The most common source of pain and dysfunction in the lower limb of the athlete is musculoskeletal in origin; nevertheless, vascular pathology may also present in a similar fashion. Sports that involve frequent repetitive motions or high-impact collisions have the highest incidence of vascular pathology.
Vascular issues in athletic patients may be difficult to diagnose for several reasons. First, most athletes are young and otherwise in good health, making vascular disease an unlikely concern in the differential diagnosis. Second, an injured athlete’s signs and symptoms may have plausible musculoskeletal etiologies, which could present in an identical fashion. Provocative testing and appropriate imaging are thus often required for the diagnosis of underlying vascular pathology. Third, a clinician may not be entirely comfortable with the typical presentation of vascular pathology in the lower limbs, details of the vascular physical examination, and inclusion criteria for vascular pathology in the differential diagnosis.
Underlying vascular issues should be suspected in any athlete who presents with limb pain, early-onset fatigue, limb swelling, limb discoloration, or skin color changes. Familiarity with provocative physical examination maneuvers and imaging modalities is essential to confirm most vascular diagnoses. Moreover, simulation of an athlete’s sport-specific positioning, motions, and level of exertion during vascular testing can uncover underlying pathology and can mean the difference between confirming or missing the diagnosis.
Vascular pathology that remains undetected for a prolonged period may have devastating consequences for the athletic patient, including retirement, loss of limb function, or even limb amputation. Consequently, familiarization with the spectrum of traumatic and nontraumatic vascular knee injuries may facilitate early detection, diagnosis, and treatment and provide an improved prognosis for the athletic patient. The intent of this chapter is to review common vascular knee injuries in athletes and provide sports medicine practitioners with a reference for the presentation, evaluation, and clinical management of lower extremity sports-related vascular injuries, including a guide to return to sports when appropriate.
Tibial-femoral knee dislocation is a severe injury with the potential for limb-threatening vascular compromise. Although historically traumatic knee dislocations are considered to be rare injuries, in recent years they have been reported more frequently. The popliteal vessels, which cross the popliteal fossa, anchored above and below the joint by the adductor hiatus and the soleus muscle, respectively, are particularly vulnerable to injury from knee dislocation ( Fig. 108-1 ). Knee dislocations are defined in terms of the tibial displacement with respect to the femur and can be characterized as anterior, posterior, lateral, and rotatory.
Anterior Knee Dislocations
Anterior dislocations are the most common, constituting 50% to 60% of all knee dislocations. Forced hyperextension is the primary mechanism of injury causing anterior dislocation of the knee. In his 1963 landmark study, Kennedy reproduced anterior knee dislocations using cadaver knee specimens subjected to various degrees of hyperextension and elucidated the vascular trauma incurred during forced hyperextension. Rupture of the popliteal artery occurs at an average of 50 degrees of hyperextension. However, at angles below the threshold of arterial rupture, stretching that results in injuries to the tunica intima, contusion, laceration, transection, or avulsion of the popliteal vessels may still occur. Intimal tearing increases the likelihood for arterial occlusion and thrombosis. The poor collateral circulation surrounding the knee joint, as well as the soft tissue injury, further increases the risk for ischemia as a result of acute popliteal occlusion. Damage to the popliteal artery occurs in 40% of anterior knee dislocations. Moreover, stretching of the tibial nerve within the popliteal fossa may cause paresthesia in the lower leg, which is often a finding associated with knee dislocation and popliteal artery injury.
Posterior Dislocation of the Knee
Posterior dislocation of the tibia on the femur accounts for approximately 33% of knee dislocations and may also be a source of potential neurovascular injury. Kennedy’s hallmark study revealed that much greater forces are required to induce posterior knee dislocations compared with the anterior knee dislocations, such as those that occur in the classic “dashboard injury.”
Injury to collateral ligaments in association with damage to the PCL results in posterior dislocation and multidirectional instability that increases the likelihood of damage to the neurovascular structures within the popliteal fossa. Green and Allen reported that 44% of posterior dislocations had associated injury to the popliteal vessels. Posterior displacement of the tibia directly translates force onto the popliteal artery and vein, with a high likelihood of vessel transection.
