There are ~ 280k THA per year, with an estimated THA revision at 5 yrs is 4.1% [1]. Most common reason is instability (22.5%), loosening (19.7%), infection (14.8%) [2]. Addressing THA pain and other complications is best done via algorithmic approach. 

Pain is the most common symptom for nearly all complications.  Pain over greater troch (troch bursitis?, maybe too much offset), pain with hip flexion (iliopsoas tendonitis?, maybe too little anteversion); start up pain (loosening?: thigh pain is stem loosening, deep buttock or groin pain is acetabular); pain at all times of the day (infection?).  Maybe no improved pain since surgery, consider extrinsic causes (back or knee, peripheral vascular disease, sciatic nerve irritation, meralgia paresthetica, malignancy).  Persistent pain since surgery could also be intrinsic (infection, unstable implant – failed integration, malpositioned component). 

On exam.  Watch the gait.  Limp? Due to muscle weakness or pain or LLD.  Abductor deficiency is seen most commonly with the direct lateral approach.  When considering LLD, watch out for a fixed pelvic obliquity from adductor contractures or spinal disease which cause apparent, not true LLD.  Look at the incision for signs of warmth, redness.  Take the leg through ROM to look for instability or impingement.  Pain with resisted hip flex is iliopsoas tendonitis. 

1. Osteolysis (Aseptic Loosening)


Aseptic Loosening of implants is caused by osteolysis.  It is most significant factor limiting longevity of THA. Revision for loosening is 4x higher than next leading cause (dislocation at 13.6%), and its particularly problematic in younger patients [2].

While osteolysis is the primary cause of loosening, infection must be part of the differential diagnosis.

Osteolysis is bone resorption caused by the body’s response to particulate debris generated as the THA implant wears out.  Motion between any two components of the prosthesis (ie the femoral head and the acetabuluar liner, the head-neck junction of the femoral stem, or the liner and shell of the acetabulum) generates debris that floats around the joint.  This debris stimulates a host response.  Particles of metal, poly, or cement can all cause osteolysis, albeit different types of reaction.  

Historical Perspective: Osteolysis was first described by Harris in 1976 and it was attributed to “cement disease” [3], because it was observed around the femoral component, and this was what started the drive for cementless implants.  Yet after significant R&D, and development of cementless implants, osteolysis was still seen around the implants [4], and the histology was similar between cemented [5] and cementless implants [6].  Surgeons then looked for another cause of osteolysis and recognized that it was produced by wear particles.

stages of osteolysis 

1) Debris production (ie poly wear) is the initial stage (we talk about metal debris in a separate section because it behaves totally differently, see section).  Particulate debris in THA is produced by Abrasive and Adhesive wear (whereas the TKA produces delaminating wear: small fissures form within the poly). 

▪ Adhesive wear is two surfaces bonding together causing the softer material to “peel” off as a thin film onto the harder surface during motion.

Volumetric wear is a specific type of adhesive wear, and it occurs as the femoral head articulates with the cup liner, and the amount of wear is proportional to the femoral head radius squared (therefore larger femoral head = more wear..this is why the initial Charnley implants, which used conventional poly, used a size 22 femoral head).  Linear wear is caused by focused stress on a isolated part of the poly due to abnormal loading.  

▪ Abrasive wear occurs when a harder surface (which is never completely smooth) cuts or ploughs through a softer surface, like a cheese grater.  Both cause particle formation.  Most wear occurs superiorly in the cup (or at the rim in cases of impingement). 

The conventional PE wear from articulating with a Cobalt-chrome head is 0.10 mm/year. The ultramolecular weight poly (UMWPE, also known as highly-crosslinked poly) wear is about 0.02 mm/year.  What is the difference between conventional and UMWPE?  The quality of PE depends on the consolidation of PE (the shape is formed using compression molding), the preparation (irradiation causes extensive cross-linking which decreases susceptibility to oxidation and wear), and the packaging (poly is sterilized in inert gas to prevent free-radical formation…although it can oxidize over time within the body, which is the reason some poly contains Vit. E,, which theoretically eats up the free radicals generated with oxidation) [7] [8]. 

The debris then travels in the joint fluid and reacts with any area of bone that is in contact with the fluid (this is an important concept when considering whether to place acetabular screws as this hardware effectively increases the surface area of bone in contact with synovial fluid…referred to as the “effective joint space” [5], this concept also highlights the value of circumferential porous coating in the femoral stem, because it reduces the effective joint space by causing bone ingrowth and blocking the path of joint fluid around the implant). 

2) Immune Reaction & Bone Loss. Poly debris activates macrophages to initiate an inflammatory response by releasing the standard cytokines (ie TNF-alpha, RANKL, IL-6, and IL-1) that stimulate osteoclast activity, inhibit osteoblast activity, and promote progressive bone loss around the prosthesis.  Osteolysis is typically progressive.  Its often asymptomatic until catastrophic failure, which occurs in the form of sudden implant loosening or an acute periprosthetic fracture (due to severe bone loss, the bone breaks under minimal stress).  

Because osteolysis is a chronic issue that causes acute complications, it must be monitored with serial radiographs for progressive changes every 3 to 6 months.  Signs of large lytic lesions, significant progression, or loose implants are the indications for revision surgery (even in the absence of symptoms).  

clinical correlate: Plain x-rays typically underestimate the size of osteolytic lesions, with lytic lesion only visible on x-ray once 20-30% of acetabular bone loss has occurred [9]. 

3) Implant Loosening. There is no universal definition of loosening.  Many consider x-ray evidence (progressive radiolucency or implant migration) sufficient to diagnose loosening, while many require clinical decline to be included for diagnosis.  Lets consider the clinical and radiographic signs.

clinical correlate:  Loosening is considered when patients report “start-up” pain (pain with their first steps, which gradually resolves, suggesting that the implant moves, then settles into a stable position during weight bearing). 

-X-ray. The femur and pelvis have been divided into zones called Gruen Zones, which help to identify areas of osteolysis. The inter-oberver reliability is somewhat suspect and therefore, these zones are mainly for academic purpose and less useful clinically.  In general serial x-rays are performed,and changes in implant positioning, such as stem subsidence, provides the best evidence. The accepted diagnostic criteria for loosening is progressive radiolucency or implant migration.

▪ Radiolucent lines that progress >2 years after surgery, or new radiolucent lines over 1 mm are significant signs of loosening.  Thinning is not the only sign to look for.  Focal areas of high cortical density (radiopaque lines), especially around the collar or at the end of the stem, indicate non-uniform stress (ie pedestal formation at the calcar), which suggest loosening [10][11]. But remember that not all cortical thinning is osteolysis (age-related thinning, or stress shielding also cause thinning). Also, in a cementless implant, a “spot weld” found at the distal end of the stem is a sign of stable fixation.  In the acetabulum there are 3 zones of radiolucency, however, radiolucencies isolated to one or two zones is less specific.  Leopold et al found nonprogressive lucencies in over 50% of revised components that were performing well clinically. 

▪ Migration. Femoral component migration is best evaluated by comparing the position of the stem relative to the calcar on serial x-rays. Acetabular component migration (superior or medial) should similarly be examined. A loose acetabulum may also demonstrate changes in version or inclination. 

▪ Cement Implants. In cemented implants debonding or cement fracture will precede loosening (cement implants can loosen by fatigue fracture where cracks propagate into pre-existing pores of the cement mantle).  However debonding doesn’t always cause loosening.  For example, a supero-lateral lucency around the stem < 2 mm does not indicate loosening. Different with cemented implants. Changes at the bone-cement interface can just be remodeling rather than loosening, however, radiolucency at the implant-cement interface is loosening.  If there is rapid osteolysis or bone disintegration then be suspicious of infection.

Cemented Femur: look for complete radiolucent line and implant migration.  An incomplete radiolucent line of 50-99% implant is only possibly loose.  Progressive radiolucent line around cement-bone interface is probably loose.  If radiolucency is <50% is unlikely loose if nonprogressive. The loosening rates for a cemented femur are impressively low, going back to the Charnley stem, survivorship at 20 years was over 95%, at 25 years about 89% and at 30 years about 82%.  

Femur side cememtless: many demonstrate some level of subsidence from initial position, and early subsidence < 5 mm usually leads to integration without problem, and the proximal taper allows for stable fit. 

Cementless Acetabulum: circumferential radiolucent line >2 mm or implant migration. 


Surgery? The decision to operate and the type of revision surgery is controversial.  First we must ask whether all osteolyis needs surgery? In the case of a loose implant, the answer is yes…revise the loose components.  But what about osteolysis with stable implant and an asymptomatic patient? Less clear.  The decision to operate on an asymptomatic hip depends on a few variables: rate of progression (delta); location of osteolysis; type of implant.  A number of studies have examined the timing for surgical intervention [12 - 15], there is no consensus statement, but there are guidelines. Even a few small areas of integration can keep a cup stable and thus patients remain asymptomatic despite expansile lesions [12] [15]. Yet progressive osteolysis will continue to reduce the area of integration until failure inevitably occurs.  Thus, in general, lesions that progress over 3-6 month period should be revised.  Femoral osteolyisis similarly remains asymptomatic until extensive synovitis occurs or impending fracture. 

Femoral Implant Revision.

Osteolysis causes different degrees of bone loss.  The Paprosky Classification was established to grade the severity of bone loss, which in turn guides treatment (different grades of bone loss require different implants to achieve stability).  

Acetabular Implant Revision:

An asymptomatic acetabular osteolysis with significant periprosthetic bone loss maybe be treated with a) implant removal and revision or b) implant retention with bone grafting of the defect and head/liner exchange.  Gross loosening of the acetabuluar cup requires full revision of the components.  Similarly to the femoral side, osteolysis of the acetabulum causes different degrees of bone loss.  There is also a Paprosky Classification for Acetabular Osteolysis to grade the severity of bone loss, which in turn guides treatment (different grades of bone loss require different implants to achieve stability).  

An asymptomatic acetabular osteolysis with significant periprosthetic bone loss maybe be treated with a) implant removal and revision or b) implant retention with bone grafting of the defect and head/liner exchange.

▪ Head/liner exchange may be considered if the components are well aligned [16].  Yet despite well aligned components there is still a 10% re-revision rate for liner exchange [17] vs. 2% re-revision rate after the cup is revised [18].  Yet other studies have found less significant differences in revision rates when the implants are well positioned [19].  In cases of malpositioned components, which may be accelerating wear, complete implant revision is probably indicated.

▪ Cup Revision: Many surgeons will fully revise a cup with significant osteolysis, all surgeons should revise a malpositioned cup with osteolysis and revise any loose cup.  The cup is loose if there is >2 mm of migration observed on serial x-ray, or if there are any signs of rotational changes, any screw breakage, or a radiolucent line (>1 mm) seen in all 3 zones [20] [21].  Acetabular components fail in two ways.  The either rock up and roll out posteriorly.  These are more often associated with posterior column defects and pelvic dissociation.  Failure can also occur when components roll up and in causing a superior medial defect.

