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 Table of Contents  
Year : 2012  |  Volume : 1  |  Issue : 3  |  Page : 155-160

Paraplegia is not a diagnosis: Spinal tuberculosis deserves a place on the clinical radar screen: Awakening call to clinicians

1 Division of Pulmonary Medicine & Infectious Diseases, SBAH-CITY Rehabilitation Hospital & Medical Centre, Riyadh, Saudi Arabia
2 Division of Orthopaedic Surgery Rehabilitation Hospital & Medical Centre, Riyadh, Saudi Arabia

Date of Web Publication28-Feb-2017

Correspondence Address:
Liaqat Ali Chaudhry
Consultant Pulmonologist, Supervisor of House Physicians, A/Consultant Infectious Diseases, Chairman IPC Committee, SBAH-CITY Rehabilitation Hospital & Medical Centre, P.O. Box 64399, Riyadh 11536, Qasim High Way, Exit 6, Banban
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

DOI: 10.1016/j.ijmyco.2012.07.008

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Disseminated Tuberculosis(TB) occurs through lymphohaematogenous dissemination of M. tuberculosis. Although it is more common in young children and those who are having risk factors like having acquired or innate immunodeficiency, weak immune system being on immunosuppressive treatments; it can also occur in immunocompetent indviduals with heavy load of infection. Inhalation being the commonest mode of entry of the pathogen results in pulmonary tuberculosis being the commonest seat of primary infection,other systems commonly involved as extra-pulmonary sites are lymphnodes, bone, brain, peritonium and genitalia depending on the amount of relative blood supply and lymphatics. We present here case of a young female who was immunocompetent, having fever, progressive lower limb weakness and loss of bowel and bladder control, becoming bed bound, and admitted in our hospital for rehabilitation with a diagnosis of paraplegia.

Keywords: Tuberculosis (TB), Pott's disease, Magnetic radio imaging (MRI) tuberculoma, Paraplegia, Activities of daily life (ADLS)

How to cite this article:
Chaudhry LA, Zamzami M, Fakharudin SK. Paraplegia is not a diagnosis: Spinal tuberculosis deserves a place on the clinical radar screen: Awakening call to clinicians. Int J Mycobacteriol 2012;1:155-60

How to cite this URL:
Chaudhry LA, Zamzami M, Fakharudin SK. Paraplegia is not a diagnosis: Spinal tuberculosis deserves a place on the clinical radar screen: Awakening call to clinicians. Int J Mycobacteriol [serial online] 2012 [cited 2022 Jan 27];1:155-60. Available from: https://www.ijmyco.org/text.asp?2012/1/3/155/201243

  Introduction Top

Tuberculosis (TB) still remains an emerging international health problem despite advances in the methods of diagnosis and treatment; it is still prevalent in developing countries and on the increase in developed ones. Skeletal involvement occurs in approximately 10% of all patients with extra-pulmonary TB. Primary lesions are usually in the lungs in a large majority of the patients [1],[2]. Multifocal tuberculosis is characterized by the presence of large multifocal tuberculosis areas in the same or different adjacent or distant organs. Lack of thinking about tuberculosis and facing difficulty in confirmation of multifocal tuberculosis may lead to a delay in diagnosis or initiating empirical anti-TB treatment, with very devastating and often irreversible complications [3],[4],[5]. Bone and joint involvement in tuberculosis is uncommon. While osteoarticular tuberculosis most commonly occurs in the vertebral column. Multifocal bony lesions may occur as a result of dissemination from a pulmonary or an osseous focus [6]. Osteoarticular tuberculosis is estimated to affect about 2% of patients with tuberculosis. Of patients afflicted with skeletal tuberculosis, 50% present with spinal lesions, 30% have hip or knee disease, and 20% are infected at other, less well-known sites, such as the pubis, wrist, shoulder, and sacroiliac joint. In particular, sacroiliac joint involvement has been reported in 7.7% of patients with skeletal tuberculosis [7]. This study presents the case of a 21-year-old single Saudi female recently admitted to SBAH-CITY Rehabilitation Hospital and Medical Centre, Riyadh, Saudi Arabia, for rehabilitation with a diagnosis of Paraplegia, double incontinent and bedridden.

