Hip fracture principally affects the frailest in society, many of whom are care dependent, and are disproportionately at risk of contracting COVID-19. We examined the impact of COVID-19 infection on hip fracture mortality in England. We conducted a cohort study of patients with hip fracture recorded in the National Hip Fracture Database between 1st February 2019 and 31st October 2020, in England. Data were linked to Hospital Episode Statistics to quantify patient characteristics and comorbidities, Office for National Statistics mortality data, and Public Health England's SARS-CoV-2 testing results. Multivariable Cox regression examined determinants of 90-day mortality. Excess mortality attributable to COVID-19 was quantified using Quasi-Poisson models. Analysis of 102,900 hip fractures (42,630 occurring during the pandemic) revealed that amongst those with COVID-19 infection at presentation (n=1,120) there was a doubling of 90-day mortality; hazard ratio (HR) 2.05 (95%CI 1.86–2.26), while for infections arising between 8–30 days after presentation (n=1,644) the figure was even higher at 2.52 (2.32–2.73). Malnutrition [1.44 (1.19–1.75)] and non-operative treatment [2.89 (2.16–3.86)] were the only modifiable risk factors for death in COVID-19 positive patients. Patients with previous COVID-19 initially had better survival compared to those who contracted COVID-19 around the time of their hip fracture; however, survival rapidly declined and by 365 days the combination of hip fracture and COVID-19 infection was associated with a 50% mortality rate. Between 1st January and 30th June 2020, 1,273 (99.7%CI 1,077–1,465) excess deaths occurred within 90 days of hip fracture, representing an excess mortality of 23% (20%–26%), with most deaths occurring within 30 days. COVID-19 infection more than doubled early hip fracture mortality; the first 30-days after injury were most critical, suggesting that targeted interventions in this period may have most benefit in improving survival.
We aimed to identify genes associated with the development of ALVAL at relatively low levels of wear. At our unit all patients undergoing revision of a MoM hip prosthesis have periprosthetic tissue samples graded for ALVAL. Explants undergo volumetric wear testing of the bearing and taper surfaces. We identified patients with moderate/severe ALVAL who had been exposed to lower than the median wear rate of all recorded patients who had developed ALVAL (<3mm3/year). This was termed the “ALVAL” group. We then identified all patients whose tissues had shown no signs of ALVAL. The patients in the two groups were sent buccal DNA collection kits. DNA was examined using next generation sequencing. Alleleic frequencies in the two groups were compared using Fisher's test and compared to a background UK population group (n=8514). We then conducted binary logistic regression with patient age, sex, primary source of debris (taper/bearing) and HLA genotype as the predictors. With the hypothesis that a cobalt/albumin metalloprotein acts as the epitope, we used validated binding prediction software to determine the relative affinities of the binding grooves created by different DQA1/DQB1 genetic combinations for albumin derived peptides. Given the protection that male sex and younger age appears to confer against ALVAL, we hypothesized that testosterone peptides may compete for these binding sites.Introduction
Methods
There are limited published data detailing the volumetric material loss from tapers of conventional metal-on-polyethylene (MoP) total hip arthroplasties (THAs). Our aim was to address this by comparing the taper wear rates measured in an explanted cohort of the widely used Exeter THA with those measured in a group of metal-on-metal (MoM) THAs. We examined an existing retrieval database to identify all Exeter V40 and Universal MoP THAs. Volumetric wear analysis of the taper surfaces was conducted using previously validated methodology. These values were compared with those obtained from a series of MoM THAs using non-parametric statistical methodology. A number of patient and device variables were accounted for using multiple regression modelling.Aims
Patients and Methods
We have encountered patients who developed large joint fluid collections with massive elevations in chromium (Cr) and cobalt (Co) concentrations following metal-on-metal (MoM) hip arthroplasties. In some cases, retrieval analysis determined that these ion concentrations could not be explained simply by the wear rates of the components. We hypothesized that these effects may be associated with aseptic lymphocyte-dominated vasculitis-associated lesion (ALVAL). We examined the influence of the ALVAL grade on synovial fluid Co and Cr concentrations following adjustment for patient and device variables, including volumetric wear rates. Initially restricting the analysis to include only patients with one MoM hip resurfacing device, we performed multiple regression analyses of prospectively collected data. We then repeated the same statistical approach using results from a larger cohort with different MoM designs, including total hip arthroplasties.Objectives
Patients and Methods
We sought to determine whether cobalt-chromium alloy (CoCr) femoral
stem tapers (trunnions) wear more than titanium (Ti) alloy stem