Treatment based on Paprosky Classification.  Cavitary defects = loss of the cancellous bone, which is loss of cancellous bone.  Segmental defects = loss of the structural support of the acetabulum (cortical bone) and has a greater effect on implant stability

2. Metal-on-Metal

The history of Metal-on-Metal (MoM) implants goes back before Charnley, to the McKee-Farrar implant, which showed binary outcomes: either early failure due to loosening or excellent long-term survivorship > 20 years.  In fact, 110 of these hips were reexamined in 1990s and showed no signs of loosening [22].  Yet there were too many early failures and the design fell out of favor and paved the road for Charnley’s metal-on-poly design.  Yet two decades later, surgeons re-examined the MoM design because of that subgroup that showed excellent long-term function.  The potential for superior longevity with MoM was appealing at a time when poly implants were failing because osteolysis (a result of poor quality PE).  Improved technology in biologic fixation and implant manufacturing suggested a promising low-wear alternative to metal-on-poly implants, with the hope of improving wear rates and overcoming the barrier to long-term survivorship.  MoM quickly became incredibly popular in the USA, with over 50% of THA using this combination as recently as 2006.  As we know, the story doesn’t end well.

Registry data (out of Europe) started showing a 2-3x higher failure rates compared to metal-on-poly.  These failures were correlated with significant adverse tissue reaction from the metal particles generated by wear [23] [24].  While the overall wear rates are lower than metal-on-poly, the metal debris is considerably more reactive, and can lead to macroscopic muscle necrosis (abductor injury is particularly concerning), significant osteolysis, and large sterile cystic masses (called “pseudotumors”). Metallosis is defined as macroscopic staining, necrosis/fibrosis of periprosthetic tissue, and is associated with solid soft tissue masses, aseptic cysts, and significant soft tissue necrosis.  The terms ARMD (Adverse Reaction to Metal Debris) or ALTR (adverse local tissue reaction) are similar broad terms to encapsulate these soft tissue lesions [25]. The end result is that many designs were recalled and MoM has fallen out of favor.

Mechanics of Metal Wear. 

The success of metal-on-metal devices depends on a fluid-film layer that develops between components.  This film provides continuous lubrication and dramatically reduces wear (hip simulators showed encouraging wear rates < 10 μm).  Mid-polar contact and high bearing conformity are necessary for this layer to form.  The major factors involved with establishing a proper environment for fluid-film layer include: head size, cup position, amount of carbon in the metal, and the "clearance" (difference in diameter between the femoral head and the cup liner, with a goal of < 100 μm). 

Yet, outside the lab, real issues like improper sizing or cup malpositioning leads to intermittent disruption of this film layer causing spikes in friction causing spikes in torque forces causing motion at the head-neck junction causing wear called “trunionosis”.  This wear occurs through fretting and crevice corrosion (not abrasion). 

▪ Fretting: this is a mechanical wear from repetitive surface motion.  It occurs at any junction between two contacting surfaces.

▪ Pitting corrosion: Stainless steel and Titanium implants withstand corrosive wear by creating a “passive layer” which a non-reactive film of chromium oxide that forms when a metal is exposed to oxygen.  Yet when this surface layer is depleted by Fretting, the metal is exposed directly to the free radicals within the aqueous environment causing a chemical reaction that leads to breakdown of the metal. 

Interestingly the majority of wear in MoM is believed to occur at the head-neck junction (trunion), not at the femoral-acetabular articulation where other forms of wear originate. This theory is supported by comparing the metal resurfacing hips (which lack a head-neck junction) with THA, and which showed low ion levels in resurfacing hips despite large size femoral heads [29-30]. Of note, metal debris is still generated in resurfacing hips which indicates that wear occurs at multiple sites in a THA. 

The wear generates significantly more particles (13-500x more) and smaller in size (0.1-0.5 μm), and these particles attract lymphocytic reaction (unlike the macrophages in poly wear).  The plasma cells, B-lymphocytes release cytokines that create massive fibrin exudate and soft tissue injury.

Etiology of Tissue Injury 

There are two causes of this significant tissue reaction.

1) Cytotoxic local tissue effect of metal (accounts for vast majority)

2) Hypersensitivity reaction (especially seen in patients that experience groin pain without elevated metal ions) [26]. Diagnosis is the major problem because is no good test for hypersensitivity, (skin patch testing or lymphocyte transformation testing are questionable).  There is no direct evidence to link patients with metal allergy to higher failure or revision of TJA, and therefore the association between symptoms and allergy is only theoretical, and therefore the diagnosis of metal hypersensitivity in the face of persistent pain and synovitis is a diagnosis of exclusion.  There is a much higher chance of indolent infection and therefore full infectous work up (esr, crp, joint aspiration, possibly repeat aspiration or alpha-defensin), no need to obtain metal ion levels because they are typically elevated in patients with normal functioning implants. Patch testing and in vitro lymphocyte testing can be ordered to look for hypersensitivity, however, they are not proven to be reliable tests. [27, 28]. 

The key to determining the severity of an ALVAL (aseptic lymphocyte-dominated vasculitis associated lesion, which appears as a type IV hypersensitivity reaction in 0.3% of patients, more in females) lesion is multifold, different from an ALTR (adverse local tissue reaction).  Obtain cobalt and chromium levels. If elevated, then repeat the test.  If remains elevated then get soft tissue imaging.  Currently get annual follow up for any symptomatic patient.  Also annual follow up for any asymptomatic patient with a recalled hip, or a THA with a head >36 mm. Cobalt is certainly the more toxic of the two metals. Not all patients respond to the same levels of metal ions, each patient has a different threshold before they begin to demonstrate symptoms of metal hypersensitivity. 

mom implant.jpg


Knowing that MoM hips can potentially lead to very severe complications, how should surgeons approach these patients, and when should they intervene?  Should all MoM THA be revised?  Its believed that significant ARMD occurs in 1% of cases within 5 years.  Therefore revision everyone subjects a lot of patients to unnecessary surgery, however, not revising problematic MoM THA in a timely manner places patients at progressively higher risk for long-term complications. 

Currently, not all MoM hips are revised, and the decision to revise is based on a number of variables.  Importantly, there is not a single good test to detect problematic MoM hips, there is not a great predictive model.  The decision to revise is based on a number of variables (implant type, metal ion levels, symptoms, cup position), which help to risk stratify patients. 

Metal Ion levels.  There is no direct correlation between blood ion levels and metallosis (and this is probably the biggest issue to date with diagnosis of metallosis) [32-34].

Gross features of metallosis typically appear when blood cobalt metal ion levels >20 ppb in the blood, or even >17 ppb [35]. Yet ARMD can certainly occur in patients under these levels.  

Therefore, can metal ion levels be used to make decisions about revision? In the UK, the FDA-equivalent MHRA (Medicines and Healthcare Products Regulatory Agency) recommends that doctors obtain metal ion levels every 3 months, and if the patient is both symptomatic and levels >7 ppb…then revision.  To confuse the matter further ARMD can occur secondary to hypersensitivity at very low ion levels. Elevated ion levels may affect patients beyond their hip replacement, and case reports exist of neurologic and cardiac morbidities associated with high levels of metal ions [36].  To date, there are no studies correlating metal ions with carcinogenesis [37], although it remains a concern due to the effect of cobalt on DNA in laboratory studies and some argue that the over numbers are not high enough to detect cancer risk if it exists [38]…and for this reason MoM is avoided in women of childbearing age).

Symptoms.  Clinical symptoms of groin pain are suggestive of loosening, and trendelenburg gait is suggestive of abductor injury, with often indicate ARMD.  ARMD can also occur in symptomatic patients, despite low levels of metal ions.  Therefore, even in patients with MoM and low metal ion levels, the next step is to obtain a MARS MRI (metal-artifact reducing sequence magnetic resonance imaging) to look for signs of pseudotumor (which is indicative of ARMD). It is always important to rule out infection in any case of painful THA.  When obtaining an aspiration, a manual cell count must be performed because metal debris is mistaken for WBCs by the counting machine causing the number to be falsely elevated. 

What about asymptomatic patients with elevated ion levels? ARMD certainly can occur in asymptomatic patients, one study found pseudotumors in 60% of asymptomatic, and 57% of symptomatic patients, indicating that symptoms alone is not reliable [39]. 

Other patient risk factors include obesity and female gender (possibly related to increased risk of hypersensitivity).

Implants. Certain implants have higher rates of metallosis (such as the ASR by DePuy, Durom by Zimmer, Recap by Biomet).  Additionally, all implants are at increased risk for metallosis with malpositioning, specifically high inclination angle (> 50°) which causes edge loading, and increased combined anteversion (> 40°) which causes posterior impingement, both of which causes micro-separation and thus disruption of the fluid film layer. Other implant related risk factors is a large femoral head size in MoM THA (>28 mm), or a small head size in MoM hip resurfacing (< 50 mm). 


Revision surgery is recommended for signs of ARMD.  Studies suggest that pathology only worsens with time, and therefore revision of components should be performed in a timely manner. 


trunnionosis what is the trunnion in tha what is a morse taper for the femoral stem

Trunnionosis is a form of metal-on-metal wear that generates metal debris and has been shown to cause ARMD (adverse reaction to metal debris).   Trunnion wear is believed to be the underlying source of MoM implants, however, it continues to be the focus of investigation in Metal-on-Poly implants too.  Trunnionosis is increasingly a concern as surgeons continued to see the classic ARMD (ie pseudotumor) associated with MoM THA in metal-on-poly and ceramic implants.  Surgeons started to investigate how this could be occurring when there is no MoM interaction at the femoral head – cup interface. It appears that despite changing the metal cup, the primary source of metallosis (even in MoM hips) was the head-neck taper, and this metal-on-metal connection still exists in the Metal-on-Poly design.  This wear is particularly elevated in the “dual modular designs” (meaning that there is a junction at both the head-neck and the neck-body).  The extra implant articulations are sites of increased motion that can generate wear particles.  There was a dramatically increased incidence of ARMD in these implants [40], and some (ie Stryker ABG/Rejuvinate) were recalled.

Trunnionosis is a clear risk in the dual modular designs, but it is also emerging as a risk in standard THA.  Retrieval studies examined the head-neck junction of multiple THA designs and have identified varying degrees of taper corrosion.  Taper corrosion is the mechanically assisted crevice corrosion.  The mechanical micromotion between the neck and neck destroys this electrochemical barrier that coats the neck taper (fretting corrosion), allowing fluid into the small porous which destroys the metal (called fretting assisted crevice corrosion).  Mild to moderate fretting is seen in about 80% of heads (female side); and 50% of trunnions (male side), meaning this type of wear is fairly common overall.

Trunnionosis appears to be a particular problem in large femoral heads (> 36 mm heads) because larger heads create a greater lever arm at the head-neck junction, thus increasing micromotion.  The excellent wear characteristics of highly-crosslinked poly has allowed the use of larger diameter heads to improve stability without the risks of volumetric wear, however, trunnionosis may be a previously unrecognized side effect. 


Instability is the 2nd leading cause of THA revision (22% of revisions nationally [2]) and remains a notable problem despite some implant advances, such as dual mobility cups.  The risk of dislocation in primary THA is roughly 1% at 1 month, 2% at 1 year, then an additional 1% every 5 years (7% at 25 years). [41, 42] . The risk of dislocation in revision THA is significantly higher: 5-7% within the first year.   

