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Rheumatology grand rounds loosening of a revision total hip replacement in a 60-year-old woman with longstanding rheumatoid arthritis clinicopathologic conference.

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ARTHRITIS & RHEUMATISM
Vol. 38, No. 9, September 1995, pp 1315-1324
0 1995, American College of Rheumatology
1315
RHEUMATOLOGY GRAND ROUNDS
LOOSENING OF A REVISION TOTAL HIP REPLACEMENT IN
A 60-YEAR-OLD WOMAN WITH
LONGSTANDING RHEUMATOID ARTHRITIS
Clinicopathologic Conference
ELLEN M. GRAVALLESE (Moderator), BARBARA N. WEISSMAN (Radiologist),
GILBERT BRODSKY (Pathologist),and JAMES MAGUIRE (Consultant)
DON L. GOLDENBERG (Discussant)
Presentation of case
A 60-year-old woman with a 30-year history of
deforming, rheumatoid factor-positive rheumatoid arthritis
(RA) presented with a 1-year history of pain in the right
groin. For the 3 years prior to admission, she had been
treated with oral methotrexate, 7.5 mg/week, and prednisone, 7 mg/day. Previous medical therapy for RA included
nonsteroidal antiinflammatory drugs (NSAIDs), diseasemodifying antirheumatic drugs (DMARDs; hydroxychloroquine sulfate, sulfasalazine, gold sodium thiomalate, and
penicillamine), and multiple courses of steroids in low dosage. She had undergone multiple surgical procedures of her
joints, including a right total hip replacement (THR) 20 years
previously, with a cemented cobalt-chrome femoral prosthesis and an ultra high molecular weight (UHMW) polyethylene acetabular component. Seven years prior to admission,
she underwent a revision surgery because of loosening of the
acetabular component. A porous-ingrowth metal shell with a
UHMW polyethylene liner was used. Pathologic specimens
from the revision hip surgery revealed synovial tissue with
fibrotic changes and a histiocytic infiltrate.
Moderator: Ellen M. Gravallese, MD: Associate Rheumatologist and Associate Pathologist, Brigham and Women’s Hospital,
and Assistant Professor of Medicine, Harvard Medical School,
Boston, MA.
Radiologist: Barbara N. Weissman, MD: Director, Musculoskeletal Section, Department of Radiology, Brigham and Women’s Hospital, and Professor of Radiology, Harvard Medical School.
Pathologist: Gilbert Brodsky, MD: Pathologist, Brigham
and Women’s Hospital, and Assistant Professor of Pathology,
Harvard Medical School.
Consultant: James H. Maguire, MD: Associate Professor of
Medicine, Harvard Medical School, Brigham and Women’s Hospital.
Discussant: Don L. Goldenberg, MD, FACP: Chief of
Rheumatology, Newton-Wellesley Hospital, Newton, MA, and Professor of Medicine, Tufts University School of Medicine, Boston.
Additional surgical procedures were a left total knee
replacement 6 years prior to admission, left THR 3 years
prior to admission, and right subtalar and talonavicular
fusion 2 years prior to admission. Because of persistent right
groin pain, she presented to her orthopedic surgeon 4
months prior to admission. Pelvis and hip radiographs were
performed.
Dr. Ellen Gravallese: Dr. Weissman, would you
review the radiographic studies at this time?
Dr. Barbara Weissman: Previous radiographs
of the hands of this patient showed features typical of
RA, with carpal bone erosion, metacarpophalangeal
(MCP) joint space narrowing, and osteoporosis. Radiographic examination of the right hip 3 years prior to
admission demonstrated a cemented femoral component in varus position with a 2-mm lucent zone along
the lateral, proximal cement-bone interface. Medially,
there was thinning of the cortex, resorption of the
medial femoral neck, and osteopenia of the proximal
medullary bone. Because the lucent zone did not
completely surround the stem of the component, the
femoral stem was thought not to be loose. The uncemented bone-ingrowth acetabular component showed
no radiographic evidence of loosening. The acetabular
bone was thin.
