A Clinical Review on Spinal Epidural Abscess: Epidemiology, Pathophysiology, Diagnosis, and Management for Emergency Medicine and Hospitalist Physicians

Abstract

Description

Spinal epidural abscess (SEA), a critical surgical emergency, demands prompt recognition and intervention to prevent severe complications and fatalities. The incidence of SEA is notably increasing, particularly among individuals with diabetes, intravenous drug use, or a history of invasive spinal procedures. Although SEA can manifest through various clinical symptoms, the presence of its classic triad—back pain, fever, and neurological deficits—is noteworthy despite its occurrence in only 10% to 13% of cases. Identifying this triad is vital due to its high specificity for SEA, which is essential to guiding swift diagnostic and therapeutic actions in a condition where early intervention is critical.

Magnetic resonance imaging is pivotal in diagnosing SEA, offering unmatched sensitivity and specificity compared to other imaging techniques. Immediate empirical antibiotic therapy and timely neurosurgical consultation, when required, form the foundation of SEA treatment. The prognosis significantly depends on the patient’s initial neurological status, underlying health conditions, and the timeliness of their presentation, diagnosis, and treatment initiation.

Given the complexity of SEA and the high risk of diagnostic delays, managing this condition involves substantial medicolegal considerations. Enhanced comprehension of SEA is imperative for improving patient outcomes and reducing health care resource burdens. Prompt and accurate diagnosis and appropriate interventions are essential for effectively managing this urgent condition.

Introduction

Spinal epidural abscess (SEA) is defined as an accumulation of purulence between the duramater— the outermost layer of the meninges covering the brain and spinal cord—and the vertebral column. This condition often stems from bacterial or fungal infections and poses a significant risk of permanent neurological deficits or death if not promptly and appropriately addressed. Unfortunately, SEA is frequently misdiagnosed, with about 62% of cases initially overlooked.¹ The thoracic and lumbosacral regions are the most common sites for SEA development, with their comparatively expansive and infection-prone adipose tissue.

The expanding abscess can exert pressure on critical spinal structures, leading to rapid progression and potentially devastating neurological consequences, including paralysis. Since its first description by Sir Percival Pott in 1761, our understanding of SEA has significantly evolved.² Yet, it poses substantial clinical challenges, underscoring the need for a current, evidence-based review.²

The significance of SEA in emergency medicine and hospitalist care extends beyond its incidence; its timely and accurate diagnosis is crucial for favorable patient outcomes. Despite its relative rarity, there has been a noteworthy increase in the prevalence of SEA in recent years.³ The condition’s nonspecific symptoms often resemble less severe issues, such as neck or back pain, complicating its diagnosis. Delays in recognizing and treating SEA can result in irreversible harm, permanent disability, or fatality.

Diagnostic delays have detrimental effects on patient outcomes and carry medicolegal consequences. The rise in litigation against emergency and hospitalist practitioners over alleged diagnostic and treatment delays in SEA cases underscores the urgency of its swift identification and management.

In this review, we delve into SEA’s prevalence, diagnostic methods, treatment options, and prognosis, aiming to provide a comprehensive, evidence-based perspective. Our objective is to equip health care professionals with the knowledge to identify and address SEA promptly. To achieve this, we focus on several key aspects. We begin by discussing strategies to distinguish SEA’s often vague symptoms from more benign conditions. We then evaluate the most effective diagnostic tools for its timely detection. Furthermore, we analyze the immediate treatment approaches and their effectiveness. Finally, we assess how these elements influence patient prognosis, recovery, and potential long-term complications.