Risk factors

▪ Patient based risk factors include females, prior hip surgery (2x increased risk), neuromuscular disease, inability to comply with hip pre-cautions such as alcohol abuse (4x increased risk) and cognitive impairment (such as dementia), older age (especially those over 80 years old), and THA for treatment of osteonecrosis or acute femoral neck fracture (the idea being that an acute need for hip arthroplasty does not give the capsule and surrounding tissue time to thicken and act as a strong soft tissue support as seen in gradual osteoarthritis progression). [43] [44]           

▪ Surgical based risk factors relate to the approach (controversial) as well as the components and their positioning (also controversial). 

Femoral head size.  Remember that larger head size increases both jump distance and arc before motion before impingement and therefore, in theory, decreases dislocation risk.  In general, the rate of dislocation from primary THA is steadily declining since the 90s, and this correlates with the gradual increase in average femoral head size.  Furthermore, one study demonstrated that larger femoral heads were associated with lower dislocations, particularly when using the posterolateral approach (with a 12% dislocation risk in 22-mm heads at 10 years vs. 6.9% for 28-mm heads vs. 3.8% for 32-mm heads [41]).

The benefit of increasing femoral head size to treat instability during revision THA has also been demonstrated [45] [46].  Both the combined theoretic and academic evidence supports the correlation between increased femoral head size and stability.

Yet a larger head size is not all sunshine and theres no free lunch in medicine.  Although highly cross-linked poly doesn’t appear to generate greater volumetric wear with larger head sizes [47]…there does appear to be a correlation between femoral head size and torque at the head-neck trunion, with risk of increased metal debris. Additionally, larger head size requires larger cup size, which in turn requires greater acetabular bone resection (some studies promoting larger heads utilized thinner metal cups as the bone-conserving solution, yet these metal-on-metal implants have since fallen out of favor).  

Component Positioning. The components must be positioned so that implant arc of motion is centered in the patients functional hip motion. The classic paper by Lewinnek describes the safe-zone of component positioning: Cup inclination 40° ± 10°,  Combined Cup-Stem anteversion 35° ± 10° (see basic concepts) [48].  In theory, this safe zone maximizes hip range of motion before impingement occurs (impingement causes the femoral head to lever out of the joint).  However, studies comparing component positioning in stable vs. dislocated hips have shown no difference in component placement [49, 50]. While its agreed that a general adherence to standard cup version and inclination is important to prevent dislocation, these studies demonstrate that positioning is not the only variable at work…patient related factors have a big impact on stability and the true “safe zone” may not be the same for all patients.  The role of pelvic tilt has become integral to this conversation of a “physiologic safe zone”.  

biomech 2.5 cup.jpg

Soft tissue envelope. Dislocation rates for the posterior approach decrease dramatically when the soft tissue is repaired.  Furthermore, many argue that the Anterolateral and Direct Anterior improve hip stability by preserving soft tissue.   

Yet the Abductor Complex remains the most important soft tissue restraint to dislocation. 

The Abductor complex pulls the head into the socket, and its absence leads to instability that is the hardest to control.  Increasing the hip offset places greater tension on the abductors and can increase stability.  Alternatively, a greater trochanteric advancement, performed by Charnley in all his THA, will increase tension on the abductor complex by moving its insertion point distally. 

In the revision setting, fracture of the greater trochanter can lead to “troch escape” whereby the entire abductor complex insertion migrates proximally taking tension off the muscle and causing a Trendelenberg gait and hip instability.

Surgical Approach. The effect of surgical approach on risk for instability remains controversial.  The importance of the soft tissue envelop for stability is well recognized. 

The posterior approach without soft tissue repair has the highest rate of dislocation (between 4-9%, which is 6-8x higher than an anterolateral approach, “Watson-Jones”), however, with meticulous soft tissue repair, dislocation rates approach to levels comparable to other surgical approaches [51]. One study showed that components were 3x more likely to be within the safe zone in a posterior approach, and yet there remained a significantly higher dislocation rate [49].  This presents an interesting contrast with regard to these 2 important variables for hip stability.  One may argue that great emphasis is placed on component positioning, because this is something that surgeons can control and can measure postoperatively.  Yet increasing evidence highlights the greater importance of soft tissue in preserving hip stability.

The Direct Anterior approach (“Smith-Peterson”) may have a lower risk of dislocation compared to posterior, but this remains controversial [52] [53] [54]. The DA preserves soft tissue and avoids abductor release, which likely promotes greater stability (although it is associated with higher rates of intraoperative femur fracture). The role of hip precautions in with the DA approach is not required, suggesting increased stability due to less soft tissue injury [55]. 


Many surgeons abide by the three strikes and your out rule; meaning surgical intervention is required if the hip dislocates more than 3 times.  Planning for surgery requires looking at leg lengths, offset, the abductor strength, and implant position (a CT to best evaluate version if thats a concern [58]).

Most 1st time dislocations are managed nonoperatively with the goal of limiting hip flex to 40°, maintainat least 10° abduction, and prevent internal rotation. While theres no good evidence to suggest that a brace reduces dislocation rates, they may have some benefit in reminding some patients to be mindful and can thus be worn for 4-6 weeks after dislocation[57].  

Operative options depends on the problem, but always remember that instability is main complication following revision surgery, so it can be easy to get caught chasing your tail if your not effective at identifying and solving the problem. 

If the components are well positioned, then look for soft tissue insufficiency.  A larger femoral head can increase jump distance, or an elevated rim can provide a buttress to prevent posterior dislocation (but it risks component impingement and dislocation in the countercoup direction).  Increasing offset can help by placing abductors under greater tension.  This can be achieved through an offset liner, or by changing the femoral component to a High Offset neck (which has a neck angle of 115°, as compared to 125-135° in a standard neck, which increases the abductor lever arm but also affects leg lengths).  A trochanteric advancement similarly places the abductors under greater tension, but has notable complications (troch escape syndrome). 

A more severe abductor deficiency (which should be evaluated with Trendelenburg Test, and EMG) may require a constrained liner for low demand patients…low demand is key because the constraint decreases joint motion and transfers increased force to the component-bone interface and thus increases loosening rates).  Dual mobility cups also provide stability for severe abductor deficiency, and have promising results, particularly in the more active population (although there is concern for higher rates of debris generation with the two articulations). 


The timing of dislocation relative to the index procedure is important. The majority occur in the first 4-6 weeks (60%) and the prognosis is better with earlier dislocations, with an 33% risk of further dislocation.  In comparison, dislocations occurring after 6 weeks postop (called a “late dislocation”) have a 55% recurrence risk [56]. Incidence of repeat dislocation increases with sequential dislocations.

3. Periprosthetic Fracture

intraop Periprosthetic fracture

postop periprosthetic fracture

The lifetime risk of a periprosthetic fracture (PPF) is relatively low, the Mayo Registry [59] [60] reported rates of 0.3% in cemented stems and 5.4% in press-fit stems, while other reports suggest about 1% for primary THA and 4% for revision THA.  It appears that press fit implants have a higher risk of fracture, although it appears an age-related correlation, whereby patients older than 70 years had a 2.9x risk compared with younger patients, and those over 80 years had a 4.4x risk [61] as compared to cemented stems, which have no age correlation [62].

The key determinants of treatment include: 1) Fracture location, 2) Implant Stability; 3) Bone Stock. These 3 factors are the key points of the Vancouver Classification, which guides treatment decisions [63] [64].

Fracture location.  Location falls into three regions.  1) metaphyseal.  2) diaphyseal at the level of the implant; 3) diaphyseal but below the implant. Location is important because it helps determine whether the implant is loose… 

Is the Implant Loose? This is the million dollar question. Fractures of the greater troch (Vancouver A) generally do not cause implant loosening.  Fractures completely distal to the tip of the stem (Vancouver C) similarly do not cause implant loosening.  In such cases, the implant is retain and the fracture is treated as an isolated incident. 

In contrast, fractures along the length of the prosthesis (Vancouver B), usually, but not always ,cause implant loosening.  The challenge is that its not always easy to identify loosening.  And it is critical to identify an implant that is loose because, if its missed, the revision surgery will fail.  In fact, studies show higher revision rates for Vancouver B1 fractures (“stable implant”), compared to Vancouver B2 fractures (“loose implant”)…probably because many of the B1 fractures were not truly stable and the implant was subtly loose, and they were misdiagnosed and subsequently failed because they underwent the wrong surgery.  Therefore, a fracture around the implant should be considered loose until proven otherwise.   

Loosening is evaluated both pre-op and intra-op.  Preop evaluation involves looking at the x-rays and comparing them to pre-fracture x-rays for signs of subsidence. Intraop evaluation involves attempting to remove the stem.  The general idea is: “If you can knock it loose, then it was loose to begin with”.  Also, if the fracture has occurred within 6 weeks of the index procedure, the stem is loose a priori because ingrowth requires at least 6 weeks to occur.   

Bone stock.  Assessing the bone stock is critical in selecting the proper prosthesis.  Periprosthetic fracture most commonly occur in the elderly with significant osteoporosis, or in people with significant osteolysis, which has made the bone thin and highly susceptible to fracture.   If the stem is loose and needs revision, it is critical to select the proper implant based on bone stock, because remember that many femoral implants will fail without the proper bone stock [65]. The Vancouver Classification takes bone stock into account, yet the Paprosky Classification is the best guide for correlating bone stock with implant selection. For a full discussion of Femoral Bone Loss, see the section on Osteolysis. 

-Type A: usually due to osteolysis.  Subclass based on Greater Troch vs. Lesser Troch.  Greater Troch with <2.5cm displacement is protected weight bearing 3 months.  >2.5 cm, risks nonunion, thus ORIF [66]. Lesser troch fx is rare, little consequence, just treat symptoms [67]

-Type B: Fracture around the stem.  First determine implant stability, look for loss of height or loss of offset due to implant subsidence, often best to compare to pre-fracture x-ray. 

B1 is a stable implant, and req. ORIF [68].  However, theres shown a higher failure rate with B1 vs. B2 which suggests that many B1 were actually unstable and misdiagnosed, and therefore its critical for the surgeon to fully evaluate the implant during surgery to determine stability, must prove its stable. [69] [70]  

B2 is loose implant, req. revision to long-stem that bypasses the fracture by 2 cortical diameters.  Its best to place a cerclage calbe at the most proximal aspect of intact distal femur to ensure that there are not hairline fractures that could propagate distally and prevent fixation.  Use a tapered fluted stem rather than a cylindrical stem (decreases intraop fractures).  Excellent healing rates. [71] 

The third type a B3 takes into account the bone stock.  These are periprosthetic fractures with poor bone stock and loose implant, and thus require long-stem and allograft or a modular proesthesis, and are considerable more challenging to treat. 

If there is more than 4-6 cm of scratch-fit in the diaphysis then use an extensively porous-coated component, but use noncemented tapered fluted stem if there is <4 cm scratch-fit diaphysis. 

-Type C: Occurs distal to stem, ignore the stem and perform ORIF, such as using LISS plate, overlap with stem of implant to ensure no stress risers.

Outcome. The functional outcome after successful fracture fixation is generally poor [72], with scores worse than THA revision for aseptic loosening [73]. Furthermore, the 1-year mortality rate is about 11% (as compared to 2.9% after elective THA, [74]). Looking at the age-related association with this complication, it appears that older and older patients, with weaker and more osteoporotic bone, and are more medically frail, experience this complication.  Therefore, the high mortality rate may be less an indication of the injury severity versus an indication of the unhealthly patients that suffer this complication.  

