Spinal Epidural Abscess

Etiology

In patients presenting with spinal epidural abscess, bacteria enter the epidural space resulting in a suppurative infection. Most often, the bacteria enter the epidural space through a hematogenous spread. Risk factors for spinal epidural abscess include an immunosuppressed state (i.e., diabetes mellitus, alcoholism, cirrhosis, end-stage renal disease, HIV infection), intravenous drug abuse, direct instrumentation (i.e., acupuncture, paraspinal or epidural injection, lumbar puncture, CNS surgery), and bacteremia. Diabetes mellitus is the most common risk factor associated with spinal epidural abscess. However, intravenous drug use and epidural catheter placement are becoming increasingly important and frequent risk factors in the development of this disease process.[6][7]

Epidemiology

SEA is an uncommon diagnosis. The incidence of SEA is approximately 2 to 8 cases per 10,000 hospital admissions.[2][8] Their incidence has recently increased because of the expanded utilization of invasive spinal procedures, the increasing age of the population, and increasing rates of intravenous drug use.[9][10]

A systematic review of 12 studies comprising 1099 patients revealed:

• Mean age of involvement of 57.2 years
• Male to female ratio of 1.66:1
• Intravenous drug abuse is the most frequently (22%) associated risk factor
• Diabetes (27%) is the most commonly associated medical comorbidity
• Staphylococcus aureus (63.6%) is the most common causative organism
• The lumbar spine (48%) is the most common location of involvement
• Back pain (67%) followed by motor weakness (52%) are the most common presenting symptoms
• 60% of patients are managed surgically.[1]

Pathophysiology

Mechanisms of Formation of SEA

• Hematogenous dissemination- in almost half of the cases with primary nidus from the skin, soft tissue, and urinary or respiratory tract infections.[2][8] Skin abscesses and furuncles were the most common source of infection.[11]
• Contiguous spread- in 10 to 30% of cases, e.g., vertebral osteomyelitis or psoas muscle abscess.[8]
• Direct inoculation-Neurosurgical interventions, lumbar puncture, epidural analgesia, and other invasive procedures in 15% of SEA.[2][8][12]
• Idiopathic in around 20% of cases.

Pathogenesis of Effects of SEA

• Direct mechanical compression
• Ischaemic
• Septic thrombophlebitis, and
• Inflammatory process mediated through bacterial toxins.[2][8][12]

Most commonly occurs within the thoracic and lumbar regions owing to the following factor:

• Larger epidural space
• An abundance of infection-liable fat, and
• The presence of low pressure vertebral venous system (Batson) communicates freely with the abdominal and pelvic venous systems.[2][8][12]

Abscess Locations

• Anterior - secondly to pyogenic spondylitis or discitis
• Posterior - following hematogenous dissemination.
• Circumferential.[2]

Etiology Behind SEA

• Staphylococcus aureus is seen in almost two-thirds of cases. S. aureus is also responsible for many other clinical mimickers, such as osteomyelitis, diskitis, sepsis, and endocarditis. MRSA infection is commonly observed among patients with implantable spinal or vascular devices.
• Coagulase-negative staphylococci, such as epidermidis, follow spinal procedures.
• Gram-negative bacteria, particularly Escherichia coli (urinary tract infection) and Pseudomonas aeruginosa (intravenous drug users).
• Rarely anaerobic actinomycosis or nocardiosis, mycobacteria, candida, aspergillus, echinococcus).[2][8][12]

History and Physical

Clinical Presentations

Hallmark triad comprised of back pain, fever, and neurological deterioration is observed only in 8 to 15% of cases.[2][8]

Almost two-thirds present have back pain as the presenting symptom.[11] Pain may be elicited through palpation or percussion of spinous processes overlaying spinal epidural abscess. Pain also may be produced through straight leg raise from compression of spinal nerve roots. As this disease progresses, patients will develop neurologic deficits consistent with spinal cord or cauda equina compression: urinary retention, bowel incontinence, anesthesia (perianal and saddle anesthesia), motor weakness, or paralysis.

