Vascular Diseases
General Approach to the Vascular Patient
Because the vascular system involves every organ system in our body, the symptoms of vascular disease are as varied as those encountered in any medical specialty. Lack of adequate blood supply to target organs typically presents with pain; for example, calf pain with lower extremity (LE) claudicating, postprandial abdominal pain from mesenteric ischemia, and arm pain with axillosubclavian arterial occlusion. In contrast, stroke and transient ischemic attack (TIA) are the presenting symptoms from middle cerebral embolization as a consequence of a stenos internal carotid artery (
Appropriate history should be focused on the presenting symptoms related to the vascular system (Table 1). Of particular importance in the previous medical history is noting prior vascular interventions (endovascular or open surgical), and all vascular patients should have inquiry made about their prior cardiac history and current cardiac symptoms. Approximately 30% of vascular patients will be diabetic. A history of prior and current smoking status should be noted.
The patient with carotid disease in most cases is completely asymptomatic, having been referred based on the finding of a cervical bruit or duplex finding of stenosis. Symptoms of carotid territory TIAs include transient monocular blindness (amaurosis), contra lateral weakness or numbness, and dysphasia. Symptoms persisting longer than 24 hours constitute a stroke. In contrast, the patient with chronic mesenteric ischemia is likely to present with postprandial abdominal pain and weight loss. The patient fears eating because of the pain, avoids food, and loses weight. It is very unlikely that a patient with abdominal pain who has not lost weight has chronic mesenteric ischemia.
The patient with LE pain on ambulation has intermittent claudicating that occurs in certain muscle groups; for example, calf pain upon exercise usually reflects superficial femoral artery (SFA) disease, while pain in the buttocks reflects iliac disease. In most cases, the pain manifests in one muscle group below the level of the affected artery, occurs only with exercise, and is relieved with rest only to recur at the same location, hence the term window gazers disease. Rest pain (a manifestation of severe underlying occlusive disease) is constant and occurs in the foot (not the muscle groups), typically at the metatarsophalangeal junction, and is relieved by dependency. Often, the patient is prompted to sleep with their foot hanging off one side of the bed to increase the hydrostatic pressure.
Specific vascular examination should include abdominal aortic palpation, carotid artery examination, and pulse examination of the LE (femoral, popliteal, posterior tibial, and dorsalis pedis arteries). The abdomen should be palpated for an abdominal aortic aneurysm (AAA), detected as an expansible pulse above the level of the umbilicus. It also should be examined for the presence of bruits. Because the aorta typically divides at the level of the umbilicus, an aortic aneurysm is most frequently palpable in the epigastrium. In thin individuals, a normal aortic pulsation is palpable, while in obese patients even large aortic aneurysms may not be detectable. Suspicion of a clinically enlarged aorta should lead to the performance of an ultrasound scan for a more accurate definition of aortic diameter.
The carotids should be auscultated for the presence of bruits, although there is a higher correlation with coronary artery disease (CAD) than underlying carotid stenosis. A bruit at the angle of the mandible is a significant finding, leading to follow-up duplex scanning. The differential diagnosis is a transmitted murmur from a sclerotic or stenotic aortic valve. The carotid is palpable deep to the sternocleidomastoid muscle in the neck. Palpation, however, should be gentle and rarely yields clinically useful information.
Upper extremity examination is necessary when an arteriovenous graft is to be inserted in patients who have symptoms of arm pain with exercise. Thoracic outlet syndrome can result in occlusion or aneurysm formation of the subclavian artery. Distal embolization is a manifestation of thoracic outlet syndrome; consequently, the fingers should be examined for signs of ischemia and ulceration. The axillary artery enters the limb below the middle of the clavicle, where it can be palpated in thin patients. It usually is easily palpable in the axilla and medial upper arm. The brachial artery is most easily located at the antecubital fossa immediately medial to the biceps tendon. The radial artery is palpable at the wrist anterior to the radius.
For LE vascular examination, the femoral pulse usually is palpable midway between the anterior superior iliac spine and the pubic tubercle. The popliteal artery is palpated in the popliteal fossa with the knee flexed to 45° and the foot supported on the examination table to relax the calf muscles. Palpation of the popliteal artery is a bimanual technique. Both thumbs are placed on the tibial tuberosity anteriorly and the fingers are placed into the popliteal fossa between the two heads of the gastrocnemius muscle. The popliteal artery is palpated by compressing it against the posterior aspect of the tibia just below the knee. The posterior tibial pulse is detected by palpation
After reconstructive vascular surgery, the graft may be available for examination, depending on its type and course. The in situ LE graft runs in the subcutaneous fat and can be palpated along most of its length. A change in pulse quality, aneurysmal enlargement, or a new bruit should be carefully noted. Axillofemoral grafts, femoral-to-femoral grafts, and arteriovenous access grafts usually can be easily palpated as well.
Noninvasive Diagnostic Evaluation of the Vascular Patient
There is increasing interest in the use of the ankle-brachial index (ABI) to evaluate patients at risk for cardiovascular events. An ABI <0.9 correlates with increased risk of myocardial infarction and indicates significant, although perhaps asymptomatic, underlying peripheral vascular disease. The ABI is determined in the following ways. Blood pressure (BP) is measured in both upper extremities using the highest systolic BP as the denominator for the ABI. The ankle pressure is determined by placing a BP cuff above the ankle and measuring the return to flow of the posterior tibial and dorsalis pedis arteries using a pencil Doppler probe over each artery. The ratio of the systolic pressure in each vessel divided by the highest arm systolic pressure can be used to express the ABI in both the posterior tibial and dorsalis pedis arteries (Fig. 1).
Segmental Limb Pressures
By placing serial BP cuffs down the LE and then measuring the pressure with a Doppler probe as flow returns to the artery below the cuff, it is possible to determine segmental pressures down the leg. These data can then be used to infer the level of the occlusion. The systolic pressure at each level is expressed as a ratio, with the highest systolic pressure in the upper extremities as the denominator. Normal segmental pressures commonly show high thigh pressures 20 mmHg or greater in comparison to the brachial artery pressures. The low thigh pressure should be equivalent to brachial pressures. Subsequent pressures should fall by no more than 10 mmHg at each level. A pressure gradient of 20 mmHg between two subsequent levels is usually indicative of occlusive disease at that level. The most frequently used index is the ratio of the ankle pressure to the brachial pressure, the ABI. Normally the ABI is >1.0, and a value <0.9 indicates some degree of arterial obstruction and has been shown to be correlated with an increased risk of coronary heart disease.1 Limitations of relying on segmental limb pressures include: (a) missing isolated moderate stenoses (usually iliac) that produce little or no pressure gradient at rest; (b) falsely elevated pressures in patients with diabetes and end-stage renal disease; and (c) the inability to differentiate between stenosis and occlusion.2 Patients with diabetes and end-stage renal disease have calcified vessels that are difficult to compress, thus rendering this method inaccurate, due to recording of falsely elevated pressure readings. Noncompressible arteries yield ankle systolic pressures of 250 mmHg or greater and an ABI of >1.40. In this situation, absolute toe and ankle pressures can be measured to gauge critical limb ischemia. Ankle pressures <50 mmHg or toe pressures <30 mmHg are indicative of critical limb ischemia. The toe pressure is normally 30 mmHg less than the ankle pressure, and a toe-brachial index of <0.70 is abnormal. False-positive results with the toe-brachial index are unusual. The main limitation of this technique is that it may be impossible to measure pressures in the first and second toes due to pre-existing ulceration.
In patients with noncompressible vessels, segmental plethysmography can be used to determine underlying arterial occlusive disease. Cuffs placed at different levels on the leg detect changes in leg volume and produce a pulse volume recording (PVR) when connected to a plethysmograph (Fig. 2). To obtain accurate PVR waveforms the cuff is inflated to 60 to 65 mmHg to detect volume changes without causing arterial occlusion. Pulse volume tracings are suggestive of proximal disease if the upstroke of the pulse is not brisk, the peak of the wave tracing is rounded, and there is disappearance of the dicrotic notch.
Although isolated segmental limb pressures and PVR measurements are 85% accurate when compared with angiography in detecting and localizing significant atherosclerotic lesions, when used in combination, accuracy approaches 95%.3 For this reason, it is suggested that these two diagnostic modalities be used in combination when evaluating PAD.
Radiological Evaluation of the Vascular Patient
Ultrasound
Ultrasound examinations are relatively time consuming, require experienced technicians, and may not visualize all arterial segments. Doppler waveform analysis can suggest atherosclerotic occlusive disease if the waveforms in the insonated arteries are biphasic, monophasic, or asymmetrical. B-mode ultrasonography provides black and white, real-time images. B-mode ultrasonography does not evaluate blood flow; thus, it cannot differentiate between fresh thrombus and flowing blood, which have the same echogenicity. Calcification in atherosclerotic plaques will cause acoustic shadowing. B-mode ultrasound probes cannot be sterilized. Use of the B-mode probe intraoperatively requires a sterile covering and gel to maintain an acoustic interface. Experience is needed to obtain and interpret images accurately. Duplex ultrasonography entails performance of B-mode imaging, spectral Doppler scanning, and color flow duplex scanning. The caveat to performance of duplex ultrasonography is meticulous technique by a certified vascular ultrasound technician, so that the appropriate 60° Doppler angle is maintained during insonation with the ultrasound probe. Alteration of this angle can markedly alter waveform appearance and subsequent interpretation of velocity measurements. Direct imaging of intra-abdominal vessels with duplex ultrasound is less reliable because of the difficulty in visualizing the vessels through overlying bowel. These disadvantages currently limit the applicability of duplex scanning in the evaluation of aortoiliac and infrapopliteal disease. In a recent study, duplex ultrasonography had lower sensitivity in the calculation of infrapopliteal vessel stenosis in comparison to conventional digital subtraction or computer tomography angiography.4 Few surgeons rely solely on duplex ultrasonography for preoperative planning in LE revascularizations. However, in the hands of experienced ultrasonographers, LE arteries can be assessed accurately by determining the significance of velocity criteria across the arterial stenosis. Duplex scanning is unable to evaluate recently implanted polytetrafluoroethylene (PTFE) and polyester (Dacron) grafts because they contain air, which prevents ultrasound penetration.
