After receiving this report, the hospitalist contacted neurosurgery services. Shortly thereafter the patient underwent unilateral laminotomy with bilateral canal decompression on hospital day 5. He was discharged home on hospital day 10 without any neurological deficits, and continued IV antibiotics as an outpatient for an additional 5 weeks.
Discussion
Only a minority of patients with SEA present with the classic triad of back pain, fever, and progressive neurological findings associated with this condition.1Careful history-taking therefore is essential to identify high-risk patients. Risk factors for SEA include diabetes, IV drug abuse, immunosuppression, chronic renal failure, liver disease, alcoholism, indwelling catheter, recent invasive spinal procedure, recent vertebral fracture, cancer, and distant site of infection.1-3,5,7,11
Leukocytosis (WBC >10×109/L) is only found in two-thirds or less of patients with SEA at the time of admission.1,3,12 Inflammatory markers such as CRP and ESR are more sensitive but not specific to SEAs.1,2,5,7,11-13
An MRI study with gadolinium is the diagnostic modality of choice over computed tomography myelography to assess for SEAs due to its noninvasive nature and ability to better delineate the extent of disease.5,7,14 An MRI of the entire spine is recommended to delineate longitudinal and paraspinal extension as SEA can traverse multiple vertebral levels.15 While awaiting the results of blood cultures, patients should be treated with broad spectrum antibiotics that include coverage of the most common etiology of SEA, S aureus.1,3,4,7,11,13 While some cases of SEA may be managed medically, the emergency physician should always treat SEA as a neurosurgical emergency and obtain consultation with the appropriate services (eg, neurosurgery, infectious disease, neurology radiology).1,5
Our patient represents an unusual case of SEAs in that he presented with S aureus bacteremia while afebrile, along with back pain and tachycardia. He subsequently developed SEA, which was recognized only through serial MRI studies. The patient’s tachycardia alone could have been easily attributed to pain and anxiety associated with the ED environment. As such, he could have easily been discharged home with a prescription [for] nonsteroidal anti-inflammatory drugs and/or muscle relaxers for pain management—though it is likely that he would have returned to the ED 3 days later with persistent and even worsening symptoms, during which he would have undergone additional testing, possibly MRI, which would have revealed the missed SEA.
Our case clearly demonstrates that no SEA was present at the time of the patient’s visit. Thus, the proverbial “missed SEA” may not have been overlooked but rather had not yet developed.
Studies show that half of all patients with SEAs are not diagnosed until after two or more visits to the ED.1,11 The literature posits that most cases are misdiagnosed at the time of initial evaluation. It has even been postulated that “misdiagnosis of spinal epidural abscess is the rule rather than the exception.”1 Although our patient was eventually diagnosed with a SEA, it was not present on the first MRI taken during the initial evaluation.
Summary
Unlike the rules of quantum mechanics and the paradox of Schrödinger’s cat, SEA follows a progression of disease.3,7,16 There is no superposition—the MRI is either positive or negative. However, excellent care requires the practitioner to know the risk factors of SEA, apply the appropriate screening tests, obtain MRI when necessary, and if diagnostic uncertainty remains, discuss with the patient or family signs and symptoms to monitor as well as reasons to return for re-evaluation.