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Spinal Cord Compression

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Last Update: February 13, 2023.

Continuing Education Activity

Spinal cord compression can result from a myriad of both atraumatic and traumatic causes. The spinal column is vulnerable to a variety of compressive phenomena, such as the expansion of blood products, neoplastic disease, infectious collections, or protrusion of bone or intervertebral disc within the limited area of the fat-filled spinal epidural space and meninges. This activity reviews the evaluation and management of atraumatic spinal cord compression and highlights the roles of the emergency physician, neurosurgeon, and interprofessional team in treating patients with this condition.


  • Identify the etiology of spinal cord compression.
  • Outline the appropriate evaluation of spinal cord compression.
  • Review the management options available for spinal cord compression.
  • Discuss interprofessional team strategies for improving care coordination and communication to advance spinal cord compression and improve outcomes.
Access free multiple choice questions on this topic.


Spinal cord compression can result from a myriad of both atraumatic and traumatic causes. The spinal column, comprised of numerous soft tissue and bony structures, is built to provide the body’s structural support and protect the spinal cord and exiting nerve roots. The encased spinal cord depends upon this stability. However, it is simultaneously vulnerable to a variety of compressive phenomena, such as the expansion of blood products, neoplastic disease, infectious collections, or protrusion of bone or intervertebral disc within the limited area of the fat-filled spinal epidural space and meninges. A simplified overview of spinal anatomy is discussed below: 

The spine is comprised of 33 vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral (fused), and 4 coccygeal (fused). The 26 non-fused portions of the spine are separated by cartilaginous intervertebral disks and supported by ligaments, including the anterior longitudinal ligament and posterior longitudinal ligament. Each neural foramen (nerve root exit site) is bounded superiorly by a pedicle, immediately inferiorly by a disc space, posteriorly by facet joints, and anteriorly by the vertebral body.

The spinal cord is approximately 40 cm in length, extending from the foramen magnum to the L1-L2 vertebrae. The cervical and lumbar enlargements of the spinal cord, responsible for innervation to the upper and lower extremities, span from C5-T1 and L2-S3, respectively. The spinal cord tapers down to its caudal tip, the conus medullaris, between T10-L1, where the non-neural filum terminale then extends downward to the S2 vertebra. Paired lumbosacral nerves extend caudally, comprising the cauda equina until exiting the spinal column at their corresponding foramina.

Vascular supply to the spinal cord includes the anterior spinal artery, supplied superiorly by the vertebral arteries, and paired posterior spinal arteries. The anterior spinal artery provides approximately two-thirds of the blood supply to the spinal cord, and the paired posterior spinal arteries provide the remaining one-third. The anterior and posterior spinal arteries receive additional blood flow from radicular arteries, the largest of which is the artery of Adamkiewicz originating from the aorta. The artery of Adamkiewicz is most commonly located between the T8-L4 levels on the left side.

The spinal epidural space is bordered anteriorly by the vertebral body and posteriorly by the dura mater. It contains fat, arteries, and venous plexus. The epidural space is larger along the thoracolumbar spine, corresponding to a higher likelihood of spinal epidural abscess in this region.


Spinal cord compression can occur from a wide range of underlying conditions. This article will focus on atraumatic causes of spinal cord compression, including degenerative spondylosis with myelopathy, metastatic disease of the spine, primary spinal cord malignancy, spinal epidural abscess, and spontaneous or iatrogenic spinal epidural hematoma.


Myelopathy, or neurologic deficit(s) due to disease of the spinal cord, most commonly results from degenerative changes (spondylosis) involving the intervertebral/uncovertebral discs, facet joints, or vertebral bodies resulting in spinal stenosis in the cervical or lumbosacral spine. Cervical spondylosis is the most common cause of myelopathy in adults above the age of 55, and the incidence of myelopathy with this condition is approximately 5% to 10%.

