Image Quiz

Acute Paraplegia After Vertebroplasty in an Eighty-two-Year-Old Woman (continued)

Answer: Epidural hematoma compressing the cauda equina and conus medullaris from T11-L2.

For larger view, click on image Fig. 2	Fig. 3	Fig. 4
Fig. 2 A representative axial computed tomography image of T12 acquired after the vertebroplasty. Note the absence of structural definition in the spinal canal, indicative of the hemorrhage. This image is the only one of all axial images of T12 showing a possible discontinuity in the medial cortex at the base of the left pedicle. A small amount of cement can be seen in the epidural space on the right side, possibly filling some veins. The trajectory of the trocar needle is clearly visible in the right pedicle. Fig. 3 A representative axial computed tomography image of L1 acquired after the vertebroplasty. Again, the intraspinal structures cannot be distinguished. There is cement filling of the central draining vein and cement draining into a lateral vein on the left side of the vertebral body. Fig. 4 Sagittal T2-weighted magnetic resonance image of the lumbar spine and part of the thoracic spine acquired after vertebroplasty. The epidural hemorrhage is clearly visible extending from T11 to L2 and compressing the cauda equina and conus medullaris. Also note the massively dilated bladder as a result of the paraplegia.

The patient was immediately returned to the operating room for an emergency spinal cord decompression. When the spinal canal was entered less than three hours after the initial onset of leg pain, a hematoma under pressure drained from the intraspinal space. A left-sided hemilaminectomy from T11 to L2 was performed, and the hematoma was evacuated. No intraspinal injury, fracture at the pedicle root, cement extravasation, or arterial bleeding source could be identified. Intraoperative hemostasis proved challenging because of a very congested venous plexus and profusely bleeding cancellous bone from the hemilaminectomies. Sealing of all bleeding bone with bone wax and hemostasis with bipolar coagulation, gelatin sponges, and silver nitrate cellulose was performed. Nevertheless, during the procedure, the patient lost 3 L of blood, requiring cell-saver autotransfusion and the administration of packed red-blood cells and fresh-frozen plasma. Postoperatively, she immediately had partial return of sensory and motor function. Within forty-eight hours, there was complete recovery of all neurological function. The patient remained in the intensive care unit for several days to monitor the cardiac and pulmonary systems, and she made a complete recovery. Fourteen days after the vertebroplasty, the patient was walking and did not require any pain medications. She was transferred to a rehabilitation facility from where she was discharged home three weeks later.

Discussion

Analysis of the case of this patient does not reveal a clear single cause for the complication, but there are several factors that may have been responsible in combination. First, low-dose aspirin was not discontinued until five days prior to the procedure. After that period, >50% of the platelets in the circulation should have been functional, since it is generally accepted that 10% of circulating platelets are replaced within twenty-four hours. There is no definitive evidence that antiplatelet medications increase the risk of an epidural hematoma after neuraxial anesthesia, which, on the basis of the scale of the intervention, might be considered a procedure comparable with uncomplicated vertebroplasty. A period of five days between the discontinuation of aspirin and spinal anesthesia procedures is recommended by some authors on empirical grounds, and a period of between several days and one week is considered sufficient for endoscopic spinal arthrodesis in the United States. A recent survey among German spinal surgeons found that the average period between the discontinuation of aspirin to the time of elective spinal surgery was 6.9 days (range, zero to twenty-one days). This indicates that some surgeons would have considered a five-day period insufficient. In our patient, a preoperative bleeding time was not performed, since there had been no clinical signs of impaired platelet function and no history of prolonged bleeding. Standard coagulation tests had been normal, and an array of platelet function tests after the complete recovery of the patient showed no underlying abnormality. Nevertheless, the possibility that a low platelet turnover, which may occur in an older person, might have prolonged the effect of platelet inhibition cannot be ruled out. Second, the hypertensive period prior to the procedure could have caused a spontaneous spinal epidural hematoma. Such hematomas are rare, and less than 300 cases have been reported. Among the suspected causes are hypertension, the use of low-molecular-weight heparins, and pregnancy with and without preeclampsia. Vascular malformation is also considered as a cause of a spontaneous epidural hematoma, but no evidence of a vascular malformation was seen in our patient. In many cases, no apparent reason has been found. The blood pressure in our patient at the beginning of the procedure was slightly elevated, but this level would not qualify as a hypertensive crisis. In addition, the close time relationship between an invasive procedure and the epidural hematoma makes a spontaneous hematoma unlikely. Third, the obstruction of transosseously draining veins in two adjacent vertebrae might have caused regional venous congestion, which is what we observed during surgery. Neurological deficits resulting from epidural venous obstruction have been described; however, none of those patients presented with acute paraplegia but rather with slowly developing symptoms as a consequence of myelopathy or nerve root irritation. In our patient, the paraplegia was clearly caused by a hematoma, but venous congestion might have exacerbated the bleeding caused by other factors. Fourth, the increase in local temperature by the curing cement might have caused thermal damage to epidural vessels. There is discussion as to whether temperatures at the posterior border of vertebrae during vertebroplasty reach levels that can cause tissue damage. Since, in T12 (Fig. 2), there was a considerable volume of cement close to the epidural space and some cement filling the epidural veins, thermal damage and subsequent bleeding cannot be ruled out. Fifth, angulation of the trocar needle while attempting to enter the left pedicle at T12 might have caused a fracture at the pedicle root, directly causing intraspinal bleeding from the cancellous bone or by injuring the epidural venous plexus at that location. We examined the left pedicle root of T12 during surgery and did not see or feel a fissure or fracture, but visibility was impaired because of the bleeding. The discontinuity of the pedicle seen in Figure 2 could also have been associated with the original vertebral fracture. In either case, it seems unlikely that such a small injury alone would have caused such an extensive hematoma.

An epidural hematoma is an extremely rare occurrence, but it should be remembered that vertebroplasty, while in general a very safe procedure, carries risks similar to those of open spinal surgery. If such emergencies cannot be addressed in a timely fashion, permanent neurological deficits may result. We therefore recommend that vertebroplasty and similar procedures should be performed only in settings where emergency spinal surgery is available. As a consequence of the case of our patient, our current policy is to discontinue aspirin at least seven days prior to elective open spinal surgery and minimally invasive spinal procedures. In addition, we routinely perform preoperative bleeding times in these patients.

Reference

1. Birkenmaier C, Seitz S, Wegener B, Glaser C, Ruge MI, von Liebe A, von Schulze Pellengahr C. Acute paraplegia after vertebroplasty caused by epidural hemorrhage. A case report. J Bone Joint Surg Am. 2007;89:1827-31.