tapers (trunnions) when used in a large diameter (LD) metal-on-metal
(MoM) hip arthroplasty system. We performed explant analysis using validated methodology to
determine the volumetric material loss at the taper surfaces of
explanted LD CoCr MoM hip arthroplasties used with either a Ti alloy
(n = 28) or CoCr femoral stem (n = 21). Only 12/14 taper constructs
with a rough male taper surface and a nominal included angle close
to 5.666° were included. Multiple regression modelling was undertaken
using taper angle, taper roughness, bearing diameter (horizontal
lever arm) as independent variables. Material loss was mapped using
a coordinate measuring machine, profilometry and scanning electron
microscopy.Aims
Patients and Methods
Modular un-cemented acetabular components are used in over 50% of UK hip replacements. Mal-seating of hard liners has been reported as a cause of failure which may be a result of errors in assembly, but also could be affected by deformation of the acetabular shell on insertion. Little information exists on in vivo shell deformation. Previous work has confirmed the importance of shell diameter and thickness upon shell behaviour, but mostly using single measurements in models or cold cadavers. Exploration of deformation and its relaxation over the first twenty minutes after implantation of eight generic metal cups at body temperature. Using a previously validated cadaveric model at controlled physiological temperature with standardised surgical technique, we tested the null hypothesis that there was no consistency for time dependent or directional change in deformation for a standard metal shell inserted under controlled conditions into the hip joint. Eight custom made titanium alloy (TiAl6V4) cups were implanted into 4 cadavers (8 hips). Time dependent cup deformation was determined using the previously validated ATOS Triple Scan III (ATOS) optical measurement system. The pattern of change in the shape of the surgically implanted cup was measured at 3 time points after insertion. We found consistency for quantitative and directional deformation of the shells. There was consistency for relaxation of the deformation with time. Immediate mean change in cup radius was 104μm (sd 32, range 67–153) relaxing to mean 96 μm (sd 32, range 63–150) after 10 minutes and mean 92 μm (sd 28, range 66–138) after 20 minutes. This work shows the time dependent deformation and relaxation of acetabular titanium shells and may aid determining the optimal time for insertion of the inner liner at surgery.
Concerns have been raised that deformation of
acetabular shells may disrupt the assembly process of modular prostheses.
In this study we aimed to examine the effect that the strength of
bone has on the amount of deformation of the acetabular shell. The
hypothesis was that stronger bone would result in greater deformation.
A total of 17 acetabular shells were inserted into the acetabula
of eight cadavers, and deformation was measured using an optical
measuring system. Cores of bone from the femoral head were taken
from each cadaver and compressed using a materials testing machine.
The highest peak modulus and yield stress for each cadaver were used
to represent the strength of the bone and compared with the values
for the deformation and the surgeon’s subjective assessment of the
hardness of the bone. The mean deformation of the shell was 129
µm (3 to 340). No correlation was found between deformation and
either the maximum peak modulus (r² = 0.011, t = 0.426, p = 0.676) or
the yield stress (r² = 0.024, t = 0.614, p = 0.549) of the bone.
Although no correlation was found between the strength of the bone
and deformation, the values for the deformation observed could be
sufficient to disrupt the assembly process of modular acetabular
components. Cite this article:
Abnormal wear of cobalt-containing metal-on-metal
joints is associated with inflammatory pseudotumours. Cobalt ions
activate human toll-like receptor 4 (TLR4), which normally responds
to bacterial lipopolysaccharide (LPS) in sepsis. Activation of TLR4
by LPS increases the expression of chemokines IL-8 and CXCL10, which
recruit leukocytes and activated T-cells, respectively. This study
was designed to determine whether cobalt induces a similar inflammatory
response to LPS by promoting the expression of IL-8 and CXCL10.
A human monocytic cell line, derived from acute monocytic leukaemia,
was treated with cobalt ions and expression of IL-8 and CXCL10 measured at
mRNA and protein levels. Cobalt-treated macrophages showed a 60-fold
increase in IL-8 mRNA, and an eightfold increase in production of
the mature chemokine (both p <
0.001); expression of the CXCL10
gene and protein was also significantly increased by cobalt (both
p <
0.001). Experiments were also performed in the presence of
CLI-095, a TLR4-specific antagonist which abrogated the cobalt-mediated
increase in IL-8 and CXCL10 expression. These findings suggest that cobalt ions induce inflammation similar
to that observed during sepsis by the simultaneous activation of
two TLR4-mediated signalling pathways. These pathways result in
increased production of IL-8 and CXCL10, and may be implicated in
pseudotumour formation following metal-on-metal replacement. Cite this article:
