(a) Cervical spine T1-weighted MRI, (b) cervical spine T2-weighted MRI, (c) thoracic spine T1-weighted MRI, (d) thoracic spine T2-weighted MRI. Long arrows = epidural hematoma, short arrows = spinal cord infarction d c 

(a) Cervical spine T1-weighted MRI, (b) cervical spine T2-weighted MRI, (c) thoracic spine T1-weighted MRI, (d) thoracic spine T2-weighted MRI. Long arrows = epidural hematoma, short arrows = spinal cord infarction d c 

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Spinal epidural hematomas are rare conditions. Although the exact cause remains unknown in up to 40% of cases, anticoagulation therapy, neoplasm, thrombolytic therapy, internal jugular vein thrombosis, and prolonged Valsalva maneuvers associated with pregnancy may be contributing factors. The source of bleeding appears to be the dorsal internal ver...

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... the patient's mental status improved on posttransplant day 10, it became clear that she was plegic in both lower extremities. Magnetic resonance imaging (MRI) of the cervical, thoracic, and lumbar spine [ Figure 1] demonstrated epidural hematoma located dorsally at the foramen magnum, and both ventrally and dorsally from C7 to T6. The hematoma was hyperintense on both T1-and T2-weighted sequences, consistent with extracellular methemoglobin (late subacute hemorrhage, >7 days). ...

