Spinal epidural abscess consist of purulent or granulomatous collections contained within the spinal epidural space and over- lying or encircling the spinal cord, roots, and nerves. Infection may be localized or may extend widely, at times involving the length of the spinal canal. In one large series an average extent of 4.3 bony segments was reported.
This is a rare type of infection — one twentieth as common as bacterial meningitis, in our experience. Although persons of any age are susceptible, it occurs more frequently in young adults..
Etiology and Pathogenesis.
Staphylococcus aureus is involved in more than 90 per cent of cases, but group A streptococci, other streptococci, pneumococci, Brucella, Salmonella, and various other gram-negative organisms may be responsible. M. tuberculosis is an important cause of chronic chronic epidural infections in areas where tuberculosis is prevalent; occasionally fungi and parasites may be recovered from epidural granulomas. There is a primary infective site remote from the spine in most cases. This usually involves the skin, and furuncles, boils, and cellulitis are the common underlying infections. Less often infections of the upper respiratory tract, genitourinary system, or bone may be responsible.
Hematogenous or lymphatic spread of infection to the highly vascular epidural space is postulated. Occasionally the responsible organism may be cultured from the blood. Minor injury to the back frequently antedates the symptoms of epidural abscess, and trauma may in some way determine the site of infection.
The lack of restraining fibrous tissue in the epidural fat allows the infection to spread caudally and rostrally, and epidural abscesses may extend into the extraspinal tissues; in contrast, the dura is rarely penetrated. In less than half the cases the spine and adjacent soft tissues are primarily affected, and the infection spreads secondarily to the epidural space. Only in tuberculous infections is primary osteomyelitis the rule. Epidural abscess may rarely complicate a lumbar puncture, myelography, or spinal operation.
The purulent material or granulomatous tissue is usually most abundant over the posterior aspect of the spinal cord. When the primary lesion is in a vertebral body, intervertebral disc, or some other anterior structure, the abscess may be predominantly ventral. Epidural abscess occurs most commonly in the thoracic region, but may develop at any level of the spinal axis. The lesion may be purulent or granulomatous.
The mechanism of neural dysfunction in spinal epidural abscess is uncertain. Since the lesion occupies space, direct compression of spinal cord, roots, and nerves is a prime consideration, but the small size of many epidural abscesses, in association with severe impairment of neural function, demands consideration of other possibilities. The most plausible of these and the one for which there are some supporting facts is a vasculitis with secondary venous and arterial occlusions resulting in infarction of neural tissues.
Clinical Manifestations of Spinal Epidural Abscess.
Heusner has divided the clinical picture into four phases: spinal ache, root pain, weaknesses (voluntary muscles, sphincters, sensibilities), and paralyses.
The spinal ache, characteristically maximal at the level of the major pathologic process, soon spreads axially and may also include the paravertebral regions. Restricted movement of the spine, especially in the anteroposterior plane, is common. A functional or even a structural scoliosis may develop. The spines overlying the disease process are tender to percussion; pain so induced may be exquisite, particularly when there is vertebral caries. Signs of sepsis (fever, leukocytosis) are prominent, except in the more chronic cases. The diagnosis is rarely made at this stage.
Within two or three days (acute cases) nerve roots inevitably become encased by the purulent material, and radicular pains develop. Meningeal signs are present in most cases, and headache is a common symptom. At times reflex activity at the level of the involved segment may be depressed. An erroneous diagnosis of “neuritis” or “shingles” is frequently made, but at this stage of illness the combination of clinical symptoms and signs should permit an accurate diagnosis.
The characteristic feature of this phase of the illness is progressive impairment of neural functions below th«.- level of the lesion, the exact syndrome depending upon the site of maximal damage. If the abscess overlies the spinal cord, spastic weakness, heightened reflexes, and a sensory level over the trunk are to be expected. There may be urinary urgency and incontinence.
Abscesses in the lumbosacral* region exert their effects on spinal roots and nerves, giving rise to dysesthesias in dermatomes supplied by the implicated nerves, along with appropriate pareses and depressed stretch reflexes. Pain is usually excruciating and nuchal rigidity extreme. The kin and soft tissues overlying the abscess may be swollen, warm, and red. High fever and signs of systemic toxicity are often present.
The diagnosis may be made as late as this with reasonable anticipation that prompt laminectomy and drainage of pus or removal of granulomatous tissue will effect considerable if not total recovery.
Within hours or at most a few days, severe or even total paralysis of nervous functions below the site of the lesion supervenes. Immediate surgical treatment is mandatory at this stage. Procrastination may vitiate the effect of any subsequent therapeutic measures, for enduring paralyses are usual if the patient remains paraplegic for more than a few hours. When an epidural abscess remains unrecognized and untreated, death occurs in 25 to 33 per cent of cases.
It is axiomatic that the foregoing analysis of the clinical features of subdural abscess is arbitrary and somewhat artificial, since the various stages may merge one into the other. Yet, considered in this way the early stages are stressed and the importance of prompt diagnosis and treatment is underscored.
Spinal epidural abscess demands consideration in the patient with sepsis, back pain, and even minimal neurologic symptoms and signs. Confirmatory evidence may be obtained by tapping the epidural space with an ordinary spinal needle. This is most safely done in the lumbar area. Gentle suction is applied with a small (2 ml.) syringe while slowly advancing the needle. If no purulent material is obtained, the stylet should be replaced in the needle and the subarachnoid space entered.
The cerebrospinal fluid is characteristically clear and xanthochromic. It may be acellular, but more often a few cells or a moderate pleocytosis (lymphocytes predominating) will be found. Normal sugar content and elevated cerebrospinal fluid protein arethe rule (several hundred to more than 2000. mg. per 100 ml.). A partial or complete manometric block below the lesion is found in most cases.
An acute viral, postinfectious, syphilitic, or necrotizing myelitis may produce a neurologic syndrome similar to that seen in stage 4 of a’ spinal epidural abscess, and may be associated with symptoms and signs of infection and cerebrospinal fluid pleocytosis. There may be back pain in acute myelitis, but the duration of illness is compressed in time. Furthermore, xanthochromic cerebrospinal fluid and manometric block are unusual in myelitis.
They are seen, however, in progressive adhesive arachnoiditis, which may be confused with subacute or chronic epidural infections. Spinal caries, demonstrable by roentgenography in less than 20 per cent of cases of spinal epidural abscess, suggests the correct diagnosis. In questionable cases a myelographic study will confirm the presence of a space-occupying intraspinal lesion. Rarely, malignant tumors, especially lymphomas that lodge in the epidural space, may present with fever, backache, neurologic signs, and spinal block. Chronic epidural abscess in which evidence of an inflammatory disease is meager or wanting will, on occasions, be confused with the more benign intraspinal tumors.
Treatment Of Spinal Epidural Abscess.
Prompt laminectomy with drainage of purulent material or removal of granulomatous tissue and the administration of appropriate antimicrobial drugs constitute proper therapy. The antimicrobials must be continued in high doses for a minimum of six weeks when pyogenic osteomyelitis is present.