Spinal Cord Infections

Infections involving the spinal canal include epidural abscesses (infection in the epidural space), meningitis (infection of the meninges), subdural abscesses (infections of the subdural space), and intramedullary abscesses (infections within the spinal cord).[1] Because the first 3 infections are discussed elsewhere (see Epidural and Subdural Infections, Meningitis), this article addresses only intramedullary abscesses.

Intramedullary spinal cord abscesses are extremely rare lesions. Since the original description in 1830 by Hart, approximately 100 cases have been reported. Their rarity, compared with brain abscesses, has been attributed to the relatively lower volume of the spinal cord and its particular blood supply.

Mechanisms of infection include (1) hematogenous spread from an extraspinal focus of infection, (2) contiguous spread from an adjacent focus of infection, (3) direct inoculation (ie, penetrating trauma, postneurosurgery), and (4) cryptogenic mechanisms (ie, no documented extraspinal focus of infection). In a 1998 review of 25 cases, hematogenous spread accounted for 8%, contiguous spread accounted for 24%, direct inoculation accounted for 4%, and 64% were cryptogenic.[2] In children, the abscesses are associated with prior anatomic spinal canal defects, such as dermal sinus tracts, which result from the incomplete partition of epithelial ectoderm and neuroectoderm in early fetal life.

Bacteria, such as staphylococci and streptococci, are the most common organisms responsible for these infections. Infections may also be caused by viral, fungal, or parasitic organisms. A diverse list of pathogens include, but are not limited to, cysticercosis, Mycobacterium tuberculosis, Listeria monocytogenes, Toxoplasma gondii, Nocardia asteroides, Histoplasma capsulatum, brucellosis, and the tapeworm spargana.

Initially, the area of the bacterial nidus is infiltrated with polymorphonuclear cells, leading to a suppurative myelitis. This evolves into central necrosis and liquefaction, which can spread along the long spinal tracts. Although the average extent of the process before 1975 was 6 vertebral levels, the average current length appears to be 3 levels. This change may be due to earlier detection and more effective antibiotics. At the periphery of this infectious process, fibroblasts proliferate and the central purulent area eventually becomes encapsulated by fibrous granulation tissue. The most commonly affected area is the dorsal thoracic spinal cord.

Frequency

International

Various reviews of the literature describe different numbers, with a range of approximately 80-100 cases since the first description in 1830. In a 2003 review, only 38 pediatric cases were identified in the medical literature since 1830.[3]

Mortality/Morbidity

Although the first reported cases had high mortality rates, prognosis has improved significantly with the advent of antibiotics.

The mortality rate without surgical intervention is practically 100%, and those patients who died despite surgery almost exclusively were affected in the preantibiotic era.

The current mortality rate (cases reported in the last 2 y) is 8-12%, although 70% of survivors had persistent neurologic deficits.

In a review of 38 pediatric cases, 20% died, 60% had residual neurologic deficits, and only 20% recovered without sequelae.[3]

A study of veterans with traumatic spinal cord injury shows the need for preventative strategies, particularly for managing cardiovascular complications, to decrease mortality.[4]

Race-, sex-, and age-related demographics

Ethnic preference does not appear to exist, although some geographic differences are present. All intramedullary paracoccidioidomycosis cases were reported in Brazil.

In one study in which sex was reported, spinal cord infections were 2.5 times more common in males than in females.

All ages are affected though children younger than 5 years are more likely affected.[5]

Female patients are affected mainly in the first 4 decades of life, whereas the incidence among male patients is distributed more evenly, with a peak in the third decade of life (see the image below).

Menezes and VanGilder have classified patients by the duration of symptoms into acute, subacute, and chronic categories.[6] In one study, the average time from the onset of symptoms to diagnosis was 46 days, with a range of 0-540 days.

Patients in the acute category present with symptoms lasting less than 1 week. Patients who present acutely have a clinical picture of transverse myelitis (with rapid onset of motor and sensory loss) and sphincter disturbances. Pain is common, and fever with signs of concomitant infection typically is present.

Patients in the subacute category present with symptoms that are 1-6 weeks old. The clinical picture resembles that of a chronic presentation.

