Further Outpatient Care
Once the patient with spinal cord hemorrhage has been treated, whether medically, via interventional radiology, or surgery, rehabilitative care can begin, depending on the nature of the spinal cord injury. Usually such care is initiated in an inpatient rehabilitation setting.
After the patient is discharged from inpatient care, outpatient therapies continue. Medical treatments are frequently necessary for the late complications of spinal cord hemorrhage, especially spasticity, pain, and neurogenic bladder.
It is not unusual for patients to have residual myelopathy, weakness, or bladder dysfunction even after receiving optimal intervention to stop the cause of hemorrhage and even decompress the spinal cord.
As with other types of spinal cord injury, outpatient follow-up is also important to identify any new or unexpected sequelae (such as urinary tract infection; deep venous thrombosis), and to monitor the progress of recovery and rehabilitation. Patients may experience significant improvements in strength and sensation, but these again depend on factors such as extent and level of injury, and existing comorbidities. [29, 31, 32, 33, 34, 35, 36, 37]
Deterrence/Prevention
Given the varying etiologies of spinal cord hemorrhage, efforts at prevention would depend on the causative factor. For instance, the pros and cons of lumbar puncture in patients with hematologic disorders or in those treated with anticoagulants (as well as the risks of reversing anticoagulation) should be carefully considered.
Prognosis
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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 |
