Hyperemic maximal venous outflow unmasks symptomatic lower extremity venous obstruction
Article Outline
Venous obstruction is an underappreciated and often unrecognized component of the pathophysiology of symptomatic chronic venous disease (CVD). Moreover, standard methods used to detect venous obstruction, such as maximal venous outflow, are inadequate as they typically test patients at rest and in the supine position when the pathophysiology of CVD is defined in the upright patient performing exercise. This report describes a patient with incapacitating venous claudication in whom standard noninvasive venous function tests were normal and whose phlebography was interpreted as showing no evidence of venous obstruction. A postocclusive reactive hyperemic technique was used to unmask significant outflow obstruction, leading to operative correction and subsequent symptom resolution.
Venous valve insufficiency and luminal obstruction are the core components of ambulatory venous hypertension, which is the underlying pathophysiology of chronic venous disease (CVD).1, 2, 3 Venous valve function is reliably evaluated noninvasively and can be quantified.2, 3, 4 Unfortunately, venous obstruction as a component of symptomatic CVD is underappreciated and often unrecognized because of our inability to detect obstruction.3, 4, 5, 6, 7, 8, 9 Maximal venous outflow (MVO) techniques of the lower extremity have been used to detect alterations in venous outflow. Initially MVO abnormalities served as a pathophysiologic surrogate for the noninvasive diagnosis of acute deep venous thrombosis (DVT).3, 4, 5, 6, 7, 8, 9 Further in-depth evaluation with phlebographic comparison demonstrated that resting physiologic studies generally were insensitive to venous obstructions that did not occlude a major deep vein.3, 4, 5, 7, 8 The unrecognized irony is that all techniques of MVO study the patient at rest with the leg elevated, whereas the pathophysiology of CVD is defined in the upright patient during exercise.10, 11
We report a patient with incapacitating venous claudication in whom all noninvasive tests of venous function were normal and whose ascending phlebogram was interpreted as showing no significant obstruction. Postocclusive reactive hyperemia (PORH) augmented arterial inflow, which increased the volume of venous outflow, thereby unmasking significant outflow obstruction on MVO evaluation. This led to further in-depth evaluation and subsequent operative correction and symptom resolution.
Case report
A 38-year-old woman presented with disabling symptoms of bursting left leg pain occurring soon after beginning ambulation. She had no history of DVT or pulmonary embolism and was never treated with anticoagulation. Two years earlier she was found to have a May-Thurner syndrome and had a left common iliac vein stenosis treated with balloon angioplasty and stenting. Her left leg symptoms of pain and edema continued, which led to ligation and stripping of her left great saphenous vein. Persistent symptoms were attributed to valve incompetence of her common femoral and femoral veins. Operative banding of her left common femoral vein just above the profunda and the femoral vein just below the profunda with polytetrafluoroethylene (PTFE) wraps was performed to restore valve competence. Unfortunately, her symptoms worsened postoperatively, and she suffered debilitating calf pain after walking only several steps. She was asymptomatic in the supine position.
Noninvasive evaluation and ascending phlebography prior to referral were essentially non-revealing. Reports indicated that there was no evidence of venous obstruction.
Repeat duplex ultrasonography showed no evidence of DVT, with a slight increase in venous velocity in the left common femoral vein. Air plethysmography demonstrated a normal calf muscle ejection fraction of 50%, a normal residual volume fraction of 24%, and a slightly abnormal venous filling index (3.1%). MVO at rest revealed a venous volume of 94 ml and a 1-second venous outflow of 41.4 ml, which calculated to an outflow fraction (OF) of 44.1%, considered normal (Fig 1). In order to study venous outflow during increased arterial inflow (attempting to simulate the pathophysiologic condition of exercise-induced venous hypertension), the principle of PORH was used. Arterial occlusion, confirmed by loss of pedal Doppler signals in continuous wave Doppler, was achieved with a standard 12-cm sphygmomanometer cuff inflated to suprasystolic pressure at the distal thigh, producing lower leg ischemia. Reduction of the cuff pressure to 70 mmHg allowed hyperemic arterial inflow to the lower leg while permitting continued venous occlusion. Venous filling was observed until lower leg volume plateaued, at which time the cuff was rapidly released as venous outflow was recorded on the plethysmograph. Three minutes of tourniquet occlusion at the thigh resulted in a postocclusive hyperemic volume of 92 ml. The 1-second outflow volume dropped to 14 ml producing a 16% OF (Fig 1), significantly lower than expected in normals 12 and that observed in the same patient at rest. This observation justified repeat phlebographic evaluation of the patient.
