# Massive Acute Spinal Subdural Hematoma Causing Sudden Onset Paraplegia in a Patient on Anticoagulation

Authors: Jacob Kosarchuk; Courtney Lewis; Martin H. Pham
Journal: Case Reports in Surgery
 (2020)

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## Abstract

Spinal subdural hematoma (SSDH) is a rare but known entity that can cause severe and irreversible motor, sensory, and autonomic dysfunction if not decompressed in a timely manner. We present here a 74-year-old female on anticoagulation who developed sudden onset back pain with rapidly progressive paraplegia. On neurologic exam, she was completely flaccid in the bilateral lower extremities with absent sensation from the umbilicus down. Imaging demonstrated a massive extra-axial spinal hematoma from T12 to S1 that initially was believed to be epidural in origin. She was taken emergently to the operating room for a T11-L5 decompressive laminectomy, and dural opening demonstrated a thick subdural clot encasing the conus and cauda equina confirming the subdural pathology. Despite decompression and partial evacuation of the subdural hematoma, she did not recover neurologic function.


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## Body

## 1. Introduction

Spinal subdural hematoma (SSDH) is a rare but known entity that can cause severe and irreversible sensorimotor and autonomic dysfunction if not decompressed in a timely manner [1–4]. We report here a case of a massive thoracolumbar SSDH in the setting of therapeutic anticoagulation causing acute-onset paralysis.


## 2. Literature Search

A literature search was performed to determine if SSDHs of this size and severity of symptoms were reported elsewhere. We searched PubMed using the terms “spinal subdural hematoma,” “massive spinal subdural hematoma,” “acute spinal subdural hematoma,” with the qualified “AND anticoagulation,” “AND warfarin,” “AND heparin,” “AND aspirin,” “AND apixaban,” “AND rivaroxaban,” “AND dabigatran,” with article-type filters for case reports, clinical studies, clinical trials, comparative studies, observational studies, reviews, and systematic reviews. We also performed reviews of citations within articles we found. Our initial search yielded 1,066 articles. After filtering for atraumatic or nonprocedural SSDH, we found 202 articles. Those that did not reference an anticoagulant in the title or body of the article were excluded, leaving a total of 24 articles.


## 3. Case Report

We present here a 74-year-old female on anticoagulation who developed sudden onset back pain and rapidly progressive flaccid paraplegia. On neurologic exam, she was completely flaccid in the bilateral lower extremities with absent sensation from the umbilicus down. Magnetic resonance imaging (MRI) demonstrated a massive ventral spinal subdural hematoma from T12 to S1 (Figure1). Due to these findings, she was taken emergently to the operating room for decompression and evacuation.Figure 1
T2-weighted MRI of the lumbar spine demonstrating ventral hypointensity relative to CSF, compressing the conus and cauda equina.


## 4. Operation

A T11-L5 laminectomy was performed for complete epidural decompression. Dural opening demonstrated a thick subdural clot encasing the conus and cauda equina (Figure2). A partial evacuation was performed focusing on the proximal hematoma at the spinal cord and conus; the rest of the clot distal at the cauda equina was partially removed with a combination of direct evacuation and irrigation due to the difficult consistency of the clot encasing the cauda equina roots.Figure 2
Operative microscope views of the dorsal thoracolumbar spinal dura. Note the mottled appearance of the dural sac (a). Opening of the dural sac (b, c) demonstrates thick clotted blood intradurally. The massive volume of the subdural blood has filled the intradural space and obliterated all egress of cerebrospinal fluid (d).
(a)(b)(c)(d)


## 5. Postoperative Course

Postoperatively, she did not have any recovery of strength or sensation. She was monitored as an inpatient for 3 days and subsequently discharged to an acute rehabilitation center. At six months follow-up, there has been no recovery of neurologic function.


