Vascular Disease: Diagnostic and Therapeutic Approaches available in Hardcover
Vascular Disease: Diagnostic and Therapeutic Approaches
- ISBN-10:
- 1935395165
- ISBN-13:
- 9781935395164
- Pub. Date:
- 04/01/2011
- Publisher:
- Cardiotext Publishing
- ISBN-10:
- 1935395165
- ISBN-13:
- 9781935395164
- Pub. Date:
- 04/01/2011
- Publisher:
- Cardiotext Publishing
Vascular Disease: Diagnostic and Therapeutic Approaches
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Overview
Internationally recognized authorities in vascular medicine Michael R. Jaff and Christopher J. White have joined with leading experts to produce a book that comprehensively and uniquely addresses vascular disease. The editors' clinical approach, combined with the work of contributors nationally renowned in their respective fields, make this work useful and practical to both clinicians and interventionalists alike. Vascular Disease: Diagnostic and Therapeutic Approaches bridges vascular and endovascular medicine to provide practicing physicians of multiple backgrounds — as well as trainees, students, and anyone involved in the treatment of vascular diseases — an essential overview of the diagnostic approaches and state-of-the-art treatments or arterial and venous diseases.
Product Details
| ISBN-13: | 9781935395164 |
|---|---|
| Publisher: | Cardiotext Publishing |
| Publication date: | 04/01/2011 |
| Pages: | 600 |
| Product dimensions: | 7.30(w) x 10.20(h) x 1.30(d) |
Read an Excerpt
Vascular Disease
Diagnostic and Therapeutic Approaches
By Michael R. Jaff, Christopher J. White
Cardiotext Publishing, LLC
Copyright © 2011 Michael R. Jaff and Christopher J. WhiteAll rights reserved.
ISBN: 978-1-935395-16-4
CHAPTER 1
Taking a Vascular History and Physical Examination
Peter C. Spittell and John A. Spittell Jr.
Introduction
Since peripheral vascular disorders can be due to either local or systemic disease, and significantly affected by comorbid conditions (eg, diabetes mellitus and cardiopulmonary disease), it is essential that a complete medical history be reviewed in addition to the specific details of the vascular complaint. Attention to demographic data — family history, occupation, current or previous illness, surgery, and/or medication — can facilitate prompt and accurate diagnosis, even of complaints or clinical findings that are unusual or perplexing. Questionnaires are useful in providing the patient time to think and record such demographic information and can facilitate this part of the medical history.
The growing availability and reliance on "high-tech" medicine in place of "high-touch" medicine should not limit attention paid to inquiring about specific historical points when evaluating any symptom or symptom complex. Time relationships of the complaint (onset, progression) should be established as accurately as possible. Exact location and severity of the symptom(s) and any modifying factors, as well as the degree of disability imposed by the symptom(s), are essential details. Results of previous investigations of the complaint(s) — noninvasive laboratory studies, imaging procedures, and biopsies of various types — and of treatment are basic to a complete vascular history.
Evaluating Pain
Painful extremities are not necessarily the result of a peripheral vascular disorder. Pain due to circulatory problems can be persistent or intermittent.
Persistent severe pain in any extremity is the hallmark of severe ischemia of that extremity — sudden arterial occlusion, ischemic ulceration, and severe chronic limb ischemia, all conditions readily confirmed and distinguished from neurologic and orthopedic disorders by the vascular examination. The pain of sudden arterial occlusion may be associated with, or even replaced by, other symptoms of acute ischemia — numbness, tingling, coldness, and/or paresis. Pain due to severe chronic ischemia is constant, worse at night, and difficult to control with medication; at times dependency on the extremity will give partial relief of the pain due to severe ischemia, and if prolonged in an attempt to get some relief, may result in an edematous, ruborous cold foot (Figure 1.1). Ulceration due to ischemia is characteristically severely painful, distinguishing it readily from the other common types of ulceration of the extremity (Table 1.1). The pain due to acute venous thrombosis is generally mild and relieved by local heat and analgesics. Lymphedema is painless unless complicated by acute lymphangitis/ cellulitis, with the pain being proportionate to the extent of the inflammation and relieved by local heat and control of the infection.
