• Neuroradiol J · Jun 2010

    Hydromyelia secondary to spinal epidural abscess. A case report.

    • R Saponiero, A Toriello, G Locatelli, N Narciso, L Posteraro, M P Panza, A N Napoli, F Romano, and N D Pugliese.
    • Neuroradiological Unit, S. Giovanni di Dio e Ruggi d'Aragona Specialist Universitary Hospital; Salerno, Italy - renato-saponiero@sangiovannieruggi.it.
    • Neuroradiol J. 2010 Jun 1;23(3):339-42.

    AbstractSpinal epidural abscess (SEA) is a rare condition that can be fatal if untreated. Risk factors are immunocompromised states as well as spinal procedures including epidural anesthesia and spinal surgery. The signs and symptoms of SEA are nonspecific and can range from low back pain to sepsis. The treatment of choice is surgical decompression followed by four to six weeks of antibiotic therapy. The most common causative organism in SEA is staphylococcus aureus and spread is usually haematogenous or contiguous from psoas, paraspinal or retropharyngeal abscesses. The exact mechanism by which an epidural abscess causes spinal cord damage is unclear. In fact, the damage is often out of proportion to the degree of compression demonstrated radiologically. There is only a report of a patient with syrinx formation secondary to epidural abscess. We describe the case of a 48-year-old woman with a two-week history of thoracic back pain and evidence of dorsal SEA probably from contiguous psoas abscess. Neurological examination revealed flaccid paraplegia and loss of sphincter control. A spinal MRI scan with Gd-enhancement revealed focal high intensity signal in the T2-weighted and FLAIR images at the level of the vertebral bodies in segments D3-D11. The patient was treated with posterior decompression and drainage of the SEA, but with a poor outcome. Six weeks after the onset of symptoms, an MRI scan showed a newly-formed hydromyelia formation from D4 to D8. The case reported is the second to describe hydromyelia formation secondary to epidural abscess and a poor outcome, experiencing partial improvement without recovery. For this reason, we confirmed that the essential problem of SEA lies in the need for early diagnosis, because the early signs and symptoms may be vague and the "classic" triad of back pain, fever and variable neurological deficits occur in only 13% of patients by the time of diagnosis. Only timely treatment will avoid or reduce permanent neurological deficits before massive neurological symptoms occur. The clear message is that a high index of suspicion and modern imaging techniques are essential.

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