Polymyalgia Rheumatica and Giant Cell Arteritis

Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are two related, immune-mediated, inflammatory conditions that occur in the elderly. PMR coexists in 40% of patients with GCA. Similarly, 10% of PMR patients develop GCA at some point during their disease course. The relation between PMR and GCA is further demonstrated by their preference for similar patient populations, linkage to the same HLA haplotypes, similar cytokine patterns in temporal artery biopsies, and similarities in anatomic involvement on PET imaging.^1-3 PMR and GCA represent two extremes of a disease spectrum.

Polymyalgia rheumatica

Definition

Bruce is credited with the first description in 1888 of PMR, which he described as “senile rheumatic gout.”⁴ However, Barber coined the term polymyalgia rheumatica in 1957, and it has become the universally accepted name for this condition.⁵

PMR is characterized by proximal, symmetrical musculoskeletal pain and stiffness. Symptoms of systemic inflammation are also common. A dramatic response to low-dose corticosteroids can be a valuable diagnostic tool in patients for whom the diagnosis is uncertain. The lack of response to prednisone raises the possibility of a paraneoplastic process manifesting with proximal pain and stiffness. In patients who have a dramatic response to treatment there is still a need for caution because some patients (~11%) with an initial PMR-like presentation evolve into a phenotype that is more that of rheumatoid arthritis and, less often, other systemic rheumatic illnesses.⁶

Epidemiology

PMR has a predilection for patients older than 50 years. The mean age at onset is 73 years, and women are affected more often than men. Its annual incidence in Olmstead County, Minnesota, a population with mostly Scandinavian heritage, is 59 per 100,000. The annual incidence of the disease increases with age.⁷ Whites of northern European descent have a higher incidence of disease than people of African American or Latin American descent.^8,9

Pathophysiology

Much has been learned about PMR and GCA, but their cause remains unknown. Their cause is likely multifactorial, resulting in the interplay of age, environment, and genetic susceptibility. The suggestion that PMR may be a forme fruste of GCA was first advanced in the 1950s and 1960s.⁵ The pathophysiology for both diseases is similar, with abnormalities of cellular immunity leading to vessel and systemic inflammation. Sixteen percent to at least 20% or more of PMR patients demonstrate arteritis on histologic examination, requiring the diagnosis to be changed to GCA.¹⁰ Cytokines such as interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-α are important in the development of inflammation in GCA.¹¹Messenger RNA (mRNA) for interferon-gamma (IFN-γ) and IFN-γ protein, a product of Th1 lymphocytes, is found in the arterial wall of GCA patients. This suggests that IFN-γ may be a necessary element in the development of vasculitis. The classic histologic features of GCA, which include inflammatory cells involving the adventitia of a muscular artery and migrating toward the media and intima, consist of Th1 cells, dendritic cells, and macrophages.⁹

Signs and Symptoms

Most patients describe subacute onset of symptoms that remain persistent over time. Seventy percent to 95% of patients report symmetrical shoulder girdle pain and stiffness. Fifty percent to 70% report neck and pelvic girdle pain. Concurrent pain in the upper arms and thighs is common and is usually worse in the morning. Shoulder and leg discomfort can lead to difficulty dressing, hair grooming, and rising from a chair. One third of patients have flulike symptoms described as fever, malaise, anorexia, or weight loss.¹²

Physical examination findings may reveal pain that limits active range of motion in the shoulders and hips. Passive range of motion should be normal. Despite subjective symptoms of muscle weakness, muscle strength testing should be normal unless it is affected by examination discomfort or by another condition.¹² Approximately 50% of patients have been said to present with distal extremity abnormalities including swelling of the knees, wrists, or metacarpophalangeal joints. Other reported findings include soft-tissue swelling; pitting edema of the hands, ankles, and feet; and median nerve compression. However, these findings are typical of inflammatory joint disease and not PMR. The examiner should direct the evaluation along other lines in attempting to define another diagnosis. Frank synovitis of the hands or feet should suggest rheumatoid arthritis or another inflammatory arthropathy. Thus, further laboratory and imaging may be needed to differentiate the two. (See the chapter “Rheumatoid Arthritis”).

Diagnosis

The diagnosis of PMR is based primarily on clinical features. Elevated acute phase reactants provide secondary support for the diagnosis. The erythrocyte sedimentation rate (ESR) is greater than 40 mm/hr in 90% of cases. Other laboratory findings include an elevated C-reactive protein (CRP), normocytic normochromic anemia, thrombocytosis, and elevated alkaline phosphatase. Elevation of muscle enzymes, such as creatine kinase and aldolase, is not a feature of PMR and should prompt consideration of an alternative diagnosis.

In 1979, Bird and colleagues proposed diagnostic criteria for PMR (Table 1). Patients who fulfilled any three criteria or had one criterion along with vasculitis on a temporal artery biopsy were considered to have PMR.¹³ In 1984, Healy proposed that patients older than 50 years, seronegative for rheumatoid factor, and any three clinical features (neck, shoulder, or pelvic girdle pain, morning stiffness, elevated ESR, or rapid response to low-dose steroids) have PMR.¹⁴ Although these criteria should serve as guidelines for the diagnosis of PMR, most authorities agree that no single feature is necessary to diagnose it in all cases. The features noted in these criteria are common enough that if patients present without these symptoms or have a suboptimal response to corticosteroids, the diagnosis should be reconsidered. Conditions that can mimic PMR include malignancies, chronic infections, drug reactions, and other rheumatic conditions such as seronegative rheumatoid arthritis or polymyositis.⁶

