Laboratory Studies
The following laboratory studies may aid in diagnosis:
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CBC with platelets
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Prothrombin time (PT)/INR and activated partial thromboplastin time (aPTT) – to exclude coagulopathy
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CSF studies (cell count, glucose, protein, oligoclonal bands, etc.) are helpful if infectious, inflammatory or demyelinating etiologies are expected
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CSF xanthochromia
Imaging Studies
Spinal MRI
Cervical, thoracic, or lumbar spinal MRI is the preferred test to confirm presence and delineate location of hemorrhage. This may indicate the underlying pathology, for instance, with enhancement.
CT myelography
An alternative when clinical suspicion is high and MRI is not available, or the patient who is not able to tolerate MRI. CT myelogram shows fluid collections (such as EDH, SDH) and is also useful for CSF leak detection. In general, CT is not as sensitive as MRI for non-boney structures. CT alone may or may not show acute hematomyelia.
Procedures
Lumbar puncture
If hemorrhage extends into the cerebrospinal fluid (CSF), the CSF sample is usually bloody appearing or xanthochromic, and protein content is increased. Xanthochromia is the yellowish discoloration of CSF due to the presence of bilirubin, which is the result of RBC lysis and subsequent heme breakdown occurring over time. An initial “bloody tap” (in the absence of a preceding hemorrhagic event) should clear and not be xanthochromic.
Xanthochromia may be present as early as 4 hours post hemorrhage, but usually takes about 12 hours to occur, after the appearance of blood within the subarachnoid space. It may persist up to four days after the original hemorrhage. Detection of xanthochromia is done by visual inspection pre- and post CSF centrifugation, which eliminates red blood cells. Mass spectroscopy of CSF may also be useful, for detection of bilirubin and to rule out other possible causes of xanthochromia (such as high protein content, or melanin). This is especially useful when the suspicion for SAH is high and the imaging findings are negative due to the time elapsed since the hemorrhage, or with smaller amounts of blood. [23]
Spinal angiography
This may be helpful in delineating the size, location, configuration, and blood flow of a spinal vascular malformation, such as AVM or AVF.
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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.
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.
| 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 |
| 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 |
