What would you do? Case challenges in knee surgery: Four knee arthroplasties presenting with effusions

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Available online at www.sciencedirect.com

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What would you do? Case challenges in knee surgery: Four knee arthroplasties presenting with effusions Kelly G. Vince, MDa,n, Harry Tsigaras, FACSb, and David G. Morgan, FRACSc a

Department of Orthopedic Surgery, Whangarei Hospital; Northland District Health Board, Whangarei, New Zealand Cabrini Health Melbourne, Melbourne, Australia c St. Andrew's Hospital, Ipswich, Queensland, Australia b

article info

abstra ct

Keywords:

Four total knee arthroplasty patients present with effusions from excess synovial fluid,

knee arthroplasty

pus, or blood. “Which fluid” and “why” are the important questions. Recent Guidelines for

complications

Diagnosis of Periprosthetic Infection from the American Academy of Orthopedic Surgeons

revision

provide a useful diagnostic algorithm. Leukocyte counts and differential, plus culture, are

sepsis

emphasized. Suspected inflammatory arthropathy led to an “anchoring bias” in the first

pigmented villonodular synovitis

case. Unsuspected bone loss posed a challenge in our second case, and the final cases

effusion

suffered effusions from instability, often a difficult diagnosis to establish.

infection

DR. VINCE: Welcome to the “Case Challenges in Knee Surgery.” We have 37 minutes to learn from a superb faculty: David Backstein from the University of Toronto, David Blaha from Ann Arbor, MI, Bill Maloney from Stanford, William Mihalko from Memphis, and Arun Mullaji from Mumbai. Today we will evaluate four total knee arthroplasties (TKAs) complicated by effusions.

1.

Case one

Our first case is provided by an overseas colleague who felt they learned a lot from this difficult experience. The case is instructive to all of us. Dr. Blaha, what is your differential diagnosis for a total knee arthroplasty (TKA) with recurrent effusions? DR. BLAHA: First is infection and the second is loosening. After that, instability. DR. VINCE: Excellent! Infection, loosening, and instability.

& 2013 Elsevier Inc. All rights reserved.

DR. VINCE: There are of course, three types of fluid we might find in an arthroplasty: pus, synovial fluid, or blood. So perhaps a fourth problem might be recurrent hemarthrosis [1–6] and a fifth might be inflammatory arthropathy, specifically gout [7,8]. The first patient is a 70-year-old male, former elite athlete who, at 6 ft 5 in. (196 cm), is tall and also heavy. He had an open meniscectomy in the 1960s and developed tricompartmental degenerative joint disease with a varus deformity. Pain and instability lead to the need for arthroplasty. His medical problems include a pacemaker and chronic warfarin for arrhythmia. He underwent a cemented posterior stabilized arthroplasty, and the surgical team was impressed by extensive hemosiderin-stained synovitis and laxity of the medial complex on completion of the arthroplasty. The surgeon expressed concern that the reconstruction required a 17-mm tibial polyethylene insert, which is thicker than the 10–12-mm components he generally uses.

Moderator: Kelly G. Vince, Whangarei, New Zealand. Panelists: David Backstein, MD, FRCS(C), MEd: Toronto, Ontario, Canada; J. David Blaha, MD: Ann Arbor, MI; William J. Maloney III, MD: Stanford, California; William M. Mihalko, MD, PhD: Memphis, TN; Arun Mullaji, FRCS(Ed), MS: Mumbai, India. n Address reprint requests to Kelly G. Vince, MD, Department of Orthopedic Surgery, Whangarei Hospital, Private Bag 9742, Whangarei 0148, New Zealand. E-mail address: [email protected] (K.G. Vince). 1045-4527/$ - see front matter & 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1053/j.sart.2013.08.013

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David Blaha, if you saw a colleague in the lunch room who had just finished a TKA, and was surprised to have used a 17mm thick modular polyethylene insert, and was worried about instability, what would be your advice? DR. BLAHA: I would review the case to see if the patient had rheumatoid arthritis, to explain synovitis and laxity. DR. VINCE: Yes. DR. BLAHA: You don’t ordinarily need a 17-mm poly. I would look carefully at the X-rays, to see if anything could have been done differently. DR. VINCE: Arun, you deal with the biggest deformities these days. Does the 17-mm poly mean you've done something wrong? DR. MULLAJI: Not necessarily, but it could. It might mean you took off too much bone for a bad deformity. If you started with a lax medial collateral ligament (MCL) and resected the standard amount of bone, then you would need a very thick insert. (Moderator comment: MCL laxity would be common with a valgus deformity.) DR. VINCE: Does anyone have a dissenting opinion? Dr. Mihalko? DR. MIHALKO: You have to make sure there wasn’t an MCL tear during surgery. DR. BACKSTEIN: Did the 17-mm poly actually make the knee stable or just make the surgeon feel a little more comfortable? DR. VINCE: Good point. I think the surgical team on this case was happy with the stability. I would reassure the surgeon that for a knee with significant varus “pseudo-laxity” and a big deformity, the surgeon must release the MCL for correction. An

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extensive medial release, requires thicker poly to stabilize the arthroplasty. After all, you must lengthen the medial side to equal the stretched-out lateral side in a varus knee. The bigger the deformity, the bigger the poly [9)]. Bill Maloney? DR. MALONEY: You’re right. If I use a 17-mm insert, I go back, to see if I took more tibia than I should have. Maybe in this varus deformity, if a surgeon cut the tibia to the base of a deficient condyle, it might have been better to make a standard cut and rebuild the defect with bone graft or metal augments. (Moderator comment: The classic recommendation dating back to John Insall’s 1984 textbook is to make the standard tibial resection in cases with tibial bone defects and then build up the deficiency rather than cutting to the base of a defect.) [10]. The other group of patients is those with laxity, like the valgus knee that hyperextends. You have to be careful with the tibial resection there because you may need a 20-mm thicker insert to stabilize the joint. DR. VINCE: Certainly. I wouldn’t want to do a valgus knee without a 17-mm or thicker poly in the theater. The knee in this case had hypertrophic, livid synovium (Fig. 1A) that impressed the surgical team as pigmented villonodular synovitis (PVNS) [11,12]. Does anybody have insight into PVNS as an indication for arthroplasty? Does it bother you? DR. BACKSTEIN: It doesn’t bother me. We work closely with a tumor group and may do a front-and-back approach for bad PVNS cases [13]. The tumor guys take it out from the back, and I do a stabilized total knee from the front. DR. VINCE: When was the last time you needed a front-andback approach for total knee replacement? Is it very common?

