Epidemiology of Total Ankle Arthroplasty: Trends in New York State.

The rate of total ankle arthroplasty (TAA) is increasing in the United States as its popularity and indications expand. There currently is no national joint registry available to monitor outcomes, and few studies have addressed the challenges faced with TAA. The purpose of this study was to evaluate the incidence, complications, and survival rates associated with TAA using a large statewide administrative discharge database. Individuals who underwent primary TAA from 1997 to 2010 were identified in the Statewide Planning and Research Cooperative System database from the New York State Department of Health. The age, sex, comorbidities, state of residence, primary diagnosis, and readmissions within 90 days were analyzed for patients with an ICD-9-CM procedure code of 81.56 (TAA). Failure of a TAA implant was defined as revision, tibiotalar arthrodesis, amputation, or implant removal. During the 14-year period, 420 patients underwent 444 TAAs (mean patient age of 61 years, 59% women, mean Charlson-Deyo comorbidity score of 0.45, and 86% New York State residents). The primary diagnosis was 37.4% osteoarthritis, 34.3% traumatic arthritis, and 15.5% rheumatoid arthritis. Surgery for failure was associated only with a younger age (56.5 vs 62 years, P=.005). The rate of subsequent failure procedures following TAAs performed in New York State was 13.8%. The incidence of TAAs is steadily increasing. The overall survival rate in New York State is better than rates reported in other national registries, but it is not yet comparable to those of hip and knee replacements. [Orthopedics. 2016; 39(3):170-176.].

Analysis of Total Ankle Arthroplasty Survival in the United States Using Multiple State Databases.

UNLABELLED: The aim of this study was to evaluate survivorship and risk factors for failure of total ankle arthroplasty (TAA) in the United States using large statewide, multipayer databases of inpatient discharges. TAA patients from 2005 to 2009 were identified from the Healthcare Cost and Utilization Project databases for 5 states (California, Florida, Nebraska, North Carolina, and Utah) and the New York Department of Health Statewide Planning and Research Cooperative System database. Patient demographics and clinical characteristics were extracted, and a multivariable logistic regression model was developed to assess risk factors for 90-day all-cause readmission and failure. Failure was defined as revision, arthrodesis, amputation, or implant removal. During the period of interest, 1545 patients received 1593 TAA. The coded etiology of arthritis was primary osteoarthritis (n = 854, 55.2%), posttraumatic arthritis (n = 466, 30.2%), rheumatoid arthritis (n = 129, 8.4%), and other (n = 96, 6.2%). The 5-year survival rate was 90.1%. Patients with a coded diagnosis of rheumatoid arthritis (odds ratio [OR] = 2.18; 95% confidence interval [CI] = 1.04-4.01) or who were readmitted within 90 days of TAA (OR = 3.41; 95% CI = 1.67-6.97) had significantly increased risk of failure. Risk factors for readmission were Charlson-Deyo Score ≥2 (OR = 3.05; 95% CI = 1.51-6.15) and increased length of stay during the arthroplasty (OR = 1.30; 95% CI = 1.16-1.47). LEVELS OF EVIDENCE: Therapeutic, Level IV: Observational study.

Investigating the relationship between ankle arthrodesis and adjacent-joint arthritis in the hindfoot: a systematic review.

BACKGROUND: Ankle arthrodesis traditionally has been regarded as the treatment of choice for many patients with end-stage ankle arthritis. However, a major reported risk of ankle arthrodesis is adjacent-joint degeneration. There are conflicting views in the literature as to the causative link between ankle arthrodesis and progression to adjacent-joint arthritis. Recent studies have challenged the causative link between arthrodesis and adjacent-joint arthritis, purporting that preexisting adjacent-joint arthritis is present in many patients. The aim of the present study was to systematically review the available literature to determine if there is sufficient evidence to support either hypothesis. METHODS: A literature search of the EMBASE and PubMed/MEDLINE databases (1974 to present) was performed. A total of twenty-four studies were included for review. The studies were reviewed, and the relevant information was extracted, including research methodology, postoperative outcomes in the adjacent joints of the foot, and whether pre-arthrodesis radiographs and medical records were available for analysis. RESULTS: The twenty-four manuscripts included eighteen clinical studies, five biomechanical studies, and one gait-analysis study. The majority of biomechanical studies showed altered biomechanics in the fused ankle; however, there was no clear consensus as to whether these findings were causes of adjacent-joint arthritis. In studies assessing clinical outcomes, the reported prevalence of subtalar joint arthritis ranged from 24% to 100% and the prevalence of talonavicular and calcaneocuboid arthritis ranged from 18% to 77%. Correlation between imaging findings of arthritis in adjacent joints and patient symptoms was not established in a number of the clinical studies reviewed. CONCLUSIONS: There is no true consensus in the literature as to the effects of ankle arthrodesis on biomechanics or whether ankle arthrodesis leads to adjacent-joint arthritis. Similarly, a correlation between postoperative imaging findings and clinical presentation in this cohort of patients has not been conclusively demonstrated.

