Range of motion after total knee arthroplasty in hemophilic arthropathy

Abstract

BackgroundOutcomes of total knee replacement in cases of hemophilic patients are worse than in patients who undergo operations due to osteoarthritis. Previous publications have reported varying rates of complications in hemophilic patients, such as infection and an unsatisfactory range of motion, which have influenced the survival of prostheses. Our retrospective study evaluated the data of hemophilic patients regarding changes in the development of the range of motion.MethodsThe data and clinical outcomes of 72 total knee replacements in 45 patients with hemophilia types A and B were reviewed retrospectively. Patients were operated between 1998 and 2013. All of the patients were systematically followed up to record the range of motion and other parameters before and after surgery.ResultsThe mean preoperative flexion contracture was 17° ± 11° (range, 0°-40°), and it was 7° ± 12° (range, 0°-60°) postoperatively. The mean flexion of the knee was 73° ± 30° (range, 5°-135°) before the operation and 80° ± 19° (range, 30°-110°) at the last follow-up. The mean range of motion was 56° ± 34° (range, 0°-130°) before the operation and 73° ± 24° (range, 10°-110°) at the last follow-up.ConclusionsStatistical analysis suggested that the range of motion could be improved until the 9th postoperative week. The patient should be operated on until the flexion contracture reaches 22° to obtain a contracture < 15° postoperatively or until the contracture reaches 12° to obtain less than 5°. The operation generally does not change the flexion of the knee in cases of hemophilic patients, but it reduces the flexion contracture and therefore improves the range.

Primary total knee arthroplasty in hemophilic arthropathy

“…Goddard et al reported the range of flexion and flexion contracture improved from 68° to 79° and 9.6° to 4.7°, respectively (62). Similar results were published by Kubes et al and Silva et al where TKA surgery decreased the average flexion contracture from 17° to 7° and 18° to 8° and improved the average preoperative flexion range from 73° to 80° and 59° to 75°, respectively (35,63). Finally, a meta-analysis by Moore et al showed an average decrease of 9.7° in flexion contracture and an increase 15° in flexion after TKA surgery (53).…”

“…The prevalence of PJI in the non-hemophilic population is around 1% (85,86). However, most studies have shown significantly higher rates of PJI in PWH with prevalence ranging from 5% to 17% (21,35,66,67). The reason behind the increased infection rate in the hemophilic population is still unknown (72); nevertheless, there are several explanations that have been proposed including poor skin condition caused by coagulation factor administration, immunosuppression, bacteremia from contamination during repeated intravenous self-administration of coagulation factor concentrate, increased incidence of postoperative hematoma or concomitant HIV or HCV infection (53,87).…”

“…Tourniquet use is still widespread for TKA in the hemophilic population. The tourniquet can be either inflated during the entire procedure, only during component cementing or until beginning of wound closure (34,35,36,37).…”

Bilateral Pseudoarthrodesis

“…Moreover, functional outcomes of TKR in hemophilic patients have also shown suboptimal improvement in motion. The surgery was reported to have little effect on the flexion of the knee but reduced flexion contracture, which overall seemed to improve the ROM 16 .…”

How much preoperative flexion contracture is a predictor for residual flexion contracture after total knee arthroplasty in hemophilic arthropathy and rheumatoid arthritis?

“…Kubes et al. [ 30 ] reported that hemophilic patients should be operated before the preoperative flexion contracture reaches 22° to obtain a contracture < 15° postoperatively or before the preoperative contracture reaches 12° to obtain a contracture < 5°. In HA, repeated intraarticular bleeding occurs with subsequent intraarticular deposition of hemosiderin and iron, which leads to upregulation of proinflammatory cytokines and, consequently, synovial hypertrophy and articular destruction [ 31 ].…”