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Complications of total hip arthroplasty

Complications of total hip arthroplasty
Literature review current through: Jan 2024.
This topic last updated: Mar 10, 2022.

INTRODUCTION — Most complications associated with total hip arthroplasty (THA) are infrequent and can be prevented if anticipated or treated readily when recognized. Complications associated with any major surgical procedure, including those related to anesthesia, comorbid medical conditions, medications, and allergic reactions, can also occur.

Perioperative as well as intermediate and late complications following THA are reviewed here. The indications for, alternatives to, and surgical technique for THA are presented separately. (See "Total hip arthroplasty".)

PERIOPERATIVE COMPLICATIONS — The major perioperative complications directly associated with total hip arthroplasty (THA) are discussed below.

Other complications associated with any major surgery such as anesthesia-related risks, allergic and other medication reactions, and those related to comorbid medical conditions are discussed separately. (See "Overview of anesthesia" and "Perioperative anaphylaxis: Clinical manifestations, etiology, and management" and "Cardiovascular problems in the post-anesthesia care unit (PACU)".)

Intraoperative fracture — Most intraoperative fractures occur on the femoral side during stem insertion. The incidence of femoral fracture during THA ranges from 0.1 to 1 percent for cemented components and from 3 to 18 percent for uncemented components [1-3].

Factors that increase the risk of fracture during primary arthroplasty include female sex, older age, osteopenia, inflammatory arthropathies, and cementless stem fixation. The use of longer-stem cementless implants during revision surgery is an additional risk factor for fracture [4].

Some fractures may not require further intervention or can be treated with wires or cables. Other, more extensive fractures may require more complex solutions including component revision, bone grafting, and/or supplementary hardware (eg, plates and screws).

Nerve injury — The incidence of nerve injury in primary THA ranges from 1 to 2 percent [5]. Injury to the sciatic nerve is most common, especially in the posterior approach, but the lateral femoral cutaneous, femoral, obturator, and superior gluteal nerves may also be injured. The peroneal division of the sciatic nerve is more susceptible to injury than the tibial division.

Risk factors for nerve injury include previous hip surgery, developmental dysplasia of the hip, lengthening of the extremity, obesity, female sex, and surgical approach. The risk of which nerve can be damaged varies with regard to surgical approach. The anterior approach appears to be associated with a higher risk for nerve injury, especially lateral femoral cutaneous and femoral nerve injuries, but it is also associated with other benefits [6]. (See "Total hip arthroplasty", section on 'Incision and exposure'.)

Nerve injury is most commonly identified in the early postoperative period once the patient has recovered from anesthesia. (See "Traumatic peripheral neuropathies", section on 'Sciatic neuropathies' and "Traumatic peripheral neuropathies", section on 'Peroneal neuropathies' and "Foot drop: Etiology, diagnosis, and treatment".)

The cause of nerve injury is unknown in over 50 percent of cases [7]. Known causes include compression due to hematoma or hardware, direct trauma (eg, retractor), transection, excessive lengthening of the extremity, ischemia (from pressure or traction), thermal injury secondary to cement, pericapsular analgesia injection, and dislocation [7].

When a suspected nerve injury is present, the wound should be inspected for large hematoma. Radiographs should be obtained and inspected for evidence of excessive lengthening, dislocation, and hardware position (eg, screws). The use of metal artifact reduction sequence (MARS) magnetic resonance imaging (MRI) or ultrasound of the pelvis and sciatic nerve may be helpful in identifying potential sources of neural compromise, including hematoma in the gluteal space and extradural impingement [8].

Treatment depends on the cause of nerve injury. If discovered immediately postoperatively, flexion of the hip and knee will reduce tension on the sciatic and femoral nerves. Surgical exploration is indicated for suspected nerve palsies caused by large hematoma, excessive limb lengthening, and nerve laceration. For other unidentifiable causes, observation is usually appropriate, especially if waiting for the analgesia injection to wear off. If foot drop is present, an ankle-foot orthosis should be used during rehabilitation. (See "Traumatic peripheral neuropathies", section on 'Sciatic neuropathies' and "Traumatic peripheral neuropathies", section on 'Peroneal neuropathies' and "Foot drop: Etiology, diagnosis, and treatment".)

Prognosis for recovery is variable and is directly correlated with the degree of nerve injury and duration of symptoms. Mixed sensory and motor losses have the poorest prognosis. Isolated peroneal injury has a better prognosis than complete sciatic palsy. Complete recovery occurs in approximately 41 percent, and another 44 percent have only a mild deficit [9]. Approximately 15 percent have a poor outcome characterized by weakness requiring an ankle-foot orthosis and persistent dysesthesia. (See "Overview of lower extremity peripheral nerve syndromes".)

Leg length discrepancy — The incidence of leg length discrepancy following THA varies widely, ranging from 1 to 27 percent [10]. There is no universal consensus on what constitutes a significant inequality [11]. Some surgeons define a significant difference as 2 cm or more. Others define a significant difference as one that adversely affects patient function.

Regardless of which definition is used, special attention to this issue needs to be made perioperatively. During THA, every attempt is made to equalize leg lengths and/or restore normal leg length. Some amount of lengthening may be necessary to restore the native capsule tension due to the reduction in head size from the native head diameter to the prosthetic head diameter [12]. (See "Total hip arthroplasty", section on 'Managing limb length discrepancy'.)

Postoperatively, leg lengths should be measured and compared with those taken preoperatively. There is wide variability in patient perception of postoperative leg length. Numerous factors affect perceived postoperative leg length, and true leg length should be differentiated from apparent discrepancy. Some patients may perceive a discrepancy when true leg lengths are in fact equal. This apparent (or functional) leg length discrepancy may be due to hip muscle weakness in the early postoperative period and often resolves within a few months. These patients should be counseled regarding this, and physical therapy should emphasize progressive strengthening and stretching to help the patient return to a normal gait pattern.