The principal intermittent pain in peripheral vascular disorders is intermittent claudication, which always indicates an inadequate arterial blood supply (usually evident on physical examination) to contracting muscles. While patients use various terms to describe their intermittent claudication — eg, "aching," "cramping," "tightness" — it is brought on only by exercise and is relieved promptly by rest; in the case of occlusive arterial disease of a lower extremity, whatever its cause, intermittent claudication occurs with walking and is relieved promptly by standing still. A significant number of patients will be asymptomatic or have atypical leg symptoms, therefore a typical history of intermittent claudication has a high specificity but a low sensitivity. Determining the amount of walking that causes the person's intermittent claudication provides an estimate of the severity of the occlusive arterial disease, although the degree of functional limitation can vary depending on the collateral circulation, exercise capacity, and comorbid conditions. Furthermore, the location of the distress of intermittent claudication is a rough indication of the level of the occlusive arterial disease in the affected part. Thus, intermittent claudication in the arch of the foot as may be seen in Buerger's disease suggests occlusive arterial disease at or above the ankle, while intermittent claudication located in the thigh or buttock indicates occlusive arterial disease of the iliac artery or aorta. Unusual locations of intermittent claudication, such as jaw claudication, which may occur in giant cell arteritis, or arm claudication, which can occur with occlusion of the subclavian artery, are useful indicators of the location of the occlusive arterial disease.
An intermittent type of pain that mimics true intermittent claudication is pseudoclaudication due to lumbar spinal stenosis. When symptomatic lumbar spinal stenosis exists in the absence of symptomatic occlusive arterial disease, clinical differentiation of true intermittent claudication from pseudoclaudication is not difficult (Table 1.2); but, when both occlusive arterial disease of the lower extremities and lumbar spinal stenosis coexist and are symptomatic, historical differentiation may not be possible so that evaluation with exercise tests in the vascular laboratory, imaging of the lumbar spine by computed tomography angiography (CTA) or magnetic resonance angiography (MRA) may be necessary to determine which is the more serious and symptomatic of the 2 conditions.
The occurrence of muscle cramps during rest, often during sleep ("nocturnal leg cramps"), does not indicate occlusive arterial disease in the extremity though patients may consider them such and seek evaluation because of them.
Color change of the extremity(s) or digit(s), both permanent and intermittent, are usually easy to diagnose clinically if sufficient details are elicited historically. For example, some questions useful clinically in the differential diagnosis of primary Raynaud's phenomenon (Raynaud's disease) from secondary Raynaud's phenomenon are shown in Table 1.3. Another vasospastic disorder, livedo reticularis, can be primary or secondary to a variety of disorders, but as a rule, the secondary types of livedo reticularis are of recent onset. The constant discoloration of the hands and occasionally the feet that occurs in the benign vasospastic acrocyanosis, seen in some young women, distinguishes it from Raynaud's phenomenon.
Since leg edema has many different causes, both systemic and regional, it is useful to have an organized historical approach to categorize its type; the answers to the following 8 questions usually differentiate regional from systemic types of edema:
1. When did the edema begin?
2. Is the swollen extremity painful?
3. Does the edema recede overnight?
4. Are there associated cardiac symptoms?
5. Is there any evidence of renal disease?
6. Is there evidence of chronic hepatic disease?
7. Are there any bowel or significant weight changes?
8. What medications, if any, is the person taking?
Important to keep in mind are the frequent causes of drug-induced edema, such as dihydropyridine calcium channel blockers. The regional types of edema of vascular origin — venous and lymphatic — are usually easy to differentiate from lipedema (Figure 1.2), a leg enlargement that is lipodystrophic in origin (Table 1.4).
The Vascular Examination
The vascular examination should include examination of the ocular fundus and the skin as well as the arterial, venous, and lymphatic systems. These will be covered in order.
