Spine Infection

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Chapter 197 Spine Infection

Kyle I. Swanson, Kene Ugokwe, Seth M. Zeidman, Thomas B. Ducker, Gregory R. Trost

Postoperative Spine Infection

Infectious complications of spine surgery are not uncommon and occur in 0.5% to 12% of patients.¹^–⁹ Infections can range from limited superficial wound infections or isolated discitis to more serious deep subfascial wound infections, osteomyelitis, epidural abscess, or meningitis. Postoperative infection results in an increase in health-care costs and increases the risk of poor outcomes, including persistent pain, permanent neurologic deficit, and death.¹^–¹¹ Some of the risk factors associated with surgical site infections include patient age,^12,¹³ obesity,^9,¹⁴^–¹⁸ diabetes,¹⁸^–²⁰ urinary incontinence,⁹ alcoholism, extended steroid use, tobacco use,¹⁸ poor nutritional status,¹² prior infection, prior surgery, prolonged hospitalization prior to surgery,¹⁸ complete neurologic deficit,^21,²² trauma,²³ tumor resection,⁹ prior radiation therapy,²⁴ and the presence of more than three comorbid diseases.⁹

The rate of postoperative infection is in large part determined by the type of operation. Surgeries without bone grafting or instrumentation have a lower rate of infection. The incidence of infection after intervertebral disc procedures is between 0.5% and 1%.^25,²⁶ There is uncertainty whether microdiscectomy with the use of an operative microscope increases the infection rate.²⁷ The rate of infection with laminectomy without fusion is estimated to be around 1.5% to 2%.^16,²⁶ The incidence of infection is higher when grafting and instrumentation are used,²⁸ which was first documented in a case series involving the use of Harrington instrumentation for fusion in scoliosis surgery.⁵ The increased risk has many components, including addition of a foreign body; lengthier, more complicated surgeries; increased blood loss; and the use of prolonged retraction. Instrumented fusion of the lumbar spine carries an infection risk of approximately 2.8% to 6%.^16,^18,^26,²⁹ Surgery after spine trauma carries a 10% risk of postoperative infection.²³

Ventral operations have a markedly lower incidence of infection than dorsal approaches, likely due in part to the injury caused by the use of prolonged retraction in dorsal approaches. The addition of a combined anterior and dorsal approach does not seem to increase the risk of infection over that for a dorsal approach alone.^23,³⁰ Other surgical factors that have been shown to increase the risk of postoperative infection include increased blood loss (>1 L),¹⁸ use of blood transfusion,¹⁹ prolonged surgical time (>3 hours),³¹ multilevel surgical fusions extending to the sacrum,³² and spinal fluid leak.¹⁸ The use of drains has not been shown to increase the risk of infection.³³ Participation of residents or fellows in the surgical team is not associated with an increased risk of infection.³⁴

The optimal method of dealing with surgical site infections is prevention. Prophylactic antibiotics have been shown convincingly to decrease the rate of postoperative infection, and their use is recommended by published clinical guidelines for all spine operations.^35,³⁶ A large meta-analysis found a statistically significant decrease in the rate of postoperative spine infection in those patients given preoperative antibiotics versus controls (2.2% vs. 5.9%).³⁷ Prophylactic antibiotics should be given prior to the start of incision, should be redosed for prolonged procedures, and should not be continued for more than 24 hours. First- or second-generation cephalosporins, such as cefazolin or cefuroxime, adequately cover the most common causes of surgical site infection and are recommended for most patients. Patients with cephalosporin allergies can be given vancomycin or clindamycin. Vancomycin should be used for patients colonized with methicillin-resistant Staphylococcus aureus (MRSA).^29,³⁵

One large prospective case-controlled study found that the rate of discitis after microdiscectomy was significantly decreased when a gentamicin-soaked collagen sponge was placed in the cleared disc space versus the rate for historical controls (0% vs. 3.7%).³⁸ The benefit of prophylactic local antibiotics for discectomy procedures is in part due to the poor penetration of IV antibiotics into the relatively avascular intervertebral disc.³⁹ The use of irrigation solution with antibiotics such as bacitracin and gentamycin, or dilute iodine, is widespread, but there is not good evidence demonstrating additional benefit over irrigation with just saline.^35,⁴⁰ Use of chlorhexidine-alcohol instead of povidone-iodine for preoperative skin cleansing has been shown to decrease surgical site infections in randomized controlled trials.⁴¹ In a Cochrane review, alcohol-based rubs were found to be equivalent to aqueous chlorhexidine-based scrubs for preoperative hand antisepsis, with aqueous povidone-iodine–based scrubs being inferior.⁴² Operating rooms with vertical laminar airflow have been demonstrated to decrease infections in dorsal spine fusion surgery.⁴³ Double-gloving; frequent release of retractors to prevent ischemia; and copious, frequent irrigation are reasonable, though unproven, strategies for also minimizing postoperative infection.^29,⁴⁴

