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Venous pathophysiology in the lower extremity manifests as a spectrum of disorders (see Section 23, Chronic Venous Disorders). Reporting standards published first in 1994 and revised in 2004 recognized pathophysiologic assessment as a key feature in assessing patients with chronic venous disease (CVD) properly, as well communicating results to the venous care community. , The 2014 joint Society for Vascular Surgery/American Venous Forum clinical practice guideline on venous leg ulcer (VLU) management recommends all patients with this most severe CVD sequela be classified according to their Clinical class, Etiology, Anatomy and Pathophysiology (CEAP). Figure 24.1 demonstrates common clinical and anatomic features associated with CVD. Patients with less severe CVD manifestations benefit from whole limb venous physiologic evaluation as well. Categorizing the pathology is critical to directing the patient’s clinical course, as well as establishing treatment success and failure.
Duplex ultrasonography is often the first-line diagnostic tool applied in CVD. Grayscale B-mode combined with Doppler insonation allows direct, real-time visualization of vein segments to detect flow limitation or valvular reflux. Color flow duplex is an accurate, noninvasive, easily repeated test (see Ch. 25 , Vascular Laboratory: Venous Duplex Scanning). Anatomic information obtained from B-mode imaging reveals structural pathology from the iliac bifurcation distally, depending on patient body habitus, while Doppler waveform analysis with provocative maneuvers provides insight on flow characteristics. The latter evaluation is reported as “reflux time.” Venous duplex scanning provides further details on this assessment. Reflux time is a surrogate for pathophysiology with different values accepted to correlate with obstruction, valvular incompetence or a combination of both depending on the anatomic location. Danielsson et al. demonstrated duplex-calculated reflux time did not correlate with CEAP classification, while a more thorough physiologic evaluation with plethysmography did. Another concept that has fallen out of favor, valve closure time, has similarly been suggested not to correlate with disease severity.
Consequently, complete clinical evaluation in CVD patients necessitates applying physiologic noninvasive testing in addition to duplex scanning. Several techniques exist and are employed with varying frequency dependent on local practice patterns. This chapter describes each technique’s application and interpretation, as well as limitations.
The first reported venous pressure measurement in a walking subject was reported in 1936. Pollack and Wood are largely credited with standardizing the recording method and identifying the contribution of defective vein valves to alterations in venous ankle pressures. Several contributors defined the relationship between vein and lower leg muscle over the next two decades, resulting in the unicameral model. Essentially, calf muscle contraction propels blood heart-ward through the deep and superficial venous systems, creating a pressure drop below the knee, termed “calf diastole.”
Classically, the dorsal foot vein (DFV) is accessed percutaneously with the patient at rest and a baseline, or standing leg, pressure recorded by a transducer. Patients then perform 10 tiptoe stands; the resultant pressure changes are graphed against time. That pressure recorded after the last exercise – generally the nadir – is the ambulatory venous pressure (AVP). Calf diastole is the time required to achieve 90% baseline pressure, also called venous refill time (VRT or VFT).
A recent study of 76 limbs in 38 normal patients suggested a subtle revision to the unicameral model. The polycameral model considers the deep and superficial lower leg compartments, as well as the dorsal foot, as separate physiologic units. Great saphenous vein (GSV) and DFV AVP were noted to be different, suggesting AVP monitoring via the DFV does not accurately reflect pressure changes in the GSV.
Figure 24.2A depicts a normal subject’s venous pressure-time curve during AVP monitoring.
A normal AVP results in a minimum 50% decrease in venous pressure relative to baseline, while calf diastole lasts a minimum of 20 seconds. Pathophysiology associated with CVD introduces multiple alterations to the normal tracing ( Fig. 24.2B ). Valvular insufficiency in superficial or deep veins leads to a shorter duration for calf diastole. Obstruction would result in a pressure increase from baseline. Combined disease incorporates both an increased exercise pressure and decreased calf diastole time.
These parameters correlate with CEAP class, particularly increasing AVP. Deep venous insufficiency produces higher AVPs than does superficial insufficiency, while combined deep vein incompetence and iliofemoral obstruction produced the highest AVP values.
The polycameral model suggests perforators draining from the superficial to deep vein system during calf diastole results in AVP discrepancies when monitored via the GSV versus the DFV, perhaps explaining the significant proportion – up to 25% – of patients with ulcers despite normal AVP values. A phlebotomy tourniquet application during monitoring interrupts the contribution from superficial venous insufficiency. Correction to normal AVP and calf diastole times suggests superficial disease, while continued abnormal values suggests deep system pathology. Column interruption duration (CID) reflects the interval from calf blood ejection to flow reappearance by Duplex, providing the opportunity to evaluate both deep and superficial vein valves independently and provide a more accurate estimate of their individual contributions to whole limb CVD.
Venous hypertension may result from venous obstruction, or calf muscle pump dysfunction, in addition to valvular incompetence. Deficiencies in calf muscle pump function may occur without anatomic CVI. Araki et al. demonstrated no difference in the degree of valvular incompetence determined by duplex between patients with active or healed venous ulcers and those with no prior ulceration. Decrease in EF and increase in RVF was observed in C6 patients compared with C4 and C5. These findings suggest that venous ulceration might be aggravated by the combination of valvular incompetence and poor calf muscle pump function. In addition, ankle range of motion was decreased in C4–6 limbs when compared to normal limbs; similar deterioration was observed at higher CEAP classes. A normal EF, >60%, was associated with a low incidence of ulceration in the presence of reflux and an abnormal EF, whereas an EF <40%, was found in limbs with active ulceration and minimal reflux.
Conceptual evolution from the unicameral model to the polycameral model of CVD remains controversial and unvalidated. The ability to quantify the contribution superficial, deep, and foot vein incompetence promises to supplant AVP as the physiologic CVD gold standard. Duplex imaging would also eliminate the need to access the DFV, which can be challenging in patients with extensive ulceration or skin changes often present in CVD.
Quantitative assessment of venous disease by AVP has been thought of as the “standard” to which other modalities should be compared. Nicolaides and Zukowskii demonstrated that AVP reflects global hemodynamics within an extremity, while correlating linearly with clinical disease severity. Unfortunately, AVP cannot reliably localize hemodynamic abnormalities beyond the deep and superficial systems, nor differentiate obstruction from reflux. Since AVP requires cannulating a foot vein, patients often prefer noninvasive testing methods that produce comparable data.
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