eMedicine Specialties > Emergency Medicine > Cardiovascular

Peripheral Vascular Disease

Everett Stephens, MD, Assistant Clinical Professor, Department of Emergency Medicine, University of Louisville

Updated: Jan 5, 2009

Introduction

Background

Peripheral vascular disease (PVD) is a nearly pandemic condition that has the potential to cause loss of limb or even loss of life. Peripheral vascular disease manifests as insufficient tissue perfusion caused by existing atherosclerosis that may be acutely compounded by either emboli or thrombi. Many people live daily with peripheral vascular disease; however, in settings such as acute limb ischemia, this pandemic disease can be life threatening and can require emergency intervention to minimize morbidity and mortality.

Pathophysiology

PVD, also known as arteriosclerosis obliterans, is primarily the result of atherosclerosis. The atheroma consists of a core of cholesterol joined to proteins with a fibrous intravascular covering. The atherosclerotic process may gradually progress to complete occlusion of medium and large arteries. The disease typically is segmental, with significant variation from patient to patient.

Vascular disease may manifest acutely when thrombi, emboli, or acute trauma compromises perfusion. Thromboses are often of an atheromatous nature and occur in the lower extremities more frequently than in the upper extremities. Multiple factors predispose patients for thrombosis. These factors include sepsis, hypotension, low cardiac output, aneurysms, aortic dissection, bypass grafts, and underlying atherosclerotic narrowing of the arterial lumen.

Emboli, the most common cause of sudden ischemia, usually are of cardiac origin (80%); they also can originate from proximal atheroma, tumor, or foreign objects. Emboli tend to lodge at artery bifurcations or in areas where vessels abruptly narrow. The femoral artery bifurcation is the most common site (43%), followed by the iliac arteries (18%), the aorta (15%), and the popliteal arteries (15%).

The site of occlusion, presence of collateral circulation, and nature of the occlusion (thrombus or embolus) determine the severity of the acute manifestation. Emboli tend to carry higher morbidity because the extremity has not had time to develop collateral circulation. Whether caused by embolus or thrombus, occlusion results in both proximal and distal thrombus formation due to flow stagnation.

Clinical

History

The primary factor for developing peripheral vascular disease (PVD) is atherosclerosis.

• Other maladies that often coexist with PVD are coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation, transient ischemic attack, stroke, and renal disease. Studies have suggested that even asymptomatic peripheral arterial disease (PAD) is associated with increased CAD mortality.¹
• Risk factors for PVD include smoking, hyperlipidemia, diabetes mellitus, and hyperviscosity.
• Other etiologies for developing PVD may include phlebitis, injury or surgery, and autoimmune disease, including vasculitides, arthritis, or coagulopathy.
  • PVD rarely exhibits an acute onset; it instead manifests a more chronic progression of symptoms.
  • Patients with acute emboli causing limb ischemia may have new or chronic atrial fibrillation, valvular disease, or recent MI, whereas a history of claudication, rest pain, or ulceration suggests thrombosis of existing PVD.
  • Radiation-induced PAD is becoming more common, perhaps due to the efficacy of current antineoplastic treatment and increased survival.²
• Intermittent claudication may be the sole manifestation of early symptomatic PVD. The level of arterial compromise and the location of the claudication are closely related as follows:
  • Aortoiliac disease manifests as pain in the thigh and buttock, whereas femoral-popliteal disease manifests as pain in the calf.
  • Symptoms are precipitated by walking a predictable distance and are relieved by rest.
  • Collateral circulation may develop, reducing the symptoms of intermittent claudication, but failure to control precipitant factors and risk factors often causes its reemergence.
  • Claudication may also present as the hip or leg "giving out" after a certain period of exertion and may not demonstrate the typical symptom of pain on exertion.
  • The pain of claudication usually does not occur with sitting or standing.
• Ischemic rest pain is more worrisome; it refers to pain in the extremity due to a combination of PVD and inadequate perfusion.
  • Ischemic rest pain often is exacerbated by poor cardiac output.
  • The condition is often partially or fully relieved by placing the extremity in a dependent position, so that perfusion is enhanced by the effects of gravity.
• Leriche syndrome is a clinical syndrome described by intermittent claudication, impotence, and significantly decreased or absent femoral pulses. This syndrome indicates chronic peripheral arterial insufficiency due to narrowing of the distal aorta.
• The patient's medications may provide a clue to the existence of PVD.
  • Pentoxifylline is a commonly used medication specifically prescribed for PVD.
  • Daily aspirin commonly is used for prevention of cardiac disease (CAD), but PVD often coexists, to some degree, in patients with CAD.

