Approach

All patients are treated with empiric and subsequent culture-directed definitive antibiotic therapy. For patients with neurologic deficit, decompressive surgery is essential. In these patients, the single most important predictor of the final neurologic outcome is the patient's neurologic status immediately before decompressive surgery.[30]​ Transfer patients with suspected spinal epidural abscess (SEA) to a higher level of care. This may be required to obtain imaging studies (e.g., contrast-enhanced magnetic resonance imaging [MRI] or computed tomography [CT] myelogram), and access to a spine surgeon for removal of SEA.

Medical management versus surgical management

There is debate about the merits of medical versus surgical management for patients with SEA without neurologic deficit, and evidence is limited. There has been a move towards increased use of medical management for this population, but it is important to select patients carefully.[9][30][41][42][43]​ Factors that may increase the risk of treatment failure of medical management include: MRSA as the causative organism; diabetes mellitus; cervical or thoracic SEA; history of intravenous drug use; age >50 years; C-reactive protein (CRP) level >115 mg/L; white blood cell (WBC) count >12.5 cells/mm³.[6][9]

Antibiotic therapy

Antibiotic therapy should be started without delay, as soon as cultures from blood, purulent material, and other possible sources of infection have been obtained.[2][28]

Empiric therapy

Empiric antibiotic therapy should be started and continued until the causative agent is identified. Every attempt to obtain bacteriologic specimens should be completed first. Antibiotics include agents active against Staphylococcus aureus, including MRSA, streptococci, and aerobic gram-negative organisms.[2][30][44]​ A suggested regimen is vancomycin plus either a third- or fourth-generation cephalosporin (e.g., cefotaxime, ceftriaxone, cefepime, or ceftazidime) or piperacillin/tazobactam. In patients at high risk of Pseudomonas species infection (e.g., history of intravenous drug use), ceftazidime, cefepime, or piperacillin/tazobactam is recommended.[2]

Patients with risk factors for fungal SEA should also receive an antifungal agent such as voriconazole or amphotericin B.[2]

Definitive therapy

Identification and prompt treatment of the causative organism is paramount. The definitive choice of antibiotic depends on the results of microbiologic culture and susceptibility testing. Once the etiologic agent is identified, treatment is tailored to the sensitivity of the specific strain if possible.[2][30]

Total duration of antibiotic treatment varies from 4 weeks to 16 weeks, depending on several factors such as comorbidities and concurrent presence of vertebral osteomyelitis.[2] Most patients receive a minimum of 2 to 4 weeks of parenteral antibiotics, which may be extended if vertebral osteomyelitis is suspected.[2][9][30] This will be followed by oral antibiotics.

  • Antibiotic regimens for methicillin-sensitive S aureus infection most commonly include nafcillin or a first-generation cephalosporin (e.g., cefazolin).

  • Antibiotic treatment of choice for MRSA infection is vancomycin. Some experts recommend adding rifampin to vancomycin.[45] Second-line options include trimethoprim/sulfamethoxazole and linezolid.[45][46] These may be used due to vancomycin allergy/intolerance or if there is a need to switch to an oral antibiotic earlier than planned (e.g., due to social reasons, patient’s refusal to receive intravenous antibiotics, or lack of intravenous access).

  • Antibiotic therapy for infection with aerobic gram-negative bacilli is usually a third- or fourth-generation cephalosporin (e.g., cefotaxime, ceftriaxone, cefepime, or ceftazidime) or piperacillin/tazobactam. When Pseudomonas species infection is suspected, cefepime, ceftazidime, or piperacillin/tazobactam is recommended. 

  • Mycobacterium tuberculosis infection: patients should receive 6 months to 1 year of appropriate antituberculous therapy. See Pulmonary tuberculosis and HIV-related opportunistic infections.

Monitoring

Throughout the course of antibiotic treatment, the patient should be monitored at least every 2 weeks for evidence of refractory infection. Serial monitoring of WBC count, CRP, and erythrocyte sedimentation rate (ESR) is recommended to assess treatment response.[9][47]​ Rising WBC count, CRP, or ESR may suggest treatment failure. In these patients, imaging with enhanced MRI of the whole spine should be repeated to evaluate any residual spinal infection. If MRI shows an enhancing bone/epidural space, repeat cultures should be taken and alternative antibiotic agents considered, based on in vitro microbial susceptibility testing. MRI should also be repeated if new symptoms of concern (e.g., back pain, weakness, or paresthesia) develop.[9][48]​ Surgical consultation should be sought for these patients.[12][42][43]

Patients with underlying comorbidities (e.g., diabetes mellitus, intravenous drug use, HIV infection) or with preexisting systemic infections (e.g., infective endocarditis) are at greater risk of chronic spinal infection. In such patients, resistant or unusual pathogens (e.g., fungi) should also be considered.[49][50]

Medical therapy can be associated with moderately high failure rates and close observation is needed, especially for patients with cervical spine lesions.[9][42][43][51]

Surgical treatment

Surgery is indicated when the patient presents with progressive neurologic deficit or does not respond to antibiotic therapy.[9][14][15][16]​​​​[43][44]​​​​[52]​​​​​​[53]

The type of surgical approach is guided in part by the imaging results. Surgery is usually performed with an open technique allowing for cord decompression, epidural irrigation, and sampling of the tissues for microbial diagnosis. For example, a focal posteriorly placed collection will yield to a single- or double-level laminectomy. For patients with less disabling symptoms, CT-guided needle aspiration of intradiscal/intra-osseous lesions may be performed.

One study reported a 30-day mortality rate after surgery for SEA of 3.7%, with most deaths occurring within 2 weeks of surgery. Independent risk factors for mortality included older age, diabetes mellitus, hypertension, respiratory comorbidities, renal comorbidities, metastatic cancer, and thrombocytopenia.[13]​ Another study identified five prognostic predictors of 30-day reoperation after surgery for SEA: cervical spine abscess, preoperative urinary incontinence, ventral location of abscess relative to thecal sac, preoperative wound infection, and leukocytosis (WBC >15,000/microL). Albumin levels <2.6 g/dL were also associated with a significant risk of reoperation within 90 days.[54]

While it is recognized that delayed surgery (24-36 hours following onset of neurologic symptoms) is less effective than surgery performed early, it may still be considered for source control or if neurologic symptoms are progressive and there is evidence of cord function.[5][55] Reviews have emphasized the essential role that timing of surgery can play in outcomes.[2][9][43][56]

Supportive therapy

Correction of hypotension

Patients with evidence of septic shock require correction of hypotension. The aim is to maintain BP >100 mmHg systolic; adequate urine output (0.5 mL/kg/hour); central venous pressure at 8 to 12 mmHg; mean arterial pressure 65 mmHg or more; and central venous saturation (superior vena cava) 70% or more or mixed venous oxygen saturation 65% or more. Treatment consists of central line placement and volume resuscitation. Vasoactive agents are recommended only if hypotension is refractory to adequate volume resuscitation. Consult a specialist for guidance on suitable vasopressor/inotrope regimens. Selection of appropriate vasoactive agents should only take place under critical care supervision, and may vary according to clinician preference and local practice guidelines.

See Shock.

Prevention of venous thromboembolism

Patients at increased risk of thrombosis should be given prophylaxis to prevent venous thromboembolism and possible pulmonary embolism.[57] Treatment should begin no later than 72 hours after presentation. Pharmacologic prophylaxis should be used unless contraindicated; nonpharmacologic measures (e.g., graduated compression stockings, intermittent pneumatic compression devices) may be used for patients at high risk for bleeding.[57]

See Venous thromboembolism (VTE) prophylaxis.

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