4. DVT

Deep Venous Thrombosis (DVT)  remains a significant concern in TJA because it can lead to Pulmonary Embolism, one of the few life-threatening complications after TJA (its the 2nd cause of mortality following cardiac events) [128] [129]. All patients undergoing TJA are deemed “High-Risk” for VTE complication, although patient risk factors allow for further stratification of risk of VTE.  

Incidence of DVT.  There is a significant difference between the rate of overall DVT versus the rate of symptomatic DVT.  A recent Japanese study examined VTE rates at Postop Day 10 via doppler of all TJA patients and found a significant discrepancy between rates of overall and symptomatic VTE in both THA and TKA [124].  In THA, overall vs. symptomatic DVT 12.6% vs. 0.2%.  In TKA overall vs. symptomatic was 24.3% vs. 0.9%.   A similar study from Europe also identified a large difference DVT [130].  Older studies using venograms to evaluate for DVT similarly found overall DVT rates between 20 – 60%, with over 50% occurring in calf veins.  In general, the overall rate of VTE varies widely (often reported around 20 - 40%, despite DVT prophylaxis), while the rate of symptomatic VTE is roughly 5% (ranges between 1 – 10%). PE occurs in 1-2% of patients, and fatal PE occurs in about 1 in 1,000 cases (0.1%).

 Thromboprophylaxis has dramatically reduced the incidence of VTE.  In patients receiving no VTE prophylaxis, the overall rate of VTE varies from 40 – 60% [133] [134] [135], significantly higher than the aforementioned rates in patients treated with prophylaxis. The overall rate of PE in patients without anticoagulation is 0.5-2.0% PE and 0.1-0.5% fatal PE.  

Health care management studies, looking at VTE rates beyond TJA procedures, have also found this large disparity between symptomatic and silent DVT, and remark “the more you look, the more you find”...reflecting a correlation between aggressive VTE monitoring (using Doppler surveillance) and higher VTE rates [131], similar to the "Observer Effect" - the measurement of a system cannot be made without affecting the system.  

As a result, while advances in doppler technology and compression protocols have improved DVT detection to reliably replicate gold standard invasive vascular studies [132], AAOS, AAHKS and ACCP guidelines discourage the routine use of Doppler screening in all TJA patients because the significance of DVT, particularly in the asymptomatic patient, is unclear.  The true incidence of VTE is high, yet because a large percentage are clinically silent (between 50-80%), the rate of clinically significant VTE is very low.  

TKA is generally associated with a higher rate of overall and symptomatic DVT.  It is also possible that the use of tourniquets in TKA increase hypercoaguability and are thus partially responsible for increased rates. Its also possible that normal postoperative symptoms in TKA (such as lower leg swelling, bruising, and pain) are mistaken for DVT symptoms, leading to higher rates of DVT screening and thus higher rates of “symptomatic DVT”.  

Timing of VTE.  When does VTE occur in the postoperative period?  This is also debatable.  While many argue the thrombotic event occurs soon after surgery (when the pro-coagulation pathway), other data suggests that it occurs a few days after surgery. 

Januel et al. reported symptomatic VTE rate of 0.53% in THA and 1.09% in TKA while patients were hospitalized postop [136].   Risk of PE was 0.14 to 0.27%. Other studies have found slightly higher rates of PE with 0.6% in THA and 1.47% in TKA during the hospital course [137]. Parvizi et al reported that 80% of PE occurred within 3 days of index surgery [138].  Yet other reports suggest 70% of VTE is diagnosed after hospital discharge. A study of 5,000 patients found the average DVT in THA occurred at 21 days, and PE at 34 days, while the average TKA DVT occurred at 20 days, and PE at 12 days [133].  The variability between studies highlights the general challenge in identifying clinically significant VTE.


AAOS, AAHKS do not provide treatment recommendations.  ACCP does provide treatment recommendations.  The challenge is that much of the data on VTE treatment, and risk of DVT progression, is not specific to TJA, but rather extrapolated from studies on other surgeries.  It is therefore unclear how these recommendations translate to TJA cases. Orthopedic surgeons must weigh the benefits of treatment with the known risks of bleeding that comes with prolonged anticoagulation of a postop patient.  The ACCP treatment recommendations do not appear to balance this risk/benefit ratio as they are not speaking specifically to TJA cases.

How do we know which DVTs are significant and which need to be treated? Do we treat all DVTs the same? It is challenging to reconcile the large disparity in numbers: 20-40% overall DVT (high prevalence) and 5% symptomatic DVT (moderate prevalence), 1% PE (low prevalence) and 0.1% fatal PE (very low prevalence).  

Do we care about DVTs themselves, or do we really only care about DVTs because of their risk of becoming a PE?  Are DVTs accurate markers for patients at risk for PE? The risk, the actual number of DVTs that propagate to PE is incompletely understood.  DVTs are not created equally.  A large above-knee DVT is different than a small calf vein DVT.

Lotke et al. used venograms and V/Q scans to correlate the relationship between DVT and PE [164].  They found, similar to other studies, that despite DVT prophylaxis, a high incidence of infrapopliteal DVT (IDVT), nearly 50% of patients [165].  These thrombi were 2.5x more common in TKA, yet the overall rate of PE was the same in THA and TKA.  These findings suggest a low correlation between IDVT and PE risk. It suggests that IDVT are not clinically significant. In contrast, there was a significant correlation between Popliteal/Femoral Vein DVT and PE, likely due to the larger caliber of these veins and thus larger sized clots.  Larger clots are more prone to propagate.

Yet the picture is not so clear for these isolated calf DVTs. Haas et al. studied over 1000 TKA patients with venography and V/Q scans, found a similar rate of 50% calf DVT, and found a significantly greater risk of symptomatic and overall PE in patients with calf DVT compared to patients without clot. Of the 655 patients with calf DVT, 11 (1.7%) had symptomatic PE, while only 1 (0.2%) of 498 patients without clot presented with a symptomatic PE [166]. Thus the treatment of calf DVTs remains controversial.

If the goal of VTE treatment is prevent the devastating complication of a symptomatic PE, is DVT even the best marker for PE risk? Other studies have demonstrated that cancer, congestive heart failure, and thrombophilia disorders have a much higher correlation with PE risk, with PE occurring in up to 10 – 30% of cases [129]. Parvizi et al reported on >26,000 TJA cases and found 1.1% risk PE with 0.2% fatal PE.  Risk factors for PE include obesity, higher Charlson Comorbidity Index, presence of DVT, TKA (vs. THA), COPD, and depression [167]. Bohl et al. found similar risk factors[168]. Thus DVT appears to be one of many risk factors.  It appears that there are many factors that influence how to treat a DVT.

Returning to the ACCP guidelines, VTE treatment recommendations are:

2.3.3. In patients with acute isolated distal DVT of the leg who are managed with initial anti- coagulation, we recommend using the same approach as for patients with acute proximal DVT (Grade 1B).

They do not distinguish between size or location of the clot.  The emphasis is on the fact that any patient being anticoagulated, that still presents with a clot, should be considered at higher risk for propagation.  Again however, this does not appear to be specific to orthopedic/TJA patients.

5. Prosthetic Joint Infection

Periprosthetic Joint Infection (PJI) is a cause of significant morbidity and mortality.  The preoperative patient optimization protocols (see preop optimization) were created in a large degree to minimize infection risk due to its correlation with obesity, diabetes, metabolic syndrome, malnutrition, smoking, and s.aureus colonization. While PJI in THA (0.3 – 1.3% primary, and 3% in revision THA) is less common than TKA (1 – 2% primary, and 6% in revision TKA), it remains an important complication.  Additionally, PJI should always be a part of the differential diagnosis when evaluating postop patients for pain, loosening, instability or even periprosthetic fracture. 

What is a PJI?  This seems obvious: the prosthesis is infected with a microorganism. Yet diagnosis of PJI is far more challenging in reality because positive cultures are not a reliable means of diagnosis, with reports suggesting that cultures are only 60% sensitive. There are other complicating factors.  For example, what if you see “gross purulence” around the implant, can you just say that its infected?  The answer is that “gross purulence” alone (with other tests negative) is not enough to diagnose an infection because many of the MoM soft tissue reactions appear very similar to “gross purulence” and osteolysis from poly wear can also appear as purulence, an thus will fool a surgeon’s into treating an infection.  So if you cannot trust your eyes and you cannot trust cultures, what can you hang your hat on to say that a joint replacement is infected?

The Musculoskeletal Infection Society (MSIS) Diagnostic Criteria was developed to formalize the diagnosis process [75]. , It offers a good foundation for PJI diagnosis.  Yet controversy remains even with this algorithm, specifically regarding what cutoffs should be used for certain lab values (cutoff values are essentially a compromise between sensitivity and specificity and there are no absolutes, outliers always exist).

Infection is diagnosed as 1 major criteria (either sinus tract or 2 cultures of the same bacteria), or 3 out of 5 minor criteria (elevated ESR/CRP, elevated synovial cell count or Leukocyte Esterase, elevated PMN%, one culture, positive histology)


Identifying symptom duration and time from index procedure are two critical forks in the diagnostic and treatment pathways [76].  PJIs are best understood by separating them at these time points.  First see what category the patient get sectioned into and then work them up accordingly. For example, an early infection (surgery < 4 weeks prior) compared to a late infection, the CRP cut off jumps from 10 to 95 mg/L, while cell count jumps from 3,000 to 10,000, and PMN% increases from 60-70% to over 80%.  This is why it is critical to know the date of surgery before interpreting any results. 

When patient presents with concern for infection, knee swelling, fevers, pain, erythema, drainage, etc.  The first step is to obtain blood work including ESR, CRP.  If inflammatory markers are elevated, then obtain aspiration.  If inflammatory markers are not elevated, but there is notable concern based on the h&p, then aspirate as well (remember the blood work is only about 90% sensitive).  In cases of acute onset of symptoms, it is believed that the bacteria is limited to the joint fluid, while chronic symptoms suggest the bacteria has had time to adhere to the prosthesis (biofilm) and invade the interface between bone and implant.

ACUTE EARLY.  Acute postoperative infection is onset of symptoms 4 weeks from the index procedure. The distinction of an early infection is important because the cutoff values for many of the tests used to diagnose a PJI change in the early postoperative period.  Synovial leukocyte levels do not normalize for about 6 weeks, and therefore WBC cell counts for aspiration are elevated at baseline.  Furthermore, the systemic inflammatory markers are elevated.  It takes around 3 weeks for CRP to normalize, and over 6 months for ESR to normalize.

Diagnostic values.  Elevated CRP in the early postoperative period is > 95 mg/mL.  Aspiration cell count over 10,000 and 89% PMN are considered elevated.

Treatment see below.

LATE. Onset of symptoms more than 4 weeks from the index procedure, but usually it occurs years after surgery.   A late infection occurs when the inflammatory phase of the primary surgery has resolved and is no longer a confounding variable when interpreting the lab results. The lab values can also be used in patients with inflammatory arthritis. Acute Late (Hematogenous).  This is acute onset (< 3 days) of symptoms long after the index procedure (> 4 weeks). Patients seen in the office after acute onset of symptoms need to be worked up quickly to maximize the benefit of surgical intervention if they are showing signs of PJI. Acute onset of symptoms suggest the bacteria has not formed a biofilm, although bacteria form the biofilm at different rates (with all bacteria forming biofilm by 4 weeks).

