Continued...

Discussion:

Intervertebral discitis, the association of fever and point tenderness over the disk. The administration of a PPD test was given to rule out tuberculosis affected back pain, progressive loss of intervertebral disk height, and erosion of adjacent vertebral end plates (3), is an uncommon entity. It is estimated that there are 1 to 2 cases of childhood discitis in a hospital that evaluates 32,500 patients a year. Discitis has a biphasic age distribution, with a higher incidence early in childhood and a subtler peak during adolescence (1). The pathogenesis of discitis is not clearly understood. Its propensity to develop in the pediatric population is believed to be due to anatomical changes that occur with age. In early childhood, vascular channels within the cartilaginous region of the intervertebral disk space as well as intraosseous arterial anastomoses allow for a hematogenous route of infection. With age, the intervertebral disk gradually devascularizes. After the age of 30, it is thought that disc inflammation is secondary to direct invasion (i.e. paravertebral abscess, vertebral osteomyelitis). Although it widely held that discitis is caused by an infection, typically a blood borne bacterial or viral infection of low virulence (4), the infectious agent is not always clear since most cultures are sterile and many patients recover without antimicrobial therapy (1). Culture of the intervertebral disk by needle biopsy are positive more often than blood cultures. However, all cultures, blood or disk space, are negative in most patients (50%-70%). This has led some to believe that discitis may be caused by a partial dislocation of the epiphysis, secondary to a flexion injury (5). When cultures are positive, the most common organism is Staphylococcus aureus. Discitis occurs most often in patients under the age of 5 who have no or low-grade fever. Discitis is uncommon in children 8 years or older (1). The affected disk is usually in the lumbar region, which causes a progressive limp or the inability to walk. The affected disk shows evidence of decreased height 2-4 weeks into the illness with variable degrees of damage to the vertebral end plates (1). However, some patients present with severe back pain, high fever, and bacteremia, which is commonly seen in osteomyelitis. Other patients show much milder symptoms even though bacteria is isolated from blood cultures; still others, show few signs and symptoms and no evidence of infection (3). The clinical manifestations may vary with age. Infants may refuse to eat and be fussy, toddlers may refuse to walk, while adolescents typically complain of back, abdominal, or pelvic pain. However, the spine is characteristically held stiff or in a splinted position, with a tendency to avoid flexing the lumbar spine. The area of inflammation should be evident on physical examination. The lumbar lordosis is commonly reversed and may be associated with paravertebral muscle spasms. The presence of fever is variable (3).

