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Radiological case of the month: Athos D. Patsalides, MD; Anastasios Raptis, MD, PhD; Nicholas J. Patronas, MD.

CASE SUMMARY

A 60-year-old man with hormone refractory adenocarcinoma of the prostate presented with deep venous thrombosis (DVT) in the lower extremities. He was subsequently treated with heparin and warfarin sodium (Coumadin, Bristol-Myers Squibb Co., Princeton, NJ). Three days later, he complained of headache and weakness of both lower extremities and the left upper extremity. Neurologic examination was significant for weakness and decreased sensations to light touch in both of the lower limbs and the left upper limb. Hyperactive deep tendon reflexes and bilateral extensor plantar reflexes were present.

[FIGURE 1 OMITTED]

DIAGNOSIS

Acute spinal epidural hematoma

IMAGING FINDINGS

MR images of the cervical and thoracic spine showed an epidural mass, which did not enhance after contrast administration. The mass appeared isointense with the spinal cord on T1-weighted (T1W) (Figure 1A) and hypointense on T2-weighted (T2W [not shown]) images. There were no bone abnormalities that were suggestive of tumor metastasis.

The heparin drip was discontinued, and protamine sulfate and fresh frozen plasma were administered. Neurosurgical consultation was obtained, and considering his medical status, it was elected to follow the patient closely rather than proceed with neurosurgical decompression. During the following few days, the patient's neurological symptoms and signs gradually resolved. A follow-up magnetic resonance (MR) scan 2 weeks later showed complete resolution of the epidural hematoma (Figure 1B).

DISCUSSION

The incidence of spinal epidural hematomas (SEH) is 0.1 per 100,000 per year, and it affects men more often than women. (1) The causes of SEH fall into 3 main categories: 1) Posttraumatic, following vertebral fractures, obstetrical birth trauma, epidural anesthesia, lumbar puncture, spinal surgery, and stab wounds; 2) a variety of predisposing conditions, such as anticoagulant therapy (recognized to be the most common predisposing factor), coagulation disorders, arteriovenous malformation, cavernous angiomas, spinal cord neoplasm, pregnancy, Paget's disease, hypertension, and collagen vascular disorder; and 3) spontaneous, for which no predisposing factors can be identified. According to Beatty and Winston, (2) bleeding from one of the epidural arteries is the most likely source of spontaneous SEH.

Typically, patients with SEH experience a sudden severe pain at the level of hemorrhage, which may radiate to the limbs. (3) The radicular pain may precede the spinal pain. A rapid development of neurological symptoms follows because of compression of the spinal cord or the cauda equina. Motor and sensory deficits develop, and patients may have urinary retention. The symptoms are usually progressive and may result in permanent neurological disability or even death due to respiratory failure if emergent neurosurgical intervention is delayed. These clinical features may resemble those of epidural neoplasia, transverse myelitis, dissecting aortic aneurysm, congenital cysts, spondylitis, epidural abscess, vertebral fractures, spinal cord infarction, and acutely ruptured disc. (4,5) In this case, the patient's history, the clinical and imaging findings, and the symptom evolution over time established the diagnosis of epidural hematoma.

From the imaging point of view, important pathologies in the epidural space of the spine that must be differentiated from SEH include spinal subdural hematomas, epidural metastases, epidural abscesses, epidural lipoma, and congenital cysts.

* Spinal subdural hematomas are rare lesions that occur when extravasated blood accumulates in the preexisting subdural space. Typically, they extend over a long segment of the spinal canal, obliterating the subarachnoid space around the cord.

* Epidural metastases are usually associated with bone destruction and are visible as homogeneous enhancement in postcontrast MR images.

* Epidural abscesses are often associated with diskitis and/or osteomyelitis of the spine. The discs and the affected vertebrae show high signal intensity on T2W imaging and low signal intensity on T1W imaging. On postcontrast scans, homogeneous enhancement is observed in the epidural space during the initial stages of the inflammatory process caused by phlegmon on granulation tissue. Later, after liquefaction has taken place, fluid collections can be discerned within the enhancing abnormality of the epidural space. Abnormal increased enhancement is always observed in the affected disc or vertebrae.

* Epidural lipoma is characterized by focal accumulation of fatty tissue with high signal on T1W and low signal on fat-suppression T2W techniques. (1,6)

* Congenital cysts in the spinal canal are characterized by loculated fluid collections with signal intensities similar to that of cerebrospinal fluid on both T1W and T2W techniques. They present with mass effect but show no abnormal enhancement.

With the advent of MRI, epidural hematomas are now diagnosed more readily. The extent of these lesions in the spinal canal can be accurately assessed, and the degree of compromise of the spinal canal and spinal cord compression can easily be measured. Previously reported cases of spontaneous resolution of SEH (4,6-9) document the benign natural history of this complication, even when the hematoma extends over several vertebral segments. Thus, early enthusiasm for surgical management of SEH has gradually subsided, and a more conservative approach has been adopted. These reports have shown that the parameters that favor nonsurgical treatment include stable and nonprogressive neurological deficit of a mild degree and absent or only minimal cord compression.

CONCLUSION

We present a patient who developed an epidural hematoma of the cervical canal during anticoagulant therapy. The hematoma resolved with conservative management. The authors emphasize that nonsurgical treatment is appropriate for such patients, providing that the neurological status is stable and nonprogressive.

REFERENCES

(1.) Holtas S, Heiling M, Lonntoft M. Spontaneous spinal epidural hematoma: Findings at MR imaging and clinical correlation. Radiology. 1996;199:409-413.

(2.) Beatty R, Winston KR. Spontaneous cervical epidural hematoma. J Neurosurg. 1984;61:143-148.

(3.) Duffill J, Sparrow OC, Millar J, Barker CS. Can spontaneous spinal epidural haematoma be managed safely without operation? A report of four cases. J Neurol Neurosurg Psychiatry. 2000;69:816-819.

(4.) Clarke DB, Bertrand G, Tampieri D. Spontaneous spinal epidural hematoma causing paraplegia: Resolution and recovery without surgical decompression. Neurosurgery. 1992;30:108-111.

(5.) Pear BL. Spinal epidural hematoma. Am J Roentgenol Radium Ther Nucl Med. 1972;115:155-164.

(6.) Boukobza M, Guichard JP, Boissonet M, et al. Spinal epidural hematoma: Report of 11 cases and review of the literature. Neuroradiology. 1994;36:456-459.

(7.) Saito S, Katsube H, Kobayashi Y. Spinal epidural hematoma with spontaneous recovery demonstrated by magnetic resonance imaging. Spine. 1994;19:483-486.

(8.) Lefranc F, David P, Brotchi J, De Witte O. Traumatic epidural hematoma of the cervical spine: Magnetic resonance imaging diagnosis and spontaneous resolution. Case report. Neurosurgery. 1999;44:408-411.

(9.) Kumar R, Gerber C. Resolution of extensive spinal epidural haematoma with conservative treatment. J Neurol Neurosurg Psychiatry. 1998;65:949-950.

Prepared by Athos D. Patsalides, MD, and Nicholas J. Patronas, MD, National Institutes of Health, Warren Grant Magnuson Clinical Center, Diagnostic Radiology Department, Bethesda, MD; and Anastasios Raptis, MD, PhD, Department of Internal Medicine, Section of Bone Marrow Transplantation, Rush-Presbyterian-St. Luke's Medical Center, Chicago, IL.
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Author:Patsalides, Athos D.; Raptis, Anastasios; Patronas, Nicholas J.
Publication:Applied Radiology
Article Type:Clinical report
Geographic Code:1USA
Date:Feb 1, 2006
Words:1118
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