  Case report Top

A 21-year-old single Saudi female, bedridden, was admitted on 24-6-2012 for rehabilitation with chief complaints of inability to stand and walk for one and half years owing to progressive weakness of her lower limbs with complete paraplegia and loss of bladder and bowel control being managed with diapers. Increased frequency of seizures in the recent past and a running fever at the time of admission not responding to antibiotics given empirically by the treating team without localization of infection before being referred for my opinion on 1-7-2012.

She is known to have corpus callosum atrophy discovered at age 3 years owing to delayed psychosocial development, mental retardation and a diagnosed epileptic at age 6 years old. She has been ambulant up until one and half years ago. With progressive lower limb weakness and a fever over the last few years, she has been admitted to various hospitals, but was never diagnosed as having multifocal disseminated tuberculosis as a real underlying cause of her paraparesis and exaggeration of her seizures in the recent past.

On general physical examination, this young, well-built female shy and feeble-minded lying supine in bed, dependent for activities of daily life (ADL), being cared for by her mother, BP=100/70, HR=88, RR=18, O2SAT=96%, T=37.8 °C, booking weight=58.5kg, BCG scar present at left deltoid, pallor +, no clubbing or jaundice, no lymphadenopathy, Oropharynx clear, and no gum hypertrophy. Both the patient and her mother deny any respiratory complaints now or in the past, no history of contact with an index case of tuberculosis. No past history of blood transfusion or surgery. No clinical signs of DVT. She is double incontinent requiring diapers.

Systemic review: Palpable gibbous noted at the back of lower thoracic spine, chest auscultation and cardiovascular system was unremarkable, no organomegaly, history of constipation in recent 3 months requiring laxatives and suppositories as required. Neuro-muscular examination revealed spastic paraparesis of both lower limbs with 0–1/5 power. Upper limbs were normal. Palpable relatively hard nodular mass without fluctuation about 2.5 × 3cm in the left lower quadrant of left breast present for 1 month according to her mother. She had normal menstrual history.

Past history of treatment with anti-epileptic medications since age 6 years and has recently been on Tab.depaqene (sod-valporate) 200 mg po bid, and Tab. Lamictal 125 mg po bid started as 2nd epileptic in our hospital for, on the one hand, raised liver enzymes ALP & GGT as a result of depaqene and on the other hand for intractable seizures.

Lab work: WBC=6.7, N=55, L=33, M=10, E=1, RBC=4.2, Hb=9.7, MCV=73, MCH=27.4, PLT=700,ESR=76, BUN=4.6, Scr=90, NA=143, K=4.5, CL=102, ALP=191, GGT=228, AST=15, ALT=12, S.T.iron=1.19, TIBC=51.09, S. Ferritin=87.5, Brucella serology negative, Hepatitis B & C viral profile reported normal, HIV serology nonreactive, PPD=24 mm Blister formation, Urine microscopy and culture reported normal. Widal test, stool & Blood culture reported normal. Gastric aspirate and induced sputum D/S AFB × 3 reported negative. Mycobacterial culture on sputum sent to France awaited. Latest liver profile showing AlkP=109, GGT=224, AST=35, ALT=48 and FBC showing WBC=8.28, RBC=4.8, Hb=11.4, Hct=36, MCV=75.3, MCH=23.4, MCHC=32 has shown improvement.

Portable chest X-ray: [Figure 1] reported unremarkable. F.F. Bronchoscopy: [Figure 2] , largely normal endobronchial tree, except posterior segment of left lower lobe showing signs of inflammation, brushings were taken and this area was lavaged. Bronchoalveolar lavage D/S AFB reported negative, but Mycobacterial culture sent to France is awaited.
Figure 1: Portable chest X-ray.

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Figure 2: F.F. Bronchoscopic view.

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MRI-axial view [Figure 3] and [Figure 4] showing huge cold abscess with thoracic vertebrae 9, 10, 11 destruction (Pott's Disease), same changes shown in MRI-sagittal view [Figure 5] showing compression of spinal cord and aorta pushed forward by the cold abscess; involvement of left sacroiliac joint and iliac bone is shown in [Figure 6]; CT-scan chest [Figure 7] and [Figure 8] showing pre-vertebral huge collection of cold abscess continuous with left-sided encysted chronic empyema, and bilateral lung infiltrates more so on left side, CT-Chest – [Figure 8], Pre-vertebral huge cold abscess mass continuous with left empyema pushing the aorta forward at thoracic 9, 10, 11 level with destruction of these thoracic vertebrae and compression of spinal cord (Pott's disease), Multiple enlarged para-aortic abdominal lymphadenopathy, Inflamed left fallopian tube. MRI Brain – [Figure 9] shows brain cortical tuberculoma in the right frontal lobe, [Figure 10] showing marked induration of 24 mm with blister formation to PPD 2 TU RT-23.
Figure 3: Axial view.