Postoperative wound infections can be classified as early onset (occurring <1 month after surgery) or late onset (occurring >1 month after surgery). Late-onset infections include isolated discitis and infections of instrumented fusions by indolent organisms. Staphylococcus aureus is responsible for approximately 50% to 75% of infections, followed by S. epidermidis, gram-negative organisms, and multimicrobrial infections.^16,²⁶ Late-onset infections associated with instrumentation are more likely to be caused by more fastidious organisms such as S. epidermidis, Priopionibacterium acnes, or Corynebacterium^44,⁴⁵

One of the chief symptoms of a surgical site infection is pain, which is often initially attributed to the surgery itself. Pain that continues to worsen days after the surgery or returns after initial relief of symptoms should raise suspicion for infection. Patients with an infection frequently, but certainly not always, have fever. A careful evaluation of other causes of fever should be undertaken, including a chest radiograph to evaluate for pneumonia or atelectasis, urinalysis to check for urinary tract infection, and possibly a lower extremity Doppler ultrasound to rule out deep vein thrombosis. The possibility of drug fever should also be explored. Other constitutional signs of infection include chills, sweating, malaise, and anorexia. Frank sepsis with hypotension and organ failure warrants emergent exploration if there is any concern for wound infection.

The most frequent sign of postoperative spine infection is wound drainage, which in one series was present in 93% of cases.²⁶ Often patients with infection are discharged home after an apparently normal recovery and return because of drainage and associated swelling, tenderness, erythema, and wound dehiscence. The average time of presentation for a postoperative spine infection is 2 weeks, though it can be days for aggressive organisms, such as Clostridium perfringens, or years for indolent infections.²⁶

New or worsening neurologic deficits, such as numbness, urinary or bowel dysfunction, weakness, or paralysis, are ominous signs and should raise suspicion for epidural hematoma or abscess. Postoperative spinal epidural abscess is a neurosurgical emergency that can lead to rapid decline if not promptly diagnosed and treated with antibiotics and surgical drainage.⁴⁶

Late-onset infections often provide fewer clinical signs or symptoms, with worsening pain generally being the only complaint. Discitis frequently manifests more than a month after discectomy as increasing pain in an afebrile patient with a normal-appearing incision. Symptoms of infection of the disc space can be misdiagnosed as recurrent disc herniation, or patients may be dismissed as hysterical or malingering. Worsening pain in a patient with a history of spine surgery should be evaluated for possible infection.

Laboratory studies are an important adjunct in diagnosing infection, especially when the wound site does not show obvious signs. Patients often demonstrate leukocytosis, with or without associated neutrophilia, but a large portion of cases will have a normal white blood cell count and differential. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels are much more sensitive, though nonspecific, markers of inflammation and are almost always significantly elevated with infection. Care must be taken in interpreting these levels since they are initially elevated after any surgery. In uninfected postoperative patients, CRP typically peaks on postoperative day 2 and returns to normal levels between days 5 and 14. ESR peaks around day 5 and can remain elevated for weeks after surgery.^47,⁴⁸ ESR and CRP levels are particularly helpful in diagnosing late-onset infections in patients with minimal signs or symptoms besides worsening or persistent pain, such as postoperative discitis.

Blood cultures should be obtained in all patients in whom a surgical site infection is suspected. Cultures of the skin or drainage site are rarely helpful because they culture normal skin flora. Needle aspiration cultures are much more reliable, and intraoperative cultures are the best option. Since most patients will need surgical debridement, the best course of action is to wait for the results of intraoperative cultures before starting antibiotics. For late-onset infections, it is especially important to continue cultures for at least 7 to 15 days to increase the chance of growing indolent organisms such a P. acnes.⁴⁵ When surgery is not indicated, as in suspected isolated discitis, and blood cultures are negative, then a percutaneous biopsy should usually be obtained to confirm the diagnosis and guide treatment.

Plain radiography, CT, and MRI can be useful in diagnosing postoperative infection, but their utility is often clouded by the similarities in imaging findings between infection and normal postoperative inflammation. Radiographs can demonstrate retained foreign bodies, disc space narrowing that develops with discitis after 7 to 10 days, erosion of vertebral end plates, or vertebral collapse.⁴⁹ Loosening of implants can also be revealed, which is often a sign of late-onset infection.⁵⁰ CT reveals many of these same features but with superior anatomic detail.

