By David Backstein, MD
Periprosthetic infection is a devastating complication that occurs in 1% to 2% of patients after total hip arthroplasty. Diagnosis requires obtaining a thorough history from the patient and conducting a thorough examination combined with appropriate investigations. The differential diagnosis includes aseptic loosening, trochanteric bursitis, iliopsoas impingement, or pain from extrinsic sources such as the spine. Effective use of available testing modalities is critical to making the diagnosis. Investigations may include hematologic studies, imaging studies, and intraoperative frozen-section analysis as well as synovial fluid white blood-cell count, culture, and Gram stain.
The first sign of an infection about a total hip prosthesis is usually pain, often at night or at rest. Radiographs may demonstrate loosened components, progressive radiolucencies, focal lysis of bone, and periosteal new-bone formation. The erythrocyte sedimentation rate and C-reactive protein level are nonspecific tests but can provide critical information. In a recent study of patients who were undergoing revision total hip arthroplasty, Schinsky et al. found that no hip in a patient with a preoperative erythrocyte sedimentation rate of <30 mm/hr and a C-reactive protein level of <10 mg/dL was determined to be infected1. This corroborates earlier work that indicated that the combination of a normal erythrocyte sedimentation rate and C-reactive protein level is reliable for predicting the absence of infection2. A synovial fluid cell count of >3000 white blood cells/mL has been shown to be the most predictive perioperative testing modality in the diagnosis of infection about a total hip prosthesis when combined with an elevated erythrocyte sedimentation rate and C-reactive protein level3. The results of frozen-section analysis are generally considered positive in the presence of at least ten polymorphonuclear cells per high-power field. Technetium-99 scans may be helpful in the diagnoses of chronic infection; however, they are nonspecific. Indium-111 leukocyte scanning alone is more accurate; however, the combination of these two tests improves the accuracy for detecting infection. Newer tests, such as polymerase chain reaction, have thus far shown large discrepancies with regard to sensitivity and positive predictive values and are probably not yet ready for routine use.
Treatment with implant removal, thorough débridement, extended use of intravenous antibiotics, and second-stage reimplantation remains the gold standard treatment option for infection about a total hip prosthesis. While successful outcomes after single-stage revision have been reported in some studies, the best results continue to be obtained when there is a minimum span of six weeks between excision and reimplantation, with eradication of infection in approximately 85% of hips4.
Schinsky MF, Della Valle CJ, Sporer SM, Paprosky WG. Perioperative testing for joint infection in patients undergoing revision total hip arthroplasty. J Bone Joint Surg Am.2008;90:1869-75.901869
2008
[PubMed][CrossRef]
Spangehl MJ, Masri BA, O'Connell JX, Duncan CP. Prospective analysis of preoperative and intraoperative investigations for the diagnosis of infection at the sites of two hundred and two revision total hip arthroplasties. J Bone Joint Surg Am.1999;81:672-83.81672
1999
Hanssen AD, Rand JA. Evaluation and treatment of infection at the site of a total hip or knee arthroplasty. Instr Course Lect.1999;48:111-22.48111
1999
Parvizi J, Ghanem E, Azzam K, Davis E, Jaberi F, Hozack W. Periprosthetic infection: are current treatment strategies adequate? Acta Orthop Belg.2008;74:793-800.74793
2008
Dealing with Heterotopic Ossification
By Vincent D. Pellegrini Jr., MD
Introduction
Heterotopic ossification is the abnormal formation of lamellar bone in nonosseous soft tissues; as such, it is histologically distinct from dystrophic calcification1.
Clinical Presentation
Most commonly, heterotopic ossification occurs as a sequel to surgically induced trauma about the hip, especially in association with total hip arthroplasty or operative repair of acetabular fractures. The radiographic prevalence of heterotopic ossification following total hip arthroplasty is reported to be as high as 90%; as many as 8% of patients experience a compromise in clinical function that may be manifested as pain, decreased range of motion, or frank ankylosis1. Known risk factors include male sex, prior heterotopic ossification, hypertrophic or posttraumatic arthritis, diffuse idiopathic skeletal hyperostosis, ankylosing spondylitis, and traumatic brain injury or other conditions of the central nervous system.
Pathophysiology
Our understanding of the pathophysiology of heterotopic ossification is largely speculative. Pluripotent mesenchymal stem cells are induced to differentiate down osteoprogenitor cell lines within sixteen hours of the inciting event, with a peak in cellular activity at less than thirty-six hours. Efforts at preventing the formation of the osseous tissue are futile if initiated beyond ninety-six hours after the inciting event. Cells are thought to derive from the local tissues, and pathologic formation of bone passes reliably through a pathway of endochondral ossification. The ectopic bone is metabolically hyperactive.
Prophylaxis
Effective prophylaxis must be initiated within five days of operation or injury. Bisphosphonate therapy delays mineralization of osteoid matrix; following the discontinuation of bisphosphonates, ectopic bone can be seen on radiographs as proceeding to ossification in an unimpeded manner. Nonsteroidal anti-inflammatory agents effectively prevent the formation of heterotopic bone but are poorly tolerated by elderly patients and have systemic effects that delay ingrowth into prosthetic surfaces. Limited-field external beam radiation is highly effective as a prophylaxis; it can be administered as a single preoperative or postoperative treatment and its effects are precisely localized to the operative area2,3. Wound complications have not been observed with a single treatment of 600 to 800 rad (6 to 8 Gy), and the late appearance of sarcoma has not been reported at these doses.
Treatment
Surgical removal of ankylosing ectopic bone about the hip is infrequently required. Postoperative prophylaxis is essential to avoid recurrence; full-field radiation is highly effective and minimizes marginal-field bone growth1.
Pellegrini VD Jr. Management of heterotopic ossification. In: Lieberman JR, Berry DJ, editors. Advanced reconstruction: hip. The Hip Society. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2005. p 247-56.
2005
Pellegrini VD Jr, Konski AA, Gastel JA, Rubin P, Evarts CM. Prevention of heterotopic ossification with irradiation after total hip arthroplasty. Radiation therapy with a single dose of eight hundred centigray administered to a limited field. J Bone Joint Surg Am.1992;74:186-200.74186
1992
[PubMed]
Schneider DJ, Moulton MJ, Singapuri K, Chinchilli V, Deol GS, Krenitsky G, Pellegrini VD Jr. Inhibition of heterotopic ossification with radiation therapy in an animal model. Clin Orthop Relat Res.1998;355:35-46.35535
1998
[CrossRef]
Avoiding Limb-Length Inequality
By Raymond H. Kim, MD
Limb-length inequality is an undesirable complication of total hip arthroplasty and is associated with numerous adverse effects, including gait alterations, low-back pain, patient dissatisfaction, and even litigation. Konyves and Bannister1 noted that lengthened limbs were also associated with lower clinical hip scores. Limb-length discrepancy can result from a poor preoperative patient evaluation as well as intraoperative technical errors with regard to the level of resection of the femoral neck, the prosthetic neck length, or the failure to restore offset.
Preoperatively, patients should be carefully assessed for a true limb-length discrepancy due to hip disease, which should be distinguished from a false limb-length discrepancy due to hip contractures or pelvic obliquity due to spinal disease2. The evaluation should also assess for coxa vara, acetabular protrusion, and a marked preoperative flexion contracture of the hip, any of which may place the patient at increased risk for postoperative limb-length inequality. Physical examination of the patient should include measurement from the anterior superior iliac spine to the medial malleolus on both lower limbs as well as an assessment of symmetry of the iliac crests to evaluate for preexisting limb-length discrepancies or pelvic obliquity.
Accurate preoperative planning and templating of radiographs is critical to the proper selection and positioning of the component. Various methods have been described for radiographic templating, with use of the greater and lesser trochanters, the inter-ischial and the inter-teardrop lines, and the center of the femoral heads as reference points. The goal of preoperative templating is to restore the normal vertical as well as horizontal offset of the hip. If the anatomy of the diseased hip is extremely distorted, the normal contralateral hip may be used to template the position of the component. Templating should begin with placement of the acetabular component in order to restore the hip center, followed by a determination of the correct femoral component size and, finally, adjustment of the seating level of the femoral component to reestablish proper length and offset.
Intraoperatively, the use of a reproducible method of evaluating limb length is critical in order to determine the relative change in length after the trial components are in place. Several techniques have been described for assessing limb length. Palpation of the heels and patellae is a crude method that is heavily dependent on proper patient positioning. When palpating the patellae, the operatively treated limb should feel relatively short if the limb lengths are equalized. More accurate means of assessing limb lengths intraoperatively include measuring the distance between fixed pins into the ilium and greater trochanter3, measuring from the lesser trochanter to the femoral head center, and referencing the infracotyloid groove to a mark on the greater trochanter.
Postoperatively, patients with limb-length inequality can be treated nonoperatively with observation or shoe lifts. Operative treatment may be indicated if there is intolerable hip or back pain due to the length discrepancy or if there is nerve injury. Operative options include modular head change, liner exchange, and full component revision. Shortening of the limb may compromise hip stability and may require use of a constrained liner or even trochanteric advancement.
Limb-length inequality can best be avoided by careful preoperative patient assessment, meticulous preoperative radiographic templating, and use of a reproducible method for intraoperative measurement.
Konyves A, Bannister GC. The importance of leg length discrepancy after total hip arthroplasty. J Bone Joint Surg Br.2005;87:155-7.87155
2005
[PubMed][CrossRef]
Jasty M, Webster W, Harris W. Management of limb length inequality during total hip replacement. Clin Orthop Relat Res.1996;333:165-71.333165
1996
Bose WJ. Accurate limb-length equalization during total hip arthroplasty. Orthopedics.2000;23:433-6.23433
2000
Neurovascular Complications Associated with Total Hip Arthroplasty
By David G. Lewallen, MD
Neurologic complications following total hip arthroplasty vary in severity from neurapraxia (peripheral nerve intact, not functioning) to axonotmesis (endoneurial tube intact, myelin disrupted) to neurotmesis (complete disruption). Most nerve injuries are in the operatively treated leg, but pressure or traction can cause nerve injury in the contralateral leg or in the upper extremities.
Deficits are usually noted immediately after surgery, but delayed onset is possible even when due to intraoperative events. Nerve injury can manifest days after surgery as a result of direct pressure or formation of a hematoma. Deficits seen several weeks or longer after surgery can be due to migration of implants or hardware. It is very important that the neurologic status be documented immediately after surgery so that the time of onset of any nerve deficit is clear.
Nerve deficits are clinically evident in 0.6% to 1.3% of patients who have undergone primary total hip arthroplasty1,2. Subclinical injury, as evidenced by electromyography, occurs in as much as 70% of patients who have undergone hip arthroplasty3. More than 90% of clinically evident nerve palsies involve the sciatic nerve, followed in percentage of frequency by the femoral and obturator nerves. Superior gluteal nerve injury is possible during surgical approaches that split the gluteus medius, if the split extends more than 5 cm proximal to the tip of the trochanter2,4. Approximately 50% of sciatic palsies involve the peroneal division only, with the rest involving both the peroneal and tibial divisions. A twofold or higher incidence of nerve palsy has been reported in female patients3.
To avoid nerve injury, careful surgical technique is important and includes meticulous retractor placement and avoidance of excessive limb-lengthening (4 cm or greater). Use of nerve monitoring is controversial, as such monitoring has not been documented to reduce the risk of nerve palsy.
Nerve recovery is variable and relates to the severity of injury. Surgical exploration is contraindicated unless a strong suspicion exists that there was direct nerve injury (transection or impingement by cement, screws, or suture). Isolated peroneal palsy is associated with a better prognosis than complete sciatic palsy is, but nearly 80% of all palsies will be associated with incomplete recovery. In a large single institutional review of nerve palsies, most patients did not achieve full recovery, with improvement occurring as long as twenty-four months after injury1. Retained motor function or early return of function within days suggests a higher rate of good final outcome4.
Vascular complications due to total hip arthroplasty, although rare, are potentially catastrophic and may be arterial, venous, or both. Structures at risk are the femoral, obturator, common, and external iliac and profunda femoris vessels. Manifestations include hemorrhage, thrombosis, arteriovenous fistula, and false aneurysm formation. The incidence approximates 0.2% to 0.3% of arthroplasties2. Injury can be caused by any sharp implements, such as scalpels, retractors, and osteotomes. Familiarity with the four-quadrant system for dividing the acetabular cavity and the safe zones for screw placement is very important to avoid injury from screws or drills5,6. Vascular injury can also occur during extraction of intrapelvic cement and medially migrated sockets. Preoperative studies, including arteriography, can be helpful in identifying the proximity of vascular structures to implants. Intrapelvic control of vessels prior to component removal may be helpful.
Knowledge of vascular anatomy and contingency planning can prevent catastrophic events or allow their successful management. Appropriate surgical draping for potential adjunctive incisions, such as the ilioinguinal approach for emergent control of intrapelvic vascular injury, can be lifesaving. The availability of a vascular surgeon can be important in complex cases during which vascular repair or ligation may be necessary.
Farrell CM, Springer BD, Haidukewych GJ, Morrey BF. Motor nerve palsy following primary total hip arthroplasty. J Bone Joint Surg Am.2005;87:2619-25.872619
2005
[PubMed][CrossRef]
Lewallen DG. Neurovascular injury associated with hip arthroplasty. Instr Course Lect.1998;47:275-83.47275
1998
Weber ER, Daube JR, Coventry MB. Peripheral neuropathies associated with total hip arthroplasty. J Bone Joint Surg Am.1976;58:66-9.5866
1976
Schmalzried TP, Amstutz HC, Dorey FJ. Nerve palsy associated with total hip replacement. Risk factors and prognosis. J Bone Joint Surg Am.1991;73:1074-80.731074
1991
Keating EM, Ritter MA, Faris PM. Structures at risk from medially placed acetabular screws. J Bone Joint Surg Am.1990;72:509-11.72509
1990
Wasielewski RC, Cooperstein LA, Kruger MP, Rubash HE. Acetabular anatomy and the transacetabular fixation of screws in total hip arthroplasty. J Bone Joint Surg Am.1990;72:501-8.72501
1990