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A 51-year-old woman with low back pain

Issue: October 2013

ByBrandon J. Erickson, MD

ByRachel M. Frank, MD

ByJonathan Howard, MD

ByHoward S. An, MD

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A 51-year-old woman with a history of coronary artery disease who had a renal transplant 4 years prior for IgA nephropathy and was on immunosuppression medication when she presented to the clinic with complaints of acute on chronic low back pain. She reported an insidious onset of pain approximately 1 year prior, and denied a history of trauma or falls.

She described her pain as a deep ache made worse with activity, especially during bending and twisting, that alleviated with lying supine in bed. She reported normal bowel and bladder function and denied weakness, paresthesias, fevers, chills, weight loss and night sweats. The patient was born in Thailand, immigrated to the United States 15 years prior, and reported traveling to Hong Kong and Thailand 6 months prior to presentation.

 

Sanjeev Bhatia

 

Andrew R. Hsu

Physical examination

On physical examination, the patient endorsed mild tenderness to palpation at the level of L1 to L3 that was greater on the right side. She was neurovascularly intact with full motor strength to knee flexion, extension, dorsiflexion, plantar flexion and extensor hallicus longus function bilaterally. Her sensation was intact to light touch in the L4 to S1 distributions bilaterally. She was able to stand up straight, but could not flex forward past 10° without reproduction of her pain. She could extend backward 15° without pain and was able to ambulate with a normal gait.

Figure 1. Initial AP (A), lateral (B), flexion (C) and extension (D) radiographs demonstrate anterior vertebral collapse of L2-L3 consistent with possible discitis, osteomyelitis or tuberculosis.

Images: Erickson BJ, et al.

Figure 2. AP (A), lateral (B) and axial (C) CT scans demonstrate bony destruction of the L2-L3 vertebral bodies.

Diagnostic studies

Radiographs, CT and MRI of the spine were obtained and are shown in Figures 1-3. A chest radiograph was also performed and revealed no acute abnormalities. Her laboratory values, including erythrocyte sedimentation rate (ESR), serum C-reactive protein (CRP) and serum white blood cell (WBC), were within normal limits.

Figure 3. T2-weighted MRI lateral and axial cuts before (A, C) and after contrast (B) demonstrate L2-L3 discitis with extension into the epidural space with abscesses noted in the right psoas muscle.

What is your diagnosis?

See answer on next page.

Spinal tuberculosis

Spinal tuberculosis, also known as Pott’s disease, requires a high index of suspicion and a thorough history to diagnose in its early stages. Patients typically present with complaints of vague back pain, rarely accompanied by neurologic deficits. A recent history of international travel, especially to Asia or South America, as well as a history of living abroad for an extended period of time, should raise the index of suspicion. A history of homelessness, incarceration or immunocompromised conditions place patients at high risk for tuberculosis. Patients may also report recent fevers, weight loss or night sweats; however, these symptoms are nonspecific, and — as seen in the current case — are not always present.

Diagnostic work-up typically involves imaging of the chest and spine, laboratory studies and administration of a PPD (purified protein derivative) skin test. Initial radiographs may show destruction of the anterior aspect of the vertebral body, most commonly in the thoracic and lumbar spine. If the disease has progressed, radiographs may show destruction of consecutive levels or demonstrate skip lesions as the pathogen spreads beneath the anterior longitudinal ligament (ALL). This may lead to a kyphotic deformity. Anterior vertebral body destruction with preservation of the disc space separates tuberculosis (granulomatous infection) from other, pyogenic infections. The posterior spinal elements are rarely involved; but if they are, the likelihood the patient will present with a neurologic deficit is much greater. Advanced imaging, such as MRI, will typically reveal a cold abscess (that develops so slowly there is no inflammation accompanying it) around the vertebral lesion, disc destruction and vertebral collapse.