Epidemiology of SEA

Although relatively low, the incidence of SEA in the United States has steadily increased. Current estimates suggest about 5 to 8 cases per 10 000 hospital admissions, nearly doubling over the past 2 decades.^4–7 This rise can be attributed to improved diagnostic capabilities, notably in neuroimaging,⁸ as well as to demographic shifts, such as an aging population, the growing prevalence of comorbidities (eg, diabetes), and an increase in invasive spinal procedures.⁹

Risk factors for SEA encompass demographic variations, comorbidities, and social determinants of health. Age plays a significant role; individuals over 50 years of age are more prone to SEA due to an increased prevalence of comorbid conditions, age-related immune decline, and heightened susceptibility to infections. ³ Males are more frequently affected, often related to higher rates of risk factors, such as substance misuse.¹⁰ Racial disparities are evident as well, with the African American population showing higher incidence rates, influenced by socioeconomic factors and limited health care access.⁹

The presence of certain comorbid conditions elevates the risk for SEA. This includes diabetes mellitus, HIV/AIDS, and chronic renal disease. Patients with malignancies, especially those undergoing chemotherapy or radiation therapy, face an increased risk due to compromised immunity.

Specific spinal factors also heighten SEA risk. These include undergoing invasive spinal procedures, like surgeries or interventions, as well as a history of spinal trauma, such as fractures or injuries.¹¹

Moreover, social determinants, such as homelessness and lower socioeconomic status, associated with increased substance misuse, limited health care access, and higher infection exposure, contribute to SEA risk.¹² Intravenous drug use or alcoholism further elevate this risk.¹³

Pathophysiology and Etiology of SEA

Spinal epidural abscess arises when infectious agents, such as bacteria, fungi, or, less commonly, parasites infiltrate the epidural space surrounding the spinal cord and nerve roots. Three primary mechanisms contribute to SEA development: hematogenous spread, contiguous spread, and direct inoculation.

Hematogenous spread is responsible for about half of SEA cases. Pathogens, like Staphylococcus aureus, including methicillin-resistant Staphylococcus aureus (MRSA), travel from systemic infections to the vascularized anterior aspect of the spinal cord, causing infection. Typical sources include endocarditis, skin and soft tissue infections, urinary tract infections, and pneumonia.¹³

Contiguous spread, accounting for roughly a third of SEA cases, involves the direct invasion from infections, like osteomyelitis, intervertebral discitis, and complicated skin or soft tissue infections, in adjacent anatomical structures.⁶ In some cases, the infection source remains unidentified.³

Direct inoculation occurs through invasive spinal procedures, such as epidural injections, lumbar punctures, or spinal surgery, which introduce infectious organisms. Risk factors include poor aseptic techniques and pre-existing bacterial colonization.¹⁴

Staphylococcus aureus is the predominant causative agent in SEA, including MRSA strains, especially prevalent in patients with implantable spinal or vascular devices. Other causative agents include coagulase-negative staphylococci, gram-negative bacteria like Escherichia coli and Pseudomonas aeruginosa, and, less frequently, anaerobic bacteria, mycobacteria, fungi, or parasites.³

The rising prevalence of MRSA highlights the importance of vigilant diagnosis and management, particularly in patients with spinal or vascular devices.³ Accurate knowledge of SEA’s microbiological profile is vital for selecting appropriate antimicrobial therapy and interventions, aiming for the best patient outcomes.

Following infection establishment, the body’s inflammatory response leads to abscess formation in the epidural space. If untreated, the abscess expands, exerting pressure on spinal structures and causing neurological symptoms. Initial symptoms typically include local pain due to nerve root irritation, progressing to radicular pain, weakness, and sensory loss. In severe cases, particularly in lumbar SEAs, bowel or bladder dysfunction may occur.

Early detection and intervention are critical to prevent permanent neurological deficits. A thorough understanding of SEA’s pathophysiology and etiology is essential, especially for emergency medicine and hospitalist physicians who often encounter these cases.

Clinical Manifestations of SEA

Typical Signs and Symptoms

SEA manifests with various symptoms, predominantly back or neck pain, fever, and neurological deficits. Recognizing these common signs is crucial for early intervention.

Back or Neck Pain: This is the most frequently reported symptom, reported in about 75%–85% of SEA patients.¹³ The pain, typically localized to the spinal level of the abscess, is often severe and gradually intensifies. Movement or actions, like coughing and sneezing, can exacerbate it. Physical examination may reveal localized tenderness, muscle spasms, or nerve root irritation signs, such as a positive straight leg raise test in lumbar abscesses.

