Continuing Education Activity

A spinal epidural abscess is a serious infection of the central nervous system that typically presents with back pain, fever, and neurological deficits. This condition is difficult to diagnose and demands a high index of suspicion, as delays in recognition can lead to significant morbidity and mortality. Prompt evaluation and treatment are essential when a diagnosis is suspected, with modern imaging techniques, such as computerized tomography and magnetic resonance imaging, playing a critical role in detection and assessment. The combination of clinical vigilance and advanced radiological tools enables timely intervention, which is crucial for improving patient outcomes and preventing permanent neurological damage.

Through this course, participants understand how to assess and manage spinal epidural abscesses while appreciating the importance of collaboration across specialties. The activity demonstrates how radiologists, neurologists, infectious disease specialists, and surgical teams collaborate to provide accurate diagnoses, effective treatments, and coordinated care. Integrating expertise from multiple disciplines improves patient outcomes through faster recognition of disease progression, more effective treatment strategy selection, and more efficient recovery monitoring. This interprofessional approach ensures that complex infections such as spinal epidural abscesses are addressed with precision and urgency.

Objectives:

• Identify red-flag symptoms such as rapidly progressing weakness, sphincter dysfunction, or sepsis that mandate urgent escalation of care.
• Determine the timing of surgical intervention versus conservative management based on neurological status, abscess location, and comorbid conditions.
• Evaluate patient outcomes by monitoring neurological function, infection clearance, and long-term spinal stability.
• Review the importance of coordination among interprofessional teams that monitor for complications and treat patients with spinal epidural abscesses.

Introduction

A spinal epidural abscess (SEA) is a suppurative central nervous system infection involving the space between the spinal dura mater and the vertebral periosteum.[1] Giovanni Morgagni first described SEA in 1761.[2] Although classically, patients with spinal epidural abscesses present with midline back pain, fever, and neurologic deficits, other presentations of this disease process can be highly variable. A spinal epidural abscess is challenging to diagnose without a strong index of clinical suspicion.[3] If untreated, spinal epidural abscesses can lead to severe neurological morbidity and even mortality. As a result, any suspicion of this condition warrants immediate evaluation and timely intervention.[4][5][6] Diagnosing and managing spinal epidural abscesses are greatly aided by modern radiological techniques, including computerized tomography and magnetic resonance imaging (MRI).

Etiology

In cases of spinal epidural abscess, bacteria invade the epidural space and produce a suppurative infection, most commonly through hematogenous dissemination. Risk factors for spinal epidural abscess include an immunosuppressed state (ie, diabetes mellitus, alcoholism, cirrhosis, end-stage renal disease, HIV infection), intravenous drug abuse, direct spinal instrumentation (ie, acupuncture, paraspinal or epidural injection, lumbar puncture, central nervous system surgery), and bacteremia. Diabetes mellitus is the most common medical comorbidity 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 spinal epidural abscess.[7][8][9]

Epidemiology

SEA is a relatively rare condition, with an estimated incidence of 2 to 8 cases per 10,000 hospital admissions.[2][10] The incidence has risen in recent years due to the broader use of invasive spinal procedures, the aging of at-risk populations, and the growing prevalence of intravenous drug use.[11][12]

Results from a systematic review of 12 studies comprising 1099 patients revealed:

• The mean age of affected patients is 57.2 years.
• The male-to-female ratio is 1.66:1.
• Intravenous drug abuse represents the most frequent associated risk factor, occurring in 22% of cases.
• Diabetes mellitus is the most common medical comorbidity, present in 27% of patients.
• Staphylococcus aureus is the leading causative pathogen, identified in 63.6% of cases.
• The lumbar spine is the most frequent site of involvement, accounting for 48% of cases.
• Back pain (67%) is the most common presenting symptom, followed by motor weakness (52%).
• Surgical management is required in approximately 60% of patients.[1]

