Clinical benefits of intra-articular anakinra for arthrofibrosis.

Published online

Journal Article

Postoperative inflammation and stiffness, as well as the struggle to achieve full range of motion (ROM), following knee surgery is a significant clinical challenge. Interleukin-1 is a crucial mediator of the inflammatory response and development of pathological conditions leading to chronic inflammation. We hypothesized that intra-articular injection of intra-articular anakinra, an IL-1 antagonist, would result in sustained improvements of chronic refractory arthrofibrosis and limited arthrofibrosis of the knee joint. We retrospectively reviewed 8 patients who underwent injection of intra-articular anakinra, 200 mg. Four patients (3 women, 1 man) had intra-articular anakinra for treatment of chronic refractory arthrofibrosis, and 4 patients (4 women) had intra-articular anakinra for limited arthrofibrosis. All 4 of the refractory arthrofibrosis patients had failed conservative treatment with intensive physical therapy, corticosteroid injections, and anti-inflammatory medication. Three of the 4 patients had failed a prior manipulation under anesthesia with lysis of adhesions. All 4 reported improvement in ROM (10°-45°) and swelling, with 75% reporting improvement in pain. Seventy-five percent of these patients returned to prior activity level. All 4 of the limited arthrofibrosis also failed similar attempts at conservative treatment, and 2 of the 4 had failed a prior manipulation under anesthesia with lysis of adhesions. After intra-articular anakinra, all 4 reported improvement in ROM (20°-45°) and swelling, with 80% reporting improvement in pain. Seventy-five percent of these patients were able to return to prior activity level. We found intra-articular anakinra to be effective in this small cohort of patients with refractory arthrofibrosis and limited arthrofibrosis.

Full Text

Duke Authors

Cited Authors

  • Brown, CA; Toth, AP; Magnussen, B

Published Date

  • December 1, 2010

Published In

Volume / Issue

  • 33 / 12

Start / End Page

  • 877 -

PubMed ID

  • 21162510

Pubmed Central ID

  • 21162510

Electronic International Standard Serial Number (EISSN)

  • 1938-2367

Digital Object Identifier (DOI)

  • 10.3928/01477447-20101021-09

Language

  • eng

Conference Location

  • United States