Computed Tomography Angiography
Computed tomography angiography (CTA) is a noninvasive, contrast-dependent method for imaging the arterial system. It depends on IV infusion of iodine-based contrast agents. The patient is advanced through a rotating gantry, which images serial transverse slices. The contrast-filled vessels can be extracted from the slices and rendered in three-dimensional format (Fig. 3). The extracted images can also be rotated and viewed from several different directions during postacquisition image processing. This technology has been advanced as a consequence of aortic endografting. CTA provides images for postprocessing that can be used to display the aneurysm in a format that demonstrates thrombus, calcium, lumen, and the outer wall, and allows “fitting” of a proposed endograft into the aneurysm (Fig. 4). CTA is increasingly being used to image the carotid bifurcation, and as computing power increases, the speed of image acquisition and resolution will continue to increase. The major limitations of multidetector CTA are use of contrast and presence of artifacts caused by calcification and stents. CTA can overestimate the degree of instent stenosis, while heavy calcification can limit the diagnostic accuracy of the method by causing a ”blooming artifact.”5 The artifacts can be overcome with alteration in image acquisition technique. There are no randomized trials to document the superiority of multidetector CTA over traditional angiography, but there is emerging evidence to support the claim that multidetector CTA has sensitivity, specificity, and accuracy that rival invasive angiography.
Magnetic resonance angiography (MRA) has the advantage of not requiring iodinated contrast agents to provide vessel opacification (Fig. 5). Gadolinium is used as a contrast agent for MRA studies, and as it is generally not nephrotoxic, it can be used in patients with elevated creatinine. MRA is contraindicated in patients with pacemakers, defibrillators, spinal cord stimulators, intracerebral shunts, cochlear implants, and cranial clips. Patients with claustrophobia may require sedation to be able to complete the test. The presence of metallic stents causes artifacts and signal dropout; however, these can be dealt with using alternations in image acquisition and processing. Nitinol stents produce minimal artifact.6 Compared to other modalities, MRA is relatively slow and expensive. However, due to its noninvasive nature and decreased nephrotoxicity, MRA is being used more frequently for imaging vasculature in various anatomic distributions.
Diagnostic Angiography
Diagnostic angiography is considered the gold standard in vascular imaging. In many centers, its use is rapidly decreasing due to the development of noninvasive imaging modalities such as duplex arterial mapping, CTA, and MRA. Nevertheless, contrast angiography still remains in widespread use. The essential aspects of angiography are vascular access and catheter placement in the vascular bed that requires examination. The imaging system and the contrast agent are used to opacify te target vessel. Although in the past this function has largely been delegated to the interventional radiology service, an increasing number of surgeons are performing this procedure and following the diagnostic imaging with immediate surgical or endovascular intervention. There are several considerations when relying on angiography for imaging.
Approximately 70% of atherosclerotic plaques occur in an eccentric location within the blood vessel; therefore, images can be misleading when trying to evaluate stenoses because angiography is limited to a uniplanar “lumenogram.” With increased use of intravascular stent deployment, it has been also noted that assessment of stent apposition and stent position in relation to surrounding branches may be inaccurate. Furthermore, angiography exposes the patient to the risks of both ionizing radiation and intravascular contrast. Nevertheless, contrast angiography remains the most common invasive method of vascular investigation for both diagnostic and therapeutic intervention. The angiogram usually provides the final informatioeeded to decide whether or not to proceed with operation or endovascular interventions.
Digital subtraction angiography (DSA) offers some advantages over conventional cut-film angiography, such as excellent visualization despite use of lower volumes of contrast media. In particular when multilevel occlusive lesions limit the amount of contrast reaching distal vessels, supplemental use of digital subtraction angiographic techniques may enhance visualization and definition of anatomy. Intra-arterial DSA uses a portable, axially rotatable imaging device that can obtain views from different angles. DSA also allows for real-time video replay (Fig. 6). An entire extremity can be filmed with DSA, using repeated injections of small amounts of contrast agent to obtain sequential angiographic images, the so-called pulse-chase technique.
Preoperative Cardiac Evaluation
The most important and controversial aspect of preoperative evaluation in patients with atherosclerotic disease requiring surgical intervention is the detection and subsequent management of associated CAD. Several studies have documented the existence of significant CAD in 40 to 50% or more of patients requiring peripheral vascular reconstructive procedures, 10 to 20% of whom may be relatively asymptomatic largely because of their inability to exercise. Myocardial infarction is responsible for the majority of both early and late postoperative deaths. Most available screening methods lack sensitivity and specificity to predict postoperative cardiac complications. There have been conflicting reports regarding the utility of preoperative dipyridamole-thallium nuclear imaging or dobutamine-echocardiography to stratify vascular patients in terms of perioperative cardiac morbidity and mortality. Iearly one half of patients, thallium imaging proves to be unnecessary because cardiac risk can be predicted by clinical information alone. Even with coronary angiography, it is difficult to relate anatomic findings to functional significance, and hence, surgical risk. There are no data confirming that percutaneous coronary interventions or surgical revascularization before vascular surgical procedures impacts mortality or incidence of myocardial infarctions. In fact, coronary angiography is associated with its own inherent risks, and patients undergoing coronary artery bypass grafting or coronary percutaneous transluminal angioplasty (PTA) before needed aortoiliac reconstructions are subjected to the risks and complications of both procedures.
The Coronary Artery Revascularization Prophylaxis trial showed that coronary revascularization in patients with peripheral vascular disease and significant CAD, who are considered high risk for perioperative complications, did not reduce overall mortality or perioperative myocardial infarction. Additionally, patients who underwent prophylactic coronary revascularization had significant delays before undergoing their vascular procedure and increased limb morbidity compared to patients who did not. Studies do support improvement in cardiovascular and overall prognosis with medical optimization of patients. Therefore, use of perioperative beta blockade, as well as use of antiplatelet medication, statins, and angiotensin-converting enzyme (ACE) inhibitors is encouraged in vascular patients
AORTOILIAC OCCLUSIVE DISEASE
The distal abdominal aorta and the iliac arteries are common sites affected by atherosclerosis. The symptoms and natural history of the atherosclerotic process affecting the aortoiliac arterial segment are influenced by the disease distribution and extent. Atherosclerotic plaques may cause clinical symptoms by restricting blood flow due to luminal obstruction or by embolizing atherosclerotic debris to the LE circulation. If the aortoiliac plaques reach sufficient mass that impinge on the arterial lumen, obstruction of blood flow to lower extremities occurs. Various risk factors exist that can lead to the development of aortoiliac occlusive disease. Recognition of these factors and understanding this disease entity will enable physicians to prescribe the appropriate treatment strategy that may alleviate symptoms and improve quality of life.
On clinical examination, patients often have weakened femoral pulses and a reduced ABI. Verification of iliac occlusive disease is usually made by color duplex scanning that reveals either a peak systolic velocity ratio of 2.5 or greater at the site of stenosis and/or a monophasic waveform. Noninvasive tests such as pulse volume recording (PVR) of the LE with estimation of the thigh-brachial pressure index may be suggestive of aortoiliac disease. MRA and multidetector CTA are increasingly being used to determine the extent and type of obstruction. DSA offers the interventionalist the benefit of making a diagnosis and the option of performing an endovascular treatment in a single session. Angiography provides important information regarding distal arterial runoff vessels as well as the patency of the profunda femoris artery (PFA). Presence of pelvic and groin collaterals is important in providing crucial collateral flow in maintaining lower limb viability. It must be emphasized, however, that patients should be subjected to angiography only if their symptoms warrant surgical intervention.
Degenerative hip or spine disease, lumbar disc herniation, spinal stenosis, diabetic neuropathy, and other neuromuscular problems can produce symptoms that may be mistaken for vascular claudication. Such cases can be distinguished from true claudication by the fact that the discomfort from neuromuscular problems often is relieved by sitting or lying down, as opposed to cessation of ambulation. In addition, complaints that are experienced upon standing suggest nonvascular causes. When confusion persists, the use of noninvasive vascular laboratory testing modalities, including treadmill exercise, can help establish the diagnosis.
The principal collateral pathways in severe aortoiliac artery occlusive disease or chronic aortic occlusion that may provide blood flow distal to the aortoiliac lesion include: (a) the SMA to the distal IMA via its superior hemorrhoidal branch to the middle and inferior hemorrhoidals to the internal iliac artery (39%); (b) the lumbar arteries to the superior gluteal artery to the internal iliac system (37%); (c) the lumbar arteries to the lateral and deep circumflex arteries to the common femoral artery (CFA) (12%); and (d) Winslow’s pathway from the subclavian to the superior epigastric artery to the inferior epigastric artery to the external iliac arteries at the groin (Fig. 7). In general, treatment indications for aortoiliac artery occlusive disease include disabling claudication, ischemic rest pain, nonhealing LE tissue wound, and LE microembolization that arise from aortoiliac lesions.
Fig. 7. Pertinent collateral pathways are developed in the event of chronic severe aortoiliac occlusive disease. As illustrated in this multidetector computed tomography angiography, these collaterals include epigastric arteries (large white arrows), an enlarged inferior mesenteric artery (white arrowhead), and enlarged lumbar arteries (black arrows).
Disease Classification
Based on the atherosclerotic disease pattern, aortoiliac occlusive disease can be classified into three various types (Fig. 8). Type I aortoiliac disease, which occurs in 5 to 10% of patients, is confined to the distal abdominal aorta and common iliac vessels (Fig. 9). Due to the localized nature of this type of aortic obstruction and formation of collateral blood flow around the occluded segment, limb-threatening symptoms are rare in the absence of more distal disease (Fig. 10). This type of aortoiliac occlusive disease occurs in a relatively younger group of patients (aged in their mid-50s), compared with patients who have more femoropopliteal disease. Patients with a type I disease pattern have a lower incidence of hypertension and diabetes, but a significant frequency of abnormal blood lipid levels, particularly type IV hyperlipoproteinemia. Symptoms typically consist of bilateral thigh or buttock claudication and fatigue. Men report diminished penile tumescence and may have complete loss of erectile function. These symptoms in the absence of femoral pulses constitute Leriche’s syndrome. Rest pain is unusual with isolated aortoiliac disease unless distal disease coexists. Occasionally patients report a prolonged history of thigh and buttock claudication that recently has become more severe. It is likely that this group has underlying aortoiliac disease that has progressed to acute occlusion of the terminal aorta. Others may present with “trash foot” that represents microembolization into the distal vascular bed
Type II aortoiliac disease represents a more diffuse atherosclerotic progression that involves predominately the abdominal aorta with disease extension into the CIA. This disease pattern affects approximately 25% of patients with aortoiliac occlusive disease. Type III aortoiliac occlusive disease, which affects approximately 65% of patients with aortoiliac occlusive disease, is widespread disease that is seen above and below the inguinal ligament (Fig. 12). Patients with “multilevel” disease are older, more commonly male (with a male-to-female ratio of 6:1), and much more likely to have diabetes, hypertension, and associated atherosclerotic disease involving cerebral, coronary, and visceral arteries. Progression of the occlusive process is more likely in these patients than in those with localized aortoiliac disease. For these reasons, most patients with a type III pattern tend to present with symptoms of advanced ischemia and require revascularization for limb salvage rather than for claudication. These patients have a decreased 10-year life expectancy when compared to patients with localized aortoiliac disease.
