Delayed paraplegia following correction of severe thoracolumbar kyphotic deformity by posterior vertebral column resectionos4_

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1 Orthopaedic Surgery (2010), Volume 2, No. 1, CASE REPORT Delayed paraplegia following correction of severe thoracolumbar kyphotic deformity by posterior vertebral column resectionos4_ Jing Li MD, Guo-hua Lv MD, Xiao-bin Wang MD, Bing Wang MD, Chang Lu MD Department of Spine Surgery, The Second Xiangya Hospital of Central South University, Changsha, China Key words: Kyphosis; Lumbar vertebrae; Neurological manifestation; Thoracic vertebrae Introduction Decompensation in the sagittal plane of the spine leads to specific complaints such as pain, cardiopulmonary compromise, limitation of the activities of daily living and neurological impairment. Along with the development of new instrumentation and spinal surgical techniques, correction of severe and rigid thoracolumbar kyphosis is now commonly being performed 1. Vertebral column resection represents a new level for treating sharp angular kyphotic deformity, but on the other hand this technique is often associated with significant bleeding and has an increased risk of neural injury 2. The etiology of neurologic injury during surgical correction of kyphosis is thought to be vascular, hypotensive, neural element stretch, or direct trauma to the neural elements. Typically, neurological deficits caused by correction of severe thoracolumbar kyphotic deformity occur acutely during surgery or immediately after surgery. Delayed paraplegia, due to various reasons, has been reported by a few researchers in scoliosis surgery 1,3 7. To the authors knowledge, there is no report in the literature describing delayed postoperative paraplegia following vertebral column resection for thoracolumbar kyphosis deformity. In the current study, the authors report a rare case of delayed paraplegia following correction of a 93 kyphosis in a 44-year-old woman with Scheuermann s disease. Case report History and examination A 44-year-old woman, who had had progressive worsening of thoracolumbar kyphosis from the age of 16 years, Address for correspondence Xiao-bin Wang MD, Department of Spine Surgery, the Second Xiangya Hospital of Central South University, Middle of Renmin Road, Changsha, China Tel: ; Fax: ; wxbspine@ yahoo.com.cn Received 12 August 2009; accepted 09 October 2009 DOI: /j x presented with a severe kyphosis accompanied by severe leg and back muscle fatigue and pain over the past three years. The patient had intermittent claudication due to back and leg muscle fatigue and pain and had received no prior medical care. General and neurological examination revealed that she had good muscle tone, normal sensation and reflexes. Her head and neck exhibited a forward posture. There was no bowel or bladder dysfunction. Upright anteroposterior and lateral radiographs demonstrated a 93 kyphosis from T 8 to L 2 with mild coronal scoliosis (Fig. 1). Preoperative extension radiographs revealed a fixed kyphosis. A total spine magnetic resonance imaging (MRI) failed to demonstrate any parenchymal signal change or intraspinal abnormality that might complicate correction of her kyphosis. Preoperative testing revealed a mild impairment of ventilatory function, with a forced vital capacity (FVC) of 2.3 L, forced expiratory volume in one second (FEV 1) of 1.8 L, and total lung capacity (TLC) of 3.3 L. The corresponding preoperative percentages of the predicated normal values were 78% for FVC, 69% for FEV 1, and 76% for TLC. Surgical procedure The patient was placed in a prone position and a posterior midline incision made. Pedicle screws were placed bilaterally in the proximal four (T 8 T 11) and the distal three levels (L 2 L 4). Coronal and lateral radiographs were performed immediately after screw insertion to confirm acceptable placement of the screws. The patient then underwent posterior vertebral resection of T 128, and Ponte Smith Petersen facetectomies from T 9 to L 29. The deformity was gradually corrected with repeated additional compression and shortening of the vertebral column along a precontoured rod. Finally, autologous bone was inserted from the posterolateral side to fill the resection gap and provide anterior arthrodesis. During the operation, 24.5 unit (4900 ml) of allogenic red blood cells, and 550 ml of fresh frozen plasma were transfused to compensate for the intraoperative blood loss of 4500 ml. The mean arterial pressure was maintained at 71

2 72 J Li et al, Delayed paraplegia after VCR procedure Figure 1. (A) Upright anteroposterior radiographs showing mild coronal scoliosis. (B) Lateral radiographs demonstrating a 93 kyphosis from T 8 to L mm Hg. The total operation time was 10 h, and the course of anesthesia was uneventful. Surgery was completed without intraoperative complications. Intraoperative neurophysiologic monitoring of the spinal cord was not available, and an intraoperative wake-up test revealed no motor impairment of the patient s lower extremities. Postoperative course The patient retained full motor strength and normal deep reflexes in her lower extremities. As the time taken to regain consciousness and commence spontaneous respiration after anesthesia was prolonged, the patient was admitted to the Intensive Care Unit (ICU) and maintained on a ventilator. It was not possible to take postoperative X-rays, but motor strength, pinprick sensation and deep reflex status the next morning were found to be stable. The patient s heart rate, blood oxygen saturation, and body temperature were almost normal. Postoperative hypoxemia was not noted. However, during the first day in the ICU, the estimated blood lost into her wound drainage bag was 6010 ml. The total volume of transfused fluid was ml, consisting of 18.5 unit (3700 ml) of allogenic red blood cells, and 1700 ml of fresh frozen plasma. Because of her severe blood loss, the patient had prolonged hypotension, and a low hemoglobin and hematocrit, her hemoglobin decreasing from 11.7 g/l to 5.6 g/l, and hematocrit from 39.9% to 18.2%. The extent of blood loss was unusual and active bleeding was thought to be unlikely. Initially we used a hemostat, a vasopressor agent (dopamine) and fluid replacement to manage the bleeding and increase the patient s arterial pressure. Thirteen hours later (the next morning), the mean arterial pressure had increased (Fig. 2) and the amount of blood in her wound drainage bag had markedly decreased, so emergency surgical revision was not undertaken. Twenty-five hours after surgery, the ICU physicians noticed that the patient had developed paraplegia. Physical examination revealed a flaccid paraparesis (0/5) in both lower extremities with absence of knee and ankle reflexes. The patient s had no sensation below the umbilicus level. By this time, her hemoglobin had decreased to 5.6 g/l and her hematocrit was 18.2%. High-dose methylprednisolone (30 mg/kg bolus followed by 5.4 mg kg-1 h for 23 h) was administered -1 without delay and emergency surgical revision undertaken. No intraspinal hematoma or hardware malposition was identified, however the spinal cord was grossly swollen and the dura looked redundant between T 11 and L 1. The laminae of T 11 and L 1 were resected to decompress the spinal cord. An X-ray film taken three days after revision surgery confirmed acceptable placement of the screws with correction of the hyperkyphosis to 32 (Fig. 3). MRI failed to demonstrate any compromise of the spinal canal, but showed an area of hyper-intensity below the T 6 vertebra on T 2-weighted images, indicating a medullary lesion with spinal ischemia (Fig. 4A). The patient returned for final follow-up 6 months after surgery. Her neurological status had improved slightly, with persisting paraplegia below the3 inguinal level. MRI revealed that the high-intensity signal had disappeared (Fig. 4B). Discussion Neurological deficits represent the other side of the coin of surgical correction of spinal deformity. The many reasons for such defects include factors both intrinsic and extrinsic to the spinal cord and column itself 1,10. Scoliosis or kyphosis with congenital spinal abnormalities, such as syringomyelia, are the main candidates for this kind of complication. The severity and rigidity of the curve, as well as the degree of kyphotic deformity, also contribute to the risk of neurological complications during corrective procedures 10,11. Vertebral column resection has been described for tumors, spondyloptosis, excision of hemivertebrae and spinal deformities. While this proce-

3 Orthopaedic Surgery (2010), Volume 2, No. 1, Figure 2. Blood pressure fluctuations in the first 25 h after surgery. dure has made the treatment of serious and rigid spinal deformities possible, it has concomitantly increased the risk of neurological complications 2. An important factor determining the degree of risk is the specific level of kyphosis correction. The distinctive vascular anatomy of the spinal cord in the thoracic region contributes to a high risk of neurological lesion when operating in this area. Compared with the cervical spine, the thoracic spine has a less liberal blood supply. Therefore, both in terms of absolute quantity and volume per square centimeter, the blood supply to the thoracic nervous tissue is inferior, which contributes to the potential for ischemic cord injury in this region 12. Another vascular characteristic of the spinal cord is the artery of Adamkiewicz, or the major anterior segmental medullary artery, which originates from intercostal or lumbar vessels near the intervertebral foramen between the T 7 and L 4 levels. Although the concept of the major anterior segmental medullary artery has been challenged and disputed, it is extremely important in regards to spinal cord supply, as it is the principle blood supply to the lower anterior two-thirds of the spinal cord Whena neurologic deficit is induced during spinal distraction, it is thought to be caused by occlusion or spasm of this artery 15. When a neurological deficit occurs following scoliosis surgery, it may be acute or delayed in development. Spinal cord injury may be caused by corrective distraction measures, ischemia or canal compromise (by implants or hematoma). Delayed neurological deficits several hours after spinal surgery are uncommon, and are usually attributable to the latter two reasons. The etiology of spinal cord ischemia is multifactorial and includes vascular division, traction, arterial or venous embolization, and segmental vessel ligation. In addition, systemic hypotension, anemia, or local edema can exacerbate the effects of poor perfusion of the spinal cord 1,7. To the authors knowledge, 15 cases of delayed neurological deficit following uneventful surgery or spinal deformity have previously been described in the literature. Although the causes of such deficits are potentially related to many factors, ischemia induced by hypotension is the most commonly reported 7,11,16 20, followed by postoperative haematoma 3,6,10, vascular origin 1,4, anemia 10, instrumentation compression 10, and hypokalaemia 5. MRI of the spine is the best option for localizing the exact cause of paraplegia. The options for treatment in these cases are: (i) high-dose methylprednisolone; (ii) blood transfusion; (iii) vasopressor agents and fluid replacement; (iv) emergency decompression; (v) removal of the instrumentation.

4 74 J Li et al, Delayed paraplegia after VCR procedure causing the delayed postoperative paraplegia. Johnston et al. also reported two cases of delayed paraplegia resulting from neural ischemic and edema after correction of complex spinal deformities with sublaminar wiring 19. Sublaminar segmental spinal instrumentation was used in both cases, and both patients had permanent paraplegia at the last follow-up. Othman et al. reported a case of correction of Scheuermann s kyphosis with T 4 L 2 pedicle screw placement and multilevel Smith-Peterson osteotomies 17. During the operative procedure, the patient s mean arterial pressure dropped precipitously to 50 mm Hg, and percutaneous neurogenic mixed evoked potentials (NMEP) and somatosensory evoked potentials (SSEP) were acutely lost bilaterally. Once normal blood pressure had been restored, the SSEP and NMEP data returned. A wake-up test performed after deformity correction indicated no neurological deficit. Cervellati et al. reported a case of severe kyphoscoliosis complicating spinal muscular atrophy type The patient suddenly became paraplegia 26 h after correction of the deformity using the Hartshill technique. Spinal cord ischemia, with a significant decrease in hemoglobin to 5.6 g/l, was the main cause of the neurological deficit. MRI revealed a Figure 3. X-ray films after revision surgery confirming acceptable placement of the screws with correction of the hyperkyphosis to 32. Most spinal surgeries are assisted by a state of induced hypotension to minimize blood loss, but unchecked and persistent hypotension may lead to inadequate perfusion of the spinal cord, resulting in spinal cord ischemia. Both in experimental animals 21 and during aortic surgery in humans 22,23 profound hypotension has been documented to cause neurological deficits. The incidence of paraplegia due to hypotension after surgery for correction of spinal deformity has not been well documented. One case of paraplegia caused by significant intraoperative hypotension during anterior spinal fusion surgery has been reported 16, and in another case intraoperative neurophysiologic monitoring data disappeared 17, but in the other cases reported, the onset was somewhat delayed 7,11, Taylor et al. have shown a clear and reversible relationship between spinal cord function and postoperative hypotension 7. In the case reported by these authors, the postoperative blood pressure fell to the same level as during surgery, causing loss of spinal cord function. Once normal arterial pressure had been restored by transfusion, neurologic function recovered rapidly without any surgical revision. The authors proposed that hypovolemia with consequent reduced cardiac output were the main factors Figure 4. (A) MRI showing an area of hyperintensity below the T 6 vertebra on T 2-weighted images. (B) Six months after the operation, the high-intensity signal had partially disappeared.