Laboratory studies, including ESR and serum CRP are often elevated, while serum WBC may be normal. Approximately one-third of patients with spinal tuberculosis (TB) have normal chest radiographs and approximately 20% of patients will have a negative PPD test. Thus, while laboratory studies, radiographs and PPD testing can be of some assistance, a high index of suspicion in the absence of convincing objective data must be maintained in these cases. The definitive diagnosis for spinal TB requires a biopsy.

 

Brandon Erickson

 

Rachel M. Frank

In this case, radiographs and CT revealed anterior vertebral body destruction at the L2-L3 levels. Interestingly, the MRI findings did reveal L2-L3 discitis with extension into the epidural space. Her ESR, CRP and WBC count were within normal limits, and no PPD was placed. Given her vague complaints of low back pain, her travel history and imaging findings, the diagnosis of spinal TB was strongly considered. A fluoroscopically guided biopsy and aspiration of the L2-L3 disc approximately 1 week after her initial presentation confirmed the diagnosis of mycobacterium TB.

Discussion and management

Howard An

Management of spinal TB varies depending on the initial clinical presentation. The literature supports initial nonoperative management in the setting of a stable patient who presents without neurologic symptoms. The initial treatment strategy should consist of an infectious disease (ID) consult and initiation of anti-TB medications, typically incorporating some combination of isoniazid, rifampin, pyrazinamide and ethambutol. Antibiotic choices are specific to the specific strain or sensitivity of TB as well as to the patient’s ability to tolerate the potential side effects. Patients should be followed closely with frequent neurologic exams to monitor for the possibility of disease progression, although medical treatment is successful in approximately 90% of cases.

Initial presentation with neurologic deficits or the progressive development of such symptoms — including weakness, paresthesias or abnormal gait — warrants more aggressive treatment with surgical intervention. The initial description of surgical treatment for spinal TB was the Hong Kong procedure, which involves debridement of any infected bone, decompression and correction of the kyphotic deformity. More recent trends have included the addition of posterior instrumentation for additional stabilization. While surgical treatment must be individualized for every patient, typical techniques incorporate a combination debridement, decompression and fusion with instrumentation. A focus on the debridement portion is of utmost importance in an effort to eradicate the local disease, and particular attention should be given to any involved bone, musculature and surrounding pseudomembranous tissue.

 

Figure 4. Immediate postoperative AP (A) and lateral (B) radiographs demonstrate anterior iliac crest strut graft from L2-L3 and T12-L4 posterior spinal hardware in appropriate position and alignment.

Postoperatively, the patient is maintained on an aggressive antibiotic regimen as guided by the ID specialists. Long-term clinical outcomes following surgical intervention for spinal TB reveal favorable outcomes, especially when drug therapy is combined with surgical intervention.

Follow-up

In this case, the patient was diagnosed with spinal TB on the basis of her biopsy results. She was started on antibiotic therapy with isoniazid, rifabutin, pyrazinamide and ethambutol at the recommendation of the ID consultant. Two months into treatment, the patient developed increasing back pain, right quadriceps and iliopsoas weakness, and progressive difficulty with gait. Given the progression of symptoms, despite aggressive antibiotic therapy (especially the neurologic deterioration), the patient was indicated for surgical intervention. The procedure was uncomplicated and included incision and drainage of the epidural abscess, partial L2-L3 transpedicular corpectomy, L2-L3 anterior strut graft with iliac crest allograft, L2-L3 laminectomy and discectomy, and T12-L4 posterior spinal fusion with instrumentation (Figure 4). It should be noted that the iliac crest graft was used for the posterolateral fusion, spanning the instrumentation and fusion, and the iliac crest wound was closed before getting into the infected area to avoid contamination. This is extremely important to minimize the postoperative risk of infection. Postoperatively, the patient continued isoniazid and rifabutin for 9 months. Her clinical examination improved. At her 6-week follow-up visit, she had full, symmetric strength of her bilateral lower extremities with no complaints.