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2010 Case #3

History: A 22 year-old male presented with a history of 1-month of mild lumbar pain that increased with physical activity, with progressive onset of paresthesias over the next two months and difficulty in walking due to subjective muscle weakness.

Epidemiology: Construction worker, born in Ancash in the Peruvianhighands and lives in Lima. No history of travel, no previous or currentTB contact known. No HIV risk factors.

Physical Examination: Afebrile, alert and oriented, normal vitalsigns. No rash, no lymphadenopathy, normal thoracic and cardiovascularexaminations. The abdomen was distended and diffusely tender making fullexamination difficult but no peritoneal signs were present. A painful masswas felt occupying almost all of the left hemi-abdomen. Bilateral abdominalpain on hip flexion was elicited. Lumbar pain at L4-5 without sensory deficitsbut with mild left leg weakness. No pathological reflexes were observed(clonus, Babinski). Normal sphincter tone.

Laboratory Results: Hematocrit 34%; WBC 15600 (no bands, 79% neutrohils,15% lymphocytes). Platelets 761,000. Normal renal and liver function. HIVnegative. Brucella agglutination negative. MRI (T2 image) is shown in Image A.

Skeletal tuberculosis is thought to result from hematogenous dissemination from a primary site and occurs 6 months to 3 years after primary infection; but cases associated with relapsing disease have been reported. Spinal TB accounts for more than 50% of all skeletal cases. It is seen more in children in developing countries but mainly occurs in adults in developed countries. The disease process begins in an intervertebral disc and usually spreads anteriorly to the adjacent vertebrae. Destruction of the anterior endplates ensues with anterior collapse leading to a wedge deformity. Cold abscesses may occur and may drain through adjacent skin. Lower thoracic vertebral location is the most common, followed by a lumbar location, as in our patient.

Clinical presentation of isolated Pott’s disease is with chronic back pain that is initially non-specific. Undiagnosed progression to severe disease leads to spinal cord compression and neurologic deficit. Differential diagnosis of the clinical syndrome and spinal lesion seen in our patient includes other forms of bacterial osteomyelitis and metastatic cancer. The spinal lesions of advanced brucellosis include bridging osteophytes, simultaneous with the presence of both osteoblastic lesions and loss of bony mass in the same vertebrae [see Gorgas Case 2001-02].

Salmonella infection or staphylococcal infections may cause spondylitis and paravertebral abscess but concomitant high fever and systemic illness would be seen. A common feature in these pyogenic vertebral infections is bone remodeling and new bone formation, which was not observed in this patient. Isolated paravertebral abscesses are most often caused by staphylococci and enteric organisms in the developed world, but tuberculosis and brucellosis which cause cold abscesses are reportedly more common causes of paravertebral abscesses in the developing world. Abscesses, due to extension of spinal TB, through the psoas sheath is frequently bilateral and may drain to the lumbar area or anteriorly to the groin or thigh. Pyomyositis has recently become more common in non-tropical countries in HIV patients and may occur in the psoas muscle.

Medical therapy of Pott’s disease is with standard regimens of anti-tuberculous drugs but for at least 9 months, but more prolonged therapy is recommended in patients with extensive bone destruction and paravertebral extension. In Pott’s disease, controversy exists as to the need for any reconstructive surgical intervention or fusion procedure in patients without neurologic deficit, with many published studies either way. None of the studies of shorter course chemotherapy have included enough patients with Pott’s disease to make any conclusions possible. Patients with acute neurologic deficits within the previous 12-24 hours should definitely have surgery. With longer standing neurologic deficit there is not well-controlled data to show better outcomes with surgery, but where neurosurgical intervention is accessible it is often undertaken in conjunction with medical therapy. Steroids should be considered for very severe paraplegia, especially in the acute stage. Spinal surgery is recommended when marked neurological deficit is present related to severe kyphosis or free bone in the medullary channel; large abscess causing respiratory obstruction; worsening neurologic deficit; and progression of spine deformity or posterior involvement.