Medical Care
Medical therapies for spinal cord hemorrhage are limited.
If the bleed is caused by a coagulopathy, reversal of the bleeding tendency is crucial. Examples include fresh frozen plasma and vitamin K or prothrombin complex concentrate for warfarin-induced bleeds, protamine sulfate for heparin-induced bleeds, platelet transfusions for thrombocytopenia, specific clotting factor concentrates or fresh frozen plasma for clotting factor deficiencies such as hemophilia and Christmas disease. The optimal treatment to reverse the effects of the new oral anticoagulants is unknown.
Another potential medical treatment, drug therapy for cord edema, is unproved.
Surgical Care
Depending on etiology (deduced from history, lab work, and imaging) and clinical findings (such as the presence or progression of neurological deficits), surgery may be indicated for hemorrhage affecting the spinal cord. Surgery would not be expected to reverse the damage already caused by infarction.
In general, surgery should be strongly considered in spinal subdural hemorrhage and epidural hemorrhage. Patients with these conditions may benefit from immediate decompressive operation if associated neurological signs and symptoms are present (e.g., weakness, paresthesiae, loss of sphincter control, positive Babinski, etc.). [24, 25]
It should be noted, however, that even emergency surgery cannot guarantee full return of function, and management decisions are made on a case-by-case basis. If coagulopathy is present, it may need to be corrected, and the patient may require medical stabilization.
Spinal vascular lesions may be approached by catheter-based interventional techniques, such as embolization or coiling.
Endovascular embolization for AVF or combined embolization followed by surgical resection for AVM may be indicated for patients with spinal SAH. [1] The decision of embolization vs. surgery or whether or not to perform any intervention is complex and depends on the presence of neurologic symptoms, acuity of symptom presentation and hemorrhage, location of the AVM (ventral vs. dorsal; proximity to critical spinal cord tracts), and location and number of feeding arteries and draining veins, presence of nidus, and any associated fistulas.
Even if significant obliteration is achieved by endovascular embolization, an AVM may still require operative resection. In the case of partial embolization, surgery is usually performed. The long-term clinical outcome of patients treated for AVMs (by endovascular intervention, surgery, or both) varies according to the nidus versus fistulous type of AVM. Patient outcomes are usually better in the latter type, which may depend on the degree of obliteration, and inherent hemodynamic differences between the two types. [26]
Consultations
The following consultations may prove helpful:
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Neurosurgeon – acute
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Neurologist – acute
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Interventional neuroradiologist – acute
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Hematologist – acute (if indicated)
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Urology – as needed
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Rehabilitation physician – long term
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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 |