The most commonly used classification system of iliac lesions has been set forth by the TASC II group with recommended treatment options. This lesion classification categorizes the extent of atherosclerosis and has suggested a therapeutic approach based on this classification (Table 3 and Fig. 13). According to this consensus document, endovascular therapy is the treatment of choice for type A lesions, and surgery is the treatment of choice for type D lesions. Endovascular treatment is the preferred treatment for type B lesions, and surgery is the preferred treatment for good-risk patients with type C lesions. In comparison to the 2000 TASC II document, the commission has not only made allowances for treatment of more extensive lesions, but also took into account the continuing evolution of endovascular technology and the skills of individual interventionalists when stating that the patient’s comorbidities, fully informed patient preference, and the local operator’s long-term success rates must be considered when making treatment decisions for type B and type C lesions
General Treatment Considerations
There is no effective medical therapy for the management of aortoiliac disease, but control of risk factors may help slow progression of atherosclerosis. Patients should have hypertension, hyperlipidemia, and diabetes mellitus controlled. They should be advised to stop smoking. Most patients are empirically placed on antiplatelet therapy. A graduated exercise program may improve walking efficiency, endothelial function, and metabolic adaptations in skeletal muscle, but, there is usually minimal improvement in patients with aortoiliac disease who are treated with these measures. Failure to respond to exercise and/or drug therapy should prompt consideration for limb revascularization. Patients with buttock claudication and reduced or absent femoral pulses who fail to respond to exercise and drug therapy should be considered for revascularization because they are less likely than patients with more distal lesions to improve without concomitant surgical or endovascular intervention.
Surgical Reconstruction of Aortoiliac Occlusive Disease
Aortobifemoral Bypass
Surgical options for treatment of aortoiliac occlusive diseases consist of various configurations of aortobifemoral bypass (ABF) grafting, various types of extra-anatomic bypass grafts, and aortoiliac endarterectomy. The procedure performed is determined by several factors, including anatomic distribution of the disease, clinical condition of the patient, and personal preference of the surgeon.
In most cases, ABF is performed because patients usually have disease in both iliac systems. Although one side may be more severely affected than the other, progression does occur, and bilateral bypass does not complicate the procedure or add to the physiologic stress of the operation. ABF reliably relieves symptoms, has excellent long-term patency (approximately 70 to 75% at 10 years), and can be completed with a tolerable perioperative mortality (2 to 3%).
Technical Considerations for Aortobifemoral Bypass
Both femoral arteries are initially exposed to ensure that they are adequate for the distal anastomoses. The abdomen is then opened in the midline, the small intestine is retracted to the right, and the posterior peritoneum overlying the aorta is incised. A retroperitoneal approach may be selected as an alternative in certain situations. This approach involves making a left flank incision and displacing the peritoneum and its contents to the right. Such an approach is contraindicated if the right renal artery is acutely occluded, because visualization from the left flank is very poor. Tunneling of a graft to the right femoral artery also is more difficult from a retroperitoneal approach, but can be achieved. The retroperitoneal approach has been reputed to be better tolerated than midline laparotomy for patients with multiple previous abdominal operations and with severe pulmonary disease. Further proposed advantages of the retroperitoneal approach include less GI disturbance, decreased third-space fluid losses, and ease with which the pararenal aorta can be accessed. There are randomized reports, however, that support and refute the superiority of this approach. A collagen-impregnated, knitted Dacron graft is used to perform the proximal aortic anastomosis, which can then be made in either an end-to-end or end-to-side fashion using 3-0 polypropylene suture. The proximal anastomosis should be made as close as possible to the renal arteries to decrease the incidence of restenosis from progression of the atherosclerotic occlusive process in the future.
An end-to-end proximal aortic anastomosis is necessary in those patients with an aortic aneurysm or complete aortic occlusion extending up to the renal arteries (Fig. 14). Although in theory, the end-to-end configuration allows for less turbulence and less chance of competitive flow with still patent host iliac vessels, there have not been consistent results to substantiate differences in patency between end-to-end and end-to-side grafts. Relative indications for an end-to-side proximal aortic anastomosis include the presence of large aberrant renal arteries, an unusually large IMA with poor back-bleeding, suggesting inadequate collateralization, and/or occlusive disease involving bilateral external iliac arteries. Under such circumstances, end-to-end bypass from the proximal aorta to the femoral level devascularizes the pelvic region because there is no antegrade or retrograde flow in the occluded external iliac arteries to supply the hypogastric arteries. As a result of the pelvic devascularization, there is an increased incidence of impotence, postoperative colon ischemia, buttock ischemia, and paraplegia secondary to spinal cord ischemia, despite the presence of excellent femoral and distal pulses.
An end-to-side proximal aortic anastomosis can be associated with certain disadvantages, which include the potential for distal embolization when applying a partially occlusive aortic clamp (Fig. 15). Furthermore, the distal aorta often proceeds to total occlusion after an end-to-side anastomosis. There may also be a higher incidence of aortoenteric fistula following construction of end-to-side proximal anastomoses because the anterior projection makes subsequent tissue coverage and reperitonealization of the graft more difficult. The limbs of the graft are tunneled through the retroperitoneum to the groin, where an end-to-side anastomosis is fashioned between the graft and the bifurcation of the CFA using 5-0 polypropylene suture. Endarterectomy or patch angioplasty of the profunda femoris may be required concurrently. Once the anastomoses have been fashioned and the graft thoroughly flushed, the clamps are removed and the surgeon carefully controls the degree of aortic occlusion until full flow is re-established. During this period the patient must be carefully monitored for hypotension. Declamping hypotension is a complication of sudden restoration of aortic flow, particularly following prolonged occlusion. Once flow has been re-established, the peritoneum is carefully reapproximated over the prosthesis to prevent fistulization into the intestine.
Despite the presence of multilevel disease in most patients, a properly performed aortobifemoral operation can provide arterial inflow and alleviate claudication symptoms in 70 to 80% of patients; however, 10 to 15% of patients will require simultaneous outflow reconstruction to address distal ischemia and facilitate limb salvage. The advantage of concomitant distal revascularization is avoidance of reoperation in a scarred groin. As a rule, if the profunda femoris can accept a 4-mm probe and if a No. 3 Fogarty embolectomy catheter can be passed distally for
Aortic Endarterectomy
Aortoiliac endarterectomy is rarely performed, as it is associated with greater blood loss, greater sexual dysfunction, and is more difficult to perform. Long-term patency is comparable with aortobifemoral grafting, and thus it remains a reasonable option in cases in which the risk of infection of a graft is excessive, because it involves no prosthetic tissue. Aortoiliac endarterectomy was useful when disease was localized to either the aorta or CIAs; however, at present, aortoiliac PTA, stents, and other catheter-based therapies have become first-line treatments in this scenario. Endarterectomy should not be performed if the aorta is aneurysmal because of continued aneurysmal degeneration of the endarterectomized segment. If there is total occlusion of the aorta to the level of the renal arteries, aortic transection several centimeters below the renal arteries with thrombectomy of the aortic cuff followed by graft insertion is easier and more expeditious when compared to endarterectomy. Involvement of the EIA makes aortic endarterectomy more difficult to complete because of decreased vessel diameter, increased length, and exposure issues. The ability to establish an appropriate endarterectomy plane is compromised due to the muscular and inherently adherent nature of the media in this location. There is a higher incidence of early thrombosis and late failure with extended aortoiliofemoral endarterectomy when compared to bypass grafting as a result of recurrent stenosis.
An axillofemoral bypass is an extra-anatomic reconstruction that derives arterial inflow from the axillary artery to the femoral artery. This is a treatment option for those patients with medical comorbidities that prohibit an abdominal vascular reconstruction. It may be performed under local anesthesia and is used for limb salvage. Extra-anatomic bypasses have lower patency when compared to aortobifemoral, and therefore, are seldom recommended for claudication. Before performing this operation, the surgeon should check pulses and BP in both arms to ensure that there is no obvious disease affecting flow through the axillary system. Angiography of the axillosubclavian vasculature is not necessary, but can be helpful if performed at the time of aortography. The axillary artery is exposed below the clavicle, and a 6- to 8-mm externally reinforced PTFE graft is tunneled subcutaneously down the lateral chest wall and lateral abdomen to the groin. It is anastomosed to the ipsilateral distal at the CFA bifurcation into the superficial femoral and profunda femoris arteries. A femorofemoral crossover graft using a 6- to 8-mm externally reinforced PTFE graft is then used to revascularize the opposite extremity if necessary. Reported patency rates over 5 years vary from 30 to 80%. Paradoxically, although it is a less complex procedure than aortofemoral grafting, the mortality rate is higher (10%), reflecting the compromised medical status of these patients.
Iliofemoral Bypass
One option for patients with unilateral occlusion of the distal common iliac or external iliac arteries is iliofemoral grafting (Fig. 16). Long-term patency is comparable to aortounifemoral bypass and because the procedure can be performed using a retroperitoneal approach without clamping the aorta, the perioperative mortality is less.
Femorofemoral Bypass
A femorofemoral bypass is another option for patients with unilateral stenosis or occlusion of the common or EIA who have rest pain, tissue loss, or intractable claudication. The primary (assisted) patency at 5 years is reported to be 60 to 70%, and, although this is inferior when compared to aortofemoral bypass, there are physiologic benefits, especially for patients with multiple comorbidities, because it is not necessary to cross-clamp the aorta. There are no studies supporting the superiority of unsupported or externally supported PTFE over Dacron for choice of conduit. The fear of the recipient extremity stealing blood from the extremity ipsilateral to the donor limb is not realized unless the donor iliac artery and donor outflow arteries are diseased. Depending on the skills of the interventionalist/surgeon, many iliac lesions classified as TASC II B, C, or D caow be addressed using an endovascular approach, thus obviating the need to perform a femorofemoral bypass. Additionally, femorofemoral bypass can be used as an adjuvant procedure after iliac inflow has been optimized with endovascular methods.
