Neurovascular Injury in Total Knee Arthroplasty


Introduction

Neurovascular injury is a rare, but distressing and debilitating complication of total knee arthroplasty (TKA). Arthroplasty surgeons must take an active role in understanding the risk factors and have knowledge of the anatomy that plays a pivotal role in reducing the incidence of these complications.

A spectrum of vascular complications have been reported, including arterial thrombosis, arteriovenous fistula formation, transection of the popliteal artery, and pseudoaneurysm formation. Postoperative vascular complications are reported to occur in 0.03% to 0.5% of TKAs. Arterial injury following TKA can lead to wound healing complications, prosthetic joint infections, amputation, and mortality. Due to the relatively poor vascularity of the skin surrounding the knee, any arterial injury can increase the potential for deep infection. In patients with preexisting arterial insufficiency, postoperative arterial complications can occasionally necessitate limb amputation. In some series, the rate of amputation after TKA with arterial complications is as high as 25% to 43%. It is key for surgeons to perform a thorough examination prior to TKA and to understand the vascular risks associated with TKA.

Nerve injuries following TKA are relatively uncommon complications but may lead to significant patient morbidity. Patients may develop a postoperative foot drop or even neuropathic pain as a consequence of nerve injury that can lead to long-term patient disability. Nerve injury following TKA may also lead to litigation by the patient. The most common nerve injury following TKA is a peroneal nerve palsy. Other nerve injuries reported in the literature include femoral or saphenous nerve palsy, lumbar plexus neuropathy, sacral plexopathy, and sciatic neuropathy. These complications are extremely rare and often are reported in isolated case reports of these uncommon complications. ,

The incidence of peroneal nerve palsy following TKA is believed to range from 0.3% to 1.3%. , , However, smaller retrospective studies have reported the rate of peroneal nerve palsy to be from 0% to 10%. The true incidence of peroneal nerve palsy may actually be underreported or undiagnosed, as patients may have a subclinical palsy that may be diagnosed only with electrodiagnostic testing. At this time, no prospective data have been reported on the incidence of postoperative peroneal nerve palsy. Patients with peroneal nerve palsy will present with variable symptoms, including paresthesias or dysesthesias in the peroneal nerve dermatomal distribution and decreased motor control of the nerves innervated by the common peroneal nerve (typically presents with ankle dorsiflexion weakness). Patients commonly present with decreased sensation over the dorsum of the foot and/or weakness of the foot and ankle.

Complex regional pain syndrome (CRPS) is a condition defined by high levels of pain, abnormal blood flow regulation, skin sweating, and edema and joint stiffness. The incidence of CRPS following TKA ranges, with studies quoting rates as high as 21%. Inconsistent diagnostic criteria have been used in studies, and it is generally accepted that the true incidence of CRPS following TKA is around 0.8%. The diagnosis is difficult, as no imaging or diagnostic modalities are specific for CRPS.

The purpose of this chapter will be to review the potential neurovascular complications following TKA. Specifically, we will review the predisposing factors, rate, presentation, and treatment of vascular injuries and nerve injuries following TKA.

Vascular Injuries in Total Knee Arthroplasty

Preoperative Risk Factors and Assessment

Due to the success of TKA and improved postoperative quality of life, the indications for TKA have expanded to include patients with significant preexisting comorbidities, including peripheral vascular disease. , Patients with a history of claudication, resting leg pain, or previous history of arterial ulcers are at elevated risk for arterial complications after TKA. Patients who have previously undergone vascular bypass surgery, including cardiac bypass surgery or patients with concerning examination findings such as asymmetric pulses or leg or toe ulceration should be referred for vascular assessment and optimization prior to TKA.

Vascular complications may also be more common in patients in whom the femoral or popliteal artery may be tethered. This is may be the underlying mechanism in patients who have previously had surgery in proximity to the TKA or in patients with a previous history of knee trauma. In one series, 71% of patients who had a vascular injury had a previous surgery in proximity to the TKA. , Patients undergoing revision TKA are more than twice as likely to have a vascular injury compared with patients undergoing a primary TKA.