Physical

A systematic examination of the peripheral vasculature is critical for proper evaluation.

• Peripheral signs of peripheral vascular disease are the classic "5 P's":
  • Pulselessness
  • Paralysis
  • Paraesthesia
  • Pain
  • Pallor
• Paralysis and paraesthesia suggest limb-threatening ischemia and mandate prompt evaluation and consultation.
• Assess the heart for murmurs or other abnormalities. Investigate all peripheral vessels, including carotid, abdominal, and femoral, for pulse quality and bruit. Note that the dorsalis pedis artery is absent in 5-8% of normal subjects, but the posterior tibial artery usually is present. Both pulses are absent in only about 0.5% of patients. Exercise may cause the obliteration of these pulses.
• The Allen test may provide information on the radial and ulnar arteries.
• The skin may have an atrophic, shiny appearance and may demonstrate trophic changes, including alopecia; dry, scaly, or erythematous skin; chronic pigmentation changes; and brittle nails.
• Advanced PVD may manifest as mottling in a "fishnet pattern" (livedo reticularis), pulselessness, numbness, or cyanosis. Paralysis may follow, and the extremity may become cold; gangrene eventually may be seen. Poorly healing injuries or ulcers in the extremities help provide evidence of preexisting PVD.
• The ankle-brachial index (ABI) can be measured at bedside. Using Doppler ultrasonography, the pressure at the brachial artery and at the posterior tibialis artery is measured. The ankle systolic pressure is divided by the brachial pressure, both measured in the supine position. Normally, the ratio is more than 1. In severe disease, it is less than 0.5.
• A semiquantitative assessment of the degree of pallor also may be helpful. While supine, the degree of pallor is assessed.  
  • If pallor manifests when the extremity is level, the pallor is classified as level 4.
  • If not, the extremity is raised 60°. If pallor occurs within 30 seconds, it is a level 3; in less than 60 seconds, level 2; in 60 seconds, level 1; and no pallor within 60 seconds, level 0.

Differential Diagnoses

Workup

Laboratory Studies

• Routine blood tests generally are indicated in the evaluation of patients with suspected serious compromise of vascular flow to an extremity. CBC, BUN, creatinine, and electrolytes studies help evaluate factors that might lead to worsening of peripheral perfusion. Risk factors for the development of vascular disease (lipid profile, coagulation tests) can also be evaluated, although not necessarily in the ED setting.
• An ECG may be obtained to look for evidence of dysrhythmia, chamber enlargement, or MI.
• Elevated levels of inflammatory blood markers such as D dimer, C-reactive protein, interleukin 6, and homocysteine have been linked to decreased lower extremity tolerance of exercise.³ Higher levels of activity in daily life have been shown to decrease these levels.⁴ The applicability to practice in Emergency Medicine is unknown. 

Imaging Studies

• Plain films are of little use in the setting of PVD. Doppler ultrasonographic studies are useful as primary noninvasive studies to determine flow status. Upper extremities are evaluated over the axillary, brachial, ulnar, and radial arteries. Lower extremities are evaluated over the femoral, popliteal, dorsalis pedis, and posterior tibial arteries. Note the presence of Doppler signal and the quality of the signal (ie, monophasic, biphasic, triphasic). The presence of distal flow does not exclude emboli or thrombi because collateral circulation may provide these findings.
• Magnetic resonance imaging (MRI) may be of some clinical benefit due to its high visual detail. Plaques are imaged easily, as is the difference between vessel wall and flowing blood. MRI also has the benefits of angiography to provide even higher detail and can replace traditional arteriography. The utility of MRI is limited in the emergency setting, often due to location of the device and the technical skill required to interpret the highly detailed images.
• Computerized tomography (CT) can be of use to the emergency physician since it does not have the time and availability constraints of MRI. Although noncontrast studies can be useful to image calcification and arteriosclerosis, contrast studies are most useful to image arterial insufficiency. Renal function should be confirmed before contrast administration, since PVD often coexists with risk factors for contrast-induced renal failure.

