Journal of the Neurological Sciences 284 (2009) 190–191
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Journal of the Neurological Sciences j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / j n s
Spinal epidural hematoma after intravenous thrombolysis for acute ischemic stroke Leonard L.L. Yeo, Joline Si Jing Lim, Vijay K. Sharma ⁎ Division of Neurology, Department of Medicine, National University Hospital, 5 Lower Kent Ridge Road, 119074 Singapore
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Article history: Received 25 January 2009 Received in revised form 11 April 2009 Accepted 14 April 2009 Available online 2 May 2009 Keywords: Thrombolysis Spinal hemorrhage Ischemic stroke
a b s t r a c t Intracranial bleeding is an important and dangerous complication associated with thrombolytic therapy for acute ischemic stroke. Spinal hemorrhage has been reported after systemic thrombolysis for various conditions other than acute ischemic stroke. Our patient presented with an acute ischemic stroke and showed signiﬁcant clinical recovery during intravenous thrombolysis. CT scan of the brain, performed about 6 h later due to neurological deterioration did not reveal any bleeding or a new infarction. However, an acute epidural hematoma was noted on MRI of the cervical spine. She was treated conservatively and showed a satisfactory recovery. We report, probably the ﬁrst case of spinal epidural hemorrhage after systemic thrombolysis for acute ischemic stroke. Spinal hemorrhage should be considered as a differential diagnosis for neurological worsening after intravenous thrombolysis for acute ischemic stroke, especially when the brain imaging studies do not reveal an appropriate intracranial pathology. © 2009 Elsevier B.V. All rights reserved.
1. Introduction Intravenously administered tissue plasminogen activator (IV-TPA) improves outcome in acute ischemic stroke (IS) and, remains the only approved therapeutic agent within 3 h of symptom-onset . Thrombolytic therapy may result in intracranial hemorrhage in a signiﬁcant proportion of patients. However, neither the older pivotal trial  nor the newer trial with an extended therapeutic timewindow  reported any signiﬁcant extracranial bleeding. Spinal hemorrhage after TPA therapy has been rarely , if ever, described in the literature in English language. To our best knowledge, we report probably the ﬁrst case of spinal epidural hemorrhage (SEH) after IVTPA therapy for acute IS.
2. Case report A 62-year old Chinese woman presented 80 min after right-sided weakness of sudden-onset. She did not suffer from any known cardiovascular risk factors. She was noted to be conscious with bloodpressure 140/80 mmHg, mild dysarthria and right-hemiparesis (power Medical Research Council-MRC grade 3) with National Institute of Health Stroke Scale (NIHSS) of 8 points. An emergently performed unenhanced computed tomography (CT) of the brain did not show any bleeding. With no contraindications, thrombolytic therapy with IV-TPA in standard dose (0.9 mg/Kg body-weight) was initiated at 120 min after symptomonset. She showed clinical improvement and NIHSS decreased to 4 points by the end of TPA infusion. ⁎ Corresponding author. Tel.: +65 67724126; fax: +65 68723566. E-mail address: [email protected]
(V.K. Sharma). 0022-510X/$ – see front matter © 2009 Elsevier B.V. All rights reserved. doi:10.1016/j.jns.2009.04.016
Her blood-pressure remained within the recommended range. About 6 h later, she complained of sudden severe pain in her right shoulder and deteriorated neurologically (power in right-extremities MRC grade 1 and NIHSS 11 points). No intracranial bleeding was seen on the repeated brain CT. CT angiography of the aorta and its major branches, performed in view of severe shoulder and upper back pain, did not show any evidence of arterial dissection. Subsequent magnetic resonance imaging (MRI) of the brain revealed a small acute infarction in left pons. MRI of the cervical spine, performed next day, revealed an epidural hematoma at C4–C7 level with cord edema (Fig. 1). Since her shoulder pain had subsided and some neurological improvement (power MRC grade 3 and NIHSS 6 points) was noted, we decided against any surgical intervention. Upon further evaluation, she denied any history of neck pain or injury in the recent past. Her platelet count (264,000 /µL), prothrombin time (13 s), activated partial thromboplastin time (32 s) and ﬁbrinogen (274 mg/dL) levels were within normal limits. No antithrombotic agents were started. She continued to show gradual improvement and MRI of the cervical spine performed on day 6 conﬁrmed partial resolution of the SEH. Upon discharge on day 7, she was able to walk with a stick (NIHSS 3 points).