Table 1: Often-Cited Diagnostic Criteria for Polymyalgia Rheumatica

Authors and Year Proposed	Proposed Criteria	Requirement for Making Diagnosis
Bird et al. (1979)	Age ≥65 yr Bilateral shoulder pain and stiffness Acute or subacute onset (<2 wk) ESR >40 mm/hr Depression and/or weight loss Bilateral tenderness in upper arm muscles Morning stiffness >1 hr	Any three of these criteria, or any one plus positive temporal artery biopsy
Jones and Hazelman (1981)	ESR >30 mm/hr or CRP >6 mg/L Shoulder and pelvic girdle pain Exclusion of rheumatoid arthritis or other inflammatory arthropathy, myopathy, malignancy Morning stiffness >1 hr Rapid response to corticosteroids	All criteria must be met
Chuang et al. (1982)	Age ≥50 ESR >40 mm/hr >1 mo bilateral aching and stiffness of at least two of the following areas: Neck or torso, shoulders or proximal arms, hips or proximal thighs Exclusion of other causes	All criteria must be met
Healey (1984)	>1 mo of neck, shoulder, or pelvic girdle pain (any two areas) Morning stiffness >1 hr Elevated ESR (≤40 mm/hr) Exclusion of other diagnoses Rapid response to daily, low-dose steroid therapy (e.g., prednisolone ≤20 mg)	All criteria must be met

CRP, C-reactive protein; ESR, erythrocyte sedimentation rate.
© 2004 The Cleveland Clinic Foundation.

Treatment

The first successful use of corticosteroids in patients with PMR was reported by Kersley in 1951.⁵ Since that time, it has remained the cornerstone of therapy for PMR. Prednisone or prednisolone is the most commonly used corticosteroids. Starting doses range from 15 to 20 mg per day. A dramatic response to therapy with near-total relief of symptoms should occur within 1 to 5 days. Lack of a dramatic response to corticosteroids should prompt physicians to reconsider the diagnosis. A gradual decline of the acute phase reactants should be expected but should never be the sole gauge of therapy. After an adequate response to corticosteroids has been achieved, the initial dose should be maintained for 1 month before beginning a slow taper to the lowest effective dose. One to 2 years of treatment with corticosteroids should be expected, and a few patients require low-dose prednisone for several years.¹⁵

Disease flares during the corticosteroid taper are common and often require temporary increases in therapy. Disease flares can occur in the presence of normal acute-phase reactants. Increases in acute phase reactants mandate an evaluation to be sure that comorbid conditions are not responsible for such changes. Isolated increases in acute-phase reactants should lead to more careful monitoring and not to reflexive increases in corticosteroids doses.¹⁶

Corticosteroids are the cornerstone of therapy, but they are not without side effects. Most patients have at least one relapse as corticosteroids are tapered, and adverse events occur in almost every patient. The role of immunosuppressive agents other than corticosteroids in PMR is controversial. Methotrexate has been studied in two randomized, double-blind, controlled trials. Van der Veen and colleagues reported that patients randomized to take oral methotrexate (10 mg/week) had the same number of relapses and received the same total cumulative prednisone dose compared with patients who received placebo.¹⁷ Caporali and colleagues reported that patients randomized to oral methotrexate (10 mg/week) for 48 weeks had fewer relapses and required lower cumulative prednisone doses than patients who took placebo.¹⁸ However, further review of the patients who received methotrexate revealed that they had the same number of relapses while they were taking prednisone as did patients who received placebo. Furthermore, the number of corticosteroid-related adverse events was equal in both treatment groups and the total cumulative prednisone dose reduction achieved by taking methotrexate in place of placebo equaled only about 1 mg/day.¹⁹

TNF-α, a cytokine produced by macrophages and T-lymphocytes, appears to play a significant role in the inflammatory process of PMR and GCA. In one pilot study, 3 mg/kg of intravenous infliximab was administered as adjunctive therapy to patients on corticosteroids. This therapy allowed 12 months of remission in three out of four patients treated with the drug.²⁰ These results were not seen in a recent double-blind, randomized, placebo-controlled study by the same author. Patients who received 3 mg/kg of infliximab at the same dosing intervals as used for rheumatoid arthritis over 22 weeks experienced the same number of weeks in remission as those who received placebo. No difference was seen in the duration of corticosteroid therapy or in the total number of patients who were able to discontinue corticosteroids between the groups.²¹

Outcomes

Adequate treatment with corticosteroids allows most patients to remain symptom free. Patients who have PMR need continued follow-up to monitor for drug-related toxicities and for possible progression to GCA. The development of a new headache or visual changes should prompt immediate medical evaluation and institution of higher doses of corticosteroids. Bilateral upper- and lower-extremity blood pressures should be obtained periodically. Differences between contralateral extremity pressures of 10 mm Hg or more should be considered abnormal. Bruits over carotid, subclavian, or femoral arteries may be due to either atheromatous disease or GCA and require further evaluation by vascular imaging.

Giant cell arteritis

Definition

GCA is a vasculitis characterized by granulomatous inflammation of medium-sized and large arteries. Inflammation is seen more commonly in the extracranial branches of the carotid arteries and other primary branch vessels of the aortic arch. Less often, internal branches of the carotid are affected, most notably the ophthalmic and posterior ciliary arteries; stenosis or occlusion of these arteries can cause loss of vision. At least one out of five patients develop large-vessel inflammation that can lead to branch vessel (e.g., most often subclavian) stenosis and less often aneurysmal dilation of the aorta (especially aortic root) or branch vessels.²² GCA is the most common vasculitis in whites older than 50 years. It has a predilection for people of northern European heritage. Women are affected at least twice as often as men.⁹