Radiographs at the time of presentation 4
months prior to admission (Figure 1) showed no
change in the appearance of the right femoral component. There was, however, new thinning and disruption of the medial acetabular cortex with protrusio
deformity, and a faint soft-tissue mass was visible
1316
RHEUMATOLOGY GRAND ROUNDS
sent for Gram stain and aerobic and anaerobic cultures. Gram stain showed a few polymorphonuclear
leukocytes and no organisms. Aerobic and anaerobic
cultures showed no growth.
Chest radiograph at the time of admission revealed linear scarring in the right upper lobe and right
lung base. The cardiac and mediastinal silhouettes
were normal, and there was no adenopathy or pleural
effusion. There was scoliosis, and resorption of the
right distal clavicle consistent with RA.
A second revision arthroplasty was planned. Over
the 6 weeks prior to admission, the patient noted significant
worsening of her right groin pain, and new pain in her right
thigh and knee. She also noted generalized malaise and
fatigue, but denied having any weight loss, fever, or chills.
Radiographs of the right pelvis and hip showed increasing
Figure 1. Anteroposterior radiograph of the right hip at presentation (4 months prior to admission), demonstrating disruption of the
medial acetabular cortex (arrowhead), with a faint soft-tissue mass
(arrows) and protrusio deformity. There is no apparent loosening of
the femoral component.
adjacent to the acetabulum. Lucency of the lateral
acetabular bone around the prosthesis was also suggested.
Aspiration arthrography was performed, and no
fluid could be aspirated initially. The injected contrast
material extravasated through the acetabular defect
and formed multiple small collections in the area of the
previously seen soft-tissue density (Figure 2). The
curvilinear nature of the contrast collections was suggestive of contrast flowing around more solid tissue,
which is seen, for example, in patients with synovitis.
The contrast material was also noted to flow around
the most proximal cement of the femoral component.
The injected contrast material was reaspirated, and
Figure 2. Arthrogram of the right hip demonstrating extravasation
of contrast material throueh the acetabular defect. The irreeular
distribution of the contrast suggests synovitis.
.,
.,
REVISION THR LOOSENING
medial migration of the acetabular component, with worsening protrusio deformity. She was admitted to the hospital for
revision THR on the right.
Medications on admission were atenolol 100 mg/day,
acetylsalicylic acid 325 mglday, prednisone 7 mdday, methotrexate 7.5 mg/week, hydrochlorothiazide 25 mg/day, triamterene 50 mglday, and iron and calcium supplements. Her
medical history was notable for longstanding essential hypertension, coronary artery disease with a history of myocardial infarction 10 years previously, chronic sinusitis, and
a history of bronchiectasis in the left and right lower lobes,
confirmed by bronchogram, with recurrent respiratory infections requiring more than 1 year of suppressive antibiotics.
Her last course of antibiotics was over 2 years prior to
admission. She was raised on a farm and has no significant
history of travel outside the United States. She was never a
cigarette smoker.
On physical examination, her temperature was
99.7"F, blood pressure 120/80mm Hg, pulse 68 beatdminute,
and respirations 14hinute. Findings of her general physical
examination were unremarkable. Musculoskeletal examination revealed deformities of the fingers and toes consistent
with RA, and synovitis, with limitation of motion and pain
on motion of the shoulders, elbows, and knees, and warmth
and synovial thickening of the MCP joints, proximal interphalangeal joints, wrists, and metatarsophalangeal joints.
Examination of the right hip revealed pain on movement and
significantly decreased range of motion. Active flexion was
decreased to 20" and limited by pain. Passive flexion was to
I#", with 30" of external rotation and 25" of internal rotation.