Vascular Injury from Knee Dislocation
When knee dislocation is diagnosed or suspected, one of the primary jobs of the clinician is to determine if concomitant injury to the popliteal artery and/or vein has occurred. Failure to recognize popliteal artery injury and restore vessel continuity after knee trauma is a potential cause of lower extremity amputation. Consequently, early recognition of vascular injury remains paramount for limb salvage. During a knee dislocation, the popliteal vessels are at risk for injury because of their anatomic location ( Fig. 108-1 ). The superficial femoral artery traverses past the tendinous hiatus of the adductor magnus muscle and continues as the popliteal artery. Five smaller collateral vessels branch off of the popliteal artery as it crosses the knee joint within the popliteal fossa: the medial and lateral superior geniculate, middle geniculate, and medial and lateral inferior geniculate arteries. The popliteal artery exits the popliteal fossa anchored below the knee joint by the soleal arch before dividing into the anterior and posterior tibial arteries. The genicular arteries form an intricate network of collateral vessels surrounding the contiguous ends of the femur and tibia. This circumpatellar network is divided into superficial and deep plexuses. The superficial plexus is located between the fascia and skin and forms three well-defined arches, one above the upper border of the patella and two below the patella. The deep plexus forms a close network of vessels that surround the articular surfaces of the femur and tibia. The network of genicular anastomoses provides the leg with collateral circulation, which is abundant in number but small in vessel caliber. Frequently the collateral vessels are injured or disrupted in conjunction with the popliteal artery during knee dislocation as a result of soft tissue injury.
The anterior and posterior tibial veins converge to form the popliteal vein at the lower border of the popliteus muscle. Occasionally the popliteal vein is duplicated and present on both the medial and lateral aspects of the popliteal artery. Proximal to the popliteal fossa, the popliteal vein traverses the adductor hiatus and continues as the femoral vein.
Injury to the popliteal artery has been reported to occur in approximately 30% of all complete knee dislocations. Types of arterial damage sustained during dislocations of the knee may include injury to the tunica intima, avulsion injury, occlusions, aneurysm generation with secondary thrombosis, embolization, rupture, and transection. Although trauma to the popliteal vessels is easily detected in cases of open knee injuries, identification of neurovascular injury as a result of blunt knee dislocation or instability may be delayed or missed entirely. Clinical indicators of vascular trauma after knee dislocation are classified as hard or soft signs ( Table 108-1 ). Hard signs demand immediate vascular repair and include pulse deficits, acute limb ischemia, active hemorrhage, and pulsatile hematoma. Hallmark signs of acute limb ischemia include pain, paresthesia, loss of sensation or motor function, pallor, and pulselessness in the distal extremity of the affected limb. In the presence of these hard signs, a diagnosis of vascular injury is strongly suggested, and treatment should involve immediate vascular repair. Alternatively, soft signs of injury to the popliteal artery after knee dislocation warrant further diagnostic evaluation and monitoring. These signs include small hematomas, reduced pedal pulses and ankle pressures, neural deficits from injury to the tibial nerve or its branches, and early hemorrhaging that has ceased. When soft signs are present, imaging of the popliteal vessels is required to assess the extent of vascular trauma.
|Type of Sign||Indicator|
|Hard||Pulse deficits in pedal pulses with an ankle brachial index <0.5|
|Distal ischemia (pain, paresthesia, pallor, and other symptoms of acute ischemia)|
|Active hemorrhage and pulsatile bleeding|
|Evidence of compartment syndrome|
|Soft||Small hematoma that does not change in size|
|Hemorrhage that has ceased|
|Reduced ankle pressure <0.9 but >0.5|
|Neural deficits from injury to the tibial nerve|
Vascular injuries associated with knee dislocations result from excessive stretching or transection of the popliteal vessels ( Fig. 108-2 ). Common vascular injuries following anterior knee dislocations include intimal tears and the formation of intimal flaps. In such patients, blood flow through the artery may not be appreciably altered, and consequently patients may present without any hard signs of vascular trauma. Nevertheless, the presence of intimal tears and flaps increases the risk of thrombosis and embolization. Moreover, extensive intimal injuries accelerate vessel wall damage over time, and patients who initially lack symptoms of vascular compromise may begin to exhibit diminished popliteal flow. Some authors suggest that posterior knee dislocations more commonly result in transection of the popliteal artery, with resultant acute limb ischemia. Blood flow through the popliteal artery becomes significantly diminished ( Fig. 108-3 ), and patients present with immediate hard signs of vascular injury such as active hemorrhage, expanding hematoma, bruits in the distal arterial circuitry, and signs of acute ischemia such as pain, paresthesia, poikilothermia, pallor, and pulselessness. These signs indicate significant vascular compromise that demands immediate operative intervention and vascular repair.
Physical Examination and Testing
The high rate of popliteal artery injury associated with knee dislocations, combined with the possibility of delayed presentation of symptoms of vascular trauma as a result of knee dislocation, demands that diagnostic evaluation for vascular integrity be performed for all patients suspected of having a knee dislocation. The diagnosis of knee dislocation itself is based on the mechanism of injury obtained from the history, physical examination, and radiographic findings. Frequently, patients may present with the knee already reduced. Because the risk for arterial injury is the same in both the reduced and dislocated knee, clinical suspicion of popliteal artery damage should remain high in such patients. Absence of hemarthrosis in patients suspected of having had a knee dislocation does not decrease the risk for vascular injury.