Diagnostic. Blood work: CRP > 10 mg/L, ESR > 30. Aspiration: WBC count > 1,700; PMN > 80%

Chronic Late. This is gradual onset of symptoms (> 3 days), long after the index procedure (> 3 weeks).  In the case of chronic symptoms it is believed that bacteria has formed a biofilm (all bacteria form biofilm by 4 weeks).  Biofilm is a layer 15% cells and 85% glycocalyx (formal name: exopolysaccharide glyocalyx) that makes the infection 1,000 – 1.5k more resistant to antibiotics. Furthermore, there is no reliable way to remove biofilm once formed.  Thus, chronic infections require removal of the infected implants


Inflammatory markers. The ESR is an acceptable marker for late infections, however, it cannot be used in the immediate postop period (“acute early” infections) because ESR requires up to 6 months to return to normal.  It is therefore falsely elevated.  CRP in contrast returns to normal around 3 weeks, and can often be used in the decision making algorithm [77].  Even in possible late PJI, the ESR is only a questionably valuable marker, and therefore, it must be positive in conjunction with the CRP to achieve a sensitivity and specificity over 90%.

ESR and CRP levels are important precursors to joint aspiration for a few reasons.  ESR and CRP are highly sensitive and therefore, if they fall within a normal range, its ok to stop the work up for infection unless highly suspicious. There is the risk of introducing bacteria into a THA with aspiration and therefore, every patient with a fever and a THA should not get an aspiration.  Additionally, no test is perfect and some aspirations can be falsely positive.  However, aspirations that are preceded by inflammatory markers influences the positive predictive value and thus reduces the risk of unnecessary major surgery [78].

Aspiration. What is a significant cell count upon aspiration.  This remains controversial.  A WBC count suggestive of infection is considerably lower than for a native knee because there is less synovial lining for neutrophils to penetrate the joint.  Studies have suggested a cell count > 3,000 is indicative of a late infection [79]. Other studies suggest an even more sensitive cutoff of 1,700 cells, with anything over 65% PMNs [80].  These values however can only be used in late infections (> 6 weeks from index procedure) because synovial leukocyte levels do not normalize until then.  Therefore in Early infections the recommended cutoff is a cell count of 27,800, 89% PMN (and CRP > 95 mg/mL) [81]. 

Notice that gram stain is not part of the MSIS criteria.  The sensitivity is too low to be helpful and should not be included in the work up [82].

Intraoperative culture: In cases of revision surgery, a single positive culture is insufficient to diagnose an infection.  These findings should be used in conjunction with other tests for diagnosis.


The goal of treatment is eradication.  This goal is challenging because bacteria form a biologic matrix around the hardware components that prevents antibiotics from reaching the bacteria.  The duration of infection (time since symptom onset) and type of bacteria both determine how advanced this glycocalyx matrix has become, and thus whether the components need to be removed.  The success of differing treatments depends on the type of bacteria and the duration of infection.  Lets look at treatment for each of PJI groups.

Acute Early Infection.  Consider I&D with poly exchange, followed by 6 weeks of IV antibiotics [83].  Studies suggest a 50% cure rate in the acute period.  However, there is a high failure rate with MRSA [84], reported around 85% failure, and therefore, 2-stage revision should be considered based on bacteria[85, 86]. 

Acute Hematogenous Infection.  Approached the same as an acute early infection (due to similar impact of bacteria and timing on matrix formation). It is best to prevent late infections by giving antibiotics before dental procedures (although the correlation between dental work and acute hematogenous infection is unclear because the organisms cultured in the synovium are rarely the same ones commonly found in the mouth).  [87]

Chronic late infection. The standard treatment is a 2-stage exchange.  The emphasis in the first stage is removing all infected material, performing an extensive debridement, opening the tibial and femoral canals, and placing an antibiotic spacer [88].  The second stage is implanting hardware that offers stable, functional knee.  The cure rate is about 80-95% (depending in part on the organism). 

STAGE 1. Dr. Duncan performed a lot of the primary groundwork investigating the elution of antibiotics in cement [64, 89-95]. Currently there is significant variability in the literature with regards to antibiotic spacer dosing, but these incremental changes derive from the initial work by Duncan et al.

The antibiotic spacer contains variable types and amounts of antibiotic.  The standard is 3-6 g of vancomycin and 1.2 g of tobramycin per package of cement.  The combination increases the rate of elution into the knee.  Thicker cement, like palacos, elutes the abx more rapidly, and thus it creates a higher concentration of antibiotic in the joint, and also in the blood stream and it therefore must be monitored closely.  Simplex does not elute as well and therefore it can have higher concentration of abx without worrying about toxic levels.  Spacers also come in two forms: static vs. dynamic. Static spacers should be held in place with a styman pin that goes up the femoral and tibial canals to prevent the spacer from being extruded from the joint and eroding through soft tissue, such as the patellar tendon.  The more popular type is a dynamic spacer.  This has the advantage of allowing for knee ROM to prevent stiffness once replant occurs.   

The spacer remains in place for 6 - 8 weeks.  Following Stage 1, the patient receives IV antibiotics for 6 weeks. Serial ESR/CRP is performed and should trend down (but often fails to normalize) [96].  

A repeat knee aspiration is performed around 8 weeks (after 2 weeks off antibiotics), and a cell count of 3,000 should be utilized as a cutoff for response to intervention.   

STAGE 2: Reimplantation of TKA.  Often times a more contrained design is required due to soft tissue attenuation or destruction during the process of irradicating the infection, and the bone loss associated with removing implants. 

One-stage exchange for chonic late infections is commonly used in Europe, but is not the standard in the United States.  In this technique, the components are explanted and a vigorous I&D is performed (read: significant tissue debridement, almost skeletonizing the remaining bone: collateral ligaments are often resected, and the revision TKA is a rotating hinge). The patient is then re-prepped, re-draped, and new components are placed.  In these cases, the bacteria is always known preoperatively, its typically not performed for MRSA infections, and it is performed in generally healthier patients.

Avoid I&D in chronic late infections due to high failure rate and added damage to the soft tissue envelope with multiple I&Ds, which may risk outcomes for 2-stage [97].  One study found worse outcomes in patients with failed I&D who then required a 2-stage procedure, suggesting that either an I&D independently impedes recovery from further surgical procedures or it merely selects patients with a more virulent organism (already resistant to I&D) who are therefore more likely to fail 2-stage. 

The entire process of revision surgery with abx spacer and final replant takes its toll on the patient.  Revision for TJA has higher mortality rate than other revisions [98]. Overall, the results for revision TJA for infection isn’t terrific, but functional spacers have improved results. [99]

JAAOS Review Infection TKA:[103]; [104]


Infections are clearly very challenging and thus the key is prevention.  Optimize patients.  Take precautions in the OR to minimize risk.  Give preoperative antibiotics.  Number needed to treat to prevent 1 infection is only about 50 patients. [105].  About 10% of Americans believe they are allergic to penicillin, while only 10% of those patients have any true reaction, and most can safely receive any beta-lactam antibiotic [106].  This is an important fact because Ancef (cefzolin) has a proven track record of offering good coverage [107]. Drug distribution in obese patients decreases due to the greater volume of tissue.  It may lead to unacceptably low blood levels, and thus doses should be increased in the obese patient.  High doses of ancef can be administered rapidly, however, vancomycin must be infused slowly (90 – 120 minutes) to avoid the potential complication of red man syndrome, and thus may complicate the timing of a surgical day.  The question of whether vancomycin should be used in high risk patients?   

6. Thigh Pain

Thigh pain is a symptom seen in loosening (secondary to osteolysis, infection) and in some cases of press fit THA. The pain is anterolateral and mid-thigh (corresponding to the level of the stem tip). The cause of pain in press-fit THA is imperfectly understood but thought to be associated with the mismatch between implant and bone modulus of elasticity…larger stem sizes, stainless steel stems, straight designs are more rigid [174]. Thigh Pain is treated nonoperatively for 18 – 24 months before considering surgery, and yet stem revision for unknown pain is controversial [175]. Surgery involves cortical strut graft with cerclage wiring to host bone while retaining the femoral stem (if its well fixed) [176].  The strut increases the rigidity of the host bone and decreases the modulus mismatch of the implant and host bone.  Results are successful.  

Thigh pain is also common in the anatomic femoral stems, which may not fully control rotation, or may not full ingrowth and lead to focal point loading.  Rates of thigh pain are reported up to 30%. 

7. Medical Complications & Readmissions

While TJA procedures are becoming better managed from a pain and blood loss standpoint, there remains a low, but important risk of mortality inherent in the fact these are large surgical procedures in a relatively old patient population. 

Courtney et al. examined 1,012 patients undergoing primary THA or TKA and found that 84% of medical complications occurred within 24 hours postop and 90% occurred within 4 days.  These patients had higher incidence of major comorbidities such as CHF, CAD, COPD, and liver failure. Older age was an additional risk factor [169].  In contrast however, a similar study that examined the timing of major postoperative complications found that over 90% occurred within the first 4 days of surgery yet almost 60% of cases occurred in patients without significant comorbidities [170].  Overall, it appears that cardiac failure was the most common cause of mortality, pulmonary embolism was the second. 

Identifying patient risk factors is an important part of pre-operative preparation for TJA. Large national databases have been used recently to further identify risk factors for medical complications.

Age (>80), diabetes, BMI > 40, and ASA class (>3, indicator of comorbidities) were all associated with increased risk of 30 day morbidity and mortality after TKA [171]. Age and cardiac disease were associated with 30 day risk in THA [172].

Looking specifically at cardiac complications, hypertension and coronary artery disease comorbities as well as age > 80 were risk factors.[173].   

These studies highlight the importance of preoperative screening to identify the risk factors that place a patient at risk for medical complications in the acute postoperative period and require hospital monitoring.

Medical complications are also associated with hospital readmission.


1. Bozic, K.J., et al., Risk of complication and revision total hip arthroplasty among Medicare patients with different bearing surfaces. Clin Orthop Relat Res, 2010. 468(9): p. 2357-62.

2. Bozic, K.J., et al., The epidemiology of revision total hip arthroplasty in the United States. J Bone Joint Surg Am, 2009. 91(1): p. 128-33.

3. Harris, W.H., et al., Extensive localized bone resorption in the femur following total hip replacement. J Bone Joint Surg Am, 1976. 58(5): p. 612-8.

4. Maloney, W.J. and W.H. Harris, Comparison of a hybrid with an uncemented total hip replacement. A retrospective matched-pair study. J Bone Joint Surg Am, 1990. 72(9): p. 1349-52.

5. Schmalzried, T.P., M. Jasty, and W.H. Harris, Periprosthetic bone loss in total hip arthroplasty. Polyethylene wear debris and the concept of the effective joint space. J Bone Joint Surg Am, 1992. 74(6): p. 849-63.

6. Schmalzried, T.P., et al., Polyethylene wear debris and tissue reactions in knee as compared to hip replacement prostheses. J Appl Biomater, 1994. 5(3): p. 185-90.