If a significant true leg length discrepancy remains, the patient may require a shoe lift to equalize the limb lengths. It is advised to wait until full recovery has occurred before applying a shoe lift. Some patients with a true discrepancy may not notice an inequality that exists. But, with significant inequality in the absence of correction, a limp, low back pain, and/or the need for a cane are more common.

Vascular injury — Vascular injury, while quite rare during THA, can be a serious complication. The incidence of vascular injury ranges from 0.2 to 0.3 percent [13].

Major vessels that may be injured include the iliac and femoral vessels, profunda femoris artery, obturator artery, and superior gluteal artery. Intraoperative injuries are often lacerations or punctures of vessels. Injuries that may be recognized postoperatively include arteriovenous fistula, arterial thrombosis, and pseudoaneurysm [14].

Causes of vascular injury include the use of retractors, osteotomes, bone saw, or a scalpel near vascular structures; cerclage wiring; excessive dissection or traction on tissues; and acetabular screw placement. An acetabular quadrant system warns against the placement of screws in the anterosuperior quadrant, where the risk of injuring the external iliac artery or vein is increased, and anteroinferior quadrant, where the risk of injuring the obturator nerve, artery, or vein is increased [15].

In cases of vascular injury, control of bleeding intraoperatively must be performed. For minor injury, simple measures such as direct pressure (eg, for venous injury), ligation, or electrocautery may be effective. However, more severe vessel injury may require additional dissection to expose the vessel to repair it, sometimes necessitating consultation with a vascular specialist.

Venous thromboembolism — Venous thromboembolism (VTE) is one of the complications following THA that presents the highest risk of mortality. Those who have undergone THA are in the highest risk group of postsurgical patients (table 1). Stasis due to torsion of the lower limb during surgery, reaming of the long bones, as well as intimal injury, has been implicated in the etiology of thromboembolic events following THA, but the precise etiology remains uncertain. Due to the high risk of deep vein thrombosis (DVT) without prophylaxis, standard protocol following THA typically uses some form of pharmacologic prophylaxis along with early mobilization. Prophylactic regimens and recommendations for preventing postoperative venous thromboembolic disease are presented separately. (See "Prevention of venous thromboembolism in adults undergoing hip fracture repair or hip or knee replacement".)

In a meta-analysis of randomized trials and observational studies including 21,369 patients receiving thromboprophylaxis after THA or hemiarthroplasty, the pooled rate of symptomatic postoperative VTE prior to hospital discharge was 0.53 percent (95% CI 0.35-0.7 percent); symptomatic DVT occurred in 0.26 percent (95% CI 0.14-0.37 percent), and pulmonary embolism (PE) occurred in 0.14 percent (95% CI 0.07-0.21 percent) [16]. (See "Prevention of venous thromboembolism in adults undergoing hip fracture repair or hip or knee replacement", section on 'Risk assessment'.)

The incidence of postoperative DVT has decreased over time [17]. However, despite pharmacologic prophylaxis, the rate of PE has remained relatively constant [18]. In a retrospective analysis, the risk for symptomatic PE after primary THA was 0.4 percent [19]. The risk of postoperative fatal PE was 0.02 percent. Independent risk factors for symptomatic PE included elevated body mass index (BMI), higher Charlson Comorbidity Index, chronic obstructive pulmonary disease, atrial fibrillation, anemia, depression, and presence of postoperative DVT.

Prevention is the key to minimizing the risk of thromboembolism following THA, and while some form of prophylaxis is warranted, the challenge for the orthopedic surgeon is minimizing the risk of bleeding and hematoma formation due to prophylactic anticoagulation [20]. (See "Total hip arthroplasty", section on 'Minimizing blood loss'.)

The approach to diagnosis and treatment of VTE is presented separately. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and "Overview of the treatment of proximal and distal lower extremity deep vein thrombosis (DVT)" and "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults" and "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity".)

Surgical site infection — Surgical site infection (SSI) is classified as superficial incisional, deep incisional, or organ/space (ie, involving the prosthetic implant) (table 2). SSI after THA is reported to occur in 0.4 to 2.2 percent of cases, with reported rates varying depending on whether superficial and deep infections are included together [21,22]. Superficial incisional infection following THA occurs in the perioperative period and is usually fairly easy to diagnose as it is usually visibly evident at the wound. Clinical signs of infection may include fever, pain at the surgical site, erythema, swelling, and wound discharge. However, it can be difficult to differentiate between superficial and deep infection. Superficial SSI may be amenable to local wound treatment and antibiotics but can progress to involve the deep tissue layers. Prevention of SSI and the general approach to evaluating and treating SSI is presented separately. Deep infection is described briefly below and in more detail elsewhere. (See 'Prosthetic joint infection' below and "Overview of control measures for prevention of surgical site infection in adults" and "Overview of the evaluation and management of surgical site infection", section on 'Superficial surgical site infection'.)

Bone cement implantation syndrome — Bone cement implantation syndrome (BCIS) is a rare but potentially fatal complication of THA that is associated with the use of polymethylmethacrylate cement. It is characterized by a variety of clinical features including hypoxia, hypotension, neurologic symptoms, cardiac arrhythmia, and possibly cardiac arrest [23]. A number of potential mechanisms have been proposed to account for this phenomenon. The main cause is believed to be embolization of fat and marrow debris. Other contributing causes may be cement monomer toxicity, anaphylatoxin release, and prostaglandin release.

The incidence of acute hypotension associated with the use of cement is less than 5 percent [1]. A significant drop in systolic blood pressure (20 mmHg or more) can occur during the insertion of a cemented femoral component. Use of a long-stem femoral component is a significant risk factor [24].

