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Gorgas Case 2016-04

Epidemiology: Born and lives in Paruro (3 hours from Cusco), farmer, with a past medical history of alcoholism, otherwise healthy. No known TB contact.

Physical Examination: BP=120/60 HR=76 RR=24 sO2=90%, afebrile. Overall pallor. Chest: bilateral basal rhonchi. Cardiovascular: normal. Abdominal: soft non-tender, no organomegaly. Musculoskeletal: tender, protuberant mass at the level of L1 (Image A). Genitourinary: 2 firm 2X2 cm tender nodules adjacent to left testicle with irregular borders. Neurological: sensory deficit right > left in lower extremities following the L1 distribution (hip girdle and groin area). Motor: decrease of strength in hip flexors (right>left), knee extensor and ankle dorsiflexors (right more than left). Reflexes: Clonus 1+ right ankle.

Discussion: Urine smear with 2+ AFB; culture positive for MTB susceptible to all 1st line TB drugs. Lumbar spine X-ray (Image B, arrow a) showed L1-L2 collapse with partial destruction of vertebral bodies and total destruction of the intervertebral disc (Image B, arrow b). MRI of the lumbar spine (Image C, T2 weighted) shows a protruding ill-defined heterogeneous mass at L1-L2 (Image C, arrow a) causing posterior spinal cord compression  (Image C, arrow b) and without new bone formation. Severe destruction (Image D, T1 weighted) of vertebral bodies L1, L2 (Image D, arrow b) and surrounding tissue inflammation (Image D, arrow a) is seen. In TB spondylitis, the disease process begins in an intervertebral disc and spreads via the anterior ligament to affect the anterior aspects of the adjacent vertebrae. Destruction of the anterior endplates ensues with anterior collapse leading to a wedge deformity seen clinically (Image A), as is well demonstrated in this case, as the spinal deformity known as a gibbus. Tissue obtained by biopsy or needle aspirate and examined histologically and by culture is generally required for diagnosis. AFB smears are usually negative. CT and appropriate neurosurgical experience for invasive diagnosis is not available at this hospital.

Complete destruction of vertebral bodies and the intervertebral disc is seen almost exclusively in infectious processes. Salmonella infection or staphylococcal infections may cause spondylitis and paravertebral abscess but concomitant high fever, leukocytosis, and significant 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. Brucellosis, another bacterial cause of spondylitis is not present in this part of Peru as goats are not raised at this altitude; anterior destruction and gibbus is not seen. 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]. Malignancy is limited to the vertebral bodies without impinging the intervertebral disc.

Tuberculosis is caused by 3 related organisms Mycobacterium tuberculosis, M africanum, and M bovis. Of these, M tuberculosis is by far the most common [Reichman LB, Hershfield ES, editors. Tuberculosis: a comprehensive international approach. New York: Marcel Dekker; 1993]. Vertebral TB is the most common form of skeletal TB [Spine. 1997; 22(15):1791-1797], whereas male genital TB is an uncommon form of extrapulmonary TB [Urol Clin North Am. 2003;30(1):111- 121]. The initial route of entry of M. tuberculosis is usually the respiratory tract, followed by hematogenous dissemination. Secondary hematogenous seeding can occur from a silent focus elsewhere in the body (eg gut, kidney, and tonsil). 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 with 50% involving the thoracic spine, 25% cervical and 25% the lumbar spine [WJ Bone Joint Surg Am. 1996 Feb; 78(2):288-98].

Pott’s (named after first description of TB spondylitis by the British surgeon Sir Percivall Pott, 1714-1788) disease usually presents with chronic back pain that is initially non-specific. Pain increasing in severity over weeks to months is seen in association with muscle spasm. Constitutional symptoms (fever, weight loss) are present less than 40% of cases [Int Orthop. 2012 Feb;36(2):221-31, J Neurosurg. 1995 Aug;83(2):243-7]. Cord compression with muscle weakness and loss of bladder and bowel control is the most serious complication and occurs in up to 30% of patients. Genitourinary TB (GU TB) is insidious, usually presenting with malaise and lower urinary tract symptoms including dysuria and hematuria. [Am J Respir Crit Care Med. 2000 Apr;161(4 Pt 1):1376-95, Am J Med. 1977 Sep;63(3):410-20, Medicine (Baltimore). 1974 Sep;53(5):377-90] Systemic symptoms are rare. Pyuria and hematuria are present in more than 90% of cases and serum creatinine is usually normal. Ureteral stricture could occur and may cause obstructive uropathy. It could also cause chronic epididymitis or prostatitis and infertility if seminal vesicles and ejaculatory ducts in men and fallopian tube in women are involved. The diagnosis of GU TB is by demonstration of the bacilli in urine in patient with dysuria, sterile pyuria, hematuria and/or radiological findings suggestive of TB.

Medical therapy of Pott’s disease is with standard regimens of anti-TB drugs for at least 9 - 12 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. Recommendations for a surgical procedure include (1)Patients with spinal disease and advanced neurological déficits, (2)Patients with spinal disease and worsening neurological deficits progressing while on appropriate therapy, (3)Patients with spinal disease and kyphosis >40 degrees at the time of presentation and (4)Patients with a cold abscess in the chest wall.

Medical therapy for GU TB is generally the same as that for pulmonary TB and 6 months duration is successful in eradicating drug susceptible TB. Upper urinary tract obstruction during treatment might occur with significant worsening during the first weeks of treatment due to inflammation followed by fibrosis and consequent obstruction of collecting system. Aside from decompression other surgical interventions should be delayed for at least 4 weeks after initiation of drug therapy.

Our patient has been started on the standard 4-drug initiation regimen of daily INH, rifampin, ethambutol, and pyrazinamide in addition to dexamethasone for the cord compression syndrome. Surgical evaluation and discussion of approaches to further spine stabilization is ongoing.