Figure 1 – (A) Arthroscopic image virtually identical to the findings at primary arthroplasty for the case under discussion. (The surgeon who has graciously shared this case did not obtain photos at the initial surgery.) This image was ultimately diagnosed as recurrent hemarthrosis but the differential diagnosis included PVNS. (This image was provided from another surgery by another surgeon, Alejandro Gonzalez Della Valle—The Hospital for Special Surgery New York, NY.) (B) Summary of findings from Bedair et al. “The diagnosis of early postoperative TKA infection using synovial fluid analysis”[14]. As leukocyte counts in synovial fluid are expected to be elevated in the early period after surgery. Aspiration was not regarded as a reliable indication of early periprosthetic infection, until this paper demonstrated clear differences between infected and non-infected cases, even in the early period after surgery. The bar on the right shows that all non-infected cases had fewer than 27,800 WBC/ll of synovial fluid. This has been recommended as a “cutoff” to indicate that no infection is present. However, the bar on the left (infected cases) shows that some had WBC concentrations between 10,700 and 27,800/ll indicating an area of uncertainty. Aspiration of an arthroplasty with a problem wound in the early postoperative period is sound practice, as it also provides material for culture and sensitivity and should be performed before antibiotic prophylaxis or therapy is initiated. (C) Anteroposterior and (D) lateral radiographs 7 months after primary TKA, when an ultrasound-guided aspiration was performed. The patient originally presented for total knee arthroplasty with what was thought to be osteoarthritis and a significant varus deformity. Intra-operative findings were highly suggestive for PVNS. The postoperative course was complicated by pain and persistent effusions. These “spot” views to confirm needle positioning, nonetheless indicate a suspicious area under the anterior femoral flange and perhaps under the medial tibial plateau. (E) Axial and (F) frontal projections of a CT scan performed 7 months after TKA. The interpretation includes synovial thickening. No mention was made of what might be interpreted as uniform radiolucencies about the tibial stem consistent with sepsis (arrows). The surgical team was committed to PVNS as the explanation for persistent effusions and this may have influenced the interpretation of the study. Current AAOS guidelines for the diagnosis of periprosthetic infections would have been highly advantageous in avoiding cognitive impediments, such as “anchoring bias.” The tenth AAOS guideline states that “We are unable to recommend for or against computed tomography (CT) or magnetic resonance imaging (MRI) as a diagnostic test for periprosthetic joint infection.” (G) AP radiograph 21 months after TKA. There is a disturbing and distinct radiolucency under the medial tibial component with radiolucencies extending across to the lateral plateau. (H) Lateral radiograph demonstrating extensive radiolucencies under the anterior femoral flange and posterior condyles highly suggestive of loosening. The tibial interface appears to have osteolysis as well. (I) AP and (J) lateral radiograph at 21 months showing the resection arthroplasty with an antibiotic-impregnated articulating spacer, plus intra-medullary antibiotic-impregnated “dowels” to deliver additional antibiotics that were placed once multiple cultures grew propionibacteria at 16 months after TKA.

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DR. BACKSTEIN: One last year, and one coming up in a month, for PVNS that has failed all other forms of treatment. DR. VINCE: David Blaha, any thoughts on PVNS? DR. BLAHA: Persistent hemorrhage into the joint looks just like PVNS so you must send a specimen to the pathologist to confirm the diagnosis. Even then it can be difficult to diagnose. DR. VINCE: Key point. The histopathology may not necessarily be definitive. At four weeks after TKA, this patient

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achieved 0–901 of flexion with a 151 quadriceps lag, a large effusion, and satisfactory radiographs. Dr. Mihalko, does anything seem unusual to you in this clinical presentation at four weeks? Any problems there? DR. MIHALKO: The large effusion will give you the quads lag, and 0–90 is within average. DR. VINCE: I’m not upset yet either. Anybody with thoughts? Would anyone do an aspiration at this point? DR. MIHALKO: I wouldn’t, no.

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DR. VINCE: What if the wound looked bad? What would it take to make you aspirate a knee at four weeks? Arun? DR. MULLAJI: I think if the patient complained of pain. DR. VINCE: But at four weeks don’t most patients have some pain? DR. MULLAJI: Pain and fever. DR. VINCE: Fever? Yes. So if the patient were febrile, with a painful swollen knee, you might aspirate. Fair enough. David Backstein, what would make you aspirate a TKA at four weeks after surgery? DR. BACKSTEIN: Some wound issue—signs or symptoms of infection. DR. VINCE: Do you like cell counts from the aspirated fluid? DR. BACKSTEIN: Yeah. DR. VINCE: What do you think about cell counts in the early phase after surgery? DR. BACKSTEIN: There’s some guidance now. Craig Della Valle was an author on a paper studying aspirations in the first few weeks after TKA [14]. DR. VINCE: Indeed, that is a key study. Many people shy away from early aspiration because they expect all white cell counts will be elevated by the surgery. This is the data from the paper you mention (Fig. 1B). They reported 78 aspirations performed within 6 weeks of TKA. All non-infected knees had white cell counts less than 27,000/ml and all the infected cases had counts greater than 10,000. The paper recommended a cutoff at 27,800 to diagnose infection. Not a bad guideline [14]. Back to our case. By three months, the patient had 1201 of flexion, no quads lag, and a moderate effusion. We all agree that there would be a reason to aspirate if the patient was febrile or had wound problems with the effusion, but perhaps not in this case at this time. The other argument not to aspirate an arthroplasty has been pre-existing inflammatory arthropathy, with the rationale: “it’s a case of PVNS, so I can’t possibly get meaningful cell counts.” Here is another study showing reliable levels of WBCs in the synovial fluid of TKAs to indicate infection even in the presence of rheumatoid disease or other inflammatory arthropathies [15] (Table 1). By five months, the patient had 1301 of flexion and a large effusion. An aspiration yielded 50 cc’s of reportedly “clear fluid” that was not sent for analysis. A dexamethasone injection was given. Arun, when would you put cortisone into a TKA?

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DR. MULLAJI: I wouldn’t. DR. VINCE: After a patient has received an arthroplasty, you would never inject cortisone into the joint? DR. MULLAJI: Yeah. DR. VINCE: Fair enough. DR. MULLAJI: Unless they complained of point tenderness, when I might inject that spot, outside the joint. DR. VINCE: Understood. DR. MULLAJI: Otherwise, I wouldn’t put cortico-steroids into the knee. DR. VINCE: Let’s go down the panel. David Blaha? DR. BLAHA: I know that some surgeons inject cortisone into an arthroplasty, but I can’t convince myself to. I sit on my hands until the temptation goes away. DR. VINCE: Okay. Bill Maloney? DR. MALONEY: I wouldn’t do it unless we had a negative culture. We do do it sometimes in patients having difficulty with motion, but in a patient like this with a large effusion, I would not. And I’m also worried he’s got 1301 of flexion with a large effusion. That says this may be an unstable knee. (Moderator comment: A negative culture, may be a false negative, and does not eliminate the possibility of infection. That would require a low cell count and low percentage of polymorphonucleocytes as per AAOS guidelines) [16]. DR. VINCE: Okay. Unstable in any particular way? DR. BLAHA: Can be in any number of ways: AP instability, midflexion instability, collateral ligament instability. You know, classically the midflexion—so-called midflexion instability—will give you recurrent effusions, anterior knee pain, and difficulty rising from a chair and doing stairs. (Moderator comment: The panelist is probably referring to “flexion instability” as documented by Pagnano, Schwab, and colleagues [17,18]. So-called “midflexion” instability is frequently invoked but has not been satisfactorily described as a clinical entity in primary arthroplasty distinct from flexion instability [19,20]). DR. VINCE: Leo Whiteside describes intra-articular cortisone injection at the time of manipulation under anesthesia for stiffness. Does anybody on the panel do that? (Moderator comment: This finding does not seem to have been published.) DR. MALONEY: I learned from Leo. I use 80 mg of DepoMedrol with our manipulations, but I have not gone as high as Leo’s current doses.

