F-18 FDG PET brain imaging in symptomatic arthroprosthetic cobaltism

Abstract

Purpose Imaging studies of cobalt toxicity from cobalt-chromium alloy arthroprosthetics have focused on the local intra-articular and peri-articular presentation from failing joint replacements. Most studies investigating neurological findings have been small case series focused on the clinical findings of memory loss, diminished executive function, tremor, hearing and vision loss, depression, and emotional lability. This study utilizes software-based quantitative analysis of brain metabolism to assess the degree of hypometabolism and areas of susceptibility, determine if a pattern of involvement exists, and measure reversibility of findings after prosthetic revision to cobalt-free appliances. Methods Over 48 months, 247 consecutive patients presenting to an orthopedic clinic with an arthroprosthetic joint containing any cobalt-chromium part were screened with whole blood and urine cobalt levels. A clinically validated inventory of 10 symptoms was obtained. Symptomatic patients with a blood cobalt level above 0.4 mcg/L or urine cobalt greater than 1 mcg/ L underwent F-18 FDG PET brain imaging. Analysis was performed with FDA-approved quantitative brain analysis software with the pons as the reference region. Control group was the normal brain atlas within the software. Results Of the 247 consecutively screened patients, 123 had blood and urine cobalt levels above the threshold. The 69 scanned patients had statistically significant regional hypometabolism and higher symptoms inventory. Fifty-seven patients were retained in the study. Distribution of hypometabolism was in descending order: temporal, frontal, Broca's areas, anterior cingulate, parietal, posterior cingulate, visual, sensorimotor, thalamic, and lastly caudate. Metal-on-metal (MoM) and metal-on-plastic (MoP) joint replacements produced similar patterns of hypometabolism. Of 15 patients with necessary revision surgery, 8 demonstrated improved metabolism when later re-scanned. Conclusion All scanned patients had regions of significant hypometabolism. Neurological toxicity from elevated systemic cobalt levels following arthroprosthetic joint replacement has a pattern of regional susceptibility similar to heavy metals and solvents, differing from classical dementias and may occur at blood and urine cobalt levels as low as 0.4 mcg/L and 1 mcg/L, respectively. Presently accepted thresholds for cobalt exposure and monitoring may need revision. Quantitative F-18 FDG PET brain imaging may aid in the decision process for treatment options and timing of possible medical versus surgical intervention.

Corrosion of Polished Cobalt-Chrome Stems Presenting as Cobalt Encephalopathy

“…Focal brain hypometabolism on QFDGPETBI consistent with ACE was found in all cases (Fig. 2) [14]. The primary indication for revision surgery was suspected neurocobaltism [11].…”

“…Since 2015, all patients presenting to his practice with a hip with a CoCr component are screened for cobaltism with a urine cobalt and a Cobaltism Symptom Inventory. The women consented to have their redacted information used for this case report, and they are part of the senior author's larger study cohort of 68 patients with arthroprosthetic cobalturia who underwent QFDGPETBI [14]. Our clinic first recognized the utility of QFDGPETBI to diagnose ACE in 2015, and we routinely use this diagnostic modality for patients with cobalturia experiencing neurologic or constitutional decompensation [14,15] At presentation, radiographs showed well-fixed components with minimal polyethylene wear, and the patients noted new minor exercise-related hip soreness.…”

“…The women consented to have their redacted information used for this case report, and they are part of the senior author's larger study cohort of 68 patients with arthroprosthetic cobalturia who underwent QFDGPETBI [14]. Our clinic first recognized the utility of QFDGPETBI to diagnose ACE in 2015, and we routinely use this diagnostic modality for patients with cobalturia experiencing neurologic or constitutional decompensation [14,15] At presentation, radiographs showed well-fixed components with minimal polyethylene wear, and the patients noted new minor exercise-related hip soreness. All subjects had elevated urine cobalt and progressive symptoms consistent with neurocobaltism, most commonly cognitive decline, fatigue, and tremor [11].…”

“…Quantitative-F 16 DG-PET-CT brain imaging (QFDGPETBI) appears to have utility in confirming the diagnosis of arthroplasty cobalt encephalopathy (ACE). A recent report noted a pathognomonic pattern of quantitative brain hypometabolism in 57 neurologically symptomatic arthroprosthetic patients with elevated urine cobalt (!1 ppb), the majority of whom were implanted with metal-on-plastic (MoP) hips [14]. We report 3 cases of severe PCoCrCFS corrosion in women with ACE implanted with well-fixed Zimmer (Warsaw, IN) Heritage stems.…”

“…We report 3 cases of severe PCoCrCFS corrosion in women with ACE implanted with well-fixed Zimmer (Warsaw, IN) Heritage stems. The major indication for revision surgery was cobaltism; all patients underwent QFDGPETBI that showed the characteristic pattern of quantitative hypometabolism described for ACE [14].…”