Prevalence

In the United States, GCA affects about 18 of 100,000 people older than 50 years. The epidemiologic characteristics of GCA are similar to those of PMR. The incidence of GCA is much higher in the northern latitudes, with a mean age at onset of 74 years. GCA and PMR might represent opposite ends of a disease spectrum, with many patients presenting features of both diseases. Approximately 40% of GCA patients have concurrent features of PMR at some point during their disease course.²³

Pathophysiology

Figure 1: Click to Enlarge

The cause of GCA is unknown, but vessel inflammation is cell mediated and not autoantibody induced. Dendritic cells, macrophages, and Th1-lymphocytes enter the vessel wall via the vasa vasorum and spread through the arterial adventitia.²⁴ A small fraction of activated T lymphocytes in the artery wall become clonally expanded. The cause for the clonal expansion is unknown but may be from a yet-unidentified neoantigen present in the arterial wall.²⁵ A broad range of proinflammatory cytokines, growth factors, and metalloproteinases are associated with inflammatory cell migration throughout the arterial media and intima. This panarterial inflammation leads to arterial damage, intimal proliferation, and ultimately luminal narrowing (Fig. 1). The luminal narrowing is responsible for ischemic events (loss of vision, stroke, and claudication). Understanding how these cytokines participate in inflammation will lead to better-targeted therapies in both GCA and PMR.²⁶

Signs and Symptoms

Headache is the most common symptom in GCA and occurs in 63% to 87% of patients. Systemic symptoms including fever, weight loss, and myalgias occur in 50% of patients.²⁷ Other symptoms include scalp pain, jaw pain while chewing, and arm or leg claudication. Vision loss, the most dreaded complication of GCA, occurs in more than 30% of patients.²⁸Anterior ischemic optic neuropathy is the most common cause of blindness. Twenty-seven percent of patients develop either an aortic aneurysm or large artery stenosis at some point during their disease course. Six percent of patients who develop an aortic aneurysm present with symptoms consistent with a dissection of the aneurysm.²² Extremity claudication occurs when aortic branch vessels, such as the subclavian artery, become critically narrow. Stroke and vision loss can occur without any preceding symptoms; however, patients can present with insidious nonspecific symptoms before the diagnosis of GCA is made. Forty percent of patients present with symptoms not considered classic for GCA. These symptoms can include cough, throat pain, or tongue pain.

A thorough physical examination may reveal a prominent, tender temporal artery. Evaluation of the artery may reveal a decreased pulse and a nodular appearance. Asymmetrical extremity blood pressures or pulses, bruits over subclavian or carotid arteries, or a murmur of aortic insufficiency suggests aortic or primary aortic branch involvement.

Diagnosis

Similar to PMR, no serologic test is diagnostic for GCA. Diagnosis is based on clinical symptoms in the presence of abnormal acute-phase reactants. More than 90% of patients have an elevated ESR. An elevated CRP, alkaline phosphatase, and platelets are not uncommon. Temporal artery biopsy is considered the standard diagnostic test for GCA. The sensitivity of biopsy, in series from medical practitioners, in detecting GCA is about 50%.²⁹ The yield of biopsy is a function of pretest probability, which might explain why some ophthalmology and other series, in which visual abnormalities were common, have yields as high as 80%.³⁰ Biopsy of the contralateral temporal artery adds very little to the sensitivity of the test.³¹

Figure 2: Click to Enlarge

Imaging of the vessel lumen with arteriography or magnetic resonance arteriography (MRA) may reveal aortic or arterial branches with stenoses or aneurysms (Fig. 2). The subclavian arteries, carotid arteries, and ascending aorta are the most commonly affected areas. Other arterial branches, such as the mesenteric and renal arteries, can also be affected. Vascular PET imaging with ¹⁸F-fluorodeoxyglucose may reveal vessel uptake in GCA as well as PMR. It is a more sensitive marker for disease than biopsy, but its diagnostic specificity is still in the process of being defined.³²

Treatment

Corticosteroids are the drug of choice for the treatment of GCA. They quickly reduce symptoms and decrease risk of visual complications from 60% to 14%.³³ Therapy with corticosteroids should start when GCA is first suspected. Waiting to start corticosteroids until after a temporal artery biopsy could result in irreversible loss of vision.

The optimal initial dose of prednisone is unclear, but most authorities agree that the initial dose should be between 40 and 60 mg/day. Doses of at least 60 mg are preferred when presenting features include ophthalmic or neurologic complications. Some authorities advocate intravenous methylprednisolone at doses of 1000 mg a day for 3 to 5 days in patients presenting with blindness.^33-35 The initial oral dose of corticosteroids should continue for 1 month before taper is considered. Many tapering schedules exist but few have been studied in clinical trials. One general rule is to taper by 10% to 20% every 2 weeks.⁹ Treatment duration is different for each patient. Long-term therapy is required in most patients. It is not unusual for corticosteroid therapy to extend beyond 4 years.^36-38

The efficacy of methotrexate in Wegener's granulomatosis and Takayasu's arteritis has led to its use in three randomized, double-blind, placebo-controlled trials for GCA. Jover and colleagues reported that patients randomized to methotrexate doses of 10 mg/week had fewer relapses and lower cumulative steroid doses compared with those who received placebo. However, a difference in relapse rates was only noted after 1 year of disease. There was no advantage to methotrexate in the first year. In addition, patients who received methotrexate had the same number of steroid-related side effects as those who received placebo.³⁹ Hoffman and colleagues conducted the only multicenter, randomized, double-blind, placebo-controlled trial of methotrexate at doses of 15 mg each week. Their conclusions did not support the use of methotrexate as adjunctive therapy with corticosteroids. Patients who were randomized to receive methotrexate did not have reduced disease activity, cumulative corticosteroid doses, or corticosteroid-related toxicities.⁴⁰ Spiera and colleagues reported similar results.⁴¹ The use of adjunctive methotrexate as a steroid-sparing agent in patients with GCA remains a controversial issue.

