Spinal Epidural Abscess

More Back Pain
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Diagnosis and reasoning

The presentation of this elderly lady is complex, combining both acute and subacute problems. The history of a fall earlier, the subsequent back pain, and the neurological signs in the lower limbs suggest spinal cord compression secondary to a spinal fracture. This is confirmed by the x-ray of the lumbosacral spine, which shows involvement of the T12 vertebra. Reduced ambulation in the elderly is a serious problem, as this predisposes towards hypostatic pneumonia. The risk is even higher in this patient, considering the history of diabetes (which impairs immunity). This is an important differential to consider when analyzing the high fever of recent onset. Another possibility is a urinary tract infection, given that she has a neurogenic bladder causing urinary stasis (the urinary incontinence is due to overflow incontinence). However, her chest x-ray and urinalysis are normal - excluding these possibilities. In addition, the full blood count shows a profound neutrophil leukocytosis, indication that an infection is almost certainly present - although the focus is unclear. At this point, one other possible focus of infection remains - the site of the vertebral fracture. The hematoma which would have formed there initially is an excellent culture medium for bacteria, predisposing her to spinal infections such as osteomyelitis or paraspinal or epidural abscess formation. An MRI of the spine is advisable to assess this possibility - and in this patient reveals features suggestive of a spinal epidural abscess (SEA). Note that drainage is required to confirm this diagnosis - and surgical drainage is the treatment of choice in the majority of patients. There is one more important aspect to her management. The possibility of a hyperglycemic hyperosmolar state (HHS) or diabetic ketoacidosis (DKA) should be suspected in all diabetic patients who are drowsy and confused - and vigilance should be doubled if an obvious infection is additionally present. However, in this patient, the normal electrolytes and only mildly elevated capillary blood sugar exclude these diagnoses. IV antibiotics should be started empirically as soon as the diagnosis is suspected. In addition, tight glycemic control with insulin is essential to control the infection. CT guided aspiration is an option in patients with minimal or no neurological signs. Corticosteroids are contraindicated as they will impair glycemic control and potentially worsen the infection.


A spinal epidural abscess (SEA) is a rare but severe infection of the epidural space. It is a neurological emergency which can be fatal if left untreated. The incidence is 2.8 cases per 10,000 admissions, with a male predominance. Typically, the age of onset is over 50 years, but patients of any age may be affected. The spinal epidural space is a space between the dura and the ligamentum flava and periosteum of the vertebral bodies, pedicles and laminae. Posteriorly, it contains fat, small arteries and the venous plexus; anteriorly, the epidural space is a potential space with the dura tightly adherent to the vertebral bodies and ligaments. As might be imagined, SEAs occur more frequently in the larger posterior space. As they increase, they usually extend along the dural sheath, involving several spinal segments. The three basic mechanisms by which an abscess can form in the epidural space are hematogenous spread, direct extension from an infected contiguous structure and iatrogenic inoculation. In case of hematogenous spread, skin and soft tissue infections are most frequently responsible. Other common sources include the respiratory tract, genitourinary system, abdominal viscera, oral cavity and, in endocarditis, the heart valves. Intravenous (IV) drug abuse has been suspected as another important mechanism via which hematogenous spread may occur. Direct extension usually originates from vertebral osteomyelitis or psoas muscle abscess. Iatrogenic causes include invasive procedures such as surgery, lumbar puncture, epidural analgesia and nerve blocks. Note that in 30% to 40% of the cases, no source can be identified. In addition, most patients with SEA have one or more predisposing conditions such as an underlying disease (especially diabetes mellitus, alcoholism or HIV infection), spinal abnormalities or spinal trauma. The clinical manifestations of SEA are variable, with the classic triad of symptoms being spinal pain, fever and neurological deficits. However, relentless, localized back pain most often the first symptom and is experienced by the vast majority of patients. The severity of neurologic compromise varies, ranging from a monoradiculopathy to a complete cord lesion. The progression of symptoms and clinical findings of SEA have been described in four stages: spinal pain; nerve root pain and spinal tenderness; motor weakness, loss of sensation, impaired sphincter control; and complete paralysis. The diagnosis of SEA must be made promptly, as a delay in treatment can lead to irreversible neurological impairment and even death. SEA may be suspected on the basis of clinical findings, while laboratory data and imaging studies may provide supportive evidence. However, drainage is the only means of confirming the diagnosis. The majority of patients have a leukocytosis and essentially all patients have an elevated ESR. Blood cultures should always be obtained and allow early isolation of the causative microbe in two thirds of patients. A search for potential causes of bacteremia may be carried out by performing urine cultures and echocardiography. Imaging of the spine is essential when the diagnosis of SEA is clinically suspected. MRI is the procedure of choice as it accurately localizes the abscess while also delineating its extension (which is essential for planning surgery). CT myelography may be used where MRI is not available. Diagnostic procedures that penetrate the spinal canal should generally be avoided. The causative microbe can be confirmed by obtaining specimens via surgical drainage. While Staphylococcus aureus is the most frequently isolated pathogen, a vast variety of other organisms (including mycobacteria, fungi and parasites) have been implicated. The principles of management are drainage of the abscess and eradication of the microorganism - and this is accomplished by a combination of medical and surgical therapy. Empirical antibiotic therapy should be commenced as soon as the diagnosis is suspected, and altered (if necessary) once culture results are available. Emergency surgical drainage (with simultaneous decompression of the spinal cord) is mainstay of treatment in the overwhelming majority of patients. However, medical management alone may be considered in patients who present with minimal neurologic deficit or are poor candidates for surgery. During and after treatment, these patients require frequent evaluation of neurological status and follow-up laboratory and imaging studies. The single most important predictor of the final neurologic outcome is the patient's neurologic status immediately before surgery. If adequately decompressed, the outcome is usually as good if not better than the preoperative condition. About 5% of patients with SEA die, usually because of uncontrolled sepsis, evolution of meningitis or other underlying illnesses.

Take home messages

  1. SEA is a neurological emergency characterized by the triad of fever, spinal pain and neurological deficits.
  2. Many patients have a predisposing medical condition, spinal abnormalities or spinal trauma. IV drug abusers are also at risk.
  3. Prompt diagnosis is a must - the longer the delay in initiating treatment, the worse the ultimate neurological outcome.
  4. Emergency surgical drainage and decompression is the treatment of choice.

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  1. Medical vs Surgical Management of Spinal Epidural Abscess : Archives of Internal Medicine, 2004
  2. Spinal Epidural Abscess in Adults: American Academy of Orthopaedic Surgeons, 2004.
  3. Spinal epidural abscess : NEJM, 2006
  4. Spinal epidural abscess in clinical practice: QJM, 2008
  5. Successful treatment of extended epidural abscess and long segment osteomyelitis: Surgical Neurology, February 2008