Patients suspected of having BCIS are typically managed with aggressive volume resuscitation, supplemental oxygen, and supportive care.

INTERMEDIATE AND LONG-TERM COMPLICATIONS

Prosthetic joint infection — Prosthetic joint infection (PJI) can be a morbid and costly complication following total hip arthroplasty (THA). The incidence of deep infection (table 2) following primary THA is approximately 1 percent [25,26]. It is important to note that while perioperative measures are important for preventing surgical site infection (SSI), other factors may contribute to a delayed onset of PJI (eg, bacteremia). (See "Prevention of prosthetic joint and other types of orthopedic hardware infection".)

The diagnosis of PJI, which can be difficult, is based on a combination of clinical examination, serum and synovial fluid laboratory studies, microbiologic culture (from peripheral blood and joint fluid), findings at surgery, and histologic analysis of periprosthetic tissue [27]. Two positive cultures of the same organism from joint aspirate (or a surgical specimen) or the presence of a sinus tract with evidence of communication to the joint are the major criteria that define the presence of deep infection [27,28]. Since these criteria are not always readily available or present, a scoring system has been developed and validated to help with determining the presence of infection (table 3) [27,28]. For inconclusive preoperative scoring or cases where no fluid can be obtained from the joint, the presence of purulence, histologic findings, or a single positive culture may assist in the diagnosis. (See "Prosthetic joint infection: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

Deep SSI and PJI may sometimes be successfully managed with antibiotics and debridement while retaining the prosthesis. However, if the implant is loose or if the infection is well established, removal of the implant is often required. Reimplantation can either be performed during the same surgical procedure or can be delayed until the infection has been cleared with a course of antibiotics. The microbiology, clinical manifestations, treatment, and prevention of PJI, in general, are presented in more detail separately. (See "Prosthetic joint infection: Epidemiology, microbiology, clinical manifestations, and diagnosis" and "Prosthetic joint infection: Treatment".)

Dislocation — Dislocation is the most common indication for early revision. The overall incidence of instability or dislocation in primary THA is typically below 5 percent [29,30]. The majority of dislocations occur posteriorly, typically with flexion, adduction, and internal rotation of the limb (image 1). Anterior dislocations are less frequent and typically occur with extension, adduction, and external rotation of the limb. The surgical approach can influence the direction of dislocation.

Dislocation of a THA is not a subtle phenomenon. Patients will typically experience a significant "pop" or "clunk" with immediate pain. There is often shortening and rotation of the affected limb (typically, external rotation with anterior dislocation; internal rotation with posterior dislocation). Weightbearing is usually not possible because the ball is no longer in the socket.

Historically, the dislocation rate following a posterolateral approach was greater compared with a modified lateral approach. Using a posterior capsular repair when performing a posterolateral approach can reduce the dislocation rate to less than 1 percent [31,32]. This is similar to using the modified lateral approach, which has a dislocation rate of less than 1 percent [33]. In a large contemporary study of over 16,000 THAs, the adjusted risk of dislocation within two years of THA was 0.17 percent for the lateral approach, 0.74 percent for the direct anterior approach, and 1.74 percent for the posterior approach [29].

Besides surgical approach, other factors influencing the rate of dislocation include implant design, implant orientation and alignment, status of the soft tissues (particularly the abductors), and the inter-relationship between the spine, pelvis, and hip [34,35]. Patient factors associated with increased risk of dislocation include female sex, advanced age, Parkinson disease, alcohol abuse, and history of previous hip procedures [36-38].

Dislocation can be diagnosed with plain radiography. Computed tomography (CT) scan may be performed after reduction to assess the alignment of the components.

Treatment depends on identification of the cause and direction of dislocation. Following dislocation, initial attempts are typically made to reduce the dislocation under sedation or anesthesia. If closed reduction is unsuccessful, then open surgical reduction or revision is required. Most first-time dislocations can be managed with simple closed reduction. Following closed reduction, strict dislocation precautions are usually recommended based on the direction of dislocation. Occasionally, a hip abduction brace is used to reinforce dislocation precautions. The data supporting brace use are not encouraging, with roughly 60 percent of patients continuing to dislocate in spite of using a brace [39]. If the patient experiences recurrent dislocations or if component malposition is identified, surgical intervention is typically recommended [40].

For dislocations related to implant failure, implant malalignment, excessive soft tissue laxity, or recurrent instability, surgical treatment is often necessary. A success rate of 80 percent can be expected for reoperations in which the specific cause of the dislocation has been well defined. The highest reported success rates have been with constrained acetabular components [41] or the use of a dual mobility construct [42]. However, late mechanical failure and loosening have been observed in these groups of patients.

Osteolysis and wear — Osteolysis is a process in which bone is resorbed as a biologic response to particulate debris. The incidence of osteolysis depends on many factors including implant design and materials, type of fixation (cemented or uncemented), and surgical technique. With traditional bearing surfaces, the incidence has varied widely, ranging from 17 to 63 percent within 10 years postoperatively [43]. However, later-generation bearing surfaces have demonstrated much improved results with later midterm studies showing no osteolysis at all [44,45]. However, longer follow-up is needed to determine the true incidence of osteolysis with later generation devices.

The common factor leading to osteolysis is mechanical wear and the resultant production of particulate debris, including polyethylene, metal, ceramic, and acrylic bone cement (typically in the micron or submicron range). A higher particle load is associated with a greater osteolytic response [46]. The process begins as wear particles from the hip implant are phagocytosed by macrophages that become activated. These activated macrophages release osteolytic factors and stimulate osteoclasts to dissolve surrounding bone [47].

Periprosthetic osteolysis is typically asymptomatic unless it progresses to aseptic loosening (see 'Aseptic loosening' below). When osteolysis is accompanied by pain, it generally reflects loss of implant fixation or a pathologic fracture. Pain may also be the result of reactive synovitis.

