Infected pseudotumor following metal-on-metal total hip arthroplasty: a case report with diagnostic challenges and implications for surveillance guidelines

Introduction

There are many possible clinical presentations due to the presence of metal wear in the periarticular region in metal-on-metal (MoM) prostheses. These presentations can range from simple metallosis or aseptic lymphocytic vasculitis-associated lesion (ALVAL), which is a specific histological pattern found in patients with MoM prostheses and due to the presence of metal ions in the articular capsule (1), to the final stage of this disease, which is pseudotumor (2). Pseudotumor is a soft-tissue mass associated with MoM implants, and this mass is neither malignant nor infective in nature (3).

All these presentations were subsumed under the designation adverse reaction to metal debris (ARMD), introduced by Jameson, which covers all failures due to metal wear, associating pain, sterile effusion, and the presence of macroscopic metallosis or necrosis (4).

The main differential diagnosis of this rare and misleading complication is periprosthetic joint infection (PJI), and both can be associated.

Multiple studies have revealed that the infection rate is higher in MoM prostheses than in other friction couples (5).

We report a case of an undiagnosed specific complication in a patient presenting with a pelvic pseudotumor in a MoM THA. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-266/rc).

Case presentation

Patient medical history

We report the case of a 75-year-old Caucasian man with a MoM total hip arthroplasty (THA) (Zimmer Biomet) consisting of a non-cemented AVENIR size 4 stem, a 62-mm cementless DUROM acetabular component, and a large diameter head (LDH) 56 + 4 head, implanted via a posterior approach in 2006 (Figure 1).

Figure 1 Patient anteroposterior radiograph of the pelvis showing his MoM THA. MoM, metal-on-metal; THA, total hip arthroplasty.

The patient had a medical history of hypertension, diabetes mellitus, dyslipidemia, and paroxysmal supraventricular tachycardia treated with rivaroxaban.

He was also diagnosed with prostatic adenocarcinoma in 2015, treated with radiotherapy, chemotherapy, and hormonal therapy, and was considered in remission.

In 2018, the patient presented with deep venous thrombosis (DVT) involving the iliac, femoral, and popliteal veins, associated with pulmonary embolism, treated with anti-Xa inhibitor (rivaroxaban).

Since the DVT, the patient progressively developed a massive lymphedema of the entire right lower limb.

Both the DVT and lymphedema were initially attributed to his prostate cancer and its treatment.

It is important to note that the radiologists and physician fortuitously detected psoas muscle bursitis on a computed tomography (CT) scan performed in 2019 during cancer surveillance. However, neither the treating physician nor the radiologist raised concerns about this finding and no further investigation or MoM-specific surveillance had been implemented (Figure 2).

Figure 2 CT scan from 2019 highlighting bursitis of the right iliopsoas tract (red arrow) compared to the left iliopsoas tract in the left side (yellow arrow). CT, computed tomography.

Recent medical issue

In February 2023, the patient developed erysipelas of the right lower limb superimposed on his preexisting lymphedema, accompanied by acute pain in the right gluteal region radiating to the posterior thigh and leg, resulting in complete functional impairment. The patient also presented with fever, prompting admission to the rheumatology department for further evaluation.

Two sets of blood cultures were obtained and revealed Streptococcus agalactiae bacteremia. Serum laboratory tests demonstrated significantly elevated inflammatory markers, with a C-reactive protein (CRP) level of 301.2 mg/L and an erythrocyte sedimentation rate (ESR) of 59 mm/h. A spine magnetic resonance imaging (MRI) was subsequently performed, revealing lesions suggestive of infectious spondylodiscitis.

The patient was then initially placed on ceftriaxone for one week, however, due to progressively worsening right hip pain, a contrast-enhanced pelvic CT scan in the portal venous phase (using iodinated contrast medium, 90 mL of Iomeron 350 mg/mL) was performed days later. This demonstrated a massive iliopsoas muscle collection measuring 17.5 cm × 12 cm in the transverse plane and extending 22 cm in length. The collection featured thick walls, multiloculated morphology, and contained gas locules—findings highly suggestive of an infectious process (Figure 3).

Figure 3 CT scan from February 2023 showing the rim enhancing fluid collection within the right iliopsoas muscle, abutting the prothesis and consistent with an infected pseudotumor (white arrow). CT, computed tomography.

Cobalt serum levels were measured and revealed elevated blood cobalt levels (6.23 µg/L) (normal value <0.45 µ/L).

