Delayed Diagnosis of Acute Spontaneous Spinal Epidural Hematoma 333 Fig. 6. Operative finding: The spinal cord is compressed by hema- toma and blood clot. No other vascular abnormality. sory loss. His physician ordered MRI. MRI scan showed an epidural hematoma with spinal cord compression from T11 to L2 (Fig. 4, 5). His physician consulted department of ortho- pedic surgery. At 24 hr after symptom onset, we examined the neurologic status. The patient’s neurologic status showed a complete motor loss except a right iliopsoas muscle power trace, L1-2 dermatome hypesthesia, L3 below dermatome anesthesia, perianal sense (-), patella tendon reflex (-/-), and ankle jerk (-/-). His coagulation profiles showed PT: 1.3 (0.9- 1.10 INR), aPTT: 34.8 (28-40 sec). We performed the bilat- eral decompressive laminectomy from T 12 to L2 immedi- ately. A large posterolateral hematoma was found within the epidural space (Fig. 6). Postoperative MRI shows extended dural sac and cord but no neurologic improvement was noted after surgery. On follow-up 12 months, his neurologic status showed a complete motor loss except the right iliopsoas, quadriceps, tibialis anterior muscle power trace, no sensory recovery, no bladder function, and no deep tendon reflex. DISCUSSION Spontaneous spinal epidural hematoma occurs infrequently. Approximately 350 cases have been reported in the medical literature, and the annual incidence has been estimated at 0.1 per 100,000. Predisposing factors such as inherited coag- ulopathy, spinal vascular malformation, anticoagulant thera- py, therapeutic thrombolysis, and epidural analgesia, have been implicated, along with hypertension and antiplatelet therapy (1, 2). The clinical course is characteristic: without preceding trauma, patients experience an acute onset of local discomfort or pain, sometimes with radicular paresthesia. Within hours, signs of spinal cord compression appeared, and paraplegia and loss of sensory function progress. Despite the clinical syndrome of SSEH is relatively characteristic, its exact diagnosis may be difficult. Differential diagnosis includes spinal abscess, tumor, ischemia, transverse myelitis or acute vertebral disc disease (3). Because the results of operative decompression of the spinal cord mainly depend on the duration of the symptoms, the time lost for diagnostic measures may have negative influ- ence on the functional outcome. Therefore, immediate neu- roradiologic confirmation of the clinical diagnosis is neces- sary. Currently, MRI has been used as the first choice of diag- nostic method for spinal emergencies because it allows rapid evaluation of large parts of the vertebral column and the spinal cord. The prognosis of neurologic deficits predominantly depends on the time interval between the onset of symptoms and the surgical decompression (2-6). In our patients, surgery was delayed because patient and physician made light of symp- tom. So the preoperative neurologic status was aggravated, and unfortunately as a result no improvement of symptom showed. Both the patient and the doctor should not take early, but mild, signs lightly which may result in delayed diagno- sis, like our two cases. In SSEH, the small signs such as minor pain and slight discomfort appear, followed by rapid neuro- logical disorder, thus, these small signs should be considered prudently and immediately carry out MRI to make quick and accurate diagnosis before the patient’s neurological state is aggravated. The prognosis appears to be related to the severity of the preoperative neurologic deficit and early operation for rapid decompression of the spinal cord is crucial. Lawton et al. (7) confirmed the relationship between neurologic recovery, the timing of surgery (operation time) and the preoperative neurological status. They showed functional recovery to cor- relate inversely with the duration of spinal cord compression and the degree of severity. Our patients’ symptoms evolved rapidly and by the time of surgical decompression, 24 hr after onset, he was completely paraplegic. There was no postopera- tive improvement. There is a evidence to suggest that func- tional recovery might have been better if the preoperative deficit was less severe. Surgery performed more than 12 hr after symptom onset is unlikely to be successful (6). Immediate drainage is recom- mended by most surgeons. In our patients, no improvement in the neurologic status was seen after surgery. We thought that this unsuccessful result was due to the complete paraple- gia preoperatively which was caused by delayed diagnosis. The time interval between onset of symptoms and surgery is determined by how long it takes for a patient to recognize symptoms and enter into the medical system, and how long it takes for the physicians to recognize clinical signs and obtain radiological studies. Although physicians can do nothing about the patient’s response time, they can accelerate the diag-