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DELAYED POST-OPERATIVE NEUROLOGICAL DEFICIT AFTER POSTERIOR SPINAL FUSION FOR ADOLESCENT IDIOPATHIC SCOLIOSIS: POSSIBLE ASSOCIATION WITH POST OPERATIVE ANAEMIA

7th Congress of the European Federation of National Associations of Orthopaedics and Traumatology, Lisbon - 4-7 June, 2005



Abstract

A 14 year-old-female, underwent a T3-L3 instrumented posterior spinal fusion for a double major curve. Surgery under controlled hypotensive anesthesia was uneventful, with normal somatosensory and motor potentials. After instrumentation, patient underwent a normal wake-up test. The preoperative haemoglobin and haematocrit was 15.1g/dl with 41%, respectively. Estimated blood loss was 400cc and postoperative haemoglobin and haematocrit were 9.7g/dl and 31% respectively. Clinical examination was normal immediately postoperatively, on the first postoperative day and the beginning of the second postoperative day. At the end of POD 2, the patient started to feel both lower extremities “heavy” and sensitive to touch. She developed generalized proximal lower extremity weakness and was unable to stand. She was also unable to void after catheter removal. At this stage, her hemoglobin had dropped from 10 g/dl on POD 1 to 7.3 g/dl. Her haemoglobin fell to 6.2 g/dl the next day with a haematocrit of 18%. No significant bleeding was noticed, and other than lightheadedness, no haemodynamic changes were noted. Transfusion was performed correcting the haemoglobin to 9.3 g/dl and haematocrit to 27%. Compressive etiology was ruled out by post-operative myelogram-CT. Patient was discharged on POD 13 and was neurologically intact at three month follow-up. Discussion: Delayed neurological deficits have been reported, and are associated most frequently with epidural haematomas. Postoperative hypotension as the etiological factor has been reported only in an adult patient. As cord compression was ruled-out the only event we can correlate with the beginning of the neurological deficit is the unexplained acute drop in haemoglobin levels on the second day, possibly impairing normal cord oxygenation. If this is not the case, we would have to accept false negative results for the three standard methods currently available for spinal cord monitoring during surgery. In this case, the normal postoperative neurological exams, performed during the first 48 hours after surgery, and the subjective symptoms the patient experienced associated with the beginning of motor deficit, leads us to conclude that the injury happened on the second day in relation to the postoperative anaemia. Although we believe children tolerate low levels of haemoglobin, transfusion policies might have to be reconsidered as the cord may be transiently at risk for ischemic events after deformity correction.

Theses abstracts were prepared by Professor Roger Lemaire. Correspondence should be addressed to EFORT Central Office, Freihofstrasse 22, CH-8700 Küsnacht, Switzerland.