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We report on two patients with myelopathy and progressive paraparesis due to vertebral hemangioma who were successfully treated by direct puncture and perfusion of the hemangioma with absolute ethanol. In one patient complete elimination of the hemangioma required a second injection of absolute ethanol. Myelopathy remitted in both patients. The technique permits the devascularization of vertebral hemangiomas as an alternative to surgery or radiation therapy.
Case Reports
The injection of ethanol into vertebral hemangiomas is part of a clinical research protocol on the evaluation and treatment of patients with spinal vascular abnormalities (protocol 93N-0150) that was approved by the institutional review board of the National Institute of Neurological Disorders and Stroke. Informed consent was obtained from each patient.
Patient 1
Patient 1 was a 54-year-old woman who had had progressive weakness of the lower extremities, worse on the right, for one year. She could walk only a few steps using a walker, and her gait was slow and spastic. Hypalgesia was present below the midchest. Clonus was present at the knees and ankles. Bilateral Babinski signs were present. Magnetic resonance imaging (MRI) of the spine demonstrated an enhancing lesion of the fourth thoracic vertebra that extended into the epidural space and compressed the spinal cord (Figure 1A). A myelographic block at the T4 level confirmed the presence of severe cord compression. Computed tomographic (CT) scanning revealed the typical honeycombed appearance of a vertebral hemangioma. On spinal arteriography, selective injection into the fourth right intercostal artery opacified a vascular lesion of the T4 vertebra (Figure 1B). Additional feeding arteries arose from the right and left second and third intercostal arteries. Embolization of several nutrient arteries of the hemangioma with 250-to-355-microm particles of polyvinyl alcohol (Ivalon, Contour Emboli, Interventional Therapeutics, South San Francisco) moderately reduced the vascular stain. Complete embolization was not possible, however, because a medullary artery supplying the spinal cord originated from one of the arteries supplying the hemangioma (Figure 1B). The patient had no neurologic improvement after transcatheter embolization.
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A CT scan performed while 10 ml of iopamidol was being injected through the needle demonstrated the opacification of hemangiomatous vessels involving the body and posterior elements of the vertebra. Rapid blood flow caused the contrast medium to clear quickly from the hemangioma. We excluded the possibility that the iopamidol was entering the subarachnoid space by taking additional axial CT cuts through the adjacent spinal levels. We then injected 10 ml of absolute ethanol into the hemangioma in increments of 2 ml every 5 to 10 minutes. The patient had transient thoracic pain during the injection. Occlusion of the hemangioma was confirmed by the prolonged retention of contrast medium in the vertebral body and by the cessation of blood flow through the biopsy needle.
Within a week of the ethanol injection, the patient's walking and leg strength began to improve. A second ethanol injection was performed 10 weeks after the first to obliterate residual hemangioma seen on MRI. After the second injection the epidural enhancement and mass effect disappeared (Figure 1D). Arteriography revealed no abnormal vascular stain. Within a month of the second injection the patient was walking without assistance. Her spasticity diminished, and she resumed her duties as a ward nurse within two months after treatment. The spasticity resolved completely within six months.
Patient 2
The second patient, a 64-year-old woman, had a three-month history of bilateral weakness and pain in the lower extremities. The pain intensified when she walked more than 6 m (20 ft). She walked with an anteflexed posture. Weakness was restricted to the proximal leg muscles. Spinal MRI revealed cord compression from an enhancing lesion of the 12th thoracic vertebra (Figure 2A). Spinal CT performed at another hospital showed a typical vertebral hemangioma.
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Discussion
Vertebral hemangiomas are congenital vascular malformations, not true neoplasms, consisting of vessels reminiscent of embryonic capillaries or veins17,18,19. They are subclassified histologically as capillary or cavernous hemangiomas, according to vessel size20. Arteriovenous shunting does not occur in hemangiomas, unlike congenital arteriovenous malformations, which, lacking capillaries, act as low-resistance arteriovenous shunts19. Vertebral hemangiomas may grow into the epidural space, compress the spinal cord, and produce slowly progressive myelopathy. Arteriovenous malformations, by contrast, originate intradurally and, by nature of their pathophysiology rather than their growth, produce either slowly progressive myelopathy from spinal cord ischemia, venous congestion or thrombosis, or acute myelopathy from intramedullary hemorrhage. MRI of the spine clearly differentiates hemangiomas from arteriovenous malformations. Hemangiomas originate in the vertebra, and spinal arteriovenous malformations generally originate intradurally.
Transarterial particulate embolization occludes feeding vessels but does not destroy the hemangioma, because an intervening capillary bed separates the feeding arteries from the hemangioma3,12,13,14,15. Another drawback of transarterial embolization is the risk of spinal cord infarction when a common artery supplies the hemangioma and the spinal cord,14 as was the case in Patient 1. By contrast, direct intralesional injection of ethanol should confine thrombosis to the hemangioma, because the capillary bed prevents retrograde flow into the feeding arteries17.
Direct intravertebral injection of acrylic has been used to treat pain from vertebral hemangiomas that are confined to the vertebral body21. Acrylic does not destroy the hemangioma, however, and when vertebral hemangiomas expand into the epidural space, the injection of acrylic can aggravate cord compression22,23. Unlike methylmethacrylate, which occupies space and creates a permanent, incompressible cast of the hemangioma, ethanol scleroses the hemangioma to a smaller size and is cleared rapidly.
A framework of thickened vertebral trabeculae prevents compression fracture in most patients with vertebral hemangioma20. Absolute ethanol eradicates the hemangioma but preserves the trabecular support and vertebral stability. Further stabilization of the vertebra with spinal instrumentation, bone fusion, or methylmethacrylate is unnecessary.
Proper technique is required for the successful and safe delivery of the ethanol. The transpedicular approach is a useful alternative to a paraspinal approach, because it avoids the pleural and retropleural spaces24 and injury to the intercostal artery and permits access to the posteromedial portion of the vertebral body. CT guidance facilitates the cannulation of small thoracic pedicles, ensures precise needle placement, and reduces the risk of neurologic injury. Test injections with contrast medium elucidate the morphologic features and volume of the hemangioma and minimize the risk of subarachnoid ethanol injection. Injecting the ethanol slowly prevents retrograde flow from the hemangioma through the capillary bed and into the feeding arteries. Local anesthesia and mild sedation allow neurologic monitoring during the procedure.
Further experience with percutaneous injection of ethanol is needed to define its place in the treatment of vertebral hemangiomas and other vertebral lesions. Unlike open surgery, ethanol injection averts vertebral resection, operative blood loss, and lengthy convalescence. Unlike intraarterial alcohol, which cannot be used more than once because it occludes the feeding arteries, and unlike radiation, which is limited by constraints on dosage, intralesional ethanol injection can be repeated as necessary to obliterate residual hemangioma.
Source Information
From the Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke (J.D.H., E.H.O.), and the Department of Radiology, Warren B. Magnuson Clinical Center (J.L.D.), National Institutes of Health, Bethesda, Md.
Address reprint requests to Dr. Heiss at the Surgical Neurology Branch, National Institutes of Health, Bldg. 10, Rm. 5D-37, 9000 Rockville Pike, Bethesda, MD 20892.
References
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Extract |
Full Text
N Engl J Med 1996;
334:1340-1341, May 16, 1996.
Correspondence
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