Hematomyelia after epidural anesthesia: a rare complication with putative multifactorial and occult etiology

Abstract

Subarachnoid hemorrhage (SAH) and spinal hematomas are considered serious but rare complications of spinal pathology. They occur after spinal anesthesia, especially in patients with risk factors such as autoimmune diseases, blood coagulation pathology, anticoagulant treatment, vascular malformations, intramedullary or spinal cord tumors, or can be multifactorial. Usually, anticoagulant therapy represents an additional factor regarding spinal SAH (SSAH) or spinal hematomas. None of the direct oral anticoagulants has a higher chance of producing a spinal hemorrhage. The diagnosis can be established based on the clinical picture of SSAH or myelopathy syndrome, completed with magnetic resonance imaging (MRI). In this study, we present the latest data from the literature regarding SSAH and hematomas and compare them with the data of a 77-year-old man with a history of atrial fibrillation, on oral anticoagulant treatment, who developed a SSAH and spinal hematoma after elective surgery for an inguinal hernia.

Keywords: hematomyelia; regional anesthesia; subdural hematoma.

Figure 1

(A) Sagittal section, increased T2 signal in the lower cervical spine; MRI of the cervicothoracic spine; (B) Sagittal section, T1 isosignal in the lower cervical medulla; cervicothoracic spine MRI; (A and B) Appear suggestive of intramedullary bleeding; (C) Sagittal section, increased T2 signal in the thoracic medulla; MRI cervicothoracic spine (appears suggestive of myelitis); (D) Sagittal section, T1 isosignal on thoracic medulla; cervicothoracic spinal MRI (appear suggestive of intra-medullary bleeding). MRI: Magnetic resonance imaging

Figure 2

Native brain CT showing bilateral parieto-occipital subarachnoid hemorrhage. CT: Computed tomography

Figure 3

Spinal cord pathology: (A) Overall transversal image of the thoracal spinal cord revels massive hemorrhage in the subdural space as well as necrosis and diffuse hemorrhagic infiltrate in the parenchyma (HE staining); On a detailed area from the central core of the spinal cord (rectangle in A, enlarged in B–E), blood vessels still show intact endothelial cells as revealed by IHC for CD34 (B), while only faint silhouettes of ballooned neurons are left based on IHC for NeuN, with (arrows) or without (arrowhead) remnant nuclei (C); A rich mononuclear inflammatory infiltrate is present, composed mostly of macrophages (CD68) (D) and T-lymphocytes (CD3) (E). (A) Slide scan; (B–E) ×100. CD: Cluster of differentiation; HE: Hematoxylin–Eosin; IHC: Immunohistochemistry; NeuN: Neuronal nuclei.

Figure 4

Microscopy of the cerebral and cerebellar cortices: (A) Cerebral cortex showed hemorrhagic exudate in the leptomeninges; (B) Blood vessels with stasis and perivascular and pericellular edema; (C) Moderate perivascular gliosis as revealed by anti-GFAP antibody IHC, ×200; (D) Cerebellar cortex presented with stasis, hemorrhage and fibrin accumulation in the leptomeninges; (E) Numerous macrophages identified by anti-CD68 antibody IHC in the leptomeningeal exudative and cellular reaction, ×200; (F) Fragmented GFAP-positive extensions but without remnant cell bodies surrounding the hemorrhage areas. HE staining: (A, B and D) ×200. CD68: Cluster of differentiation 68 (marker of macrophages); GFAP: Glial fibrillary acidic protein (marker of astrocytes); HE: Hematoxylin–Eosin; IHC: Immunohistochemistry