Other Tests

• The ankle-brachial index (ABI) is a useful test to compare pressures in the lower extremity to the upper extremity. Blood pressure normally is slightly higher in the lower extremities than in the upper extremities. Comparison to the contralateral side may suggest the degree of ischemia.
• The ABI is obtained by applying blood pressure cuffs to the calf and the upper arm. The blood pressure is measured, and the systolic ankle pressure is divided by the systolic brachial pressure. Normal ABI is more than 1; a value less than 0.95 is considered abnormal. This test can be influenced by arteriosclerosis and small vessel disease (eg, diabetes), reducing reliability. Progressive PAD, indicated by ABI decline of greater than 0.15, has been associated with increased cardiovascular disease risk.⁵
• Transcutaneous oximetry affords assessment of impaired flow secondary to both microvascular and macrovascular disruption. Its use is increasing, especially in the realm of wound care and patients with diabetes. Transcutaneous oximetry has not been studied extensively in emergent occlusion.

Procedures

• The criterion standard for intraluminal obstruction has always been arteriography, although this is both potentially risky and often unobtainable in the emergency setting. The delay associated with obtaining arteriography in the setting of obvious limb ischemia can delay definitive treatment to deleterious effect. If time allows, arteriography can prove useful in discriminating thrombotic disease from embolic disease.

Treatment

Prehospital Care

Prehospital care for peripheral vascular disease (PVD) involves the basics: control ABCs, obtain intravenous access, and administer oxygen. Generally, do not elevate the extremity. Note and record distal pulses and skin condition. Perform and document a neurological examination of the affected extremities.

Emergency Department Care

Attention to the ABCs, intravenous access, and obtaining baseline laboratory studies should occur early in the ED visit. Obtain an ECG and chest radiograph.

Treatment of either thrombi or emboli in the setting of peripheral vascular disease is similar. Empirically, initiate a heparin infusion with the goal of increasing activated partial thromboplastin time to 1.5 times normal levels. Acute leg pain correlated with a cool distal extremity, diminished or absent distal pulses, and an ankle blood pressure less than 50 mm Hg should prompt consideration of emergent surgical referral.

In some cases of emboli, intra-arterial thrombolytic agents may be useful. The exact technique of administration varies, in both dosage and time of administration. Remember that intra-arterial thrombolysis remains investigational. Obviously, such thrombolytic therapy is contraindicated in the presence of active internal bleeding, intracranial bleeding, or bleeding at noncompressible sites.

Consultations

Early surgical consultation in patients with acute limb ischemia is prudent. Depending on the case, the surgeon may involve interventional radiology or proceed operatively. Emboli may be treated successfully by Fogarty catheter (ie, an intravascular catheter with a balloon at the tip). The balloon is passed distal to the lesion; the balloon is inflated, and the catheter is withdrawn along with the embolus. This technique most commonly is used for iliac, femoral, or popliteal emboli.

Definitive treatment of hemodynamically significant aortoiliac disease is usually by aortobifemoral bypass. Its 5-year patency rate is approximately 90%. Those patients in whom PVD becomes significant, however, often have a plethora of comorbid medical conditions, such as cardiovascular disease, diabetes, and chronic obstructive pulmonary disease, which increase procedural morbidity and mortality. Axillobifemoral bypass and femoral-femoral bypass are alternatives, both of which have lower 5-year patencies but have lower procedural mortality.

Some areas of arteriostenosis can be revascularized with percutaneous transluminal coronary angioplasty (PTCA). If the occlusion is complete, a laser may be useful in making a small hole through which to pass the balloon. Restenosis is a concern with PTCA, particularly for larger lesions. Stents and lasers are still considered experimental.

Medication

The goal of pharmacotherapy is to reduce morbidity and to prevent complications.

Anticoagulants

Anticoagulants reduce thrombin generation and fibrin formation and minimize clot propagation.

Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.

Dosing

Adult

80 U/kg IV bolus, followed by infusion of 18 U/kg/h

Pediatric

Administer as in adults

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity

Contraindications

Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

In neonates, preservative-free heparin is recommended to avoid possible toxicity (gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock; recent neurosurgery (within 6 wk), major surgery within 48 h, known bleeding diathesis, childbirth within 24 h, thrombocytopenia

Follow-up

Further Outpatient Care

• Patients who have significant peripheral vascular disease but whose illness is not so severe or acute that it requires inpatient treatment may be discharged with appropriate follow-up. However, counsel these patients regarding the potential effects of various activities and medications on the course of their illness. Advise patients to stop smoking and to avoid cold exposures and medications that can lead to vasoconstriction, including medications used for migraines and over-the-counter medications.
• Some recreational drugs (eg, cocaine) may have a deleterious effect on peripheral arterial tone, and beta-blockers may exacerbate the condition.
• Consultation with providers who will be following the patient after ED discharge is advised when making decisions regarding the discontinuation of medications used for chronic medical conditions.