Prevention of vascular injuries following TKA begins with a thorough history and neurovascular examination by the orthopaedic surgeon preoperatively. A history should be obtained to identify previous vascular operations, such as bypass surgery or aortic aneurysm repair, which indicates a diagnosis of peripheral vascular disease. Further, the patient’s history should be obtained to identify any symptoms of claudication or ischemic sequelae in either of the lower limbs. During the physical examination, the surgeon should assess skin integrity, compare pedal pulses to the contralateral extremity and palpate the popliteal fossa to rule out a popliteal artery aneurysm. Previous incisions signifying arterial bypass should be noted, as arterial bypass patency and function needs to be assessed by duplex ultrasound prior to TKA. Radiographs should be assessed for calcifications below the level of the femoral artery and in the popliteal artery ( Fig. 10.1 ).

Fig. 10.1, Preoperative lateral radiograph of the right knee demonstrating arterial calcification.

If the surgeon has any concern for arterial insufficiency, ankle-brachial indices (ABIs) should be determined. If the ABI is less than 0.9, the patient is at increased risk for arterial complications and needs a preoperative vascular surgery consultation. Patients with an ABI of less than 0.5 need assessment by a vascular surgeon with an angiogram. Patients with an ABI of less than 0.5 may need bypass surgery that should be performed prior to TKA. It is imperative to recognize that vascular injuries can occur as the result of an undiagnosed vascular problem or in patients with unrecognized risk factors.

Intraoperative Considerations—Tourniquet Use

In patients with increased risk of vascular complications following TKA, consideration should be given to not using a tourniquet. In patients with calcified arteries and peripheral vascular disease, the force generated by the tourniquet could increase the risk for both thrombosis and embolization, with subsequent occlusion of a distal artery. The force generated by the tourniquet could fracture a calcified artery because a calcified artery has lost its elasticity, which can lead to a subsequent intimal tear. Anchoring of the superficial femoral artery proximally with a tourniquet and stretching of the vessel distally during knee manipulation can lead to possible arterial injury or embolization as well. ,

Best available evidence demonstrates no difference in functional outcomes, blood loss, or complications after TKA in patients undergoing primary TKA with or without the use of a tourniquet. For patients with radiographic evidence of calcification of the popliteal or femoral artery, recommendations have been given that TKA should be performed without a tourniquet. In patients with diminished pedal pulses, similar recommendations have been given that TKA should be performed without a tourniquet. , Patients with identified risk factors should undergo evaluation by a vascular surgeon prior to TKA. Patients needing vascular intervention should undergo such intervention prior to the planned TKA.

In patients with a lower limb arterial bypass, patency and function needs to be assessed by the vascular surgeon and duplex ultrasound performed preoperatively. Two recommendations have been given for patients with the femoropopliteal bypass. The surgeon can perform the TKA without a tourniquet, or a 5000-U intravenous bolus of heparin can be administered prior to tourniquet use and reversed with protamine sulfate at the end of the surgery. Patients with a prosthetic arterial bypass may be at particularly high risk for graft thrombosis.

Mechanism of Vascular Injury

The majority of vascular complications after TKA are associated with indirect vessel injury in patients with an already diseased artery. , Indirect trauma typically occurs as a result of stretching or tearing of a vessel, which during a difficult knee can occur during dislocation, manipulation, or during hyperextension of the joint. Direct trauma occurs through use of a posterior retractor that has the potential to injure the popliteal artery, injury from the oscillating saw during the resection of the proximal tibia or posterior femoral condyles, or during a posterior capsular release.

Vascular injuries can be classified into four categories: (1) acute arterial occlusion, (2) pseudoaneurysm formation, (3) arterial severance, and (4) arteriovenous fistula formation.

Acute Arterial Occlusion

Acute arterial occlusion is a rare, but limb-threatening complication after TKA. The most often affected vessel is the popliteal artery. Occlusion or thrombosis leads to limb ischemia that causes irreversible damage, which often requires amputation if not identified promptly and treated appropriately. Few cases of this devastating complication have been reported; however, surgical intervention is often required by a vascular surgeon in the treatment of arterial occlusion or thrombosis.

