Pathophysiology and Etiology
Microbial pathogens may enter the epidural space via:
- Contiguous spread from vertebral osteomyelitis or psoas abscess (about 30% of cases)
- Hematogenous dissemination (about 25% to 50% of cases)
- Direct inoculation (eg, during spinal or epidural anesthetic procedures or surgery)
- The mechanism is unknown in the remainder of cases.
As the pyogenic process progresses longitudinally in the epidural space, damage to the spinal cord can be from one or a combination of factors:
- Direct compression
- Thrombosis and thrombophlebitis of nearby veins
- Arterial blood supply interruption
- Bacterial toxins and inflammatory mediators
Less common pathogens:
- Coagulase-negative staphylococci, such as Staphylococcus epidermidis, are usually related to spinal instrumentation.
- Aerobic gram-negative rods, such as Escherichia coli, often arise from an infection in the urinary tract.
- Pseudomonas aeruginosa is associated with IV drug users.
- Other rare etiologic agents are anaerobic bacteria, agents of actinomycosis or nocardiosis, mycobacteria, fungi, or parasites (ie, Echinococcus and Dracunculus).
The median age of onset of SEA is approximately 50 years, and the prevalence appears to be greatest between age 50 and 70, but SEA can occur at any age. The incidence has been higher in males in some studies.
Predisposing medical history:
- Diabetes mellitus
- Human immunodeficiency virus (HIV) infection
- Alcohol use disorder
- Renal insufficiency
- Spinal abnormality, injury, or intervention – degenerative joint disease, trauma, surgery, drug injection, placement of epidural stimulators or catheters, nerve acupuncture, epidural analgesia, nerve block
- Potential local or systemic source of infection – skin and soft-tissue infections, vertebral osteomyelitis, urinary tract infection, sepsis, indwelling vascular access infections, tattooing, intravenous drug use
The clinical findings in patients with SEA may develop acutely within hours to days (usually after hematogenous seeding), or more chronically over weeks to months (usually in association with vertebral osteomyelitis or another contiguous focus of infection).
The initial manifestations are often nonspecific. The classical diagnostic triad consists of fever, spinal pain, and neurologic deficits. However, only some patients, 2% to 37%, have all three components at presentation.
Fever occurs in 60% to 70% of patients, but may be infrequent (range 32% to 70%). The specific neurologic signs depend on the level of spinal cord involvement.
Pain is the most consistent symptom (70% to 90% of cases) and is usually accompanied by local tenderness at the affected level.
The clinical course in most patients with SEA progresses through four clinical stages:
- Stage 1 – Backache at the level of the affected spine
- Stage 2 – Nerve root pain
- Stage 3 – Spinal cord dysfunction
- Stage 4 – Paralysis
Epidural abscesses that are enclosed within the bony confines of the skull or spinal column can expand and cause increased intracranial pressure in the brain or compressive symptoms in the spinal cord, leading to severe symptoms, permanent complications, or even death, depending on the site of central nervous system involvement.
Intracranial Epidural Abscess
- Cranial epidural abscess occurs less commonly than SEA.
- Fever and headache are the usual complaints, but patients may also be asymptomatic.
- Gradenigo's syndrome can occur when the cranial epidural abscess is near the petrous bone involving cranial nerves V and VI. Unilateral facial pain and weakness of the lateral rectus muscle are observed.
- The initial focus is usually in the paranasal sinuses, middle ear, or mastoids, where the causative organisms are likely to be microaerophilic or anaerobic streptococci and/or other anaerobes such as Propionibacterium and Peptostreptococcus species.
- Intracranial epidural abscess (IEA) may also occur after trauma, fetal scalp monitoring, halo pin penetration, and craniotomy, where the most likely infecting organisms are staphylococci, especially S. aureus, and gram-negative bacteria