The ocular fundus provides a unique opportunity to view and assess arteries and veins. Findings that are relevant to vascular disorders include the cholesterol plaque (Figure 1.3), which indicates atherosclerosis of the ascending, or arch, portion of the thoracic aorta or the ipsilateral carotid artery; there is an increased frequency of stroke in persons with asymptomatic retinal cholesterol emboli. Noting engorged retinal veins (Figure 1.4), seen in polycythemia vera, may explain the occurrence of a patient's arterial or venous thrombosis. A rare heritable disorder of elastic tissue frequently associated with occlusive peripheral, coronary, and cerebral arterial disease, pseudoxanthoma elasticum, has a classic ocular fundus finding of angioid streaks (Figure 1.5). The important secondary and correctible cause of hypertension, coarctation of the aorta, may be "tipped off" by very tortuous retinal arterioles (Figure 1.6), though this is not an absolute association.
Like the ocular fundus, the skin can be a valuable source of clinical diagnostic findings. After noting the color, temperature, and hair growth of the skin, attention to some other specific "vascular" points is useful. Venous stars (Figure 1.7) in the skin of the upper arm or anterior chest indicate occlusion or obstruction of a major mediastinal vein (which may also present with nonpulsatile distention of a jugular vein). A useful maneuver in the evaluation of a swollen limb is comparing the texture of the skin of the back of one's hand (Figure 1.8) to the texture of the skin of the swollen limb; the skin in lymphedema is palpably thickened. Other diagnostically valuable skin lesions are the xanthomata in lipid disorders, telangiectasia in scleroderma (Figure 1.9), and the "plucked chicken" skin in the face, neck, and axilla in pseudoxanthoma elasticum (Figure 1.10). Four common types of ulceration of the skin of the extremity are seen in persons with vascular disease, and each has enough characteristic features to readily allow identification on examination (see Table 1.1).
Evaluation of the peripheral arterial system should include palpation of the carotid arteries and of the subclavian, brachial, radial, and ulnar arteries in the upper extremity, and the abdominal aorta and femoral, popliteal, posterior tibial, and dorsal pedis arteries in the lower extremity. Having a system of grading of each artery's pulsation is useful — eg, 0 indicates absence of pulsation, 4 indicates normal pulsation, and 1, 2, and 3 indicate degrees of impairment of pulsation. There are many other grading scales, with some advocating 0 being absent, 1 being palpable but diminished, and 2 being normal. A widened or aneurysmal pulse should be described as such, and not be given a number. The abdominal aorta should be examined and if a palpable pulsatile mass is evident, further screening tests for abdominal aortic aneurysm are warranted. Routinely palpating and comparing the timing of the pulsation of the radial arteries simultaneously will prevent missing the "delayed pulsation" of the radial artery ipsilateral to an occluded subclavian artery, so-called subclavian steal (Figure 1.11); identifying the subclavian steal can be quite important in the potential coronary bypass patient since the ipsilateral internal mammary artery would not be a good choice for revascularizing a coronary artery unless the subclavian artery lesion is corrected prior to coronary artery surgery. A similar and important "delay" of a femoral artery pulsation compared to a radial artery pulsation in the person with coarctation of the aorta will be evident if simultaneous palpation of the radial and femoral arteries is always included in the arterial examination.
Following the peripheral arterial examination, a clinically useful maneuver is elevation of the lower extremities to 60° above the level and observing any change in color of the skin of the soles of the feet. If no pallor develops in 60 seconds of elevation the arterial circulation is normal or minimally occluded; however, if definite pallor of the skin of the sole of the foot develops within 60 seconds of elevation (Figure 1.12) of the extremity, there is significant occlusive arterial disease in the extremity. Confirmation can be obtained by having the patient hang the extremities dependent to observe the time for color to return to the skin (normal, 10 seconds; ischemia, 15 or more seconds), and for the superficial veins to fill (normal, 15 seconds; ischemia, 20 or more seconds). When the extremity is severely ischemic, with dependency a deep rubrous color — dependent rubor (see Figure 1.1) — will develop. These elevation-dependency tests provide a rapid office or bedside clinical evaluation of the peripheral arterial circulation.