Pathophysiology

Mechanisms

• Hematogenous spread occurs in nearly half of cases, with primary infections commonly arising from the skin, soft tissues, or the urinary and respiratory tracts.[2][10] Skin abscesses and furuncles are the most common source of infection.[13]
• Direct contiguous extension results in 10% to 30% of cases, eg, vertebral osteomyelitis or a psoas muscle abscess.[10]
• Direct inoculation is responsible for approximately 15% of cases, usually after neurosurgical procedures, lumbar puncture, epidural anesthesia, or other invasive spinal interventions.[2][10][14]
• Idiopathic cases represent about 20% of infections, where no clear source of infection can be identified. 

Pathogenesis

• Direct mechanical compression
• Ischemia
• Septic thrombophlebitis
• Inflammatory process mediated through the release of bacterial toxins [2][10][14]

Spinal epidural abscesses most frequently develop in the thoracic and lumbar regions, largely because these areas contain a larger epidural space, a higher volume of infection-prone adipose tissue, and the Batson venous plexus. This low-pressure vertebral venous network freely communicates with the abdominal and pelvic venous systems.[2][10][14]

Abscess Locations

• Anterior due to pyogenic spondylitis or discitis
• Posterior from hematogenous dissemination
• Circumferential [2]

Etiology

• Staphylococcus aureus is seen in almost two-thirds of cases.[15] S aureus is also responsible for many other clinical infections, such as osteomyelitis, diskitis, sepsis, and endocarditis. Methicillin-resistant S aureus (MRSA) infection is commonly observed among patients with implantable spinal or vascular devices.
• Coagulase-negative Staphylococcus epidermidis after spinal procedures.
• Gram-negative bacteria, such as Escherichia coli, are commonly associated with urinary tract infections, and Pseudomonas aeruginosa is often found in intravenous drug users.
• Rarely, Actinomyces, Nocardia asteroides, Mycobacterium tuberculosis, Candida albicans, Aspergillus fumigatus, and Echinococcus granulosus can cause SEA.[2][10][14]

History and Physical

Clinical Presentation of Spinal Epidural Abcess

The hallmark presentation triad, comprised of back pain, fever, and a neurological deficit, is observed in only 8% to 15% of cases.[2][10] Approximately two-thirds of patients have back pain as the presenting symptom.[13] Pain may be elicited through palpation or percussion of the spinous processes overlaying the spinal epidural abscess. Pain may also be produced through the straight leg raise test from compression of the spinal nerve roots. As the disease progresses, patients develop neurologic deficits consistent with spinal cord or cauda equina compression that include urinary leakage, constipation, anesthesia (perianal and saddle anesthesia), motor weakness, or paralysis.

Four stages have been described in the natural history of spinal epidural abcess:

1. Back pain, fever, or spine tenderness
2. Radicular pain and nuchal rigidity
3. Neurological deficits 
4. Paralysis [10]

   • Stage 4 is observed in roughly 34% of patients.[16]

Red flags

• Unexplained fever
• Neurological deficits
• Active infective pathology [17]

Risk factors

• Diabetes mellitus
• Intravenous drug use
• Indwelling vascular catheter
• Recent spinal intervention
• Immunosuppressed state
• Infective pathology elsewhere [13][18]

A model-based study that considered age, fever, antimicrobial usage within 30 days, presence of back/neck pain, and a history of drug abuse showed an area under the curve value of 0.88.[19] Back pain combined with fever and elevated serum inflammatory markers can be used as an algorithmic approach to advocate for obtaining a contrast-enhanced MRI study of the spine.[20]

Evaluation

Evaluation of SEA

First-line imaging

• MRI with gadolinium enhancement is the imaging modality of choice, with sensitivity >90%.[10][21] This delineates the extent of the lesion, guides management, and distinguishes SEA from other conditions.
• On noncontrast MRI, paraspinal edema has the highest sensitivity (97%) compared with psoas muscle edema (54%), bone marrow edema (65%), and disc edema (66%).[22] On multivariate analysis, only paraspinal and bone marrow edema remain significant predictors.[22]
• SEA typically spans 3 to 4 vertebral segments but may involve the entire spine. The avascular necrotic center often produces a ring-enhancing pattern.[2][14]

