYMPTOMS | ||||||||||||||||||||||||||||||||
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TABLE 1.3 DIFFERENTIATING EMBOLISM FROM THROMBOSIS AS THE ETIOLOGY OF LIMB ISCHEMIA | ||||||||||
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