Her laboratory evaluation prior to right hip surgery
revealed a white blood cell (WBC) count of 5,600/mm3, with
76% polymorphonuclear leukocytes, 6% monocytes, and
18% lymphocytes. The hematocrit was 31.1% with a mean
corpuscular volume of 94.5 pm3 (normal 80-95). The platelet
count was normal. Her electrolyte levels were normal, blood
urea nitrogen was 32 mgldl, and serum creatinine was 1.3
mg/dl. Her serum albumin level was 3.7 g d d l (normal
3.2-5.3), and serum uric acid was 8.5 mg/dl. Alkaline phosphatase was 105 IU/liter (normal 3 6 1 18), aspartate aminotransferase was 25 IU/liter (normal 9-30), alanine aminotransferase was 21 IU/liter (normal 7-52), lactic acid
dehydrogenase was 251 IU/liter (normal 107-231), and total
bilirubin was 0.2 mg/dl. The urinalysis findings were normal
except for the presence of rare hyaline casts.
The patient was taken to the operating room for a
right revision THR. Intraoperatively, the hip capsule appeared thickened, and a small amount of purulent material
was released upon entering the hip capsule. Upon removal of
the screws holding the acetabular cup in place, considerable
metallic debris was noted around the periphery of the cup,
and purulent material was also noted along the screw tracks.
Discussion
Dr. Don Goldenberg: The patient described
here represents an all too common problem for rheumatologists and orthopedic surgeons: the evaluation of
1317
a possibly infected joint prosthesis. Total joint replacement surgery has been the single most important
therapeutic advance in the rheumatic diseases during
the past 25 years. By 1990, it was estimated that
approximately 120,000 THRs were performed in the
United States each year (1). Infection continues to be
the most serious complication of joint replacement
surgery. Since the 1960s, the incidence of prosthetic
joint infection has dramatically fallen, from a rate as
high as 13% to less than 1% for primary operations in
most series (1-3). Improved surgical techniques and
prostheses and the use of perioperative antibiotics
have helped decrease the incidence of infection. This
is especially true for early perioperative infections,
presumably introduced at the time of surgery (3).
Late prosthetic joint infections occurring more
than 1 year after implant continue to be an important
problem. These infections often present indolently, as
in this patient, and are very difficult to differentiate
from aseptic joint loosening. To better elucidate this, I
would like to review the case history.
This patient had severe, deforming, and active
RA. She had been maintained on multiple NSAIDs
and DMARDs, and for the previous 3 years, had been
taking modest doses of prednisone and methotrexate.
Patients with RA are at greater risk of prosthetic joint
infection than are patients with osteoarthritis (OA)
(4-6). Prednisone and methotrexate therapy may further increase the risk of infection. There is significant
debate whether methotrexate should be temporarily
discontinued at the time of joint replacement surgery
(7-10). Concern that patients taking methotrexate in
the perioperative period may have a greater incidence
of wound infections must be balanced by concern over
possible exacerbation of RA during the time that the
methotrexate is withheld.
The single most important risk factor for infection in this patient was the fact that she was undergoing a revision arthroplasty (1 1). This was her third
right hip arthroplasty, the first THR having been done
20 years earlier and a revision done 7 years earlier.
Patients undergoing revision arthroplasty are 8 times
more likely to develop infection than those undergoing
primary arthroplasty (5). The rate of infection increases with each subsequent surgical revision (2,3).
There was no report of microbiologic culture of
samples from the second hip surgery, but pathologic
specimens revealed synovial tissue with fibrotic
changes and a histiocytic infiltrate, characteristic of
aseptic joint loosening. The longer the time from the
initial implant, the greater the risk of both aseptic and
1318
septic joint loosening (1). Aseptic loosening over time
may cause inflammation, provoked by fragments of
metal, polyethylene, or cement, and increased vascularity. At a mean of 6 years after joint implant,
sepsis is the cause of joint loosening in only 1 4 % of
cases (3). However, this is still a substantial problem
since the rate of revision or reoperation due to failure
of fixation is 10-30% after 10 years (1).
Thus, the index of suspicion for infection of the
right hip prosthesis was high in this patient. Unfortunately, as exemplified by this case, the definitive
diagnosis ofjoint sepsis is often difficult. Most patients
present with slowly progressive joint pain, as this
patient did. Radiographic evidence ofjoint loosening is
usually present, but does not allow one to distinguish
aseptic from septic causes (2). Radiographs in this
patient 4 months prior to admission demonstrated
loosening of the acetabular component, with medial
migration and new disruption of the acetabular cortex.
