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Knee stiffness is a common complication associated with trauma or surgery and has been extensively studied.1-3 Risk factors include injury severity, timing of surgery, delayed postoperative rehabilitation, prolonged immobilization, infection, complex regional pain syndrome, and technical errors during intraarticular and extra-articular reconstructive procedures. Extra-articular stiffness may be caused by muscular fibrosis and contracture, heterotopic ossification, or myositis ossificans. The inflammatory response to injury or surgery can cause fibrosis, resulting in restricted knee motion. Anterior interval scarring, contracture of the posterior capsule or suprapatellar pouch, and diffuse arthrofibrosis may contribute to knee stiffness, lead to alterations in the biomechanics of the joint, and cause pain.4-6 Specific releases can be performed for each fibrotic region. Familiarity with the diagnosis and arthroscopic management of these disorders may lead to improved outcomes in this patient population.
Pathophysiology of Arthrofibrosis
The exact etiology of intra-articular tissue fibrosis is unknown, but several theories exist. Platelet-derived growth factor and transforming growth factor-beta 1 are inflammatory cytokines produced by the inflamed synovium that promote the proliferation of fibroblasts and extracellular matrix proteins, the inhibition of proteolytic enzymes, and the production of collagen. These cytokines are present in intra-articular scar tissue and in the synovial fluid of patients with joint trauma, as well as in fibrosis in the kidney, liver, and lung.7-9 Additionally, vascular endothelial growth factor is present in the infrapatellar fat pad.8 This factor is released after injury to the fat pad and may lead to vascular ingrowth and scarring.4 Another theory posits that injury, whether induced by trauma or surgery, produces hemorrhage and subsequent fibrosis due to the maturation of localized clotting and induction of progenitor cells.
Nonsurgical Management Prevention is the most effective means of avoiding motion loss following knee injury or surgery. Initially, modalities such as ice, compression, elevation, aspiration of effusion, electrical stimulation, physical therapy, nonsteroidal antiinflammatory drugs, and a shortterm course of oral corticosteroids can be used to decrease knee pain and inflammation and maintain motion.10 Flexion is more easily obtained than extension, thus, efforts should be directed toward maintaining extension. Isometric strengthening of the quadriceps helps to restore extension and prevents atrophy. Early patellar mobilization prevents adhesion formation and contracture of the patellar tendon. Surgery for an acute injury is best performed after inflammation, edema, and pain have decreased and range of motion (ROM) has normalized. Preoperative and postoperative immobilization should be kept to a minimum; early knee mobilization following surgery is recommended. Additional intervention is indicated in patients who fail initial nonsurgical treatment. Several authors have recommended isolated manipulation of the knee under anesthesia within 6 to 12 weeks postoperatively in patients who have not regained full ROM following surgery.10,11 However, this modality has recently fallen out of favor due to the risk of intraarticular hemorrhage and subsequent postoperative scarring, as well as complications such as excessive tibiofemoral and patellofemoral compression with the risk of chondral damage or fracture, rupture of the patellar tendon, distal femoral fracture, and complex regional pain syndrome.12,13
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