Diagnostic evaluation of vascular integrity in the lower limb is critical to determining a method of treatment ( Fig. 108-4 ). Serial measurements of pulse quality in both the posterior tibial and dorsalis pedis arteries should be performed because the pulse may be diminished or absent after an upstream arterial injury. Studies reveal that clinical evaluation of peripheral pulses accurately identifies the existence of vascular lesions after knee dislocation with a specificity of 91%. Although the presence of pulse abnormalities is sufficient to rule in the existence of vascular lesions, a low sensitivity of 79% means that vascular injury may exist in the absence of peripheral pulse deficits. In addition to digital pulse evaluation, serial measurements of the ankle brachial index (ABI) enable the clinician to qualitatively assess deficits in distal perfusion induced by vascular trauma. ABI values <0.9 indicate the presence of vascular injury requiring surgical intervention with 95% to 100% sensitivity and 80% to 100% specificity.
In patients presenting with pulse abnormalities and associated ischemic syndrome, surgical intervention and revascularization is the primary priority, and imaging may be performed to determine the location and severity of vascular compromise. In this context, imaging aids in determining the surgical approach and should be performed in the operating room to minimize warm ischemia time. Previous studies have found that approximately 3 hours are saved when arteriographic imaging is performed in the operating arena. In patients with pulse abnormalities in the absence of ischemia, imaging is mandatory to determine if intervention and vascular repair are required.
Historically, arteriography has served as the gold standard for symptomatic vascular lesions after knee dislocation. This form of imaging allows the examiner to identify the location and extent of injury and the presence of intimal flap tears both within the popliteal artery and its distal branches. However, the invasive nature of angiography has led to a trend in recent years toward less invasive and safer imaging modalities. Moreover, arteriography is not fully reliable as an imaging tool. Studies have reported 1% to 6% false-negative rates, which can delay patient treatment, and 2.4% to 7% false-positive rates, which can result in unnecessary surgical intervention. In the Lower Extremity Assessment Project study, it was reported that patients with hard signs of vascular injury can be treated effectively without arteriographic imaging before surgery.
In recent years, duplex ultrasonography has become a mainstay of the rapid evaluation of vascular pathology resulting from suspected popliteal artery injury and can be used to analyze flow through the popliteal vessels in real time in the emergency department or operating room ( Fig. 108-4 ). Studies assessing the diagnostic value of duplex scanning as a means of noninvasive imaging in persons with lower limb trauma reported a diagnostic sensitivity of 95%, a specificity of 99%, and a diagnostic accuracy of 98%. The rapidity with which duplex scanning can be performed makes it an ideal tool for visualization of vascular trauma, particularly in patients with vascular compromise who are awaiting operative intervention.
Computed tomographic angiography (CTA) and magnetic resonance angiography (MRA) also can be used to visualize intimal tears when duplex ultrasound results are equivocal.
Warm ischemia time remains the single most important variable that determines functional outcome in patients with a popliteal artery injury resulting from knee dislocation. Prompt diagnostic evaluation, including imaging to determine the extent of vascular injury, and operative intervention to restore adequate distal perfusion in the hypoperfused patient are essential for successful treatment and limb salvage. Warm ischemia times greater than 6 hours can cause irreversible neurologic injury and muscle necrosis distal to the site of blood flow obstruction, and the rate of amputation in patients who experience a delay in arterial reconstruction exceeding 8 hours has been reported to be 85%. Consequently, any delay of imaging and immediate intervention in cases of limb ischemia increases morbidity and worsens patient prognosis.
Immediate surgical repair is obligatory as soon as vascular trauma is confirmed. The principles of surgical intervention in patients with popliteal artery injuries include (1) rapid restoration of arterial blood flow to the distal extremity, (2) removal of thrombus in the distal artery, and (3) alleviation of compartment syndrome, which may exacerbate distal ischemia. Whether vascular or orthopaedic reconstruction should be performed first remains an area of debate, with the appropriate sequence of repair depending on the time course of injury and the severity of the ischemia. If the patient presents with prolonged warm ischemia time or severe deficits in distal perfusion, prompt vascular repair and restoration of arterial flow is indicated before orthopaedic management. In such cases, however, secondary orthopaedic procedures may damage newly repaired vascular structures. Consequently, the order of repair should be determined on a case-by-case basis, with special consideration given to the extent and severity of ischemia in the presenting patient.
