Complications after Total Knee Arthroplasty

2.1 Vascular injuries

Although arterial injury during knee replacement is rare, it may have serious results from limb loss to mortality. Arterial injuries can be seen as thromboembolism, direct vascular laceration, pseudoaneurysm, and arteriovenous fistula [3]. The incidence is reported to be 0.03–0.2% in the literature [4].

Vascular injuries may develop due to the thermal effect of cement polymerization, joint manipulations, dislocations, and excessive manipulation [5]. Considering the issue as specific to the total knee arthroplasty, care should be taken against vascular injury during posterior cruciate ligament and posterior capsular release during femoral condylar cutting. Atypical localization of vascular structures due to changes in adhesions and normal anatomy in revision cases increases the risk of vascular injury twice as compared to primary cases [6]. Nowadays, increasing procedures of TKA bring about the possibility of vascular injuries although they are rare. Therefore, it is necessary to take precautions against vascular injuries that may develop, to identify risky patients and to make an early diagnosis. For this, a good anamnesis and physical examination are essential. It is important to examine the presence of hypertension, diabetes, smoking, and vascular claudication. Coldness of the extremities to be operated during physical examination, skin atrophy and thinning, prominent vascular structures, ulcerative wound, and distal arterial pulse weakness are the findings that need attention. In addition to these findings, the presence of vascular calcifications in radiological scanning, a history of bypass, and an ankle-brachial index below 0.9 are other findings that should be considered. No tourniquet should be used in patients with the abovementioned conditions [7]. Embolism and arterial insufficiency may develop due to tourniquet effect in patients with vascular disease and atheroma plaque in the superficial artery [8]. It has been shown that during the manipulation of the superficial femoral artery fixed during tourniquet effect, intimal damage may occur [9]. Improper placement of retractors can also cause damage by direct mechanical trauma [10]. Particularly during insertion of the posterior retractor, a 1 cm area in the lateral portion of the midline was identified as a risky area [11]. In a cadaver study, neurovascular structures on the tibial side were mapped on a clock diagram. Accordingly, the popliteal vein at 12 o’clock, the popliteal artery at 1 o’clock, and the anterior tibial artery at 2 o’clock for the left knee were shown as in place [12]. Cautious use of the saw between 11 and 3 o’clock defined in the tibial cutting is important in protecting vascular structures [12].

If vascular injury is suspected the tourniquet should be deflated, and bleeding control should be performed before the incision is closed. The possibility of arterial injury should be taken into consideration in the presence of excessive and pulsatile bleeding and in the absence of peripheral pulses. Although recent studies suggest bleeding control after routine tourniquet deflation prior to incision, its benefit is controversial [13]. The surgeon should perform a postoperative peripheral pulse examination routinely, suspect acute ischemia in the presence of cold and delayed distal capillary filling, and request cardiovascular consultation [14]. Acute ischemia cases with delayed diagnosis of 4–6 hours cause irreversible damage. Prophylactic fasciotomy is performed after revascularization [14].

Pseudoaneurysm may present with pulsatile swelling in the popliteal fossa due to direct damage to the popliteal artery during surgery. Doppler ultrasonography is useful in the diagnosis. In the treatment, excision of the lesion and repair with vascular graft is applied after embolization [15]. Arteriovenous fistula is less common. It usually occurs due to injury to the medial and lateral geniculate arteries and its branches. It may present with pulsatile swelling in the popliteal region that gives “trill.” Hemarthrosis or pseudoaneurysm may develop. Ultrasound and angiography are used for diagnosis [16]. The detected lesions should be evaluated together with cardiovascular surgery, and treatment should be planned. Embolization, lesion excision, and graft repair are treatment options [15].