Arterial occlusion is often the result of thrombosis, fascial obstruction, or embolization of an atheromatous plaque due to damage of a previously diseased vessel ( Fig. 10.2 ). The use of a tourniquet in patients with peripheral vascular disease defined by calcified vessels, diminished pedal pulses, history of bypass surgery, or a previously existing vascular graft or injury has been implicated as a cause of arterial or graft occlusion. , , , Embolization can be the result of dislodgement of a previously diseased vessel due to knee manipulation or use of a tourniquet. Distal blood flow is then compromised, which creates an opportunity for thrombosis formation. Lack of blood flow from the use of a tourniquet can also increase the risk for thrombosis formation in previously diseased vessels. Popliteal artery occlusion has also been related to obstruction by soft tissues due to correction of a severe flexion contracture. , Acute occlusion of the popliteal artery has also been linked to direct injury of the popliteal artery as a result of the intimate relationship between the posterior tibia and popliteal artery. ,

Fig. 10.2, Anteroposterior and lateral angiography demonstrating thrombosis of a popliteal artery after TKA.

Mixed results have been published on the outcomes of patients with acute arterial occlusion following TKA. The most common treatment for popliteal artery occlusion is either isolated thrombectomy or arterial bypass. Thrombectomy is one of the most frequently described treatments for occlusion of the popliteal artery, but conflicting results range from full patient recovery to amputation and patient mortality. Arterial bypass has also been described as a treatment modality in patients with arterial occlusion, but complications ranging from prosthetic graft infection to amputation have been reported. , The most important factor in patient outcomes is prevention and rapid recognition to decrease the time from injury to vascular repair or reperfusion.

It is unclear at this time whether prophylactic fasciotomies should be performed at the time of revascularization in patients after an arterial injury following TKA. Many vascular surgeons may want to perform prophylactic fasciotomies after revascularization, but this may subject patients to multiple additional surgeries and has been shown to possibly place patients at increased risk for periprosthetic joint infection. Further research needs to be conducted to determine what “normal” compartment pressures are after total joint arthroplasty and how to best determine the need for fasciotomies after revascularization.

Arterial Pseudoaneurysm Formation

The close proximity of the popliteal artery during a TKA places it at significant risk for direct injury. Arterial pseudoaneurysm formation after TKA is a rare and typically late complication. Pseudoaneurysm, otherwise known as a false aneurysm , forms after TKA typically as a result of a partial injury to the popliteal artery. During the initial insult, a hematoma forms around the artery, and fibrin and connective tissue organize and undergo endothelialization, with formation of a central cavity. This central cavity communicates with the damaged popliteal artery, forming a false aneurysm ( Fig. 10.3 ). This is in contrast to a true aneurysm, in which the blood is contained within a true arterial wall.

Fig. 10.3, Angiography demonstrating a popliteal artery pseudoaneurysm following TKA.

To our knowledge, only a few case studies have reported this complication at this time. The early identification and diagnosis of an aneurysm after TKA is essential in preventing long-term complications, including limb ischemia or hemorrhage. However, many aneurysms remain subclinical and are not identified until 1 to 6 months after an arterial injury. , All reported cases have occurred as a result of injury to the popliteal artery or inferior geniculate artery, with popliteal artery pseudoaneurysms being the most common. The orthopaedic surgeon needs to be aware of this condition, as patients with a pseudoaneurysm may present with nonspecific symptoms that may be confused with a postoperative deep vein thrombosis (DVT) or hematoma in the early postoperative period. Patients may present with limb ischemia or swelling, a pulsatile mass, bruit, hemarthrosis, or hemorrhage. , If there is concern for aneurysm formation postoperatively, an urgent vascular surgery consultation is needed with further evaluation with angiography to confirm the diagnosis.

Multiple treatment modalities have been described for the treatment of pseudoaneurysms after TKA. Reconstruction with a saphenous or synthetic graft has been described but is associated with a complication rate as high as 25%. Endovascular treatment with a covered stent or percutaneous treatment of pseudoaneurysms with thrombin is the mainstay of treatment. Treatment options depend on the size of the pseudoaneurysm, typically with stent placement reserved for larger lesions and thrombin injections used for the treatment of small pseudoaneurysms. However, many vascular surgeons do not recommend the use of covered stents across highly mobile joints due to the high rate of stent occlusion at midterm follow-up. Percutaneous injection of thrombin has shown good results in the treatment of pseudoaneuryms. Recurrence of the pseudoaneurysm is a concern with percutaneous thrombin treatment as well as the risk of systemic thrombin release, which can lead to distal thrombosis or embolization.

Further long-term studies need to be done to determine the best treatment modality for pseudoaneurysms after TKA. The orthopaedic surgeon needs to be aware of this possible complication, as limb ischemia from delayed diagnosis of a pseudoaneurysm can place the patient at significant risk for poor wound healing, possible infection, or amputation.

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