Differentiation between discitis and vertebral osteomyelitis is difficult early in the disease course as the two entities are considered by some to be different stages of the same disease spectrum. However, vertebral osteomyelitis typically occurs in older children, with a peak incidence in adolescence, who present with fever and complain of lumbar, thoracic, or cervical back pain. The patient is more likely to be ill appearing and have a higher, longer lasting fever at the time of diagnosis compared to the patient with discitis. Radiographic evidence, which also lags behind clinical symptoms, shows rarefaction of the involved vertebral body followed by deterioration of bone, typically from the anterior region of the vertebral body. MRI is the diagnostic study of choice for patients with suspected vertebral osteomyelitis since it is 96% sensitive and 93% specific on evaluation for this disease (1). Radiographic evidence for discitis lags behind clinical signs and symptoms. Radiographs are usually interpreted as normal shortly after the onset of clinical symptoms; however, subtle changes that are evident early in the disease process (i.e. end plate demineralization or irregularity) are often detectable in retrospect. Two to four weeks into the disease process, progressive narrowing of the intervertebral disc is evident. If the radiographs demonstrate the characteristic changes associated with discitis, this supports the diagnosis of discitis. MRI may be more definitive. Radionuclide scans may be useful in the early detection of vertebral infections, such as discitis and osteomyelitis. One study demonstrated that bone scans allowed for an earlier diagnosis of disc space infection relative to non-scanned patients, with an average time after admission of 3 days compared to 11 days for the non-scanned group (5). However, bone scans cannot differentiate between different disease states and must be interpreted alongside other clinical and diagnostic studies. It has been suggested, in the advent of MRI, that nuclear bone scans should only be used in very young patients in whom localization of symptoms to the spine cannot be done solely on physical examination (1). CT can facilitate the diagnosis of discitis by confirming the presence of disc narrowing and vertebral end plate destruction earlier in the course of the disease (4). However, like nuclear bone scans and lab studies, CT typically provides nonspecific information (1). Thus, it is especially useful when clinical evidence of infection associated with back pain and neurologic symptoms are present. CT is also better at demonstrating areas of inflammation than a conventional radiograph. MRI is the imaging study of choice for discitis. It is more sensitive, 96%, than either bone scans or CT in the diagnosis of disc space infections. Characteristic changes include irregularity and destruction of the vertebral end plates and body, increased signal intensity on T2 weighted images, bone destruction within adjacent vertebrae which are evident as low intensity signals on T1 weighted images and high intensity signals on T2 weighted images, and soft tissue changes on all images (6). If the patient shows constitutional symptoms and is suspected of having a bacterial cause of infection, initial treatment with immobilization and appropriate antibiotics is indicated. The most common bacterial isolate in discitis is Staph aureus; however, cultures should guide antibiotic therapy. A minimum of 4-6 weeks of antibiotic therapy should be initiated if a patient has a positive culture, elevated WBC, or persistently elevated ESR. In patients who show minimal symptoms and who have normal labs, the use of antibiotic therapy is less clear. Immobilization in such cases may be sufficient treatment (3). Recommendations for immobilization include the use of strict immobilization with a spica cast or modified immobilization with bed rest with early mobilization in a halo vest (7). It is recommended that a brace be worn for 3 months following mobilization (5). Operative procedures are indicated in patients who do not respond to initial therapy, when there are negative blood or closed biopsy cultures, neurologic deficit, paravertebral abscess, and progressive spinal deformity (7). In children, aggressive surgical treatment is rarely needed, except in the cases of tuberculosis or other caseating diseases that are not responding to antibiotics (8). Patients treated surgically typically have a more rapid resolution of symptoms which may be secondary to decompression of the infected disk space (9). Gebhard and Brugman have shown that percutaneous discectomy of the infected disc is effective in relieving symptoms, obtaining a bacterial diagnosis, and helped to eliminate the infection (9). Discitis usually carries a good prognosis. Mortality is extremely low, approaching zero, and recurrence is uncommon. However, residual back pain, limited spinal mobility and neurologic deficit can occur (7). In a study by Bernard et al., which followed up 35 children (an average of 17 years after they had intervertebral discitis), 43% had residual back pain, 91% had normal flexion of the lower back, 86% had markedly restricted lumbar extension, and 80% had a narrowing of the vertebral canal. These results did not seem to be influenced by the type of treatment the patients received (10). It was also suggested that the incidence of back pain increased with age.

References:

1. Fernandez M, Carrol CL, Baker CJ. Discitis and Vertebral Osteomyelitis in Children: An 18-Year Review. Pediatrics 2000;105 (6):1299-1304
2. Maguire JH. Osteomyelitis. In: Braunwald E, Fauci AS, Hauser SL, Isselbacher KJ, Kasper DL, Longo DL, Martin JB, Wilson JD (eds). Harrison's Principles of Internal Medicine, 14th Edition CD-ROM. McGraw-Hill, New York, 1998, pp824-827.
3. Wood GW. Infections of the Spine. In: Behrman RE, Kliegman RM, Jenson HB (eds). Nelson Textbook of Pediatrics, 16th ed. W.B. Saunders Co., Philadelphia, 2000, pp3094-3119.
4. Garcia FF, Semba CP, Sartoris CC, Sartoris DJ. Diagnostic Imaging of Childhood Spinal Infections. Orthopaedic Review 1993;22 (3):321-327.
5. Glazer PA, Hu SS. Pediatric Spinal Infections. Orthopedic Clinics of North America 1996;27(1):111-123.
6. Ozuna RM, Delamarter RB. Pyogenic Vertebral Osteomyelitis and Post Surgical Disc Space Infections. Orthopedic Clinics of North America 1996;27(1):87-94.
7. Harris LF, Haws FP. Disc Space Infection. Alabama Medicine 1994;63(7):12-14.
8. Wood II GW. Infections of the Spine. In: Canale ST (ed). Campbell's Operative Orthopaedics, 9th ed., Mosby Inc., St. Louis, 1998, pp3094-3119.
9. Gebhard JS, Brugman JL. Percutaneous Discectomy for the Treatment of Bacterial Discitis. Spine 1994;19(7):855-857. 10.Jansen BR, Hart W, Schreuder O. Discitis in Childhood, 12-35-year Follow-up of 35 Patients. Acta Orthop Scand 1993;64(1):33-36

Copyrighted:Radiology Cases in Pediatric Emergency Medicine Volume 7, Case 1 Loren Yamamoto, MD, MPH s, Professor of
Pediatrics,University of Hawaii John A. Burns School of Medicine..Loreny@hawaii.edu

Back to Case

More cases..

Last created on 01-07-2006