Presentation
History
The presentation of all types of spinal cord hemorrhage varies based on the acuity of the hemorrhage as well as the longitudinal and cross-sectional extent of the hemorrhage and its rate of expansion. The following descriptions are typical, but not absolute.
Intramedullary hemorrhage / hematomyelia
Clinical presentation may include the following:
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Sudden, severe, localized back pain, with or without radicular pain
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Pain is usually centered in back or neck, and often radiates in the dermatomal distribution of the level of the hemorrhage
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Hemiparesis, paraparesis, or quadriparesis
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Sensory loss below the hematoma
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Loss of sphincter control
Spinal SAH
Clinical presentation may include the following:
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Sudden, severe, localized spinal pain with or without radicular pain
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Headache
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Meningismus
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Acute onset of neck, thoracic, or back pain was described as “le coup de poignard” or “the strike of the dagger” by Michon is a hallmark of SAH of the spine (Michon 1928).
Spinal EDH and SDH
Clinical presentation may include the following:
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Sudden, severe, localized back pain (mostly in cervical and thoracic regions due to higher prevalence of hemorrhage in these region) with or without radicular pain
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Hemiparesis, paraparesis, or quadriparesis
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Sensory loss below the hematoma
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Loss of sphincter control
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Physical
Intramedullary hemorrhage / hematomyelia
Physical examination may reveal the following:
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Myelopathy (e.g., Brown-Séquard syndrome, central cord syndrome, transection syndrome, conus medullaris syndrome) with or without radiculopathy.
Spinal SAH
Physical examination may reveal the following:
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Varying degree of myelopathy (e.g., Brown-Séquard syndrome, transection syndrome, conus medullaris syndrome, cauda equina syndrome) with or without radiculopathy.
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Menigismus might be present and may point to concurrent presence of cranial SAH
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Cranial neuropathies
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Papilledema
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May have cutaneous angioma or bruit over the spine in case of AVM and dural AVF, respectively
Spinal EDH and SDH
Physical examination may reveal the following:
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Myelopathy (e.g., Brown-Séquard syndrome, transection syndrome, conus medullaris syndrome, cauda equina syndrome) with or without radiculopathy.
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Causes
Intramedullary hemorrhage / hematomyelia
Causes may include the following:
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Trauma
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Vascular malformations
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Bleeding diatheses
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Anticoagulants
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Hemorrhage into tumor
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Venous infarction
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Spinal radiation
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Gower's intrasyringal hemorrhage
Spinal SAH
Causes may include the following:
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Spinal angioma
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Spinal artery aneurysm
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Intracranial aneurysm
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Bleeding diatheses
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Anticoagulants
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Polyarteritis nodosa
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Hemorrhage into tumor
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Trauma
Spinal EDH
Causes may include the following:
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Spontaneous
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Trauma
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Liver disease with portal hypertension
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Bleeding diatheses
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Lumbar puncture
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Epidural anesthesia
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Epidural vascular malformation
Spinal SDH
Causes may include the following:
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Bleeding diatheses
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Anticoagulants
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Trauma
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Lumbar puncture
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Vascular malformations
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Spinal surgery
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Spontaneous
Previous
Media Gallery
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A 60-year-old female presented with gradual onset of worsening back pain, lower extremity weakness, and paresthesia (over 6-8 days). She was found to have a spinal arteriovenous malformation in the thoracic region. A sagittal T2 MRI section of thoracic spine showed a heterogeneous, non-enhancing intradural extra-medullary mass (red arrow) displacing the spinal cord in the thoracic spine spanning from lower cervical to T11. The mass may represent AVM with corresponding hemorrhage. The hemorrhage involved late subacute intramedullary with some chronic component.
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Spinal angiography in the same 60-year-old female patient as above further characterized the AVM and the feeding arteries which were successfully embolized. Also noted are the tortuous subarachnoid spinal veins (yellow arrows) which increased pressure on the cord and contributed to the development of Foix-Alajouanine syndrome.
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A 62-year-old male presented with a sudden onset of severe back pain, lower extremity weakness, and loss of sensation. A sagittal thoracic T2 MRI showed an intradural mass in the lower thoracic region, along with hemorrhage (red arrow). The hemorrhage contained both chronic and subacute and is contained to the subdural space.
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Spinal angiography on the same 62-year-old male patient showed a dissecting aneurysm of the recurrent radicular medullary branch of artery of Adamkiewicz originating from the left T10 and supplying the anterior spinal artery. It was subsequently treated via endovascular embolization.
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4
Tables
- Table 1. Summary of intramedullary spinal cord hemorrhage etiologies, with history and associated clues, common imaging findings, and representative management. Adapted from Leep, Hunderfund, & Wijdicks (2009).
- Table 2. Commonly used anticoagulants and antiplatelet agents, and the antidotes used to reverse their effects. Antidotes may be used in patients who have had a hemorrhage, are actively bleeding, in preparation for surgical intervention, or are at high risk for further hemorrhage.
Table 1. Summary of intramedullary spinal cord hemorrhage etiologies, with history and associated clues, common imaging findings, and representative management. Adapted from Leep, Hunderfund, & Wijdicks (2009).
| Etiology | History clues | Imaging findings | Management |
|---|---|---|---|
| Spinal trauma | MVA, falls, sports | Associated injury to bony and/or ligamentous structures | Spine stablization/decompression; debated rolde of steroids |
| Spinal AVM | Sudden onset of neurological deficits, severe back pain, and meningismus | Abnormal vessels with flow voids | Endovascular embolizations vs. surgical resection |
| Spinal cavernoma | Family or personal history of cavernomas | “Popcorn”-like lesions with associated hemosiderin rings | Possible surgery if recurrent bleeds |
| Coagulation deficits | History of warfarin, heparin, or other medications; elevated PTT or INR; sudden onset of deficits; genetic causes; liver or autoimmune disease; malignancy | Possible air-fluid levels | Anticoagulation reversal; correction of deficient coagulation factor(s); treatment of underlying problem |
| Spinal cord tumor | Progressive neurological deficits; known history of cancer (especially renal cell carcinoma) | Mass effect with spinal cord enlargement; contrast enhancement | Surgical resection; radiation for malignancy |
Table 2. Commonly used anticoagulants and antiplatelet agents, and the antidotes used to reverse their effects. Antidotes may be used in patients who have had a hemorrhage, are actively bleeding, in preparation for surgical intervention, or are at high risk for further hemorrhage.
| Anticoagulant/antiplatelet agent | Antidote |
|---|---|
| Heparin (UFH and LMWH) | Protamine sulfate |
| Warfarin | Vitamin K, fresh frozen plasma (FFP), prothrombin protein concentrate (PPC), Factor VII concentrate Note: PPC and Factor VII have effects within minutes; FFP and Vitamin K require hours–days to take full effect. |
| Direct factor X inhibitors (Fondaparinaux, Apixaban) | Four factor PCC Oral activated charcoal Andexanet alfa |
| Novel oral anticoagulants (NOAC) | Four factor PPC Oral activated charcoal Idarucizumab (Praxbind) for dabigatran reversal +/- platelet transfusion for clopidogrel and ticagrelor |