Adjunct imaging

• Plain radiographs and computed tomography may show disc space narrowing and bone lysis.[14]
• Nuclear medicine techniques (indium-biotin scans, F-fluorodeoxyglucose PET) can reveal increased radiotracer uptake, though their role is adjunctive.[2][14]
• Myelography is no longer recommended.[13]

Laboratory evaluation

• Erythrocyte sedimentation rate >30 mm/hr and C-reactive protein >10 mg/L have >95% sensitivity for SEA.[2]
• Cerebrospinal fluid (CSF) analysis may show elevated protein and pleocytosis, but cultures are positive in only 25% of cases. Due to the risks of meningitis or subdural spread, CSF sampling is reserved for select cases, typically when myelography is performed.[13][14]
• Blood cultures have a high diagnostic yield and are positive in nearly all patients with positive CSF cultures.[10][14]
• Computed tomography-guided aspiration and open or minimally invasive sampling produce culture positivity in 78.8% to 90.5% of cases.[2]

Treatment / Management

Treatment of SEA

Neurological progression

• The rate of progression between stages is highly variable.[14]
• Transition from stage III to IV is often rapid, typically occurring within 24 hours.[14]
• The presenting neurologic status is the most significant factor influencing clinical outcomes.[2][14] 

Standard of care

• Early surgical drainage combined with systemic antibiotics remains the treatment of choice.[10][14]
• Surgery generally involves decompressive laminectomy and débridement, performed as early as possible.[10][14]

Surgical Management

• The first successful decompressive laminectomy for SEA was performed by Barth in 1901 for a thoracic abscess.
• Indications for urgent surgery with antibiotics include [1]

  • Progressive neurological deterioration
  • Spinal instability
  • Persistence of infection despite antibiotics
• Preferred approach: Decompressive laminectomy and debridement plus antibiotics [9][10][18]
• Special considerations:

  • Laminotomy may be used in children.[13]
  • Spinal instrumentation can be performed to prevent postoperative instability and appears safe without major infectious complications.[19] 
• Computed tomography–guided aspiration is an option for patients who are neurologically intact or medically frail.[2]

Nonsurgical Management

Criteria for conservative management

• Minimal or no neurological deficits
• Causative organism identified (via blood culture or computed tomography-guided aspiration)
• Ability for close clinical monitoring [14]

Medical management may also be chosen in cases of:

• Patient refusal of surgery
• High operative risk
• Late presentation with paralysis greater than 24–36 hours (low likelihood of recovery)
• Extensive panspinal infection [14]

Key points

• More patients are treated medically than in the past (40% vs 12.7%), largely due to earlier diagnosis and presentation with back pain/fever rather than neurologic deficits.[1]
• However, failure rates exceed 40%, with morbidity including up to 22% risk of permanent paralysis and high mortality.[2]
• Poor antibiotic penetration into the necrotic abscess center contributes to limited efficacy.[2]

Antibiotic therapy

• Pending culture results

  • Staphylococci: Penicillins, first or second-generation cephalosporins
  • MRSA: Vancomycin
  • Gram-negative bacilli: Third or fourth generation cephalosporins [2][14]
• Duration: 4 to 8 weeks, covering the risk of concurrent osteomyelitis [2]
• Route: Intravenous therapy (recommended for bioavailability and compliance) [14]
• Required: Removal of infected implants (eg, spinal cord stimulators) [14]

Predictors of poor outcome

• Preexisting neurological deficits
• Age older than 65
• Diabetes mellitus [23]

Differential Diagnosis

The differential diagnosis for SEA should include the following: 