After multidisciplinary review and based on the modified Musculoskeletal Infection Society (MSIS) criteria and International Consensus Meeting (ICM) on Musculoskeletal Infection guidelines (6), the diagnosis was revised to PJI with an infected, metal debris-induced pseudotumor of the iliopsoas muscle.

The diagnosis of pseudotumor was retained based on the constellation of clinical, biological and imagery findings.

Metal artifact reduction sequence (MARS)-MRI, which is considered the gold standard for the evaluation of ARMD (7) was not performed in this case.

Given the acute septic presentation, positive blood cultures, and the need for urgent surgical management, CT imaging was favoured for rapid assesment of abscess formation and surgical planning. The absence of MARS-MRI is acknowledged as a limitation of this report.

Similarly, the elevated serum cobalt level was considered as one element supporting the diagnosis of ARMD, but not as the sole determinant. The decision to proceed with revision surgery was not made solely on the basis of this elevation, particularly as the level remained below the commonly cited 7 µg/L threshold often used to prompt revision. In any case, a formal indication for revision surgery was present, which is the PJI.

The diagnosis of spondylodiscitis was ultimately excluded based on spine MRI reassessment by a musculoskeletal radiologist and the convergence of clinical and paraclinical findings. The initially seen lesions on spine MRI were ultimately consistent with arthritic spinal changes. In addition, retrospective review of CT scans performed in 2019 revealed a pre-existing cystic mass consistent with a pseudotumor, initially described as psoas bursitis.

From patient perspective, this was an acute infectious episode that led to hospitalization and major revision surgery, which he perceived as a sudden and severe deterioration in a THA that was functioning normally for years, especially given that he had no progressive functional impairment which would be linked to his THA and he was reassured by his physicians about his chronic lower limb swelling.

A schematic timeline summarizing the clinical course, diagnostic steps, and management decisions is provided in Figure 4.

Figure 4 Timeline of events. CT, computed tomography; DVT, deep venous thrombosis; MoM, metal-on-metal; PJI, periprosthetic joint infection; THA, total hip arthroplasty.

Surgical management and progression

The patient underwent a two-stage revision of his THA. During the first stage, we performed prosthesis removal with multiple bacteriological samples, and placement of a Palacos cement spacer one week after symptom onset. Intraoperative cultures grew Streptococcus agalactiae, and the patient received a 3-month course of antibiotic therapy (amoxicillin).

Pathological examination confirmed the diagnosis of metal-induced pseudotumor, demonstrating fibrinous exudate, macrophage infiltration with metal debris deposition, and multiple suppurative foci confirming infection also (Figure 5).

Figure 5 Capsular fibrosis with macrophage and giant cell reaction on metal debris with evidence of infection (Morawietz III). ALVAL, aseptic lymphocytic vasculitis-associated lesion.

The surgical wound completely healed with no signs of inflammation in 2 weeks.

After 3 months of antibiotic therapy leukocyte count was 4,700 G/L and CRP level was 5.8 mg/L.

Pelvic imaging revealed significant reduction in pseudotumor size (Figure 6).

Figure 6 Scan plan showing shrinking of the collection and pseudotumor (red arrow).

The patient subsequently underwent the second-stage revision, receiving a THA with a 59-mm Smith & Nephew acetabular reinforcement device and a cemented 53-mm dual mobility Capitole-Evolutis acetabular component with a 28-mm metal head on polyethylene cup and non-cemented femoral stem Evolutis Stemsys size 12 (Figure 7).

Figure 7 Radiographs showing post op aspect after second stage revision.

Perioperative biological lab cultures grew Staphylococcus capitis and Staphylococcus epidermidis, prompting treatment with rifampicin and doxycycline.

At 29 days postoperatively, the patient showed excellent outcomes with no inflammatory signs at surgical sites, leukocyte count was 3,900 G/L and CRP level at 27.7 mg/L.

Unfortunately, the patient died 2 days later. The cause of death could not be determined as the family declined autopsy.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent for publication of this case report and accompanying images was not obtained from the patient or the relatives after all possible attempts were made.

Discussion

Our patient presented with a rare but well-described complication of MoM arthroplasty.

The aim of the article is not to make judgements about the initial management, especially because we were not able to obtain the real cause of death, however we believe that the data we presented is solid enough to provide a good understanding of the evolution. We also believe that a better understanding and sensibilization for all relevant healthcare professionals for this specific complication can help to improve patient outcomes this prompted us to review the literature and try to summarize it.