## 6. Literature Review Results

Our review of the literature resulted in 202 articles discussing atraumatic and nonprocedural iatrogenic SSDH. They included case reports, reviews on management of SSDH, and reviews on imaging diagnosis of SSDH. We found 24 case reports on SSDH in patients who had been anticoagulated (Table1). There was an even distribution of male and female patients (12 males and 12 females) found in this literature review, and the average age was 63.06 years with a range of 38 to 80 years old (Table 2). The majority of patients in the series had atrial fibrillation as a comorbidity (15/24), with others including stroke (2/24), cardiovascular and disease (3/24), venous thromboembolism (2/24), cardiac valve replacement (2/24), and other (1/24). 2/24 were on low molecular weight heparin (LMWH), 4/24 were on aspirin (in combination therapies), 10/24 were on warfarin, 2/24 were on clopidogrel, 1/24 was on ticlodipine, 3/24 were on apixaban, 4/24 were on rivaroxaban, and 1/24 was on dabigatran. 13/24 patients had multilevel or diffuse SSDH, 9/24 were confined to the thoracic region and 1/24 to the lumbar region, and none had purely cervical or sacral SSDH. 19/24 had no associated subarachnoid hemorrhage (SAH), 4/24 had definite SAH, and 1/24 had indeterminate SAH. 5/24 patients did not improve, 13/24 partially improved, 5/24 fully recovered, and 1 patient died of a cardiac arrest. 16/24 patients received operative intervention, and 8/24 received conservative treatment (including the patient that died). Of the patients that did not improve, all 5 underwent surgical intervention. 10/13 in the partial improvement had surgery compared to 3/13 who were managed conservatively. 4/5 patients who fully recovered were managed conservatively, and 1/5 was operated on.Table 1
Results and summary of the case reports identified in the literature search.
Patient characteristicsSexMaleFemale1212AgeAverageMinMax63.063880ComorbiditiesA-fibStrokeCVDPE/DVTValve replacementOther1523221Agent usedLMWHASAWarfarinClopidogrelTiclodipineApixabanRivaroxabanDabigatran241021341Location of bleedCervicalThoracicLumbarSacralMultilevel091013Associated SAHYesNoIndeterminate1941InterventionOperativeNonoperative168RecoveryNo improvementSome improvementFull recoveryDeath51351Recovery vs. interventionNo improvementSome improvementFull recoveryDeathOpNon-OpOpNon-OpOpNon-OpOpNon-Op501031401Table 2
Characteristics of patients in the literature review.
Author and yearAge (years)SexLocationPresenting symptomsAnticoagulant/antiplateletRisk factorsSAHTreatmentOutcomeMiller 200467MT11-S1Progressive loss of sensation, bilateral leg weakness, back pain, urinary retentionWarfarinAtrial fibrillationNoneT10-L2 laminectomyNo recoveryCha 200572FT3-T6Bilateral lower extremity paraplegia, sensory loss, urinary retention, back painLMWH, ASALaryngeal cancer, NSTEMINoneT3-T5 laminectomyMinimal recoveryChau 200852MC7-L1Bilateral lower limb weakness, decreased lower extremity sensation, bowel and bladder dysfunctionLMWHSalmonella typhi, reactive arthritis, type II diabetesNoneT11-T12 laminectomyPartial recoveryBadge 200978FT3-T12Nausea, giddiness, headache, back pain, progressive L lower extremity weakness and ataxiaWarfarinAtrial fibrillationNoneT5 laminectomyImprovedMete 201042MT6-L5Sudden headache and backache, agitation, paraparesis, meningismusWarfarinCardiac pacemaker, h/o cardiac bypassYesConservativeDeath (cardiac arrest)Payer 201059MT2-T9Left-dominant paraparesis below T8, weakness, sphincter dysfunctionASA, clopidogrelCardiac stentingNoneConservativeFull strength recovery at 1 year, improvement in ataxia, paresthesia, urge incontinenceWang 201267FL4-S1Back pain, bilateral radiating leg pain, bifrontotemporal headache, bilateral lower extremity weakness and numbnessASA, clopidogrelAtrial fibrillation, concomitant SDHNoneConservative (SSDH), burr hole craniotomy (SDH)Full recovery at 1 yearBruce-Brand 201376ML1-L4Sudden onset severe low back pain, lower extremity weaknessWarfarinAtrial fibrillation, type II diabetes, HTN, dyslipidemiaNoneT12-L4 laminectomyPartial recovery at 6 monthsCastillo 201569MT3-conusBack pain, bilateral lower extremity paraplegia, bowel and bladder dysfunctionRivaroxabanAtrial fibrillationNoneCervical and lumbar drainsNo recovery at 6 monthsDargazanli 201572MT6-T8Interscapular back pain, rapidly progressive bilateral lower extremity paraplegia, decreased lower extremity sensation to pain and temperature L > RRivaroxabanAtrial fibrillationNoneT6-T8 laminectomyNo improvement at 6 monthsFrioui 201565FT12-L1Back pain, paraparesis, urinary retentionUnclear anticoagulantAtrial fibrillation, HTNNoneConservativeNeurological recovery observed at 24 h. Persistent urinary retention at 1 yearJung 201553FC7-T6Sudden onset headache, nausea, vomiting, meningismus, bilateral lower extremity sensory loss and weakness, back painWarfarinAortic valve replacementYesC7-T6 laminectomyImprovement in anal tone and bladder functionZaarour 201558MC7-T2Interscapular back pain, progressive bilateral lower extremity weakness and numbnessRivaroxabanAtrial fibrillation, type II diabetes, HTN, dyslipidemia, recent THA with spinal anesthesiaNoneInitially conservative, C7 corpectomy at HD4ImprovedSiasios 201638FDiffuseSevere neck and back painWarfarinRecent C-section, PENoneConservativeFull recovery at dischargeWolfe 201767MCervicothoracicLeft lower extremity weakness, urinary retentionDabigatranAtrial fibrillation, endocarditis, PCKD s/p transplant, BPH, OSA, melanomaYesConservativeFull recovery in 2 daysAkiyama 201771MT7-S12 weeks history bilateral lower leg pain, dysesthesia, paraparesis, urinary disturbance, and feverTiclodipineL cerebral infarct, unruptured L MCA aneurysmsNoneL3-L4 laminectomyImprovedBunevicius 201768MT2-T6Left-sided chest and back pain, L leg weakness, and R leg numbnessWarfarinAtrial fibrillationNoneT3-T6 hemilaminectomyPartial improvementBang 2018Middle agedFThoracolumbarLower extremity weakness after assault∗∗RivaroxabanAtrial flutterNoneLaminectomyNo improvementColell 201875FDiffuseBilateral lower extremity weakness L > R, decreased sensationApixabanAtrial fibrillation, HTNNoneLaminectomyImproved at 6 monthsGirithari 201857FT4-T8Back pain, headache, vomiting, bilateral lower extremity weakness, urinary retentionWarfarinDVTNoneLaminectomyNo improvement at 6 monthsMchaourab 201868MT1-T5Back pain, urinary retention, headache, neck stiffness, vomiting, bilateral limb weakness, and ataxiaApixabanAtrial fibrillationPossibleConservativePartial improvementArain 201980FT4-T9Bilateral lower extremity paraplegia, incontinenceWarfarinAtrial fibrillationNoneT3-T11 laminectomyPartial improvementArdebol 201967FT4-T7Back pain, progressive bilateral lower extremity paraplegia, bowel and bladder dysfunctionApixabanAtrial fibrillationNoneT4-T7 laminectomyFull recovery at 1 yearWeiner 201942FL1-S1Vaginal pain, back pain radiating down the right leg, left leg weakness, frontal headacheWarfarin, ASARheumatic heart disease, mechanical mitral valve, CVA, concomitant SDH, concomitant arachnoiditisYesCraniotomy for SDH, conservative for SSDHFull recovery at 1 month


