Femoral artery ischemia during spinal scoliosis surgery detected by posterior tibial nerve somatosensory-evoked potential monitoring

• Published in: Spine (Philadelphia, Pa. 1976) Vol. 25; no. 11; p. 1457
• Main Authors: Vossler, D G, Stonecipher, T, Millen, M D
• Format: Journal Article
• Language: English
• Published: United States 01.06.2000
• Subjects: Adolescent; Evoked Potentials, Somatosensory; Femoral Artery; Humans; Intraoperative Complications - prevention & control; Ischemia - diagnosis; Ischemia - etiology; Leg - blood supply; Male; Monitoring, Intraoperative; Nerve Compression Syndromes - diagnosis; Nerve Compression Syndromes - etiology; Scoliosis - surgery; Spinal Cord - surgery; Tibial Nerve - blood supply; Tibial Nerve - physiology
• ISSN: 0362-2436
• DOI: 10.1097/00007632-200006010-00021

A case report of unilateral leg ischemia caused by femoral artery compression detected using posterior tibial nerve somatosensory-evoked potentials during spinal scoliosis instrumentation surgery. To report a rare cause of intraoperative unilateral loss of all posterior tibial nerve somatosensory-evoked potential waveforms. Failure to obtain adequate popliteal fossa, spinal, subcortical, and cortical potentials during posterior tibial nerve somatosensory-evoked potential spinal cord monitoring usually results from technical factors or chronic conditions affecting the peripheral nerve. A 16-year-old boy with thoracic scoliosis had normal posterior tibial nerve somatosensory-evoked potentials both before surgery and in the operating room immediately after anesthesia induction and prone positioning on a four-post spinal frame. One hour after the start of surgery, a minimal amplitude reduction of the right popliteal fossa potentials appeared. Fifteen minutes later, the amplitudes of the popliteal fossa, subcortical, and cortical potentials evoked by right posterior tibial nerve stimulation became substantially reduced. Subsequently, all waveforms were lost. Malfunction of the right posterior tibial nerve stimulator was initially suspected, but when proper function was verified, a search for other causes of this loss led to discovery of leg ischemia. The patient was repositioned on the spinal frame, and all posterior tibial nerve somatosensory-evoked potentials waveforms began to reappear 7 minutes later. There was no postoperative clinically detectable complication. Although technical malfunction should always be suspected when all intraoperative somatosensory-evoked potential waveforms are initially seen and subsequently lost, one should also consider the possibility that intraoperative ischemia due to limb positioning could be the etiology.