Contrasted CT and MRI both have excellent sensitivity for identifying fluid collections, but it can sometimes be difficult to differentiate between abscess and postoperative seroma or hematoma. Either modality helps differentiate superficial from subfascial infections. Contrasted MRI is the best study for determining postoperative epidural abscess.⁵¹ MRI with contrast is also the study of choice for diagnosing discitis and osteomyelitis. T1-weighted images reveal hypointensity of the disc and vertebral body. On T2-weighted images, the involved bone and disc are hyperintense due to edema and the involved disc demonstrates a loss of the intranuclear cleft.⁵² Areas of inflammation enhance with contrast administration.⁴⁹ Unfortunately, many of the same MRI signal findings are seen with normal postoperative changes.⁵³ Radionuclide studies, such as gallium/bone (technetium) scintigraphy, can be useful when MRI is contraindicated or nondiagnostic due to artifact from implants.^49,⁵⁴

Treatment consists of targeted antibiotics and surgery in nearly all cases, though there are a few exceptions. There is a significant difference between the treatment of spine infections in the presence of grafting and instrumentation versus simple decompression procedures. The treatment is also different for early-onset infections versus that for late-onset infections in the setting of instrumentation. Some very superficial wound infections or stitch abscesses can be treated with empirical antibiotics alone, but there must be no evidence of deeper infection or significant systemic signs of infection. Ensuring adequate nutrition is vital for the successful treatment of all postoperative infections.^12,⁵⁰

Isolated postoperative discitis often presents later than other postsurgical infections with worsening back pain, elevated ESR/CRP, and characteristic findings on radiograph and MRI. Discitis can frequently be treated successfully with 4 to 6 weeks of IV antibiotics alone. This requires obtaining bacterial diagnosis via blood cultures or percutaneous biopsy. Spontaneous fusion across the disc space usually occurs after resolution of the infection. Many surgeons recommend bracing to minimize pain. Surgery for debridement of the disc space is indicated in the setting of new or worsening neurologic deficits, significant associated infection (especially epidural abscess), and progression of infection and bony involvement or worsening pain despite antibiotics.

Surgical debridement is warranted for most other surgeries that do not involve bone graft or instrumentation. This is especially true for subfascial infections. Exploring below the fascia is recommended for all but the most superficial of infections. All necrotic, infected, and foreign material, such as sutures, must be completely debrided. Cultures should be obtained and sent for Gram stain and aerobic, anaerobic, and fungal cultures. Once culture specimens have been sent, empirical broad-spectrum antibiotics, such as vancomycin and a third-generation cephalosporin, can be started. The wound should be copiously irrigated with large volumes, with many institutions using 9 L of bacitracin-containing irrigation.^26,⁵⁰ Pulse-lavage irrigation may improve debridement.

Primary closure over a drain can frequently be used for more superficial infections; however, deeper infections should usually be left open to heal via secondary intention or with a delayed closure. Vacuum-assisted closure (VAC) dressings have been increasing in popularity and are purported to decrease nursing requirements and aid in healing, but no good trials have yet proved their benefit over traditional gauze packing.⁵⁵^–⁵⁷ Repeat debridement at 48 to 72 hours can be beneficial for treating septic or immunocompromised patients or in the setting of infections caused by multiple organisms or those associated with extensive myonecrosis.^26,^29,⁵⁰ Tailored IV antibiotics are continued for 4 to 6 weeks.

Infections after instrumented spine fusions require the same aggressive debridement and irrigation. For early infections, almost all published reports advocate leaving the spinal instrumentation and viable bone graft in place in order to maximize the chance of fusion.1–3,24,26,29,30 ^,32 ^,50 ^,58 ^,59 Loose instrumentation and nonviable bone graft should be removed. Surgical wounds should usually be left open to heal by secondary intention or with delayed closure. Repeat irrigation and debridement is occasionally needed for reasons listed earlier. Levi et al. reported success using an irrigation-suction system for postoperative care.³⁰ IV antibiotics selected based on culture and sensitivies are continued for at least 6 weeks. In addition, Kowalski et al. found a significant decrease in the late recurrence of infection in patients treated with oral suppression therapy for at least 6 months after an initial course of IV antibiotics.²⁴

Late infections after instrumented fusion are usually the result of more fastidious organisms that are capable of creating a glycocalyx covering on implanted hardware that is resistant to antibiotics and the normal immune response.⁶⁰ Surgical treatment involves debridement, irrigation, and removal of hardware.^24,^60,⁶¹ Fortunately, in most cases bony fusion has already occurred, as assessed on CT or intraoperatively, and the hardware is no longer needed for stabilization. Patients with late infections who have implants left in place have a significantly higher risk of treatment failure.²⁴ Postoperatively, patients should be monitored closely for evidence of pseudarthosis or deformity that would warrant repeat instrumented fusion. After removal of hardware, debridement, and irrigation, the wound can typically be closed over a drain, and appropriate antibiotics are continued for 6 weeks,^24,⁶¹ although one group reported good outcomes with just 2 days of IV antibiotics followed by 7 days of oral antibiotics.⁶⁰