Figure 3: Click to Enlarge

The finding of abundant TNF-α in GCA arteries (Fig. 3) has led investigators to study TNF-α inhibition as a potential disease modulator in GCA. Hoffman and colleagues reported results of a multicenter, randomized, double-blind, placebo-controlled trial of intravenous infliximab as adjunctive therapy to corticosteroids in patients with newly diagnosed GCA.⁴²The study was stopped at 22 weeks when infliximab was shown to not improve durability of remission or reduce cumulative steroid doses. The results of this study suggest that although TNF is found in abundance in affected vessels, it might not play a critical role in the pathogenesis of GCA. Other mediators might play more important roles in disease propagation.

Aspirin (ASA) is known to reduce the risks of ischemic stroke and myocardial infarction.^43,44 No prospective trial has ever been done to see if antiplatelet therapy reduces the risk of cranial ischemic complications in patients with GCA. A recent review of 175 GCA patients by Nesher and colleagues observed that patients who took low-dose ASA (100 mg/day) were five times less likely to present with visual complications or stroke.⁴⁵ A second report by Lee and colleagues showed similar results in patients on antiplatelet or anticoagulant therapy.⁴⁶ Sixteen percent of GCA patients taking ASA, warfarin, or clopidogrel developed an ischemic event compared with 48% of patients not on this therapy (P < 0.0005). Bleeding complications were not increased in the patients on antiplatelet or anticoagulant therapy. The authors concluded that adjunctive low-dose ASA should be considered in all patients with GCA who have no contraindications for its use.

Outcomes

Some studies have found that the overall mortality in patients with GCA is similar to that of age- and gender-matched controls. Other studies have noted an increase in mortality, particularly from cardiovascular events. There is agreement that patients with GCA are at higher risk of death from the complications of aortic aneurysms. Thoracic aneurysms are 17 times more likely to occur in GCA patients and can occur at any time during the disease course. Fifty percent of patients with aortic aneurysms experience dissection or rupture of their aneurysm.^22,47-49 Cost-benefit data are not available. Because the risks of aortic catastrophes are well documented, we recommend careful auscultation for aortic valve murmurs or bruits, which should be followed by MRA or CT angiography to determine the nature and seriousness of the aortic lesion. Size of the lesion, hemodynamic consequences, and change over time per sequential imaging determine the need for surgical interventions.

Nearly every patient treated with long-term corticosteroids develops complications related to therapy. Sixty percent develop severe adverse events such as corticosteroid-induced diabetes, avascular necrosis, glaucoma, or vertebral fractures.⁵⁰Corticosteroid-induced osteoporosis is a well-known complication of long-term steroid use. Medications such as calcium, vitamin D, and anti-resorptive agents should be considered in every patient who will receive corticosteroids for more than 3 months. Screening for osteoporosis with bone densitometry at the induction of corticosteroid therapy (and at regular intervals) is as important an intervention as prescribing steroids to prevent blindness.

Summary

• Clinicians should inquire about headache, jaw pain, and vision loss in all PMR patients at every clinic visit because 10% will develop GCA at some point during their disease course.
• Lack of a response to corticosteroids or the inability to taper below 20 mg/day should raise the possibility of a paraneoplastic process in patients with GCA.
• Isolated increases in acute phase reactants in GCA and PMR should never lead to reflexive increases in corticosteroids doses but lead to more careful monitoring for a disease flare.
• Aortic aneurysms occur in about one of five patients with GCA and should be periodically screened for in every patient.
• Corticosteroids remain the standard of care for the treatment of GCA and PMR.

References

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Total Hip Arthroplasty

The total hip arthroplasty (THA), a common procedure performed in many acute care hospitals, is used in cases of severe joint damage resulting from osteoarthritis, rheumatoid arthritis, and avascular necrosis. It is one of the most successful and cost-effective interventions in medicine.After THA surgery, many patients typically are able to return to participation in activities that were too painful before surgery.

Indications

The most common indications for a THA are as follows:

• Pain. Pain is the principal indication for hip replacement. This includes pain with movement and pain at rest. A significant amount of pain may be reliably relieved as early as 1 week after surgery.
• Functional limitations. Capsular contractions and joint deformity cause a decreased ROM in the hip with subsequent functional restrictions.
• Loss of mobility. There are certain patient subgroups in which joint stiffness, without hip pain, is an indication for surgery. These groups include patients with ankylosing spondylitis.
• Radiographic indications of intra-articular disease. Although radiographic changes are considered in the decision to operate, the more significant determinant is the severity of symptoms. Arthroplasty of the hip is considered in the presence of osteoarthritis, aseptic necrosis, congenital abnormalities, rheumatoid arthritis, and Paget's disease, among others.

Contraindications for THA, both absolute and relative, include but are not limited to the following:

• Active infection.
• Inadequate bone stock or periarticular support.
• Younger age. Although most THAs are performed in patients between 60 and 80 years of age, hip replacement is occasionally performed in younger patients including those in their teens and early 20s.
• Obesity.
• Planned return to high-impact sports or occupations.
• Arterial insufficiency.
• Neuromuscular disease.
• Mental illness.

Procedure

The hip is a polyaxial synovial joint consisting of a modified ball and socket articulation between the acetabulum of the pelvis and the head of the femur. Both portions of this articulation are replaced during total hip arthroplasty. A bipolar prosthesis consisting of an outer metal shell that articulates with acetabular cartilage via a snap-fit attachment to the ball of the femoral component is often used. A number of factors determine the procedure used by the surgeon including surgeon familiarity and comfort, patient size, and scars from previous surgery or trauma.

