The treatment choice for each patient depends on a number of variables including whether the infection is superficial or deep, the time since surgery, the condition of the soft tissues, host factors, the infecting organism and whether or not the implants are well fixed. Treatment goals consist of eradication of infection, pain relief and functional recovery. There are a number of therapeutic options available to the surgeon.

These options are:

A detailed description of these therapeutic options is beyond the scope of this chapter (see Chaps.​ 59 and 60).

Pain may result from abnormal stresses placed both upon the soft tissues and the knee joint. The exact nature of the instability needs to be determined as patients with patellofemoral pain, maltracking, flexion contracture or weak quadriceps may all describe their symptoms as instability. Instability may occur in flexion, extension, mid-flexion, globally and hyperextension following TKR [3]. There are a number of causes for instability depending on whether this occurs early or late after TKR (see Table 35.1).

Conservative measures such as weight loss in obese patients should be instituted where applicable. Extra-articular deformities or deformity affecting the hip or foot should be corrected prior to any knee reconstruction. Hyperextension instability is a difficult problem to manage, especially in the presence of underlying quadriceps weakness which should ideally be addressed preoperatively. Hinge-type TKRs preventing hyperextension may be used, but owing to their restricted motion, forces at the implant-bone interface are high and they may fail prematurely. True quadriceps paralysis may be better served with arthrodesis than revision.

Extensor mechanism complications are a common cause of pain and poor outcome following TKR. They include tendon rupture, patellar fracture, patellofemoral instability, patellar clunk syndrome, polyethylene wear and peripatellar adhesions.

Partial avulsion can be managed with bony reattachment using either suture anchors or through drill holes using Vicryl tape. Rerupture of primary repair is common, especially if a late repair was performed. Therefore, augmentation with either semitendinosus tendon autograft or synthetic ligaments such as the Leeds-Keio device may be undertaken [4–6].

Repair should be performed as soon as possible. The method of repair depends on the level of the tear and quality of patellar bone stock. Mid-substance rupture may be managed with end-to-end repair using sutures. Bony avulsion may be repaired using suture anchors or drill holes through the patella. If there is any extensor mechanism deficiency, augmentation with allograft or synthetic ligament may be required; augmentation using synthetic ligament offers the advantage of early rehabilitation.

Patellofemoral instability may be secondary to “overstuffing” of the patellofemoral joint, malrotation of the femoral and/or tibial components and failure to medialise the patella or lateralise both the femoral and tibial components. Asymmetrical patellar resection or soft tissue imbalance may also impair patellofemoral tracking [8]. The cause of the instability is generally a structural one and therefore management is predominately surgical [9].

If the components are correctly aligned, patellofemoral tracking may occasionally be improved with a lateral retinacular release [7, 10]. This procedure may disrupt the blood supply to the patella and complications including patellar fracture and avascular necrosis of the patella, and postoperative pain and swelling have been reported [11, 12]. Patellar blood supply may be better preserved using outside-in mesh expansion of the lateral retinaculum [13].

Mild component malrotation may be better addressed with proximal or distal extensor mechanism realignment than complete component revision. Proximally, good results have been reported with vastus medialis obliquus advancement and medial plication combined with lateral release [14, 15]. Distal realignment with tibial tubercle osteotomy and medialisation may also improve patellofemoral instability [16, 17] taking care to create a long, distally tapered osteotomy to prevent a stress-riser.

Treatment depends on the extensor mechanism integrity, stability of the patellar component fracture configuration and quality of the bone. A useful treatment algorithm for these fractures has been proposed by Ortiguera and Berry [18]. Type I fractures with a stable implant and intact extensor mechanism may be managed nonoperatively and usually have a good outcome. Type II fractures with an intact implant but with extensor mechanism disruption require surgical intervention using either open reduction internal fixation or partial patellectomy. Results following surgical fixation of displaced patellar fractures have been poor [18]. For type IIIa fractures, characterised by a loose patellar component with reasonable bone stock, component revision is preferable, while type IIIb fractures with loose patellar component and poor bone stock require removal of the component or total patellectomy.

Optimising range of motion is possibly the most poorly understood ingredient of TKR. Unfortunately, stiffness frequently leads to pain and functional restriction. Factors predisposing to stiffness are listed in Table 35.2 and may be classified as preoperative, intraoperative and postoperative.

Pain control is essential if stiffness is to be prevented. Poorly controlled pain leads to reduced range of motion and subsequent adhesion formation. Yercan et al. [20] have suggested that manipulation under anaesthesia (MUA) for stiffness may be reduced from 9 to <1 % by adequate pain control.

Management requires careful assessment and diagnosis of the underlying cause. Specialist knee physiotherapist input is helpful often in combination with a pain specialist if pain is felt to be a contributory factor. Treatment options for stiffness include physiotherapy, MUA, arthrolysis and revision TKR. The indications and timing of MUA are controversial. In our unit, we undertake MUA after 6 weeks postoperatively when there has been failure to regain preoperative range of motion or failure to progress after appropriate physiotherapy. Stiff, posterior cruciate ligament (PCL)-retaining TKR’s which are otherwise well balanced and aligned may benefit from arthroscopic PCL release performed at 3–6 months postoperatively [21].

Revision TKR for stiffness should only be undertaken if a clear technical error has been identified [19, 20].

The clinical assessment and diagnosis of these are discussed earlier in the chapter. Popliteus tendon impingement is amenable to arthroscopic release of the femoral attachment of the tendon, while fabellar impingement may be treated reliably with fabellar excision [22].

Nowadays, with modern PCL-retaining design, this complication is rarely seen. The historical incidence has been shown to be up to 3.5 %; most patients with recognised clunk syndrome require surgical intervention, and excellent results can be expected using a superolateral portal to undertake arthroscopic resection [23].

The most common non-coagulopathic cause for recurrent haemarthrosis is impingement of the entrapped synovium. This may be managed nonoperatively [1]; however, synovectomy may be undertaken if this fails. This can be performed either open or arthroscopically and may be combined with surgical embolisation if a bleeding vessel is identified [24, 25].