MoM THA had been introduced by Wiles in 1958, then by McKee, Chen and Farrar in the 1960s. Initially, it was abandoned due to high failure rates but was reintroduced in the 1980s with second-generation MoM thanks to considerable advances in metallurgy, tribology and biomechanics to address complications and loosening seen in metal-on-polyethylene THA (8).

We can distinguish MoM prostheses with small heads and standard heads (28 and 32 mm respectively) from prostheses with large heads (36 mm and larger).

Small head prostheses can also be divided in two groups: high-carbon heads and low-carbon heads.

Low-carbon heads are made of an alloy composed of 0.05% of carbon while high carbon heads are made of an alloy of 0.2% of carbon (9). It seems that heads with a high concentration of carbon present less loosening (10).

Multiple risk factors have been identified in ARMD. Female patients, age over 40 years, large femoral head prostheses (>36 mm), cup inclination over 50° and high acetabular cup anteversion appear to be risk factors of developing ARMD (10,11), but not metal hypersensitivity (7).

It is important to note that the presence of metal debris around the articular region in MoM THA, particularly with DUROM cups, results from corrosion causing metal wear at the head-neck junction of a total hip implant in addition to metal loss from bearing surfaces (12).

The intra-articular presence of metal ions in MoM prostheses can present as simple metallosis or as an ALVAL, but it can also result in a more impressive picture, such as a pseudotumor (2).

These presentations were grouped under the term ARMD, referring to failures caused by intra articular metal wear debris (2).

It represents a local immune reaction caused by chromium and cobalt debris release in the articulation, but it is also caused by the direct toxicity of metal ions (13).

These metal ions are small enough to be disseminated throughout the body to involve a type IV lymphocyte-mediated hypersensitivity reaction (2) and more specifically CD4+ T cells, while a non-specific immune reaction to other debris is mediated by macrophages and giant cells (14-16).

It is also important to know that patients with metal ions in the periarticular region and blood will not necessarily develop ARMD as there are many other factors such as genetics and age that play a significant role in metal hypersensivity (14).

Pathological findings characteristic of ALVAL and pseudotumor include vasculitis, perivascular and intramural capillary lymphocyte infiltration with endothelial swelling, localized hemorrhage, and necrosis (14). These findings were observed in our case, confirming the diagnosis of metal debris-induced pseudotumor.

ARMD incidence is about 6.5% for all types of MoM prostheses (4) and it is the source of 0.6% of failures among all types of THA (2), but if we look more closely to failure rate in MoM THA, the incidence is higher.

In a retrospective study, Grübl et al. reported a 98.6% survivorship rate for MoM THA at 10 years (17). A prospective study of 99 MoM THAs by Neumann et al. also found 10-year survivorship rates of 98% for the stem and 96% for the acetabular cup (8).

But a study by Higuchi et al., nuances all these findings, reporting that radiographic osteolysis rates are significantly higher in MoM bearing surfaces compared to ceramic on ceramic at 10-year follow-up but without more revisions (18). This study raises questions about the consequences of this osteolysis on long-term prosthesis survivorship beyond 10 years.

A more recent study by Holappa et al., reports a survivorship of 89.6% at 10 years and 82.9% at 14 years with a revision rate of 13.4% and 55.9%, these revisions were for ARMD while ARMD prevalence was 12.4% (19).

Varnum, referring to the Nordic Arthroplasty Register Association, reports a higher revision rate for MoM prostheses compared to polyethylene on metal prostheses (20). Moreover, studies based on the Australian Arthroplasty register and the British Arthroplasty register have made the same observation (21,22).

In a systematic review, Drummond et al. report that about one in five MoM prostheses will need a revision surgery at 10 or 13 years, especially for large-head prostheses (>36 mm) (23). Palazzuolo et al. find that the most frequent cause of failure in MoM THA is ARMD with a frequency of 59% at 13-year follow-up (24).

The main reasons for hip prosthesis revision related to ARMD are ALVAL and pseudotumor. These two complications are often misdiagnosed. The primary differential diagnosis is PJI (4).

In another study, Lainiala et al. report that the survivorship of revisions for MoM THA was 69% (25).

Biological monitoring in MoM prostheses is done by serum dosage of chromium and cobalt. We consider that cobalt blood level is high when it is superior to 7 µg/L but a cobalt serum level between 2 and 7 µg/L in symptomatic patients is an indication to push investigations and have regular monitoring (26).

Serum cobalt level was elevated at 6.23 µg/L in our patient, exceeding normal values but remaining below the commonly cited 7 µg/L threshold often used to prompt revision surgery. According to current guidelines, cobalt levels between 2 and 7 µg/L should be considered indeterminate and interpreted in conjunction with clinical symptoms and imaging findings rather than as standalone diagnostic criteria. In this case, the cobalt level was therefore supportive—but not confirmatory—of ARMD, contributing to the overall diagnostic assessment.

Although X-rays is the first test to run in symptomatic patients, it lacks effectiveness to detect ARMD.

Ultrasound seems to be more accurate with a sensitivity of approximately 100% and a specificity of 96% (7). MRI with artefacts treatment (MARS) is an excellent exam with a sensibility of 92% and a specificity of 100% (7).

Our patient did not have MARS MRI as a set of arguments converged toward the diagnosis of ARMD and additionally the PJI was obvious so the patient needed revision surgery in all cases.

Guidelines for monitoring patients with MoM THA from different scientific and orthopedic societies (26-29) are summarized in a clinical algorithm (Figures 8,9).

Figure 8 Guideline for asymptomatic patient with MoM THA (10). MARS, metal artifact reduction sequence; MoM, metal-on-metal; MRI, magnetic resonance imaging; THA, total hip arthroplasty.

Figure 9 Guideline for monitoring patient with symptomatic MoM THA (10). MARS, metal artifact reduction sequence; MoM, metal-on-metal; MRI, magnetic resonance imaging; THA, total hip arthroplasty.

Concerning systemic effects of metal debris, multiple secondary effects have been reported as renal failure (30), cardiac dysfunction and central neurologic disturbances such as tremor and cognitive disorders, and peripheral neurologic disorders such as deafness and optic neuropathy with visual disturbance (31).

There is no evidence currently of any established in vivo clear link between the presence of metal debris and the emergence of cancer or fetal malformation, even if there is no doubt about cytotoxic, genotoxic and mutagenic effects of metal ions in vitro. However, even though those studies are comforting, we must be careful because of the very known latency of some cancers, especially because of the fact that these implants are generally put in young patients because of their high activity level (32).

We have found in literature some cases of patients presenting pelvic localization of metal-induced pseudotumor. Abdul reports a case of pelvic localization and abdominal symptomatology that have needed a revision surgery (33). Filho reports another case of pelvic localization with urinary symptomatology that also needed revision surgery (34). Mak also reports a case of metal-induced pseudotumor with pelvic localization (35). DeFrang reports a case of a persistent lymphedema of the lower limb secondary to cystic mass compressing the femoral vein; this cystic mass was due to polyethylene debris (36).

It is important to remember that our patient himself had a chronic lymphedema of the whole lower limb that had been initially put down to his radiotherapy for prostatic adenocarcinoma, and this lymphedema regressed after surgery. After reviewing old CT scans of our patient with radiologists specialized in osteoarticular imagery, we can confirm that the pseudotumor was compressing the iliac vein and the lymphatic vessels, explaining the history of thrombosis and chronic lymphedema (Figure 10).

Figure 10 CT scan done in 2019 showing the compression of the iliac vein (red arrow with white border) by the pseudotumor (white arrow). CT, computed tomography.

This case highlights the role of cognitive bias and diagnostic anchoring in complex clinical presentations. The patient’s history of prostate cancer likely contributed to anchoring bias, leading to the attribution of deep vein thrombosis and chronic lymphedema to oncologic causes. Additionally, early imaging findings described as psoas bursitis were not integrated into an MoM-specific surveillance framework, and serum metal ion levels were not assessed at that time. These factors may have contributed to delayed recognition of ARMD. This observation underscores the importance of systematic follow-up protocols and periodic re-evaluation of prior assumptions in patients with MoM THA.

The coexistence of ARMD-associated pseudotumor and infection in this case warrants careful consideration. While intraoperative cultures and histopathological findings confirmed infection, the temporal and causal relationship between ARMD and PJI cannot be definitively established. One plausible hypothesis is that chronic metal debris–induced tissue necrosis created a locally immunocompromised environment, predisposing the pseudotumor to secondary infection. Conversely, a primary PJI may have extended into a pre-existing pseudotumor. Given the delayed diagnosis and overlapping clinical features, both mechanisms remain possible and should be considered in similar clinical scenarios.