Since the radial artery is at times being considered for access or use as a conduit, for percutaneous coronary angiography or interventional procedures, the adequacy of the collateral circulation in the hand can be reliably evaluated with the Allen test (Figure 1.13). The Allen test has been modified to provide a timed end point to evaluate the adequacy of the collateral circulation in the hand by the ulnar artery; timing of the return of color to the thenar eminence and thumb while the radial artery compression is maintained and the compression of the ulnar artery is released is the end point of this modification. The Allen test is also useful for the diagnosis of thromboangiitis obliterans (Buerger's disease) (Figure 1.14), the purpose for which the test was originally described by Allen.
Auscultation for bruits over large arteries (carotid, subclavian, renal and femoral, and the abdominal aorta) is an essential part of a complete arterial examination. Bruits usually indicate turbulence of flow due to stenosis upstream; most bruits are systolic but occasionally the systolic bruit will extend into diastole as a result of an arterial stenosis in the range of 80% — a significant clinical finding (Figure 1.15).
Many physicians have included performance of the ankle-brachial index (ABI) in their offices or clinic evaluations since the ABI has become the objective standard for diagnosis; furthermore, the ABI detects clinically occult disease in a significant number of patients. A normal ABI (at rest) is 1.0 to 1.4, an ABI ≤ 0.9 is abnormal and not only confirms the diagnosis of lower-extremity arterial occlusive disease but an abnormal ABI is also associated with a higher risk of mortality (BARI trial), future cardiovascular morbidity and mortality (HOPE trial), and increased risk of stroke.
Determining the ABI before and after standard exercise (eg, active pedal plantar flexion, an office-based exercise study, or treadmill walking) provides an accurate estimate of any arterial insufficiency and the functional impairment it is imposing.
Many examiners have difficulty adequately examining the popliteal artery, so some useful points about this aspect of the vascular examination are warranted. From a clinical point of view, the popliteal artery begins in the lower medial thigh at the point where the superficial femoral artery exits the adductor tendon, and it then extends distally to the level of the knee joint, where it is located at the junction of the lateral and medial vertical thirds of the knee. The "clinical" popliteal artery ends where it trifurcates, about 1 inch below the knee joint in the middle of the upper calf. The reason for emphasizing the "clinical" popliteal artery is that popliteal artery aneurysm can occur at the upper, middle, and/or lower portions of the artery (Figure 1.16) and could be overlooked unless all portions of the artery are examined.
The subclavian vessels can be compressed in the thoracic outlet, most often in the space between the uppermost rib (a cervical rib or the first rib) and the clavicle (Figure 1.17), resulting in variable symptoms and complications. Compression of the subclavian artery can be demonstrated by performance of the thoracic outlet maneuvers (active and passive costoclavicular, hyperabduction, and scalene maneuvers) and noting a change in the amplitude of the radial artery on the side of the maneuver. Ultrasonography of the subclavian artery during thoracic outlet maneuvers can document compression of the subclavian artery and of the subclavian vein.
Many venous disorders of the extremities are easy to evaluate and/or diagnose by careful physical examination (eg, varicose veins and chronic deep venous insufficiency) while others, particularly acute deep venous thrombosis, require noninvasive or venographic procedures for accurate diagnosis.
Examination for varicose veins should be done with the patient standing. The competency and course of superficial veins can be determined by compressing the vein at various levels while simultaneously palpating the vein distally for any impulse; transmission of the impulse distally for 20 cm indicates venous valvular incompetence. The presence of deep venous valvular incompetence is suggested by the presence of dependent edema, stasis pigmentation, and chronic indurated cellulitis (Figure 1.18), but in their absence deep venous valvular insuf- ficiency can be detected by noninvasive vascular laboratory studies. Varicose veins and other signs of localized increased venous pressure can be a sign of arteriovenous fistula. In the case of congenital arteriovenous fistula in the extremity, the clinical signs can vary from the presence of a birthmark to increased size of the extremity, varicose veins, and "hot" venous ulceration (Figure 1.19). Acquired arteriovenous fistula in extremity vessels can produce signs of increased venous pressure in the extremity (Figure 1.20) in addition to pulsatile varicose veins and the typical multiple pitched bruit on auscultation near or over the fistula.