The first successful THA was developed by John Charnley in the 1960s. This procedure involved a transtrochanteric lateral approach. Three other approaches have evolved since: the anterolateral approach, the direct lateral approach, and the posterolateral approach. Controversy remains as to which approach results in the lowest complication rate.

• Anterolateral approach. There are numerous variations of the anterolateral approach. All variations approach the hip through the interval between the tensor fascia lata and the gluteus medius muscle. Some portion of the hip abductor is released from the greater trochanter, and the hip is dislocated anteriorly.

• Direct lateral approach. The direct lateral approach leaves the posterior portion of the gluteus medius attached to the greater trochanter. Because the posterior soft tissues and capsule are left intact, this approach is preferred in the more noncompliant patients to prevent postsurgical dislocation.

• Posterolateral approach. The posterolateral approach gains access to the hip joint by splitting the gluteus maximus muscle. The short external rotators are then released, and the hip abductors are retracted anteriorly. The femur is then dislocated posteriorly. Although the posterior approach may allow for maintenance of abductor strength, it generally results in a higher postsurgical dislocation rate.

Both the anterolateral and the posterolateral approaches appear to result in decreased blood loss and fewer hematomas when compared with the transtrochanteric approach. The advantages of the anterolateral approach are the lower dislocation rates and the excellent acetabular exposure. The disadvantage of the anterolateral approach is an increase in antalgic gait (at least temporarily). Although several studies imply weakening of the abductor muscles as a result of the anterolateral approach, only one study has found a statistically significant increase in weakness of the abductors with this approach.

Although the posterolateral approach has remained essentially unchanged, the anterolateral approach has been modified by several surgeons to decrease gluteus medius disruption and, it is hoped, to decrease postoperative abductor muscle dysfunction and resultant limp. However, no studies from the past decade have yet compared abductor muscle dysfunction in the posterolateral approach versus a modified anterolateral approach. In obese patients or those undergoing revision surgery who have excessive scar tissue, the aforementioned surgical approaches may not provide adequate exposure. In these circumstances, a trochanter osteotomy can be performed. After the prosthesis has been inserted, the trochanter is reattached by wires or screws.

A number of criteria must be met for the long-term success of the implant. These include adequate fixation, adequate strength and wear resistance, and biological and biomechanical compatibility.

• Fixation. Two types of fixation are recognized: cemented and cementless. Methylmethacrylate cement has the useful property of approximately 90% of its polymerization occurring during the first 10 minutes following application. The acrylic cement's resistance to compression load is usually adequate to allow weight-bearing as tolerated (WBAT) on the affected extremity early in the rehabilitation program often on the first or second postoperative day. However, there are a number of disadvantages to the traditional method of cementing. These include poor tensile and compressive strengths of the acrylic cement, and the high incidence of component loosening in younger, more active patients.Cementless technology was introduced as a strategy to improve the results of cemented hip replacement in the 1970s. Excellent bone ingrowth has been demonstrated in porous-coated implants inserted without cement provided there is good bone quality. Bone in growth occurs during the first six postoperative weeks. Whether the patient is restricted to nonweightbearing (NWB) status or allowed to partially weight-bear (PWB) is determined by the surgeon and may depend on the mechanical fixation of the prosthesis within the acetabulum and femur. There is no universal agreement on indications for cementless versus cemented hip replacement. However, it is generally agreed that the primary indication for a cementless THA is the young, active individual, usually younger than age 65 physiologically.
• Adequate strength and wear resistance. In the early years of hip replacement, fracture of the femoral stem was a problem. This problem has been resolved largely by the use of improved metal processing. Polyethylene wear undoubtedly has been the major long-term problem of THA. The use of a ceramic femoral head has been advocated, especially in young, active patients, because it produces less polyethylene wear compared with a conventional metal femoral head.
• Biological compatibility. The primary fixation mode of cementless acetabular components is mechanical and is dependent on a physical interlock between the cup and the reamed acetabulum.Secondary fixation is biological and is achieved by means of bone growth onto or into the substrate at the implant-bone interface. The fixation surface of cementless metal-backed sockets typically consists of a porous coating of beads or fiber metal, a titanium plasma-sprayed surface, various sintered surface textures, or a bioactive ceramic coating such as hydroxyapatite or tricalcium phosphate. For long-term stability, it is essential that this direct bond between the implant and the bone be maintained. The production of particulate wear debris from implant materials and subsequent osteolysis has been recognized as the major cause of long-term failure in THA. Using cell cultures, Vermes and colleagues demonstrated that metallic particulate debris affected osteoblast function through two distinct mechanisms: a direct negative effect on cellular function by the phagocytosis itself, and an effect mediated through cytokines that cause a downregulation of procollagen gene expression along with decreased cell proliferation. Moreover, this study demonstrated that osteoblasts stimulated by particulate debris produced interleukin-6 and prostaglandin E2, leading to the activation of osteoclast function.
• Biomechanical compatibility. Prosthetic impingement resulting from poor positioning, the head–neck ratio, and the presence of a modular head with an extended sleeve has been implicated in decreasing the postsurgical ROM at the hip after THA. Additional factors, such as osseous impingement and soft-tissue tension, can further decrease the range.