Radiographically, osteolysis appears as endosteal, intracortical, or nonlinear cancellous bone destruction. Lesions can become quite large and expansile, especially on the acetabular side. Bone loss is often significant by the time osteolysis appears on plain radiographs (image 2). CT scanning with metal artifact suppression can provide better visualization of osteolytic defects than plain radiographs and are useful in determining the size of lesions.

To decrease wear and subsequent osteolysis, much attention has been directed toward the elimination of possible sources of wear and particulate debris. The most common source of such debris is polyethylene from the articulation between the femoral head and acetabular liner. Highly cross-linked polyethylene with improved resistance to wear has been developed as a possible solution.

The treatments available for osteolysis are surgical. Indications for surgery include extensive osteolysis with a loose component, impending or actual pathologic fracture or the presence of symptoms. Most patients who undergo surgical revision for osteolysis are asymptomatic. Revision is directed at updating the prosthesis to a modern bearing to prevent further bone loss. Delaying surgical intervention until symptoms are present or implants become loose can make the revision surgery more difficult. Exchange of the acetabular liner and removal of granulomatous tissue has the potential to decrease wear and slow the progression of osteolysis without subsequent component loosening [48-50].

Aseptic loosening — Aseptic loosening is the most common indication for late revision after THA [51]. The incidence of aseptic loosening is highly variable. Improvements in bearing surface wear characteristics, implant design, surgical technique, and patient selection have all led to a decreasing incidence.

Aseptic loosening is most often caused by wear of the prosthetic components (see 'Osteolysis and wear' above). The risk of aseptic loosening leading to revision THA is approximately 1 percent per year [52]. Other etiologies include poor initial stability of the implant, suboptimal implant design (retrospective assessment), patient factors (eg, age, weight, activity level, underlying diagnosis), and failure of fixation. In cementless implants, poor host response and lack of biologic integration may be causes. In cemented implants, suboptimal cement technique or cement fatigue/fracture may be a cause.

Although periprosthetic osteolysis may be asymptomatic, aseptic loosening is often associated with pain. Loosening of the femoral component typically causes deep-seated aching in the proximal to middle aspect of the femur that is worse with weightbearing and better with rest or unloading the hip. The radiographic appearance may include a radiolucent line at the implant bone interface, a pedestal at the tip of the stem, or migration on sequential radiographs. CT or bone scan may also be used to help diagnose aseptic loosening. Bone scan should be limited to evaluation of implants that have been in place more than two years since increased uptake on bone scan can be seen even around well-fixed arthroplasty implants within the first one to two years. (See 'Osteolysis and wear' above.)

Aseptic loosening must be differentiated from PJI. Various tests have been used to try to differentiate these two disorders. The most definitive is joint aspiration and culture. In some cases, bone or tissue biopsy is necessary to clarify the etiology. Intraoperative cultures at the time of revision arthroplasty may also be indicated in some cases. (See "Prosthetic joint infection: Epidemiology, microbiology, clinical manifestations, and diagnosis" and "Prosthetic joint infection: Treatment".)

Sequelae from metal-on-metal wear debris — Metal-on-metal (MOM) wear debris has been associated with numerous complications including early implant failure due to accelerated bearing surface wear, adverse local tissue reactions (ALTR), and metal hypersensitivity reactions [53-59]. Metal wear debris can originate from any implant region where one metal surface is in contact with another metal surface. This is most often associated with the bearing surfaces of a MOM implant, including THA, hip resurfacing, or when using dual mobility cups [60]. Metal wear debris may also originate from the metal taper (trunnion), where a metal head is secured to the stem or a modular neck-body junction in a dual-taper stem [61,62]. (See "Total hip arthroplasty", section on 'Bearing surface'.)

The most common of the MOM wear debris complications is an ALTR, in which the metal wear debris creates problems locally. This can lead to a mass around the prosthesis (sometimes referred to as a "pseudotumor") consisting of increased joint fluid in and around the joint, thickened synovium, and/or local tissue necrosis, which can be extensive. These cases often require revision arthroplasty. Approximately one million patients worldwide have received MOM implants, the majority of which were placed between 2003 and 2010, but because of these issues, the use of MOM implants has fallen out of favor [63]. MOM implant usage is mostly limited to hip resurfacings for which there is not an equivalent alternative.

Management recommendations for patients with MOM implants by regulatory agencies differ between countries, and devices available in one country are not necessarily available in another. Our approach to management of patients with MOM implants is broadly consistent with recommendations made by the US Food and Drug Administration (FDA) and the Medicines and Healthcare products Regulatory Agency (MHRA) and are as follows [57,64,65]:

For asymptomatic patients (those without hip pain, swelling, or dysfunction), we suggest routine orthopedic evaluation (at least once every five years). Follow-up includes:

Physical examination with functional assessment

Evaluation for asymptomatic local swelling or masses

Cobalt and chromium levels are typically obtained and compared with baseline postoperative levels

For patients who develop symptoms suggestive of hip dysfunction such as pain, swelling, or gait abnormality, we suggest measurement of cobalt and chromium ions, imaging with ultrasound or MRI using metal artifact reduction sequence (MARS). If surgical revision is not deemed necessary in such patients, we suggest that this evaluation be repeated every 6 to 12 months.

It is not known what constitutes an acceptable elevation of metal ions in the bloodstream with these patients. It may be that a rising metal ion level is of greater concern than a specific threshold. The degree of ALTR may differ from patient to patient and may be implant specific.

Periprosthetic fracture — Periprosthetic fracture (fracture in proximity to the implant) is a postoperative complication with an incidence of less than 1 percent following primary THA [2,3]. Periprosthetic fractures occur most often on the femoral side at sites of weakened bone, such as near osteolytic lesions or areas where stress risers exist (eg, cortical perforation).