Obturator Bypass
An obturator bypass is used to reconstruct arterial anatomy in patients with groin sepsis resulting from prior prosthetic grafting, intra-arterial drug abuse, groieoplasm, or damage from prior groin irradiation. This bypass can originate from the CIA, EIA, or uninvolved limb of an ABF. A conduit of Dacron, PTFE, or autologous vein is tunneled through the anteromedial portion of the obturator membrane to the distal superficial femoral or popliteal artery. The obturator membrane must be divided sharply so as to avoid injury to adjacent structures, and care must be taken to identify the obturator artery and nerve that pass posterolaterally. After the bypass is completed and the wounds isolated, the infected area is entered, the involved arteries are débrided to healthy tissue, and vascularized muscle flaps are mobilized to cover the ligated ends. There have been varied results in terms of patency and limb salvage for obturator bypass. Some authors have reported 57% 5-year patency and 77% 5-year limb salvage rates, whereas others have shown a high rate of reinfection and low patency requiring reintervention.
Thoracofemoral Bypass
The indications for thoracofemoral bypass are (a) multiple prior surgeries with a failed infrarenal aortic reconstruction and (b) infected aortic prosthesis. This procedure is more physiologically demanding than other extra-anatomic reconstructions because the patient must not only tolerate clamping the descending thoracic aorta but also performance of a left thoracotomy. The graft is tunneled to the left CFA from the left thorax posterior to the left kidney in the anterior axillary line using a small incision in the periphery of the diaphragm and an incision in the left inguinal ligament to gain access to the extraperitoneal space from below. The right limb is tunneled in the space of Retzius in an attempt to decrease kinking that is more likely to occur with subcutaneous, suprapubic tunneling. Thoracofemoral bypass has long-term patency comparable to aortofemoral bypass.
Complications of Surgical Aortoiliac Reconstruction
With current surgical techniques and conduits, early postoperative hemorrhage is unusual and occurs in 1 to 2% of cases. It is usually the result of technical oversight or coagulation abnormality. Acute limb ischemia (ALI) occurring after aortoiliac surgery may be the result of acute thrombosis or distal thromboembolism. The surgeon can prevent thromboembolic events by (a) avoiding excessive manipulation of the aorta, (b) ensuring adequate systemic heparinization, (c) judicious placement of vascular clamps, and (d) thorough flushing before restoring blood flow. Acute thrombosis of an aortofemoral graft limb in the early perioperative period occurs in 1 to 3% of patients.112 Thrombectomy of the graft limb is performed through a transverse opening in the hood of the graft at the femoral anastomosis. With this approach, it is possible to inspect the interior of the anastomosis and pass embolectomy catheters distally to clear the superficial femoral and profunda arteries. Various complications may be encountered following aortoiliac or aortobifemoral reconstruction (Table 4).
Intestinal ischemia following aortic reconstruction occurs in approximately 2% of cases; however, with colonoscopy, mucosal ischemia, which is a milder form, is seen more frequently. The surgeon can identify patients who require concomitant revascularization of the IMA, hypogastric arteries, or mesenteric arteries by examining the preoperative arteriogram for the presence of associated occlusive lesions in the celiac axis, the superior mesenteric arteries, or both. Likewise patients with patent and enlarged IMA or a history of prior colonic resections will benefit from IMA reimplantation.
In a comprehensive review of 747 patients who had aortoiliac operations for occlusive disease, secondary operations for late complications such as reocclusion, pseudoaneurysms, and infection were necessary in 21% of cases over a 22-year period. The most frequent late complication is graft thrombosis. Limb occlusion occurs in 5 to 10% of patients within 5 years of the index operation and in 15 to 30% of patients 10 years or more after the index operation. Anastomotic pseudoaneurysms occur in 1 to 5% of femoral anastomoses in patients with aortofemoral grafts. Predisposing factors to pseudoaneurysm formation include progression of degenerative changes within the host artery, excessive tension at the anastomosis, and infection. Due to the associated risks of thrombosis, distal embolization, infection, and rupture, anastomotic aneurysms should be repaired expeditiously.
Infection following aortoiliac reconstruction is a devastating complication that occurs in 1% of cases. Femoral anastomoses of aortofemoral reconstructions and axillofemoral bypasses are prone to infection. Use of prophylactic antibiotics and meticulous surgical technique are vital in preventing contamination of the graft at the time of implantation. If infection appears to be localized to a single groin, one may consider the treatment strategies of graft preservation, aggressive local wound débridement, antibiotic solution irrigation, and soft tissue coverage with rotational muscle flaps. This nonexcisional treatment approach may be useful in selective cases of localized femoral graft infection. Most patients with infected aortoiliofemoral reconstructions usually require graft excision and revascularization via remote uncontaminated routes or the use of in situ replacement to clear the infective process and maintain limb viability. Aortoenteric fistula and associated GI hemorrhage are devastating complications, with a 50% incidence of death or limb loss. The incidence of aortoenteric fistula formation appears to be higher after an end-to-side proximal anastomosis, because it is more difficult to cover the prosthesis with viable tissue and avoid contact with the GI tract with this configuration. Treatment of aortoenteric fistula requires resection of all prosthetic material, closure of the infrarenal abdominal aorta, repair of the GI tract, and revascularization by means of an extra-anatomic graft.
Epidemiology of Chronic Peripheral Venous Disease
The term chronic venous disease, or more specifically of interest here, chronic peripheral venous disease (CPVD) has been used more generally to refer to either visible and/or functional abnormalities in the peripheral venous system. The most widely used classifi cation of such abnormalities is the CEAP (Clinical, Etiological, Anatomic, Pathophysiologic), which includes both anatomic (superfi cial, deep, or perforating veins) and pathophysiologic (reflux, obstruction, both) categories.
The CEAP classification was created by an international committee of clinical experts, and reflects the clinical situation in patients typically referred to a vascular specialist for clinically significant venous disease. In contrast to the clinical situation, population studies of CPVD typically have focused on broader categories determined by visual inspection only. The three major categories of interest have been varicose veins (VV), chronic venous insufficiency (CVI), and venous ulcers. However, there has not been a standard definition of these categories. VV has been defined bothincluding and excluding telangiectasias (spider veins), and at differing levels of visible disease severity. CVI typically has been defined by skin changes and/or edema in the distal leg. Venous ulcers, both active and healed, have been defined by visual inspection and subjective inference as to etiologic origin.
Two studies have now reported results on defined free-living populations with simultaneous assessment of both visible abnormalities and functional impairment by Duplex ultrasound.
The Duplex examination for the San Diego Population Study (SDPS) determined both obstruction and reflux, whereas the o.
Although these discrepancies occurred in a minority of cases, they were frequent enough to lead us to separately classify visible and functional CPVD in each limb evaluated in the SDPS. Specially, we classified each limb into four visible categories: normal, telangectasias/spider veins (TSV), VV, and trophic changes (TCS), the latter category being one or more of hyperpigmentation, lipodermatosclerosis, or active or healed ulcer. The presence/absence of edema was not by itself a criterion for TCS. For functional disease, we determined the presence of obstruction and reflux separately for the superficial, perforating, and deep systems. The presence of either reflux or obstruction in superficial or deep veins was categorized as functional disease, and because of small numbers, abnormalities of the perforating veins were considered as deep disease. Three functional categories were defined: normal, superficial functional disease (SFD), and deep functional disease (DFD). Here, the term “functional” is essentially interchangeable with “anatomic.” Also, in this population study obstruction was uncommon, and virtually all legs with obstruction also had reflux, such that SFD and DFD essentially refer to reflux.
In addition to separately assessing edema, we asked about a history of superficial venous thrombosis (SVT) and deep venous thrombosis (DVT), with or without pulmonary embolism.
AGE AND CVPD
Using mutually exclusive categories for both visible and functional CVPD, we found a graded relationship with increasing age for VV, with those aged 70–79 years having nearly twice the prevalence of those aged 40–49 years. TSV also increased with age, but this difference was obscured by the mutually exclusive categories with increasing numbers of participants with TSV also having VV or TCS at older ages. TCS showed the most dramatic age-related increase, with the oldest age group having more than four times the prevalence of the youngest.
These findings for visible disease are consistent with most previous population studies, which generally have found a linear increase in TSV or VV with age (reviewed in Reference 4). Earlier studies typically defined CVI only by venous (assumed) ulcers, and reported exponential increases in CVI with age, findings similar to the dramatic age increase we reported for the broader TCS category.
For functional CVPD, SFD was more than twice as common and DFD was 64% more common in the oldest age group. SFD showed both a higher prevalence and a steeper age gradient than did DFD.
The only other population data on functional disease were from the
Edema was strongly age-related as expected, but history of SVT and DVT were somewhat less so, perhaps reflecting selective recall bias in older participants.
Nonetheless, our data for DVT overall are quite similar to the lifetime prevalence in a large population-based study.
GENDER AND CPVD
For visible disease, we found nearly twice as much VV in women as in men, but TCS were 50% more common in men. These findings for VV are consistent with earlier studies, but earlier studies also have suggested a small excess of CVI in women, in contrast to our findings for the broader category of TCS. However, more concordant with our findings, the
Edema was about 50% more common in men than women, consistent with a 50% greater history of DVT in men. The
ETHNICITY AND CPVD
The SDPS reported data for four ethnicities, nonHispanic White, Hispanic, African-American, and Asian. Non-Hispanic Whites showed the highest prevalence of CPVD, with only 14.3% with a normal examination. Non-Hispanic Whites had the highest rates of TSV, TCS, and DFD, and the second highest rates (after Hispanics) of VV and SFD. African-Americans and Asians had a somewhat lower prevalence of CPVD. Consistent with the visible and functional findings, Non-Hispanic Whites also had the highest rates of edema and DVT by history, and Hispanics the highest rate of SVT by history.
Several previous studies have suggested a higher prevalence in developed than developing countries, although these studies are not entirely consistent. The SDPS is the first population study to evaluate multiple ethnic groups who were residents of the same geographical area.
RISK FACTORS FOR CPVD
Age was positively consistently related to all levels of visible and functional disease in both sexes. In comparison with non Hispanic whites (NHW), African-American Asian had less TSV and VV in both sexes, less TCS in men, and less DFD in women. Our results thus confirm that older age and NHW ethnicity are risk factors for CPVD.
Family history of venous disease based on subject recall was a risk factor for all levels of visible and functional disease. Although this finding could be biased, it is consistent with many other studies, although not all.
Ankle motility was a risk factor for visible disease SFD in women and for TSV in men. It was protective for women with DFD and men with SFD. The association of increasing laxity in connective tissue with venous disease corroborated previous research.
The protective associations could reflect increased ankle motility leading to decreased venous pressure by increasing pumping action.