2.2 Neurologic complications

Nerve injuries are rare during TKA. Peroneal nerve injury is the most common of these [17]. Sacral plexopathy and sciatica neuropathy are also seen, although rarely [18]. Risk factors for neurological injury are [19]:

• Flexion deformity

• Advanced valgus deformity

• Presence of an intra-articular hematoma

It has been shown that the risk of nerve injury is increased in patients with rheumatoid arthritis [20]. However, none of these risk factors is directly related to nerve injury [18]. Nerve injury is associated not only with the surgical procedure but also with the anesthesiologist-induced regional anesthesia [21]. Hypertension, diabetes, nerve compression history, presence of tethered cord, and rheumatoid arthritis in the patients increase the risk of neural complications secondary to regional anesthesia [22]. The duration of tourniquet use was associated with nerve injuries. According to this, in the tourniquet applications exceeding 2 hours, the risk of peroneal and tibial nerve injuries including 89% peroneal nerve was determined as 7%. All of these have been shown to get recovery. In procedures exceeding 2 hours, the 10–30-minute break and deflation of the tourniquet reduces the complication rate [19]. Although there is a minimal effect on the functional results of the patients effect on the functional results of the patients during the follow-up, paresthesia and numbness are seen in the distal and lateral site of incision due to the injury of the infrapatellar branch of the saphenous nerve. It is seen in the literature at a rate of 25–76%, and most of these recover spontaneously [23]. Nerve injuries are difficult to detect intraoperatively. In the presence of postoperative nerve injury, physical therapy should be planned immediately. EMG examination is recommended after 3 months [20]. If no improvement is observed, nerve exploration may be planned in the future.

2.3 Extensor mechanism injuries

The extensor mechanism in the knee joint consists of quadriceps muscle group, quadriceps tendon, patella, patellar retinaculum, patellar tendon, and tuberositas tibia. Extensor mechanism integrity may be impaired during surgery [20]. Although extensor mechanism injuries occur more frequently postoperatively, they may also occur intraoperative. The incidence is reported to be between 1 and 12% [24]. The treatment of extensor mechanism injuries is quite difficult and the results are not satisfactory.

2.4 Medial collateral ligament injury

During total knee replacement, medial collateral ligament (MCL) is important for soft tissue stabilization and coronal plan stability. The incidence of iatrogenic MCL injury is 2.2–2.7% [35]. In the case of surgical injuries, direct repair, constrained prosthesis use, and even revision at the same session are among the options [36]. Unrecognized MCL injuries during surgery cause early instability. This leads to early implant wear and consequently the need for early revision. Therefore, it is important to diagnose and repair the injury during surgery [37]. Sudden instability in the valgus stress test during knee stabilization indicates MCL injury. Injury may occur from femoral insertion, within the tendon or tibial insertion [38]. Primary repair technique varies according to injury level. Fixation with screw is recommended if MCL injury occurs from its femoral insertion site. Otherwise, if it is through tendon, repairing with insoluble suture technique is recommended. Finally, if MCL injury occurs from its tibial insertion site, both insoluble suture anchor technique and fixation with staple technic are recommended [39, 40]. Factors that increase the risk of medial collateral ligament injury during surgery are as follows [39]:

• Using a larger saw blade than femoral condyle

• Delayed excision of medial side osteophytes

• Performing challenging manipulations of varus-valgus

• Patients with flexion contractures [39]

Patient-related risk factors include obesity and severe deformities [41, 42].

A certain algorithm has not yet been established for the treatment of iatrogenic MCL injuries that occur intraoperative. Many treatment methods with disadvantages and advantages have been used [39, 43, 44]. The traditional method is using constrained prosthesis. However, in this method, it was shown that the stress load on the implant increased and direct repair and treatment with non-constrained prosthesis were recommended instead. In addition, augmentation or increase in polyethylene thickness has been proposed [45]. In one study, it was shown that the risk of instability was 57% in the use of non-constrained prostheses independent of the repair technique after MCL injury [37]. In a 2016 study, four treatment modalities were compared after MCL injury. These are the use of non-constrained prosthesis only, the use of non-constrained prosthesis with primary repair, the use of non-constrained prosthesis only, and the use of constrained prosthesis with primary repair. In 23 patients, the most appropriate treatment method according to the knee community scoring was found to be the use of constrained prosthesis only [46]. However, due to the small number of patients, larger series of studies are needed to determine which treatment is most appropriate.