7. Muratoglu, O.K., et al., Ex vivo wear of conventional and cross-linked polyethylene acetabular liners. Clin Orthop Relat Res, 2005. 438: p. 158-64.

8. Manning, D.W., et al., In vivo comparative wear study of traditional and highly cross-linked polyethylene in total hip arthroplasty. J Arthroplasty, 2005. 20(7): p. 880-6.

9. Puri, L., et al., Use of helical computed tomography for the assessment of acetabular osteolysis after total hip arthroplasty. J Bone Joint Surg Am, 2002. 84-A(4): p. 609-14.

10. Zicat, B., C.A. Engh, and E. Gokcen, Patterns of osteolysis around total hip components inserted with and without cement. J Bone Joint Surg Am, 1995. 77(3): p. 432-9.

11. Udomkiat, P., Z. Wan, and L.D. Dorr, Comparison of preoperative radiographs and intraoperative findings of fixation of hemispheric porous-coated sockets. J Bone Joint Surg Am, 2001. 83-A(12): p. 1865-70.

12. Schmalzried, T.P., V.A. Fowble, and H.C. Amstutz, The fate of pelvic osteolysis after reoperation. No recurrence with lesional treatment. Clin Orthop Relat Res, 1998(350): p. 128-37.

13. Hozack, W.J., et al., Relationship between polyethylene wear, pelvic osteolysis, and clinical symptomatology in patients with cementless acetabular components. A framework for decision making. J Arthroplasty, 1996. 11(7): p. 769-72.

14. Hozack, W.J., P.S. Bicalho, and K. Eng, Treatment of femoral osteolysis with cementless total hip revision. J Arthroplasty, 1996. 11(6): p. 668-72.

15. Kavanagh, B.F., et al., Pelvic osteolysis associated with an uncemented acetabular component in total hip arthroplasty. Orthopedics, 1996. 19(2): p. 159-63.

16. Maloney, W.J., 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(11): p. 1628-34.

17. Restrepo, C., et al., Isolated polyethylene exchange versus acetabular revision for polyethylene wear. Clin Orthop Relat Res, 2009. 467(1): p. 194-8.

18. Lie, S.A., et al., Isolated acetabular liner exchange compared with complete acetabular component revision in revision of primary uncemented acetabular components: a study of 1649 revisions from the Norwegian Arthroplasty Register. J Bone Joint Surg Br, 2007. 89(5): p. 591-4.

19. Koh, K.H., et al., Complete acetabular cup revision versus isolated liner exchange for polyethylene wear and osteolysis without loosening in cementless total hip arthroplasty. Arch Orthop Trauma Surg, 2011. 131(11): p. 1591-600.

20. Massin, P., L. Schmidt, and C.A. Engh, Evaluation of cementless acetabular component migration. An experimental study. J Arthroplasty, 1989. 4(3): p. 245-51.

21. Hodgkinson, J.P., P. Shelley, and B.M. Wroblewski, The correlation between the roentgenographic appearance and operative findings at the bone-cement junction of the socket in Charnley low friction arthroplasties. Clin Orthop Relat Res, 1988(228): p. 105-9.

22. Jacobsson, S.A., K. Djerf, and O. Wahlstrom, Twenty-year results of McKee-Farrar versus Charnley prosthesis. Clin Orthop Relat Res, 1996(329 Suppl): p. S60-8.

23. Porat, M., et al., Causes of failure of ceramic-on-ceramic and metal-on-metal hip arthroplasties. Clin Orthop Relat Res, 2012. 470(2): p. 382-7.

24. Ebramzadeh, E., et al., Failure modes of 433 metal-on-metal hip implants: how, why, and wear. Orthop Clin North Am, 2011. 42(2): p. 241-50, ix.

25. Haddad, F.S., et al., Metal-on-metal bearings: the evidence so far. J Bone Joint Surg Br, 2011. 93(5): p. 572-9.

26. Campbell, P., et al., The John Charnley Award: a study of implant failure in metal-on-metal surface arthroplasties. Clin Orthop Relat Res, 2006. 453: p. 35-46.

27. Anand, A., F. McGlynn, and W. Jiranek, Metal hypersensitivity: can it mimic infection? J Arthroplasty, 2009. 24(5): p. 826 e25-8.

28. Luetzner, J., et al., Serum metal ion exposure after total knee arthroplasty. Clin Orthop Relat Res, 2007. 461: p. 136-42.

29. Steffen, R.T., et al., The five-year results of the Birmingham Hip Resurfacing arthroplasty: an independent series. J Bone Joint Surg Br, 2008. 90(4): p. 436-41.

30. Mabilleau, G., et al., Metal-on-metal hip resurfacing arthroplasty: a review of periprosthetic biological reactions. Acta Orthop, 2008. 79(6): p. 734-47.

31. Pandit, H., et al., Pseudotumours associated with metal-on-metal hip resurfacings. J Bone Joint Surg Br, 2008. 90(7): p. 847-51.

32. Williams, D.H., et al., Prevalence of pseudotumor in asymptomatic patients after metal-on-metal hip arthroplasty. J Bone Joint Surg Am, 2011. 93(23): p. 2164-71.

33. Steele, G.D., et al., Early failure of articular surface replacement XL total hip arthroplasty. J Arthroplasty, 2011. 26(6 Suppl): p. 14-8.

34. Kwon, Y.M., et al., "Asymptomatic" pseudotumors after metal-on-metal hip resurfacing arthroplasty: prevalence and metal ion study. J Arthroplasty, 2011. 26(4): p. 511-8.

35. De Smet, K., et al., Metal ion measurement as a diagnostic tool to identify problems with metal-on-metal hip resurfacing. J Bone Joint Surg Am, 2008. 90 Suppl 4: p. 202-8.

36. Tower, S.S., Arthroprosthetic cobaltism: neurological and cardiac manifestations in two patients with metal-on-metal arthroplasty: a case report. J Bone Joint Surg Am, 2010. 92(17): p. 2847-51.

37. Keegan, G.M., I.D. Learmonth, and C.P. Case, Orthopaedic metals and their potential toxicity in the arthroplasty patient: A review of current knowledge and future strategies. J Bone Joint Surg Br, 2007. 89(5): p. 567-73.

38. Visuri, T., et al., Cancer risk after metal on metal and polyethylene on metal total hip arthroplasty. Clin Orthop Relat Res, 1996(329 Suppl): p. S280-9.

39. Hart, A.J., et al., Circulating levels of cobalt and chromium from metal-on-metal hip replacement are associated with CD8+ T-cell lymphopenia. J Bone Joint Surg Br, 2009. 91(6): p. 835-42.

40. Cooper, H.J., The local effects of metal corrosion in total hip arthroplasty. Orthop Clin North Am, 2014. 45(1): p. 9-18.

41. Berry, D.J., et al., Effect of femoral head diameter and operative approach on risk of dislocation after primary total hip arthroplasty. J Bone Joint Surg Am, 2005. 87(11): p. 2456-63.

42. Berry, D.J., et al., The cumulative long-term risk of dislocation after primary Charnley total hip arthroplasty. J Bone Joint Surg Am, 2004. 86-A(1): p. 9-14.

43. Paterno, S.A., P.F. Lachiewicz, and S.S. Kelley, The influence of patient-related factors and the position of the acetabular component on the rate of dislocation after total hip replacement. J Bone Joint Surg Am, 1997. 79(8): p. 1202-10.

44. Woolson, S.T. and Z.O. Rahimtoola, Risk factors for dislocation during the first 3 months after primary total hip replacement. J Arthroplasty, 1999. 14(6): p. 662-8.

45. Sikes, C.V., et al., Instability after total hip arthroplasty: treatment with large femoral heads vs constrained liners. J Arthroplasty, 2008. 23(7 Suppl): p. 59-63.

46. Amstutz, H.C., M.J. Le Duff, and P.E. Beaule, Prevention and treatment of dislocation after total hip replacement using large diameter balls. Clin Orthop Relat Res, 2004(429): p. 108-16.

47. Lachiewicz, P.F., et al., Femoral head size and wear of highly cross-linked polyethylene at 5 to 8 years. Clin Orthop Relat Res, 2009. 467(12): p. 3290-6.

48. Lewinnek, G.E., et al., Dislocations after total hip-replacement arthroplasties. J Bone Joint Surg Am, 1978. 60(2): p. 217-20.

49. Abdel, M.P., et al., What Safe Zone? The Vast Majority of Dislocated THAs Are Within the Lewinnek Safe Zone for Acetabular Component Position. Clin Orthop Relat Res, 2016. 474(2): p. 386-91.

50. Esposito, C.I., et al., Cup position alone does not predict risk of dislocation after hip arthroplasty. J Arthroplasty, 2015. 30(1): p. 109-13.

51. Kwon, M.S., et al., Does surgical approach affect total hip arthroplasty dislocation rates? Clin Orthop Relat Res, 2006. 447: p. 34-8.

52. Sheth, D., et al., Anterior and Anterolateral Approaches for THA Are Associated With Lower Dislocation Risk Without Higher Revision Risk. Clin Orthop Relat Res, 2015. 473(11): p. 3401-8.

53. Barnett, S.L., et al., Is the Anterior Approach Safe? Early Complication Rate Associated with 5090 Consecutive Primary Total Hip Arthroplasty Procedures Performed Using the Anterior Approach. J Arthroplasty, 2015.

54. Berend, K.R., et al., Primary and revision anterior supine total hip arthroplasty: an analysis of complications and reoperations. Instr Course Lect, 2013. 62: p. 251-63.

55. Restrepo, C., et al., Hip dislocation: are hip precautions necessary in anterior approaches? Clin Orthop Relat Res, 2011. 469(2): p. 417-22.

56. von Knoch, M., et al., Late dislocation after total hip arthroplasty. J Bone Joint Surg Am, 2002. 84-A(11): p. 1949-53.

57. Dewal, H., et al., Efficacy of abduction bracing in the management of total hip arthroplasty dislocation. J Arthroplasty, 2004. 19(6): p. 733-8.

58. Pierchon, F., et al., Causes of dislocation of total hip arthroplasty. CT study of component alignment. J Bone Joint Surg Br, 1994. 76(1): p. 45-8.

59. Berry, D.J., Epidemiology: hip and knee. Orthop Clin North Am, 1999. 30(2): p. 183-90.

60. Thomsen, M.N., et al., Fracture load for periprosthetic femoral fractures in cemented versus uncemented hip stems: an experimental in vitro study. Orthopedics, 2008. 31(7): p. 653.

61. Cook, R.E., et al., Risk factors for periprosthetic fractures of the hip: a survivorship analysis. Clin Orthop Relat Res, 2008. 466(7): p. 1652-6.

62. Thien, T.M., et al., Periprosthetic femoral fracture within two years after total hip replacement: analysis of 437,629 operations in the nordic arthroplasty register association database. J Bone Joint Surg Am, 2014. 96(19): p. e167.

63. Masri, B.A., R.M. Meek, and C.P. Duncan, Periprosthetic fractures evaluation and treatment. Clin Orthop Relat Res, 2004(420): p. 80-95.

64. Brady, O.H., et al., The reliability and validity of the Vancouver classification of femoral fractures after hip replacement. J Arthroplasty, 2000. 15(1): p. 59-62.

65. Paprosky, W.G., N.V. Greidanus, and J. Antoniou, Minimum 10-year-results of extensively porous-coated stems in revision hip arthroplasty. Clin Orthop Relat Res, 1999(369): p. 230-42.