Lower limb injury was a risk factor in women for DFD. Coughlin et al., in a case-control study, found serious lower limb trauma to be a risk factor for CVI.
CVD-related factors, such as angina, PTCA, hypertension, and diastolic pressure were associated with less TSV, SFD, and DFD for men and women and less VV for men. Although some studies have found a relationship between atherosclerosis and venous disease, others have not.
The reason for any protective effect of cardiovascular disease and hypertension on CPVD is not readily apparent, although venous vasoconstriction and microthrombosis could conceivably be involved.
Hours spent walking or standing was positively associated with VV, TCS, and SFD in men and women. Fowkes et al. found that walking was a risk factor for women with venous insufficiency when age-adjusted, but less so when multiply adjusted. They found walking to be related to lessened risk of venous insufficiency in men. Our data indicate that standing was a strong risk factor for venous disease in women. This is concordant with a number of studies, and contrasts with some other studies.
Weight, height, waist, and BMI, defined as weight in kg divided by height squared in meters squared, were positively associated with TCS, and DFD in men and VV, TCS, and SFD in women. Weight, waist circumference, the waist/hip ratio, and body mass index are all measures of adiposity.
A number of studies have found an association of obesity with venous disease. Gourgou et al. found a relationship in both men and women with VV. Our finding of increased waist circumference in men with TCS was consistent with findings that both obesity and male gender were associated with CVI and with the finding that weight was an independent risk factor for CVI in multivariate analysis In contrast, Coughlin et al. and Fowkes et al. both found that obesity was not a factor in venous insufficiency among women. Fowkes et al. extended this finding to men as well. Other studies also have found no association between obesity and venous disease.
However, the
During exercise the venomuscular pump is activated, which leads to a transient decrease in venous pressure, which should be protective for venous disease. This is consistent with our results in men.
HRT duration or parity was positively associated with all levels of visible and functional disease in women. Gourgou et al. found increasing VV prevalence with increasing numbers of births. Coughlin et al. found that multiparity was associated with varicose veins in pregnant women.
Some studies have found that the changes are effected with only one pregnancy. The increase of CPVD with HRT duration may indicate yet another underexamined systemic effect of HRT.
Our data indicate that age and family history were the strongest risk factors for CPVD, and neither is subject to intervention. Other significant findings on inherent factors included associations with connective tissue laxity and height. CVD-related factors were associated with lower rates of venous disease. Among volitional factors important findings were a relationship of CPVD with central adiposity, positional factors such as hours spent standing or sitting, exercise, and selected hormonal factors in women. In contrast with prior studies, we found no relationship with dietary fiber intake. In women but not men we confirmed the importance of a previous lower limb injury for DFD.
VENOUS ANATOMY, PHYSIOLOGY, AND PATHOPHYSIOLOGY
ANATOMY
The venous system in the lower extremities can be divided, for purposes of understanding, into three systems: the deep system, which parallels the tibia and femur; the superficial venous system, which resides in the superficial tissue compartment between the deep muscular fascia and the skin; and the perforating or connecting veins, which join the superficial to the deep systems. It is because these latter veins penetrate anatomic barriers, they are called perforating veins.
Although the superficial veins are the targets of most therapy, the principal return of blood flowfrom the lower extremities is through the deep veins. In the calf, these deep veins are paired and named for their accompanying arteries.
Therefore, the anterior tibial, posterior tibial, and peroneal arteries are accompanied by their paired veins, which are interconnected. These crural veins join and form the popliteal vein. Occasionally the popliteal veins as well as more proximal deep veins are also paired like the calf veins.
As the popliteal vein ascends, it becomes the femoral vein. Formerly, this was called the superficial femoral vein, but that term has been abandoned. Near the groin the femoral vein is joined by the deep femoral vein, and the two become the common femoral vein, which ascends to become the external iliac vein proximal to the inguinal ligament.
Ultrasound imaging has shown that the superficial compartment of the lower extremities consists of two compartments, one enclosing all the structures between the muscular fascia and the skin, and the other, within the superficial compartment enclosing the saphenous vein and bounded by the muscular fascia inferiorly and the superficial fascia superiorly, is termed the saphenous compartment (see Figure 1). The importance of this anatomic structure is underscored by its being targeted during percutaneous placement of endovenous catheters and the instillation of tumescent anesthesia.
The main superficial veins are the great saphenous vein and the small saphenous vein. These receive many interconnecting tributaries, and these tributaries may be referred to as communicating veins. They are correctly called tributaries rather than branches of the main superficial veins. The great saphenous vein has its origin on the dorsum of the foot.
It ascends anterior to the medial malleolus of the ankle and further on the anteromedial aspect of the tibia. At the knee, the great saphenous vein is found in the medial aspect of the popliteal space. It then ascends through the anteromedial thigh to join the common femoral vein, just below the inguinal ligament. Throughout its course, it lies within the saphenous compartment. The small saphenous vein originates laterally from the dorsal venous arch of the foot and travels subcutaneously behind the lateral malleolus at the ankle. As it ascends in the calf, it enters the deep fascia and ascends between the heads of the gastrocnemius muscle to join the popliteal vein behind the knee . In fact, there are many variations of the small saphenous vein as it connects both to the popliteal vein and to cranial extensions of the saphenous vein, as well as connections to the posteromedial circumfl ex vein (vein of Giacomini).
The third system of veins is called the perforating vein system. As indicated earlier, they connect the superficial and deep systems of veins. There is a fundamental fact, which confuses understanding of perforating veins. This relates to flow direction. Some perforating veins produce normal flow from the superficial to the deep circulation, others conduct abnormal outflow from the deep circulation to the superficial circulation. This is termed perforating vein reflux. Any of these perforating veins may demonstrate bidirectional flow
In the leg, the principal clinically important perforating veins are on the medial aspect of the ankle and leg, and are found anatomically at approximately
Conversely, when they are dysfunctional, they allow muscular compartment pressure to be transmitted directly to unsupported cutaneous and subcutaneous veins and venules.
VENOUS PHYSIOLOGY
It is estimated that 60 to 75% of the blood in the body is to be found in the veins. Of this total volume, about 80% is contained in the veins that are less than 200 μm in diameter. It is important to understand this reservoir function as it is related to the major components. The splanchnic venous circulation and the veins of the skin are richly supplied by the sympathetic nervous system fibers, but muscular veins have little or none of these. The veins in skeletal muscle, on the other hand, are responsive to catecholamines.
Although arterial pressures are generated by muscular contractions of the heart, pressures in the venous system largely are determined by gravity. In the horizontal position, pressures in the veins of the lower extremity are similar to the pressures in the abdomen, chest, and extended arm. However, with the assumption of the upright position, there are dramatic changes in venous pressure. The only point in which the pressure remains constant is the hydrostatic indifferent point just below the diaphragm. All pressures distal to this point are increased due to the weight of the blood column from the right atrium. When assuming the upright position, there is an accumulation of approximately 500 ml of blood in the lower extremities, largely due to reflux through the valveless vena cava and iliac veins. There is some loss of fluid into the tissues, and this is collected by the lymphatic system and returned to the venous system.
Venous valves play an important role in transporting blood from the lower extremities to the heart. In order for valve closure to occur, there must be a reversal of the normal transvalvular pressure gradient. A pressure and generated velocity flow exceeding 30 cm/second leads to valve closure. Direct observation of human venous valves has been made possible by specialized ultrasound techniques.
Venous flow is not in a steady state but is normally pulsatile, and venous valves undergo regular opening and closing cycles. Even when fully opened, the cross-sectional area between the leaflets is 35% smaller than that of the vein distal to the valve. Flow through the valve separates into a proximally directed jet and vortical flow into the sinus pocket proximal to the valve cusp. The vortical flow prevents stasis and ensures that all surfaces of the valve are exposed to sheer stress. Valve closure develops when the vortical flow pressure exceeds the proximally directed jet flow.
The role of venous valves in an individual quietly standing is not well understood. Pressures in the superficial and deep veins are essentially the same during quiet standing, but as Arnoldi has found, the pressure in the deep veins is
Normally functioning perforating vein valves protect the skin and subcutaneous tissues from the effects of muscular contraction pressure. This muscular contraction pressure may exceed 100 to 130 mmHg.
Intuitively, the role of venous valves during muscular exercise is obvious, since their major purpose is to promote antegrade flow from superficial to deep. Volume and pressure changes in veins within the calf occur with muscular activity. In the resting position, with the foot fl at on the floor, there is no flow. However, in the heel strike position, the venous plexus under the heel and plantar surface of the foot (Bejar’s plexus) is emptied proximally. Blood flows from the foot and ankle into the deep veins of the calf. Then, calf contraction transports this blood into the deep veins of the thigh, and henceforth, blood flow proceeds to the pelvic veins, vena cava, and ultimately to the heart all due to the influence of lower extremity muscular contraction.
PATHOPHYSIOLOGY
Abnormal functioning of the veins of the lower extremities is recognized clinically as venous dysfunction or, more commonly, venous insufficiency. Cutaneous telangiectases and subcutaneous varicose veins usually are grouped together under the title Primary Venous Insufficiency, and limbs with skin changes of hyperpigmentation, edema, and healed or open venous ulceration are termed Chronic Venous Insufficiency (CVI).
Primary Venous Insufficiency
Explanations of venous pathophysiology as published in reviews, texts, and monographs are now for the most part out of date. The new science as we now know it is incorporated in the following summary.
A dysfunctional venous system follows injury to vein walls and venous valves. This injury is largely due to inflammation, an acquired phenomenon. Factors, which are not acquired, also enter into such injury. These include heredity, obesity, female gender, pregnancy, and a standing occupation in women. Vein wall injury allows the vein to elongate and dilate thus producing the visual manifestations of varicose veins. An increase in vein diameter is one cause of valve dysfunction that results in reflux. The effect of persistent reflux through axial veins is a chronic increase in distal venous pressure. This venous pressure increases as one proceeds from the inguinal ligament past the knee to the ankle.
Prolonged venous hypertension initiates a cascade of pathologic events. These manifest themselves clinically as lower extremity edema, pain, itching, skin discoloration, and ulceration.
The earliest signs of venous insufficiency often are elongated and dilated veins in the epidermis and dermis, called telangiectasias. Slightly deeper and under the skin are fl at, blue-green veins of the reticular (network) system. These may become dilated and elongated as well . And finally, still deeper but still superficial to the superficial fascia are the varicose veins themselves. All of these abnormal veins and venules have one thing in common: they are elongated, tortuous, and have dysfunctional venous valves.
This implies a common cause, which is inflammation.
