Concurrent spontaneous spinal and tentorial subdural hematomas in an older patient receiving anticoagulation treatment: a case report

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J Korean Soc Geriatr Neurosurg. 2025;21(2):90-93

Publication date (electronic) : 2025 October 29

doi : https://doi.org/10.51638/jksgn.2025.00108

Joo Hyung Shin¹, Hyung Cheol Kim^,2

¹Department of Neurosurgery, Bundang Jesaeng Hospital, Seongnam, Korea

²Department of Neurosurgery, Jiwoo Hospital, Seongnam, Korea

Corresponding Author: Hyung Cheol Kim, MM Department of Neurosurgery, Jiwoo Hospital, 183 Sujeong-ro, Sujeong-gu, Seongnam 13290, Korea Tel: +82-31-756-8355; Fax: +82-31-756-5455; E-mail: ns.kimhc@gmail.com

Received 2025 August 19; Accepted 2025 September 22.

Abstract

Introduction

Spinal subdural hematoma (SDH) is a rare clinical entity, and its concurrent manifestation with intracranial SDH is exceptionally rare. These hematomas may occur due to trauma, medical procedures, or spontaneously [1,2]. Spontaneous SDHs are typically associated with vascular malformations or coagulation disorders, particularly in patients receiving anticoagulation therapy [3,4]. While spinal SDH alone is uncommon, its coexistence with intracranial SDH further complicates diagnosis and management [1,5]. The presence of simultaneous hemorrhagic lesions in both spinal and intracranial compartments poses a diagnostic challenge and raises concern regarding the underlying pathophysiology and systemic bleeding tendency.

While several reports have described concomitant spinal and intracranial subdural hematomas, most involved younger or trauma-related cases. To our knowledge, few cases have been documented in elderly patients with chronic anticoagulation therapy and thrombocytopenia. This makes our case particularly relevant for geriatric neurosurgical practice.

Case Report

A 70-year-old woman presented to the neurology outpatient clinic with a one-month history of persistent bilateral buttock and posterior calf pain. The pain was radiating and dull in nature, without sensory deficits or weakness. She denied any history of trauma, fever, or systemic illness. Initially, she was diagnosed with peripheral artery occlusive disease and received medical treatment, which was ineffective.

Her past medical history included mitral valve replacement 27 years ago and a diagnosis of left atrial thrombus three years earlier, for which she was maintained on long-term warfarin therapy. On admission, laboratory tests showed prothrombin time (international normalized ratio, INR) 2.07, activated partial thromboplastin time 43.7 seconds, and a platelet count of 69,000/μL, indicating a bleeding tendency [3]. The patient did not exhibit any signs of altered consciousness, cranial nerve deficits, or bowel and bladder disturbances.

Lumbar spine magnetic resonance imaging (MRI) revealed a SDH from L1 to S1 (Fig. 1). Additional brain imaging, including computed tomography (CT), revealed a tentorial subdural hematoma (Fig. 2). There were no signs of mass effect or midline shift. Due to the high risk of thromboembolic events from the existing left atrial thrombus, complete cessation of anticoagulation was not advisable. Therefore, warfarin was discontinued and replaced with subcutaneous enoxaparin as bridging therapy.

Fig. 1.

Lumbar spine magnetic resonance imaging, with sagittal T2- and T1-weighted images showing a crescent-shaped subdural hematoma extending from L1 to S1 (arrows). The lesion is located in the dorsal subdural space without significant cord compression.

Fig. 2.

Brain computed tomography: axial image demonstrating a tentorial subdural hematoma (arrows) along both tentoria cerebelli. No evidence of midline shift or mass effect was observed.

The patient was managed conservatively with close clinical and radiological monitoring during hospitalization. Bed rest was advised, and analgesics including acetaminophen and tramadol were administered as needed. She was monitored daily for any neurological deterioration. Ten days later, follow-up brain CT and lumbar MRI showed near-complete resolution of both spinal and intracranial SDHs (Figs. 3, 4). The patient's pain significantly improved, and no new neurological symptoms were observed.