Table 1 – Summary of findings from Cipriano et al. “Serum and Synovial Fluid Analysis For Diagnosing Chronic Periprosthetic Infection in Patients with Inflammatory Arthropathy.” Aspirated Fluid Arthropathy Type

Noninflammatory Inflammatory

ESR

32 30

CRP

15 17

WBC/ml

Polymorphonucleocytes (%)

3450 3444

78 75

The utility of all serum and synovial tests for predicting chronic periprosthetic loint infection was similar for patients with noninflammatory and inflammatory arthritis. The optimal cut-offs for ESR, CRP, synovial fluid leukocyte counts, and differentials are similar and so aspiration of fluid from arthroplasties is a reasonable practice when trying to diagnose periprosthetic infection, irrespective of type of arthropathy. i.e., elevated values in patients with inflammatory arthropathy and problem arthroplasties should not be attributed to the underlying pathology. Periprosthetic infection is a real concern.

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DR. VINCE: Okay. Is that going to be a patient with a large effusion? DR. MALONEY: No. DR. VINCE: So that would be injection into a stiff TKA, one that does not have an effusion. The General Practitioner (GP) in this case repeated the aspiration yielding 75 cc that again were not sent to the laboratory. A few days later, the lower limb began swelling. Two duplex scans, 11 days apart, were negative for thromboembolic disease (TED) but did show an accumulation of fluid in the knee. David, is there anything else that you might do at this point? It’s six months. He still has an effusion. DR. BACKSTEIN: Is he symptomatic? DR. VINCE: He’s not happy. That’s why he keeps coming back and the knee is swollen. DR. BACKSTEIN: I would consider an angiogram to see if there may be bleeding into the knee. DR. VINCE: Okay. David Blaha, anything else you might do at this point? DR. BLAHA: If I’m convinced he doesn’t have a DVT to explain swelling as opposed to an effusion, and if he doesn’t have infection—I’ve tried a PCL substituting brace to see if this would decrease the swelling and improve comfort. If it does, that supports the diagnosis of instability. DR. VINCE: David Blaha, I would like to amplify your important point about infection. That you would like to make sure first that he doesn’t have infection. DR. BLAHA: Very important to rule it out first. DR. MALONEY: Kelly, you said the repeat aspiration was “clear,” but you did not give us any lab values. Is the culture negative? DR. VINCE: Excellent point. That’s because the sample was not sent to the lab. What are your thoughts about aspirating fluid from a TKA and putting it in the trash? DR. MALONEY: Every time we aspirate fluid, we send it to the lab. DR. VINCE: All aspirated specimens to the lab, with rare exception? Any disagreement? (none) DR. BACKSTEIN: I would be upset that the GP had aspirated one of my total knees. DR. VINCE: Yes, I agree. What about sedimentation rate and CRP? Would you recommend these tests in a patient whose TKA was swollen? DR. BLAHA: Yes. DR. VINCE: Why did you guys forget this in our discussion? DR. BLAHA: The first thing I said was that you must rule out infection. I understood that had been done in this case. DR. VINCE: Yes apologies David, but very good that we make the point emphatically: infection should be ruled out first. Would you say that ESR and CRP would be a good way to begin evaluating for infection? DR. BLAHA: Absolutely. Yes. DR. VINCE: We all agree to consider infection first in this case. However, the team caring for this patient believed the diagnosis was PVNS and concluded that the ESR and CRP would be elevated because of inflammatory arthropathy. Is that a reason not to order these tests? What do you think, David Backstein? DR. BACKSTEIN: You can’t come to that conclusion and not rule out infection by some other means.

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DR. VINCE: So with the data we have, an ESR of 97 and a CRP of 186 at 6 months after TKA, what should we do? DR. BACKSTEIN: Aspirate the knee, and send the fluid off for cell count, differential, and culture. DR. VINCE: Right. The famous “three tests in one.” An aspiration was performed in this case, under ultrasound guidance, but not all three tests were requested. The differential for leukocytes was “95% granulocytes” but no absolute leukocyte count was included. The culture was negative. Can we relax with a negative culture? Dr. Mihalko, can you relax with a negative culture? (Fig. 1C and D). DR. MIHALKO: No. We know cultures are not full proof there will be false-negatives. DR. VINCE: Right. I think we must adopt the standardized habit of sending every synovial fluid specimen for all three tests: cell count, differential, and culture. I know the first time in a new hospital, I’ve always gone to the lab myself, presented the specimen, asked them how they plan to do the tests, and explained to the technicians what I need. Sometimes it has helped to give the lab staff references from our literature, and we’ve learned from each other. Arun, does your laboratory give you the kind of information that you require? DR. MULLAJI: No. They still haven’t got around to doing the cell counts. DR. VINCE: They don’t do cell counts? DR. MULLAJI: No. DR. VINCE: Okay. Anybody? Bill Maloney, your laboratory, they do cell counts for you? DR. MALONEY: Yes, sir. DR. VINCE: I would say that once you become accustomed to cell count data, you rely on them. They are very reassuring. Back to our patient, a CT arthrogram was performed. (Fig. 1E and F). I imagine the requisition for the study would have specified “PVNS” so the radiologist was likely to report synovial thickening, and reinforce the diagnosis—one that may or may not be correct. Arun, what you do think about this? This is an image to guide the aspiration. Any thoughts? (Fig. 1C and D). DR. MULLAJI: There’s clearly an effusion with what appears to be air bubbles in the joint. I’m worried that if they have not injected air at the time of the arthrogram, the air is particularly worrisome. DR. VINCE: Fair enough. I think they did inject air. Bill Maloney, there’s a cross-section of the CT arthrogram. Would you do a CT scan in a patient like this? DR. MALONEY: No. DR. VINCE: Okay. Would anybody do a CT scan in a patient like this? DR. BACKSTEIN: If there was pain that I couldn’t explain, and I’ve ruled out infection, yeah, I probably would. DR. VINCE: Looking for what information? DR. BACKSTEIN: for (tibial or femoral component) malrotation [21] DR. VINCE: Right. I certainly agree with you, David. But you and I would only request the CT scan after multiple aspirations, all had negative cell counts, negative differentials, and negative cultures. If there was still unexplained pain, only then would you and I be looking at rotational positioning [22]. Agreed? DR. BACKSTEIN: Agreed.