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Figure 4: Axial view, contrast.

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Figure 5: Sagital view.

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Figure 6: Left sacroiliac joint bone lesions.

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Figure 7: CT-chest, empyema.

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Figure 8: CT-chest.

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Figure 9: Brain tuberculoma on MRI.

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Figure 10: Induration to PPD 2TU-RT-23.

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  Impression Top

(1) Delayed psychosocial development with mental retardation due to atrophy of Corpus callosum discovered at age 3 years; (2) known epileptic since age 6 years with recent acceleration in seizures; (3) Anemia of chronic disease with associated iron deficiency; (4) Misdiagnosis of multifocal disseminated tuberculosis, including Pott's disease, causing paraplegia, involving lungs, brain cortical tuberculoma of the right frontal lobe, left pleura encysted chronic empyema, para-aortic abdominal lymphadenopathy, thoracic spine vertebrae involved T-2 and destruction of T-9, 10, 11 leading to spinal cord compression with complete paraplegia and double incontinence.

  Started empirical anti-tuberculous therapy on 1-7-2012 as follows Top

Tab, INH 300 mg po od before breakfast, Tab. Rifampicin 600 mg po od before breakfast, Tab. Ethambutol 1200 mg po od, Tab. Pyrazinamide 1500 mg po od, inj. streptomycin 1 g I/M od for 30 days, Tab. vit B6 40 mg po od, inj. cleaxane 40 mg sub. cut od, Tab. Valporate sodium (Depaqene) 500 mg od, SYP. Ferose 90 mg po od, Tab. Paracetamol 1 g prn q8h, inj. Dexamethasone 12 mg im od for 3 weeks, started on Tab. Lamictal 125 mg po bid.

She tolerated treatment well and clinical response to the empirical anti-tuberculous therapy was good and quick; her fever subsided after 2 weeks of treatment. Her alkaline phosphatase and GGT were raised even before starting anti-TB medications on admission; it was most likely due to valproate sodium as discussed and agreed by the clinical pharmacist, which was tapered while dose of Lamictal was gradually increased. Transaminases were normal before starting anti-tuberculous treatment and remained stable till to date at completion of 25 days of treatment and recommended her immediate transfer to an acute care hospital for the urgent spinal and thoracic surgical intervention.

The patient was discussed in the family and multidisciplinary team meeting; they were told that the patient had no rehabilitation potential at the present time, base line essential investigations were completed and she was started on empirical anti-TB treatment with a very strong possibility of disseminated multifocal tuberculosis which has responded to empirical anti-TB treatment; the patient needs an immediate transfer to an acute care hospital, because at this stage this patient has class-III spinal tuberculosis with a huge pre-vertebral cold abscess, and left-sided encysted chronic empyema requires urgent surgical intervention which at present is a diagnostic as well as therapeutic priority. Thus she was transferred to an acute care hospital.

  Discussion Top

TB has caused disease in humans for thousands of years. TB may date from the domestication of cattle in ancient Egypt. Mummies that have been dated from 5000 BC to 1000 BC show angular kyphosis that strongly suggests TB of the spine. One highly specific example of this deformity occurs in the body of the Egyptian priest Nesperhan (1000 BC), which also shows the large psoas abscess that often accompanies TB of the spine [8]. Robert Koch in March-1882 proved that Tuberculosis causes the multifaceted disease and after his discovery, the milestones of diagnosis and treatment continued to accumulate [9] with the development of the tuberculin skin test in 1891, X-ray diagnosis in 1896 and the vaccine of Bacille Calmette Guerin (BCG) in 1921. Curative treatment for TB was developed during the 1940s and early 1950s, and treatment for prevention of future disease was developed during the 1960s [10].

