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Symptoms: Back Pain, Inability to Stand

Barrett, Whitney MD; Smith, Travis MD

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doi: 10.1097/01.EEM.0000532175.68949.d5
    Spinal Epidural Abscess
    Spinal Epidural Abscess:
    A normal spine x-ray.
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    Figure
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    A 57-year-old homeless man with a past medical history of hepatitis C and renal cancer after a partial nephrectomy presented with back pain for three days after a ground-level fall. He described his lower back pain as constant and aching.

    His pain worsened with ambulation and sleeping on hard ground. He was seen at another emergency department twice before. The first yielded an x-ray and the second symptomatic therapy. He was seen in an urgent care center before his current presentation for the same symptoms, and was diagnosed with a urinary tract infection.

    He was taking methadone for opiate abuse, and stated that he had taken his usual dose of 345 mg by mouth one hour before presentation. He had also injected heroin the night before. He was able to walk out of the urgent care center earlier and to go to a methadone clinic, but he came to the ED because he could no longer walk. He denied fever, numbness/tingling, bowel or bladder incontinence, dysuria, and urinary retention.

    His vital signs were normal, and his oral temperature was 37.3°C. He was thin but in no acute distress. He was markedly somnolent and fell asleep frequently during the visit. His pupils were miotic, he had no neck tenderness or stiffness, and he was tender to palpation of the midline high lumbar spine and over the paralumbar muscles. His lower-extremity exam was notable for normal reflexes and tone but 4/5 strength bilaterally throughout with an indeterminate Babinski's sign bilaterally. He was unable or unwilling to stand.

    What additional lab tests would be useful in further risk-stratifying this patient? What imaging study could guide management of this patient?

    Find the diagnosis and case discussion on p. 26.

    Diagnosis: Spinal Epidural Abscess

    Spinal epidural abscess (SEA) is considered a rare disease, but has been increasing in incidence from about 0.5 per 10,000 admissions this past century to 3-8 per 10,000 admissions now. This may be related to the increasing age of the population, total number of spinal procedures, rising IV drug abuse, prevalence of acquired immunodeficiency syndrome, and improving sensitivity of imaging modalities. About three-quarters of patients with SEA are over age 50 and male (2:1 has been described). (J Emerg Med 2010;39[3]:384.)

    Diagnostic delays are common due to vague symptoms and nonspecific exam findings on early presentation. Half of patients had at least one prior health care visit for similar symptoms the month before diagnosis. Three-quarters of patients were misdiagnosed on the initial ED visit. (Open Forum Infect Dis 2016;3[4]:2.) Despite diagnosis delays, SEA mortality has decreased from 80 percent to two to 20 percent likely from antibiotics and improved surgical management.

    SEA occurs when microorganisms gain access to the epidural space by hematogenous spread, direct inoculation, contiguous foci, or idiopathic causes. The mechanism for neurologic deficits in SEA, although debated, is likely related to a combination of direct compression of the spinal cord and circulatory compromise from venous stasis and arterial thrombosis in the infected area. Posterior spinal epidural abscesses are more common with the spread of distant infection. Anterior epidural abscesses are more commonly associated with discitis or vertebral osteomyelitis. (N Engl J Med 2006;355[19]:2012.)

    Early diagnosis remains elusive. Back pain is the most common presenting symptom, occurring in 70 to 100 percent of patients. The classic triad of back pain, fever, and neurologic deficits occur in only two to 37 percent of patients, depending on the study. Most patients present with variations of the “classic triad,” including symptoms like radicular or paraspinous pain. Eighty percent of patients ultimately diagnosed have at least one risk factor, which includes diabetes mellitus, IV drug use, alcohol abuse, and other immunocompromised states. Additional risk factors can be recent or remote instrumentation of the spine, epidural analgesia, nerve acupuncture, tattooing, other sites of infection, and trauma. A thorough history of symptoms and risk factors is crucial to identifying who warrants further workup.

    Figure
    Figure:
    This patient's thoracic and lumbar spine MRI showed epidural abscesses at L3-L4 and L4-L5, multiple posterior paraspinal abscesses at L3, L4, and L5, and osteomyelitis of the L3 and L4 spinous processes.

    Evaluation includes lab testing with progression to imaging, and erythrocyte sedimentation is the most helpful blood test for screening. About 80 percent of SEA patients had an ESR greater than 50 mm/hr, and all had an ESR greater than 20 mm/hr. (Open Forum Infect Dis 2016;3[4]:4.) C-reactive protein is more useful to monitor for response to treatment. Lumbar puncture should not be routinely performed because it rarely isolates the causative organism and risks spreading infection. Blood cultures are frequently positive and useful for guiding antibiotic treatment. (J Emerg Med 2010;39[3]:384.)

    MRI is the test of choice for detecting SEA with greater than 90% sensitivity and specificity. CT myelography is an invasive test that is less specific than MRI and risks contaminating the subarachnoid space, but can be considered if MRI is not possible. Routine MRI screening in ED patients with back pain is not feasible, so the provider (or institution) should consider using symptoms, risk factors, and lab results as screening tools before obtaining an MRI. A diagnostic decision tree can be found in the article by Davis, et al., in the Journal of Neurosurgery and Spine. (2011;14[6]:765.)

    SEA treatment includes early empiric antibiotics and neurosurgical consultation for surgical decompression. Antibiotics should be given as soon as blood and site-specific cultures are taken when possible, but should not be held preoperatively if sepsis or neurologic symptoms are present. A majority of SEA results from Staphylococcus. Before culture results are available, a combination of vancomycin and piperacillin/tazobactam or a third- or fourth-generation cephalosporin is recommended. Glucocorticoids may help to reduce swelling in patients with progressive neurologic compromise awaiting surgical decompression, but they have been associated with adverse outcomes and are not routinely recommended. (N Engl J Med 2006;355[19]:2013.)

    SEAs are staged based on symptoms: stage 1 by severe back pain at the level of the affected spine, fever, and local tenderness; stage 2 by nerve-root pain and neck stiffness; stage 3 by motor weakness, sensory deficit, and bladder and bowel dysfunction; and stage 4 by paralysis. Patients who receive surgery during stages 1 or 2 usually remain neurologically intact and have decreased risk of pain and radiculopathy. Patients who receive surgery in stage 3 may have no weakness or improved weakness from preoperative baseline. Patients who receive surgery in stage 4 for source control may regain some neurologic function. (J Emerg Med 2004;26[3]:285.)

    Our patient's ESR was greater than 80 mm/hr. An MRI of the thoracic and lumbar spine showed osteomyelitis, epidural abscesses, and multiple posterior paraspinal abscesses throughout the lumbar. He was started on intravenous vancomycin, cefepime, and metronidazole, and had a laminectomy performed at L3-L5 levels without complication. All of his cultures grew methicillin-sensitive Staphylococcus aureus. Antibiotics were narrowed to IV nafcillin for six weeks. On follow-up, the patient could perform his independent activities of daily living, and was scheduled to see the substance abuse team.

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