3.1 Bleeding

Bleeding is seen in varying rates between 0 and 39% after TKA [47]. This naturally increases the need for blood transfusion. Intraoperatively, care should be taken about bleeding and good bleeding control is established. Thus, the amount of bleeding is reduced to a minimum. As a result, the risks of immunological reaction due to transfusion are reduced.

Bleeding tolerance is low in patients with comorbid disease and in patients with insufficient cardiac capacity, and the risk of complications increases even in small amounts of bleeding. Preoperative blood preparation before surgery and limitation of the use of anticoagulants are among the measures that can be taken. Precautions during and after TKA surgery can reduce the amount of bleeding. These methods are as follows:

• Use of femoral intramedullary plugs [48]

• Hypotensive anesthesia [49]

• Cryotherapy and Jones bandage [50]

• Use of fibrin tissue adhesive [50, 51]

• Clamping the drain [52, 53, 54]

• Application of tranexamic acid [55]

Fibrinolysis is activated by surgical trauma and tourniquet use [56]. Increased fibrinolytic activity causes increased bleeding during TKA. Tranexamic acid shows an anti-fibrinolytic effect by inhibiting the conversion of plasmin to plasminogen [57]. Tranexamic acid can be administered in four different ways: intravenous, oral, intramuscular, and intra-articular [55]. Transition to maximum plasma levels is 30 minutes for intramuscular use, 5–15 minutes for intravenous use, and 2 hours after oral use [58]. Patients with total knee arthroplasty may be treated with a fast-acting intravenous route. Many studies have shown that administration of tranexamic acid after tourniquet deflation and postoperative dose repeat reduces the amount of bleeding and the need for transfusion [59, 60, 61]. However, many different protocols for the use of tranexamic acid have been implemented. Preoperative single dose and repeated dose every 8 hours for 3 days have been described in the literature and shown to be effective [62]. In a study conducted in 2011, tranexamic acid was administered at a dose of 10 mg/kg 10 minutes before the tourniquet was opened, and the same dose was repeated 3 hours postoperatively. Five hundred mg tranexamic acid was administered orally 3 times a day for 5 days. At the end of this study, it was shown that the amount of hemorrhage and the rate of transfusion decreased effectively [55].

3.2 Skin healing problems: superficial and deep infections

The incidence of wound problems after TKA is 1–25% [63]. The skin problems may be delayed wound healing, skin necrosis, traumatic or atraumatic separation of the lips of the wound, prolonged serous discharge at the wound site, formation of superficial or deep hematoma, allergic reaction to patch, suture material or dressing materials, bullae formation, fat necrosis, bleeding, keloid formation, and superficial or deep infection [64].

Etiologic reasons that may develop the problem before TKA should be determined in advance, and appropriate measures should be taken [65]. Presence of systemic diseases such as diabetes, hypertension, rheumatoid arthritis, and vascular insufficiency, which may adversely affect wound healing before TKA, should be questioned. Since the soft tissues around the knee are thinner than the other parts of the body, even the smallest problem that may occur at the wound site can cause serious complications. Incision planning should be made carefully in the case of a history of operation from the same place and scarring beforehand, and if necessary, plastic surgery assistance should be taken.

3.3 Deep vein thrombosis and pulmonary embolism

Deep vein thrombosis is the general name of thrombosis in the venous circulatory system. It occurs most commonly in the deep veins of the lower extremity [85]. From asymptomatic deep vein thrombosis to pulmonary embolism, which can be fatal, it can be confused with clinical manifestations of varying degrees [85]. It is one of the important complications that increase morbidity and mortality after TKA [86]. Even with mechanical or pharmacological methods, the incidence of asymptomatic DVT is 5.1%, and the incidence of symptomatic DVT is 0.4% [87]. The mortality rate due to pulmonary embolism after TKA is 0.08% [88].

