Peripheral Vascular Disease Clinical Presentation

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. PVD that coexists with CAD may indicate an increased burden of atheroma.^[1] Studies have suggested that even asymptomatic peripheral arterial disease (PAD) is associated with increased CAD mortality.^[2]
• 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.^[3]
• 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.

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.