Those in the chronic category present with symptoms of greater than 6 weeks' duration. Patients with chronic spinal cord abscesses present with signs and symptoms that are more consistent with an intramedullary tumor (ie, with a slowly progressive and stuttering neurologic deficit). Patients may complain of a radicular-type pain and are frequently afebrile.

Radiculopathic pain can present in the back, neck, extremities, or, occasionally, as abdominal or chest pain of undetermined origin. At least one reported case exists in which abdominal surgery was performed and later diagnosis proved intramedullary abscess of the spinal cord to be the origin of the problem.

A review of 25 patients, published in 1998, revealed fever in 40%, back or radicular pain in 60%, and a triad of fever, pain, and neurologic deficits in 24%.[2]

A thorough physical examination to determine the extent of the motor and sensory deficit and its levels is of primary importance to guide diagnostic modalities later. Examine the cervical, dorsal, and lumbar regions carefully looking for dermal sinuses, suggestive lesions, and signs of local infection.

First findings of intramedullary spinal cord abscess include fever (in acute forms), radiculopathic pain, and neurologic deficit.[7]

Root pain can present along a well-defined dermatome or, occasionally, as abdominal or chest pain of undetermined origin.

Palpation of the spinous processes or straight-leg raising is unlikely to elicit pain on examination.

Motor deficit usually progresses from slight paresis of one or more limbs to a flaccid paraplegia or tetraplegia with sensory loss below the level of the lesion and eventual sphincter disturbances (urinary retention or incontinence and/or loss of rectal tone).

A review of 25 patients, published in 1998, revealed the following:[2]

• Motor deficits only (24%)

• Sensory deficits only (4%)

• Motor and sensory deficits (68%)

• Brainstem dysfunction (4%)

• Urinary incontinence (56%)

• Meningismus (12%)

Presence of spinal dysraphism (congenital midline neuroectodermal defects) with persistent dermal sinus can lead to development of an intramedullary abscess by contiguity. These abscesses usually are observed early in life. In a review of 25 patients, 36% had spinal dysraphisms.[2] Tethered cord syndrome can lend itself to iatrogenic spinal cord infection and damage via a lumbar puncture.[8]

The existence of chronic conditions (eg, alcoholism, diabetes, intravenous drug use) can predispose patients to the development of this rare pathology of intramedullary abscess.

Immunosuppression (eg, AIDS) alters the bacteriology of spinal abscesses.

Organisms also can cause spinal cord infections.

A CBC count demonstrates leukocytosis only in the acute presentation (with or without neutrophilia).

Cerebrospinal fluid (CSF) analysis demonstrates the following:

• Marked pleomorphic leukocytosis, increased protein level, and decreased glucose and chloride level may be noted in the rare patients in whom the abscess has ruptured into the subarachnoid space.

• Often, mild leukocytosis (mostly polymorphonucleocytes) and protein level increase are observed.

Results from blood cultures occasionally are positive, showing the bacteriology of the underlying disease (eg, bacterial endocarditis, urosepsis).

CSF cultures usually are sterile.

Cervical, thoracic, or lumbar spine radiographs

Plain films are not helpful in diagnosing spinal cord abscesses and usually are normal.

If plain films show diskitis, osteomyelitis, or paraspinal infection, then one should suspect spread of contiguous infection into the spinal cord.

However, in patients in whom the abscess is associated with dysraphism, spina bifida can be demonstrated.

Myelography with contrast

A positive myelogram reveals an expanded spinal cord or a complete block.

Until recently, myelography was the most reliable diagnostic tool; MRI largely has replaced it.

MRI

To date, in the cases reported using MRI, the T1-weighted images exhibit decreased signal intensity. Peripheral enhancement, similar to that observed with abscesses of the brain, has been found with gadolinium.

MRI has become the preferred imaging technique, yielding not only the diagnosis but also the extent of the process.

Lumbar puncture

Do not attempt lumbar puncture if a dermal sinus is found in the lumbar area. Delay the procedure until a tethered cord syndrome has been excluded using computed tomography of the lumbar spinal canal.

Abdominal and jugular compression maneuvers with proper manometry may be indicated to establish the presence of a block to CSF flow. CSF manometer has been supplanted by neuroimaging, particularly MRI.

Jugular compression for manometric testing never should be performed if an intracranial mass is present.

Because the course of this condition is measured in days and not in hours (some patients take several months to present to medical care), patients' arrival by Emergency Medical Services (EMS) transport is unlikely.