66. Pritchett, J.W., Fracture of the greater trochanter after hip replacement. Clin Orthop Relat Res, 2001(390): p. 221-6.

67. Pike, J., et al., Principles of treatment for periprosthetic femoral shaft fractures around well-fixed total hip arthroplasty. J Am Acad Orthop Surg, 2009. 17(11): p. 677-88.

68. Parvizi, J. and D.N. Vegari, Periprosthetic proximal femur fractures: current concepts. J Orthop Trauma, 2011. 25 Suppl 2: p. S77-81.

69. Lindahl, H., et al., Risk factors for failure after treatment of a periprosthetic fracture of the femur. J Bone Joint Surg Br, 2006. 88(1): p. 26-30.

70. Lindahl, H., et al., Periprosthetic femoral fractures classification and demographics of 1049 periprosthetic femoral fractures from the Swedish National Hip Arthroplasty Register. J Arthroplasty, 2005. 20(7): p. 857-65.

71. Incavo, S.J., et al., One-stage revision of periprosthetic fractures around loose cemented total hip arthroplasty. Am J Orthop (Belle Mead NJ), 1998. 27(1): p. 35-41.

72. Beals, R.K. and S.S. Tower, Periprosthetic fractures of the femur. An analysis of 93 fractures. Clin Orthop Relat Res, 1996(327): p. 238-46.

73. Young, S.W., C.G. Walker, and R.P. Pitto, Functional outcome of femoral peri prosthetic fracture and revision hip arthroplasty: a matched-pair study from the New Zealand Registry. Acta Orthop, 2008. 79(4): p. 483-8.

74. Bhattacharyya, T., et al., Mortality after periprosthetic fracture of the femur. J Bone Joint Surg Am, 2007. 89(12): p. 2658-62.

75. Parvizi, J., et al., New definition for periprosthetic joint infection: from the Workgroup of the Musculoskeletal Infection Society. Clin Orthop Relat Res, 2011. 469(11): p. 2992-4.

76. Fehring, T.K., et al., Early failures in total knee arthroplasty. Clin Orthop Relat Res, 2001(392): p. 315-8.

77. Aalto, K., et al., Changes in erythrocyte sedimentation rate and C-reactive protein after total hip arthroplasty. Clin Orthop Relat Res, 1984(184): p. 118-20.

78. Barrack, R.L. and W.H. Harris, The value of aspiration of the hip joint before revision total hip arthroplasty. J Bone Joint Surg Am, 1993. 75(1): p. 66-76.

79. Schinsky, M.F., et al., Perioperative testing for joint infection in patients undergoing revision total hip arthroplasty. J Bone Joint Surg Am, 2008. 90(9): p. 1869-75.

80. Trampuz, A., et al., Synovial fluid leukocyte count and differential for the diagnosis of prosthetic knee infection. Am J Med, 2004. 117(8): p. 556-62.

81. Bedair, H., et al., The Mark Coventry Award: diagnosis of early postoperative TKA infection using synovial fluid analysis. Clin Orthop Relat Res, 2011. 469(1): p. 34-40.

82. Ghanem, E., et al., Periprosthetic infection: where do we stand with regard to Gram stain? Acta Orthop, 2009. 80(1): p. 37-40.

83. Segawa, H., et al., Infection after total knee arthroplasty. A retrospective study of the treatment of eighty-one infections. J Bone Joint Surg Am, 1999. 81(10): p. 1434-45.

84. Bradbury, T., et al., The fate of acute methicillin-resistant Staphylococcus aureus periprosthetic knee infections treated by open debridement and retention of components. J Arthroplasty, 2009. 24(6 Suppl): p. 101-4.

85. Deirmengian, C., et al., Open debridement of acute gram-positive infections after total knee arthroplasty. Clin Orthop Relat Res, 2003(416): p. 129-34.

86. Deirmengian, C., et al., Limited success with open debridement and retention of components in the treatment of acute Staphylococcus aureus infections after total knee arthroplasty. J Arthroplasty, 2003. 18(7 Suppl 1): p. 22-6.

87. Chen, A., et al., Prevention of late PJI. J Orthop Res, 2014. 32 Suppl 1: p. S158-71.

88. Burnett, R.S., et al., Technique and timing of two-stage exchange for infection in TKA. Clin Orthop Relat Res, 2007. 464: p. 164-78.

89. Wentworth, S.J., et al., Hip prosthesis of antibiotic-loaded acrylic cement for the treatment of infections following total hip arthroplasty. J Bone Joint Surg Am, 2002. 84-A Suppl 2: p. 123-8.

90. Penner, M.J., B.A. Masri, and C.P. Duncan, Elution characteristics of vancomycin and tobramycin combined in acrylic bone-cement. J Arthroplasty, 1996. 11(8): p. 939-44.

91. Masri, B.A., et al., Effect of varying surface patterns on antibiotic elution from antibiotic-loaded bone cement. J Arthroplasty, 1995. 10(4): p. 453-9.

92. Kendall, R.W., C.P. Duncan, and C.P. Beauchamp, Bacterial growth on antibiotic-loaded acrylic cement. A prospective in vivo retrieval study. J Arthroplasty, 1995. 10(6): p. 817-22.

93. Jackson, J., et al., The use of bone cement for the localized, controlled release of the antibiotics vancomycin, linezolid, or fusidic acid: effect of additives on drug release rates and mechanical strength. Drug Deliv Transl Res, 2011. 1(2): p. 121-31.

94. Haddad, F.S., et al., The PROSTALAC functional spacer in two-stage revision for infected knee replacements. Prosthesis of antibiotic-loaded acrylic cement. J Bone Joint Surg Br, 2000. 82(6): p. 807-12.

95. Duncan, C.P. and B.A. Masri, The role of antibiotic-loaded cement in the treatment of an infection after a hip replacement. Instr Course Lect, 1995. 44: p. 305-13.

96. Ghanem, E., et al., Staged revision for knee arthroplasty infection: what is the role of serologic tests before reimplantation? Clin Orthop Relat Res, 2009. 467(7): p. 1699-705.

97. Sherrell, J.C., et al., The Chitranjan Ranawat Award: fate of two-stage reimplantation after failed irrigation and debridement for periprosthetic knee infection. Clin Orthop Relat Res, 2011. 469(1): p. 18-25.

98. Berend, K.R., et al., Two-stage treatment of hip periprosthetic joint infection is associated with a high rate of infection control but high mortality. Clin Orthop Relat Res, 2013. 471(2): p. 510-8.

99. De Man, F.H., et al., Infectiological, functional, and radiographic outcome after revision for prosthetic hip infection according to a strict algorithm. Acta Orthop, 2011. 82(1): p. 27-34.

100. Emerson, R.H., Jr., et al., Comparison of a static with a mobile spacer in total knee infection. Clin Orthop Relat Res, 2002(404): p. 132-8.

101. Willis-Owen, C.A., A. Konyves, and D.K. Martin, Factors affecting the incidence of infection in hip and knee replacement: an analysis of 5277 cases. J Bone Joint Surg Br, 2010. 92(8): p. 1128-33.

102. Bozic, K.J., et al., Patient-related risk factors for postoperative mortality and periprosthetic joint infection in medicare patients undergoing TKA. Clin Orthop Relat Res, 2012. 470(1): p. 130-7.

103. Daines, B.K., D.A. Dennis, and S. Amann, Infection prevention in total knee arthroplasty. J Am Acad Orthop Surg, 2015. 23(6): p. 356-64.

104. Shirwaiker, R.A., et al., A clinical perspective on musculoskeletal infection treatment strategies and challenges. J Am Acad Orthop Surg, 2015. 23 Suppl: p. S44-54.

105. Hill, C., et al., Prophylactic cefazolin versus placebo in total hip replacement. Report of a multicentre double-blind randomised trial. Lancet, 1981. 1(8224): p. 795-6.

106. Frumin, J. and J.C. Gallagher, Allergic cross-sensitivity between penicillin, carbapenem, and monobactam antibiotics: what are the chances? Ann Pharmacother, 2009. 43(2): p. 304-15.

107. Ponce, B., et al., Surgical Site Infection After Arthroplasty: Comparative Effectiveness of Prophylactic Antibiotics: Do Surgical Care Improvement Project Guidelines Need to Be Updated? J Bone Joint Surg Am, 2014. 96(12): p. 970-977.

108. Bierbaum, B.E., et al., An analysis of blood management in patients having a total hip or knee arthroplasty. J Bone Joint Surg Am, 1999. 81(1): p. 2-10.

109. Carson, J.L., et al., Liberal or restrictive transfusion in high-risk patients after hip surgery. N Engl J Med, 2011. 365(26): p. 2453-62.

110. Carson, J.L., The shifting paradigm for transfusion of red blood cells. Clin Adv Hematol Oncol, 2015. 13(3): p. 152-4.

111. North, W.T., et al., Topical vs Intravenous Tranexamic Acid in Primary Total Hip Arthroplasty: A Double-Blind, Randomized Controlled Trial. J Arthroplasty, 2015.

112. Yamasaki, S., K. Masuhara, and T. Fuji, Tranexamic acid reduces postoperative blood loss in cementless total hip arthroplasty. J Bone Joint Surg Am, 2005. 87(4): p. 766-70.

113. Noticewala, M.S., et al., Predicting need for allogeneic transfusion after total knee arthroplasty. J Arthroplasty, 2012. 27(6): p. 961-7.

114. Friedman, R., et al., Allogeneic blood transfusions and postoperative infections after total hip or knee arthroplasty. J Bone Joint Surg Am, 2014. 96(4): p. 272-8.

115. Wei, W. and B. Wei, Comparison of topical and intravenous tranexamic acid on blood loss and transfusion rates in total hip arthroplasty. J Arthroplasty, 2014. 29(11): p. 2113-6.

116. Huang, Z., et al., Combination of intravenous and topical application of tranexamic acid in primary total knee arthroplasty: a prospective randomized controlled trial. J Arthroplasty, 2014. 29(12): p. 2342-6.

117. Irwin, A., et al., Oral versus intravenous tranexamic acid in enhanced-recovery primary total hip and knee replacement: results of 3000 procedures. Bone Joint J, 2013. 95-B(11): p. 1556-61.

118. Ker, K., et al., Effect of tranexamic acid on surgical bleeding: systematic review and cumulative meta-analysis. BMJ, 2012. 344: p. e3054.

119. Iwai, T., et al., Repeat-dose intravenous tranexamic acid further decreases blood loss in total knee arthroplasty. Int Orthop, 2013. 37(3): p. 441-5.

120. McCormack, P.L., Tranexamic acid: a review of its use in the treatment of hyperfibrinolysis. Drugs, 2012. 72(5): p. 585-617.

121. Gill, J.B. and A. Rosenstein, The use of antifibrinolytic agents in total hip arthroplasty: a meta-analysis. J Arthroplasty, 2006. 21(6): p. 869-73.

122. Whiting, D.R., et al., Preliminary results suggest tranexamic acid is safe and effective in arthroplasty patients with severe comorbidities. Clin Orthop Relat Res, 2014. 472(1): p. 66-72.