These findings are consistent with either septic or
aseptic joint loosening. Therefore, a hip arthrogram
with joint aspiration was performed. Unfortunately,
no synovial fluid was aspirated from the hip. A “dry
tap” should always include multiple attempts at aspiration, with repositioning of the needle as well as
repositioning of the hip. Ultrasound of such joints has
sometimes revealed loculated purulent fluid (2).
If repeated attempts at aspiration yield no fluid,
contrast material should be injected to confirm that the
needle is in the joint space and to reaspirate the
injected fluid for culture. Sterile saline may also be
injected at this time to provide more material for
culture; however, bacteriostatic solutions that might
potentially inhibit bacterial growth should be avoided.
Even when fluid is obtained during preoperative joint
aspiration, the correlation with results of intraoperative culture varies from 73% to 83% (2). In this case,
the contrast material was sent for culture and Gram
stain. The Gram stain demonstrated a few polymorphonuclear leukocytes but the aerobic and anaerobic
cultures yielded no growth. The extravasation of the
contrast material into the pelvis is consistent with the
new disruption of the medial acetabular cortex seen on
routine radiographs. It may, however, be further evidence of deep joint infection.
The patient’s pain progressed during the 6
weeks prior to admission, with radiation of pain to the
thigh and the knee. There were no systemic signs of
infection by history or by an initial examination, other
than a low-grade fever. It is of interest that the patient
did have a history of chronic upper and lower respira-
RHEUMATOLOGY GRAND ROUNDS
tory infections. However, findings of a chest radiograph taken at admission were consistent with old
pulmonary infection and did not document recent
infection. In addition, the patient had not required
antibiotics for bronchiectasis in over 2 years.
Her musculoskeletal examination demonstrated
active synovitis of multiple joints, but the pain and
decreased range of motion of the right hip were out of
proportion to that of the otherjoints. I assume that the
new pain in the right knee was actually pain referred
from the hip rather than an indication of a possible
infection involving that knee, However, it is important
to determine whether the polyarthritis described on
her examination at this time was consistent with her
active RA. If there was any evidence of new swelling
in the right knee or other joints, they should also have
been aspirated and cultured before surgery.
As is often the case, the laboratory studies were
not helpful in differentiating septic from aseptic joint
loosening. The peripheral leukocyte count was not
elevated, and the right hip radiographs demonstrated
further medial migration of the acetabular prosthesis
with protrusio deformity consistent with aseptic loosening. Although the erythrocyte sedimentation rate
(ESR) is very helpful in the evaluation of a possible
infected prosthetic joint in OA (2), it is much less likely
to be of value in a patient with active RA, who would
be expected to have a chronically elevated ESR.
Therefore, as is often the case, the presence of
infection in the prosthetic joint could not be excluded
until the time of surgery. Routine preoperative arthrography and aspiration are advocated at some centers, but the predictive value is dependent on the
clinical likelihood of infection. For example, Tigges et
a1 reported a negative predictive value of 99% for 147
preoperative aspiration cultures when compared with
operative cultures; the positive predictive value, however, was only 54% (12). Other groups have reported a
much lower positive predictive value because of the
frequent occurrence of false-positive cultures that are
not verified by culture of specimens obtained intraoperatively (13).
Gould et a1 found that all 60 hip arthrographic
aspirations performed in patients with a low index of
suspicion for infection were negative, but 5 of the 6
aspirations in cases with a high index of suspicion
were positive, 4 of which were confirmed to be the
same organism at surgery (14). Nevertheless, preoperative joint aspiration remains the most useful test in
the evaluation of possible infected prosthetic joints (15).
REVISION THR LOOSENING
A number of scintigraphic techniques have
been utilized for preoperative diagnosis of an infected
prosthetic joint. Labeled WBC scans and/or technetium sulfur colloid scans have provided the best sensitivity and specificity (2,16). However, these scans
are expensive, and may not provide a definitive diagnosis, since they depend on both the technique and the
reader, and may vary with activity of the infection.