Spontaneous Spinal Infections

Discitis

Pyogenic discitis is a bacterial infection of the intervertebral disc that is frequently associated with involvement of the adjacent vertebral end plates (spondylodiscitis). Incidence is estimated to be between 0.2 and 2.4/100,000 each year, with two peaks in age distribution: one in early childhood and another between ages 60 and 70 years.^62,⁶³ The relatively high proportion of children with pyogenic discitis is likely related to the anatomy of the disc space during development. Children still have a vascular supply into the nucleus pulposus of the disc, which allows septic emboli to lodge with the disc. The vascular supply in adults only reaches the anulus fibrosus. In the adult population, more men are affected than women.⁶⁴ Risk factors for developing discitis include invasive procedures, diabetes (11–31%), malignancy, IV drug use (IVDU), immunosuppression, alcoholism, renal failure, and cirrhosis.^62,^63,⁶⁵

The majority of cases are caused by S. aureus, with gram-negative rods, Streptococcus, and Enterococcus being the next most frequently involved organisms.^63,⁶⁴ Gram-negative organisms are more common when associated with diabetes, immunocompromise, infections of the genitourinary or gastrointestinal tracts, or IVDU.⁶⁵ Tuberculosis (TB) and brucellosis are atypical bacterial infections that can cause discitis in endemic regions and in at-risk populations. Fungal discitis is rare but should be considered in patients who are critically ill, immunosuppressed, taking multiple antibiotics, or have an indwelling catheter.⁶⁶ The most frequent location is the lumbar spine (60%), followed by the thoracic (30%) spine and the cervical spine (10%).^62,⁶⁴

In 1936, Milward and Grout were the first to describe the clinical and radiographic characteristics of interspace infection after the inadvertent introduction of microorganisms into a disc space during a lumbar puncture.⁶⁷ More than 90% of patients complain of back or neck pain.⁶² This pain often is not relieved by medications or recumbency. Radicular pain symptoms are not uncommon. Guarding against movement and a positive straight-leg raise may be present. Fever is present in approximately 60% to 70%.⁶³ Neurologic deficits, especially weakness, should raise concern for more a extensive infection such as an epidural abscess. In children, discitis often presents as a refusal to bear weight or walk.⁶⁸ The time from onset to diagnosis is often months. ESR and CRP are elevated in most patients, but leukocytosis is present in less than half of cases.⁶⁹

The differential diagnosis for discitis includes other infections of the spine and adjacent structures, trauma, osteoporotic fracture, degenerative disc disease or acute herniation, metastatic disease, and inflammatory spondyloarthopathies. Discitis is often also associated with bacterial endocarditis (3.7–15%). Echocardiography is recommended for patients with spontaneous discitis. Back pain in the setting of endocarditis or bacteremia should lead to an evaluation for discitis.⁷⁰

MRI with contrast is the image modality of choice for diagnosing spontaneous discitis, with a sensitivity and specificity greater than 90%. If an MRI is not possible, the next most sensitive studies are radioisotope scans followed by CT with contrast. Radiographs also show typical changes such as disc space narrowing and end-plate erosion, but these changes usually take several weeks to develop.⁴⁹ CT is particularly helpful for guiding percutaneous biopsy.

If possible, antibiotics should be held until cultures can be obtained. Blood cultures are positive in approximately half of discitis cases.⁶⁴ To maximize yield, three culture specimens taken at different times and locations should be obtained, ideally when the patient is febrile. If after 48 hours there is no growth, a CT-guided percutaneous biopsy should be obtained, which increases the yield to between 60% and 70%.⁶⁴ Samples should be taken from both adjacent vertebral end plates and the disc itself, and the disc space should be rinsed and aspirated. Biopsy samples are sent for histopathologic studies, aerobic, anaerobic, fungal, and mycobacterial cultures, and stains.⁶² A second percutaneous biopsy has been shown to increase yield when the first biopsy is negative.⁶⁹ Occasionally open biopsy is required to obtain a diagnosis.

Approximately three-quarters of spontaneous pyogenic discitis cases can be treated nonoperatively with IV antibiotics tailored according to the results of the cultures and sensitivities.⁶² There are no good studies comparing various antibiotic regimens, duration of antibiotic therapy, or the role of oral antibiotics after administration of IV antibiotics. Traditionally 4 to 6 weeks of IV antibiotics was recommended, but recent reports suggest there is a decreased risk of recurrence if antibiotics are used for 12 weeks, often with a switch to oral antibiotics after 6 weeks.^62,⁶⁵ Spinal immobilization for pain control, using bracing or short-term bed rest, is recommended by most surgeons.