Superficial thrombophlebitis is usually quite easily recognized by its reddened linear course, which is palpably hardened and tender, but if it does not present these classic findings, Doppler ultrasonography can readily confirm the diagnosis. Acute lymphangitis is usually easily differentiated by its associated high fever, frequently accompanied by chills, from superficial thrombophlebitis.
(Continues...)
Excerpted from Vascular Disease by Michael R. Jaff, Christopher J. White. Copyright © 2011 Michael R. Jaff and Christopher J. White. Excerpted by permission of Cardiotext Publishing, LLC.
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Table of Contents
Contents
About the Contributors, ix,Foreword by Jess R. Young, xiii,
Preface, xv,
Part 1 Evaluation of the Patient with Peripheral Vascular Disorders,
1. Taking a Vascular History and Physical Examination Peter C. Spittell and John A. Spittell Jr., 3,
Part 2 The Assessment of Peripheral Artery Disease,
2. The Diagnosis of Peripheral Artery Disease Stephen O'Connor, Thomas J. Kiernan, and Michael R. Jaff, 19,
3. Peripheral Vascular Angiography Jose A. Silva and Christopher J. White, 31,
Part 3 Aortic Arch and Supraclavicular Artery Disease,
4. Subclavian and Upper-Extremity Artery Disease Jeffrey A. Goldstein, Raghu Kolluri, and Krishna Rocha-Singh, 53,
5. Extracranial Carotid Artery Disease Christopher J. White and Michael R. Jaff, 73,
6. Vertebrobasilar Insufficiency J. Stephen Jenkins and Tyrone J. Collins, 99,
7. Hemodialysis Access Intervention John A. Bittl, 109,
Part 4 Aortic, Visceral, and Renal Artery Disease,
8. Diseases of the Thoracic Aorta Mark F. Conrad and Richard P. Cambria, 137,
9. Abdominal Aortic Aneurysmal Disease Tikva S. Jacobs and Michael L. Marin, 177,
10. Chronic Mesenteric Ischemia Jose A. Silva, 195,
11. Renal Artery Disease Christopher J. White and Michael R. Jaff, 215,
Part 5 Lower-Extremity Artery Disease,
12. Acute Limb Ischemia Kenneth Ouriel and Vikram S. Kashyap, 245,
13. Occlusive Diseases of the Abdominal Aorta and Iliac Arteries Joseph J. Ricotta II and Timothy M. Sullivan, 255,
14. Femoropopliteal Artery Disease Mitchell J. Silver and Gary M. Ansel, 267,
15. Critical Limb Ischemia: Limb Salvage, Angiogenesis Ashequl M. Islam and Kenneth Rosenfield, 287,
16. Vascular Access Complications and Treatment Stephen R. Ramee and John P. Reilly, 309,
Part 6 Nonatherosclerotic Artery Disease,
17. Thromboangiitis Obliterans (Buerger's Disease) Jeffrey W. Olin, 329,
18. Systemic Vasculitides Reena L. Pande and Joshua A. Beckman, 341,
19. Vasospastic Diseases Raghu Kolluri and John R. Bartholomew, 371,
20. Fibromuscular Dysplasia Jeffrey W. Olin, 389,
Part 7 Venous Disease,
21. Deep Venous Thrombosis and Pulmonary Embolism John A. O'Dea, Thomas J. Kiernan, and Michael R. Jaff, 407,
22. Contemporary Management of Superior Vena Cava Syndrome Andrew C. Eisenhauer, 427,
23. Uncommon Venous Disorders Jessica Nevins Morse and Bruce H. Gray, 439,
24. Chronic Venous Insufficiency and Varicose Veins Steven M. Dean and Saundra S. Spruiell, 459,
Part 8 Hypercoagulability and Uncommon Vascular Diseases,
25. Hypercoagulable States Julia A. M. Anderson and Jeffrey I. Weitz, 521,
26. Environmental and Hereditary Vascular Disorders Juzar Lokhandwala and John R. Bartholomew, 547,
Index, 561,