Preoperative scintigraphy was not performed in this
patient.
At the time of surgery, a small amount of
purulent material was released upon entering the hip
capsule, and purulent material was noted along the
track of the screws holding the acetabular cup. This, of
course, is a strong indication that the prosthesis was
infected. The purulent material and at least 3 tissue
specimens, including the capsule, should be obtained
for aerobic and anaerobic culture, including culture for
mycobacterial and fungal organisms. The initial dry
tap may relate to isolation of the bacteria within the
glycocalyx, a biofilm formed by bacteria at the cement
interface (3). This glycocalyx provides a protective
environment for bacterial growth and leads to poor
penetration of antibiotics and further difficulty with
diagnosis.
Could anything other than infection cause this
clinical picture? A foreign body reaction with formation of a synovial-like membrane at the bone-cement
interface occurs in loosened joint prostheses (17-19).
This tissue may be infiltrated with particulate cement
and polyethylene, and has been shown to express
cytokines and prostaglandin E, in high levels (20). This
foreign body reaction is now considered critical in the
pathogenesis of aseptic prosthetic joint loosening. This
process may also have contributed to the loosening of
this hip prosthesis, but would not explain the purulent
discharge from the hip capsule and around the screws.
However, the “metallic debris” described would be
consistent with aseptic loosening and with a foreign
body reaction playing a key role in the infection along
the screw tracks.
Crystal-induced synovitis may also cause
purulent-appearing drainage. Although the metallic
debris may include crystalline material, I know of no
reports demonstrating a purulent reaction caused by
metal debris. This patient did have a slightly elevated
serum uric acid level, but there was no clinical evidence to suggest gout or pseudogout.
It seems most likely that this patient had a late
prosthetic joint infection. These infections are usually
hematogenously acquired. Any of a number of aerobic
1319
and/or anaerobic bacteria could have been recovered
from the intraoperative specimen. Staphylococcus epidermidis and Staphylococcus aureus are still the most
common organisms that infect the prosthetic joint at
any stage (3). In this patient, the respiratory tract
would be a likely source of hematogenously acquired
infection and gram-negative bacilli, such as Pseudomonas, or a mixed anaerobidaerobic infection would
also be likely. In view of the abnormal findings of chest
radiography and the history of being raised in a rural
area, mycobacterial and fungal organisms should be
considered, although such microbes are rare causes of
prosthetic joint infection.
Polymeric substances, including UHMW polyethylene, may be associated with bacterial strains that
have increased resistance to bactericidal antibiotics
(2). This resistance may relate in part to the ability of
strains exposed to these substances to produce the
biofilm, glycocalyx (3,21). In vitro experiments have
demonstrated that S epidermidis organisms that were
allowed to adhere to polymethylmethacrylate discs
were more resistant to antibiotics than those bacteria
that were immediately detached from the discs (21).
Scanning electron microscopy showed an accumulation of bacteria surrounded by a glycocalyx layer.
Many bacteria may form such a protective coating.
This research has been helpful in providing further
impetus for the surgical removal of all biomaterials
whenever possible in the treatment of prosthetic joint
infections.
I assume that either the culture of the purulent
discharge or tissue specimens, or the pathologic tissue
sections demonstrated that the joint was infected. At
least half of these cultures should grow the same
organism(s) (22). At this point, the prosthesis would
usually be removed, with extensive debridement and
administration of appropriate systemic antibiotics.
Surgical alternatives would include immediate (1stage) or delayed (2- or 3-stage) revision after weeks
to months of intravenous antibiotics, or arthrodesis
or resection arthroplasty. In view of the 2 previous revisions and the patient’s persistent arthritis,
a 2-stage procedure, possibly using antibioticimpregnated bone cement, might be the most logical
choice (22).
Unfortunately, despite the marked decrease in
prosthetic joint infections during the past 20 years,
late-onset hematogenously acquired infection continues to be a major diagnostic and therapeutic problem.