An atraumatic case of extensive Achilles tendon ossification.

BACKGROUND: Ossification of the Achilles tendon is rare with most cases of ossification or calcification consisting of small, focal lesions. This pathology is usually predisposed by surgery, trauma, or other factors. CASE DESCRIPTION: A case of extensive Achilles ossification and calcification, without prior surgery or trauma, is reported. Following removal of one of the largest ossific masses reported in the literature, measuring 11.0cm×2.5cm×2.0cm with additional 6.5cm calcifications, surgical reconstruction was required. PURPOSE AND CLINICAL RELEVANCE: The objective of this report was to describe an unusual case of Achilles tendon ossification and calcification that occurred without the presence of predisposing factors. When a large gap is present after removal of the ossification, direct repair may be impossible and V-Y lengthening plus flexor hallucis longus (FHL) transfer is a viable option for pain relief and return to function.

Talonavicular arthroscopy for osteochondral lesions: technique and case series.

BACKGROUND: Traditional treatment of talonavicular osteochondral lesions (OCLs) requires an open procedure. Arthroscopic microfracture of talonavicular OCLs may provide a viable, minimally invasive approach. The purpose of this study was to describe an arthroscopic approach for treatment of talonavicular OCLs, describe the proximity of arthroscopic portals to important structures in cadaver specimens, and report magnetic resonance imaging (MRI) findings and clinical outcomes of this technique. METHODS: Five cadaver specimens were dissected so proximity of portals to adjacent tendons and neurovascular structures could be assessed. Subsequently, 3 athletic patients with OCLs of the talonavicular joint were treated with arthroscopic debridement and microfracture. Patient records and imaging studies were retrospectively reviewed. RESULTS: In the cadaver specimens, the mean distance between the neurovascular bundle and the medial border of the extensor hallucis longus (EHL) was 9.0 (range, 8 to 10) mm. The saphenous nerve was located a mean of 6.8 (range, 6 to 7) mm from the medial border of the tibialis anterior tendon. Therefore, portals were placed just medial to the EHL and tibialis anterior tendon to avoid the neurovascular bundle and saphenous nerve, respectively. In all patients, access, identification of the OCL, debridement, and microfracture were successfully performed. All patients demonstrated improvements in Foot and Ankle Outcome Scores and Short Form-12 scores and began gradual return to activity within 12 weeks following the operation. No significant complications occurred. MRI indicated signal consistent with reparative fibrocartilage in all patients. CONCLUSION: Talonavicular arthroscopy allowed visualization, curettage, synovectomy, loose body removal, and microfracture of OCLs that would have otherwise required an open approach. At early follow-up, all patients had returned to their previous activity levels. Arthroscopy of the talonavicular joint was a viable approach for microfracture of OCLs. LEVEL OF EVIDENCE: Level IV, case series.

Effect of NOS inhibition on rat gastric matrix metalloproteinase production during endotoxemia.

UNLABELLED: Matrix metalloproteinases (MMPs) degrade the extracellular matrix and contribute to LPS-induced gastric injury. MMPs are closely modulated by their activators, membrane type-MMP (MT-MMPs) and their endogenous inhibitors, the tissue inhibitors of metalloproteinases (TIMPs). As LPS-induced gastric injury is mediated in part by iNOS, and NO modulates MMP production in vitro, we hypothesized that NOS inhibition would similarly modulate LPS-induced gastric MMP production. Therefore, the purpose of these studies was to compare the effects of selective and nonselective NOS inhibition on LPS-induced gastric MMP production. METHODS: Sprague-Dawley rats were given either the nonselective NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 5 mg/kg, s.c.), a selective iNOS inhibitor, aminoguanidine (45 mg/kg, i.p.) or L-N-iminoethyl-lysine (L-NIL; 10 mg/kg, i.p.), or vehicle 15 min before saline or LPS (20 mg/kg, i.p.) and killed 24 h after LPS administration. Stomachs were assessed for macroscopic injury (computed planimetry), and gastric mucosal MMP production was assessed by gelatin zymography, in situ zymography, and Western analysis for MMP-2, MT1-MMP, and TIMP-2. (n > or = 4/group; ANOVA). RESULTS: Aminoguanidine treatment decreased LPS-induced macroscopic gastric injury as well as MMP-2 and MT1-MMP protein production while having no effect on TIMP-2 protein levels. L-NIL similarly attenuated the induction of MMP-2 and MT1-MMP by LPS. L-NAME failed to attenuate LPS induced gastric injury or MT1-MMP protein induction and increased MMP-2 levels. L-NAME similarly had no effect on gastric TIMP-2 production. CONCLUSIONS: Selective iNOS inhibition decreases gastric MMP-2 activity after LPS administration, whereas nonselective inhibition increases MMP-2 levels. The ability of selective iNOS inhibition to ameliorate LPS-induced gastric injury may be due in part to its inhibition of active MMP-2 production, whereas nonselective NOS inhibitors increase MMP-2 levels and maintain gastric injury after LPS administration.