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DR. MALONEY: But that’s usually in a stiff knee, right, Kelly? Not in a knee with 1301 of flexion. DR. VINCE: Excellent point Bill. Stiff knees certainly are associated with internally rotated components, [23] but unstable knees are also associated with malrotated components [24]. In addition, Robert Barrack has identified internal rotation of tibial and femoral components in otherwise satisfactory TKAs with anterior knee pain [22]. I am worried about the radiolucency around the keel that showed up in this CT scan. (Fig. 1E and F). A rheumatologist was consulted at this point, because the orthopedic team was convinced they were struggling with recalcitrant PVNS. Looking back on cases like this, there is often a pivotal point where a decision was made about the diagnosis and it is unlikely for a clinician to re-evaluate the entire situation from the beginning. It seemed that this happened at the primary surgery with the synovitis. By now, the rheumatologist has accepted the diagnosis and advised a radionuclide synovectomy assuming infection had been ruled out. We have all agreed on this panel that we would rule out infection, with the recent AAOS guidelines, but that information was not collected in this case. Seven months after TKA, an arthroscopic synovectomy was performed to obtain better material for culture. Cultures of aspirated synovial fluid had been negative. (Moderator comment: This seems to have been an example of “anchoring bias” [25] or the tendency in decision making to rely too heavily on the initial data encountered and then to orient all further observations around that piece of information. While diagnoses can be made more easily with shortcuts or “heuristics,” [26] a series of errors were nicely enumerated in one case study by Guidry and colleagues— anchoring heuristic, premature closure, confirmation bias, and the blind obedience heuristic [27]. These tendencies have been described clearly by Groopman, in his book “How Doctors Think”[28]. Most of those seem to have been operant in this case and could have been avoided with the AAOS guidelines for diagnosis of periprosthetic infection.) By seven months, the rheumatology consultant recommended a radionuclide synovectomy after infection had been ruled out by taking tissue specimens arthroscopically. David Backstein, what’s the role of arthroscopy in a case like this in your hands? DR. BACKSTEIN: None in my world. DR. VINCE: All right. Arun? Would you take a look inside this TKA with a “scope?” DR. MULLAJI: I think when you reach this point, you’ve done everything. I think there’s no harm in looking at it with the scope. DR. VINCE: Except that we must be very clear on what you mean by “reached this point.” The members of this panel would have aspirated three times, and sent synovial fluid each time for cell counts, leukocyte differential, and cultures. No specimen from this patient was ever sent for these investigations and arthroscopy was performed on the belief that the quality of culture material would be superior. Dr. Mihalko, what would you say is the role of arthroscopy in the assessment of total knees? DR. MIHALKO: In my practice, none. DR. VINCE: Okay. Bill Maloney. DR. MALONEY: No role.

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DR. VINCE: David Backstein, do you think synovial specimens from arthroscopy are superior to repeated aspirations? DR. BACKSTEIN: Getting tissue is helpful. I recently had a case that ended up with a diagnosis of tuberculosis (TB), and I don’t think that culture would have grown without tissue. DR. VINCE: Okay. So would you go to arthroscopy after the three aspirations, or would you go to arthrotomy? DR. BACKSTEIN: I tend to do these things open, with arthrotomy. DR. VINCE: So you would have done this open. Okay. Fluid and tissue came back from arthroscopy with a negative culture. (Moderator comment: There is concern that the necessary preservatives in arthroscopic fluids will inhibit bacterial growth of a culture specimen.) The yttrium was installed at 9 months and was supplemented at 10 months with systemic plaquenil, prednisone, and voltaren to treat the working diagnosis: PVNS. By 12 months, the patient feels “50% better” with systemic therapy, but at 14 months the effusion returns and the patient is described as “grumpy.” Methotrexate is given every week. An ultrasound to guide another aspiration reports “scant fluid and synovial thickening.” Aspirated fluid is not sent for cell count, but yields scant propionibacterium on culture. What would you make of that, Bill Maloney? DR. MALONEY: The patient has a periprosthetic infection with Propionibacterium acnes. DR. VINCE: Mm-hmm. Okay, I think we are getting somewhere. And any other thoughts? What about the fact that the report states: “scant growth”? Is that the equivalent of a “subculture” or “positive in the broth” and maybe a false positive? DR. MALONEY: P. acnes is difficult to culture, but it’s real, so you have to keep the specimen for several weeks. If the lab only keeps the specimen for five days, you may miss the diagnosis and there may only be scant growth. We’re seeing an increasing number of P. acnes infections. DR. VINCE: Dave Backstein, what are your thoughts about that particular organism? DR. BACKSTEIN: The specimen may be difficult to grow, but the micro-organism is generally sensitive to antibiotics. DR. VINCE: The cell counts would have been so very useful to validate culture reports and to alert the surgical team to the risk of infection when the first culture came back negative. A positive subculture with a normal cell count from synovial fluid can be accurately interpreted as a false positive. A positive subculture with elevated leukocyte numbers is distressing and indicates a true positive. The arthroscopy was repeated at 16 months after TKA, presumably the culture had been interpreted as a false positive. Five tissue samples grew nothing but fluid placed in “blood culture” medium grew coagulase-negative staphylococcus. The patient was the treated with seven days of intravenous antibiotics followed by six weeks of oral therapy. David Backstein, what would you do now, sixteen months after TKA, with persistent effusions, and these culture results? DR. BACKSTEIN: I worry about when he may have developed this infection after so many interventions. If infection has been there from the beginning, then my treatment will be a two-stage revision. There’s no place for an irrigation and debridement of any kind in this knee.

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Table 2 – Inflammatory Serum Tests Values in the Days Following Removal of the Infected Prosthesis, Despite the Possible Diagnosis of PVNS POD