Mortality associated with an infected joint arthroplasty varies from 5% to 20% (23). The role of antibi-
RHEUMATOLOGY GRAND ROUNDS
1320
A
B
Figure 3. Specimen obtained at revision hip replacement surgery. A, There are abundant macrophages with pale, granular
cytoplasm infiltrating the joint capsule. B, A giant cell containing a large wedge-shaped particle consistent with polyethylene is
seen.
otic prophylaxis for late prosthetic joint infections is a
subject of controversy. However, Blackburn and
Alarcon suggested that patients with RA, especially
those with risk factors that include nonarticular infections, revision implants, and possible long duration of
the implant, should receive antibiotics prior to any
procedure likely to cause bacteremia (23). Each of
those risk factors was present in this patient. Prevention and early diagnosis of prosthetic joint infections
continue to be major challenges for orthopedic surgeons and rheumatologists.
Clinical diagnosis: Infected prosthetic hip joint.
Dr. Gravallese: At the time of surgery, the
surgeon obtained a Gram stain of the purulent material, which was negative for organisms. Does this
influence your diagnosis in any way?
Dr. Goldenberg: No. Gram stains are notoriously unhelpful in these situations.
Dr. Gravallese: The operating surgeon assumed
that the hip prosthesis was infected, and both the
acetabular and femoral components were removed.
Dr. Gilbert Brodsky will present the pathology findings from this surgery and from the previous right hip
revision surgery.
Dr. Gilbert Brodsky: Tissue from the revision
surgery 7 years prior to admission showed fibrotic
synovium and capsular tissue, with a sparse infiltrate
of lymphocytes and histiocytes, as well as rare giant
cells. Histiocytes in this specimen were large, with a
pale, finely granular to clear cytoplasm. These cells
may be called “cementophages,” in that they appear
to have phagocytosed finely particulate polymethylmethacrylate. This specimen demonstrated in a limited
1321
REVISION THR LOOSENING
A
B
Figure 4. Specimen obtained at revision hip replacement surgery. A, Metal synovitis associated with the failed acetabular
prosthesis is demonstrated. There is disruption of the joint capsule surface, with underlying granulation tissue and deposition
of dark particles consistent with metal debris. B, High-power view, showing metal particles within histiocytes.
way the synovitis that can be seen in specimens from
patients with failed joint prostheses. The pathologic
process has been given many names, but I prefer the
term “detritic synovitis” (24,25). The detritus can be a
number of different materials. In addition to the “cementophage” reaction to polymethylmethacrylate,
one can see large refractile particles of polymethylmethacrylate or polyethylene, which wear off and
become embedded in the synovium. A histiocytic
reaction with foreign body giant cells surrounding the
extruded material is common. Spicules of necrotic
bone may also become embedded in the tissue (26).
One can also see a finely or coarsely granular pigmented material deposited from degeneration of the
metallic component of the prosthesis. In extreme
cases, the metal deposition can impart a slate-grey to
black color to the surface of the gross specimen
(27,28).
Similar detritic changes were noted prominently in the specimen from this patient’s most recent
hip replacement. A dense histiocytic infiltrate was
seen, with areas of granulation tissue response, necrosis, and embedded bone spicules. Fragments of probable polyethylene with a giant cell reaction were
present (Figure 3). A prominent reaction to the metallic prosthetic component, with histiocytes filled with
metallic particles, was also noted (Figure 4).
In addition to the detritic changes, there were
large areas of necrosis with peripheral palisading histiocytes, fibroblasts, and occasional giant cells, as well
as areas of central caseation. What was described
intraoperatively as “purulent material” might more
accurately have been designated as caseous necrosis
(Figure 5). Gram stain and stains for fungi were
negative in this case; however, the acid-fast stain
showed numerous acid-fast bacilli.
1322
Figure 5. Specimen obtained at revision hip replacement surgery,
showing the edge of a large granuloma with caseous necrosis in the
joint capsule.