Metastatic spinal cord compression (MSCC) develops in 2.5% to 5% of patients dying as a result of cancer, with significant variation by primary tumor type.[1] In a 2011 analysis of the Nationwide Inpatient Sample, investigators found that lung cancer (24.9%), prostate cancer (16.2%), and multiple myeloma (11.1%) comprised the majority of 75,876 hospitalizations related to MSCC.[2]

Although uncommon, the incidence of spinal epidural abscess (SEA) has increased over the past several decades. A recent study showed an incidence of 5.1 cases per 10,000 admissions at a large U.S. academic hospital.[3] Suspected causes for the increased incidence of SEA include improvement in diagnostic strategies (MRI), IV drug use associated with the opioid epidemic, and increased frequency of invasive spinal procedures in the United States.

Spontaneous spinal epidural hematoma (SSEH) remains rare, with a reported incidence of 0.1 per 100,000 and 600 reported cases in the medical literature, with an age predilection for the 4 and 5 decades of life.[4][5][6] In recent years, SSEH has received more attention in light of direct oral anticoagulant and vitamin K antagonist use for the treatment of common conditions such as non-valvular atrial fibrillation and deep venous thrombosis (DVT) or pulmonary embolism (PE). Most of our current knowledge regarding the presentation, management, and natural course of SEH stems from experience with procedure-related SEH, i.e., epidural analgesia.


Degenerative spondylosis is a general term for degenerative changes in the spine and a common cause of non-specific neck and back pain among older adults. When degenerative changes result in the narrowing of the spinal canal, myelopathy, or neurologic deficits related to spinal cord compression, can result. Stenotic damage to the spinal cord is thought to be the result of two processes: direct compression of the neural elements and ischemia related to disruption of arterial and venous structures surrounding the spinal cord.[7]

MSCC from a solid tumor typically results from hematogenous spread of malignant cells to a vertebral body. In the case of pelvic tumors, i.e., prostate cancer, Batson venous plexus is hypothesized to account for the promotion of vertebral metastasis via shunting of venous blood from the abdomen and pelvis to the epidural venous plexus during Valsalva maneuver. In approximately 10% of cases, direct spread from a paraspinal mass can occur; this is most commonly seen with lymphoma. Over time, an enlarging vertebral mass can compress the spinal vasculature, thecal sac, and spinal cord resulting in pain and neurologic deficits. Destruction of the vertebral body can also result in a compression deformity with direct compression of bony fragments on the spinal cord. The thoracic spine is most commonly implicated in MSCC, followed by the lumbar and cervical vertebral levels. Spinal cord tumors make up a rare percent of spinal malignancy, representing 4% to 10% of CNS tumors and only 1% of all cancers.

SEA most commonly results from the hematogenous spread (26% to 50% of cases). As the epidural space is a vertical sheath, SEA can spread over several vertebral levels. SEA can also occur from the extension of a contiguous soft tissue/bony infection, i.e., psoas abscess, vertebral osteomyelitis, or via direct inoculation from a spinal procedure or surgery. Risk factors for SEA include IV drug use; any condition resulting in bacteremia (i.e., dental abscess, infection of an indwelling vascular catheter, infective endocarditis); epidural catheter placement; and paraspinal analgesic/steroid injection. Other risk factors include diabetes, immunosuppression secondary to HIV or medications, alcoholism, trauma, or acupuncture. Staphylococcus aureus is identified as the causative organism in over 50% of cases; other bacterial species identified include Escherichia coli, Streptococcal species, and Pseudomonas aeruginosa. Damage can be caused either by direct compression from abscess formation or inflammatory vascular thrombosis; the latter is responsible for sudden neurologic deficits that can be observed among patients with spinal epidural abscess.

