A 66-year-old man was brought to the ED by ambulance for evaluation of severe neck pain, headache, and nausea for 3 days. He says the pain is worse and lasting longer than previous episodes.
The patient states that he had multiple similar episodes of neck pain and headache over the last several years since suffering from a spontaneous subdural hemorrhage requiring a craniotomy. Two days ago, he was seen in the ED for this pain, and told the ED provider that a muscle spasm of his neck was causing his headache and nausea. He said that his symptoms 2 days ago were similar to those in previous episodes, which were successfully treated with muscle relaxants and analgesics.
At the ED visit 2 days ago, the patient had an otherwise unremarkable physical examination and was treated symptomatically with hydromorphone, diazepam, and ondansetron. No additional workup was obtained at that time. He was discharged home with a prescription for combination acetaminophen and oxycodone.
At today's visit, the patient rates his pain as a 10 on a 0-to-10 pain intensity rating scale and says the combination acetaminophen and oxycodone did not relieve his pain. He denies any other neurologic symptoms including weakness, numbness, difficulty walking, change in vision, difficulty with thought or speech, or other systematic complaints. He has had no recent falls or head and neck trauma. He is not under the care of a chiropractor, and has not had any spinal interventions in many years.
He takes no daily medications and has no known drug allergies. In addition to the craniotomy, his surgical history includes a partial small bowel resection 4 years ago to treat an obstruction. He smokes a pack of cigarettes daily and occasionally drinks alcohol. He denies illicit drug use. His family history is remarkable for type 2 diabetes and hypertension. He has no family history of coronary artery disease, stroke, or coagulopathies.
On arrival to the ED, the patient was in moderate distress. He was sitting upright on the ambulance stretcher and moaned in pain when he was moved to the hospital bed. He preferred to sit upright rather than lie down. His vital signs were: BP, 134/80; heart rate, 114 and regular; respirations, 19; oral temperature, 38.95° C (102.1° F); and SpO2, 91% on room air. The patient appears much older than his stated age of 66 years. He had decreased range of motion in his neck with exquisite tenderness diffusely throughout the posterior cervical region without step-off, mass, or rash. The remainder of the head-ears-eyes-nose-and-throat examination was unremarkable. Heart and lung auscultation also were unremarkable with the exception of sinus tachycardia. Of note, the patient complained of increased neck pain when asked to sit forward for auscultation. A complete neurologic examination showed no abnormalities of sensation, movement, and strength. Grip strength was normal and equal bilaterally, but the patient complained of increased neck pain with abduction of either shoulder.
The patient was placed on 2 L of supplemental oxygen via nasal cannula. IV access was obtained and he was treated symptomatically with hydromorphone, ondansetron, and acetaminophen. Samples were sent for a complete blood cell (CBC) count, comprehensive metabolic panel, troponin level, and coagulation studies. An ECG and a CT angiogram of the head and neck were ordered.
The ECG revealed sinus tachycardia at a rate of 123 beats/minute. Laboratory studies were remarkable for a white blood cell count of 22,500 cells/mm3 (normal range, 4,800 to 10,800 cells/mm3), blood urea nitrogen level of 40 mg/dL (normal range, 5 to 20 mg/dL), creatinine of 1.47 mg/dL (normal range, 0.7 to 1.4 mg/dL), and glomerular filtration rate of 49 mL/min/1.73 m2. Troponin was negative. Coagulation studies were normal. Secondary to the leukocytosis, a venous lactate level was obtained and was normal at 0.6 mmol/L. Samples were sent for two sets of blood cultures and erythrocyte sedimentation rate (ESR).
Because of his renal status, the patient was hydrated with IV 0.9% sodium chloride solution before undergoing a CT angiogram of the head and neck. The CT showed no acute intracranial abnormality and no significant arterial abnormality in the head or neck. A gas-containing epidural collection was noted in the upper cervical spine, exerting significant mass effect on the spinal cord. Edema was noted in the prevertebral/retropharyngeal space (Figure 1). The radiologist recommended obtaining an MRI.