It is important to understand the Virchow triad in the pathogenesis of DVT development. There is a slowdown in blood flow (stasis), endothelial damage, and hypercoagulability [89]. The admixture of fat and bone marrow particles into the venous system after engraving of the femoral canal during TKA explains the hypercoagulability branch of the Virchow triad. Hyperflexion of the leg during surgery and anterior manipulation of the tibia with retractors explain endothelial damage. In addition, this manipulation causes obstruction of the popliteal veins and prolonged immobilization of the leg, leading to venous pooling and stasis [89].

4.1 Instability

The development of instability after TKA is the third most common cause of revision (17%) after aseptic loosening and infection [102]. Patients present with signs of pain and swelling with movement and weight loss. There may also be pain, emptiness, or abnormal friction and rattling noise in some range of motion. On the knee during walking, varus or valgus orientation and recurvatum can be seen. Anterior knee pain during sitting up is typical in flexion instabilities. The heaviest table is knee dislocation. The treatment of instability is revision surgery. However, the rate of recurrent instability after revision was 18–60% [103]. This high rate is usually due to the lack of correct identification of the cause of instability.

A clinical classification of knee instability was established. Components of this classification are flexion-extension gap mismatch, component alignment problem, isolated ligament failure, extensor mechanism failure, component loosening, and global instability [103].

4.2 Joint stiffness

One of the reasons that greatly affect patient satisfaction after TKA operations is the amount of joint range of motion. To achieve good results, a flexion range of at least 90° is required. Sixty-five degrees of flexion is required during walking; 106° of flexion is required when sitting on a chair and tying shoes. Postoperative limited and painful joint movements significantly reduce patient comfort. A flexion range of less than 90° for 6 weeks after TKA surgery is defined as a rigid knee [107].

4.3 Periprosthetic joint infections

Deep infection after TKA is the most common cause of revision. Systemic complications such as septicemia and cardiopulmonary insufficiency may also occur in patients with periprosthetic infection [117]. As a result, it increased mortality rates. Nowadays, the incidence of deep infection after TKA varies between 0.4 and 2% [74]. Factors that pave the way for infection in the postoperative period include the presence of rheumatoid arthritis, diabetes, hemophilia, malignancy, HIV, obesity, smoking, intravenous drug addiction, knee septic arthritis and osteomyelitis, prolonged surgical time, malnutrition, steroid use, and prolonged skin problems.

Antibiotic prophylaxis is the most effective method to prevent infection [118]. Prophylaxis should be administered 30–60 minutes. Before skin incision [119]. It has been shown that short postoperative antibiotherapy is more beneficial than the longer one [120].

Fewer people entering the operating room, using drapes to prevent superficial contamination, providing laminar air flow, effective sterilization of surgical instruments, and keeping the surgical time 150 minutes below are also necessary to prevent infection [121].

Risk groups of patients should be identified before the operation, and a separate planning should be made for each patient according to comorbid diseases. Antibiotic cement has been shown to reduce the infection rate in patients at risk [122]. However, it has been reported that the use of antibiotic cement in the patient group with no risk may cause premature loosening [123].

The most common organisms produced after infected knee arthroplasties are Staphylococcus aureus, coagulase negative Staphylococcus, and Streptococcusbacteria [124]. However, many microorganisms can also be active. Variations have occurred in microorganisms due to the unnecessary antibiotics used recently, and this has led to the development of resistance. Of these microorganisms, the most common isolates are methicillin-resistant Staphylococcus aureus(MRSA) and many antibiotics [125]. Fungal infections are not common, but the most common causative agents in these isolated are Candidaspecies [126].

Bacteria that cause prosthetic infection form a biofilm layer on the implant. This biofilm layer increases the virulence of the agent. In addition, it forms resistance to treatment because of its limitation on antibiotic permeability. The best antibiotic to cross the biofilm layer is rifampicin [127]. There are studies suggesting the addition of rifampicin to antibiotic treatment specific for the reproductive bacteria [127, 128].