Reconstruction of the popliteal artery can be achieved through either posterior or medial approaches. The posterior approach allows for greater visualization of structures within the popliteal fossa and is more ideally suited for treatment of lesions of the midpopliteal artery, whereas the medial approach allows easier access to distal structures of the popliteal fossa and is associated with more rapid postsurgical healing. The type of surgical repair performed depends on the extent of vascular injury and may include lateral repair, end-to-end arterial repair with interposition vein graft, repair of intimal injury by vein patch, or bypass by saphenous vein grafting. The majority of popliteal artery repairs that result from knee dislocations require venous grafting. Venous patches are used to provide structural integrity in cases of intimal tears and flaps, and greater saphenous vein grafts from the contralateral leg are used for extensive arterial resection. End-to-end repair of the popliteal artery through a posterior approach requires the least dissection of the popliteal artery and surrounding soft tissue. If the popliteal vein is also damaged after knee dislocation, venous repair is required and can be accomplished by lateral repair or interposition vein grafts. Failure to repair venous injuries is associated with an increased risk of lower extremity edema, thrombosis, and embolization, as well as limb loss. If ischemia has been present for several hours, a fasciotomy is mandatory to prevent compartment syndrome. Fasciotomy is required in the treatment of 50% to 80% of patients with injury to the popliteal artery and is associated with a significant improvement in the rate of limb salvage. Primary amputation is rarely indicated and is only used when extensive muscle necrosis is present in the distal extremity. Typically, warm ischemia times exceeding 6 hours are associated with a dramatic increase in the rate of eventual limb amputation.
Although historically all popliteal artery injuries resulting from knee dislocations have been repaired through open surgical methods, in some studies authors have reported the successful treatment of blunt popliteal artery injuries and acutely ischemic distal lower extremities with use of endovascular techniques. Proponents of endovascular repair in cases of blunt popliteal artery injury cite the usefulness of a percutaneous approach in cases in which extensive soft tissue damage to the surrounding structures of the popliteal fossa may complicate open repair. Endovascular techniques allow for visualization of the injury site, removal of any associated thrombus, protection against distal embolization, and repair of an intimal lesion. However, the durability of covered stents and endografts in the popliteal location, where excessive motion occurs, has not been established.
Patient history and presentation
Examination of pedal pulses on both the affected and contralateral limb
Bilateral ankle brachial index measurements
Imaging of the popliteal space using duplex ultrasonography
In patients presenting with hard signs of vascular injury, no further imaging is required and immediate surgical intervention is warranted
In patients presenting with soft signs of vascular injury or if the duplex scanning yields equivocal results, further imaging via magnetic resonance angiography and computed tomographic angiography scanning is necessary to establish treatment protocol
Open surgical intervention
With the patient lying prone, an S-shaped incision is made in the popliteal region
The posterior approach is preferred over the medial approach because it facilitates greater access to the neurovascular structures of the popliteal fossa with the least amount of soft tissue dissection and sparing of the saphenous vein
Skin flaps are raised to expose underlying deep fascia, which is then transected longitudinally
Care should be taken to avoid transection of the median cutaneous sural nerve
The tibial nerve is encountered first and mobilized
The popliteal vein passes through the medial and lateral heads of the gastrocnemius muscle deep in the popliteal fossa
The popliteal artery lies deeper in the popliteal space and can be followed distally
Arterial reconstruction is required if evidence of significant intimal injury, stenosis, occlusion, thrombosis, or laceration is observed
Placement of a short interposition vein graft, which is usually harvested from the ipsilateral lesser saphenous vein or contralateral saphenous vein
An alternative is a short venous bypass graft with exclusion of the occluded artery to avoid thromboembolism
Postoperative follow-up should include focused physical examinations with special attention to distal perfusion. Ankle pressures, ABI measurements, and duplex scanning should be performed to assess blood flow through the reconstructed artery within the popliteal fossa. Use of other imaging modalities such as computed tomography (CT)/CTA and magnetic resonance imaging (MRI)/MRA are generally not recommended unless symptoms of graft occlusion or diminished blood flow reappear. Follow-up should be scheduled within 4 to 6 weeks after surgery and twice annually within the first year. In subsequent years, annual follow-up is sufficient to ensure graft patency.
Postoperative complications after popliteal artery repair are centered on evaluation for delayed compartment syndrome, graft patency, maintenance of tension-free healing, and prevention of postsurgical deep vein thrombosis (DVT). Antiplatelet medications are typically prescribed for patients to prevent postsurgical graft thrombosis. Patency of the vein graft may be compromised by stenosis at the sites of venous graft-artery interface. Postsurgical follow-up should include physical examination and imaging via duplex ultrasonography to ensure graft patency and appropriate healing.