10

21

42

56

CRP ESR

38 53

8 16

9

4 5

DR. VINCE: David Blaha, what would you do at this point? It’s been 16 months of misery, effusions. DR. BLAHA: Two-stage revisions for this guy. I think he has a proven infection in the joint. DR. VINCE: Okay. By 18 months there’s a cloudy effusion, with a lucency under the tibia. The CRP is elevated at 67 and the ESR is 56. The treating physicians and surgeons have concluded that this is a periprosthetic infection and recommended a two-stage reimplantation. Everybody is coming to the same conclusion as the two Davids on our panel. This is the X-ray (Fig. 1G and H). Bill Maloney, give us some guidance on this. Does it look okay? DR. MALONEY: No. You’re starting to get a significant radiolucency under the medial tibial plateau, consistent with sepsis. Now you have a chronic periprosthetic infection, plus secondary osteomyelitis. This patient, I think, is not a good candidate for a one-stage revision even if you generally favor that approach to periprosthetic infection. This case should be done in two stages. We had a run of P. acnes infections, and they can destroy a lot of bone—worse than you see on the X-ray. DR. VINCE: Understood. Arun, how would you treat this? What’s your approach? What do you see in that X-ray picture? DR. MULLAJI: I think you can see massive erosion on the medial side of the tibia. DR. VINCE: Yep. DR. MULLAJI: There are lucencies on the lateral tibia and under both the anterior and posterior femoral flanges. The femoral component is clearly loose. DR. VINCE: I agree this prosthesis is loose. Have you ever seen osteolysis as a cause of aseptic loosening at 16 months? What are your thoughts as to the etiology of this loosening? DR. MULLAJI: Not really, this is due to infection. DR. VINCE: So if you see this picture at 16 months after TKA, it looks convincingly like sepsis. The patient was treated with removal of the components and an antibioticimpregnated spacer (Fig. 1I and J). The histopathology from the resection came back as “chronic synovitis and hemosiderin consistent with old hemorrhage.” The microbiology from tissue specimens at the prosthesis removal grew P. acnes bacteria. Eight of 10 cultures obtained at surgery were positive: seven had scant growth and one from under the tibia had moderate growth. Does that seem like an excessive number of cultures to take? Bill Maloney? DR. MALONEY: Maybe. We do five, but I can see in this situation, the surgeon wanted some answers, so I understand. DR. VINCE: Personally, I might have taken more than one from every site. After component removal, which was the first surgery of a two-stage revision, he received Rifampicin, Fusidic acid, and Penicillin. The inflammatory markers declined to normal by 56 days post-op. He reported feeling

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very well by three months, the best ever since his arthroplasty. The team was nervous about this case and they left the patient with a resection arthroplasty for 12 months. The serum ESR and CRP values progressed well with the prosthesis out (Table 2). Any reason you might extend the period of explantation, David Blaha? DR. BLAHA: No, I don’t see any reason to wait a year. If the ESR and CRP are down and the nutritional status is good, I wouldn’t wait 12 months. DR. VINCE: Yep. Got you. Dr. Mihalko? DR. MIHALKO: The only reason I would delay reimplantation would be inflammatory parameters that are not coming down. Then I would repeat the debridement and use another spacer. I wouldn’t wait for 12 months to reimplant if ESR and CRP had normal values. DR. VINCE: Fair enough. Would 12 months be helpful, Arun, in any particular infected case? DR. MULLAJI: Actually, I tend to keep my patients 6–12 months with the spacer. I don’t do second-stage revision very early, largely because most of my patients don’t have a known organism (Moderator comment: The clinical problem of culture-negative periprosthetic infection is well described.) [29–31]. DR. VINCE: Are you using an articulating spacer? DR. MULLAJI: I keep an articulating spacer so they’re walking about and moving around just like normal. DR. VINCE: Very good. And because of the concern about collateral ligament insufficiency, a hinged-type prosthesis was used for the reimplantation. Let’s review the AAOS (American Academy of Orthopedic Surgeons) Guidelines for Diagnosis of Periprosthetic Infection (Table 3) and how [16,32] adherence might have clarified this case from the beginning. I’m sure you are all familiar with these. First, the idea of stratifying the patient by risk in terms of suspicion of infection. Bill Maloney, what constitutes a higher-risk patient in your view? DR. MALONEY: The patient with morbid obesity and diabetes creates higher suspicion. A wound that doesn’t heal well or one that needed debridement early in the post-op period, a patient with a hematoma, or one who was put on antibiotics because the wound problems make me worry about a chronic low-grade infection. DR. VINCE: Right. So does risk influence your actions? (Moderator comment: The Guidelines define in detail, “higher probability of infection” and “lower probability of infection.”) [16,32]. DR. MALONEY: I treat everyone the same. If there’s any suspicion of infection, I do exactly what these guidelines say. DR. VINCE: The messages from guidelines 2 and 3 are that we should perform ESR and CRP from peripheral blood in all patients with problem arthroplasties, but aspiration is not obligatory if the inflammatory marker values are normal, unless we have stratified the patient as a high probability of infection. Aspirated synovial fluid should be sent to the laboratory for leukocyte count, leukocyte differential, and bacterial culture—the 3 essential tests, something that is essential if the ESR and CRP are elevated. Dr. Mihalko, do you agree with that? DR. MIHALKO: I agree completely. DR. VINCE: Recommendations four, five, and six pertain to hip arthroplasty.

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Table 3 – Summary of AAOS Guidelines for Diagnosis Periprosthetic Infection 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 a b c

Stratify Patients by Risk/Suspiciona Obtain ESR þ CRP for all patientsa Aspirate if ESRþCRP are elevated or suspicion high (cell count, differential, þ culture)a (Selection of THA patients for aspiration)b (When to repeat Hip aspiration)b Low-probability infection/no surgery planned/but ESR þ CRP up then re-evaluated in 3 monthsb If discrepancy between suspicion and 1st aspirate then re-aspiratec Keep off abx(antibiotics) 2 weeks before aspirationb Nuclear scan option: PPI not diagnosed/no surgery plannedb CT þ MRI: No recommendationsb Intra-operative gram stain: Opposedb Dx neither established nor excluded: Intra-operative frozen section: Recommendedb Patient being assessed for PPI: Multiple cultures at surgeryb Abx for suspected infection: opposed until aspiration is performedb Routine revision: opposed to withholding abxb

Guideline applies to both the hip and the knee. Guideline applies to the hip. Guideline applies to the knee.

Number seven recommends that problem TKAs have a repeat aspiration, for cell count, differential, and culture when there’s a discrepancy between the probability of infection and the results of an aspiration. The eighth recommendation is that all aspirations should be performed with the patient off of antibiotics for a minimum of two weeks. Number 9 was reported as a weak recommendation in favor of nuclear imaging in patients where the diagnosis of infection is suspected but has not been established by the above guidelines and where no surgery is scheduled. The tenth point was that no recommendation could be made about CT and MR imaging when infection is the question. Bill Maloney, any guidance on this? Is this what you practice? DR. MALONEY: Yeah, that’s pretty much what we do. The infectious disease (ID) people like the nuclear imaging. I don’t think it’s especially helpful in the early postoperative period. DR. VINCE: Right. DR. MALONEY: If a nuclear scan is negative, which it never is in the early postoperative phase, we can rule out infection. In that way, scans are helpful for late events (more than a year after surgery) [33,34] but not for acute infections. DR. VINCE: Arun, are you happy with these recommendations? Specifically that CT scans are not considered very useful in the workup of infection? DR. MULLAJI: Yep. DR. VINCE: Fair enough. The 11th recommendation opposes relying on intra-operative gram stains to rule out infection at revision and the 12th supports the use of frozen-section analysis at surgery when the diagnosis of infection has neither been established nor excluded. Number 13 recommends multiple cultures at surgery for patients being evaluated for infection. That was done in this case and confirmed the diagnosis. Number 14 clearly opposes the use of antibiotics unless an aspiration has been performed. What about antibiotics to prevent infection because the wound looks red? Is that reasonable? Does anyone favor antibiotics for possible superficial wound infection without an aspiration? PANEL: (No support for use of antibiotics without an aspiration.)