Response to therapy is demonstrated by diminishing pain, resolution of fever, and progressive decrease in CRP levels.⁴⁸ Radiographs should be obtained at regular intervals after initiation of treatment and should show sclerosis and osteophyte formation by 3 months if healing is occurring.⁶⁵ Patients generally progress to fusion over 6 to 12 months. Repeat MRI is generally not helpful and often initially appears worse than pretreatment scans.⁷¹ MRI should usually be reserved for patients with new or worsening neurologic symptoms to rule out expanding abscess.

Surgery is reserved for patients with neurologic deficits, especially those with associated epidural abscess and spinal cord compression, for clinical failure after conservative treatment, for treatment of spinal instability or correction of deformities, for obtaining a diagnosis by open biopsy after failed percutaneous biopsy, and occasionally for persistent pain.⁷²

Recurrence rates after a course of antibiotics are generally around 10% (0–16%).^62,⁶⁹ Chronic pain is the most common residual complication. Functional impairment and neurologic deficits occur in a minority.⁶⁴ Mortality is generally low and usually related to associated sepsis, endocarditis, or underlying disease.^63,⁶⁹

Vertebral Osteomyelitis

Infection of the bones of the spinal column—vertebral osteomyelitis—can occur after trauma, as a result of direct manipulation during surgery, via contiguous spread from adjacent structures, or via hematogenous spread from distant sources.⁷³ Vertebral osteomyelitis is relatively rare, with an estimated incidence of 2.4/100,000 people. Older adults are more likely to be affected, with the incidence increasing from 0.3/100,000 for those younger than 20 years of age to 6.5/100,000 for those older than 70.⁷⁴ There is a male predominance that also increases with age.^74,⁷⁵

Patients with vertebral osteomyelitis usually have predisposing factors, with the most common being diabetes mellitus, end-stage renal disease requiring dialysis, sepsis, endocarditis, cancer, HIV infection, immunosuppression, alcoholism, and IVDU.^73,^75,⁷⁶ Urinary tract infections followed by skin infections were the most common sources of infection.⁷⁵

A vast majority of cases of pyogenic spine osteomyelitis involve the vertebral body, with only 3% to 12% involving the dorsal elements of the spine.⁷⁷ Infection generally begins at the highly vascular end plates. Most cases involve two or more contiguous vertebral bodies and the intervening disc. Vertebral osteomyelitis occasionally manifests as the collapse of an isolated vertebral body. The lumbar spine is the most commonly involved (58%), followed by the thoracic spine (30%) and cervical spine (11%).⁷⁵ Associated epidural abscesses (17%), paravertebral abscesses (26%), and disc space abscesses (5%) are frequent.⁷³

The most common causative organism is S. aureus. Escherichia coli is the most commonly reported gram-negative organism and is especially associated in cases when genitourinary or gastrointestinal infections are the source.⁷⁵ S. aureus is the most frequent organism in IV drug users, but they also have an increased frequency of Pseudomonas aeruginosa⁷⁶ In many developing regions of the world TB is a frequent cause of chronic vertebral osteomyelitis.

There is often a substantial delay in the diagnosis of vertebral osteomyelitis due to the nonspecific nature of its presenting symptoms. In one large series the mean time to diagnosis was 1.8 months, with only a quarter of cases being diagnosed in less than a month. The same study revealed that on initial presentation only a quarter of the patients had vertebral osteomyelitis considered in the differential diagnosis. The majority of patients (86%) present with several weeks of worsening back or neck pain.⁷³ Fever has been reported in 35% to 60% of patients.^73,⁷⁸ Neurologic deficits are present in approximately a third of cases, and only around one fifth of patients have localized tenderness.⁷⁸ Rapidly worsening neurologic deficits and paralysis should raise the concern for associated spinal epidural abscess. Acute worsening of pain is often associated with vertebral collapse. Back pain in the setting of bacteremia, such as with endocarditis, should always lead to an evaluation for vertebral osteomyelitis. The differential diagnosis for vertebral osteomyelitis includes other localized spine infections, osteoporotic or traumatic fractures, spondyloarthopathies, degenerative disc disease, herniated disc, metastasis, and infections such as pancreatitis and pyelonephritis.⁷⁹

Leukocytosis is present in approximately two thirds of cases, and there is an associated neutrophilia in about a third of cases.⁸⁰ ESR and CRP measurements are much more sensitive to the presence of inflammation and are elevated in almost all cases of vertebral osteomyelitis.^48,⁸⁰ Serial CRP is more accurate than ESR for gauging response to therapy.⁴⁸ Blood cultures should be obtained in all patients with suspected vertebral osteomyelitis because 58% (range, 30–78%) of cultures will be positive.⁷⁵ Identifying the organism via blood cultures often obviates the need for more invasive procedures.

