Nicholas Kennedy1, Steven T Chambers1, Imogen Nolan1, Kate Gallagher1, Anja Werno1, Melanie Browne1, Lisa K Stamp2. 1. From the Department of Rheumatology, Immunology and Allergy, the Department of Infectious Diseases, and Decision Support, Christchurch Hospital; the Department of Pathology, and the Department of Medicine, University of Otago; Canterbury Health Laboratories, Christchurch, New Zealand.N. Kennedy, MB ChB, Clinical Immunology/Rheumatology registrar, Department of Rheumatology, Immunology and Allergy, Christchurch Hospital; S.T. Chambers, MB ChB, MD, MSc, FRACP, Professor of Infectious Diseases, Department of Pathology, and Department of Medicine, University of Otago, and Department of Infectious Diseases, Christchurch Hospital; I. Nolan, Medical student, Department of Medicine, University of Otago; K. Gallagher, infectious diseases nurse, Department of Infectious Diseases, Christchurch Hospital; A. Werno, MD, PhD, FRCPA, Medical Director, Microbiology, Canterbury Health Laboratories; M. Browne, Decision Support, Christchurch Hospital; L.K. Stamp, MB ChB, FRACP, PhD, Department of Rheumatology, Immunology and Allergy, Christchurch Hospital, and Department of Medicine, University of Otago. 2. From the Department of Rheumatology, Immunology and Allergy, the Department of Infectious Diseases, and Decision Support, Christchurch Hospital; the Department of Pathology, and the Department of Medicine, University of Otago; Canterbury Health Laboratories, Christchurch, New Zealand.N. Kennedy, MB ChB, Clinical Immunology/Rheumatology registrar, Department of Rheumatology, Immunology and Allergy, Christchurch Hospital; S.T. Chambers, MB ChB, MD, MSc, FRACP, Professor of Infectious Diseases, Department of Pathology, and Department of Medicine, University of Otago, and Department of Infectious Diseases, Christchurch Hospital; I. Nolan, Medical student, Department of Medicine, University of Otago; K. Gallagher, infectious diseases nurse, Department of Infectious Diseases, Christchurch Hospital; A. Werno, MD, PhD, FRCPA, Medical Director, Microbiology, Canterbury Health Laboratories; M. Browne, Decision Support, Christchurch Hospital; L.K. Stamp, MB ChB, FRACP, PhD, Department of Rheumatology, Immunology and Allergy, Christchurch Hospital, and Department of Medicine, University of Otago. Lisa.Stamp@cdhb.health.nz.
Abstract
OBJECTIVE: To determine the epidemiology, clinical features, and microbiology of adult native joint septic arthritis in Canterbury, New Zealand, over a 5-year period in individuals with and without an underlying rheumatic disorder. METHODS: Patients with native joint septic arthritis were identified retrospectively and classified by Newman's criteria. The clinical characteristics were described and comparisons made between those with and without underlying rheumatic disease. RESULTS: Two hundred forty-eight cases of native joint septic arthritis (mean age 60, range 16-97 yrs) were identified with an overall incidence rate of 12.0/100,000/year (95% CI 10.6-13.6). Yearly incidence increased with age to a maximum of 73.4/100,000 in those > 90 years of age. Septic arthritis was iatrogenic in 16.9% of cases while 27% had an underlying inflammatory arthritis including gout (14.9%), calcium pyrophosphate disease (8.5%), and rheumatoid arthritis (4%). Few patients were taking immunosuppressant therapy, with just 1 taking a biological agent. Staphylococcus aureus was the most commonly identified organism. Those with underlying inflammatory arthritis were significantly older (73.6 yrs vs 55.6 yrs; p < 0.001), more likely to be female (55.2% vs 26.0%; p < 0.001), and to have septic polyarthritis (16.4% vs 4.4%; p = 0.002). The 30-day mortality was 2%, increasing to 6% at 90 days. CONCLUSION: The incidence of septic arthritis in Canterbury, New Zealand, is higher than in previous studies. Crystal arthropathy commonly coexisted with infection although autoimmune arthritis and immunosuppression was less of a factor than anticipated.
OBJECTIVE: To determine the epidemiology, clinical features, and microbiology of adult native joint septic arthritis in Canterbury, New Zealand, over a 5-year period in individuals with and without an underlying rheumatic disorder. METHODS:Patients with native joint septic arthritis were identified retrospectively and classified by Newman's criteria. The clinical characteristics were described and comparisons made between those with and without underlying rheumatic disease. RESULTS: Two hundred forty-eight cases of native joint septic arthritis (mean age 60, range 16-97 yrs) were identified with an overall incidence rate of 12.0/100,000/year (95% CI 10.6-13.6). Yearly incidence increased with age to a maximum of 73.4/100,000 in those > 90 years of age. Septic arthritis was iatrogenic in 16.9% of cases while 27% had an underlying inflammatory arthritis including gout (14.9%), calcium pyrophosphate disease (8.5%), and rheumatoid arthritis (4%). Few patients were taking immunosuppressant therapy, with just 1 taking a biological agent. Staphylococcus aureus was the most commonly identified organism. Those with underlying inflammatory arthritis were significantly older (73.6 yrs vs 55.6 yrs; p < 0.001), more likely to be female (55.2% vs 26.0%; p < 0.001), and to have septic polyarthritis (16.4% vs 4.4%; p = 0.002). The 30-day mortality was 2%, increasing to 6% at 90 days. CONCLUSION: The incidence of septic arthritis in Canterbury, New Zealand, is higher than in previous studies. Crystal arthropathy commonly coexisted with infection although autoimmune arthritis and immunosuppression was less of a factor than anticipated.
Entities:
Keywords:
CRYSTAL ARTHROPATHY; EPIDEMIOLOGY; NATIVE JOINT; NEW ZEALAND; SEPTIC ARTHRITIS
Authors: Heinrich M L Mühlhofer; Susanne Feihl; Ingo J Banke; Christian Suren; Florian Pohlig; Rüdiger von Eisenhart-Rothe Journal: Orthopade Date: 2020-02 Impact factor: 1.087