Several complications are associated with THA. These include, but are not limited to the following:

• Deep vein thrombosis (DVT). DVT remains the most common and potentially lethal complication following either elective or emergency surgery of the hip in adults. Peak incidence, which is proably between 40% and 60% for distal (calf) vein thrombosis, and 20% for proximal (popliteal, femoral, and iliac) thrombosis, occurs during the second and third week postsurgery. However, the period of increased risk can be up to 3 months after surgery. Even with prophylaxis, the incidence of angiographically proven asymptomatic pulmonary embolism has been reported to be approximately 20%.
• Heterotopic ossification. Heterotopic ossification (HO) is a well-known complication of surgical approaches to the hip that involve dissection of the gluteal muscles and is the most common complication following THA. There is also a strong association between HO and spinal cord injury, with lesions occurring at multiple sites and showing a strong propensity to recur, and in patients with traumatic brain injury. The exact mechanism for heterotopic bone formation has not been thoroughly elucidated, although trauma to the muscles during surgery appears to be a major contributing factor in provoking pluripotent mesenchymal cell differentiation into osteoprogenitor cells. This process begins as soon as 16 hours after injury and is maximal at 36–48 hours. Additional reported risk factors for HO include thoracic and abdominal trauma, male gender, T-type fracture, delay in fracture fixation, and closed head injury.Differentiating early HO from lower extremity deep venous thrombosis (DVT) can prove to be extremely difficult as both conditions can present with the same symptoms of lower extremity pain, swelling, and erythema. HO and DVT have been positively associated, perhaps because the mass effect and local inflammation of HO encourage adjacent thrombus formation by venous compression and phlebitis. HO often begins as a painful palpable mass that gradually becomes nontender and smaller but firmer to palpation. Bone scan is the method of choice for earliest detection.
• Femoral fractures. Fracture of the femur in association with THA is a challenging complication that has been well described.The prevalence of these fractures has ranged from 0.1% (7 of 5400)  to 20%. Risk factors include female gender, rheumatoid arthritis, cortical perforation, osteopenia, osteoporosis, preoperative femoral deformity, a revision operation, osteolysis, and loosening of the stem.
• Dislocation. Dislocation of the total hip replacement remains a common and potentially extremely problematic complication. As many as 85% of dislocations are reported to occur within 2 months after THA.Dislocation is more common in elderly people, particularly those with impaired cognition and balance and vibration sensitivity. It occurs more commonly in women. There is also a correlation with history of trauma or developmental dysplasia of the hip. Patients with cerebral dysfunction or excessive alcohol use are also at higher risk. Dislocation rate is a factor of many other requirements including component position, technical errors, imbalance of tissues, surgical approach, and patient compliance.
• Neurovascular injury. A review of the literature reveals that the prevalence of nerve palsy following THA varies from 0.08% to 7.5%, depending on the study with an overall prevalence of 1%. The peroneal division of the sciatic nerve is involved in almost 80% of cases, with the femoral nerve and the obturator nerve involved less frequently.There are many proposed causes for neuropathy associated with THA, including direct trauma; excessive tension because of an increase in limb length, or offset, or both; bleeding, or compression, or both, by a hematoma; and unknown.

Presurgery Evaluation and Education

At many institutions, patients attend a presurgery class 7–10 days before surgery. These preoperative training sessions have been shown to improve motivation, understanding, and compliance during rehabilitation of the postsurgical patient. The class instructors usually include a case nurse, dietitian, and physical therapist.

• The case nurse reviews how to make the home safe; what to expect before, during, and after surgery; how to prevent dislocations; what medications will be used; and what type of transport is needed to bring the patient home. He or she also brings in pictures of the operating room and samples of equipment. A case nurse reviews the patient's history before admission, and a home assessment is performed 6 weeks preoperatively.
• The dietitian discusses which foods help healing, and how to cope with decreased appetite and depression that are both common after surgery.
• The physical therapist discusses the postsurgical physical therapy program and shows each patient how to use an appropriate assistive device for gait. An assessment is made of general strength, ROM, neurologic status, endurance, and safety awareness. The patient receives instruction on the early postoperative exercises, deep breathing and coughing, pertinent hip precautions, and safe transfer techniques. Upper body exercises are taught to help the patient walk with an assistive device (crutches, or walker) and to transfer. Function can be assessed using the Harris Hip Scale or a similar standard outcome measurement for the hip.

Patients and their caregivers are encouraged to ask questions and complete forms used to calculate their current function. The patients receive booklets on diet, exercise, postsurgical precautions, home safety, and discharge planning.

Postsurgical Rehabilitation

Following the surgery, thromboembolic disease (TED) hose are placed on the patient. For patients who have undergone either a posterolateral approach or a transtrochanteric approach, a triangular foam cushion is strapped between the legs to keep the hip in an abducted position. Patients at a high risk of dislocation, such as those who have undergone a postrevision arthroplasty or those with cognitive impairments, may need to wear a hip abduction orthosis that maintains the hip in abduction for 6–12 weeks. These orthoses may make ambulation difficult if the abduction is more than 5–10 degrees.

The postsurgical examination is divided into three components: patient history, the systems review, and tests and measures. The selection of examination procedures and the depth of the examination are based on the patient age, severity of the problem, the acute stage of recovery, the early phase of rehabilitation, home situation, and other relevant factors. The relevant tests and measures for this patient population include the Fatigue Severity Scale, the Harris Hip Scale, Manual muscle testing of the upper extremity (UE) and nonoperated lower extremity (LE), Elderly Mobility Scale, Braden Scale for Predicting Pressure Sore Risk, and ROM with goniometry. Reexamination is conducted on a daily basis and at discharge from the acute care phase. Indications for reexamination include new clinical findings or failure to respond to physical therapy interventions. The reexamination and discharge includes the same tests and measures used at initial examination.

Most important is to avoid during the examination those motions and positions that are contraindicated according to surgical approach:

• For the posterolateral approach, this involves avoidance of flexion of the hip beyond 90 degrees, and minimal adduction or internal rotation of the hip.
• Following a lateral or anterolateral approach, the patient should avoid extension, external rotation, and adduction across midline.

These precautions must be maintained for at least 6 weeks, or until the surgeon decides otherwise.

A review of the literature reveals inconsistent practice patterns in the physical therapy management of THA patients. The postsurgical rehabilitation program that follows is based on the consensus found.The program is divided into two components: the inpatient stay, and the outpatient course of intervention.

Phase 1: Inpatient Phase (24 Hours to Discharge)

This phase typically involves four to eight physical therapy sessions.

Table: Factors That May Modify Frequency of Visits

Accessibility and availability of resources.	Overall health status.
Adherence to the intervention program.	Pain and early movement tolerance.
Age.	Potential discharge destinations.
Cognitive status.	Premorbid conditions.
Comorbidities.	Probability of prolonged impairment, functional limitation, or disability.
Complications from surgery.	Psychological and socioeconomic factors.
Concurrent medical, surgical, and therapeutic interventions.	Psychomotor abilities.
Decline in functional independence.	Severity of the current condition.
Level of impairment.	Social support.
Level of physical function.	Stability of the condition.
Nutritional status.	Stability of vital signs.

 Twice daily visits are recommended over one daily visit. Ideally, the patient will have attended a preoperative training session. Basic physical therapy begins on postoperative day 1, provided no direct complications from the surgery have occurred. Patients should be evaluated routinely for peripheral nerve function on a daily basis. If a palsy is detected, a knee immobilizer (for femoral nerve palsy) should be used with ambulation, additional exercises focusing on strengthening the affected muscles and stretching the antagonists to prevent joint contractures should be prescribed, and the patient should be fitted with the appropriate orthotic (ankle foot orthoses [AFOs] with sciatic palsy) to allow physical therapy to proceed.

Goals

• Prevent postsurgical complications, including
  • DVT
  • postoperative infection
  • detrimental effects of immobilization
  • pulmonary embolus
• Reports of pain to be 7/10 or less. Increasing or severe buttock pain may indicate a hematoma.
• Patient to achieve an independent or minimally supervised functional level for
  • bed mobility including transfers in and out of bed
  • transfers on and off a commode
  • transfers up and down from a chair of varying heights
• Gait training at a household level with the appropriate assistive device for 100 feet, and with the least amount of assistance that renders the patient safe.
• Independence with stair negotiation (one or more steps), consistent with the patient's home environment, with appropriate assistive device and with and without a handrail.
• Independence with the home exercise program that will be performed 2–3 times a day.
• Independence with adherence to THA precautions and correct application of them into any permitted functional activity.

The patient should be repositioned every 2 hours by the nursing staff. The skin, especially on the heels, is checked regularly for breakdown. The patient is provided with information on assistive devices, such as an elevated seat, a long handled shoehorn, elastic laces, and a long handled reacher. A referral for occupational therapy may be necessary for specific instructions on activities of daily living such as dressing and bathing.

Electrotherapeutic and Physical Modalities

Modalities that reduce pain and swelling (ice and elevation) are initiated as early as possible. With the physician's permission, electrical stimulation can be used for edema reduction, muscle reeducation, and pain control.

Therapeutic Exercise and Home Program

The therapeutic exercise program typically begins within 24 hours after the surgery.

Exercises may include the following:

• Resistive exercises to the uninvolved extremities.
• Ankle pumps (not circles, so as to prevent any inadvertent rotation at the hip) for both lower extremities.
• Quadriceps sets, gluteal sets, and hamstring sets of the involved leg.
• Deep-breathing and coughing exercises.
• Leg dangling over the edge of the bed (day 2) and sitting in a hip chair. The clinician must check the patient's blood pressure and pulse during initial sitting and standing activities. If orthostatic hypotension occurs, a tilt table or a reclining, high-backed chair can be used to gradually bring the patient to an upright position.
• Active and isometric hip abduction of the involved leg (day 2).These exercises are deferred initially if a trochanteric osteotomy has been performed.
• Active assistive hip and knee flexion (heel slides) to the involved limb. These are performed while maintaining the hip ROM within the guidelines specified by the surgeon (day 2). The patient can use a sheet to help with this exercise.
• Short arc quads of the involved leg (day 2).

Functional Training

On the first day after the surgery, the clinician begins transfer training and instructs the patient with regard to bed mobility. Training includes transfers from supine to sitting on the bed, and then from sitting to standing, while observing all of the necessary hip precautions. If permitted by the surgeon, the patient can be shown how to transfer to an appropriate bedside chair. The patient is encouraged to sit on the chair for about 30–60 minutes, depending on tolerance, which can be measured using the vital signs of pulse and blood pressure, as well as subjective complaints such as light headedness or dizziness.

Gait training with crutches (younger more active patients) or walker (more elderly patients) is usually begun on the second day following surgery. The patient's assistive device is adjusted to the correct height. Close attention must be paid to these patients during gait training because of their balance deficiencies and the potential for temporary postural hypotension.

• The weight-bearing status of the patient with a noncemented THA is decided by the surgeon. It can vary from NWB to toe-touch weight bearing, to partial weight bearing (20–25 lbs pressure). Toe-touch weight bearing involves applying no more than 10% of body weight. It has been described as analogous to walking on eggshells. Partial weight bearing is a difficult concept for most patients to grasp. Using a bathroom scale, or a description such as "1/10 of body weight" (depending on the patient's weight) usually helps. Force platforms are also available to measure these forces directly and can provide beneficial feedback for the patient.
• The weight-bearing status for the patient with a cemented THA is usually partial weight bearing for 6 weeks prior to full weight bearing, although some surgeons permit weight bearing as tolerated with a walker immediately.

Normalization of the gait pattern should be taught early. Stand-to-pivot transfers should also be taught to prevent the patient from rotating at the involved hip.

Stair negotiation, based on the patient's home situation, is typically taught on day 3.

Home Care Phase (1–7 Days)

If functional independence is required before a patient returns home, the patient is typically transferred to a dedicated rehabilitation unit, or an acute or subacute care setting. If adequate home care and safe transport are available, the patient is allowed to return home.

In one study, Munin and colleagues determined certain markers that were predictive of patients who would require an inpatient rehabilitation program versus direct discharge to home. Those patients determined to be at high risk were 70 years of age or older, 51% lived alone, and many had a number of comorbid conditions. The average length of stay for comprehensive inpatient THA rehabilitation is 7–10 calendar days.

A physical home care assessment usually occurs within 24 hours after hospital discharge. During this phase, the role of the physical therapist is to address any safety concerns including moving or adjusting the height of furniture, the removal of any throw rugs, review of sitting and sleeping positions and hip precautions, and progression of home exercise program.

Weight-bearing exercises, such as seated heel raises and mini-squats against a wall are usually introduced at this time.

Phase 2: Outpatient Phase (Week 2–8) This phase typically lasts for 2–6 weeks and may involve six to nine physical therapy sessions. The staples are usually removed after 12–14 days. Goals Reports of pain to be 5/10 or less. Hip ROM to be 70–90 degrees of hip flexion. Balance and proprioception to be at 50% of the uninvolved leg, as measured by single-leg stance time, if weight-bearing status permits. Strength to be 3/5–4/5 on the involved lower extremity. A positive Trendelenburg test at the end of this phase indicates a need for additional outpatient therapy for gait training and strengthening. Patient to achieve independence with all transfers. Patient to have a normal gait pattern with a quad cane or straight came, held on the contralateral side on level surfaces. Electrotherapeutic and Physical Modalities Superficial thermal modalities may be used in this phase. Therapeutic Exercise Weakness following a THA is common and can lead to diminished protection of the implant fixation surfaces during activities. Flexibility exercises are performed within the limitations of hip precautions to the following muscle groups: Iliopsoas. Quadriceps and rectus femoris. Gastrocnemius and soleus. Hamstrings. Lower extremity strengthening exercises include NWB exercises of heel slides, hip abduction in the supine position, straight leg raises, and short arc quads weight-bearing exercises of weight shifting, modified wall slide squats to approximately 45 degrees of hip flexion, modified lunges (anterior and lateral), and step-ups and step-downs Upper extremity strengthening exercises are initiated as needed. Cardiovascular conditioning is begun with the use of an upper body ergonometer. Neuromuscular Retraining Biomechanical ankle platform system (BAPS) board exercises in sitting or standing position, with weight-bearing restrictions observed. Biased stance balance-and-reach activities involving reaching arms forward at shoulder height and waist height. Functional Training Gait training is performed on level and stairs with appropriate assistive device. The patient can be advanced to a single-point cane as and if appropriate. A four-point cane may be used as an interim device. Transfers are progressed to all surfaces, when permitted. Patients are usually permitted to drive 6–8 weeks after surgery. Driving reactions, including the delay and force of a brake application after an emergency signal, may be impaired, especially following right hip replacement. Manual Therapy Manual therapy techniques include soft tissue techniques and mobilization of the posterolateral or anterolateral hip scar mobilization contract–relax techniques within the limits of the hip precautions passive stretching of lateral hip, knee, and lumbar spine within the limits of the precautions Phase 3 (Week 9 +) Goals Reports of pain to be 2/10 or less with activity of the involved leg, and 0/10 at rest. Hip ROM to be at 90 degrees of flexion. Involved lower extremity muscle strength to be at 4/5 with manual muscle testing. Patient to be independent with ambulation, and with no gait dysfunction. Balance and proprioception to be at 80%, compared with the uninvolved leg, as measured by single-leg stance time. Patient to be independent with stair negotiation without an assistive device. Patient to demonstrate functional independence in activities of daily living. Patient to achieve return to employment or previous hobbies, as indicated. Therapeutic Exercise Phase 1 exercises are progressed, with the addition of increased resistance as appropriate. Weakness of the hip muscles has been shown to exist up to 2 years postsurgery. Therefore, the therapeutic exercise program should be continued for at least 1 year, and preferably longer, until the involved limb strength is equal to that of the uninvolved. Treadmill exercises are initiated, as well as other low-impact forms of conditioning, as appropriate. Neuromuscular Retraining Single-leg balance-and-reach exercises are performed including reaching arms forward, reaching opposite leg forward, and reaching opposite leg laterally. Mark Dutton, PT,Orthopaedic Examination, Evaluation, and Intervention 2nd edition McGraw-Hill 2008  ISBN: 0071474013  https://www.aofoundation.org/wps/portal/!ut/p/c1/04_SB8K8xLLM9MSSzPy8xBz9CP0os3hng7BARydDRwML1yBXAyMvYz8zEwNPQwN3A6B8JG55AyOSdBtYBLgZGDmZ-huaBAcYgeTx6_bzyM9N1S_IDY0od1RUBACWqcev/dl2/d1/L2dJQSEvUUt3QS9ZQnB3LzZfQzBWUUFCMUEwOEVSRTAySjNONjQwSTEwRzA!/?contentUrl=%2fsrg%2f31%2f04-Approaches%2f2008%2f31_Nr52_Appr_Direct-lateral.jsp&bone=Femur&segment=Proximal&showPage=approach&classification=31-B3&treatment=&method=Arthroplasty&implantstype=&redfix_url=1284974569031&approach=Direct%20lateral%20approach http://www.jisrf.org/total_hip_replacement.htm http://www.hopkins-arthritis.org/physician-corner/cme/rheumatology-rounds/hip_knee_arthroplasty_rheumrounds9.html