Fever: In approximately half of the patients, fever may range from low-grade to high and can be intermittent or persistent.³ While indicative of systemic inflammation, the absence of fever, especially in the elderly or immunocompromised patients, does not exclude SEA.

Neurological Deficits: As the abscess grows, neurological symptoms develop due to spinal cord or nerve root compression or vascular compromise. These may include sensory changes (numbness, tingling, loss of sensation), motor symptoms (weakness, gait difficulties, paralysis), and bowel or bladder dysfunction. Radiculopathy, causing sharp, shooting nerve pain, is also common.

The Triad of SEA: The classic triad—fever, back pain, and neurological deficits—is associated with SEA. However, it is complete at presentation in only 10% to 13% of patients, as noted by Davis et al.¹⁰

Atypical Presentations

SEA can present atypically, complicating diagnosis. Immunocompromised patients, the elderly, and those with peripheral neuropathy may not exhibit standard symptoms. Chronic back pain sufferers might not report new pain, and unusual pain patterns (abdominal pain, joint pain) can mislead diagnosis. Furthermore, patients may exhibit unusual pain patterns, such as abdominal pain, resembling intra-abdominal conditions or joint diseases in the shoulders, hips, or knees.¹⁵ Nonspecific symptoms like malaise, weight loss, or fatigue can be misleading, especially in patients with slow-progressing abscesses.

Progression of Symptoms and Potential Complications

Without treatment, SEA symptoms typically worsen over time. What begins as localized pain may evolve into widespread back discomfort, followed by radicular pain, indicating nerve irritation or compression. Progressive motor weakness is common as the condition advances. Untreated SEA can lead to severe complications, like permanent neurological deficits (paraplegia, quadriplegia, incontinence), sepsis, and disseminated infection. The mortality rate, ranging from 6% to 32%, underscores the critical need for timely diagnosis and treatment.^14–16

Diagnostic Methods for SEA

Laboratory Investigations and Their Diagnostic Value

When evaluating suspected SEA, initial laboratory tests typically include a complete blood count, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). These tests, while nonspecific, can indicate systemic inflammation or infection, thus supporting clinical suspicion of SEA.¹⁷ Blood cultures are essential in all suspected cases, yielding causative organisms in 50%–60% of patients.¹⁸ However, it is essential to recognize the limitations of these tests. For instance, an ESR of 20 mm/h or greater is observed in at least 94% of SEA cases, but neither ESR nor CRP is specific to SEA. In confirmed cases, blood cultures are positive in approximately 60% of patients, whereas cultures from the abscesses are positive in around 90% of cases, with Staphylococcus aureus being the most common pathogen (63%). The white blood cell count may be elevated or normal in SEA cases.¹²

Imaging Techniques: Magnetic Resonance Imaging and Computed Tomography Scan

Magnetic resonance imaging (MRI) is the gold standard for SEA diagnosis, offering over 90% sensitivity and specificity.¹² MRI precisely delineates the abscess, showing its location, size, and impact on the spinal cord or nerve roots. Gadolinium-enhanced MRI significantly improves diagnostic accuracy, revealing well-circumscribed, ring-enhancing lesions typical of abscesses. Though less sensitive than MRI, computed tomography (CT) scans can detect spinal abnormalities indicative of SEA, such as bone erosion, osteomyelitis, or discitis. Up to 80% of SEA cases may present with concurrent diskitis or osteomyelitis, necessitating thorough evaluation when these conditions are identified.³

CT scanners are more widely available than MRI machines. Non-contrasted CT scans can identify differential diagnoses for back pain, such as fractures or tumors. CT myelograms, used when MRI is contraindicated (eg, in patients with pacemakers), can provide valuable diagnostic insights but are less sensitive and specific than MRI. MRI’s superior sensitivity and specificity enable detailed visualization of spinal cord compression, epidural collection, and related inflammatory changes, making it the preferred imaging modality for SEA diagnosis.

Differential Diagnoses

The nonspecific symptoms of SEA and its similarities with other conditions make its diagnosis challenging. Differential diagnoses include disc herniation, vertebral fracture, spinal tumor, other infections, like vertebral osteomyelitis and discitis, and non-spinal causes, such as renal colic or abdominal aortic aneurysm. Differentiation requires a thorough assessment of clinical presentation, laboratory results, and imaging findings. The classic triad of back pain, fever, and neurological deficits is often absent at initial presentation. High suspicion for SEA is crucial, especially in patients with risk factors, such as diabetes, intravenous drug use, or recent spinal surgery. The range of differential diagnoses depends on factors such as age, immune status, and comorbidities, necessitating comprehensive evaluations, including detailed imaging and, in some cases, biopsy.

Initial Treatment Approach and Empiric Antibiotics

The management of SEA begins urgently in the emergency department or hospitalist units. Rapid recognition and immediate initiation of treatment are critical to avert severe neurological outcomes. Following blood culture collection and potential source cultures, broad-spectrum empiric antibiotics should be administered promptly. This initial anti-biotic therapy aims to cover likely causative organisms, primarily Staphylococcus aureus (including MRSA) and gram-negative bacilli, notably Escherichia coli.¹⁶ A combination of vancomycin and cefepime effectively targets staphylococci, streptococci, and gram-negative bacilli. In patients at risk for fungal infections (eg, those with immunosuppression or a history of intravenous drug use), antifungal therapy should be considered. When clinical findings, laboratory data, and imaging studies suggest SEA, a definitive diagnosis necessitates drainage procedures for confirmation.

Surgical Interventions: Indications and Techniques

Timely recognition of SEA is imperative for initiating prompt antibiotic therapy and considering surgical consultation. Indications for surgery include significant or worsening neurological deficits, severe pain not relieved by medical treatment, spinal instability due to osteolysis, or suboptimal response to antibiotic therapy.¹³ Surgical decompression is commonly performed using laminectomy, hemilaminectomy, or interlaminar fenestration. In specific cases, particularly for patients with posterior SEA without neurological deficit, those at high surgical risk, or those unresponsive to antibiotics alone, CT-guided needle aspiration in conjunction with antibiotics can be advantageous.¹¹ Antibiotic monotherapy may be considered for patients with significant surgical risks or prolonged symptom duration. The primary objectives of surgery are to control the infection source, decompress the spinal cord and nerve roots, and debride the abscess. However, neurological improvement post-surgery is less likely if paresis has been present for over 24–36 hours.¹¹

Follow-up and Long-Term Management: Antibiotic Duration and Other Considerations

The management of SEA extends beyond surgical intervention. Typically, a 4–6-week course of antibiotics is required to eradicate the infection.^7,19 This duration should be adjusted based on the patient’s response to treatment, infection severity, and the causative pathogen. Post-discharge long-term management includes surveillance with repeat imaging, pain management, physical therapy, and careful control of diabetes mellitus, renal insufficiency, immunosuppression, and other predisposing conditions.

Prognostic Factors Influencing Outcomes

The prognosis of SEA depends on multiple factors, including the speed of diagnosis and initiation of treatment, the severity and rate of neurological decline at presentation, the patient’s underlying comorbidities, and the causative organism.⁶ Prompt diagnosis and immediate treatment, encompassing antibiotic therapy and surgical intervention, are linked with improved outcomes. Poor prognostic indicators include rapid neurological deterioration or severe impairment at presentation, advanced age, the presence of sepsis or systemic inflammatory response syndrome, comorbid conditions, like diabetes or renal failure, and infections caused by MRSA.²⁰

Outcome Statistics: Recovery, Morbidity, Mortality

Despite medical advancements, SEA is associated with substantial morbidity and mortality. Mortality rates vary between 5% and 16%, escalating in cases presenting with severe sepsis or septic shock.^15–17 Post-treatment, about 20%–40% of patients suffer from residual motor deficits or chronic pain.⁷ These outcomes underscore the critical need for early detection and rapid management to optimize patient outcomes in SEA cases.