• Disc prolapse
• Degenerative spinal canal stenosis 
• Vertebral discitis and osteomyelitis
• Transverse myelitis
• Spinal cord hematoma
• Psoas muscle abscess
• Meningitis
• Urinary tract infection
• Pyelonephritis and perirenal abscess [24]
• Endocarditis [13]

Prognosis

The time frame for SEA, from the onset of symptoms to hospital admission and neurologic progression, is highly variable and unpredictable.[14] Obtaining an early diagnosis for SEA is crucial for achieving a favorable prognosis.[16] A delay in the diagnosis of SEA, which is characterized by multiple clinical visits before a definitive diagnosis and treatment is obtained, can increase residual weakness or a permanent neurologic deficit.

Irreversible paralysis still affects 4% to 22% of patients, primarily due to a delay in diagnosis and suboptimal management. Between 11% and 75% of patients are initially misdiagnosed.[14] Approximately 5% of patients die from sepsis or other related causes.[25] Additionally, 4% to 22% of patients experience irreversible paraplegia. There is limited data available in the literature regarding neurological recovery after surgery. However, recovery is variable and generally depends on multiple factors, including age, health status, medical comorbidities, and time to diagnosis. Timely treatment initiation is critical.[26]

Timely surgical intervention plays a critical role in managing spinal epidural abscess cases. When surgery is performed during stage 1 or stage 2, it significantly reduces pain and leads to neurological improvement in over 90% of cases. Even in stage 3, surgical treatment can reverse or lessen neurological deficits. In cases progressing to stage 4, operating within 36 hours of presentation may allow patients to restore some neurological function.[2][14][23] Esophageal tears and intestinal–spinal fistula must be excluded among patients with refractory or recurrent infections.[14]

There is a high risk of recurrence among patients with:

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

 The presence of a motor deficit is a risk factor for 90-day mortality.

Complications

The complications that can manifest with SEA are as follows: 

• Pressure sores
• Urinary tract infection
• Deep vein thrombosis
• Sepsis
• Meningitis
• Mortality [10][14]

If mortality occurs, it is often after sepsis or meningitis.[2] The mortality rate ranges from 1.3% to 31%.[2] However, mortality decreased from 34% during the 1960s to 15% in the 1990s.[13] Although the reported incidence of SEA has doubled over the last two decades, the associated mortality has decreased from approximately 50% to around 14%.[13][14] Mortality and paralysis were associated with a longer duration from the completion of imaging to the final radiology report.[27]

Deterrence and Patient Education

Considerations for deterrence and patient education include: 

• Vigilant outpatient follow-up, especially within the first 90 days, is critical for surgically and nonsurgically treated individuals to monitor for infection resolution, detect complications, and identify any emerging neurological deficits or fever. Study results highlight that inadequate follow-up is common, emphasizing the importance of coordinated post-discharge care.[28] 
• Rehabilitation is essential for patients with motor weakness or neurological impairment, aiding in functional recovery and reducing long-term disability.
• Patients typically require prolonged antibiotic therapy. Partnering with home health services such as infusion nurses or medication management can significantly enhance compliance and therapeutic success.
• Emotional and mental health are vital yet sometimes overlooked in SEA recovery. Patients should be encouraged to communicate any signs of depression, lack of motivation, or suicidal ideation to their healthcare providers promptly for screening and possible mental health referral.

Enhancing Healthcare Team Outcomes

Enhancing Healthcare Team Outcomes

SEA is rare in the United States but is associated with significant morbidity when it occurs. Prognosis depends on the extent of the abscess, the neurological deficits present at the time of diagnosis, and the timeliness and effectiveness of treatment. Even with appropriate therapy, many patients are left with residual neurological deficits and require long-term rehabilitation to maximize recovery. Common complications during the recovery period include pressure ulcers and deep vein thrombosis.[7][29][30]

Optimal management of SEA requires a multidisciplinary, interprofessional approach that integrates the expertise of neurosurgeons, neurologists, intensivists, infectious disease specialists, nurses, physical and occupational therapists, pharmacists, and advanced practice clinicians.[14] Each team member plays a distinct and complementary role in enhancing patient-centered outcomes:

• Physicians and advanced practitioners must rapidly recognize red flag symptoms, initiate timely imaging and laboratory workup, and coordinate surgical or medical interventions. They are responsible for balancing the urgency of treatment with ethical obligations to communicate risks, benefits, and alternatives to patients and families.
• Nurses, including inpatient and home health nurses, provide essential monitoring for complications such as urinary retention, sepsis, pressure ulcers, and deep vein thrombosis. They also reinforce medication adherence, patient education, and early recognition of new neurological deficits.
• Physical and occupational therapists are crucial in rehabilitation. They help patients recover muscle mass, mobility, and endurance, especially for those with residual motor weakness or other deficits.
• Pharmacists support safe and effective antimicrobial therapy, monitor for drug interactions and adverse effects, and provide patient education to improve adherence.
• Care coordinators and case managers facilitate smooth transitions between hospital, rehabilitation, and home care, ensuring continuity of treatment and reducing preventable readmissions.

Following discharge, many patients require ongoing physical therapy and home healthcare services. A home health nurse may need to monitor recovery and watch for delayed complications. Long-term indwelling bladder catheters are sometimes required, which increases the risk of urinary tract infections. Constipation and impaired gastric motility are common and must be addressed proactively in comprehensive care planning.[31][32]

Ethics, Safety, and Communication

Interprofessional communication and shared decision-making are critical to reducing delays and improving outcomes. Ethical responsibilities include early recognition of concerning symptoms, timely imaging, and appropriate referral to specialists. SEA is frequently misdiagnosed, with delays reported in up to 75% to 84% of cases, leading to preventable paralysis in 4% to 22% of patients.[2][14] In many instances, critical signs or symptoms were missed or not acted upon, and delays in radiology reporting further contributed to morbidity.[27]

Medicolegal Considerations

Diagnostic delays are the most common cause of malpractice claims related to SEA, with lawsuits often resulting from paralysis due to late diagnosis and treatment.[2] These findings underscore the importance of vigilance, effective teamwork, and seamless communication among healthcare professionals to improve patient safety and reduce liability.

Review Questions

• Access free multiple choice questions on this topic.
• Click here for a simplified version.
• Comment on this article.

References

1.

Arko L, Quach E, Nguyen V, Chang D, Sukul V, Kim BS. Medical and surgical management of spinal epidural abscess: a systematic review. Neurosurg Focus. 2014 Aug;37(2):E4. [PubMed: 25081964]

2.

Sharfman ZT, Gelfand Y, Shah P, Holtzman AJ, Mendelis JR, Kinon MD, Krystal JD, Brook A, Yassari R, Kramer DC. Spinal Epidural Abscess: A Review of Presentation, Management, and Medicolegal Implications. Asian Spine J. 2020 Oct;14(5):742-759. [PMC free article: PMC7595828] [PubMed: 32718133]

3.

Prabahkar D, Qazi I, Devi S, Eldahtoury S, Janjua AW. Spinal Epidural Abscess: Raising the Index of Suspicion. Cureus. 2025 Jun;17(6):e85465. [PMC free article: PMC12229139] [PubMed: 40621306]

4.

Babu JM, Patel SA, Palumbo MA, Daniels AH. Spinal Emergencies in Primary Care Practice. Am J Med. 2019 Mar;132(3):300-306. [PubMed: 30291829]

5.

Boody BS, Tarazona DA, Vaccaro AR. Evaluation and Management of Pyogenic and Tubercular Spine Infections. Curr Rev Musculoskelet Med. 2018 Dec;11(4):643-652. [PMC free article: PMC6220010] [PubMed: 30280287]

6.

Chow F. Brain and Spinal Epidural Abscess. Continuum (Minneap Minn). 2018 Oct;24(5, Neuroinfectious Disease):1327-1348. [PubMed: 30273242]

7.