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... Most cases of acute SEDH have a multifactorial etiology, including old age, uncontrolled arterial hypertension, congenital and acquired coagulopathies, platelet dysfunction or even anti-platelet medication (aspirin, clopidogrel) [14], anticoagulants [15], [16], vascular malformations, tumors, spinal surgery or spinal procedures (lumbar punctures, epidural anesthesia) [10], [17], severe hepato-renal comorbidities (cirrhosis, liver transplantation, hemodialysis) [10], [17], even intense efforts implying sustained Valsalva maneuvers (intense efforts, lifting heavy weights [8], childbirth). ...
... Most cases of acute SEDH have a multifactorial etiology, including old age, uncontrolled arterial hypertension, congenital and acquired coagulopathies, platelet dysfunction or even anti-platelet medication (aspirin, clopidogrel) [14], anticoagulants [15], [16], vascular malformations, tumors, spinal surgery or spinal procedures (lumbar punctures, epidural anesthesia) [10], [17], severe hepato-renal comorbidities (cirrhosis, liver transplantation, hemodialysis) [10], [17], even intense efforts implying sustained Valsalva maneuvers (intense efforts, lifting heavy weights [8], childbirth). ...
... In rapid deterioration of the neurological status the most appropriate management is emergency decompressive hemilaminectomy and hematoma evacuation [17]. ...
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Introduction: Epidural hematoma has a double anatomopathological topography: intracranial and/ or spinal. Its etiology is complex: post-traumatic (spinal trauma, or lumbar puncture), iatrogenic (secondary to an inadequate anticoagulation or antiplatelet treatment), congenital or acquired disorders of coagulation (leukemia, hepatic cirrhosis), secondary to intense Valsalva maneuvers (e.g. during labor, or an intense physical effort), and idiopathic. The purpose of this article is to present a clinical case of acute spinal epidural hematoma (SEDH) with atypical clinical picture and a puzzled pathophysiological mechanism, and also a brief review of the relevant literature. Case presentation: An 80-years-old male patient, with locomotor disability (bilateral congenital foot deformity), and multiple cardiovascular comorbidities (chronic atrial fibrillation (AF), dilated cardiomyopathy and contractile dysfunction (chronic heart failure, with left ventricle ejection fraction 40 %), chronically anticoagulated with a vitamin K antagonist (acenocumarol). The elderly submitted a body-level fall without cranial trauma, event followed by a short loss of consciousness (without convulsions or sphincter relaxation). He suffered a low-energy cervical fracture (C7 vertebral injury) and a posterolateral acute SEDH at C3-Th2 vertebral levels. Decompressive hemilaminectomy at the C4-Th2 levels and evacuation of the SEDH, was performed during the early sub-acute phase. The patient was transferred in our rehabilitation clinic as C4 AIS-C tetraplegia (global motor score 50/100), neurogenic bladder and bowel, with post surgical wound dehiscence (healed per secundam). The subject had a favorable neurological evolution and was discharged as C7 AIS-D tetraplegia (global motor score 81/100). Discussion: The case particularity consists in a puzzled etiopathogenetic mechanisms and difficulty to accurately indicate the chronological chain of events generating the acute SEDH. An overdosed anticoagulant therapy might be incriminated as an iatrogenic cause for a “spontaneous” SEDH, but most probably its etiology is complex, probably traumatic, consequence of the cervical spine fracture due the low-intensity biomechanical impact. The complex predisposing circumstances to accidental fall in our elderly patient were due to the: - impaired, unstable locomotor function, secondary to his bilateral congenital clubfoot deformity / disability - chronic AF, contractile dysfunction and hypodiastolic phenomena, with cardiogenic syncope and global brain ischemia or transient ischemic cerebral attack. Despite the good immediate outcomes, his future functional prognosis might be poor, due to the advanced age, severe cardiovascular pathology and the complex disturbances of the neuro-myo-artro-kinetic apparatus (major impediments of the somatic / body functions and structure). This health-related condition had severe repercussions on the subject`s activity (related to tasks and basic activities of daily living) and participation, affecting the outcome of rehabilitation, and his quality of life. Conclusions: Clinicians should consider the remote risk of SEDH (even with atypical clinical presentation) in patients with AF and anticoagulant medication. Despite a postponed decompressive intervention (imposed by the severe comorbidities), our patient neurologically improved without recurrence, following a complex neurorehabilitation program.
... Several factors contribute to the genesis of a spinal hematoma, such as vascular malformations, coagulopathies, thrombolytic drug administration, tumors, autoimmune diseases, pregnancy, excessive exercise, previous epidural anesthesia, cardiac surgery, and lumbar puncture. [2,[4][5][6][7][8]10,12,16,[18][19][20]22,23,25,[28][29][30]33,34,36] This type of lesion indiscriminately affects both sexes, all ethnicities, and all age groups. [1,3,[15][16][17]23,31] Clinical symptomatology varies from pain to sensory and/or motor deficits, hemiparesis, Brown-Séquard syndrome, incomplete or complete spinal cord syndrome, as well as cauda equina syndrome. ...
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Background: Iatrogenic or spontaneous spinal hematomas are rarely seen and present with multiple symptoms that can be difficult to localize. Most spontaneous spinal hematomas are multifactorial, and the pathophysiology is varied. Here, we present a case of a scattered, multicomponent, combined subdural and epidural spinal hematoma that was managed conservatively. Case Description: A 38-year-old woman came to the emergency department (ED) complaining of severe neck and back pain. She had undergone a caesarean section under epidural anesthesia 4 days prior to her arrival in the ED. She was placed on heparin and then warfarin to treat a pulmonary embolism that was diagnosed immediately postpartum. Her neurological examination at presentation demonstrated solely the existence of clonus in the lower extremities and localized cervical and low thoracic pain. In the ED, the patient′s international normalized ratio was only mildly elevated. Spinal magnetic resonance imaging revealed a large thoracolumbar subdural hematoma with some epidural components in the upper thoracic spine levels. Spinal cord edema was also noted at the T6-T7 vertebral level. The patient was admitted to the neurosurgical intensive care unit for close surveillance and reversal of her coagulopathy. She was treated conservatively with pain medication, fresh frozen plasma, and vitamin K. She was discharged off of warfarin without any neurological deficit. Conclusions: Conservative management of spinal hematomas secondary to induced coagulopathies can be effective. This case suggests that, in the face of neuroimaging findings of significant edema and epidural blood, the clinical examination should dictate the management, especially in such complicated patients.
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Spontaneous spinal epidural hematoma is an extraordinarily rare condition for which there are only a few hundred documented cases, none in relation to cardiac ablation procedures. This case describes a 71-year-old woman who develops lower extremity numbness and weakness due to spontaneous spinal epidural hematoma after an atrial fibrillation ablation. (Level of Difficulty: Intermediate.).
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Introduction: Spontaneous spinal epidural hematoma (SSEH) is a rare clinical entity, most often with acute symptomatic spinal cord compression and potentially permanent neurologic deficits. SSEH usually has surgical solutions and a good outcome after hematoma evacuation. Case presentation: A 61-year-old professional weight-lifting coach presented to the emergency department with sudden back pain, rapidly progressive paraparesis, and neurogenic bladder, after an intense training, 5 h previously. Magnetic resonance imaging revealed a ventral thoracic epidural hematoma with significant compression at Th3-Th6. Surgical procedure was performed within the first 12 h: decompressive laminectomy from Th3 to Th7 vertebral levels and near total epidural hematoma removal. The patient improved rapidly from Th5 AIS-C to Th7 AIS-D paraplegia with independent ambulation, after the intervention. The rehabilitation program led to further improvement of the neurologic deficits and a favorable outcome, to AIS-E. Discussion: Weightlifting has been reported as SSEH precipitating factor in young athletes. Our case is unique however, because the athlete was older. The underlying pathophysiological mechanism is represented by intravenous pressure changes and bleeding of the epidural venous plexus during a prolonged Valsalva maneuver, induced by strenuous, repeated efforts. Spondylosis, hypertension, and low doses of aspirin were incriminated as risk factors for SSEH. Prompt diagnosis, emergent decompressive intervention, early rehabilitation, and secondary prophylaxis were essential for a good outcome.