A number of classification schemes have been described, but the Vancouver classification system is often used (figure 1) [66]. Fractures are divided into type A, B, or C, as follows:

Type A (A1, A2) fractures are trochanteric in location. These are subclassified into AG (involving the greater trochanter) and AL (involving the lesser trochanter).

Type B (B1, B2, B3) fractures are located about the stem or tip of stem. These are subclassified into B1 (a well-fixed stem), B2 (a loose stem), and B3 (marked osseous deficiency or destruction).

Type C fractures are well distal to the tip of the stem.

Treatment options for periprosthetic fractures include nonoperative (eg, protected weightbearing) or surgical management (eg, revision arthroplasty, internal fixation). However, because of their inherent variability, management of periprosthetic fractures must be individualized, taking into consideration many factors including the age and physical needs of the patient, limb alignment, fracture location, fracture pattern, bone quality, location of any bone defects, type of implant fixation (cemented versus cementless), and stability of the implant.

Nonoperative treatment may be appropriate for stable fractures around well-fixed and functional implants (Vancouver type A, type B1). Otherwise, operative treatment is preferred for unstable fractures and fractures associated with loose or otherwise failed prostheses (ie, Vancouver type B2, type B3, type C). The surgical treatment of choice is usually determined by whether the stem is loose or well fixed. If the stem is loose, revision arthroplasty with a long-stem implant is the recommended treatment. Internal fixation may be indicated for unstable fractures with a well-fixed stem [67].

Implant failure or component fracture — The prevalence of implant fractures was estimated to be 0.27 percent in a retrospective survey from 1995 conducted by the American Association of Hip and Knee Surgeons [68]. Implant breakage is typically the result of deformation and fatigue fracture caused by repetitive loading (usually over the course of years). Even an incomplete fatigue fracture can progress to catastrophic failure with continued loading. In addition to inadequate fatigue strength of the metal, other factors that predispose to implant fracture are increased patient weight, high patient activity level, and poor implant fixation and stability [69,70].

Stems using modern metallurgy and manufacturing techniques have nearly eliminated stem breakage due to fatigue failure. Forged femoral components with decreased grain size, microporosity, and inclusions have greatly improved fatigue strength as compared with prior cast or annealed implants [71]. Early femoral stem designs that used stainless steel with inadequate cross-sectional area and high offset were particularly vulnerable.

Heterotopic ossification — Bone healing can be complicated by the formation of ectopic bone within skeletal soft tissues (heterotopic ossification [HO]). Following THA, HO can occur around the femoral neck and adjacent to the greater trochanter.

The incidence of HO following THA varies widely and may reach up to 90 percent for high-risk populations [72-75]. However, the incidence of clinically significant HO in the general population is thought to be lower, with estimates closer to 10 percent [72]. Risk factors for HO among patients undergoing THA are discussed separately. (See "Total hip arthroplasty", section on 'Prophylaxis for heterotopic ossification in selected patients'.)

Typical symptoms include hip stiffness and pain within a few months of surgery. Many patients with radiographically limited HO are asymptomatic. Some patients with severe HO may have signs of inflammation including fever, erythema, swelling, warmth, and tenderness. Such findings must be distinguished from wound infections or PJI.

Findings of soft tissue ossification may be visible on plain radiographs as early as three to four weeks postoperatively. Maturation of the HO may take up to one or two years. The maturation process can be monitored by serial radiographs or bone scan. Bone scanning typically shows increased uptake in the soft tissues adjacent to the hip, but these findings are not specific for HO. It is recommended to wait until one year after surgery before performing a bone scan to evaluate for HO.

The most widely accepted classification system (Brooker) includes four grades based on an anteroposterior (AP) radiograph of the pelvis and hip [76].

Grade I represents islands of bone within soft tissues about the hip

Grade II includes bone spurs adjacent to the pelvis or proximal end of the femur, leaving at least 1 cm between opposing bone surfaces

Grade III represents bone spurs adjacent to the pelvis or proximal end of the femur, leaving less than 1 cm between opposing bone surfaces

Grade IV represents radiographic ankylosis of the hip

The treatment of HO depends on symptoms and severity of HO. A comprehensive review of radiographs, patient symptoms, and physical examination will determine the ultimate need for intervention. Most early-grade HO requires no treatment at all and may be completely asymptomatic. More advanced HO may lead to pain and severe stiffness, which may require surgical excision.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Total hip arthroplasty".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Deciding to have a hip replacement (The Basics)")

Beyond the Basics topics (see "Patient education: Total hip replacement (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Complications related to total hip arthroplasty (THA) are uncommon. When complications do occur, the diagnosis and treatment are generally straightforward. Complications can be regarded as those occurring in the perioperative period and those occurring later. Perioperative complications may relate to the conduct of the operation, while those occurring later generally relate to the rehabilitation, healing, and wear and tear of the implant. (See 'Introduction' above and 'Perioperative complications' above and 'Intermediate and long-term complications' above.)

Surgical complications include bone fracture and neurovascular injury. These can often be prevented with good surgical practices. Leg length discrepancy is usually addressed while performing THA; however, some patients may have residual discrepancies, for which a shoe lift helps limit ambulation difficulties. During the placement of a cemented femoral stem, some patients may experience transient or more severe hypotension related to bone cement implantation syndrome; treatment is supportive. (See 'Intraoperative fracture' above and 'Nerve injury' above and 'Vascular injury' above and 'Leg length discrepancy' above and 'Bone cement implantation syndrome' above.)

Patients undergoing THA are in the highest risk group for venous thromboembolism (VTE), and mechanical and pharmacologic perioperative prophylaxis is recommended. Risk factors for VTE are similar to other populations. (See 'Venous thromboembolism' above and "Prevention of venous thromboembolism in adults undergoing hip fracture repair or hip or knee replacement" and "Overview of the causes of venous thrombosis".)