DR. VINCE: The 15th and final recommendation is NOT to withhold antibiotic prophylaxis at revision surgery for patients with low probability of infection or for those with an established diagnosis of infection undergoing surgery. It has been common practice, when doing a revision for any reason, to hold the antibiotics in order to take intra-operative cultures. What do you think, Bill Maloney? DR. MALONEY: We agree with the recommendations. We give the antibiotics now and no longer hold them at revision. DR. VINCE: That makes sense, as revision patients are at the highest risk of infection, and if we hold their antibiotics, we compromise the prophylaxis. One point to emerge from these guidelines is that the time to diagnose infection is before the revision surgery, during the planning phase. DR. BACKSTEIN: What if your aspirations have been negative, but you continue to suspect infection? DR. VINCE: Wouldn’t that mean you plan to take everything out anyway? DR. BACKSTEIN: But if you want deep cultures that are meaningful, wouldn’t you hold the antibiotics? DR. VINCE: Yes I would hold them, but I would not be doing a revision that day, if I were not sure of the diagnosis. I would be doing a resection arthroplasty; taking everything out, obtaining the good quality cultures you describe because I don’t have proof it’s not infected. That patient, undergoing removal only, does not have the same need for prophylaxis. DR. BACKSTEIN: But you need to identify the organism to treat them properly. DR. VINCE: I agree. I would withhold the antibiotics in that case. I would get good-quality cultures, but I wouldn’t be putting any prosthesis in that day. Even surgeons who favor a one-stage treatment for infection feel that correct identification of the micro-organism is an important part of the treatment. DR. BACKSTEIN: Right.

2.

Case two

DR. VINCE: This case surprised the surgeon at revision. A very active 56-year-old male, had a painful total knee five years

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post-op. He was initially very satisfied with the knee but now has had a year of swelling and a feeling of instability. Knee motion on presentation is slight flexion contracture, and 1301 of flexion. Arun, your thoughts on this case? What are you expecting to see? DR. MULLAJI: The fact that he’s going “up to minus five,” he’s hyperextending, so I’m thinking of instability. DR. VINCE: I’m sorry. That notation is meant to describe “lacking 51 of full extension,” specifically a flexion deformity. DR. MULLAJI: Oh, so flexion contracture of 51. DR. VINCE: Yes. Sorry. DR. MULLAJI: Okay. That’s different. Since it’s five years post-TKA, I am considering instability, perhaps early osteolysis and also infection. DR. VINCE: Fair enough. The first radiographs date from the onset of symptoms about 4 years after TKA. They include AP, lateral, flexed-view PA, and Merchant views (Fig. 2A–D). The next set of AP and lateral radiographs are taken after about one year of symptoms, at five years’ post-TKA (Fig. 2E and F). Dr. Mihalko, what do you make of these radiographs with this clinical situation? DR. MIHALKO: On the medial side of the tibia, there is a radiolucency that has worsened since the symptoms began. The lateral X-ray may have some scalloping at the interface, so that makes me worry about infection. DR. VINCE: All right. Fair enough. David Blaha, what do you make of this? DR. BLAHA: I would begin by looking first of all for infection, then make sure that the implants aren’t loose. After four years of good function, with a recent onset of an effusion, I also worry about wear. The effusion could be associated with wear particles and that radiolucency would go along with the diagnosis of osteolysis. The components don’t look loose, and so I am concentrating on infection and wear. DR. VINCE: Right. When you mention infection, I imagine we would all do the same thing that was discussed in the first case: serum for sedimentation rate (ESR), “C”-reactive protein (CRP), and then aspirate the knee, sending fluid for cell count, differential, and culture. Those investigations were all negative in this case, and the diagnosis was made of relatively routine, aseptic loosening. The decision was made for revision. Bill Maloney, any advice for the surgeon? DR. MALONEY: There’s a lot of osteolysis in the proximal tibia. You can see a large osteolytic lesion in the lateral tibial plateau (Fig. 2E). In cases like this at five years, we typically see not only articular polyethylene wear but also a lot of backside wear. So I suspect that there’s going to be a lot of wear and a lot of osteolysis. DR. VINCE: Okay. Arun, any advice for the surgeon? DR. MULLAJI: I think even on the femoral side there’s a huge amount of osteolysis around the posterior condyle. DR. VINCE: Really? DR. MULLAJI: Yeah, on the lateral view. DR. VINCE: Okay. Well spotted. DR. MULLAJI: At least that’s what it seemed on the X-ray. I would advise the surgeon to be prepared to deal with large bony defects. DR. VINCE: Okay. All right. David Backstein? DR. BACKSTEIN: So the ESR and CRP were normal?

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DR. VINCE: Yep. Yep. We can say with assurance, based on the protocol we discussed in the first case that this arthroplasty is not infected, despite the worrisome radiograph. DR. BACKSTEIN: With this implant at five years, I’d be really wondering why they had such bad poly wear. I’m suspicious that there’s some serious mechanical problem with the knee joint. DR. VINCE: He has 1301 of flexion and is a very active person who works as a manual laborer. Would that explain the wear? DR. BACKSTEIN: It’s possible that this resulted from a high level of activity, but it’s unusual. I haven’t seen it just from that alone. DR. VINCE: Would a little instability in flexion contribute to the problem? Also, this was probably not cross-linked polyethylene. DR. BACKSTEIN: Yeah. DR. MALONEY: He did well for four years with high activity, so that’s not really consistent with flexion instability, Kelly. I mean, it’s a posterior stabilized prosthesis, so, maybe the post broke to give instability, but the tibia doesn’t look subluxed. DR. VINCE: Agreed. There is no disabling flexion instability. The patella has not been resurfaced and it’s tracking centrally, indicating good rotational position (Fig. 2D). I first learned about this case while doing surgery at our hospital, and the company rep in our room showed me a cell phone picture from a surgeon colleague of mine 400 miles away asking for advice. They had planned a simple revision with primary components but were taken by surprise with the amount of bone loss. David Blaha, what’s your advice for the surgeon who is surprised at surgery by an unanticipated problem like this? What would you do at this point? DR. BLAHA: If you do revisions, you have to be ready to be surprised. You must have the posterior stabilized or the constrained condylar-type components on the shelf as part of a revision system. You may not have hinged components available, but if you knew pre-operatively that you had an intact medial collateral ligament, you wouldn’t need one. DR. VINCE: Okay. So, Bill Maloney, the surgeon just thought it was going to be a revision with primary components. Bad surprise on the surgical day. What should they do? DR. MALONEY: Put in a spacer and send the patient over to your hospital. DR. VINCE: They seemed to agree with you! They implanted an articulating spacer, with antibiotic-loaded cement that they purposefully did not fix well, in order not to burn any bridges, and pave the way for second stage even if it proved to be infected. They obtained good cultures at the time and we planned the surgery together several months later. David Backstein, any insight you can give this surgeon in retrospect? I think the surgeon’s learned a lesson. They’re going to be prepared with more gear next time. DR. BACKSTEIN: I think that the lesson is if you’re going to do revisions, you have to be prepared. DR. VINCE: Right. DR. BACKSTEIN: Or else you get burned. DR. VINCE: Arun, you looked at that lateral X-ray and immediately picked up that there were large osteolytic defects (Fig. 2E–H). Bill, you identified big defects in the tibia. (Moderator