MRI is the best imaging modality for evaluating for vertebral osteomyelitis, with a sensitivity of nearly 100% and accuracy over 90%.⁸¹ Findings associated with osteomyelitis include a low intensity on T1-weighted images with loss of the usual hyperintense signal of fat in the bone marrow, hyperintensity on T2-weighted images in the bone or adjacent disc and soft tissues indicative of edema, and enhancement with contrast of the end plates and associated abscesses. There is usually a loss of the intranuclear cleft of involved discs. End-plate destruction is a late finding.⁸¹

Radiographs and CT are beneficial in the delineation of bony destruction. Radiographs often reveal narrowing of intervertebral disc spaces, rarefaction of the vertebral body, loss of trabeculations near the end plate, or frank vertebral body collapse. Besides providing more accurate anatomic details of the bony involvement for assessment of stability, CT with IV contrast can be used for guiding percutaneous biopsy.

Combined gallium/bone scintigraphy is the most useful radionuclide study for diagnosing vertebral osteoarthritis in patients unable to have MRI due to incompatible implants or in whom MRI imaging is nondiagnostic. 2-[¹⁸F] Flouro-2-deoxy-d-glucose positron emission tomography (FDG-PET) is a promising new modality that also has a high reported accuracy. In contrast, labeled leukocyte imaging is not considered useful in the diagnosis of vertebral osteomyelitis.^54,⁸¹

The overall goal of treatment of vertebral osteomyelitis is to eliminate the infection while maintaining neurologic function and spinal stability. A majority of patients are able to obtain this goal without surgical intervention with antibiotics and spine immobilization via bracing or bed rest. The overall rate of surgery has likely been rising, and a recent systematic review found that 42% of patients had some form of surgical intervention. The reasons for surgery include open biopsy, spine stabilization (23%), drainage of associated abscess (21%), decompression of the spinal cord (13%), and correction of deformity after infection had been cleared (2%).⁷⁵ The use of instrumentation for stabilization in patients with acute infection does not appear to increase the risk of relapse when the patient has an appropriate course of antibiotics.⁸²

Antibiotics are chosen based on the results of culturing a causative organism and should be withheld prior to obtaining the culture results if possible. If blood cultures are negative, CT-guided percutaneous biopsy or open biopsy should be obtained. Aerobic, anaerobic, fungal, and mycobacterial culture specimens should be sent. Histopathology is useful in identifying granulomas that might be indicative of tuberculosis or brucellosis.⁷⁹ Antibiotics are usually continued for at least 6 weeks, but recommended courses ranging from 4 weeks to 3 months have been reported.⁸³ Longer courses should be considered in patients with complicated infections or implanted hardware. Antibiotic courses of less than 4 weeks have a higher incidence of relapse.⁸⁴ In certain instances oral regimens have been used successfully after a course of IV antibiotics. One randomized trial found similar outcomes in patients treated with a combination of an oral fluoroquinolone and rifampin and in those treated with IV antibiotics.⁸⁵

Patients should be monitored closely for failure of therapy. Failure of symptoms to improve and persistent CRP elevations at 4 weeks indicate likely treatment failure.⁴⁸ MRI obtained after starting treatment is a poor predictor of treatment outcome and should be reserved for patients in whom a change in symptoms occurs that might suggest new or worsening abscess.⁷⁹ Relapse occurs in 1% to 22% of cases and is more likely in patients with recurrent bacteremia, a chronically draining sinus, or a paravertebral abscess.⁷³

The systematic review by Mylona et al. found a mortality rate of 6%, with most deaths attributable to associated sepsis. Approximately a quarter of patients had a significant decrease in quality of life. The most common complications reported were chronic pain (28%), weakness (16%), and dysfunction of the bowels or bladder (7%).⁷⁵ Predictors of worse outcome include motor weakness or paralysis at presentation, delayed diagnosis (>2 months), and acquisition of the infection in the hospital.⁷³

Spinal Epidural Abscess

Spinal epidural abscess (SEA) is a relatively rare but extremely important clinical condition involving supportive infection in the epidural space of the spinal canal. SEA is considered a neurosurgical emergency because severe neurologic decline or death may become unavoidable if diagnosis and treatment are delayed. The mortality rate from SEA has been reported to be between 4.6% and 31%.⁸⁶

Incidence reports from longer than 2 decades ago estimated that 0.18 to 1.96 cases of SEA occur per 10,000 hospital admissions.^87,⁸⁸ However, evidence suggests that the incidence has increased as the number of susceptible patients with known risk factors, such as IVDU and HIV infection, has increased.^46,^86,⁸⁹ This apparent increase in incidence may in part be due to the fact that the diagnosis of SEA is also made easier due to the advances in medical imaging. The male-to-female ratio was previously reported to be approximately 1:1,^87,⁸⁸ but a large meta-analysis in 2000 revealed a ratio of 1:0.56.⁹⁰ This predominance is likely related to the higher incidence of trauma, alcoholism, IVDU, and other risk factors in men. SEA is more common in adults, with the majority of cases occurring from ages 30 to 60, but it can occur with any age group, with the youngest reported case being a 10-day-old patient.⁹⁰ The most common location for SEA is the thoracic spine, followed by the lumbar and lumbosacral regions.