Fig 1.
(Top) Air plethysmography demonstrates normal venous outflow in patient at rest. (Bottom) Using postocclusive reactive hyperemia techniques on the same patient reveals abnormal venous volumes, prompting further evaluation for obstruction.
Left lower extremity catheter-directed descending phlebography followed and showed a stenosis at the level of the femoral vein wrap but was initially not considered significant (Fig 2). Because of the marked abnormality of the hyperemic MVO, venous pressures were measured from the mid femoral to the common femoral vein, demonstrating a 4 mmHg pressure gradient with the patient in the supine position. The phlebogram also demonstrated an aneurysmal portion of the vein wall in the area of the previous operation.
Fig 2.
Repeat ascending phlebography shows stenosis and a venous aneurysm in the area of previous operation. These findings were not considered significant on prior evaluation.
It became evident that the femoral vein was significantly narrowed at the level of the vein wraps, resulting in venous obstruction which produced debilitating symptoms with exercise (ambulation), although at rest the patient's venous outflow measurement was normal. Reoperation with removal of the PTFE bands was recommended. Upon exploration, the PTFE bands were observed above and below the profunda femoris vein junction, thereby restricting venous outflow from the entire lower extremity. An aneurysmal portion of femoral vein wall protruded between the pieces of PTFE (Fig 3). After removal of the bands, the common femoral vein remained stenotic due to transmural sclerosis. The venous aneurysm and the first 2 cm of common femoral vein were resected. The superficial wall of the femoral vein below the profunda was incised, thereby widening a stenotic portion of the proximal femoral vein. A ringed PTFE graft was interposed with the hood of PTFE extending onto the femoral vein distally as a patch angioplasty repair of the constricted segment just below the profunda femoris vein (Fig 4).
Fig 3.
PTFE bands above and below the profunda femoris vein junction restrict outflow to the entire lower extremity.
Fig 4.
A venous aneurysm and the first 2 cm of common femoral vein are resected and a ringed PTFE graft placed to repair the constricted segment. Descending phlebography demonstrates graft patency.
The patient remained on aspirin and heparin postoperatively and received intermittent pneumatic compression while being converted to oral anticoagulation with warfarin. She was asymptomatic upon resuming ambulation the next day.
Pre-discharge descending phlebography showed spasm in the femoral vein below the interposition graft, which was secondary to catheter manipulation. The graft was patent. Venous pressures recorded a 1 mmHg gradient from the mid-femoral vein to the inferior vena cava, which is considered normal.
The patient was discharged on aspirin 81 mg and warfarin maintaining a target international normalized ratio (INR) of 2.0-3.0 for three months. Compression stockings of 30-40 mmHg ankle gradient were prescribed to further control edema. At three months follow-up, repeat resting and postocclusive reactive hyperemic MVO examinations were normal (Fig 5). At one-year follow-up, the patient remained asymptomatic, the venous outflow was normal, and compression stockings were no longer worn.
Fig 5.
Postoperatively, noninvasive studies demonstrate normal venous outflow volumes at rest and with hyperemia.
Discussion
This case illustrates the underappreciated and unrecognized problem of venous obstruction, even when it results in debilitating venous claudication. This patient's early-onset symptoms of venous claudication are atypical but can be explained by occlusion of the profunda femoris venous drainage and femoral vein drainage. Evidently this patient's venous drainage was maximally compensated at rest; therefore, early after initiation of exercise, the pressure volume hemodynamics changed and symptoms occurred.
This case confirms once again that standard methods of MVO to evaluate venous obstruction are inadequate. The pathophysiology of CVI is defined by the patient exercising in the erect position, yet testing for venous obstruction is routinely performed in the supine, leg-elevated position with the patient at rest. Hyperemic MVO “stresses” the venous system, which stimulates increased arterial inflow, similar to the exercising subject.
PORH has been used to evaluate venous obstruction in conjunction with arm-foot pressure differentials (AFPD).13 Fully compensated venous obstructions had an AFPD of <4 mmHg at rest and <6 mmHg after PORH. Raju and Fredericks13 defined obstruction as partially compensated if the AFPD was <4 mmHg at rest but >6 mmHg after PORH. Partially decompensated obstructions correlated with an AFPD >4 mmHg at rest and >6 mmHg after PORH. Paradoxically, the AFPD after PORH in fully decompensated observations was <6 mmHg. Although the presence and extent of reflux increased the likelihood of venous ulceration, grade of obstruction seemed to have no influence on the distribution of ulceration. No correlation of symptom severity to the grade of obstruction was mentioned.