If presented with a patient who requires EMS transport, oxygen, analgesia, and a position of comfort are the only treatments needed in the prehospital arena.

In patients in whom meningismus is involved, antiemetics and gentle handling are indicated.

Because this is such a rare entity, making the diagnosis in the ED is likely difficult. The emergency physician should consider the diagnosis when an infectious picture is present along with neurologic deficits originating at the spinal cord level.

Treatment goals include making an accurate diagnosis and starting antibiotics as early as possible.[9, 10]

Determining the extent of the motor and sensory deficit and its levels is important to guide diagnostic modalities later. Examine the cervical, dorsal, and lumbar regions carefully looking for dermal sinuses, suggestive lesions, and signs of local infection.

Plain radiography of the involved spinal levels occasionally can offer a clue when abnormal.

A lumbar puncture always is considered in a patient with a septic picture with neurologic involvement; however, remember that besides cell count, protein, glucose, and bacteriologic studies, manometric maneuvers can establish the diagnosis of CSF block. Again, neuroimaging (especially MRI) of the spine has made CSF manometry largely obsolete for detecting spinal canal block. If a dermal sinus is found in the lumbar region, deferring the lumbar puncture until the absence of a tethered cord syndrome can be ascertained is prudent.

Start antibiotics as soon as the bacteriologic workup samples have been obtained. Concomitant risk factors determine the most optimal antibiotic coverage for each individual patient.

The use of steroids to treat spinal cord swelling should be made in consultation with neurosurgery.

For additional information, see Spinal Cord Abscess and Spinal Cord Tumors - Management of Intradural Intramedullary Neoplasms.

The neurosurgeon should be involved early to guide the diagnostic flow toward surgery.

An infectious disease consultant can offer invaluable help regarding the best antimicrobial combination.

Consult a neuroradiologist to read the MRI with gadolinium study.

The goal of therapy is to eradicate infections. The empiric antimicrobial therapy should take into account the mechanism of infection, which helps predict the most likely infection organism or organisms.

For example, for contiguous spread through a sinus tract opening, one suggested regimen is vancomycin plus cefotaxime plus metronidazole.

For postneurosurgical complication, a suggested regimen consists of vancomycin plus ceftazidime with or without metronidazole.

For cryptogenic infection (ie, no identified primary source), a suggested regimen is ampicillin plus cefotaxime plus metronidazole. Ampicillin must be administered to cover L monocytogenes.

For hematogenous spread, the choice of antibiotics obviously depends on the primary source of infection. The optimal duration of antimicrobial therapy is not well defined. One review recommended a minimum of 4-6 weeks of parenteral therapy, with consideration of an additional 2-3 months of oral antimicrobial therapy.

Class Summary

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Vancomycin (Vancocin, Vancoled, Lyphocin)

Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci.

Cefotaxime (Claforan)

Arrests bacterial cell wall synthesis, which, in turn, inhibits bacterial growth. Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.

Metronidazole (Flagyl IV, Metro IV)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents (except for Clostridium difficile enterocolitis).

Ceftazidime (Ceptaz, Fortaz, Tazicef, Tazidime)

Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins.

Ampicillin (Marcillin, Omnipen, Principen, Polycillin-N)

Bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.

Laminectomy is the treatment of choice once the provisional diagnosis is made. Then, opening of the dura, needle aspiration of the abscess (with pus bacteriology), midline myelotomy with drainage of the cavity, abundant irrigation, and closure by layers are performed.

The dura mater preferably is closed with a graft, if needed, once decompression has been accomplished. Although marsupialization has been tried occasionally, it generally is not recommended.

In children, all cases of abscesses with concomitant isolated dermal sinus presented when the child was older than 6 months of age, which suggests that complete resection of the dermal sinus before 6 months of age may prevent the formation of intramedullary spinal cord abscess and its significant morbidity and mortality.

Complications include the following:

• Sepsis

• Neurologic sequelae (70%)

• Death

Prognosis of spinal cord infection was grim in the preantibiotic era. Currently, with prompt diagnosis, early surgery, and correct antibiotic therapy, the chances for full or almost full recovery often are very good.

Early surgery is the key to recovery for patients in the acute category.

Prognosis generally is better for patients in the chronic and subacute categories.