Fotaki A, Anatoliotaki M, Tritou I, Tzagaraki A, Kampitaki M, Vlachaki G. Review and case report demonstrate that spontaneous spinal epidural abscesses are rare but dangerous in childhood. Acta Paediatr. 2019 Jan;108(1):28-36. [PubMed: 30222897]

8.

Du JY, Schell AJ, Kim CY, Trivedi NN, Ahn UM, Ahn NU. 30-day Mortality Following Surgery for Spinal Epidural Abscess: Incidence, Risk Factors, Predictive Algorithm, and Associated Complications. Spine (Phila Pa 1976). 2019 Apr 15;44(8):E500-E509. [PubMed: 30234819]

9.

Guimarães D, Silva M, Morgado S, Reis L, Fernandes P. Beyond Risk Factors: Spinal Epidural Abscess in a Young, Healthy Patient. Cureus. 2024 Nov;16(11):e74397. [PMC free article: PMC11669180] [PubMed: 39723325]

10.

Rosc-Bereza K, Arkuszewski M, Ciach-Wysocka E, Boczarska-Jedynak M. Spinal epidural abscess: common symptoms of an emergency condition. A case report. Neuroradiol J. 2013 Aug;26(4):464-8. [PMC free article: PMC4202809] [PubMed: 24007734]

11.

Vakili M, Crum-Cianflone NF. Spinal Epidural Abscess: A Series of 101 Cases. Am J Med. 2017 Dec;130(12):1458-1463. [PubMed: 28797646]

12.

Czigléczki G, Benkő Z, Misik F, Banczerowski P. Incidence, Morbidity, and Surgical Outcomes of Complex Spinal Inflammatory Syndromes in Adults. World Neurosurg. 2017 Nov;107:63-68. [PubMed: 28757405]

13.

Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: a meta-analysis of 915 patients. Neurosurg Rev. 2000 Dec;23(4):175-204; discussion 205. [PubMed: 11153548]

14.

Darouiche RO. Spinal epidural abscess. N Engl J Med. 2006 Nov 09;355(19):2012-20. [PubMed: 17093252]

15.

Tong SYC, Fowler VG, Skalla L, Holland TL. Management of Staphylococcus aureus Bacteremia: A Review. JAMA. 2025 Sep 02;334(9):798-808. [PMC free article: PMC12663922] [PubMed: 40193249]

16.

Erşahin Y. Spinal epidural abscess: a meta-analysis of 915 patients. Neurosurg Rev. 2001 Jul;24(2-3):156. [PubMed: 11485240]

17.

Bhise V, Meyer AND, Singh H, Wei L, Russo E, Al-Mutairi A, Murphy DR. Errors in Diagnosis of Spinal Epidural Abscesses in the Era of Electronic Health Records. Am J Med. 2017 Aug;130(8):975-981. [PubMed: 28366427]

18.

Turner A, Zhao L, Gauthier P, Chen S, Roffey DM, Wai EK. Management of cervical spine epidural abscess: a systematic review. Ther Adv Infect Dis. 2019 Jan-Dec;6:2049936119863940. [PMC free article: PMC6643182] [PubMed: 31367375]

19.

Artenstein AW, Friderici J, Visintainer P. A Predictive Model Facilitates Early Recognition of Spinal Epidural Abscess in Adults. West J Emerg Med. 2018 Mar;19(2):276-281. [PMC free article: PMC5851499] [PubMed: 29560054]

20.

Tetsuka S, Suzuki T, Ogawa T, Hashimoto R, Kato H. Spinal Epidural Abscess: A Review Highlighting Early Diagnosis and Management. JMA J. 2020 Jan 15;3(1):29-40. [PMC free article: PMC7733760] [PubMed: 33324773]

21.