Long-term Sequelae and Quality of Life After Treatment

Long-term complications of SEA predominantly involve neurological issues, such as chronic pain, motor and sensory deficits, and bladder or bowel incontinence. These sequelae can lead to disability, adversely affecting patients’ quality of life and increasing health care burdens. Studies indicate that even after recovering from the acute phase, many patients with SEA continue to struggle with persistent pain and physical limitations, impacting their work capacity and overall quality of life.^7,21

Medicolegal Considerations

SEA presents a significant challenge in diagnosis, with delayed or missed diagnoses often leading to grave consequences. Newman-Toker et al. reported that about 62.1% of SEA cases are initially misdiagnosed or diagnosed late, resulting in serious harm in 22.1% of these cases.¹ The need for accurate and timely diagnosis is highlighted by the risk of permanent neurological damage or death if treatment is delayed. Additionally, the extent of neurological deficits at diagnosis closely correlates with long-term neurological recovery. Nearly half of SEA survivors endure residual neurological impairments, and 15% suffer severe outcomes, like paresis or complete paralysis.⁷ Thus, reducing diagnostic delays is essential to improve patient outcomes and minimize the morbidity and mortality associated with SEA.

SEA, although rare, is a critical consideration in patients presenting with common back pain complaints. Misdiagnosis or delays in diagnosis are frequent, leading to long-term severe consequences for the patient. Legal claims against health care providers for delayed or incorrect diagnosis and treatment, particularly in cases resulting in paralysis, highlight the importance of maintaining a high level of suspicion.¹ Prompt actions, including MRI imaging, systemic antibiotics, and neurosurgical consultation, are imperative when patients present with the triad of back pain, fever, and neurological symptoms.

Summary

Our review of SEA highlights the importance of early detection, accurate diagnosis, and prompt treatment of this potentially devastating condition. SEA poses significant diagnostic and therapeutic challenges, particularly for emergency medicine and hospitalist physicians, who are often the first to evaluate these patients.

Given SEA’s complexity, variable presentations, and increasing incidence, a high index of suspicion is crucial, especially in patients with known risk factors. This review underscores the connection between diagnostic delays, poorer outcomes, and increased litigation against health care providers, emphasizing the necessity for rapid assessment and assertive management.

Emergency medicine and hospitalist physicians must be particularly vigilant for SEA. They should consider it in differential diagnoses for patients presenting with back pain, fever, and neurological deficits, especially if diabetes, intravenous drug use, or recent spinal procedures are present.

A thorough and systematic evaluation, including appropriate imaging and laboratory tests, is critical. MRI with contrast remains the gold standard for SEA diagnosis due to its high sensitivity and specificity. A multidisciplinary approach involving neurosurgeons and infectious disease specialists early in the care process is essential for managing suspected SEA cases.

Conclusion

SEA is a serious, often misdiagnosed condition that demands swift recognition, diagnosis, and intervention. In this review, we highlighted the increasing prevalence of SEA, particularly among populations with specific risk factors. Although SEA can present with varied symptoms, the classic triad of back pain, fever, and neurological deficits is fundamental for early recognition.

We reaffirmed the critical role of imaging, particularly MRI, in diagnosing SEA while noting the challenges related to its accessibility and interpretation. This review underscores the need for health care providers, especially in emergency medicine and hospitalist settings, to maintain a high level of suspicion for SEA, as early diagnosis and treatment are directly linked to better patient outcomes.

Immediate administration of empiric antibiotics and timely neurosurgical involvement are vital in managing SEA effectively. However, questions remain about the optimal antibiotic regimen and treatment duration, highlighting areas for future research.

The prognosis for patients with SEA varies, influenced by factors like the patient’s initial neurological status, existing comorbidities, and the timeliness of therapy. Medicolegal considerations are also significant, particularly concerning the potential legal consequences of diagnostic or treatment delays. Enhancing our understanding and management of SEA is vital for improving patient outcomes and reducing its burden on health care resources and patient lives.

Funding Statement

This research was supported (in whole or in part) by HCA Healthcare and/or an HCA Healthcare-affiliated entity.