Does osteoarthritis of the ankle joint progress after triple arthrodesis? A midterm prospective outcome study.

BACKGROUND: Debate exists regarding the effect of triple fusion on the development of osteoarthritis (OA) of the ankle joint. The midterm outcome after triple arthrodesis and the prevalence of OA following triple arthrodesis are reported in this study. The role of alignment in the development of OA was investigated. METHODS: Seventy five patients (87 feet) were evaluated in 2003 and of these, 48 patients (55 feet) were available for second evaluation in 2008. X-rays of the ankles and feet were made prior to surgery, in 2003 and in 2008, and the level of osteoarthritis (OA) was graded with the Kellgren and Lawrence score. Of all postoperative X-rays, the AP and lateral talo first metatarsal angle X-rays were compared. Also, standardized digital photos were made to assess the geometry/alignment. The Foot Function Index (FFI) and the American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot score were completed. In order to investigate the role of the underlying alignment on the aggravation of ankle osteoarthritis, patients were divided into a 'varus' and a 'valgus' group based on the indication for surgery. RESULTS: The outcome scores (AOFAS and FFI) after triple arthrodesis remained stable in the present 7.5-year follow-up study. An important increase of OA of the ankle was not established, 58% of the patients showed no aggravation, 31% one-grade and 2% two-grade increase of OA. A trend was found (P=.063) towards aggravation of OA of the ankle in patients of the varus group with the highest medial arches (persistent cavovarus deformity). CONCLUSION: This study reports minor, not statistically significant, changes of the ankle joint following triple arthrodesis after 7.5 years. Clinical outcome remained stable in time. Clinical relevance It seems that triple arthrodesis as such does not lead to major osteoarthritis of the ankle, given that adequate alignment of the hindfoot is achieved. LEVEL OF EVIDENCE: Level II, retrospective study.

Release of von Willebrand factor antigen (vWF:Ag) and eicosanoids during acute injury to the isolated rat lung.

It has been suggested that the von Willebrand factor antigen (vWF:Ag) may be a clinical marker for pulmonary endothelial cell injury. An ELISA was developed for the measurement of rat vWF:Ag. Rat lungs were isolated and perfused with a recirculating, blood-free, physiologic salt solution. Circulating levels of vWF:Ag and the eicosanoids thromboxane B2 (TXB2) and prostaglandin 6-keto F1-alpha (6-keto PGF1 alpha) were measured before and after different forms of insult. The addition of phospholipase C (PLC) or hydrogen peroxide (H2O2) to the perfusate caused lung damage as manifested by pulmonary artery pressure increase and pulmonary edema. This was paralleled by significant release of vWF:Ag, TXB2, and 6-keto PGF1 alpha. Increased hydrostatic pressure caused pulmonary edema without vWF:Ag and eicosanoid release. The addition of vasopressin to the perfusate caused vWF:Ag release but no lung injury and no release of eicosanoids. It is concluded that in the rat model, vWF:Ag release is a nonspecific marker for lung injury.