F-18 FDG PET brain imaging in symptomatic arthroprosthetic cobaltism

Robert L Bridges,Stephen S Tower,Bradford D Gessner,Christina S Cho,Marc R Beck

doi:10.1007/s00259-019-04648-2

Abstract

PurposeImaging 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.MethodsOver 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.ResultsOf 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.ConclusionAll 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.

Highlights

This article is part of the Topical Collection on Neurology.Modern hip, shoulder, and knee joint replacements employ metal, ceramic, or plastic materials to replace one or both articular surfaces
Systemic cobalt toxicity most commonly affects the nervous, endocrine, and cardiovascular systems, which may result in deafness, blindness, peripheral neuropathy, thyropathy, polycythemia, cardiac failure, and, in extreme cases, death. [1,2,3,4] Profound systemic toxicity results when a fractured ceramic hip implant is revised to a CoCr femoral head, or when a CoCr ball and socket articulate (Metal-onMetal Hip)
F-18 FDG PET brain imaging has become instrumental in early detection and monitoring of neurodegenerative disease. [16,17,18,19,20,21] In 1991, Callender utilized visual interpretation of SPECT and PET imaging to identify regions of brain injury from exposure to organic solvents

Summary

Introduction

This article is part of the Topical Collection on Neurology.Modern hip, shoulder, and knee joint replacements employ metal, ceramic, or plastic materials to replace one or both articular surfaces. Periprosthetic CoCr metallosis produced by wear or corrosion of CoCr articular components (heads or sockets) or at the. [10] Patients may react with an immune response to CoCr implants by direct attack of leukocytes resulting in ARMD and systemically from circulating cobalt in the absence of significant implant wear or taper corrosion. [1,2,3,4] Profound systemic toxicity results when a fractured ceramic hip implant is revised to a CoCr femoral head, or when a CoCr ball and socket articulate (Metal-onMetal Hip). [4] Nominal cobalt exposure from wear or corrosion of modular CoCr implants or CoCr articular surfaces can cause a subtler presentation of neurologic, psychiatric, and constitutional maladies, confused with aging, and similar to the vocational manganese toxicity. Such software provides a reproducible and objective dataset without inter-observer variability in processing and interpretation of the scan. [23]

Methods

Results

Discussion

Conclusion