Patient Education

• For excellent patient education resources, visit eMedicine's Circulatory Problems Center. Also, see eMedicine's patient education article Peripheral Vascular Disease.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize severe arterial insufficiency may put the patient at risk for serious local ischemic complications. In addition, it is critical that the patient be evaluated for acute cardiac conditions that might have led to peripheral arterial ischemia. Potentially significant legal consequences may ensue if these conditions are missed.

References

1. Nakata S, Yokoi Y, Matsumoto R, et al. Long-term cardiovascular outcomes following ischemic heart disease in patients with and without peripheral vascular disease. Osaka City Med J. Jun 2008;54(1):21-30. [Medline].

2. Jurado JA, Bashir R, Burket MW. Radiation-induced peripheral artery disease. Catheter Cardiovasc Interv. Oct 1 2008;72(4):563-8. [Medline].

3. McDermott MM, Liu K, Ferrucci L, et al. Circulating blood markers and functional impairment in peripheral arterial disease. J Am Geriatr Soc. Aug 2008;56(8):1504-10. [Medline].

4. Craft LL, Guralnik JM, Ferrucci L, et al. Physical activity during daily life and circulating biomarker levels in patients with peripheral arterial disease. Am J Cardiol. Nov 1 2008;102(9):1263-8. [Medline].

5. Criqui MH, Ninomiya JK, Wingard DL, et al. Progression of peripheral arterial disease predicts cardiovascular disease morbidity and mortality. J Am Coll Cardiol. Nov 18 2008;52(21):1736-42. [Medline].

6. Aufderheide TP. Peripheral arteriovascular disease. In: Emergency Medicine: Concepts and Clinical Practice. 1998:1826-44.

7. Feldman AJ. Acute extremity ischemia and thrombophlebitis. In: Emergency Medicine: A Comprehensive Study Guide. 1996:389-94.

8. Hauser CJ, Klein SR, Mehringer CM, et al. Superiority of transcutaneous oximetry in noninvasive vascular diagnosis in patients with diabetes. Arch Surg. Jun 1984;119(6):690-4. [Medline].

9. Hedin U, Wahlberg E. Gene therapy and vascular disease: potential applications in vascular surgery. Eur J Vasc Endovasc Surg. Feb 1997;13(2):101-11. [Medline].

10. Henein MY, Anagnostopoulos C, Das SK, et al. Left ventricular long axis disturbances as predictors for thallium perfusion defects in patients with known peripheral vascular disease. Heart. Mar 1998;79(3):295-300. [Medline].

11. Howell JM. Acquired diseases of the arteries and veins. In: Emergency Medicine. 1998:203-6.

12. Levien DH. Vascular surgery. In: Introduction to Surgery. 2^nd ed. 1993:208-14.

13. Schwartz GR. Nontraumatic organ system emergencies. In: Principles and Practice of Emergency Medicine. 1992:1382-90.

14. Semashko DC. Vascular emergencies. Mt Sinai J Med. Sep-Oct 1997;64(4-5):316-22. [Medline].

15. Yousuf AM, Pai NB. Noninvasive evaluation of vascular diseases. Hosp Physician. Apr 1991;48-52.

Keywords

PVD, peripheral vascular disease, arteriosclerosis obliterans, circulation disorder, functional peripheral vascular disease, organic peripheral vascular diseases, atherosclerosis, emboli, thrombi, atheroma, vascular disease, cardiac emboli, coronary artery disease, myocardial infarction, MI, atrial fibrillation, transient ischemic attack, stroke, renal disease, smoking, hyperlipidemia, diabetes mellitus, hyperviscosity, phlebitis, autoimmune disease, vasculitides, arthritis, coagulopathy

Contributor Information and Disclosures

Author

Everett Stephens, MD, Assistant Clinical Professor, Department of Emergency Medicine, University of Louisville
Everett Stephens, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

David A Peak, MD, Assistant Residency Director of Harvard Affiliated Emergency Medicine Residency, Attending Physician, Massachusetts General Hospital; Consulting Staff, Department of Hyperbaric Medicine, Massachusetts Eye and Ear Infirmary
David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians and National Association of EMS Physicians
Disclosure: Intellicare Salary Management position; South Middlesex EMS Consortium Salary Management position

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Assistant Professor, Department of Medicine, Division of Emergency Medicine, Harvard Medical School; Associate-Chief, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Schering  Honoraria Speaking and teaching

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