Most patients with SEA have an underlying predisposing condition such as diabetes, end-stage renal disease with dialysis,⁹¹ cirrhosis, medical immunosuppression for transplant, chronic steroid therapy, HIV, malignancy and related chemotherapy, alcoholism, or previous trauma or spine intervention.^86,^88,^90,⁹² Approximately half of SEA cases are caused by hematogenous spread from a focus of infection, which can be either arterial or via the paravertebral venous plexus.⁹³ The most common source of infection is skin abscesses.⁹⁰ Other commonly reported sources include IVDU, indwelling venous or arterial catheters, dental abscesses, bacterial endocarditis, urinary tract infections, and respiratory infections. Iatrogenic introduction of disease via surgery, epidural anesthesia, or corticosteroid injection, among other causes, is another important source for the introduction of bacteria. Finally, contiguous spread to the epidural space can occur and has been reported from such sources as adjacent psoas abscesses, decubitus ulcers, abdominal infections, pyelonephritis, mediastinitis, and pharyngeal abscesses.

The most common microbial agent in SEA is S. aureus, which causes two-thirds to three-quarters of all cases.^46,^90,⁹⁴ Of concern is the increasing prevalence of MRSA, which in some reports represents almost 40% of abscesses.⁹⁵ Overall, aerobic gram-positive organisms, such as S. epidermidis, Streptococcus viridans, Enterococcus, and Propionibacterium, among others, account for nearly 80% of SEA cases.

Coagulase-negative staphylococci, such as S. epidermidis, are more common in patients who have undergone invasive spine procedures or who have implanted foreign bodies. Gram-negative organisms, such as E. coli, Enterobacter, Salmonella, Proteus, Serratia, and Pseudomonas, among others, are more likely to be involved when the source of the infection is gastrointestinal infection or urinary tract infection. Pseudomonas is more likely in patients with IVDU.⁹⁶ Multiple organisms can be found in up to 10% of abscesses. Anaerobic cultures should always be obtained since anaerobic bacteria, such as Bacteroides and Peptostreptococcus species, also rarely cause SEA.^87,⁹⁷ Other causes of SEA include atypical bacterial infections, such as TB, brucellosis, and actinomycosis, for which acid-fast bacillus staining and extended cultures may be necessary; fungal infections, such as aspergillosis, in patients who are immunocompromised; and even parasitic infections, such as echinococcosis and dracunculiasis.⁹⁰

SEA can present acutely over the course of days, with gross pus in the epidural space and signs of sepsis, or in a more chronic presentation of symptoms that develop over months, with granulation tissue in the epidural space. The organism responsible for the infection often determines the time course of presentation.

Diagnosis begins with recognition of the clinical presentation. Heusner’s classic description of the presentation of SEA in 1948 describes four stages: (1) severe back pain, local tenderness and fever; (2) signs of spinal irritation such as Kernig sign, neck stiffness, and radicular pain; (3) development of neurologic deficits such as weakness, fecal or urinary incontinence, and sensory deficits; and (4) progression of weakness to paralysis.⁹⁸ Most patients with SEA do not present with such a characteristic course and often initially present with only complaints of isolated back pain. For this reason it is very common for the diagnosis of SEA to be initially missed. The most common signs and symptoms are back pain (71%) and fever (66%),⁹⁰ and the combination should always raise the possibility of SEA. Atypical signs and symptoms such as localized tenderness to percussion, thoracic radicular pain, and pain with recumbency should also raise red flags. Symptoms of systemic infection such as chills, night sweats, or sepsis may be present.⁹⁹ New-onset neurologic deficits are more common with cervical and thoracic SEA and need to be rapidly evaluated due to the possibility of progression. Approximately one third of patients present with some degree of paralysis.⁹⁰

In a patient with back pain, the addition of laboratory tests to identify systemic signs of inflammation can greatly enhance screening for pyogenic spine infection. The leukocyte count, ESR, and CRP are often elevated, though a normal lab value by itself should never be used to rule out the possibility of SEA. The incidence of leukocytosis is approximately 68% to 78%.^100,¹⁰¹ Approximately 94% to 100% of patients have an elevated ESR.^90,¹⁰⁰ Leukocytosis and an elevated ESR are relatively nonspecific symptoms and must be interpreted in the setting of the patient’s condition as a whole. All patients thought to have SEA should also have blood cultures drawn as this can help with the diagnosis of SEA as well as identifying the offending pathogen.