Chronic Venous Insufficiency
Skin changes of hyperpigmentation, scarring from previous ulceration, and active ulcerations are grouped together under the term chronic venous insufficiency (CVI). Numerous theories have been postulated regarding the cause of chronic venous insufficiency and the cause of venous ulceration.
All the theories proposed in the past century have been disproved. An example is the theory of venous stasis, first proposed in a manuscript by John Homans of Harvard in 1916.
It was a treatise on diagnosis and management of patients with chronic venous insufficiency, and in it, Dr. Homans coined the term “post-phlebitic syndrome” to describe the skin changes of CVI. He stated that, “Over-stretching of the vein walls and destruction of the valves . . . interferes with the nutrition of the skin . . . there-fore, skin which is bathed under pressure with stagnant venous blood will form permanent open sores or ulcers.”
That statement, like many others that describe venous conditions and their treatments, is steeped in dogma and is short of observational fact. The erroneous term stasis ulcer honors that misconception, as do the terms venous stasis disease and stasis dermatitis.
Alfred Blalock, who later initiated cardiac surgery, disproved the stasis theory by studying oxygen content from varicose veins and normal veins.
He pointed out that the oxygen content of the femoral vein in patients with severe chronic venous insufficiency was greater than the oxygen content of the contralateral nonaffected limb. Because oxygen content was higher, some investigators felt that arteriovenous fi stulas caused venous stasis and varicose veins.
That explanation, though disproved, has some basis in fact since the entire thermal regulatory apparatus in limbs depends on the opening and closing of arteriovenous shunts. These shunts are important as they explain some terrible accidents that happen during sclerotherapy when sclerosant entering a vein is shunted into the arterial system and distributed in its normal territory.
Microsphere investigations have failed to show any shunting and the theory of arteriovenous communications has died despite the fact that these shunts actually exist and do open under the influence of venous hypertension.
Hypoxia and its part in causation of chronic venous insufficiency was investigated throughout the last 25 years of the twentieth century. English investigators thought that a fi brincuff, observed histologically, blocked transport of oxygen and was responsible for skin changes of CVI at the ankles and distally.
That theory has been abandoned even though a true periarteriolar cuff is easily identified histologically.
The two elements that make up all the manifestations of lower extremity venous insufficiency are failure of the vein valves and vein walls and skin changes at the ankles, both of which are related to venous hypertension.
Failure of Vein Walls and Valves
Our work suggests that venous hypertension causes a shear stress dependent leukocyte-endothelial interaction, which has all the manifestations of chronic inflammation.
These are leukocyte rolling, firm adhesion to endothelium, and subsequent migration of the cells through the endothelial barrier into parenchyma of valves and vein walls.
There, macrophages elaborate matrix metalloproteases, which destroy elastin and possibly collagen as well. Vein walls become stretched and elongated. Vein valves become perforated, torn, and even scarred to the point of near total absence. These changes are seen both macroscopically and angioscopically.
Similar changes have been produced in the experimental animal by constructing an arteriovenous fistula to mimic the venous hypertension of venous dysfunction in humans.
Skin Changes
The second manifestation of chronic venous insufficiency is expressed in the skin where leukocytes also are implicated in the observed changes. There is evidence that leukocyte activation in the skin, perhaps related to venous hypertension, plays a major role in the pathophysiology of CVI. Thomas, working with Dormandy, reported that 25% fewer white cells and platelets left the dependent foot of the patients with venous hypertension. When the foot was elevated there was a significant washout of white cells but not platelets, suggesting platelet consumption within the microcirculation of the dependent foot. They concluded that the decrease in white cell exodus was due to leukocyte trapping in the venous microcirculation secondary to venous hypertension. They further speculated that trapped leukocytes may become activated, resulting in release of toxic metabolites causing damage to the microcirculation and overlying skin. Apparently, the primary injury in the skin is extravasation of macromolecules and red blood cells into the dermal interstitium. Red blood cell degradation products and interstitial protein extravasations are potent chemoattractants and represent the initial chronic inflammatory signal responsible for leukocyte recruitment.
The important observations of Dormandy’s group were historically the first to implicate abnormal leukocyte activity in the pathophysiology of CVI.
The importance of leukocytes in the development of dermal skin alterations was further emphasized by Coleridge Smith and his team. They obtained punch biopsies from patients with primary varicose veins, lipodermatosclerosis, and patients with lipodermatosclerosis and healed ulcers. They counted the mediaumber of white blood cells per high power field in each group but there was no attempt to identify the types of leukocytes. In patients with primary varicose veins, lipodermatosclerosis, and healed ulceration there was a median of 6, 45, and 217 WBCs per mm2, respectively. This demonstrated a correlation between clinical disease severity and the number of leukocytes in the dermis of patients with CVI.
The types of leukocytes involved in dermal venous stasis skin changes remain controversial. T-lymphocytes, macrophages, and mast cells have been observed on immunohistochemical and electron microscopic examinations.
The variation in types of leukocytes observed may reflect the types of patients investigated. The
SYMPTOMS OF PRIMARY VENOUS INSUFFICIENCY
It is well known that the presence and severity of symptoms do not correlate with the size or severity of the varicose veins present. Symptoms usually attributable to varicose veins include feelings of heaviness, tiredness, aching, burning, throbbing, itching, and cramping in the legs (see Table 2). These symptoms are generally worse with prolonged sitting or standing and are improved with leg elevation or walking. A premenstrual exacerbation of symptoms is also common. Generally, patients find relief with the use of compression in the form of either support hose or an elastic bandage. Weight loss or the commencement of a regular program of lower extremity exercise may also lead to a diminution in the severity of varicose vein symptoms. Clearly, these symptoms are not specific, as they may also be indicative of a variety of rheumatologic or orthopedic problems. However, their relationship to lower extremity movement and compression is usually helpful in establishing a venous origin for the symptoms. Significant symptoms suggestive of venous disease should prompt further evaluation for valvular insufficiency and calf muscle pump dysfunction. If a venous etiology is suspected but all examinations are negative, repeat examination during a symptomatic period is warranted and often fruitful.
The recent development of an extremely painful area on the lower leg at the ankle associated with an overlying area of erythema and warmth may be indicative of lipodermatosclerosis, which may be associated with insufficiency of an underlying perforator vein, and examination for this lesion should be performed. Lipodermatosclerosis may precede ulceration and has been shown to be improved by stiff compression and certain pharmacologic interventions. Patients with a history of iliofemoral thrombophlebitis who describe “bursting” pain with walking may be suffering from venous claudication. In these patients an evaluation for persistent hemodynamically significant obstruction, possibly treatable with angioplasty and stenting, may be in order.
PHYSICAL EXAMINATION
Using no special equipment, the practitioner can obtain a degree of information regarding overall venous out flow from the leg, the sites of valvular insuffi ciency, the presence of primary versus secondary varicose veins, and the presence of DVT. The screening physical examination consists of careful observation of the legs. Any patient with the following conditions should be examined more fully: large varicose veins; bulges in the thigh, calf, or the inguinal region representative of incompetent perforating veins (IPVs) or a saphena varix; signs of superficial venous hypertension such as an accumulation of telangiectasias in the ankle region (corona phlebectatica); or any of the findings suggestive of venous dermatitis (pigmentation, induration, eczema). This includes patients with obvious cutaneous signs of venous disease such as venous ulceration, atrophie blanche, or lipodermatosclerosis. An obvious but often forgotten point is the necessity of observing the entire leg and not confining the examination simply to the area that the patient feels is abnormal.
Finally, because the veins of the leg empty into the pelvic and abdominal veins, inspection of the abdomen is very important, since dilation of veins on the abdominal wall or across the pubic region suggests an old iliofemoral thrombus. Dilated veins along the medial or posterior aspect of the proximal thigh or buttocks most often arise from varicosities involving the pudendal or other pelvic vessels, and these can be of ovarian reflux origin.
CLINICAL TESTING
Historically important tests of venous function have been part of the physical examination of venous insufficiency (see Table 3). These tests have been laid aside largely because of their lack of specificity and sensitivity. The continuouswave Doppler examination has replaced most of these tests, and confirmatory duplex testing has relegated them to an inferior role. However, the educated physician who treats venous insufficiency must have knowledge of these tests and their physiologic background, such as the Trendelenburg test or Brodie-Trendelenburg test.
Trendelenburg Test
A tourniquet may be placed around the patient’s proximal thigh while the patient is standing. The patient then assumes the supine position with the affected leg elevated 45 degrees. The tourniquet is removed, and the time required for the leg veins to empty, which is indicative of the adequacy of venous drainage, is recorded. When compared with the contralateral leg, the method just described may demonstrate a degree of venous obstructive disease. Another approach is to elevate the leg while the patient is supine and to observe the height of the heel in relation to the level of the heart that is required for the prominent veins to collapse. Unfortunately, neither procedure is sufficiently sensitive nor accurate and does not differentiate acute from chronic obstruction, thus being of minimal assistance in current medical practice.
Cough Test
One hand is placed gently over the GSV or SFJ, and the patient is asked to cough or perform a Valsalva maneuver. Simply palpating an impulse over the vein being examined may be indicative of insufficiency of the valve at the SFJ and below to the level of the palpating hand.
Percussion/Schwartz Test
One hand is placed over the SFJ or SPJ, and the other hand is used to tap very lightly on a distal segment of the GSV or SSV. The production of an impulse in this manner implies insufficiency of the valves in the segment between the two hands. Confirmation of the valvular insufficiency can be achieved by tapping proximally while palpating distally. This test can also be used to detect whether an enlarged tributary is in direct connection with the GSV or SSV by palpating over the main trunk and tapping lightly on the dilated tributary, or vice versa. The presence of a direct connection results in a palpable impulse being transmitted from the percussing to the palpating hand. As might be expected, these tests are far from infallible.
Perthes’ Test
The Perthes’ test has several uses, including distinguishing between venous valvular insufficiency in the deep, perforator, and superficial systems and screening for DVT. To localize the site of valvular disease, the physician places a tourniquet around the proximal thigh with the patient standing. When the patient walks, a decrease in the distension of varicose veins suggests a primary process without underlying deep venous disease because the calf muscle pump effectively removes blood from the leg and empties the varicose veins. Secondary varicose veins do not change caliber (if there is patency of the deep venous system) because of the inability to empty blood out of the veins as a result of impairment of the calf muscle pump. In the setting of a current DVT, they may increase in size. If there is significant chronic or acute obstructive disease in the iliofemoral segment, the patient may note pain (venous claudication) as a result of the obstruction to outflow through both the deep and superficial systems. The Perthes’ test is now of more historical than actual clinical importance.
