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.

Twenty million North Americans have cobalt-chrome arthroprosthetic components, and 1 million have metal-on-metal hip replacements. 1 Cobalt is a mitochondrial toxin-encephalopathy and cardiomyopathy (cobaltism) may occur from iatrogenic, industrial, dietary, or arthroprosthetic cobalt exposure. 2,3 In unexposed populations, the 95th percentile of cobalt levels in urine and blood are 1 part per billion (ppb) and 0.4 ppb, respectively. 3 Wear and corrosion of cobalt-chrome joint implantations can result in periprosthetic tissue inflammation or necrosis, also known clinically as adverse reactions to metallic debris. 1,4 Periprosthetic cobalt-chrome metallosis is disseminated systemically and may result in arthroprosthetic cobaltism. 1,3,4 Systemic cobalt dissemination can result in brain hypometabolism and atrophy; patients with levels of cobalt in blood as low as 1.1 ppb and in urine as low as 4.1 ppb are reported as having cobalt encephalopathy. 5,6 MethodsThis cohort study analyzed redacted data from 1 orthopedic clinic. The institutional review board at the University of Alaska Anchorage designated the study to be exempt, and patients provided written informed consent for this study. Patients with a suspected hip, knee, or shoulder replacement containing cobalt-chrome were screened with a spot screening of cobalt in urine. Levels of cobalt in blood were then determined for patients with cobalt levels in urine 1 ppb or higher. Patients were designated as cobalt-positive if cobalt levels in urine were 1 ppb or higher or if levels in blood were 0.4 ppb or higher. The reference laboratory test results threshold for reporting cobalt in urine and blood are generally 1 ppb and 0.5 ppb, respectively. Patients with cobalt levels below the reporting threshold in either were assigned half the threshold value. All P values were from 2-sided tests and results were deemed statistically significant at P < .05. Analysis was conducted using Prism version 9.1.1 (GraphPad). This study followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guideline. ResultsA total of 241 patients were screened (mean [SD] age at time of cobalt determination, 68.1 [9.3] years; median duration of exposure to any cobalt-chrome implantation, 11.6 years [range, 2.0-33.2 years]; 117 [48.5%] women); 138 (57%) tested cobalt-positive (mean cobalt level in urine, 12.6 ppb; median, 1.2 ppb). Eleven subjects had no cobalt-chrome implantation (because zirconia and cobaltchrome femoral-heads are indistinguishable radiographically), none of whom were cobalt-positive.Paired cobalt levels in urine and blood (144 patients) correlated significantly (cobalt in blood = 0.25 × cobalt in urine; P < .001). Paired joint-fluid and urine cobalt (57 patients) correlated significantly (joint fluid = 20 × cobalt in urine; P < .001). Patients were classified by type, location, number, and brand of their implantation (Table ). These classes were risk-grouped based on mean cobalt levels in urine (ie, extreme, greater than 20 ppb; high...

Adverse reactions to metallic debris from corrosion of polished cobalt-chromium–cemented femoral stems are reported. Cobaltism (systemic cobalt poisoning) has not been reported from this phenomenon. Three patients presented to their surgeon for ongoing care 10-20 years after primary metal-on-plastic hip arthroplasty with the same polished cobalt-chromium–cemented femoral stems (Heritage, Zimmer). Urine cobalt was elevated, and the patients had symptoms consistent with cobaltism. Quantitative-F 16 DG-PET-CT brain imaging was performed showing generalized and focal brain hypometabolism consistent with cobalt encephalopathy. At revision, all stems were well fixed and grossly corroded. At 1 year after revision, cobalturia and cognitive symptoms were resolved or improved. Mechanically assisted crevice corrosion at the polymethylmethacrylate interface is a complication of polished cobalt-chromium–cemented stems that can result in systemic cobalt exposure and toxic encephalopathy. Our cases had only minor periprosthetic symptoms. Patients implanted with polished cobalt-chromium–cemented stems warrant monitoring with urine cobalt. Patients with cobaltemia warrant an evaluation for toxic encephalopathy.