5 Orthopaedic Surgery (2010), Volume 2, No. 1, high-intensity signal which indicated a medullary lesion secondary to cord ischemia. The patient retained full motor strength and normal deep reflexes in the lower extremities for about 25 h after correction of kyphosis. Postoperatively, she had massive blood loss with prolonged hypotension, low hemoglobin and hematocrit. Although a dopamine infusion was maintained throughout most of the first postoperative day together with transfusion of fluid, the mean arterial blood pressure still ranged from 56 mm Hg to 68 mm Hg over the first 13 h. Her hemoglobin decreased from 11.7 g/l to 5.6 g/l, and hematocrit from 39.9% to 18.2%. Thus we deduce that the cause of the delayed neurological deficits in our case was cord ischemia caused by hypotension and anemia. Immediate revision surgery and sequential MRI confirmed spinal cord ischemia, edema and infarction above the instrumentation level. Mechanical obstruction from the hardware or a developing hematoma was ruled out. Our case illustrates that delayed ischemia following complicated spinal surgery can lead to serious irreversible neurological deficits. Altogether, during or after surgery for correction of deformity there are many potential risks to the spinal cord which can lead to neurological compromise. Such neurological deficits are usually found intraoperatively or immediately after surgery. Several-hour delayed paraplegia is uncommon. This case report suggests that hypovolemia is indeed an important causative mechanism for delayed neurologic deficits in spinal deformity correction surgery especially with the vertebral column resection technique. One should be aware of the importance of postoperative observation of spinal deformity cases in order to detect any impending neurologic deficit early. References 1. Keyoung HM, Kanter AS, Mummaneni PV. Delayedonset neurological deficit following correction of severe thoracic kyphotic deformity. J Neurosurg Spine, 2008, 8: Macagno AE, O Brien MF. Thoracic and thoracolumbar kyphosis in adults. Spine, 2006, 31 (19 Suppl.): S161 S Chang JH, Hoernschemeyer DG, Sponseller PD. Delayed postoperative paralysis in adolescent idiopathic scoliosis: management with partial removal of hardware and staged correction. J Spinal Disord Tech, 2006, 19: Stöckl B, Wimmer C, Innerhofer P, et al. Delayed anterior spinal artery syndrome following posterior scoliosis correction. Eur Spine J, 2005, 14: Kluba T, Giehl JP. A surprising cause of paresis following scoliosis correction. Eur Spine J, 2001, 10: Mineiro J, Weinstein SL. Delayed postoperative paraparesis in scoliosis surgery. A case report. Spine, 1997, 22: Taylor BA, Webb PJ, Hetreed M, et al. Delayed postoperative paraplegia with hypotension in adult revision scoliosis surgery. Spine, 1994, 19: Suk SI, Kim JH, Kim WJ, et al. Posterior vertebral column resection for severe spinal deformities. Spine, 2002, 27: Geck MJ, Macagno A, Ponte A, et al. The Ponte procedure: posterior only treatment of Scheuermann s kyphosis using segmental posterior shortening and pedicle screw instrumentation. J Spinal Disord Tech, 2007, 20: Cervellati S, Bettini N, Bianco T, et al. Neurological complications in segmental spinal instrumentation: analysis of 750 patients. Eur Spine J, 1996, 5: Wilber RG, Thompson GH, Shaffer JW, et al. Postoperative neurological deficits in segmental spinal instrumentation. A study using spinal cord monitoring. J Bone Joint Surg Am, 1984, 66: Dommisse GF. The blood supply of the spinal cord. A critical vascular zone in spinal surgery. J Bone Joint Surg Br, 1974, 56: Cheshire WP, Santos CC, Massey EW, et al. Spinal cord infarction: etiology and outcome. Neurology, 1996, 47: Lazorthes G, Gouaze A, Zadeh J. Arterial vascularization of the spinal cord. J Neurosrug, 1971, 35: Brodkey JS, Richards DE, Blasingame JP, et al. Reversible spinal cord trauma in cats. Additive effects of direct pressure and ischemia. J Neurosurg, 1972, 37: Ben-David B, Haller G, Taylor P. Anterior spinal fusion complicated by paraplegia. A case report of a falsenegative somatosensory-evoked potential. Spine, 1987, 12: Othman Z, Lenke LG, Bolon SM, et al. Hypotensioninduced loss of intraoperative monitoring data during surgical correction of Scheuermann s kyphosis: a case report. Spine, 2004, 29: E258 E Bridwell KH, Lenke LG, Baldus C, et al. Major intraoperative neurologic deficits in pediatric and adult spinal deformity patients. Incidence and etiology at one institution. Spine, 1998, 23: Johnston CE, 2nd, Happel LT, Jr, Norris R, et al. Delayed paraplegia complicating sublaminar segmental spinal instrumentation. J Bone Joint Surg Am, 1986, 68:

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