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Figure 2 – (A) AP radiograph of an active and fit 56-year-old male with a physically demanding job, about 4 years after surgery. Our panel identified radiolucencies under the tibial component suggestive of infection or aseptic loosening (arrows). (B) Lateral projection confirming these lesions. The posterior femoral bone has begun to lose its trabeculation, a sign of osteolysis. There is also subtle erosion of bone under the anterior flange (arrow). Prior radiographs were not available for comparison. (C) Flexed view PA, weight-bearing radiographs showing the right TKA and unoperated left knee. The right knee has definite and disturbing radiolucencies under the tibia consistent with sepsis and loosening. The less obvious decrease in bone density in the medial femoral condyle is very suspicious for osteolysis. (D) Merchant patello-femoral radiograph [45] showing a centrally tracking patellar that argues in favor of satisfactory rotational positioning of the femoral and tibial components [46]. The patella has not been resurfaced. (E) AP radiograph, now 5 years after TKA showing severe loss of medial femoral condylar bone that threatens the integrity of the cortex (double arrows). There is a line demarcating the border of a large osteolytic lesion in the proximal lateral tibia. (single arrow). (F) Lateral radiograph at 5 years after TKA, with cortical disruptions and incontrovertible lytic lesions in the posterior condyle (arrow). These could be due to sepsis or osteolysis. Only aspirated synovial fluid can make the distinction reliably, when evaluated for cell count, differential, and culture according to the AAOS Guidelines for the diagnosis of Periprosthetic Infection [16,32] (G) AP and (H) lateral radiographs of a “loosely cemented” primary component with antibiotic-loaded polymethyl methacrylate as an interim spacer. At revision for aseptic loosening, the planned reconstruction with primary components was not feasible due to the extent of the bone loss. A definitive revision was scheduled at a later date with full revision equipment. (I) Intra-operative photo at definitive revision showing extensive osteolytic defects that were not amenable to reconstruction with primary components. (J) AP and (K) lateral radiograph of definitive revision with diaphyseal engaging uncemented intra-medullary stems, allograft bone chips packed into large osteolytic femoral condylar defects and trabecular metal cones to enhance fixation and defect management on both tibia and femur. Note eccentric reaming technique of femur to reduce varus alignment and unload the medial compartment in a patient who has failed from medial tibial wear [47]. The stem extension is in valgus relative to the medullary canal and an offset stem has been placed to centralize the femoral component after the stem was placed up against the lateral femoral endosteum.

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comment: Conventional radiographs notoriously underestimate bone defects from osteolysis. CT scanning reveals the extent of bone loss more accurately and often more disturbingly.) Dr. Mihalko, considering reimplantation, (Fig. 2I) how would you manage these defects? What would you like to do technically? DR. MIHALKO: On the tibial side it looked like you could probably use a metaphyseal sleeve [35]. And on the medial femoral condyle there is more extensive defect than I appreciated on the radiograph. DR. VINCE: The defect has broken through the cortex leaving not much more than a shell. Anything else? DR. MIHALKO: I would be concerned that the MCL (medial collateral ligament) will no longer be attached, so I’d be ready for a hinge if necessary. DR. VINCE: Do you feel the MCL is not going to be intact or the bone’s not going to be intact. DR. MIHALKO: The bone’s not going to be intact for the revision. DR. VINCE: Is there a difference in terms of how it should be treated? DR. MIHALKO: Yes. DR. VINCE: Okay. Dave Backstein, what device would you reimplant this with, generically speaking? DR. BACKSTEIN: I’m a fan of porous cones [36]. I like using them. And I would absolutely be prepared to use a hinge. If it’s a big enough chunk of bone that I can fix, I’ll fix the epicondyle with a couple of screws, but most of the time I prefer a hinge. DR. VINCE: Okay. Bill Maloney, the bone defects, what do you think you might use, and in terms of degree of constraint, what do you want to be prepared with? DR. MALONEY: Prior to the availability of “sleeves,” we would have used a large femoral head to reconstruct the medial femoral condyle and probably impaction grafting on the tibial side [37–40]. I still use that technique in some cases. Today we would use an implant with a CCK [41] (constrained condylar knee i.e., non-linked constrained device, a non-hinge) type of articulation to protect the bone graft. We’d use (intra-medullary) stems and would either press-fit long ones or fully cement short ones. I tend to go a little bit longer with a press-fit stem in this type of case. DR. VINCE: Okay. As everyone has said, some sleeves or cones will be required for the bone defects. I used a cone augment in the reconstruction with a non-linked constrained device, not a hinge [42] (Fig. 2J and K). I packed a lot of bone graft into the medial femoral condyle, as you see up here, supplemented with the cone to hold it in place. It sounds like structural allografting is not anybody’s first choice these days, despite the size of these defects, and it’s dealer’s choice in terms of hinge or not.

3.

Case three

Here is a third, somewhat hypothetical, case that has a bearing on effusions. Let’s consider the patient with an arthritic knee and a 431 fixed flexion contracture to explore your thoughts about surgical technique (Fig. 3A and B). If a surgeon approached a knee like this, by making all the bone

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cuts according to the manufacturer’s product manual, but without any soft tissue surgery, what would they have in terms of gaps? Bill Maloney? DR. MALONEY: With a fixed flexion contracture, usually you would have a tight extension gap after the standard cuts have been performed. DR. VINCE: Tight extension gap. Okay. Everybody agrees, in a case with a fixed flexion contracture, if you don’t do any soft tissue releases and simply follow the manufacturer’s steps, you end up with a small extension gap and a normal or relatively larger flexion gap. And if you choose your tibial polyethylene insert to achieve full extension, what will the patient have. Arun? DR. MULLAJI: If you haven’t done soft tissue releases? DR. VINCE: Right. DR. MULLAJI: Then you’re going to be having a tight extension gap, and in flexion you’re going to be loose. DR. VINCE: Right. DR. MULLAJI: So either you’re going to put in a thin insert, in which case you’ll be lax in flexion. DR. VINCE: Right. DR. MULLAJI: And if you put in a thick insert, you’ll be okay in flexion, but you’re not going to be OK in extension. DR. VINCE: Right, the knee will not come to full extension and you will have a persistent, uncorrected flexion contracture (Fig. 3C–F). DR. MULLAJI: So the basic problem is the soft tissue release. DR. VINCE: Excellent description, and I think it highlights that the person who presents for TKA and who is at the greatest risk for flexion instability [17,18] is the flexion contracture patient. DR. BACKSTEIN: You have to use a good-sized femoral component for flexion contracture patients. DR. VINCE: Agreed. If you undersize the femoral component, the discrepancy between flexion and extension gaps will be increased. But in the situation described, the instruments should indicate the correct size of femoral component and the unreleased contracture would create the flexion– extension imbalance we have described resulting in “flexion instability.” This highlights the point that the patient at greatest risk for flexion instability is the patient who presents with a flexion contracture and it does not have to be as severe as 431. An older cadaver study reported that each millimeter of polyethylene was probably responsible for about 41 of motion [43].