Surgical site infection (SSI) following THA is reported to occur in 0.4 to 2.2 percent of patients. Superficial SSI occurs in the perioperative period and may be amenable to local wound treatment and antibiotics, but can progress to involve the deep tissue layers. It is important to note that while perioperative measures are important for preventing SSI, other factors may contribute to a delayed onset of prosthetic joint infection (PJI; eg, low virulent/slow-growing organism or hematogenous spread). Deep SSI and PJI may sometimes be successfully managed with antibiotics and debridement while retaining the prosthesis. However, if the implant is loose or if infection is well established, removal of the implant is often required. Reimplantation can be performed during the same surgery or can be delayed until the infection has been cleared with a course of antibiotics. (See 'Surgical site infection' above and 'Prosthetic joint infection' above and "Prosthetic joint infection: Treatment".)

Complications related to rehabilitation, implant incorporation, and longer-term implant wear and tear include prosthetic hip dislocation, osteolysis, aseptic loosening, metal-on-metal (MOM) wear debris, periprosthetic fracture, and implant failure. In spite of the potential for these problems, most patients may never require revision arthroplasty. (See 'Dislocation' above and 'Osteolysis and wear' above and 'Aseptic loosening' above and 'Sequelae from metal-on-metal wear debris' above and 'Periprosthetic fracture' above and 'Implant failure or component fracture' above and "Total hip arthroplasty", section on 'Longevity of implant'.)

Postoperative healing can be complicated by the formation of ectopic bone within skeletal soft tissues, which is known as heterotopic ossification (HO). When present following THA, HO typically occurs around the femoral neck and adjacent to the greater trochanter. HO is identified readily on plain radiography, and while many patients are asymptomatic, if symptoms become severe, surgical excision of the lesions may be necessary. (See 'Heterotopic ossification' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Thomas Thornhill, MD, Jeffrey Katz, MD, MSc, and Bill Walter, MBBS, FRACS, PhD, who contributed to earlier versions of this topic review.