Any procedure involving puncture into the spinal canal, most commonly neuraxial analgesia, can result in hemorrhage and resulting SEH formation. Although bleeding most commonly originates from the epidural venous plexus, subdural and subarachnoid hemorrhage can also be seen. SEH formation within the spinal canal results in increased pressure, spinal cord ischemia, and subsequent infarction resulting in neurologic deficits. Risk factors for procedure-related SEH include preexisting coagulopathy (i.e., anticoagulant use, advanced renal disease, thrombocytopenia, preeclampsia), procedural difficulty, advanced age, and anatomic spinal abnormalities. SSEH has achieved increased recognition concurrent with the increased use of direct oral anticoagulants and vitamin K antagonist therapy for various conditions, including venous thromboembolism, atrial fibrillation, and mechanical valve placement.

History and Physical

There is considerable overlap between "red flag" causes of back pain and risk for spinal cord compression. General red flags that should prompt consideration of spinal imaging include age more than 65, new-onset gait instability, sphincter incontinence, corticosteroid use, midline pain, and presence of spinal contusion on exam (for traumatic pathology). Red flags for specific causes of spinal cord compression will be discussed below:

Cervical spondylotic myelopathy variably results in weakness affecting the arms, legs, or both. Patients may also complain of sensory loss at the cervical or thoracic level. Spastic urinary and rectal sphincter dysfunction can be seen. On exam, lower motor neuron findings, including hyporeflexia, dermatomal sensory loss, and diminished fine motor control, may be present in the upper extremities. Upper motor neuron findings, including hyperreflexia and abnormal Babinski response, can be seen in the lower extremities. Gait disturbance is often an early finding associated with cervical myelopathy.[8][9] Lhermitte sign, an "electric shock" sensation in the neck with radiation down the spine or arms, might be elicited with forward neck flexion on the exam. Acute onset of the above symptoms following an episode of excessive neck flexion or extension should prompt suspicion for cervical myelopathy and imaging evaluation.

Based on a 2013 systematic review by Downie and colleagues, the only well-validated red flag for MSCC is a history of malignancy.[10] Back pain is the most common presenting symptom, reported by 80 to 95% of patients.[11][12] Pain is constant, aching, classically worse at night, and with Valsalva maneuver (i.e., coughing, sneezing). Radicular pain may manifest in cases of advanced disease. Motor deficits are present in 35 to 75% of patients at diagnosis (PMID: 20594024). A subset of patients with lumbosacral MSCC may present with findings suggestive of cauda equina syndrome, which is defined by characteristic neurologic deficits associated with compression of the spinal nerves below the conus medullaris. Findings might include bilateral lower extremity symptoms, lower extremity weakness in a patchy distribution, sensory deficits involving multiple dermatomes, urinary retention, overflow urinary incontinence, fecal incontinence, and gait abnormalities.

The classic tried of fever, back pain, and localized neurologic deficits for SEA are rare in clinical practice and more likely to be observed in late presentations. Fever is apparent in a wide range (30% to 75%) of cases. The combination of fever and localized back pain, particularly when worse with percussion, should prompt further diagnostic evaluation for SEA, discitis, and osteomyelitis. The absence of fever does not preclude a diagnosis of SEA; accordingly, most patients undergo more than one healthcare visit before the diagnosis is made.

Presenting symptoms and exam findings for SEH include acute-onset back pain, motor weakness, and bowel/bladder dysfunction. Interestingly, radicular pain is an uncommon complaint among patients with SEH.[13] As described above, risk factors for SEH include neuraxial analgesia and anticoagulant use; this combination of characteristic symptoms and risk factors should prompt further evaluation for SEH, preferably with MR imaging.


Suspicion for spondylotic myelopathy should prompt MR imaging evaluation. CT myelography is an alternative option and can provide a quantitative assessment of spinal canal narrowing, in addition to improved detail of bony structures and soft tissue calcification. MRI provides better detail of spinal cord pathology, is less invasive, and therefore preferred in patients presenting with suspected acute myelopathy.[8]

Gadolinium contrast-enhanced MR imaging is the gold standard for diagnosis of MSCC (sensitivity 93%, specificity 97%), and imaging of the entire spine is advised in the evaluation of this condition.[14] CT myelography is only recommended when MRI is contraindicated; x-ray is inadequately sensitive for metastatic disease and does not adequately characterize soft tissue detail. 