Four stages have been described in the natural history of the disease:

1. Stage 1 - Back pain, fever, or spine tenderness
2. Stage 2 - Radicular pain and nuchal rigidity
3. Stage 3 - Neurological deficits, and
4. Stage 4 - Paralysis[8]

Stage 4 is observed in roughly 34% of patients.[13]

Salient Red flags for SEA include:

• Unexplained fever
• Neurological deficits
• Active infective pathology[14]

Major risk factors for SEA include:

• Diabetes
• Intravenous drug use
• Indwelling vascular catheter
• Recent spinal intervention
• Immunosuppressant status
• Infective pathology elsewhere[11][15]

A model-based study comprising age, fever, antimicrobial usage within 30 days, back/neck pain, and history of drug abuse showed an area under curve (AUC) value of 0.88.[16]

Back pain alongside fever/risk factors and raised serum inflammatory markers can be used as an algorithmic approach for advocating contrast MRI study.[17]

Evaluation

The presence of paraspinal edema in non-contrast MRI has been observed to have the highest sensitivity (97%) for SEA compared to psoas (54%), bone marrow (65%), and disc edema (66%), respectively.[18] Though all these variables were significant in univariate analysis, only paraspinal and bone marrow edema were observed to be significant predictors of SEA in multivariate analysis.[18] MRI with gadolinium enhancement is the imaging armamentarium of choice.[8] MRI, with a sensitivity of more than 90%, helps delineate the extension of the lesion, helps in management strategies, as well as differentiates it from other differentials.

A plain roentgenograph or CT may reveal a narrowing of the disk and bone lysis.[12]

The necrotic center being avascular gives the characteristic ring-enhancing pattern.[2] SEA usually extends over three to four vertebral segments, but panspinal infection can occur.[12]

Serum ESR >30 mm/hr and a serum CRP >10 mg/L has sensitivity of >95% in SEA.[2]

The CSF analysis only reveals features of parameningeal inflammation showing increased proteins and pleocytosis.

Recent advances in nuclear imaging such as Indium-biotin scans and F-fluorodeoxyglucose-positron emission tomography show increased uptake.[2][12]

Myelography is no longer recommended.[11]

CSF cultures are positive only in 25% of cases, and due to concurrent risks of meningitis or subdural infection, they are now only recommended during myelography only.[11]

Blood cultures or CT-guided needle aspiration have high yields.[8] Blood cultures, however, yield a positive result in almost all patients with a positive CSF culture.[12]

Open or minimally invasive procedures cultures positivity in almost 78.8 to 90.5% of cases.[2]

Treatment / Management

The rate of progression from one stage to another is highly variable.[12] The progression from stages III to IV is often rapid, mostly within 24 hours.

There has been a consensus that surgical drainage, together with systemic antibiotics, is the treatment of choice. Surgery, comprised of decompressive laminectomy and débridement, is recommended as early as possible.[8][12](B3)

Surgical modalities:

The first successful decompressive laminectomy for a SEA was performed by Barth for a thoracic abscess in 1901. Urgent surgical intervention with systemic antibiotics has been the gold standard of SEA treatment for patients with:

• Evolving neurological deterioration
• Spinal instability
• Persistence of infection despite antibiotic treatment.[1]
(A1)

Decompressive laminectomy and debridement combined with antibiotics is the method of choice.[8][15]Laminotomy is an option for children with SEA.[11] Spinal instrumentation to prevent presumed post-operative instability can be undertaken since they are observed to be safe and free of major infective complications.[19](A1)

Element of antibiotic stewardship during management pending culture reports:

• Staphylococci-Penicillin and first or second-generation cephalosporins
• Methicillin-resistant Staphylococcus aureus (MRSA) - vancomycin
• Gram-negative bacilli - Third or fourth-generation cephalosporins[2][12]

Medical management is indicated among patients wherein:

• The patient has no or minimal neurological deficits
• The causative organism is clearly specified through blood culture of CT-guided aspiration
• The patient is stringently monitored.[12]