  1. Saleh KJ, Kassim R, Yoon P, Vorlicky LN. Complications of total hip arthroplasty. Am J Orthop (Belle Mead NJ) 2002; 31:485.
  2. Berry DJ. Epidemiology: hip and knee. Orthop Clin North Am 1999; 30:183.
  3. Della Rocca GJ, Leung KS, Pape HC. Periprosthetic fractures: epidemiology and future projections. J Orthop Trauma 2011; 25 Suppl 2:S66.
  4. Davidson D, Pike J, Garbuz D, et al. Intraoperative periprosthetic fractures during total hip arthroplasty. Evaluation and management. J Bone Joint Surg Am 2008; 90:2000.
  5. DeHart MM, Riley LH Jr. Nerve injuries in total hip arthroplasty. J Am Acad Orthop Surg 1999; 7:101.
  6. Fleischman AN, Rothman RH, Parvizi J. Femoral Nerve Palsy Following Total Hip Arthroplasty: Incidence and Course of Recovery. J Arthroplasty 2018; 33:1194.
  7. Schmalzried TP, Amstutz HC, Dorey FJ. Nerve palsy associated with total hip replacement. Risk factors and prognosis. J Bone Joint Surg Am 1991; 73:1074.
  8. Beksaç BP, Della Valle AG, Salvati EA. Acute sciatic nerve palsy as a delayed complication of low-molecular-weight heparin prophylaxis after total hip arthroplasty. Am J Orthop (Belle Mead NJ) 2009; 38:E28.
  9. Schmalzried TP, Noordin S, Amstutz HC. Update on nerve palsy associated with total hip replacement. Clin Orthop Relat Res 1997; :188.
  10. Desai AS, Dramis A, Board TN. Leg length discrepancy after total hip arthroplasty: a review of literature. Curr Rev Musculoskelet Med 2013; 6:336.
  11. Abraham WD, Dimon JH 3rd. Leg length discrepancy in total hip arthroplasty. Orthop Clin North Am 1992; 23:201.
  12. van Arkel RJ, Ng KCG, Muirhead-Allwood SK, Jeffers JRT. Capsular Ligament Function After Total Hip Arthroplasty. J Bone Joint Surg Am 2018; 100:e94.
  13. Nachbur B, Meyer RP, Verkkala K, Zürcher R. The mechanisms of severe arterial injury in surgery of the hip joint. Clin Orthop Relat Res 1979; :122.
  14. Sharma DK, Kumar N, Mishra V, Howell FR. Vascular injuries in total hip replacement arthroplasty: a review of the problem. Am J Orthop (Belle Mead NJ) 2003; 32:487.
  15. Wasielewski RC, Cooperstein LA, Kruger MP, Rubash HE. Acetabular anatomy and the transacetabular fixation of screws in total hip arthroplasty. J Bone Joint Surg Am 1990; 72:501.
  16. Januel JM, Chen G, Ruffieux C, et al. Symptomatic in-hospital deep vein thrombosis and pulmonary embolism following hip and knee arthroplasty among patients receiving recommended prophylaxis: a systematic review. JAMA 2012; 307:294.
  17. Shahi A, Chen AF, Tan TL, et al. The Incidence and Economic Burden of In-Hospital Venous Thromboembolism in the United States. J Arthroplasty 2017; 32:1063.
  18. Lieberman JR, Cheng V, Cote MP. Pulmonary Embolism Rates Following Total Hip Arthroplasty With Prophylactic Anticoagulation: Some Pulmonary Emboli Cannot Be Avoided. J Arthroplasty 2017; 32:980.
  19. Parvizi J, Huang R, Raphael IJ, et al. Symptomatic pulmonary embolus after joint arthroplasty: stratification of risk factors. Clin Orthop Relat Res 2014; 472:903.
  20. Burnett RS, Clohisy JC, Wright RW, et al. Failure of the American College of Chest Physicians-1A protocol for lovenox in clinical outcomes for thromboembolic prophylaxis. J Arthroplasty 2007; 22:317.
  21. Agodi A, Auxilia F, Barchitta M, et al. Risk of surgical site infections following hip and knee arthroplasty: results of the ISChIA-GISIO study. Ann Ig 2017; 29:422.
  22. Dale H, Skråmm I, Løwer HL, et al. Infection after primary hip arthroplasty: a comparison of 3 Norwegian health registers. Acta Orthop 2011; 82:646.
  23. Donaldson AJ, Thomson HE, Harper NJ, Kenny NW. Bone cement implantation syndrome. Br J Anaesth 2009; 102:12.
  24. Patterson BM, Healey JH, Cornell CN, Sharrock NE. Cardiac arrest during hip arthroplasty with a cemented long-stem component. A report of seven cases. J Bone Joint Surg Am 1991; 73:271.
  25. Lindeque B, Hartman Z, Noshchenko A, Cruse M. Infection after primary total hip arthroplasty. Orthopedics 2014; 37:257.
  26. Gundtoft PH, Overgaard S, Schønheyder HC, et al. The "true" incidence of surgically treated deep prosthetic joint infection after 32,896 primary total hip arthroplasties: a prospective cohort study. Acta Orthop 2015; 86:326.
  27. Parvizi J, Tan TL, Goswami K, et al. The 2018 Definition of Periprosthetic Hip and Knee Infection: An Evidence-Based and Validated Criteria. J Arthroplasty 2018; 33:1309.
  28. https://umexpert.um.edu.my/file/publication/00006143_166566_78638.pdf (Accessed on August 04, 2019).
  29. Fleischman AN, Tarabichi M, Magner Z, et al. Mechanical Complications Following Total Hip Arthroplasty Based on Surgical Approach: A Large, Single-Institution Cohort Study. J Arthroplasty 2019; 34:1255.
  30. Rowan FE, Salvatore AJ, Lange JK, Westrich GH. Dual-Mobility vs Fixed-Bearing Total Hip Arthroplasty in Patients Under 55 Years of Age: A Single-Institution, Matched-Cohort Analysis. J Arthroplasty 2017; 32:3076.
  31. Pellicci PM, Bostrom M, Poss R. Posterior approach to total hip replacement using enhanced posterior soft tissue repair. Clin Orthop Relat Res 1998; :224.
  32. White RE Jr, Forness TJ, Allman JK, Junick DW. Effect of posterior capsular repair on early dislocation in primary total hip replacement. Clin Orthop Relat Res 2001; :163.
  33. Demos HA, Rorabeck CH, Bourne RB, et al. Instability in primary total hip arthroplasty with the direct lateral approach. Clin Orthop Relat Res 2001; :168.
  34. Lee SH, Lim CW, Choi KY, Jo S. Effect of Spine-Pelvis Relationship in Total Hip Arthroplasty. Hip Pelvis 2019; 31:4.
  35. Ike H, Dorr LD, Trasolini N, et al. Spine-Pelvis-Hip Relationship in the Functioning of a Total Hip Replacement. J Bone Joint Surg Am 2018; 100:1606.
  36. Morrey BF. Difficult complications after hip joint replacement. Dislocation. Clin Orthop Relat Res 1997; :179.
  37. Leichtle UG, Leichtle CI, Taslaci F, et al. Dislocation after total hip arthroplasty: risk factors and treatment options. Acta Orthop Traumatol Turc 2013; 47:96.
  38. Gausden EB, Parhar HS, Popper JE, et al. Risk Factors for Early Dislocation Following Primary Elective Total Hip Arthroplasty. J Arthroplasty 2018; 33:1567.
  39. Dewal H, Maurer SL, Tsai P, et al. Efficacy of abduction bracing in the management of total hip arthroplasty dislocation. J Arthroplasty 2004; 19:733.
  40. Novikov D, Mercuri JJ, Schwarzkopf R, et al. Can some early revision total hip arthroplasties be avoided? Bone Joint J 2019; 101-B:97.