CLASSIFYING VENOUS DISEASE
The Swedish physician and scientist Carl von Linné published a classification of plants based on the number of stamina and pistils in
Clinical Classification
C0: No visible or palpable signs of venous disease
C1: Telangiectasias or reticular veins
C2: Varicose veins
C3: Edema
C4a: Pigmentation and/or eczema
C4b: Lipodermatosclerosis and/or atrophie blanche
C5: Healed venous ulcer
C6: Active venous ulcer
S: Symptoms including ache, pain, tightness, skin irritation, heaviness,
muscle cramps, as well as other complaints attributable to venous
dysfunction
A: Asymptomatic
Etiologic Classification
Ec: Congenital
Ep: Primary
Es: Secondary (postthrombotic)
En: No venous etiology identified
Anatomic Classification
As: Superficial veins
Ap: Perforator veins
Ad: Deep veins
An: No venous location identified
Pathophysiologic Classification
Basic CEAP:
Pr: Reflux
Pr,o: Reflux and obstruction
Pn: No venous pathophysiology identifiable
Same as basic, with the addition that any of 18 named venous segments
can be utilized as locators for venous pathology:
Superficial veins:
1. Telangiectasias/reticular veins
2. Great saphenous vein (GSV) above knee
3. GSV below knee
4. Small saphenous vein
5. Nonsaphenous veins
Deep veins:
6. Inferior vena cava
7. Common iliac vein
8. Internal iliac vein
9. External iliac vein
10. Pelvic: gonadal, broad ligament veins, other
11. Common femoral vein
12. Deep femoral vein
13. Femoral vein
14. Popliteal vein
15. Crural: anterior tibial, posterior tibial, peroneal veins (all paired)
16. Muscular: gastrocnemial, soleal veins, other
Perforating veins:
17. Thigh
18. Calf
TREATMENT OF VENOUS INSUFFICIENCY
The term venous insufficiency implies that normal functioning is deranged. Terms used to describe the various manifestations of venous insufficiency lend confusion to the general topic. Some of these terms, such as telangiectasias, thread veins, and spider veins are descriptive but imply different conditions. And it is in the chronic disorders, dominated by venous reflux through failed check valves causing hyperpigmentation, ulceration, and corona phlebectatica, where disorientation reigns. Some order can come from subscribing to a unifying theory of primary venous insufficiency and of a common theory of effects of an inflammatory cascade that clarify both situations.
The manifestations of simple primary venous insufficiency appear to be different from one another. However, reticular varicosities, telangiectasias, and major varicose veins are all elongated, dilated, and are tortuous. Investigations into valve damage and venous wall abnormalities eventually may lead to an understanding of the problem, and therefore, a solution by surgery or pharmacotherapy.
Scanning electron microscopy has shown varying degrees of thinning of the varicose venous wall. These areas of thinning coincide with areas of varicose dilation and replacement of smooth muscle by collagen, which is also a characteristic of varicose veins. Our approach to this has been to assume that both the venous valve and the venous wall are affected by the elements that cause varicose veins. We and others have observed that in limbs with varicose veins, an absence of the subterminal valve at the saphenofemoral junction is common. Further, perforation, splitting, and atrophy of saphenous venous valves have been seen both by angioscopy and by direct examination of surgical specimens.
Supporting the theory of weakness of the venous wall leading to valvular insufficiency is the observation that there is an increase in the vein wall space between the valve leaflets. This is the first and most commonly observed abnormality associated with valve reflux. Realizing these facts, our investigations have led us to explore the possible role of leukocyte infiltration of venous valves and the venous wall as part of the cause of varicose veins. In our investigations of surgical specimens, leukocytes in great number have been observed in the venous valves, and wall and monoclonal antibody staining has revealed their precise identification as monocytes. Similar findings are present in the skin of patients with venous insufficiency.
SURGICAL TREATMENT
Removal of the Great Saphenous vein (GSV) from the circulation is one of two essential steps in treating lower limb varicose veins. Incompetent valves along the GSV allow blood to reflux down the vein and into its tributaries, transmitting high pressure into smaller tributaries, which become varicose as a result. Much emphasis has been placed on the correct technique of high sapheno-femoral ligation, in which meticulous attention is paid to identifying, ligating, and dividing all the tributaries of the GSV as they join the vein in the groin. It has always been a matter of surgical dogma that overlooking any of these allows continued reflux into the residual tributary and subsequent development of recurrent varicose veins.
A number of studies have confirmed that patients in whom the GSV is stripped tend to have fewer than those undergoing simple high ligation of the Sapheno-femoral junction (SFJ). Sarin et al. studied 89 limbs in 69 patients with LSV incompetence.
Legs were randomized to SFJ ligation with or without stripping, and evaluated by photoplethysmography (PPG), duplex scanning, clinical examination, and patient satisfaction. The follow-up period was 18 months. Significant differences in favor of the stripped group were found in all four parameters at final evaluation.
Asimilar study of 78 patients (110 limbs) was reported by Dwerryhouse et al. in 1999, with a longer follow-up period of five years. This demonstrated a significantly lower reoperation rate among patients undergoing GSV stripping (6%), as opposed to 20% in those undergoing high SFJ ligation alone.
Duplex scanning showed a much lower incidence of residual reflux in the remaining GSV when the proximal vein had been stripped to the knee than when it had not. However, the patient satisfaction rate was not significantly different between the two groups. Ninety percent of the stripped groups were satisfied as opposed to 87% in the nonstripped group (p = ns).A further study from Jones et al. came to similar conclusions.
One hundred patients (133 limbs) were randomized as before. After two years, 43% of those who had not had GSV stripping demonstrated recurrent varicose veins as opposed to 25% who had. There was a statistically significant difference.
NEOVASCULARIZATION
Of great importance was the fact that duplex scanning showed that neovascularization in the groin was the commonest cause of varicose recurrence. It was often seen in the ligation group that reflux through the neovascularization entered the residual saphenous vein and perpetuated the old varices while new ones developed. The authors concluded that by stripping the GSV, one was removing the run-off into which the new vessels could drain. Again, however, the satisfaction was broadly similar between the two groups: 91% in the stripped group and 87% in the unstripped.
All these authors concluded that stripping the long GSV gave better long-term results than simple high saphenous ligation. This appears to be true in terms of objective assessment of recurrence rates and in objective measurement of post-operative venous function but is not generally reflected in patient satisfaction rates, which tend to be similar which-ever procedure is performed. This led Woodyer and Dormandy to reach a contrary conclusion—that stripping the LSV was a procedure based on surgical dogma, and one that did not confer subjective benefit to the patients so treated. This leads one to conclude that a better method of evaluation of treatment results should be developed.
NONSURGICAL TREATMENT
In recent years, endovenous ablation has been found to be safe and effective in eliminating the proximal portion of the GSV from the venous circulation, with even faster recovery and better cosmetic results than stripping. The two currently available methods used to achieve ablation of the GSV are the Closure© procedure using a radiofrequency (RF) catheter and generator (VNUS Medical Technologies, Inc.,
The major difficulty with defining success as reduction or absence of refl ux is that attempts to establish whether reflux is present in a portion of a previously closed GSV may be inaccurate. Also, most recurrent patency is seen in the proximal portion of the treated GSV. Therefore, distal compression of the closed portion of the GSV to identify reflux in a proximal segment is futile. Likewise, using the Valsalva maneuver is unreliable and lacks reproducibility. Finally, the importance of distinguishing a partially patent channel with flow, from one with reflux, is academic, since the valves are just as thoroughly destroyed as the rest of the vein wall.
INVERSION STRIPPING OF THE SAPHENOUS VEIN
One of the cornerstones of surgery for varicose veins is removal of the Great Saphenous vein (GSV) from the circulation. This can be done using minimally invasive techniques described elsewhere in this volume, but specific indications for performing saphenous surgery remain. These are largely institutional and geographic but they justify the following exposition.Indications for intervention in primary venous insufficiency are listed in Table 4 Often, it is the appearance of telangiectatic blemishes or protuberant varicosities that stimulates consultation. Ultimately, this may be the only indication for intervention.
Characteristic symptoms include aching, pain, easy leg fatigue, and leg heaviness, all relieved by leg elevation, and worsened on the first day of a menstrual peritod. Other indications for intervention for venous varicosities include superficial thrombophlebitis in varicose clusters, external bleeding from high-pressure venous blebs, or advanced changes of chronic venous insufficiency such as severe ankle hyperpigmentation, subcutaneous lipodermatosclerosis, atrophie blanche, or frank ulceration. Symptoms are frequent throughout the CEAP Classes 1 through 6. Clinical Disability Scores parallel the clinical classification.
Objectives of treatment should be ablation of the hydrostatic forces of axial refl ux and removal of the effects of hydrodynamic forces of perforator vein reflux. The latter can be accomplished by removal of the saphenous vein in the thigh and the varicose veins without specific perforating vein interruption. In
Ligation of the saphenous vein at the saphenofemoral junction has been practiced widely in the belief that this would control gravitational reflux while preserving the vein for subsequent arterial bypass. It is true that the saphenous vein is largely preserved after proximal ligation. Unfortunately, refl ux continues and hydrodynamic forces are not controlled. Less refl ux persists when the long saphenous vein has been stripped. There is a better functional outcome after stripping and fewer junctional recurrences. Randomized trials show efficacy of stripping compared to simple proximal ligation.
Earlier comparisons of saphenous ligation versus stripping were fl awed by today’s standards. Subjective evaluation was the only means of measuring outcome for a time.
Duplex scanning came into use, verifying that stripping was superior to proximal ligation; this fact was supported by PPG. Despite those facts, it was acknowledged that the period of disability after stripping was greater than that after simple ligation. In attempts to decrease disability and improve efficacy, high tie was added to saphenous vein sclerotherapy, but foot volumetry showed that radical surgery, including stripping produced superior results.
Ultimately, attention became focused on saphenous nerve injury associated with ankle to groin stripping. It was concluded that nerve injury was reduced by groin to ankle stripping (see Figure 5). Preservation of calf veins by stripping to the knee was shown to reduce nerve injury and did not adversely affect early venous hemodynamic improvement.
This fact is contraintuitive, and the subject deserves further study.Attempts to reduce nerve injury and simultaneously clean up varicose vein surgery led to use of the hemostatic tourniquet. In a study with level 1 evidence, it was shown that use of a hemostatic cuff tourniquet during varicose vein surgery reduces perioperative blood loss, operative time, and postoperative bruising without any obvious drawbacks.
