Subclinical femoral neuropathy after anterior cruciate ligament reconstruction

Background and aim of the study: Patients with anterior cruciate ligament (ACL) reconstruction and femoral catheter analgesia may develop quadriceps amyotrophy. We aimed to determine whether this amyotrophy might be related to a femoral neuropathy. Material and method: After Ethical Committee approval and patients' written informed consent, 17 patients ASA I and II scheduled to undergo ACL reconstruction were recruited. An electromyography (EMG) was performed before the operation in order to exclude a femoral neuropathy. A femoral nerve catheter was inserted before the surgery with the aid of a nerve stimulator, and 20 ml of 0.5% ropivacaine was injected. The operation was done under spinal or general anaesthesia. Postoperative analgesia was provided with 0.2% ropivacaine for 72 hours, in association with oxycodone, paracetamol and ibuprofen. A second EMG was performed 4 weeks after the ACL repair. A femoral neuropathy was defined as a reduction of the surface of the motor response of more than 20%, compared to the first EMG. A third EMG was performed at 6 months if a neuropathy was present. Results: Mean age of this group of patients was 27 years old (range 18-38 y.). Among the 17 patients, 4 developed a transient femoral neuropathy (incidence of 24%) without clinical complain. Conclusion: In this study, the incidence of subclinical femoral neuropathy after ACL reconstruction is high. This lesion may be caused by the femoral catheter (mechanical damage, toxicity of local anaesthesia) or by the Tourniquet. Further studies are needed to investigate the incidence of subclinical neuropathy, according to the type of analgesia (epidural analgesia, PCA) and surgery.

Acute painful diabetic neuropathy: an uncommon, remittent type of acute distal small fibre neuropathy.

INTRODUCTION: Acute painful diabetic neuropathy (APDN) is a distinctive diabetic polyneuropathy and consists of two subtypes: treatment-induced neuropathy (TIN) and diabetic neuropathic cachexia (DNC). The characteristics of APDN are (1.) the small-fibre involvement, (2.) occurrence paradoxically after short-term achievement of good glycaemia control, (3.) intense pain sensation and (4.) eventual recovery. In the face of current recommendations to achieve quickly glycaemic targets, it appears necessary to recognise and understand this neuropathy. METHODS AND RESULTS: Over 2009 to 2012, we reported four cases of APDN. Four patients (three males and one female) were identified and had a mean age at onset of TIN of 47.7 years (±6.99 years). Mean baseline HbA1c was 14.2% (±1.42) and 7.0% (±3.60) after treatment. Mean estimated time to correct HbA1c was 4.5 months (±3.82 months). Three patients presented with a mean time to symptom resolution of 12.7 months (±1.15 months). One patient had an initial normal electroneuromyogram (ENMG) despite the presence of neuropathic symptoms, and a second abnormal ENMG showing axonal and myelin neuropathy. One patient had a peroneal nerve biopsy showing loss of large myelinated fibres as well as unmyelinated fibres, and signs of microangiopathy. CONCLUSIONS: According to the current recommendations of promptly achieving glycaemic targets, it appears necessary to recognise and understand this neuropathy. Based on our observations and data from the literature we propose an algorithmic approach for differential diagnosis and therapeutic management of APDN patients.