After the history, clinical examination, and laboratory markers have raised the possibility of SEA, the next step is to identify or rule out the diagnosis with radiologic imaging. The most sensitive and specific imaging modality is MRI with gadolinium contrast. Plain-film radiographs, CT, and CT-myelography may be useful as adjuncts or when MRI is not possible.

MRI findings in SEA reveal an epidural mass that is hypointense to isointense on T1-weighted images and hyperintense on T2-weighted images. The abscess usually enhances with contrast administration, often as a linear rim enhancement surrounding a nonenhancing core that represents purulent material.¹⁰² More heterogeneous enhancement may be present if the abscess has more of a phlegmon consistency as opposed to liquid pus.⁴⁴ MRI is also excellent for identifying other conditions that may mimic SEA, such as spinal tumors, transverse myelitis, spinal cord infarction, or intervertebral disc herniation.

Radiographs and CT are useful for evaluating for adjacent osteomyelitis. Bony erosion or destruction may be seen on radiographs after 4 to 6 weeks of infection; however, delineation of bone involvement is appreciated much better with CT imaging. CT may show evidence of inflammation, such as stranding in the paravertebral soft tissues. After contrast administration, SEA may be identified as an enhancing epidural mass. However, there are reports of CT imaging alone missing a relatively high proportion of SEAs.¹⁰³ CT imaging can be useful for surgical planning, especially in deciding whether fusion and instrumentation will be needed after surgical debridement.

If MRI is not possible, CT-myelography can be a very useful diagnostic substitute. Prior to widespread availability of MRI, myelography and then CT-myelography were the gold standards for radiologic diagnosis of SEA. With CT-myelography contrast is directly injected into the thecal sac and an epidural mass can be identified as blockage of flow from above or below, depending on where the puncture was performed. In a direct comparison study, MRI and CT-myelography were found to be equally sensitive (91% vs. 92%).¹⁰⁴ CT-myelography is less specific than MRI and provides less information about the characteristics of the epidural mass. Moreover, CT-myelography requires an invasive procedure that can introduce infection or spread an epidural infection to a subdural space, causing a subdural empyema or meningitis.¹⁰⁵ Since SEA in the upper cervical spine is relatively rare, a lateral C1-2 puncture is often recommended to limit the chance of traversing the epidural collection during the myelogram. A myelogram also allows for the evaluation of CSF, which reveals associated meningitis in up to 15% of patients. However, most authors recommend against lumbar puncture for the purpose of CSF examination alone in the evaluation of suspected SEA due to the low specificity and risk of seeding infection.^51,^90,¹⁰⁴^–¹⁰⁶

Many conditions can present with back pain and signs and symptoms of inflammation in a manner similar to SEA. A large percentage of SEA cases are still initially misdiagnosed, leading to a delay in treatment. In a large meta-analysis, the most common initial misdiagnosis was intervertebral disc herniation, followed by meningitis, vertebral osteomyelitis, sepsis, endocarditis, and spinal tumors.⁹⁰ The differential diagnosis for SEA should also include epidural metastasis, acute transverse myelitis, subdural empyema, intramedullary abscess, epidural hematoma, autoimmune spondylitis, discitis, infections of adjacent structures (pyelonephritis, psoas abscess, etc.), vascular malformations, subarachnoid hemorrhage, and lymphoma. Acute transverse myelitis is more common than SEA and typically presents with rapidly progressing neurologic deficits without significant back pain. A history of a recent viral illness would also make acute transverse myelitis more likely.

The next step in the diagnosis of SEA after obtaining radiologic imaging is to obtain a culture of the organism causing the infection. Obtaining cultures prior to starting antibiotics is imperative to ensure the highest yield; however, this is not always possible when the patient is frankly septic. Antibiotics given prior to culture or biopsy can result in a failure to isolate a bacterial source and lead to the patient being unnecessarily treated with broad-spectrum antibiotics. The easiest method for isolation of the bacterial source involves obtaining blood culture specimens, which should be obtained from multiple sites and at different time points. Ideally, at least three separate blood specimens are obtained while the patient has spiking fevers. The yield from blood samples in the setting of SEA is between 30% and 60%.⁴⁴

If blood cultures are negative, then percutaneous needle biopsy with either fluoroscopic or CT guidance should be performed.¹⁰⁷ If the biopsy is unrevealing, a repeat percutaneous biopsy or open biopsy may be necessary. Antibiotics should be withheld, even in a patient with rapidly progressing neurologic symptoms, until an adequate sample can be obtained at the time of surgery. All biopsy samples should be sent for aerobic, anaerobic, mycobacterial, and fungal stains and cultures. Occasionally extended periods of incubation are necessary for fastidious organisms.

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