Recurrent varicose veins after surgery are acknowledged to be a major problem for patients and society. Traditionally, it was thought that the most common reason for varicose recurrence was failure to perform an adequate saphenofemoral junction dissection , or to correctly identify the saphenous vein for removal.
Duplex scans have clarified this situation and instead of technical error, some investigators are convinced that new vessel growth contributes to recurrent varicose veins. In particular, incomplete superficial surgery, at the saphenofemoral and saphenopopliteal junctions, is a less frequent cause of recurrent disease, and neovascular reconnection and persistent abnormal venous function are the major contributors tomdisease recurrence.
PREOPERATIVE PREPARATION
Over the years, much space has been given to clinical examination of the patient with varicose veins. Many clinical tests have been described. Most carry the names of now-dead surgeons who were interested in venous pathophysiology. This august history notwithstanding, the Trendelenburg test, the Schwartz test, the Perthes test, and the Mahorner and Ochsner modifications of the Trendelenburg test essentially are useless in preoperative evaluation of patients today.
The clinical evaluation can be improved by using hand-held Doppler devices. However, preoperative evaluation is best performed by means of duplex scanning and a focused physical examination. Our protocol for duplex mapping of incompetent superficial veins has been published. Although many cite cost considerations as a reason for omitting duplex evaluation, we believe that duplex scanning for venous insufficiency is in fact both simple and cost effective. Duplex mapping defines individual patient anatomy with considerable precision and provides valuable information that supplements the physician’s clinical impression.
Three principal goals must be kept in mind in planning treatment of varicose veins: 1) the varicosities must be permanently removed and the underlying cause of venous hypertension treated; 2) the repair must be done in as cosmetic a fashion as possible; 3) complications must be minimized.
Current practice of treating the source of venous hypertension, the saphenous vein alone either by EVLT or VNUS technology, is inadequate. The patient’s complaint, the varicose veins, must be addressed. This is as important as the physician’s knowledge that the sources of venous hypertension must be addressed.
To speak of permanent removal of varicosities implies that all potential causes of recurrence have been considered and that surgery has been planned so as to address them. There are four principal causes of recurrence of varicose veins, of which three can be dealt with at the time of the primary operation.
One cause of recurrent varicosities is failure to perform the primary operation in a correct fashion. Common errors include missing a duplicated saphenous vein and mistaking an anterolateral or accessory saphenous vein for the greater saphenous vein. Such errors can be eliminated by careful and thorough groin dissection. Accordingly, failure to do a proper groin dissection has long been held to be a second principal cause of recurrent varicose veins. It is now known, however, that such dissection causes neovascularization in the groin, leading to recurrence of varicose veins. A third cause of recurrent varicosities is failure to remove the greater saphenous vein from the circulation. As mentioned earlier, reasons often cited for this failure is the desire to preserve the saphenous vein for subsequent use as an arterial bypass. It is clear, however, that the preserved saphenous vein continues to reflux and continues to elongate and dilate its tributaries. This produces more and larger varicosities. A fourth cause of recurrent varicosities is persistence of venous hypertension through nonsaphenous sources—chiefly, perforating veins with incompetent valves. Muscular contraction generates enormous pressures that are directed against valves in perforating veins. Venous hypertension induces a leukocyte endothelial reaction, which, in turn, incites an infl ammatory response that ultimately destroys the venous valves and weakens the venous wall. The perforating veins most commonly associated with recurrent varicosities are the midthigh perforating vein, the distal thigh perforating vein, the proximal anteromedial calf perforating vein, and the lateral thigh perforating vein, which connects the profunda femoris vein to surface varicosities.
Finally, there is a fi fth cause of recurrent varicosities, which is out of control of the operating surgeon—namely, the genetic tendency to form varicosities through development of localized or generalized vein wall weakness, localized blowouts of venous walls, or stretched, elongated, and floppy venous valves.
SAPHENOUS SURGERY
For varicose vein surgery to be successful, two tasks must be accomplished. The fi rst is ablation of reflux from the deep to the superficial veins, including the saphenofemoral junction, the saphenopopliteal junction, and midthigh varices from the Hunterian perforating vein. Accomplishment of this task is guided by the careful preoperative duplex mapping of major superficial venous reflux.
The second task is removal or destruction of all varicosities present at the time of the surgical intervention. Accomplishment of this task is guided by meticulous marking of all varicose vein clusters. A number of options are available for surgical treatment of varicose veins. Regardless of the specific approach taken, the general technical objectives are the same: 1) ablation of the hydrostatic forces of axial saphenous vein refl ux and 2) removal of the hydrodynamic forces of perforator vein outflow.
Ankle-to-groin stripping of the saphenous vein has been a dominant treatment of varicose veins over the past 100 years. One argument against routine stripping of the leg (i.e., ankle-to-knee) portion of the saphenous vein is the risk of concomitant saphenous nerve injury. Another argument is that whereas the objective of saphenous vein removal is detachment of perforating veins emanating from the saphenous vein, which are seen in the thigh, the perforating veins in the leg are actually part of the posterior arch vein system rather than the saphenous vein system. This latter argument notwithstanding, preoperative ultrasonography frequently shows that the leg portion of the saphenous vein is in fact directly connected to perforating veins. Therefore, removal of the saphenous vein from ankle to knee should be a consideration in every surgical case.
OPERATIVE TECHNIQUE
The surgical approach taken must be individually tailored to each patient and each limb. Groin-to-knee stripping of the saphenous vein should be considered in every patient requiring surgical intervention. Iearly all patients, this measure is supplemented by removal of the varicose vein clusters via stab avulsion or some form of sclerotherapy.
Preoperative marking, if correctly performed, will have documented the extent of varicose vein clusters and identified the clinical points where control of varices is required. Incisions can then be planned. As a rule, incisions in the groin and at the ankle should be transverse and should be placed within skin lines. In the groin, an oblique variation of the transverse incision may be appropriate. This incision should be placed high enough to permit identification of the saphenofemoral junction.
Generally, throughout the leg and the thigh, the best cosmetic results are obtained with vertical incisions. Transverse incisions are used only in the region of the knee, and oblique incisions are appropriate over the patella when the incisions are placed in skin lines.
A major cause of discomfort and occasional permanent skin pigmentation is subcutaneous extravasation of blood during and after saphenous vein stripping. Such extravasation can be minimized by applying a hemostatic tourniquet after Esmarch exsanguination of the limb. The pressure in the hemostatic tourniquet should be between 250 and
The practice of identifying and carefully dividing each of the tributaries to the saphenofemoral junction has been dominant over the past 50 years. The rationale for this practice has been that it would be inadvisable to leave behind a network of interanastomosing inguinal tributaries. Accordingly, special efforts have been made to draw each of the saphenous tributaries into the groin incision so that when they are placed on traction, their primary and even secondary tributaries can be controlled. The importance of these efforts has been underscored by descriptions of residual inguinal networks as an important cause of varicose vein recurrence. Currently, however, this central practice of varicose vein surgery is under challenge, on the grounds that groin dissection can lead to neovascularization and hence to recurrence of varicosities.
Preoperative duplex studies have already demonstrated incompetent valves in the saphenous system, and a disposable plastic stripper can be introduced from above downward; alternatively, a metal stripper can be employed. Both of these devices can be used to strip the saphenous vein from groin to knee via the inversion technique. This approach should reduce soft tissue trauma in the thigh.
In the groin, the stripper is inserted proximally into the upper end of the divided internal saphenous vein and passed down the main channel through incompetent valves until it can be felt lying distally approximately
Stripping of the saphenous vein has been shown to produce profound distal venous hypertension. This occurs in virtually every operation, even when the limb is elevated. Therefore, after the stripper is placed, one should consider performing the stab avulsion portion of the procedure before the actual stripping maneuver.
Incisions to remove varicose clusters vary according to the size of the vein, the thickness of the vein wall, and the degree to which the vein is adhering to the perivenous tissues. In general, vertical incisions 1 to
Phlebectomy techniques for varicose clusters have been markedly refined by experienced workers in
Once the stab avulsion portion of the procedure is complete, the previously placed stripper is pulled distally to remove the saphenous vein. Although plastic disposable vein strippers and their metallic equivalents were designed to be used with various-sized olives to remove the saphenous vein, in fact, a more efficient technique is simply to tie the vein to the stripper below its tip so that the vessel can then be inverted into itself and removed distally. To decrease oozing into the tract created by stripping, a
Laboratory Studies
Analysis of blood, urine, or tissue is not needed to make the diagnosis of lymphedema. Such tests, however, help to define the underlying causes of lower extremity edema when the etiology is unclear.
– Liver function, BUN/creatinine levels, and urinalysis results should be checked if a renal or hepatic etiology is suspected.
– Specific markers should be checked if a neoplasm is suspected.
– CBC count with differential should be checked if an infectious etiology is being considered.
Medical Care
The goal of therapy is to restore function, to reduce physical and psychologic suffering, and to prevent the development of infection.
- The first-line treatment is complex physical therapy. This therapy is aimed at improving lymphedema with manual lymphatic drainage, massage, and exercise. It advocates the use of compression stockings (at a minimum of
40 mm Hg), multilayer bandaging, or pneumatic pumps. Leg elevation is essential. Appropriate skin care and debridement is also stressed to prevent recurrent cellulitis or lymphangitis. - In secondary lymphedema, the underlying etiology (ie, neoplasm, infection) should also be properly treated to relieve the lymphatic obstruction and to improve lymphedema.
- In cases of recurrent cellulitis or lymphangitis, long-term antibiotic therapy with agents such as penicillins or cephalosporins is sometimes used.
- Filariasis has been treated with diethylcarbamazine and albendazole.
- In cases associated with obesity, weight loss is strongly recommended.
- A few pharmacological therapies have been found to be effective in the treatment of lymphedema.
- The benzopyrones (including coumarin and flavonoids) are a group of drugs that have been found to be successful in treating lymphedema when combined with complex physical therapy. They aid in decreasing excess edematous fluid, softening the limb, decreasing skin temperature, and decreasing the number of secondary infections. The benzopyrones successfully increase the number of macrophages, leading to proteolysis and protein reabsorption. Of note, however, is that hepatotoxicity has been associated with coumarin therapy.
- Case reports have suggested effective treatment of chronic lymphedematous changes (eg, elephantiasis nostra verrucosa [ENV]) with oral and topical retinoids. These therapies are thought to help normalize keratinization and decrease inflammatory and fibrotic changes.
- Topical emollients and keratolytics, such as ammonium lactate, urea, and salicylic acid, have been recommended to improve secondary epidermal changes.
- Diuretics are not effective in treating lymphedema.