Laboratory evaluation, although not always helpful, is a routine part of the diagnostic work-up for patients with suspected SEA. The absence of leukocytosis does not reliably rule out SEA; one study showed an elevated WBC count in only two-thirds of patients with SEA.[15] C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) have also been used to risk-stratify patients with suspected SEA. A 2011 study incorporated ESR and CRP into a diagnostic algorithm for patients with suspected SEA. Those with more than one risk factor for SEA, fever, or radiculopathy underwent ESR and CRP testing; an abnormal result expedited imaging evaluation with MRI or CT myelography as appropriate. An ESR value >20 mm/hr associated with one or more SEA risk factors corresponded to sensitivity and specificity of 100% and 67%, respectively, for diagnosis of SEA. CRP was less reliable with sensitivity and specificity of 87% and 50%, respectively. In this study, implementation of the diagnostic algorithm resulted in less diagnostic delays (84% vs. 10%, p <0.001) and a reduction in motor deficits present at the time of SEA diagnosis (82% vs. 20%, p <0.001). These findings suggest a role for ESR in risk-stratifying patients with one or more risk factors for SEA, although this study has not yet been externally validated.[16]

MRI with gadolinium contrast enhancement is the gold standard imaging study for evaluation of SEA. Imaging of the full spine for skip lesions should be considered. In a retrospective study of 233 adult patients with SEA, 22 (9%) had two or more fluid collections in two separate anatomic regions. The authors formulated a prediction algorithm with risk factors for skip lesions, including the following: symptoms for seven or more days, ESR >95 mm/h, and concomitant infection outside of the spine.[17]

Treatment / Management

General Management

Generally, cervical spondylotic myelopathy is managed conservatively in early, mild stages with various treatment measures, including physical therapy, limiting high-risk physical activities, and pain control with non-steroidal anti-inflammatory agents, muscle relaxants, and other agents. Epidural steroid injections are also a mainstay of conservative treatment.[18][19] Serial neurologic exams over time may be helpful, with repeat imaging as needed for the progression of neurologic deficits. Surgical decompression should be considered for patients with moderate to severe manifestations with failure of conservative therapy. Surgical treatment should be tailored specifically to the pathology at hand and is indicated urgently in those with abrupt worsening.[7]

Urgent glucocorticoid administration for MSCC with neurologic involvement is recommended. Administration of dexamethasone results in the downregulation of vascular endothelial growth factor and prostaglandin E2, with a corresponding decrease in spinal cord edema. Glucocorticoid therapy has been shown to improve analgesia and neurologic function.[20][21] A Cochrane review demonstrated multiple adverse effects of high-dose dexamethasone (96 mg IV x 3 days, followed by a taper), including psychosis and gastric ulcer formation compared with standard-dose dexamethasone (10 mg IV bolus followed by 4 mg IV every 6 hours) without demonstrable improvement in neurologic function.[22]

Both surgical intervention and radiation treatment play a central role in the management of MSCC. Factors that may weigh into the decision for surgical management include spinal stability, neurologic deficits, and overall prognosis. The Spine Instability Neoplastic Score has demonstrated 95.7% sensitivity and 79.5% specificity in the determination of spinal stability and can be used to guide clinicians in deciding whether surgical intervention should be pursued.[23] Other validated decision aids include the Epidural Spinal Cord Compression Scale and functional/prognostic outcome scores, including the Modified Bauer Score and the New England Spinal Metastasis Score.[24][25][26][27] Depending on the level, radiosensitivity, and stability of the culprit spinal lesion, surgical management might include percutaneous kyphoplasty and vertebroplasty in addition to radiation treatment versus surgical decompression and spine stabilization, ideally with circumferential excision of an epidural tumor followed by posterior segmental fixation. Anterior reconstruction with either bone graft or bone cement should be considered for patients with vertebral body destruction. Radiation treatment alone is preferred for patients with spinal stability without neurologic deficits and those with radiosensitive tumors.

