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Epidural abscess refers to an inflammatory mass or localized collection of purulent material between the dura mater and the overlying skull in intracranial epidural abscess or the vertebral column in spinal epidural abscess (SEA).
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.
Local extension of infection from the spinal epidural space can occur or can disseminate to other sites via the bloodstream.
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
Staphylococcus aureus causes about 50% to 90% of cases. There has been an increasing proportion of methicillin-resistant S. aureus (MRSA) cases recently, although it had historically only accounted for 15% of staphylococcal spinal epidural infections.
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).
Polymicrobial infection occurs in about 5% to 10% of cases.
Demographics 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
Malignancy
Human immunodeficiency virus (HIV) infection
Alcohol use disorder
Renal insufficiency
Risk factors:
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
Signs, Symptoms, and Timeline 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
Once paralysis develops, it may quickly become irreversible. Thus, urgent intervention may be required if progression of weakness or other neurologic findings is suspected or detected.
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
Codes
ICD10CM: G06.1 – Intraspinal abscess and granuloma
SNOMEDCT: 61974008 – Epidural Abscess
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Differential Diagnosis & Pitfalls
Disk and degenerative bone disease – Back pain typically not associated with fever.
Metastatic tumors – Rapidly progressive tumors may be difficult to distinguish from SEA. Occur in the thoracic vertebra in 60% of cases. May be suggested by imaging but usually require biopsy for diagnosis.
Vertebral discitis (diskitis) and osteomyelitis – Frequently associated with SEA, and a drainable focus of infection may be missed.
Guillain-Barré syndrome (GBS) / acute demyelinating polyradiculoneuropathy – Severe low back pain, as well as bowel and bladder dysfunction and hyporeflexia that can be found in spinal cord impairment in SEA can be differentiated by the absence of a focal enhancing spinal mass lesion in acute immune-mediated polyneuropathies. Cerebrospinal fluid (CSF) analysis in GBS frequently demonstrates albuminocytologic dissociation.
Herpes zoster – Can present with unilateral pain prior to the appearance of skin lesions.
Amyloidosis and parathyroid-associated vertebral destruction – Causes of destructive lesions of the vertebra in long-term hemodialysis patients that can present with paresis or paralysis; lesions on MRI are dense and water-poor.