There are no reports of PORH being used as a stress maneuver to improve the sensitivity of noninvasive testing for venous obstruction. It is expected that venous capacitance increases following PORH, especially in patients who do not have postthrombotic venous disease. In the face of venous outflow obstruction with augmented arterial inflow, the OF would be expected to decrease, as occurred in this patient, thereby improving the sensitivity of the technique to detect any important physiologic venous outflow obstruction.
The reduced one-second outflow fraction following PORH may seem counterintuitive to some. This patient's venous stenosis was fixed, as was the volume of her venous outflow over time. Hyperemia significantly increases arterial inflow in the face of fixed venous outflow. The findings described by this patient's outflow curves are easily explained when one understands that the outflow curves measure relative volume change over time and not absolute volume. At rest, the venous outflow fraction was nearly at capacity. With hyperemia, there is significantly increased arterial inflow for an extended period of time in the face of restricted venous outflow, hence a reduced outflow fraction. Therefore, the reduced one-second outflow fraction does not mean reduced venous outflow, but rather reduced venous outflow relative to arterial inflow.
This patient had no history of DVT; therefore, with the exception of the stenotic femoral and common femoral vein, her venous system was normal and had the capability to significantly increase her venous volume capacity. This patient was unusual in that her chronic problem was solely venous obstruction. The common femoral stenosis and proximal femoral vein stenosis affected the entire lower extremity venous drainage, at least with exercise. As clear-cut as this case may seem in retrospect, standard noninvasive venous evaluation failed to detect the physiologic importance of the patient's venous obstruction, and routine ascending phlebography also failed to identify outflow obstruction as the etiology for her incapacitating symptoms.
This case illustrates the inadequacy of present methods of detecting physiologically important venous obstruction. This is a major shortcoming of current diagnostic methods that result in a misunderstanding of the pathophysiology of venous disease. Venous occlusion that is identified in symptomatic patients is generally considered important. Unfortunately, noninvasive techniques are not yet available to quantify the pathophysiologic significance of varying degrees of venous obstruction. Hyperemic MVO produces a challenge to the venous system, similar to exercise, increasing arterial inflow approximately six-fold.14 This will stress the outflow capability of the proximal veins. This preliminary observation suggests that this new technique has the potential of improving the noninvasive evaluation of venous obstruction and putting it into the proper perspective of patients with chronic venous disease.
References
- . The pathophysiology of chronic venous insufficiency. In: Rutherford RB editors. Vascular surgery. 6th ed.. Philadelphia: W.B.Saunders; 2005;p. 2220–2229
- . Classification and clinical and diagnostic evaluation of patients with chronic venous disorders. In: Rutherford RB editors. Vascular surgery. 6th ed.. Philadelphia: W.B. Saunders; 2005;p. 2230–2240
- . Investigation of chronic venous insufficiency: A consensus statement (France, March 5-9, 1997). Circulation. 2000;102:E126–E163
- . Evaluation of chronic venous disease. In: Mansour MA, Labropoulos N editor. Vascular diagnosis. Philadelphia: W.B. Saunders; 2005;p. 447–462
- The role of venous outflow obstruction in patients with chronic venous dysfunction. Arch Surg. 1997;132:46–51
- . Proximal lower extremity chronic venous outflow obstruction: recognition and treatment. Semin Vasc Surg. 2002;15:57–64
- Noninvasive tests in venous insufficiency. J Cardiovasc Surg (Torino). 1993;34:3–11
- . Air plethysmography: a clinical review. Int Angiol. 1995;14:45–52
- . Air plethysmography: the answer in detecting past deep venous thrombosis. J Vasc Surg. 2001;33:715–720
- . Detection of outflow obstruction in chronic venous insufficiency. J Vasc Surg. 1993;17:583–589
- . New approaches to the diagnosis and treatment of venous obstruction. J Vasc Surg. 1986;4:42–54
- . Can post-occlusive reactive hyperemia improve evaluation of venous obstruction in patients with chronic venous disease?. [Abstract] Phlebology. 2007;22:233–234
- . Venous obstruction: an analysis of one hundred thirty-seven cases with hemodynamic, venographic, and clinical correlations. J Vasc Surg. 1991;14:305–313
- Paolini D, Comerota AJ, Jones L. Lower extremity arterial inflow is adversely affected in patients with venous disease. In: Scientific program of the 20th Annual Meeting, American Venous Forum; February 20-23, 2008; Charleston, SC. Abstract 33.
Competition of interest: none.
PII: S0741-5214(08)00474-6
doi:10.1016/j.jvs.2008.03.038
© 2008 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
