Vascular leg pain – Pathophysiology
Lower extremity pain can arise from abnormalities in either arteries or veins. In the case of arterial disease, the tissues are insufficiently supplied with oxygenated blood because of obstruction to inflow. In the case of veins, valvular incompetence or venous obstruction result in distention and excessive hydro-static pressure in the veins and adjacent tissues. In rare instances, virtually total venous obstruction may result in sufficient reduction in outflow of blood to seriously reduce nutrient capillary inflow, resulting in tissue ischemia.
Arterial flow is capable of increasing dramatically in response to demand. During muscle contraction as with walking, metabolic byproducts build up in the muscles resulting in reflex vasodilatation and reduced vascular resistance. Compensatory inflow rapidly follows to nourish the exercising muscle. In the presence of arterial obstructive disease, compensatory inflow is retarded and the increased demands cannot be met. Ischemic claudication pain ensues which persists until demand is reduced by cessation of exercise and the supply of oxygenated blood can be replenished.
Obstruction of the main arterial channels results in enlargement of collaterals connecting the proximal relatively undiseased arterial tree with the distal underperfused tree. If the occlusion is limited to a relatively short segment of artery, such as the iliac or superficial femoral, collateral channels can usually provide sufficient flow into the distal tree to render the leg symptom-free until exercise increases demand. Such segmental disease causing intermittent claudication generally reduces the resting systolic pressure ratio between the ankle and the arm to 0.4–0.9. In situations where there are multiple obstructions in series, such as combined iliac and femoral disease, collateral flow must bridge a longer distance, with reduced blood pressure and flow to the distal bed. Such patterns, as well as patterns of severe obstruction in the more distal portion of the leg below the knee, account for most instances of ischemic pain at rest.
Resting ischemic symptoms and findings are generally associated with ankle/ brachial pressure ratios < 0.4. With acute occlusion of an essentially normal artery, there are no enlarged collaterals available at the onset of ischemia and the severity of ischemia is consequently greater than in more chronic situations where obstruction develops slowly and collaterals have had sufficient time to enlarge. Ischemia results in pain, progressing to paresthesia and numbness and finally to paralysis due to both nerve and muscle involvement as the duration and severity of ischemia increase. Symptoms of chronic arterial occlusive disease may be enhanced in the presence of anemia and reduced cardiac output.
Acute venous occlusion results in abrupt increase in pressure in veins distal to the obstruction. Collaterals naturally enlarge to carry flow into the lower pressure venous tree proximal to the obstruction. Increased pressure produces distension of the veins and increases interstitial fluid within the muscle compartments causing painful stretching of the fascia. In the presence of acute thrombosis, variable associated inflammation of the vein adjacent to thrombus adds a component of inflammatory pain. When venous outflow is virtually completely obstructed through both main channels and adjacent collaterals, as in Phlegmasia alba dolens, arterial inflow is impeded sufficiently to produce ischemic pain. With more chronic obstruction, pain is generally minimal because of the absence of inflammation and presence of large collaterals which decompress the distal veins.
In some circumstances, however, sufficient venous obstruction may be present to produce intermittent claudication based on inability of the venous tract to provide sufficient outflow for the increased amounts of arterial inflow brought on by muscle contraction. Most commonly, chronic venous insufficiency on the basis of primary valvular incompetence or previous deep vein thrombosis (DVT) results in enlargement of venous channels, increased hydrostatic pressure in the more distal portion of the leg with dependence and pressure transmission to the fascia and superficial tissues with consequent sensations of heaviness, stretching, and aching.