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Quick Consult: Symptoms: Low-Grade Fever and Hypotension

Wiler, Jennifer L. MD, MBA

doi: 10.1097/01.EEM.0000414928.07298.f4
Quick Consult

Dr. Wileris an assistant professor of emergency medicine and the medical director of reimbursement at the University of Colorado Denver School of Medicine and an adjunct assistant professor of emergency medicine at the Washington University School of Medicine in St. Louis.

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A 69-year-old man with history of diabetes was found down for an unknown time by neighbors. He is obtunded, withdrawing to pain only with his right arm when he arrives in the ED.

He has a low-grade temperature and is hypotensive. A CT scan of the brain is unremarkable, but the cervical C-spine CT scan is shown in the photograph.

What is the diagnosis, and how would you manage this condition? See next page.

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Diagnosis: Epidural Abscess

An epidural abscess is a rare but potentially life-threatening condition where pus accumulates in the epidural space, the area between the dura that covers the spinal cord and brain and the bony compartment that it is enclosed by the skull or vertebra. Two different variants of epidural abscesses exist, and are defined by their location: spinal or intracranial. Because the dura tightly adheres to the skull, epidural abscess formation in the brain results in a space-occupying lesion that can raise intracranial pressure, and is immediately life-threatening.

Spinal epidural abscesses can involve multiple vertebral levels because the dura is less adherent to the vertebral bodies. The dura is tightly adherent anteriorly to the verbral body but less so posteriorly in the space that contains vascular structures and fat. Lumbar and thoracic abscess location is most typical (the cervical spine accounts for less than 20 percent; Pain Physician 2004;7[2]:269) because the epidural space is relatively larger than in the cervical region, but abscess can extend anywhere along the dural sheath.

The average length of spread along the spinal canal is three to five levels. (Medicine [Baltimore] 1992;71[6]:369.) Spinal epidural abscess is nearly 10 times more common than intracranial epidural abscess.

Most epidural abscesses (nearly 50%) are the result of hematogenous seeding from a remote infectious source. Another 30 percent are from extension of local infection (e.g., vertebral osteomyelitis), and approximately 20 percent are from local instrumentation (e.g., lumbar puncture). Some reports say as many as 30 percent, however, are from an unknown source.

Risk factors for spinal epidural abscesses are immunocompromising conditions including diabetes mellitus or alcohol abuse, acupuncture, local instrumentation, intravenous drug abuse, spinal trauma (may be remote), renal insufficiency, and pregnancy. (N Engl J Med 2006;355[19]:2012; Neurosurg Rev 2000;23[4]:175.)

Abscess can cause spinal cord injury by direct compression, inflammatory mediated local injury, thrombosis, or acute vascular compromise. More than 50 percent of spinal epidural abscesses are caused by Staphylococcus aureus. (Neurosurg Rev 2000;23[4]:175) with methicillin-resistant (MRSA) infections on the rise. (N Engl J Med 2006;355[19]:2012.) Mycobacterium tuberculosis is fairly uncommon in the United States, but is a known etiology in developing countries. (Adv Tuberc Res 1980;20:92.)

Intracranial epidural abscesses are most commonly caused by Staphylococcus species, and are the result of intracranial trauma or instrumentation. If the infection is an extension from the sinuses or ear, then anaerobes are more common. Because the dura is adherent to the skull and the potential space limited, intracranial epidural abscesses tend to be well localized elliptical pockets of infection caused by the dura dissecting away from its bony support.

Patients with intracranial epidural abscess can have subdural extension because of seeding of venous outflow vessels in the brain. Risk factors for developing intracranial epidural abscesses are immunocompromising conditions including diabetes mellitus and alcohol abuse, post-craniotomy or head injury, neonates with fetal monitoring probes, and infections of the head including mastoiditis, sinusitis, and otitis media.

Diagnosing spinal or intracranial epidural abscesses can be challenging because of myriad possible clinical presentations and examination findings that do not follow a classic neurological impairment picture. The clinical presentation of an intracranial epidural abscess depends on the location and size of the infection. Patients can present with signs of increased intracranial pressure or local trauma from an expanding mass occupying lesion.

Symptoms are the result of the infection and the intracranial lesion. Presentation may be as severe as coma, altered mental status, and vital signs consistent with sepsis, or a focal neurologic deficit that mimics a vascular stroke. Patients with spinal epidural abscesses typically have a more indolent presentation, which makes the initial diagnosis challenging and often leads to diagnostic delays. (J Emerg Med 2004;26[3]:285.)

Local inflammation can cause pain and then motor dysfunction, sensory changes, and paralysis. Less likely, patients present altered and septic. Physical findings depend on the size and location of the abscess, but can include fever (present in less than half of patients), headache, or back pain, focal neurologic deficits, wound infection, seizure (intracranial), and local tenderness on palpation (spine lesion).

Patients may have elevated inflammatory markers (ESR, CRP, and leukocytosis), but these nonspecific findings are not always present. Blood cultures should be obtained because they are positive in nearly 60 percent of patients and can guide antibiotic therapy. MRI with gadolinium is the diagnostic imaging modality of choice to make the diagnosis of spinal and intracranial epidural abscess because it best identifies early infection and inflammation. (Semin Roentgenol 2006;41(4):363; N Z Med J 1998;111[1073]:345.)

CT scan with IV contrast can be used if MRI is not available. If epidural abscess is suspected, lumbar puncture should not be performed because it can elicit hematogenous and local spread or result in brain herniation.

The differential diagnosis of epidural abscess is extensive, and includes all etiologies of back pain, headache, sepsis, and altered mentation.

If epidural abscess is suspected or confirmed, neurosurgery should be emergently consulted, and consultation with an infectious disease specialist may be prudent. Whether to treat patients with spinal and intracranial epidural abscesses medically or surgically depends on the patient's condition, but includes treatment of the infectious agent and elimination of the abscess mass.

Broad-spectrum empiric antibiotics are the cornerstone of initial treatment, with tailored treatment initiated once the underlying pathogen has been identified. Surgical intervention can be performed for diagnostic and therapeutic treatment. Granulation tissue is commonly found at the time of surgical drainage. Permanent paralysis from spinal epidural abscess is reported to be as high as 20 percent. (Neurosurgery 1996;39[5]:958.)

Despite modern treatments, the mortality rate of from spinal epidural abscess is approximately five percent, usually from sepsis and multisystem failure. (N Engl J Med 2006;355[19]:2012.] But the mortality rates of an epidural abscess are as high as 20 percent with comorbid conditions. Delays in diagnosis and intervention are known risk factors for poor outcomes.

The cervical spine CT of this patient showed a large area of edema in the left paraspinal musculature with foci of subcutaneous gas extending from the levels of C3–5 consistent with inflammation or infection. Early goal-directed therapy was initiated in the emergency department.

He was found to have MSSA bacteremia and endocarditis. A subsequent MRI revealed a large epidural abscess extending from the cervical to the lumbar spine with evidence of spinal cord compression. Given the risks, the family decided to not pursue surgical decompression and drainage. The patient was transitioned to comfort care and expired.

© 2012 Lippincott Williams & Wilkins, Inc.