## 7. Discussion

We present the case of a massive spinal subdural hematoma in an elderly female on anticoagulation causing severe back pain and rapid-onset paraplegia. SSDH as an entity has been previously described, including in association with anticoagulation. We report here a unique case of a massive thoracolumbar SSDH that initially was believed on radiological review to be a ventral epidural hematoma in origin.Spontaneous spinal subdural hematoma (sSSDH) is a rare cause of back pain, paraplegia, and cauda equina syndrome and should be considered in a patient who is on anticoagulation, and no other precipitating events are identified [3]. The average age of patients in this case series was 63.06 years (note—one study simply reported the age as “middle aged”), which is similar to a recent study by Pereira et al. but differs from other older studies [3, 4]. We found an even distribution of males (50%) and females (50%) in this case series, which is similar to previously reported rates [1, 4]. The majority of patients in this series were on warfarin [5–14], which could be due to a higher rate or longer duration of warfarin use compared to newer novel oral anticoagulants (NOACs) and not necessarily due to the agent itself, though studies have shown lower rates of (unspecified) major bleeding events with NOACs [15–23]. We identified fewer patients on other agents (including antiplatelet therapies) that developed SSDH [14, 24–28].SSDHs are often associated with coagulopathies (iatrogenic or related to impaired innate hemostasis mechanisms) and procedural iatrogenic causes, though there is still a significant amount of SSDHs secondary to arteriovenous malformations, trauma, and idiopathic causes [3, 4, 6]. The pathophysiology of spontaneous SSDH is still unclear but is theorized to be caused by bleeding within the subdural space itself or as an extension of a subarachnoid bleed into the subdural space after an increase in intrathoracic or intra-abdominal pressure [1, 3]. Indeed, there have been cases of concomitant SAH and SSDH [7, 9, 14, 18, 21]. Important prognostic factors include neurologic status at presentation, presence of coagulopathy, performance of lumbar puncture, and associated diseases [4]. Interestingly, extension of hematoma, surgery, and presence of SAH were not found to be significant predictors of outcome.MRI is considered the gold standard in the diagnosis of SSDH, but digital subtraction angiography may be useful if spinal AVM is suspected [2]. SSDH can be managed conservatively with medical management (often including steroids), percutaneous drainage, and surgical evacuation [3, 29]. Though the literature suggests that conservative management results in better outcomes, this may be related to bias in choosing patients with less severe symptoms for medical management whereas more impaired patients are selected for surgical intervention [4].


## 8. Conclusion

SSDH is a rare but serious cause of rapid-onset back pain, sensorimotor, and autonomic deficits, and in some cases, mortality. It is often associated with iatrogenic causes including anticoagulation (as in this case) but in some instances may be idiopathic. MRI is the gold standard for diagnosis. Patients with mild or moderate symptoms can be managed conservatively, but urgent surgical decompression and clot evacuation are warranted in patients with severe symptoms to prevent permanent neurologic injury or death.



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