This is also advocated for patients despite requiring decompressive laminectomy among cohorts with:

• Lack of consent for surgery
• High operative risks
• Late presentation with paralysis of more than 24 to 36 hours with minimal chances of recovery
• Impracticality due to panspinal infection[12]

A significantly higher percentage of patients do receive medical management (40% vs. 12.7%) currently compared to historical data due to earlier diagnoses, with most of the patients presenting only with back pain and fever with absent or minimal neurological deficits.[1] The fair analysis of the comparative outcomes of medical and surgical modalities is limited by the differences in the study methodology and pooled data obtained from the retrospective studies in the historical data set, causing a significant risk of reporting bias.[1](A1)

The standard duration of antibiotics is at least four to eight weeks to cover the concurrent risk of osteomyelitis among these cohorts.[2] Intravenous therapy is justified to improve the bioavailability and compliance with therapy.[12] Removal of all the infected implants, such as the spinal cord stimulator system, is required.[12]

Medical management alone has high failure rates (more than 40%), increased morbidity (up to 22% permanent paralysis), and high mortality.[2] Moreover, the necrotic center of the abscess has less penetrance by antibiotics.[2]

Computed tomography (CT) guided aspiration is an option in patients in neurologically intact and frail patients.[2]

The most significant marker of an outcome includes the presenting neurologic status of the patient.[2][12]

The risk variables predicting failed treatment include:

• Associated neurological deficits
• Age over 65
• Concurrent diabetes[19]

Differential Diagnosis

• Disc prolapse
• Degenerative spinal canal stenosis 
• Vertebral discitis and osteomyelitis
• Transverse myelitis
• Spinal cord hematoma
• Psoas abscess
• Meningitis
• Urinary tract infection
• Pyelonephritis/ perirenal abscess
• Endocarditis[11]

Prognosis

The disease has an enigmatic tale, with both the time lapse between the onset of symptoms and hospital admission and progression to a higher stage being highly variable and unpredictable.[12] The essential problem of SEA lies in the necessity of early diagnosis.[13]

A delay in the diagnosis of SEA (defined as multiple visits before the definite diagnosis and treatment) can result in increased residual weakness or permanent neurologic deficit.

Irreversible paralysis still affects 4 to 22% of patients owing largely to delay in diagnosis and suboptimal management. 11 to 75% of them are initially misdiagnosed.[12]

Around 5% of the patients die from sepsis or other related causes.[20] Moreover, 4 to 22% of patients experience irreversible paraplegia.

There is limited data available in the literature about neurological recovery after surgery. However, the recovery is variable and generally depends on multiple factors, including age, health status, comorbidities, and time to diagnosis. Timely treatment initiation is crucial.[21]

Importance of timely surgical interventions among patients with SEA:

• Surgery during stage 1 or stage 2 reduces pain and shows improvement in above 90% of cases.
• Surgery during stage 3 may reverse or minimize neurological deficits.
• Surgery during stage 4 within 36 hours may help regain some neurological functioning.[2][12][19]

Esophageal tears and intestinal–spinal fistula need to be ruled out among patients with refractory or recurrent infections.[12]

There is a high risk of recurrence among patients with:

• History of intravenous drug use
• Bowel dysfunction at presentation
• Concurrent local wound infection
• Concurrent immunocompromised status or immunosuppressive agents.

 The motor deficit has been observed to be a risk factor for 90-day mortality.

Complications

Complications of SEA include: 

• Pressure sores
• Urinary tract infection
• Deep-vein thrombosis
• Sepsis
• Meningitis, and
• Mortality[8][12]

Mortality is mostly following sepsis or meningitis.[2] The mortality rate is between 1.3% and 31%.[2] The mortality, however, decreased from 34% during the 1960s to 15% in the 1990s.[11] Though the reported incidence of SEA has doubled in the last two decades, the associated mortality has also reduced by almost 50% to approximately 14%.[12][11] Patients who died or acquired paralysis were observed to have a longer duration (almost three times) between their imaging and final reads.[22]