Once the diagnosis of SEA is made, intravenous antibiotics are routinely given. The decision to withhold antibiotics before tissue diagnosis/culture can be made on a case-by-case basis in conjunction with neurosurgery and should only be considered in a stable patient without clinical evidence of bacteremia/sepsis. The standard regimen includes ceftriaxone, 2 g IV daily, and vancomycin, 15 to 20 mg/kg IV every 8 to 12 hours for adequate S. aureus coverage. Management of SEA usually involves surgical management with decompression. Increasing numbers of case reports and small studies have also shown a role for a trial of non-operative management with IV antibiotics and close monitoring among appropriately selected patients.

In a 2014 retrospective study of this practice, 73 out of 142 patients with SEA were successfully treated with an antibiotic-alone approach. Statistically significant factors associated with failure of non-operative management included age more than 65 years, diabetes, MRSA infection, neurologic compromise, and circumferential SEA.[28] The decision to pursue non-operative management should only be made with direct neurosurgical consultation for risk factor assessment and admission and with the individual patient's preferences in mind.

Prompt surgical decompression with laminectomy and evacuation is indicated for SEH with severe or progressive neurologic deficits. Although an exact time interval for the prevention of irreversible neurologic deficits has not been defined, most experts advise evacuation within 48 hours of symptom onset. A role for anticoagulation reversal with non-operative management has been explored in case reports but is not currently considered standard care for patients with SEH, particularly when neurologic deficits, bowel or bladder dysfunction are present.

Surgical Approaches

For the above conditions, a variety of surgical approaches exist depending on the location of the pathology. For cervical spine pathology, approaches are generally either anterior or posterior in nature. For stenosis caused by soft cervical disc herniations, anterior cervical discectomy, and fusion (ACDF) is a mainstay. Here, the anterior neck is opened through most commonly a transverse incision, and the anterior cervical spine is approached. The herniated disc is incised and removed, and either a cadaveric graft or structural allograft is inserted to promote fusion. A plate is usually placed over the construct for added stability. An additional anterior approach for pathology partly or wholly behind the vertebral body is the cervical corpectomy, whereby a similar exposure is done as in an ACDF, but the vertebral body and discs above and below are completely resected and a cage is inserted with a plate overlying the construct.[29]

For pathology posterior to the cord, such as canal stenosis from ligament hypertrophy, often posterior cervical decompression (laminectomy vs. laminoplasty) with or without fusion is preferred. Posterior cervical fusion is most often accomplished via lateral mass fusion, but pedicle screw fixation and interfacet fusion are also options at hand for the surgeon.[30] Another reason to consider a posterior cervical approach would be for anterior cord pathology associated with ossification of the posterior longitudinal ligament (OPLL). Here, it is often preferred to perform posterior cervical decompression via laminectomy or laminoplasty to avoid iatrogenic cord trauma from an anterior approach. If OPLL is suspected on MRI, CT imaging is indicated in the pre-operative setting, so this diagnosis may be made.[31]

In the thoracic and lumbar regions, posterior approaches for decompression (laminectomy, discectomy, etc.) with or without fusion remain the most common technique. However, anterior and lateral approaches are also possible. In the thoracic region, an anterior approach is possible but carries high morbidity, especially in the upper thoracic spine, and requires an access surgeon. Anterior approaches in the upper thoracic spine will also be limited by the heart and mediastinal structures. Lateral approaches to the thoracic spine may be less morbid but often will still require an access surgeon. Lateral access options include extracavitary or intracavitary and will vary depending on the pathology.[32] Another common reason to require an anterior or lateral approach to the thoracic spine includes thoracic disc herniations, anterior vertebral body tumors, or anterior vertebral body osteomyelitis with cord compression. In the thoracic spine and upper lumbar spine above the conus medullaris, avoidance of manipulation of the cord is imperative to prevent an iatrogenic neurologic deficit. [33]

