Chapter 11 The History and Physical Examination
Vascular History
Arterial Disease
Peripheral artery disease
In addition to carotid and coronary artery disease (CAD), peripheral artery disease (PAD) is one of the most common clinical manifestations of atherosclerosis. Approximately 50% of patients with PAD have symptoms, described in the following discussion as typical or atypical, and the remainder are asymptomatic. The importance of making the diagnosis of PAD, even in the absence of symptoms, derives from the prognostic information implicit with its diagnosis (see Chapter 16). Notably, patients with PAD often have coexisting coronary and cerebrovascular atherosclerosis, and are two- to fourfold more likely than patients without PAD to die of cardiovascular disease.1
Intermittent Claudication
A cardinal symptom of PAD is intermittent claudication (see Chapter 18). Claudication occurs when limb skeletal muscle ischemia is produced with effort because increased muscle energy requirements are not served by sufficient augmentation in blood supply. Symptoms develop intermittently with activity; the blood flow limitation imposed by peripheral artery stenosis typically does not compromise muscular function at rest. Claudication is variably described as aching, heaviness, burning, fatigue, cramping, and/or tightness in the affected limb. Symptoms occur with reproducible amounts of exercise: one block of walking, one flight of stairs, or 5 minutes on a bicycle, for example. Discomfort may develop in any muscular portion of the leg—buttocks, hip, thigh, calf, or foot. Areas of the limb to develop discomfort are related to the arterial segments with stenoses. Iliac artery disease typically produces hip or buttock claudication, whereas femoral artery disease causes thigh or calf claudication. Arm claudication is unusual, but may occur in patients with innominate, subclavian, axillary, or brachial artery stenosis. Cessation of activity relieves the exercising muscle’s demand-supply mismatch and enables restoration of oxidative metabolism. Therefore, patients typically report that discontinuation of activity relieves the discomfort after several minutes.
Atypical symptoms also occur and may include reduction of leg discomfort despite continued effort, gait disturbance, and slower walking speed.2 Atypical claudication may be more common than traditional symptoms because of the high frequency of other conditions present in this older age group: spinal stenosis, venous insufficiency, and degenerative join disease. Patients with intermittent claudication often slow their walking speed by a third to regulate muscle use and prolong walking distance. Thus, when a physician solicits the history of walking impairment, patients may report no change in distance walked before symptoms occur, despite a progressive decline in functional ability.3
Several questionnaires for PAD have been devised and validated. These provide a standard to accompany the interview when querying patients about symptoms of PAD. The Rose questionnaire was the initial PAD-related questionnaire, but limited diagnostic sensitivity minimized its utility.4,5 The San Diego questionnaire is a modified version of the Rose Questionnaire and a more reliable instrument to assess intermittent claudication (see Chapter 16).6 The disease-specific Walking Impairment Questionnaire has been validated and can be used to assess walking difficulty in patients with PAD. It has four subscales: severity of pain with walking, distance, speed, and stair climbing.7
Critical Limb Ischemia
Critical limb ischemia (CLI) occurs when limb blood flow is inadequate to meet the metabolic demands of the tissues at rest.8 This may result in persistent pain, especially in the acral portions of the leg (toes, ball of the foot, heel). Additional foot symptoms include sensitivity to cold, joint stiffness, and hypesthesia. As a consequence of the effects of gravity on perfusion pressure, patients may report worsening of pain with leg elevation, or even when lying in bed, and reduction in pain with limb dependency (e.g., when the feet hang over the bed onto the floor). Critical limb ischemia may cause tissue breakdown (ulceration) or gangrene.
Acute Limb Ischemia
Acute limb ischemia is most often due to embolism or in situ thrombosis (see Chapter 46).9 Other causes include arterial dissection or trauma. The presentation of acute arterial occlusion ranges from asymptomatic loss of a pulse, to worsened claudication, to sudden onset of severe pain at rest. Symptoms may develop suddenly over several hours, or over several days. Acute ischemic symptoms are more likely to occur when no or few collateral vessels are present, rather than when there is a well-developed collateral network. Acute arterial occlusion may cause symptoms in any portion of the leg distal to the obstruction. The five Ps—pain, pallor, poikilothermia, paresthesias, and paralysis—characterize the historical features and findings of patients with acute limb ischemia. Severity of symptoms does not discriminate among etiologies.
Atheroembolism
Atheroembolism is embolization of atherosclerotic debris that compromises distal arteries (TAO) (see Chapter 47). Atheroemboli vary in composition, from larger fibroplatelet particles that occlude small arteries to cholesterol emboli, nanometers in size, that occlude arterioles. Causes of atheroemboli include catheterization and cardiovascular surgery, but approximately half of such events occur without a known precipitant.10
Other Peripheral Artery Diseases
Uncommon diseases of the peripheral arteries should be considered in patients with claudication or evidence of ischemia, but whose age falls below that typically affected by atherosclerosis or in those with atypical symptoms. These diseases include thromboangiitis obliterans (TAO) (see Chapter 44), Takayasu arteritis (see Chapter 42), and giant-cell arteritis (see Chapter 43), and vascular compression syndromes, such as those affecting the thoracic outlet, iliac artery, and popliteal artery (see Chapter 62).
Patients with giant-cell arteritis (GCA) are typically older than 50 years of age. Giant-cell arteritis predominantly affects the branches of the thoracic aorta and the intracranial arteries. Some 50% of patients have constitutional symptoms related to inflammation, and 50% have coexisting polymyalgia rheumatica. The most common complaint is headache that typically affects the occipital or temporal region; it occurs in over 60% of patients with GCA. In patients with headache, scalp tenderness may be present. Partial or complete vision loss develops in 20% of patients, and approximately 50% of these individuals report amaurosis fugax (i.e., transient episodes that involve one eye and last 10 minutes or less [see Chapter 43]). Patients may present with upper limb claudication, and 40% report jaw claudication. Tongue claudication and swallowing difficulties are less common.