Final pathologic diagnoses:
1. Mycobacterial arthritiswith extensivecaseous necrosis.
2. Synovitis associated with a failed orthopedic prosthesis (“detritic synovitis”).
3. Rheumatoid arthritis.
Dr. Gravallese: I have asked Dr. James Maguire, Clinical Director, Division of Infectious Disease,
to discuss mycobacterial infections in prosthetic
joints.
Dr. Maguire: It is important to determine the
species of mycobacteria in infected prostheses because the treatment of infections due to Mycobacterium tuberculosis differs from that of infections due to
nontuberculous or so-called “atypical” mycobacteria.
In this case, further attempts to isolate an organism by
arthrocentesis and culture were unsuccessful. We suspected that the patient’s infection was due to M
tuberculosis or Mycobacterium bovis because of the
long interval between implantation and the onset of
symptoms. Tuberculous infections of prosthetic joints
generally result from reactivation of previous infection
and may occur years after implantation of the prosthesis (29-35). In contrast, infections due to nontuberculous mycobacteria tend to become apparent within a
few weeks or months of surgery, probably because
most are acquired intraoperatively ( 3 6 3 9 ) . It is of
interest that this patient gave a history of consuming
RHEUMATOLOGY GRAND ROUNDS
raw dairy products as a child and may have acquired
her infection by this route.
The published literature on mycobacterial infections of prosthetic joints is sparse. Most nontuberculous infections are due to Mycobacterium fortuitum
and Mycobacterium chelonei, fast-growing organisms
that are ubiquitous in soil and water and are introduced by intraoperative contamination, penetrating
injury, or injection (36-39). Although these organisms
are called “rapidly growing” mycobacteria, they cannot be detected in cultures until at least 4 days of
incubation. As a rule, microbiology laboratories hold
routine cultures for less than this amount of time, and
may fail to isolate these organisms unless advised in
advance to use special procedures. Infections caused
by nontuberculous mycobacteria typically present
with joint pain, swelling, or a draining sinus tract
within a few weeks or months after surgery. Late
hematogenous infections are rare, although Mycobacterium avium intracellulare was isolated from the
blood and both hip arthroplasties of a patient with the
acquired immunodeficiency syndrome who had undergone joint replacement more than 10 years earlier (40).
Removal of the prosthesis as well as prolonged
courses of antibiotics are necessary to cure infection
with nontuberculous mycobacteria. These organisms
frequently are resistant to standard antituberculous
drugs, but are susceptible to agents such as ciprofloxacin, clarithromycin, and amikacin.
M tuberculosis may infect a joint prosthesis as a
consequence of disseminated infection (41,42), by
inadvertent implantation in a joint that is actively
infected (43,44), or most commonly, by reactivation of
an old, quiescent infection. It is not understood why
osteoarticular tuberculosis reactivates after joint replacement or why some infections recrudesce within
weeks after surgery and others do so years later. It is
recommended that patients with previous tuberculous
arthritis who have never received treatment should
complete a course of prophylactic isoniazid before
surgery (45). If there is any suspicion of active infection at the time of surgery, these patients should
receive standard multidrug therapy until infection is
ruled out by smears and cultures. As illustrated by this
case, it may be difficult to recognize quiescent infection when there is no history of active disease.
Infections due to M tuberculosis are more likely
to be eradicated without removal of the prosthesis
than infections due to “atypical” mycobacteria
(46,47). Debridement of soft tissues may be necessary,
in addition to at least 9 months of multidrug therapy
1323
REVISION THR LOOSENING
with agents such as isoniazid, rifampin, pyrazinamide,
and ethambutol. There is controversy over the length
of time that should elapse following treatment of a
tuberculous joint before total joint arthroplasty is
attempted (46,47). In the present case, both the acetabular and femoral components were removed at the
time of surgery. We elected to observe the patient for
several months after completing chemotherapy before
reimplantation of the prosthesis.
ACKNOWLEDGMENT
The authors would like to thank Dr. Elinor Mody for
assistance in the preparation of this case.
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