4.4 Periprosthetic fractures

Periprosthetic fractures around the knee are fractures that occur during or after surgery within 15 cm of the knee joint or within 5 cm of the intramedullary part of the prosthesis, if any [137]. The incidence of these fractures after TKA is 0.3–2.5% for femur and 0.4 01% for tibia [138, 139].

The main risk factor related to the patient is the age of the patient. This risk is due to an increased risk of falling due to the patient’s age and osteoporosis associated with age [140]. Corticosteroid use, diseases that may increase the risk of falling with rheumatoid arthritis (epilepsy, Parkinson’s, cerebellar ataxia, myasthenia gravis) can be counted as other patient-related risk factors [141].

Intraoperative diaphyseal femoral fractures may occur due to incorrect placement of the intramedullary guide and osteopenia [142]. Unsuitable bone incisions, aggressive impaction of the ligamentous posterior stabilized femoral component, and eccentric placement of trial components are also risk factors for femoral fracture. It has been shown to increase the frequency of periprosthetic fractures due to increased resistance in flexion and rotation movements in anterior femoral notching [143]. The possibility of periprosthetic fracture is increased in revision TKA cases [144]. Periprosthetic fractures are more common due to the rotational forces of restrictive prosthesis using shear forces in the prosthesis [141].

Due to the stronger structure of the tibia, fracture development is rare.

For femoral periprosthetic fractures, there is a classification that questions fracture displacement and component fixation.

• Type 1 describes fractures with non-displaced and stable components.

• Type 2 refers to component stable fractures with displacement of more than 5 mm or angulation of more than 5°.

• Type 3 indicates loose fractures [145].

4.4.1 Treatment

4.4.1.1 Femoral fractures during surgery

The femur fractures vertically more than the metaphyseal region. A stable periosteum prevents displacement. It is followed conservatively without any additional intervention. For fractures penetrating the femoral cortex, whether or not a bone graft is used, the penetration level should be treated with a stem prosthesis that is at least twice the diameter of the femoral canal [146].

4.4.1.2 Postoperative femoral fractures

When non-displaced fractures and stable prosthesis occur after TKA, conservative treatment may be preferred. Four to six weeks of non-weight procedure, long leg plaster, or hinged orthosis is followed.

Displaced and unreducible supracondylar fractures are almost always treated surgically in the presence of adequate bone stock ( Figure 1 ) [147].

Locked compression plates are preferred for knee periprosthetic fractures [144]. Prosthetic revision should be performed in fractures that cause prosthesis loosening and malposition. In these cases, stented prosthesis of sufficient length should be placed to obtain a stable fixation of the intact bone [138]. Knee replacement revision after periprosthetic fractures is often associated with the loss of range of motion (ROM) [148].

4.4.1.3 Tibia fractures

The majority of tibial periprosthetic fractures during surgery involve the plateau region and are generally non-displaced [146, 149]. If prosthetic loosening is present, revision surgery using a stem component long enough to cross the fracture line is required [150].

Postoperative tibial fractures can be examined in four groups. In type 1 fracture, revision is recommended because tibial component will be in varus alignment. The medial defect should be closed with bone graft or metal support [150]. Type 2 fractures are treated with nonsurgical treatment if the component is stable and there is minimal displacement [149]. Displaced type 2 fractures are treated with internal fixation. If the component is unstable, it must be revised using a long tibial stem to cross the fracture line [149]. Internal fixation should be performed for type 3 and 4 fractures [145].

4.5 Aseptic loosening

The deterioration of the relationship between prosthesis and bone is defined as loosening. The loosening may be between the prosthetic cement and the cement bone. Loosening is inevitable in long-term prostheses. It is useful to distinguish the concepts of osteolysis and loosening. Without prosthesis osteolysis, loosening of the cement may occur. The mechanisms that cause loosening are micromotion, component collapse, and periprosthetic osteolysis [151].