Fig. 3.

Follow-up lumbar spine magnetic resonance imaging, with sagittal T2- and T1-weighted images obtained 10 days later, showing near-complete resolution of the subdural hematoma (arrows).

Fig. 4.

Follow-up brain computed tomography: axial image obtained 10 days later demonstrating marked resolution of the tentorial subdural hematoma (arrows).

Enoxaparin was then discontinued, and warfarin therapy was resumed under close INR monitoring. The patient was discharged with outpatient follow-up scheduled at regular intervals. During a two-month follow-up, there was no recurrence of symptoms or reformation of hematoma. She regained full mobility and was able to return to her normal daily activities.

Discussion

Spontaneous concurrent spinal and intracranial subdural hematomas are exceedingly rare, with only a few cases reported in the literature [1,3,4]. Most spinal SDHs occur secondary to trauma, lumbar puncture, or spinal surgery [2,6]. Spontaneous cases are usually related to coagulation abnormalities or anticoagulation therapy [3,4]. Our patient was particularly vulnerable due to multiple synergistic risk factors, including advanced age, long-term warfarin use, and thrombocytopenia. These conditions likely contributed to vascular fragility and an increased tendency for bleeding. Previous reports have also noted the role of reduced vascular compliance in elderly patients, which may predispose to vessel rupture even in the absence of trauma.

The pathophysiology of simultaneous spinal and intracranial SDH remains unclear. Several mechanisms have been proposed, including migration of hematoma through the subdural space along the neuraxis, intracranial pressure shifts leading to rupture of bridging veins, and independent multifocal bleeding events [2,6,7]. In anticoagulated patients, these mechanisms may be amplified by impaired hemostasis. In our case, the coexistence of both lesions in the setting of anticoagulation therapy and thrombocytopenia supports a systemic bleeding predisposition rather than a localized vascular abnormality.

Recent literature continues to underscore the rarity of concurrent intracranial and spinal SDH. Chu et al. [1] reported a case of concurrent spinal and intracranial SDHs presenting with back pain, managed conservatively. Kim et al. [3] also described a spontaneous intracranial and spinal SDH with favorable outcome. Kwon et al. [2] presented a migration phenomenon of intracranial SDH into the spine. Kokubo et al. [7] prospectively evaluated the association of lumbar and cranial SDHs, supporting the migration hypothesis. Our case aligns with these reports but is distinct in involving an elderly patient with thrombocytopenia and a high thromboembolic risk, successfully treated conservatively without surgical intervention.

The clinical presentation of spinal SDH is variable, ranging from isolated radicular pain to acute paraplegia or sphincter dysfunction [6]. Our patient presented only with radicular pain, which delayed the initial suspicion of a spinal hemorrhage. This underscores the importance of maintaining a high index of suspicion in elderly patients on anticoagulation therapy who present with atypical spinal symptoms.

The management of concurrent SDH must be individualized. Surgical decompression is warranted when there is evidence of rapid neurological deterioration or cord compression [8]. However, in the absence of neurological deficits, conservative management may be appropriate [1,3,4,7]. In our patient, the decision to avoid surgery was based on her stable neurological status and the need to maintain anticoagulation due to the presence of a left atrial thrombus. Warfarin was temporarily discontinued and replaced with low-molecular-weight heparin, which allowed hematoma resolution while minimizing thromboembolic risk. Her favorable outcome highlights the effectiveness of individualized, conservative management in selected elderly patients. Informed consent was obtained from participant included in this study.

Conclusion

In elderly patients receiving anticoagulant therapy, new-onset spinal pain may represent an underlying SDH, which can rarely coexist with intracranial SDH. Prompt imaging evaluation and recognition of this association are critical for timely diagnosis. Our case demonstrates that in the absence of neurological deficits, conservative management with tailored anticoagulation adjustment can lead to favorable outcomes. Clinicians should maintain high vigilance for this rare but clinically significant condition in anticoagulated geriatric populations.

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