At this time a consult was requested with the on-call neurosurgeon. The patient was administered IV ceftriaxone and vancomycin and had a repeat neurologic examination. The patient was neurologically intact but continued to complain of 10/10 neck pain. Additional pain medications were ordered.
After reviewing the radiographs, the neurosurgeon requested the patient undergo MRI imaging, which requires transfer to the university hospital. The neurosurgeon said the patient will need an extensive surgical drainage from an anterior approach. Serial neurologic examinations were conducted throughout the patient's ED stay. He remained neurologically intact and stable. The patient was diagnosed with a cervical epidural abscess with cord compression.
Spinal epidural abscesses are a rare but potentially fatal infection that occurs within the epidural space and the spinal cord.1 Spinal epidural abscesses occur in only 2 to 25 patients per 100,000 admitted to the hospital; however, the incidence may have increased over the last 30 years.2 Part of this increase may relate to the fact that MRI has improved the sensitivity and accuracy of diagnosis.2
Infections of the epidural space can originate from continuous spread or through hematogenous routes from a distant source.1 If untreated, the abscess grows and eventually compresses the spinal cord. Spinal epidural abscesses most commonly occur as a complication from skin infections; other causes include septicemia, vertebral osteomyelitis, IV drug use, spinal surgery, epidural anesthesia, and lumbar puncture.1,2 Staphylococcus aureus is the most common causative organism.2,3 Risk factors include IV drug use, diabetes, chronic renal failure, alcohol abuse, and immunosuppression.4 Thoracic and lumbar sites are more commonly affected than cervical sites.4
The classic clinical presentation is back pain that has localized to a tender site, fever, sweats, and rigors. Later symptoms include paralysis, sensory disturbance, and bowel and bladder disturbance.3,4 Classically, the triad of back pain, fever, and progressive neurologic deficits should increase concerns for a spinal epidural abscess, but these findings may suggest late disease.
Spinal epidural abscess is a neurologic emergency and patients should undergo an extensive workup and aggressive treatment. MRI with gadolinium of the affected spinal region is the diagnostic test of choice, but CT angiography of the neck also can provide clues to the diagnosis.4 Laboratory analysis should, at minimum, include a CBC count for leukocytosis and an ESR, which although nonspecific, is elevated in nearly all patients.4 Obtain blood cultures and culture of the abscess to determine the causative organism.3 Avoid lumbar puncture, which may disseminate the infection from the epidural space into the subarachnoid space.3
Obtain an urgent surgical consultation for decompression and start empiric antibiotics with coverage for Gram-positive and Gram-negative organisms.4 Several antibiotic regimens exist, but commonly nafcillin is given for Gram-positive coverage; vancomycin for methicillin-resistant organisms; and a third- or fourth-generation cephalosporin, such as ceftazidime or cefepime, for Gram-negative coverage.1,4 Reevaluate the antibiotic regimen after culture results are obtained.
Although surgical decompression was once considered mandatory in all patients with a spinal epidural abscess, the earlier diagnosis made possible by MRI has reduced the need for surgical intervention in some patients.1,2 Surgical decompression is still considered the mainstay of treatment in all patients with an associated neurologic deficit.2
Prognosis depends on the severity of disease progression at the time of diagnosis. The disease is thought to be fatal in 18% to 23% of patients, and patients with neurologic deficits rarely regain full function if the deficits are present for more than 36 hours before surgical intervention.4
The patient was transferred to the university hospital for further neurosurgical evaluation. He remained fully neurologically intact and due to the large size of the abscess and evidence of spinal cord compression, surgical decompression was performed via an uncommon anterior approach.
The patient completed 8 weeks of IV antibiotics, participated in occupational and physical therapy, and made a full recovery. The source of infection was never determined.