Ultraschall Med 2016; 37 - PS8_06
DOI: 10.1055/s-0036-1587902

Acute peroneal nerve injury after lateral ligamentous reconstruction

P Schwarzkopf 1, D Boeckler 2, A Goldammer 3, C Trantakis 3, K Pracht 1
  • 1Sana Klinikum Borna, Department for Anaesthesia, Intensive Care Medicine, Pain Therapy and Palliative Medicine, Borna, Germany
  • 2Sana Klinikum Borna, Department for Neurology, Borna, Germany
  • 3Sana Klinikum Borna, Department for Head and Spinal Microsurgery, Borna, Germany

A 24 year old woman with a history of anterior cruciate and lateral ligament rupture of the right knee was referred to our hospital because of acute peroneal nerve injury with foot drop and toe lifter palsy on the right site after reconstruction surgery of both ligaments in an external hospital.

Our neurosurgeon referred her to our neurosonographical consultation. Electromyography (EMG) and neurosonography of common peroneal nerve (CPN) were performed.

A complete foot lifter paralysis and an incomplete deficiency of sensory components of superficial peroneal nerve were seen. EMG of the anterior tibial muscle suggested complete denervation. It showed massive pathological spontaneous and no volitional activity. During neurosonography of the CPN a hypoechogenic structure was seen perforating and compressing CPN at the site of fibular head (picture 1 – B: yellow arrow pointing at CPN, C: black arrow pointing at perforating structure)

We strongly recommended an operative exploration of the CPN at the fibular head. During surgery which was done both by a neurosurgeon (AG) and an orthopedic surgeon it became obvious that the tendon graft of the lateral ligament perforated the CPN at the fibular head (picture 1 – A: black arrow pointing at perforating structure, yellow loops around CPN, tweezers holding CPN). The loosened tendon graft was cut and pulled under the CPN and reinserted again. The continuity of the CPN was macroscopically and electromyographically preserved – so no transplantation had to be done.

Three months after the operation the foot lifting power reached muscle strength grade (M) 4. Paresis of the toe lifter remained low, M 1 – 2, so physiotherapy was still needed.

Fig. 1