Spinal epidural hematomas (SEH) are uncommon clinical and neuroradiological findings, accounting only for 0.3–0.9% of all lesions, occupying spinal canal space.
SEH can be classified into idiopathic, spontaneous, and secondary. The most important causes of secondary SEHs are: coagulopathies, anticoagulants [2
], vascular malformations [5
], neoplasms, trauma with or without fractures [21
], medical procedures such as epidural catheterization or lumbar spinal surgery [34
]. Co-risk factors have also been described: minor trauma, chiropractic manipulation [33
], Paget’s disease, ankylosing spondylitis, rheumatoid arthritis, and cervical spondylitis [13
]. An SEH associated with unrecognized aortic coarctation has also been described; in that case, the ensuing increased pressure in the collateral circulation was blamed as the cause for the epidural bleeding [40
]. Nevertheless, for up to one-third of the SEHs, no clear etiology can be found and if associated with co-factors such as minor trauma, these are termed “spontaneous” spinal epidural hematomas (SSEH). Finally, SEHs are defined “idiopathic” when not any associated causal condition can be identified [29
SEHs can be acute or chronic. Chronic SHE is defined as spinal compression for months or years with mild symptoms and slight pain. Compared to acute SEHs, chronic forms are more rarely described in literature and are generally located in the lumbar spine [21
]. As far as we know, only 18 cases (including our two cases) of chronic lumbar SEH have been described until now (Table ). The chronic SEHs are, moreover, characterized by a slower and progressive raising of neurological focal symptoms and/or neurogenic claudication or cauda equina syndrome [21
]. Only one case with acute paraparesis has been described so far [35
We resumed all the cases published in literature of chronic (more than 1 month of symptoms) epidural lumbar spinal hematoma, spontaneous or idiopathic
A slowly progredient occurrence of symptoms in lumbar chronic SEHs is probably due to the wider spinal canal and the higher tolerance of the lumbar neurological structures of the space occupying effect of an organizing hematoma [3
]. The rarer chronic SEHs of the cervical spine described in literature have a shorter progression of neurological symptoms in comparison with the lumbar ones [14
]. Finally, in approximately 65% of SEHs, more than one vertebra is involved, and in 50% of cases, three or more.
Pathophysiologically, the bleeding source of chronic SHE could be located in the internal anterior and posterior vertebral plexus (Batson’s plexus), formed by two anterior and posterior veins extending along the entire epidural space. This plexus has extensive connection via venous rami with the external plexus through each vertebral body and the posterior vertebral elements [11
]. Considering these anatomical prerequisites, some of the previously analyzed factors in association with any circumstance able to transiently raise the venous pressure (e.g., Valsalva maneuver) can lead to bleeding and organizing hematoma. Moreover, these epidural venous plexus represent a cavo-caval shunt and, therefore, are highly sensitive to an abdominal pressure increase, as well as the intrathoracic, intraspinal, and intracranial pressure. The pressure in the epidural veins is lower than in the vena cava; the absence of valves in the epidural plexus and in the vertebral body allows blood flow in both cranial and caudal direction. The epidural venous plexus can be considered as the balancing system of the pressure/volume ratio in relation to intracranial, intrathoracic, intra-abdominal blood pressure, and volume changes. Hypothetically, a rupture of a weakened epidural vein could occur with a sudden and massive blood flow reversal from the larger caval system into the smaller vertebral veins.
Chronic SEH may also be caused by bleeding of smaller vessels inside the ligamentum flavum which could explain the almost exclusive dorsal or dorso-lateral location of this type of hematoma [36
]; the yellow ligament is largely composed of elastic tissue containing numerous small blood vessels which can be torn during forced hyperflexion. The arterial bleeding source, however, has been considered the main origin of the rarer acute forms of SEHs in the lumbar spinal tract.
As for clinical symptoms, SEH can mimic disc herniation, canal stenosis [21
] or tumor signs and they are characterized by severe axial back pain with or without acute or delayed neurological deficits [12
]. The pain onset, often related to minor strain or Valsalva-like maneuvers, can be acute or slowly progressive, especially in the rare case of chronic epidural hematoma. Signs of myelopathy, Brown-Séquard syndrome or bowel, and bladder function impairment are described in the cervico-dorsal location of SEHs [1
]; radicular symptoms are more typically reported in the lumbar SHEs and the severity of neurological impairment is also quite variable [21
]. Yet, several cases of cervical chronic SEHs presenting with radicular symptoms have been reported in the literature [23
The CT scan imaging in chronic SEH is less useful for differential diagnosis since a small ventrally located chronic hematoma can easily be confused with a large herniated disc. MRI represents the diagnostic gold standard for SEH [8
]; the T1 and T2 intensity patterns are both equally helpful in discrimination against almost all other vertebral space occupying lesions. Acute epidural hematomas typically appear hypointense in T2-weighted and isointense in T1-weighted images lesions. When the hematoma becomes chronic, the neuroradiological findings change and SEHs typically become hyperintense in both T1- and T2-weighted images. Finally, MRI is useful in identifying other lesions, which are responsible for spinal bleeding (e.g., tumors and MAVs). Angiography is not used in routine diagnostics unless the appearance of a tortuous vessel on MRI raises the suspicion of a vascular malformation.
Differential diagnosis of chronic SEH should also include other benign lumbar epidural masses, such as synovial or ligamentum flavum cysts, both of which are prone to intralesional hemorrhage, and epidural cavernous angiomas. Graziani et al. [9
] consider that the frequency of spinal epidural cavernous angiomas is probably underestimated; the inability to reveal an angioma through pathological examination not necessarily means that such lesions cannot be the source of bleeding; the failure to visualize these malformations could be related to their very small size or to thrombosis after the initial episode of hemorrhage. The very variable neurological symptoms and signs may accompany an initial pain or can develop several hours or days after the pain onset.