Pressure changes in the Kager fat pad at the extremes of ankle motion suggest a potential role in Achilles tendinopathy.

The Kager fat pad is one of the largest soft tissue structures local to the ankle joint, yet it is poorly understood. It has been hypothesised to have a role in Achilles tendinopathy. This study aimed to investigate the pressure areas in the Kager fat pad adjacent to the Achilles tendon and to assess the anatomy and deformation of the Kager fat pad in cadavers. Twelve fresh frozen cadaveric ankles (mean age 44 years, range 38-51) were mounted in a customized testing rig, enabling plantar flexion and dorsiflexion of the ankle, with the Achilles tendon loaded. A needle tipped pressure sensor was inserted in two areas of the Kager fat pad under ultrasound guidance (retrocalcaneal bursa and at 3 cm proximal from Achilles insertion). Pressure readings were recorded at different flexion angles. Following testing, the specimens were dissected to expose the Kager fat pad and retrieve it for analysis. MRI images were also taken from three healthy volunteers and the Kager fat pad deformation examined. Mean pressures significantly increased in all specimens at terminal ankle plantar and dorsi flexion in both regions (p < 0.05). The Kager fat pad was consistently adherent to the Achilles at its posterior aspect for a mean length of 7.7 cm (SD 0.27, 89% of KFP length). The most distal part of the Kager fat pad was the exception and it detached from the Achilles to give way to the retroalcaneal bursa for a mean length of 0.92 cm (SD 0.24, 11% of KFP length). The bursal space is partially occupied by a constant 'wedge' extension of Kager fat pad. The mean volume of the whole Kager fat pad was 10.6 ml (SD 3.37). Video and MRI demonstrated that the Kager fat pad undergoes significant deformation during plantar flexion as it is displaced superiorly by the Achilles, with the wedge being forced into the retrocalcaneal bursal space. The Kager fat pad does not remain static during ankle range of motion, but deforms and its pressure also changes. This observation supports the theory that it acts as a shock-absorber to the Achilles tendon and pathological changes to the fat pad may be clinically important in the development of Achilles tendinopathy.