There are a substantial number of patients who continue to complain of pain following total knee arthroplasty (TKA). There are many potential causes of continued pain, and these are broadly categorized into intrinsic and extrinsic sources. When evaluating a patient with a painful TKA, the physician begins with a thorough history and physical examination, along with the appropriate radiographs. Further workup includes laboratory analysis, specifically evaluating the inflammatory markers erythrocyte sedimentation rate and C-reactive protein, along with a synovial fluid aspirate evaluating the white blood cell count with differential and culture. Advanced imaging modalities are sometimes helpful when the diagnosis remains unclear, including stress radiographs, live fluoroscopic imaging, ultrasound, nuclear imaging, and magnetic resonance imaging. Further surgery is not advisable without a clear diagnosis, as this is associated with very poor results. Instead, serial follow-up or a referral to a specialist for a second opinion may be most appropriate.
High-intensity resistance (HIR) training has been associated with muscle hypertrophy and decreased microvascular density that might produce a blood flow limitation. The effect of HIR training on lower leg maximal blood flow and minimum vascular resistance (Rmin) during reactive hyperemia were investigated in 7 healthy males. The gastrocnemius-soleus muscles of one leg were trained using maximal isokinetic concentric contractions for 4 weeks; the nontrained leg was the control. Lower leg blood flow was measured by venous occlusion plethysmography. Lower leg muscle volume was determined using magnetic resonance imaging. Peak isokinetic torque increased in both the trained (T) and nontrained (NT) legs (p < .05). Lower leg muscle volume increased by 2% in the T leg only (p < .05). In the T leg, maximal blood flow decreased and Rmin increased (p < .05); no hemodynamic change was detected in the NT leg. It is concluded that HIR training of the calf muscles is associated with a decrease in hyperemia-induced blood flow; thereby, indicating a blood flow limitation to the calf muscles.
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