3. Discussion We report a case of SEH as a complication of IV-TPA thrombolysis in acute IS. To the best of our knowledge, such phenomenon has not been described previously in the literature. SEH is a relatively rare condition that usually occurs in patients with coagulopathies or hematological abnormalities , undergoing anticoagulation  or after thrombolytic therapy . SEH has been reported after thrombolysis for myriad reasons such as myocardial
L.L.L. Yeo et al. / Journal of the Neurological Sciences 284 (2009) 190–191
Fig. 1. Neuroimaging features after systemic thrombolysis. Saggital MRI of the cervical spine shows acute epidural hematoma on T1 (1A) and T2-weighted sequence (1B) extending from C4 to C7 vertebral levels. MRI of the brain showed a small acute infarction in left pons (1C). Epidural hematoma appears hypointense on gradient echo (1D). Axial sections on T1-weighted (1E) sequences demonstrate displacement of the spinal cord (marked S). T1-weighted axial MRI of the cervical spine (taken at the same level as 1E) repeated after 5 days shows partial resolution of the hematoma as well as the changes in its magnetic properties (1F).
ischemia, pulmonary embolism etc. However, we could not ﬁnd any published report of SEH after thrombolysis for acute IS. Signiﬁcantly lower dose of thrombolytic agent used in IS as compared to other indications could be responsible for this observation. Closest to our case is a report by Kim et al of an acute IS patient with spinal bleeding after thrombolysis . However, unlike our case, their patient developed bleeding in the subdural space. Our patient did not sustain any fall or injury to the neck, denied any neck problems in past and did not show any demonstrable coagulopathy. Therefore, systemic thrombolysis for acute IS appears as the most likely etiology. SEH, considered to be the commonest variety of spinal hematomas , usually presents acutely with back pain, pain in a radicular distribution or signs of cord compression. Prognosis in such cases is usually determined by the severity of initial neurological deﬁcits. MRI is considered as the imaging modality of choice as it can help in establishing the age of SEH also. In acute phase, CT scan can demonstrate the dura mater as pushed towards spinal cord and differentiate “hyperdense-hematoma” from “hypodense-surrounding fat”. However, the yield decreases in subacute phase as the hematoma tends to become isodense and less clearly demarcated . Management of SEH is conservative if the neurological impairment is subtle and patient does not deteriorate . Surgical decompression is indicated in patients with severe deﬁcits or rapid deterioration and an early intervention is associated with better outcomes . In our patient, pain in the right shoulder subsided rapidly and she showed rapid resolution of neurological deﬁcits, therefore we opted for the conservative measures. It is prudent to monitor the hematoma with repeat MRI scans in patients treated conservatively . Our patient
showed resolution of hematoma as well as the cord edema on a repeat MRI scan. In conclusion, we report spinal epidural hematoma as an unusual complication of systemic thrombolysis for acute ischemic stroke. Spinal epidural hematoma may be considered as a differential diagnosis for the neurological worsening in some cases after IV-TPA therapy for acute IS, especially when the brain imaging studies do not reveal an appropriate intracranial pathology. References  The National Institutes of Neurological Disorders and Stroke rt–PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995;333: 1581–7.  Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 h after acute ischemic stroke. N Engl J Med 2008;359:1317–29.  Kim SH, Choi SH, Song EC, Rha JH, Kim SR, Park HC. Spinal subdural hematoma following tissue plasminogen activator treatment for acute ischemic stroke. J Neurol Sci 2008;273:139–41.  Groen RJM, Ponssen H. The spontaneous spinal epidural hematoma: a study of the etiology. J Neurol Sci 1990;98:121–38.  Bamford CR. Spinal epidural hematoma due to heparin. Arch Neurol 1987;35:693–4.  Sawin PD, Traynelis VC, Follett KA. Spinal epidural hematoma following coronary thrombolysis with tissue plasminogen activator. Report of two cases. J Neurosurg 1995;83:350–3.  Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev 2003;26:1–49.  Post MJ, Becerra JL, Madsen PW, et al. Acute spinal subdural hematoma: MR and CT ﬁndings with pathologic correlates. AJNR Am J Neuroradiol 1994;15:1895–905.  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;69:816–9.