Thromboangiitis obliterans (Buerger’s disease) is a small- to medium-vessel vasculitis that affects the distal vessels of the arms or legs, and usually occurs before 40 years of age in cigarette smokers.11 It affects more men than women. The classic triad of TAO is claudication, Raynaud phenomenon, and superficial thrombophlebitis. Claudication of the hands or feet may progress to ulceration of the fingers or toes.11
Neurovascular Compression Syndromes
Claudication in the upper extremities raises the possibility of thoracic outlet syndrome (see Chapter 62).12 Compression of the axillary or subclavian artery by a cervical rib, abnormal insertion of the scalene anticus muscle, or apposition of the clavicle and first rib may result in arterial compression during head turning, arm use above or behind the head, or arm extension. Weakness, burning, aching, or fatigue in the arms can result. Examples of triggers include wall painting, hair washing, and housecleaning.
Popliteal artery entrapment should be considered in a young person with leg claudication but preserved pulses at rest.13 Anatomical variants in the course of the popliteal artery may result in its compression by the gastrocnemius muscle during exercise and can cause symptoms of claudication.
Vasospastic and related diseases
Raynaud phenomenon is the most common vasospastic disorder encountered in clinical practice14 (see Chapter 48). Patients typically report that the digits become pale or cyanotic during cold exposure. Fingers are most commonly affected, but the toes develop symptoms in 40% of affected individuals. Less commonly involved areas include the tongue, nose, and ear lobes. Patients may experience paresthesias or pain in the digits if ischemia persists. With rewarming and release of vasospasm, digital rubor due to reactive hyperemia may develop. A pulsating or flushed feeling may accompany the hyperemic phase. All color phases are not required for diagnosis. Indeed, with an appropriate history, the diagnosis can be made with only one color change.
Acrocyanosis is a vascular disorder characterized by bluish discoloration of the hands and feet exacerbated by cold exposure (see Chapter 49). Unlike Raynaud phenomenon, the discoloration is not confined to the digits, and pallor does not occur. Warming, however, can ameliorate cyanosis and restore normal skin color. Acrocyanosis typically occurs in persons aged 20 to 45 years, and women are affected more often than men.
Pernio is a vascular inflammatory disorder in which skin lesions and swelling occur in fingers and toes, particularly in cold moist climates (see Chapter 51). Other exposed portions of the body may be affected. The typical lesions described by the patient are pruritic and painful blisters or superficial ulcers.
Renal artery disease
No symptoms specific to renal artery stenosis are elicited by history. Unlike other end organs, symptoms of chronic renal ischemia are not localized to the kidney, but reflect systemic pathophysiological alterations that result from activation of the renin angiotensin system and disturbances of salt and water balance. Historical clues that raise suspicion of renal artery stenosis include onset of hypertension before age 30 or after age 55, malignant hypertension, hypertension refractory to three concurrently prescribed antihypertensive medications, azotemia subsequent to administration of an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker, unexplained azotemia, recurrent congestive heart failure, and episodic pulmonary edema (see Chapter 23). Renal artery stenosis should be considered in patients with these clinical clues, particularly if they have evidence of atherosclerosis in other regional circulations (e.g., CAD, PAD, aortic disease).
Mesenteric artery disease
Most patients with atherosclerosis of the celiac, superior mesenteric, or inferior mesenteric arteries are asymptomatic unless two or all three of these arteries are occluded. Symptoms of chronic mesenteric ischemia include postprandial epigastric or midabdominal pain that may radiate to the back (see Chapter 27). Onset of abdominal discomfort is 15 to 30 minutes after eating, and symptoms may persist for several hours. Patients tend to avoid food to prevent these symptoms, and weight loss ensues.
Carotid artery disease
The majority of patients with significant stenoses of the common or internal carotid arteries are asymptomatic (see Chapter 30). When they do occur, symptoms may be temporary (minutes to hours) or fixed, indicating a transient ischemic attack (TIA) or stroke, respectively. Symptoms of carotid artery disease reflect compromise of the neural territory subtended by its principal intracranial branch, the middle cerebral artery, and include contralateral hemiparesis, hemiparesthesia, and aphasia. Ipsilateral amaurosis fugax or blindness may also occur because the ophthalmic artery is supplied by the internal carotid artery.
Venous and Lymphatic Systems
Deep vein thrombosis
Patients with thrombosis of a deep vein of a limb may present with swelling or discomfort, or no symptoms at all (see Chapter 52). Symptoms are usually but not always unilateral. Historical queries should seek potential causes of deep vein thrombosis (DVT) when it is suspected. Information regarding recent trauma, surgery, hospitalization, prolonged period of immobility, cancer, thrombophilic disorder, or family history of venous thrombosis should be acquired. An uncommon cause of left leg DVT is May-Thurner syndrome, in which the left iliac vein is compressed by the right iliac artery. In patients with arm symptoms, questions should seek evidence of indwelling catheters or cancer, since these are the most common causes of upper extremity DVT. In addition, a history of repetitive arm motion should be sought when considering the possibility of Paget-Schroetter syndrome, in which compression of the axillosubclavian vein by muscular, tendinous, or bony components of the thoracic outlet may cause thrombosis. Thrombosis or extrinsic compression of the superior vena cava may cause symptoms of superior vena cava syndrome, which include headache, face and neck fullness and flushing, and bilateral arm swelling.
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