Overuse and osteopenia are the causes of patient-related loosening. Implant design may also be the cause of loosening. According to this, loosening is more likely in cementless prosthesis and constrained prosthesis. One of the most important causes of aseptic loosening is malalignment. It has been shown that a 4 mm medial collapse of the tibial component and varus deformity of more than 2° increases the likelihood of loosening [152]. In the early period, a radiolucent line is seen between the component and bone on radiography, and a collapse occurs as the loosening progresses. Loosening is more common around the tibial component [152]. In the presence of loosening around the whole component, septic loosening should be considered, and differential diagnosis should be performed.

In the case of loosening, the treatment is decided according to symptoms and progress. If pain is associated with instability and there are X-ray findings, early revision surgery is recommended for bone stock preservation.

4.6 Osteolysis

Osteolysis usually occurs due to inflammatory reactions caused by worn polyethylene particles or in the presence of infection. Metal particles can also cause osteolysis. Titanium causes more osteolysis than cobalt and chromium. Giant cells that develop against abrasive particles act by forming a membrane [153]. Particle size is important for this mechanism. The particle sizes range from 1 to 100 micrometers under the electron microscope. Large parts do not cause osteolysis [153]. There is no osteolysis if the parts are not spread to the cancellous bone, so osteolysis is not seen when the cancellous bone is properly covered with cement [154]. On the other hand, the incidence of osteolysis increases when pres-fit prosthesis is applied; screw fixation without cement is used or cement breaks [155]. Osteolysis is closely related to prosthetic design. Osteolysis usually occurs after 2 years of TKA. Occurrence is rare before 2 years [156]. Osteolysis is mostly seen in the tibia [157]. Diagnosis includes pain, joint effusion, and synovitis due to joint instability. Focal bone destruction may be seen on radiolucent line and X-ray. It can be seen that there is no continuity of trabeculae and bone cortex in cancellous bone. Therefore, control X-rays are very important in patient follow-up and must be compared with old radiographs in controls. CT and MRI can be used for osteolysis that cannot be detected on direct radiography [158].

If the lesion is small in treatment and the prosthesis is stable, observation is sufficient. Bisphosphonate and calcium supplementation can be initiated [159]. If the prosthesis is instable, two options can be applied. The first one is debridement, polyethylene replacement, and curettage, followed by impaction of the defect with bone graft. The second is revision [159].

4.7 Patellofemoral joint problems

Patellofemoral joint problems after TKA generally cause anterior knee pain. Patients’ ability to tolerate this pain rarely causes patellofemoral joint problems to be revised [160]. It should be kept in mind that not only patellar component-related procedures but also procedures involving the tibiofemoral joint may cause this problem. Even in revision surgery due to a problem of patellofemoral origin, it is often caused by a component in the tibia and femur [161]. In a study, patella and malrotation were among the eight most common causes of failed TKA [162].

Advanced valgus alignment, previous high tibial osteotomy, or tuberositas tibia osteotomy increases the rate of patellofemoral joint problems in TKA [160].

There are many points to be considered in the surgical technique to prevent patellofemoral joint problems. These are [163]:

• Component placement: If the femoral component is placed medially, anteriorly, or flexed, or if there is internal rotation and if the component is excessive in size, patellofemoral problems may occur finally. Likewise, the medialization and internal rotation of the tibial component increases the risk.

• Surgical approach type: Midvastus and subvastus interventions that protect the extensor mechanism more can reduce PF joint problems.

• Lateral release: The need for lateral retinacular release increases PF joint problems.

• Patella resection amount: When patellar component is used, resection of the patella with anterior–posterior reduction of 12 mm increases the risk of PF joint problems [164, 165].

Patellar surface replacement is controversial today. However, in a recent study, it was found that anterior knee pain was less common in patients who underwent patellar surface change than those who did not. In the same study, the causes of PF joint revision were more common in patients without patella surface changes [166].

The results in patients with patellar articular surface alteration due to persistent anterior knee pain after TKA are not as successful as those with surface replacement during primary TKA [167]. In the treatment of anterior knee pain after TKA, mechanical causes should be investigated after the exclusion of an underlying infection.