Jiang G, Sun LL, Yang ZT, Cui JF, Zhang QY, Gao CP. Primary spinal epidural abscess: magnetic resonance imaging characteristics and diagnosis. BMC Med Imaging. 2024 Oct 17;24(1):278. [PMC free article: PMC11487751] [PubMed: 39420251]

22.

Shifrin A, Lu Q, Lev MH, Meehan TM, Hu R. Paraspinal Edema Is the Most Sensitive Feature of Lumbar Spinal Epidural Abscess on Unenhanced MRI. AJR Am J Roentgenol. 2017 Jul;209(1):176-181. [PubMed: 28379730]

23.

Epstein NE. Timing and prognosis of surgery for spinal epidural abscess: A review. Surg Neurol Int. 2015;6(Suppl 19):S475-86. [PMC free article: PMC4617026] [PubMed: 26605109]

24.

Scalia G, Marrone S, Paolini F, Palmisciano P, Ponzo G, Giuffrida M, Furnari M, Iacopino DG, Nicoletti GF, Umana GE. Spinal epidural abscess due to acute pyelonephritis. Surg Neurol Int. 2022;13:159. [PMC free article: PMC9062902] [PubMed: 35509571]

25.

Kang T, Park SY, Lee SH, Park JH, Suh SW. Spinal epidural abscess successfully treated with biportal endoscopic spinal surgery. Medicine (Baltimore). 2019 Dec;98(50):e18231. [PMC free article: PMC6922448] [PubMed: 31852084]

26.

Berwick BW, Luo TD, Sun KW, Sharp RA, Birkedal JP, O'Gara TJ. Epidural Abscess in the Lumbar Spine: A Single Institution's Experience With Nonsurgical and Surgical Management. J Surg Orthop Adv. 2019 Fall;28(3):224-231. [PubMed: 31675300]

27.

King C, Fisher C, Brown PCM, Priest KC, Tanski M, Sullivan P. Time-to-completed-imaging, survival and function in patients with spinal epidural abscess: Description of a series of 34 patients, 2015-2018. BMC Health Serv Res. 2020 Feb 14;20(1):119. [PMC free article: PMC7023770] [PubMed: 32059715]

28.

MacNeille R, Lay J, Razzouk J, Bogue S, Harianja G, Ouro-Rodrigues E, Ting C, Ramos O, Veltman J, Danisa O. Patients Follow-up for Spinal Epidural Abscess as a Critical Treatment Plan Consideration. Cureus. 2023 Feb;15(2):e35058. [PMC free article: PMC10023045] [PubMed: 36938240]

29.

Chaker AN, Bhimani AD, Esfahani DR, Rosinski CL, Geever BW, Patel AS, Hobbs JG, Burch TG, Patel S, Mehta AI. Epidural Abscess: A Propensity Analysis of Surgical Treatment Strategies. Spine (Phila Pa 1976). 2018 Dec 15;43(24):E1479-E1485. [PubMed: 29916954]

30.

Shah AA, Ogink PT, Harris MB, Schwab JH. Development of Predictive Algorithms for Pre-Treatment Motor Deficit and 90-Day Mortality in Spinal Epidural Abscess. J Bone Joint Surg Am. 2018 Jun 20;100(12):1030-1038. [PubMed: 29916930]

31.

Eltorai AEM, Naqvi SS, Seetharam A, Brea BA, Simon C. Recent Developments in the Treatment of Spinal Epidural Abscesses. Orthop Rev (Pavia). 2017 Jun 23;9(2):7010. [PMC free article: PMC5505082] [PubMed: 28713526]

32.

Colston J, Atkins B. Bone and joint infection. Clin Med (Lond). 2018 Mar;18(2):150-154. [PMC free article: PMC6303448] [PubMed: 29626020]

Disclosure: Walter Hall declares no relevant financial relationships with ineligible companies.

Disclosure: Sunil Munakomi declares no relevant financial relationships with ineligible companies.

Disclosure: Fassil Mesfin declares no relevant financial relationships with ineligible companies.