  41. Shah SN, Kaye RJ, Kelly NH, et al. Retrieval analysis of failed constrained acetabular liners. J Arthroplasty 2009; 24:54.
  42. Sutter EG, McClellan TR, Attarian DE, et al. Outcomes of Modular Dual Mobility Acetabular Components in Revision Total Hip Arthroplasty. J Arthroplasty 2017; 32:S220.
  43. Harris WH. Wear and periprosthetic osteolysis: the problem. Clin Orthop Relat Res 2001; :66.
  44. Kim YH, Park JW, Kim JS. Alumina Delta-on-Highly Crosslinked-Remelted Polyethylene Bearing in Cementless Total Hip Arthroplasty in Patients Younger than 50 Years. J Arthroplasty 2016; 31:2800.
  45. Hamilton WG, McAuley JP, Blumenfeld TJ, et al. Midterm Results of Delta Ceramic-on-Ceramic Total Hip Arthroplasty. J Arthroplasty 2015; 30:110.
  46. Kobayashi A, Freeman MA, Bonfield W, et al. Number of polyethylene particles and osteolysis in total joint replacements. A quantitative study using a tissue-digestion method. J Bone Joint Surg Br 1997; 79:844.
  47. Drees P, Eckardt A, Gay RE, et al. Mechanisms of disease: Molecular insights into aseptic loosening of orthopedic implants. Nat Clin Pract Rheumatol 2007; 3:165.
  48. Terefenko KM, Sychterz CJ, Orishimo K, Engh CA Sr. Polyethylene liner exchange for excessive wear and osteolysis. J Arthroplasty 2002; 17:798.
  49. Rubash HE, Sinha RK, Paprosky W, et al. A new classification system for the management of acetabular osteolysis after total hip arthroplasty. Instr Course Lect 1999; 48:37.
  50. Maloney WJ, Herzwurm P, Paprosky W, et al. Treatment of pelvic osteolysis associated with a stable acetabular component inserted without cement as part of a total hip replacement. J Bone Joint Surg Am 1997; 79:1628.
  51. Ferguson RJ, Palmer AJ, Taylor A, et al. Hip replacement. Lancet 2018; 392:1662.
  52. Katz JN, Wright EA, Wright J, et al. Twelve-year risk of revision after primary total hip replacement in the U.S. Medicare population. J Bone Joint Surg Am 2012; 94:1825.
  53. American Academy of Orthopaedic Surgeons. Modern metal-on-metal hip implants: A technology overview. December 2, 2011. http://www.aaos.org/research/overviews/Metal_On_Metal.pdf (Accessed on March 29, 2013).
  54. Griffin WL, Nanson CJ, Springer BD, et al. Reduced articular surface of one-piece cups: a cause of runaway wear and early failure. Clin Orthop Relat Res 2010; 468:2328.
  55. Langton DJ, Jameson SS, Joyce TJ, et al. Early failure of metal-on-metal bearings in hip resurfacing and large-diameter total hip replacement: A consequence of excess wear. J Bone Joint Surg Br 2010; 92:38.
  56. Browne JA, Bechtold CD, Berry DJ, et al. Failed metal-on-metal hip arthroplasties: a spectrum of clinical presentations and operative findings. Clin Orthop Relat Res 2010; 468:2313.
  57. FDA Medical Devices: Metal-on-Metal Implants. http://www.fda.gov/medicaldevices/productsandmedicalprocedures/implantsandprosthetics/metalonmetalhipimplants/default.htm (Accessed on March 12, 2013).
  58. Pinson ML, Coop CA, Webb CN. Metal hypersensitivity in total joint arthroplasty. Ann Allergy Asthma Immunol 2014; 113:131.
  59. Sedrakyan A, Normand SL, Dabic S, et al. Comparative assessment of implantable hip devices with different bearing surfaces: systematic appraisal of evidence. BMJ 2011; 343:d7434.
  60. Galea VP, Laaksonen I, Matuszak SJ, et al. Mid-term changes in blood metal ion levels after Articular Surface Replacement arthroplasty of the hip. Bone Joint J 2017; 99-B:33.
  61. Cooper HJ, Urban RM, Wixson RL, et al. Adverse local tissue reaction arising from corrosion at the femoral neck-body junction in a dual-taper stem with a cobalt-chromium modular neck. J Bone Joint Surg Am 2013; 95:865.
  62. Cooper HJ, Della Valle CJ, Berger RA, et al. Corrosion at the head-neck taper as a cause for adverse local tissue reactions after total hip arthroplasty. J Bone Joint Surg Am 2012; 94:1655.
  63. Graves SE, Rothwell A, Tucker K, et al. A multinational assessment of metal-on-metal bearings in hip replacement. J Bone Joint Surg Am 2011; 93 Suppl 3:43.
  64. FDA Safety Communication: Metal-on-Metal Hip Implants. http://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/ucm335775.htm (Accessed on March 12, 2013).
  65. MHRA Medical Device Alert MDA/2012/036 All metal-on-metal (MoM) hip replacements. http://www.mhra.gov.uk/Publications/Safetywarnings/MedicalDeviceAlerts/CON155761 (Accessed on March 12, 2013).
  66. Duncan CP, Masri BA. Fractures of the femur after hip replacement. Instr Course Lect 1995; 44:293.
  67. Greidanus NV, Mitchell PA, Masri BA, et al. Principles of management and results of treating the fractured femur during and after total hip arthroplasty. Instr Course Lect 2003; 52:309.
  68. Heck DA, Partridge CM, Reuben JD, et al. Prosthetic component failures in hip arthroplasty surgery. J Arthroplasty 1995; 10:575.
  69. Jazrawi LM, Della Valle CJ, Kummer FJ, et al. Catastrophic failure of a cemented, collarless, polished, tapered cobalt-chromium femoral stem used with impaction bone-grafting. A report of two cases. J Bone Joint Surg Am 1999; 81:844.
  70. Chao EY, Coventry MB. Fracture of the femoral component after total hip replacement. An analysis of fifty-eight cases. J Bone Joint Surg Am 1981; 63:1078.
  71. Galante JO. Causes of fractures of the femoral component in total hip replacement. J Bone Joint Surg Am 1980; 62:670.
  72. Zhu Y, Zhang F, Chen W, et al. Incidence and risk factors for heterotopic ossification after total hip arthroplasty: a meta-analysis. Arch Orthop Trauma Surg 2015; 135:1307.
  73. DeLee J, Ferrari A, Charnley J. Ectopic bone formation following low friction arthroplasty of the hip. Clin Orthop Relat Res 1976; :53.
  74. Ritter MA, Vaughan RB. Ectopic ossification after total hip arthroplasty. Predisposing factors, frequency, and effect on results. J Bone Joint Surg Am 1977; 59:345.
  75. Hürlimann M, Schiapparelli FF, Rotigliano N, et al. Influence of surgical approach on heterotopic ossification after total hip arthroplasty - is minimal invasive better? A case control study. BMC Musculoskelet Disord 2017; 18:27.
  76. Brooker AF, Bowerman JW, Robinson RA, Riley LH Jr. Ectopic ossification following total hip replacement. Incidence and a method of classification. J Bone Joint Surg Am 1973; 55:1629.
Topic 7973 Version 29.0

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