Similar indications for anterior or lateral approaches to the lumbar spine exist, but in general, they are less morbid when compared to the thoracic spine. Anterior approaches to the lumbar spine may be selected for pathologies anterior to the dura, including vertebral body tumors, infection, or burst fractures. A relatively common approach for lumbar disc disease is the anterior lumbar interbody fusion (ALIF). ALIF is best indicated in patients with the collapse of disc space, causing foraminal stenosis without significant canal stenosis. In this technique, an indirect decompression of the neural foramina is accomplished through a wide discectomy and placement of a large graft anteriorly into the disc space. An access surgeon is almost always required by the neurosurgeon for ALIF procedures. In addition, the ALIF is best done in the lower lumbar spine (L4-S1) to avoid the major vessels anteriorly. Lateral or oblique approaches to the lumbar spine may be done for similar indications as an ALIF and frequently do not require an access surgeon by the neurosurgeon. A more common indication for a lateral approach to the lumbar spine is also disc disease without significant central canal compromise. Similar to the ALIF, indirect decompression is done in lateral or oblique approaches. Here, a coronal deformity of the spine may also be corrected. Aside from disc surgery in a lateral or anterior approach, vertebral body resections (corpectomies) with the placement of large grafts may be done for tumor, fracture, or infection. For lateral approaches to the lumbar spine, L2-L4 are, in general, most easily accessed. Levels superior to L2 are often limited by the ribs, and rib resection may be required. Levels inferior to L4 are, in general, limited by the iliac crest. In addition, anterior and lateral fusions of the thoracic or lumbar spine are also often supplemented by posterior pedicle screw fixation for additional stability when needed.[34]

Despite the above approaches, posterior approaches, especially in the lumbar spine, remain the most common. This is due to the following general reasons: ease of access, decreased morbidity, often shorter patient recovery, and versatility for the surgeon. For most degenerative lumbar pathology, a posterior approach is a good option. For lumbar claudication secondary to congenital stenosis, a simple laminectomy may be adequate. If significant disc pathology is also present, a laminectomy may be supplemented with a partial or complete discectomy. Complete discectomies may be accomplished through a posterior corridor (posterior lumbar interbody fusion [PLIF]) or a more lateral corridor (transforaminal lumbar interbody fusion [TLIF]) and need to be supplemented with disc grafts as well as pedicle screw fixation.[34][35]

As shown above, a wide variety of approaches to the cervical, thoracic, and lumbar spine are available in the armamentarium of the spine surgeon. Approaches should be selected based on the location of the pathology in the spine and its relation to the spinal canal. In addition, the surgeon should always keep in mind his or her skill level and what is safest in the surgeon's hands. Preexisting medical conditions of the patient also play a large part in selecting an approach. The best approach is often the safest approach.

Differential Diagnosis

Patients with symptomatic spinal cord compression will often present with some degree of back pain and neurologic complaints. In addition to etiologies discussed in this paper, the broad differential diagnosis should include spinal cord infarction, transverse myelitis, subarachnoid hemorrhage, aortic pathology, including dissection/aneurysm, and acute myocardial infarction.[36]

Among patients presenting with symptoms and exam findings suggestive of cauda equina syndrome, differential considerations include MSCC, leptomeningeal carcinomatosis, and non-neoplastic causes, including intervertebral disc extrusion and osteoporotic fracture.

When extrinsic spinal cord compressive disorders are ruled out based on MR or CT myelography imaging in a patient with acute neurologic deficits, inflammatory, demyelinating, or toxin-related disorders must also be considered. These might include amyotrophic lateral sclerosis (ALS), Guillain-Barre syndrome, HIV myelopathy, botulism, multiple sclerosis, or transverse myelitis and warrant further evaluation with neurologic consultation, as well as additional studies, i.e., lumbar puncture and cerebrospinal fluid analysis, electromyography (EMG).


