Spinal Cord Hemorrhage

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Background

Hemorrhage affecting the spinal cord is rare. It most commonly is caused by trauma, vascular malformations, or bleeding diatheses and can be intramedullary, subarachnoid, subdural, or epidural. Onset is usually sudden and painful, causing myelopathic signs and symptoms.

Pathophysiology

Hematomyelia is caused by bleeding within the substance of the spinal cord. The blood tends to dissect longitudinally above and below the hemorrhage, disrupting gray matter more than white matter. Spinal subarachnoid hemorrhage (SAH) may cause symptoms due to blood in the subarachnoid space or blood dissecting into the spinal cord or along nerve root sheaths. Spinal epidural hemorrhage (EDH) and subdural hemorrhage (SDH) cause compressive symptoms due to hematomas in these spaces.

Epidemiology

Frequency

United States

Hemorrhage affecting the spinal cord is rare. Spinal subarachnoid hemorrhage accounts for less than 1% of all subarachnoid hemorrhages. Spinal epidural hemorrhage occurs at least 4 times more commonly than spinal subdural hemorrhage.

Mortality/Morbidity

Spinal hemorrhage can lead to irreversible myelopathy (including conus medullaris and cauda equina syndromes) and/or radiculopathy.

Sex

The incidence of hematomyelia, spinal subarachnoid hemorrhage, and spinal epidural hemorrhage is higher in males than in females. Spinal subdural hemorrhage is more common in women (female-to-male ratio is 2:1).

Age

Spinal epidural hemorrhage has a bimodal distribution, with peaks during childhood and the fifth and sixth decades of life. Spinal epidural hemorrhage is most common in the cervical region in children and in the thoracic and lumbar regions in adults. Spinal subdural hemorrhage predominates in the sixth decade.

History

Physical

Causes

Laboratory Studies

Imaging Studies

Procedures

Medical Care

Medical therapies for spinal cord hemorrhage are limited.

Surgical Care

Consultations

Medication Summary

The goal of pharmacotherapy is to inhibit the effect of anticoagulants in patients taking such medications. Attempts to treat spinal cord swelling (edema) with mannitol or corticosteroids have not been tested in randomized, double-blind studies. If spinal cord trauma can be taken as a situation similar to cord compression, high-dose corticosteroids may be beneficial.

Protamine

Clinical Context:  Neutralizes heparin effects by forming a salt.

Phytonadione (AquaMEPHYTON, Mephyton, Vitamin K)

Clinical Context:  Promotes liver synthesis of clotting factors that in turn inhibit warfarin effects.

Class Summary

Anticoagulated patients may require a blood modifier.

Further Inpatient Care

Once the patient with spinal cord hemorrhage has been treated, whether medically, via interventional radiology, or surgery, rehabilitation can begin. Usually this is accomplished in an inpatient rehabilitation setting.

Further Outpatient Care

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.

Inpatient & Outpatient Medications

Deterrence/Prevention

Avoid lumbar puncture in patients with hematologic disorders or in those treated with prescribed anticoagulants.

Prognosis

Prognosis varies but generally is correlated with severity of deficit. A more favorable outcome is seen in patients receiving prompt diagnosis and surgical intervention.

Author

Richard M Zweifler, MD, Chief of Neurosciences, Sentara Healthcare; Professor and Chair of Neurology, Eastern Virginia Medical School

Disclosure: Nothing to disclose.

Specialty Editors

Rodrigo O Kuljis, MD, Esther Lichtenstein Professor of Psychiatry and Neurology, Director, Division of Cognitive and Behavioral Neurology, Department of Neurology, University of Miami School of Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Consulting; Sunovion Consulting fee None; Supernus Speaking, consulting; Upsher-Smith Grant/research funds None

Chief Editor

Helmi L Lutsep, MD, Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Stryker Neurovascular Consulting fee Review panel membership

References

  1. Barth A, Bougousslavsky J, Caplan LR. Spinal stroke syndromes. In: Barth A, Caplan LR, eds. Stroke Syndromes. 1995. New York: Cambridge University; 395-402.
  2. Borm W, Mohr K, Hassepass V et al. Spinal hematoma unrelated to previous srugery. Analysis of 15 consecutive cases treated in a single institution within a 10-year period. Spine. 2004;29:E555-E561.
  3. Byrne TN, Benzel EC, Waxman SG. Diseases of the Spine and Spinal Cord. Contemporary Neurology Series. New York: Oxford University Press; 2000.
  4. Domenicucci M, Ramieri A, Paolini S, et al. Spinal subarachnoid hematomas: our experience and literature review. Acta Neurochir (Wien). Jul 2005;147(7):741-50; discussion 750. [View Abstract]
  5. Geibprasert S, Krings T, Apitzsch J, et al. Subarachnoid hemorrhage following posterior spinal artery aneurysm. A case report and review of the literature. Interv Neuroradiol. Jun 2010;16(2):183-90. [View Abstract]
  6. Geldmacher DS, Bowen BC. Spinal cord vascular disease. In: Bradley WG, Daroff RB, Fenichel GM, Jankovic J, eds. Neurology in Clinical Practice Principles of Diagnosis and Management. 5th ed. Philadelphia, Pa: Butterworth-Heimann; 2008:1285-93.
  7. Groen RJM. Non-operative treatment of spontaneous spinal epidural hematomas: a review of the literature and a comparison with operative cases. Acta Neurochir (Wien). 2004;146:103-110.
  8. Gross BA, Du R, Popp AJ, Day AL. Intramedullary spinal cord cavernous malformations. Neurosurg Focus. Sep 2010;29(3):E14. [View Abstract]
  9. Karavelis A, Foroglou G, Petsanas A, Zarampoukas T. Spinal cord dysfunction caused by non-traumatic hematomyelia. Spinal Cord. May 1996;34(5):268-71. [View Abstract]
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  12. Russell NA, Benoit BG. Spinal subdural hematoma. A review. Surg Neurol. Aug 1983;20(2):133-7. [View Abstract]

T2-weighted sagittal MRI of the cervical spine shows mixed signal intensity within the spinal cord consistent with posttraumatic intramedullary hemorrhage. The hypointensity reflects deoxyhemoglobin and the hyperintensity reflects either early hemorrhage or edema. The C6 vertebral body is distracted from C7 with extensive ligamentous injury. Courtesy of Francis G. Greiner, MD, Department of Radiology, University of South Alabama College of Medicine.

T2-weighted sagittal MRI of the cervical spine shows mixed signal intensity within the spinal cord consistent with posttraumatic intramedullary hemorrhage. The hypointensity reflects deoxyhemoglobin and the hyperintensity reflects either early hemorrhage or edema. The C6 vertebral body is distracted from C7 with extensive ligamentous injury. Courtesy of Francis G. Greiner, MD, Department of Radiology, University of South Alabama College of Medicine.