123. Raphael, I.J., et al., Aspirin: an alternative for pulmonary embolism prophylaxis after arthroplasty? Clin Orthop Relat Res, 2014. 472(2): p. 482-8.

124. Migita, K., et al., Venous thromboembolism after total joint arthroplasty: results from a Japanese multicenter cohort study. Arthritis Res Ther, 2014. 16(4): p. R154.

125. Parvizi, J., et al., Does "excessive" anticoagulation predispose to periprosthetic infection? J Arthroplasty, 2007. 22(6 Suppl 2): p. 24-8.

126. Patel, V.P., et al., Factors associated with prolonged wound drainage after primary total hip and knee arthroplasty. J Bone Joint Surg Am, 2007. 89(1): p. 33-8.

127. Sachs, R.A., et al., Does anticoagulation do more harm than good?: A comparison of patients treated without prophylaxis and patients treated with low-dose warfarin after total knee arthroplasty. J Arthroplasty, 2003. 18(4): p. 389-95.

128. Poultsides, L.A., et al., Meta-analysis of cause of death following total joint replacement using different thromboprophylaxis regimens. J Bone Joint Surg Br, 2012. 94(1): p. 113-21.

129. Callaghan, J.J., et al., Prophylaxis for thromboembolic disease: recommendations from the American College of Chest Physicians--are they appropriate for orthopaedic surgery? J Arthroplasty, 2005. 20(3): p. 273-4.

130. Quinlan, D.J., et al., Association between asymptomatic deep vein thrombosis detected by venography and symptomatic venous thromboembolism in patients undergoing elective hip or knee surgery. J Thromb Haemost, 2007. 5(7): p. 1438-43.

131. Pierce, C.A., et al., Surveillance bias and deep vein thrombosis in the national trauma data bank: the more we look, the more we find. J Trauma, 2008. 64(4): p. 932-6; discussion 936-7.

132. Ozbudak, O., et al., Doppler ultrasonography versus venography in the detection of deep vein thrombosis in patients with pulmonary embolism. J Thromb Thrombolysis, 2006. 21(2): p. 159-62.

133. Bjornara, B.T., T.E. Gudmundsen, and O.E. Dahl, Frequency and timing of clinical venous thromboembolism after major joint surgery. J Bone Joint Surg Br, 2006. 88(3): p. 386-91.

134. Bergqvist, D., et al., Low-molecular-weight heparin (enoxaparin) as prophylaxis against venous thromboembolism after total hip replacement. N Engl J Med, 1996. 335(10): p. 696-700.

135. Stringer, M.D., et al., Deep vein thrombosis after elective knee surgery. An incidence study in 312 patients. J Bone Joint Surg Br, 1989. 71(3): p. 492-7.

136. Januel, J.M., 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(3): p. 294-303.

137. Ogonda, L., et al., Aspirin for thromboprophylaxis after primary lower limb arthroplasty: early thromboembolic events and 90 day mortality in 11,459 patients. Bone Joint J, 2016. 98-B(3): p. 341-8.

138. Parvizi, J., et al., Timing of Symptomatic Pulmonary Embolism with Warfarin Following Arthroplasty. J Arthroplasty, 2015. 30(6): p. 1050-3.

139. Restrepo, C., et al., Safety of simultaneous bilateral total knee arthroplasty. A meta-analysis. J Bone Joint Surg Am, 2007. 89(6): p. 1220-6.

140. Mont, M.A. and J.J. Jacobs, AAOS clinical practice guideline: preventing venous thromboembolic disease in patients undergoing elective hip and knee arthroplasty. J Am Acad Orthop Surg, 2011. 19(12): p. 777-8.

141. Falck-Ytter, Y., et al., Prevention of VTE in orthopedic surgery patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest, 2012. 141(2 Suppl): p. e278S-325S.

142. Lieberman, J.R. and M.J. Pensak, Prevention of venous thromboembolic disease after total hip and knee arthroplasty. J Bone Joint Surg Am, 2013. 95(19): p. 1801-11.

143. Anderson, F.A., Jr., et al., Prevention of venous thromboembolism after hip or knee arthroplasty: findings from a 2008 survey of US orthopedic surgeons. J Arthroplasty, 2012. 27(5): p. 659-66 e5.

144. Lee, Y.K., et al., Conflict of interest in the assessment of thromboprophylaxis after total joint arthroplasty: a systematic review. J Bone Joint Surg Am, 2012. 94(1): p. 27-33.

145. Wilson, N.V., et al., Thrombo-embolic prophylaxis in total knee replacement. Evaluation of the A-V Impulse System. J Bone Joint Surg Br, 1992. 74(1): p. 50-2.

146. Warwick, D., et al., A randomised comparison of a foot pump and low-molecular-weight heparin in the prevention of deep-vein thrombosis after total knee replacement. J Bone Joint Surg Br, 2002. 84(3): p. 344-50.

147. Pitto, R.P., et al., Mechanical prophylaxis of deep-vein thrombosis after total hip replacement a randomised clinical trial. J Bone Joint Surg Br, 2004. 86(5): p. 639-42.

148. Sugano, N., et al., Clinical efficacy of mechanical thromboprophylaxis without anticoagulant drugs for elective hip surgery in an Asian population. J Arthroplasty, 2009. 24(8): p. 1254-7.

149. Park, Y.G., et al., Incidence and Fate of "Symptomatic" Venous Thromboembolism After Knee Arthroplasty Without Pharmacologic Prophylaxis in an Asian Population. J Arthroplasty, 2016. 31(5): p. 1072-7.

150. Bozic, K.J., et al., Does aspirin have a role in venous thromboembolism prophylaxis in total knee arthroplasty patients? J Arthroplasty, 2010. 25(7): p. 1053-60.

151. Vulcano, E., et al., Aspirin for elective hip and knee arthroplasty: a multimodal thromboprophylaxis protocol. Int Orthop, 2012. 36(10): p. 1995-2002.

152. Deirmengian, G.K., et al., Aspirin Can Be Used as Prophylaxis for Prevention of Venous Thromboembolism After Revision Hip and Knee Arthroplasty. J Arthroplasty, 2016.

153. Gutowski, C.J., et al., Direct Costs of Aspirin versus Warfarin for Venous Thromboembolism Prophylaxis after Total Knee or Hip Arthroplasty. J Arthroplasty, 2015. 30(9 Suppl): p. 36-8.

154. Lotke, P.A. and J.H. Lonner, The benefit of aspirin chemoprophylaxis for thromboembolism after total knee arthroplasty. Clin Orthop Relat Res, 2006. 452: p. 175-80.

155. Eriksson, B.I., et al., Rivaroxaban versus enoxaparin for thromboprophylaxis after hip arthroplasty. N Engl J Med, 2008. 358(26): p. 2765-75.

156. Kakkar, A.K., et al., Extended duration rivaroxaban versus short-term enoxaparin for the prevention of venous thromboembolism after total hip arthroplasty: a double-blind, randomised controlled trial. Lancet, 2008. 372(9632): p. 31-9.

157. Wood, R.C., 3rd, et al., Retrospective Evaluation of Postoperative Bleeding Events in Patients Receiving Rivaroxaban After Undergoing Total Hip and Total Knee Arthroplasty: Comparison with Clinical Trial Data. Pharmacotherapy, 2015. 35(7): p. 663-9.

158. Hull, R., et al., A comparison of subcutaneous low-molecular-weight heparin with warfarin sodium for prophylaxis against deep-vein thrombosis after hip or knee implantation. N Engl J Med, 1993. 329(19): p. 1370-6.

159. Francis, C.W., et al., Prevention of deep-vein thrombosis after total hip arthroplasty. Comparison of warfarin and dalteparin. J Bone Joint Surg Am, 1997. 79(9): p. 1365-72.

160. Colwell, C.W., Jr., et al., Comparison of enoxaparin and warfarin for the prevention of venous thromboembolic disease after total hip arthroplasty. Evaluation during hospitalization and three months after discharge. J Bone Joint Surg Am, 1999. 81(7): p. 932-40.

161. Turpie, A.G., et al., Fondaparinux vs enoxaparin for the prevention of venous thromboembolism in major orthopedic surgery: a meta-analysis of 4 randomized double-blind studies. Arch Intern Med, 2002. 162(16): p. 1833-40.

162. Bauer, K.A., et al., Fondaparinux compared with enoxaparin for the prevention of venous thromboembolism after elective major knee surgery. N Engl J Med, 2001. 345(18): p. 1305-10.

163. Friedman, R.J., et al., Practice patterns in the use of venous thromboembolism prophylaxis after total joint arthroplasty--insights from the Multinational Global Orthopaedic Registry (GLORY). Am J Orthop (Belle Mead NJ), 2010. 39(9 Suppl): p. 14-21.

164. Lotke, P.A., M.E. Steinberg, and M.L. Ecker, Significance of deep venous thrombosis in the lower extremity after total joint arthroplasty. Clin Orthop Relat Res, 1994(299): p. 25-30.

165. Maynard, M.J., T.P. Sculco, and B. Ghelman, Progression and regression of deep vein thrombosis after total knee arthroplasty. Clin Orthop Relat Res, 1991(273): p. 125-30.

166. Haas, S.B., et al., The significance of calf thrombi after total knee arthroplasty. J Bone Joint Surg Br, 1992. 74(6): p. 799-802.

167. Parvizi, J., et al., Symptomatic pulmonary embolus after joint arthroplasty: stratification of risk factors. Clin Orthop Relat Res, 2014. 472(3): p. 903-12.

168. Bohl, D.D., et al., Development and Validation of a Risk Stratification System for Pulmonary Embolism After Elective Primary Total Joint Arthroplasty. J Arthroplasty, 2016.

169. Courtney, P.M., et al., Who Should Not Undergo Short Stay Hip and Knee Arthroplasty? Risk Factors Associated With Major Medical Complications Following Primary Total Joint Arthroplasty. J Arthroplasty, 2015. 30(9 Suppl): p. 1-4.

170. Parvizi, J., et al., Total joint arthroplasty: When do fatal or near-fatal complications occur? J Bone Joint Surg Am, 2007. 89(1): p. 27-32.

171. Belmont, P.J., Jr., et al., Thirty-day postoperative complications and mortality following total knee arthroplasty: incidence and risk factors among a national sample of 15,321 patients. J Bone Joint Surg Am, 2014. 96(1): p. 20-6.

172. Belmont, P.J., Jr., et al., Morbidity and mortality in the thirty-day period following total hip arthroplasty: risk factors and incidence. J Arthroplasty, 2014. 29(10): p. 2025-30.

173. Belmont, P.J., Jr., et al., Postoperative myocardial infarction and cardiac arrest following primary total knee and hip arthroplasty: rates, risk factors, and time of occurrence. J Bone Joint Surg Am, 2014. 96(24): p. 2025-31.

174. Lavernia, C., et al., Thigh pain in primary total hip arthroplasty: the effects of elastic moduli. J Arthroplasty, 2004. 19(7 Suppl 2): p. 10-6.

175. Brown, T.E., et al., Thigh pain after cementless total hip arthroplasty: evaluation and management. J Am Acad Orthop Surg, 2002. 10(6): p. 385-92.

176. Kim, Y.H. and J.S. Kim, Revision hip arthroplasty using strut allografts and fully porous-coated stems. J Arthroplasty, 2005. 20(4): p. 454-9.