4.

Case four

DR. VINCE: Now, let’s consider an unstable total knee arthroplasty in a 49-year-old female who suffered injury to her patello-femoral joint and lateral compartment in a motorcycle accident some years before. Five arthroscopic surgeries were performed over the years, each with small, temporary improvement in the knee. Eventually, a navigated cruciate retaining knee arthroplasty was performed for post-traumatic osteoarthritis. There were no wound problems after surgery. These radiographs show the post-op total knee which the patient feels is unstable (Fig. 4A and B). The mechanical axis

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Figure 3 – (A) AP of both knees showing symmetric joint space narrowing on the left knee due to severe rheumatoid arthritis. (B) Lateral radiograph of the left knee in full extension showing a 431 fixed flexion contracture. (C) Schematic drawing depicting the lateral view of an arthritic knee with a fixed flexion contracture about to undergo TKA by a measured resection technique, with no alteration to the recommended bone cuts and no soft tissue releases. (D) The standard amount of bone has been removed from the proximal tibia and equal thicknesses has been removed from the distal and posterior femoral condyles. (E) As the posterior soft tissues are tight, they have not been released in this case, and a relatively thinner spacer can be accommodated in the extension gap. (F) This relatively thin spacer, corresponding to a thin modular tibial insert, will allow excess laxity in the flexion gap. This is the typical scenario that leads to “flexion instability”: arthritis with a fixed flexion contracture that is not corrected at surgery with either posterior releases or additional resection of distal femoral bone. If a thicker polyethylene insert was selected, the knee would not extend fully. The amount of instability in flexion may be subtle at surgery, but clinically very significant to patient function later on. passes through the medial compartment, much like her normal contralateral knee (Fig. 4C). She consulted an arthroplasty specialist two years after the primary arthroplasty, having had pain since the surgery. Chronic regional pain syndrome had been considered by her original surgeon. The workup for infection as discussed above was negative. She has persistent swelling and can only walk short distances. The TKA flexes very well, but doesn’t straighten and she feels there is a “tight band” around the knee. Stairs are particularly difficult. Dr. Mihalko: How do you interpret this situation? DR. MIHALKO: I see the tibial base plate is out of alignment on the AP radiograph. This is probably an unbalanced knee that was implanted in varus.

DR. VINCE: Definitely, and the consulting surgeon described varus thrust through stance phase. David Backstein, you would interpret this as a case of? DR. BACKSTEIN: They have pain that feels like tightness? DR. VINCE: Pain, swelling, great motion but difficulty with stairs. DR. BACKSTEIN: So “midflexion instability” is generally that sort of picture. DR. VINCE: Not “flexion instability?” DR. BACKSTEIN: Yes, “flexion instability.” People call it “midflexion,” but yes, flexion instability. DR. VINCE: Yes and the surgeon reported that the posture of the foot was rotated externally and that there was a lax flexion gap.

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Figure 4 – (A) AP radiograph of a chronically painful, unstable and swollen TKA performed for post-traumatic osteoarthritis. The radiograph depicts the components symmetrically, but only by externally rotating the limb, as manifested by the disappearance of the fibular head behind the tibia. This is a TKA with internally rotated tibial and femoral components. (B) Lateral radiograph of an unstable TKA. The flexion gap was also lax. (C) Mechanical axis of TKA with varus and flexion instability. The static alignment is satisfactory in this case, but ligament imbalance was responsible for a varus thrust. (D) Computed tomography (CT) cut through the distal femur showing reasonable rotational position of the femoral component. (E) CT cut through the proximal tibia indicating internal rotation position of the tibial component. Arrow indicates the lateral position of the tibial tubercle. (F) AP radiograph of revision TKA that has restored alignment and stability with a posteriorstabilized articulation and long press fit uncemented stem extensions to guide position and augment fixation. (G) Lateral radiograph after revision for varus and flexion instability. DR. BLAHA: It could be extension instability too. DR. VINCE: Yes, absolutely, as demonstrated by the varus thrust. DR. VINCE: Bill Maloney, what do you think of the rotational position of the tibial component on this X-ray, in a patient with external rotation posture of the foot? DR. MALONEY: You have a good AP image of the implant but the tibial bone is rotated externally with the fibular head obscured behind the tibia, so the component has probably been internally malrotated when it was put in (Fig. 4A). DR. BACKSTEIN: The size of the tibial component is probably why the surgeon went into internal rotation. If they had used a smaller tibia, it would have been easier to rotate the component to a more accurate position. DR. VINCE: Bill Maloney, your description is right on target and confirmed by the CT scan, done in this case according to

the Perth Protocol, slightly different to the Berger–Rubash protocol that is used frequently in North America to quantify rotational positioning of femoral and tibial components in TKA. (Fig. 4D and E). A successful revision was performed correcting the rotational positioning problems and restoring varus–valgus stability. By restoring size and position, it was not necessary to use significant constraint as we see here with a posterior-stabilized articulation (courtesy Dr. Davis Morgan). We have come to the end of our allotted time having reviewed four knee arthroplasties complicated by swelling and effusions. The joint fluid was thought to be from persistent inflammatory arthropathy in the first case but turned out to be infection with an indolent micro-organism: P. acnes [44]. The second had effusions from polyethylene wear, with component loosening and unexpectedly large osteolytic defects at revision. The third, a hypothetical case with an

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effusion, explored the predisposing factors for flexion instability. The fourth case had persistent pain and effusions from a combination of flexion plus varus instability that was revised without a constrained implant with attention to component size and position. We have agreed that evaluation of the patient with excess fluid in a TKA is made much easier by the new guidelines from the AAOS for diagnosis of periprosthetic infection [16,32]. In short, when effusions are present, the fluid may be pus, excess synovial fluid, or blood. An aspiration with cell count, differential, and culture will provide the answer. Gentlemen, thank you very much. And Seth, thank you for the opportunity to discuss these cases at this 2012 meeting of CCJR in Las Vegas. Until next time.

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