Tuberculous lumbar spinal epidural abscess in a young adult: A case report


Tuberculous spinal epidural abscess is an uncommon pathology that needs an urgent intervention to decompress pressure on the spinal epidural sac, cord and roots, writes Ghazwan A Hasan.

Vertebral tuberculosis accounts for less than 1% of all tuberculosis infections. It is considered the most serious type of skeletal tuberculosis, with possible neurological symptoms due to compression of the neural structures. It may lead to deformity and significant vertebral structure destruction and instability.1 Spinal epidural abscess is a rare disease with a reported incidence of 1–2/10,000; tuberculosis accounts for 2% of these infections.2

Ghazwan Hasan
Ghazwan Hasan

There are only a few reported cases of tubercular spinal epidural abscess. Most of these infections are secondary to pyogenic infection.68 Treatment options depend on many factors, such as the site and severity of compression, as well as clinical presentation. Medical treatment can be offered in certain cases. Surgery is indicated when there is compression of neurological structures, failure of resolution, doubtful diagnosis, and other reasons like mechanical instability. Surgical options may vary from decompression laminectomy to multilevel laminotomy, or laminectomy with or without fixation; all this can be determined by the adequacy of decompression intraoperatively.1 Infection of the spine may lead to a wide range of problems including neurological deficit, mechanical instability and deformity.3 There are few repeated cases about tubercular spinal epidural abscess, because most of these infections are secondary to pyogenic infection.68

In a recent case, our team was able to improve lower-limb motor power and sphincter function in a 42-year-old man with lumbar spinal epidural tuberculous abscess occupying the spinal canal from L2–L5 vertebrae extending to the posterior paraspinal muscles and presenting with bilateral progressive lower limb weakness.

A teacher complaining of 15 days’ of progressive back pain, radiating to both thighs, was referred to our hospital. He subsequently developed weakness affecting both lower limbs—predominantly the left side—with urinary incontinence and constipation. These symptoms were associated with low grade fever, loss of appetite, and eventually the inability to walk.

On examination, the man looked pale and uncomfortable. He had a pulse of 95 beats per minute, blood pressure at 110/70mmHg, a temperature of 38.3 degrees centigrade, and a respiratory rate of 19 cycles per minute. By this point he was unable to walk, had severe tenderness in the back around the midline and paraspinal region, and severely limited motion of the spine. He also presented with pararesthesia below the inguinal ligaments in both lower limbs.

Laboratory tests showed haemoglobin at 11.1g/dl, a white blood cell count of 11*109 with lymphocytosis (60%), an essential sedimentation rate of 95mm/hour, C-reactive protein at 90, blood glucose of 114g/dl, blood urea at 78mg/dl, and serum creatinine at 1.3.

Short tau inversion recovery showed localised collections of pus in the canal at L3, L4 and L5 levels, with a small collection of pus at the L2–L3 level. There were also multiple pockets of pus in the paraspinal muscles.

After discussing treatment options with the patient, we decided to proceed with surgery under general anaesthesia. In a prone position using a posterior midline approach, the paraspinal muscles were dissected. We noticed multiple pockets of pus impeded the paraspinal muscles, mainly on the left side, which were evacuated. Then, a laminectomy of L3-L4 was performed, with hemi-laminectomy at L2-L3 and L4-L5. Pus was draining from these levels through the spinal canal. Samples were taken from pus, laminae bone, and soft tissue and sent for histopathological and microbiological studies.

We performed a thorough irrigation and debridement, before a drain was applied and the wound closed in layers. The patient was kept on broad spectrum antibiotics for 14 days pending results.

Upon histographic analysis, sections showed calcified mature bony trabeculae and degenerative cartilaginous tissues components in between marked haematopoietic depletion, as well as dense chronically inflamed fibrous replacement, including heavy mixed chronic inflammatory cells which include foamy histiocytic and mature lymphocytic cells infiltrate. Multiple ill-defined granulomas were seen with obvious extra bony inflammatory extension to the surrounding soft tissue and skeletal muscular tissues. Our final impression was of chronic specific tuberculous granulomatous spinal cord abscess. Anti-tuberculosis antibiotics were started after these results became available.

A follow-up MRI at one month showed abscess resolution with good decompression of the cauda equina region. The right lower limb had full motor recovery, while the left lower limb was weak on knee flexion and ankle dorsiflexion (grade 4). The patient suffered from urinary incontinence and constipation. Two months after surgery the patient had full lower limb motor recovery (grade 5), except for grade 4+ knee flexion, nocturnal incontinence, and constipation. Five months later, he had recovered motor strength in both lower limbs, as well as full control of his sphincters.

Cases of spinal epidural abcess due to tuberculosis infection have been reported in developing countries. The clinical presentation of tubercular spinal epidural abcess may be more insidious, leading to failure of early diagnosis treatment.3 Initial presentation may include back pain, low grade fevers and severe neurological deficit. However, the classical triad of fever, back pain and neurological deficits present in only 2% of tubercular spinal epidural abcess.2 The thoracic and lumbar regions are the most commonly affected.4 MRI is the diagnostic modality of choice, but CT myelogram can be performed for those who cannot undergo MRI.5

Tubercular spinal epidural abscess develops secondary to vertebral body involvement, and rarely by haematogenous spread from a primary focus in the body.9–11 Involvement of vertebral body of the lumbar spine seems to be the cause of pus collection in our case. The clinical presentation in our patient suggested compression in the cauda equine region with highest level of involvement at L2.

Tubercular SEA is amenable for both non-surgical and surgical management.3 In our case we chose the surgical treatment because of the progressive neurological deficit.

Kennedy et al concluded that early diagnosis and decompression are the most important predictive parameters of successful outcomes.312  Our case report highlights the importance of early diagnosis and early treatment of tuberculous spinal epidural abscess.


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Ghazwan A Hasan is an orthopaedic spine surgeon. Co-authors include Saif M Kani, an orthopaedic surgeon, and Ahmed Alqatub, a member of the Royal  College of Surgeons of Edinburgh, all at Iraq Shaheed Ghazi Al-Hariri Specialized Surgical Hospital, Medical City Complex, Baghdad, Iraq.