Untreated cervical spondylotic myelopathy may manifest as a slow progression of worsening gait, upper and lower extremity weakness, sensory loss, and pain.[8] Acute neurologic changes in the setting of cervical spondylosis with even a minor neck injury should prompt urgent investigation. Following surgical decompression, 50% to 80% of patients report improvement in symptoms, while a range of 5% to 30% may worsen.

Prompt identification of MSCC is crucial to attaining a favorable neurologic outcome. Multiple studies have shown that pretreatment neurologic deficits and duration of symptoms are important prognostic indicators for the preservation of ambulatory function. Accordingly, severe (1 to 2 out of 5 on motor strength testing) weakness and inability to ambulate for more than 48 hours before diagnosis are both associated with poor neurologic outcomes.[37] Fortunately, increased recognition of new-onset back pain in an ambulatory cancer patient as a red flag among primary care and emergency providers has resulted in earlier diagnosis of MSCC when comparing recent data to studies of patients with MSCC through the 1990s.[38][39]

Approximately 5% of patients with SEA die from sepsis or other complications.[15] Irreversible paraplegia occurs in up to 22% of patients.[40][41] A retrospective outcome study of 97 patients discharged from two large urban academic hospitals following treatment for SEA demonstrated a 37.1% 90-day readmission rate, with persistent infection comprising 36.1% of all readmissions. Risk factors for readmission included baseline immunosuppression, alcohol use disorder, and chronic hepatitis. Interestingly, treatment strategy (conservative vs. surgical) was not associated with a higher risk of readmission.[42]


The most feared complication of untreated spinal cord compression from any source is an irreversible neurologic deficit, including paralysis, gait impairment, sensory loss, urinary and fecal incontinence, or retention.

Surgical complications following spinal cord decompression are variable, but include iatrogenic spinal cord or nerve root injury, durotomy with subsequent cerebrospinal fluid leak, epidural hematoma, wound infection, and nonunion. These must be weighed against the perceived benefits of operative decompression, taking into account each patient's age, comorbidities, duration, and severity of symptoms.

In patients treated with conservative treatment, there is a possibility of acute paraplegia as a consequence of subtle occlusion of arteries that sustain the spinal cord. This is more possible in older patients with atherosclerosis.

Deterrence and Patient Education

Back pain is one of the more common reasons for unplanned emergency department visits, short- and long-term disability. Patients often present for care with a primary desire for pain relief. Imaging is not typically helpful for acute back pain in a patient without the aforementioned “red flag” risk factors. It will not change management for a patient with a neurologically intact exam. When caring for a patient with acute back pain, it is important to emphasize the relative value of imaging and why (or why not) it is indicated.

If a patient is deemed stable for discharge home and a plan for outpatient follow-up, one should review return precautions related to pathological and surgical causes of back pain. Symptoms suggestive of spinal cord compression might include bilateral arm or leg symptoms, weakness, numbness, urinary retention, urinary or stool incontinence, gait difficulty, or worsening midline back pain in a patient with a history of malignancy.

Enhancing Healthcare Team Outcomes

This activity reviews the evaluation and management of atraumatic spinal cord compression. It highlights the roles of the emergency physician, neurosurgeon, and inpatient care team in treating patients with this condition.

Atraumatic spinal cord compression occurs as a result of numerous possible etiologies and is notoriously difficult to identify in the early stages. Delayed diagnosis can result in permanent neurological disability or death. Practitioners should recognize that further evaluation is warranted when early symptoms, such as back pain, motor weakness, sensory deficits, or gait difficulty, are present, especially in the context of known risk factors. This will lead to improved recognition of potential abnormalities, which, in turn, will dictate treatment strategies and improve patient outcomes.

Review Questions


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Disclosure: Jennifer Singleton declares no relevant financial relationships with ineligible companies.

Disclosure: Matthew Hefner declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK557604PMID: 32491536


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