It has been reported that patients with MoM prostheses are at a greater risk of PJI than patients with other bearing surfaces prostheses (5,37).

Huang, in his study on the Australian register, found a higher rate of revision due to PJI in patients with MoM THA (36.9%) at 7 years compared to those with other bearing surfaces prosthesis (2%). He also reported that this risk is higher in the first 2 years following the surgery (5).

Leal reports a higher rate of PJI in patients with pseudotumors compared to patients with MoM hip arthroplasty but without pseudotumors (38). Judd and Noiseux found that, besides a higher risk of PJI, there is a significant prevalence of atypical germs in this population (39). Anwar showed that chromium and cobalt particles are not toxic for bacteria and rather accelerate their development in vitro (40).

This susceptibility to infections is probably due to the fact that the released debris lead to an excessive macrophage activation and production of oxygen derivatives causing local defense depletion and damage in adjacent tissues. In addition, cytokine cascade will perpetuate the inflammatory phenomena which will have as a result a local inflammatory zone with compromised immune defense and so a higher risk of infection (41).

In our case we followed the modified MSIS and ICM criteria for the diagnosis of PJI (6).

Concerning the patient death, it is well known that patients undergoing THA revision for infection experience a significant excess risk of death during the first year of surgery that persists several years after (42).

This is due to the elevated rate of medical complication following revisions surgery for PJI that can reach 15.3% generally and even 22.4% in elderly patients during the 6 months after the surgery (43).

Zmistowski et al. identified advanced age, higher Charlson Comorbidity Index, history of stroke, polymicrobial infections, and cardiac disease, as risk factors of death after revision for PJI (44), and it is important to remember that our patient was 75 years old, had history of paroxysmal supraventricular tachycardia and hypertension.

In his study, Lainiala reports a complication rate of 11% in revision surgery for ARMD among hip arthroplasty, and if we look for non-mechanical complications, we find that the three first complications are DVT, pulmonary embolism and bowel occlusion (45).

Main causes of death after arthroplasty are pulmonary embolism, cerebrovascular event, pulmonary compromise, acute myocardial infarction, cardiac complications and finally pneumonia and sepsis (46).

Our patient already had a history of pulmonary embolism and could have a recurrence which can explain the death.

He also had a history of paroxysmal supraventricular tachycardia, diabetes mellitus and dyslipidemia, which can be the cause of a cerebrovascular event or a cardiac complication.

Metal debris is known to have cardiac toxicity, and this could be an aggravating factor specially concerning his well-known cardiac disease. Moreover, it is well known that cobalt induced cardiomyopathy can persist and even worsen after revision surgery (31).

However, the preoperative cardiac evaluation did not reveal any cardiomyopathy, and the transthoracic echocardiogram was normal. We therefore believe that an acute cardiac event—such as paroxysmal supraventricular tachycardia or myocardial infarction—is a possible cause of death, given the patient’s medical history of diabetes and dyslipidemia, further aggravated by surgical stress. However, cardiac cobalt toxicity appears unlikely.

Sepsis and pneumonia also do not seem to be a cause of death for us as well as the patient was medically stable 2 days before death, there was no signs of wound inflammation and labs showed no alarming values (3,900 G/L and CRP at 27.7 mg/L).

Finally, patients with MoM prostheses seem to have higher risk of haematopoietic cancers, and this could also be a possible cause of death for our patient, but regarding the fact we have only one complete blood count at the last follow-up we cannot neither confirm or deny this hypothesis (47).

The exact cause of death could not be established, as no autopsy was performed according to the patient family wish. Beyond this individual limitation, this case highlights broader system-level challenges in the long-term surveillance of patients with MoM THA, including delayed recognition of complications and fragmented follow-up across specialties.

Conclusions

MoM THA are currently less used, but we still see them especially in cases of revision for simple loosening or in more serious and specific complications related to metal debris or infections. These complications can have multiple and intertwined manifestations and are sometimes difficult to differentiate.

It is crucial to maintain a high index of awareness in front of patients with MoM THA and follow the existing guidelines of learned societies.

Acknowledgments

We would like to thank Miss Yasmine Grassa and Miss Ons Ghali for their precious support.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-266/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-266/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-266/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent for publication of this case report and accompanying images was not obtained from the patient or the relatives after all possible attempts were made.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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