Although Pul. Tuberculosis as well as extra-Pulmonary is more common in immunocompromised individuals, it also occurs in immunocompetent patients. Pulmonary tuberculosis is more common and is the main target for national tuberculosis programs because of its epidemiological significance. Extra-pulmonary tuberculosis is seen commonly as lymphadenitis and the cervical region is the most common site; other sites are pleura as pleural effusion or empyema, the spine usually known as Pott's disease, the brain as tuberculomas or meningoencephalitis, and the joints and urogenital system may also be involved [3]. Among those having multifocal tuberculosis, lung involvement is seen in about 70% of cases. Conversely, pulmonary tuberculosis is associated with multifocal extra-pulmonary in about 30% of cases. Thoracic spine is the most common site of spinal tuberculosis as seen in this patient. Neurological deficits are common with longstanding thoracic and cervical involvement if left untreated progressing to incomplete or complete paraplegia [11]. Dissemination to the brain as observed in our patient is reported in about 15% of cases [12].

This patient was running a fever since admission and was being treated with empirical inj. meropenem 1 g IV q8h for 5 days without localizing focus of infection as the portable chest X-ray at admission was reported unremarkable and urine microscopy and culture reported negative. She continued with fever and had severe constipation with abdominal distension. The primary treating team started her on colchicine keeping in mind a possibility of Mediterranean fever and at the same time requested a CT-scan of the abdomen to rule out intestinal obstruction .At this juncture, she was referred for my opinion in view of persisting fever. I went to see the patient, but she was already in the CT-room for CT-abdomen. I suggested that the primary team include a CT-chest as well before I could see her.

To everybody's surprise the major site of pathology was in the chest and thoracic spine. Besides having complete paraplegia and double incontinence since she was one and half years old, she had a history of increased frequency of seizures in the recent past with persisting fever. She had palpable gibbous at lower thoracic spine. Her overall picture was highly suggestive of disseminated multifocal tuberculosis; therefore, she was started on empirical anti-tuberculous therapy as CAT-1. Her booking weight was 58.5kg. Next to rule out anticipated brain involvement in the patient having disseminated multifocal tuberculosis in the background of recent increased frequency of seizures, MRI-brain without contrast (family refused MRI/ CT-brain with IV contrast) was arranged which confirmed brain involvement in the form of the right frontal lobe cortical tuberculoma. Her TST with PPD-RT 23 2TU was recorded=24 mm induration with blister formation, ESR=76, and her Brucella serology reported negative. She was continued on anti-tuberculous therapy with the addition of adjuvant inj. Dexamethasone 12 mg IM for 3 weeks. She was found to have anemia of chronic disease with associated iron deficiency.

Course in the hospital

She tolerated treatment well and her response was good; she became a febrile after 2 weeks of anti-TB treatment and gained weight after 3 weeks of treatment. The final diagnosis was corpus callosum atrophy, delayed psychosocial development, accelerated epilepsy, disseminated multifocal tuberculosis involving lungs, left pleura with chronic encysted empyema, brain tuberculoma, Pott's disease involving T-2 and destruction of T-9, 10, 11 with huge pre-vertebral cold abscess complicated with complete paraplegia and loss of bowel and bladder control, anemia of chronic disease with associated iron deficiency. Possible tuberculosis of the right fallopian tube, and left breast likely fibroadenoma (or less impending cold abscess; it was a relatively hard mass without any fluctuation), left iliac bone TB. She was referred for urgent spinal and thoracic surgical intervention as it was now a diagnostic and therapeutic priority, because histopathological diagnosis still remains essential in this patient having GATA class-III spinal tuberculosis and disseminated tuberculosis complicated with complete paraplegia [13],[14].


The underlying diagnosis of disseminated tuberculosis and its associated complications, including Pott's disease, causing complete paraplegia in this patient unfortunately has been missed at various hospitals attended by the patient. If this case was diagnosed early, she would have been potentially treatable with modern anti-TB drugs, without becoming paraplegic in early stages. Paraplegia in its own right is not a diagnosis, besides trauma, it is a manifestation of various chronic spinal pathologies – tuberculosis is one of them. Diagnosis of tuberculosis, especially extra-pulmonary tuberculosis, is often delayed and is quite challenging in the absence of typical constitutional symptoms. Empirical anti-tuberculous therapy must not be delayed in severely sick patients during investigations if there is no other considerable differential diagnosis as in this case .Clinical and radiological response to empirical initial intensive phase anti-tuberculous therapy is also considered a direct evidence and clue to correct diagnosis as observed in this patient. Early diagnosis and treatment also help to avoid complications or a need for surgical treatment. In young and middle-aged adult patients presenting for the first time with progressive paraparesis and pyrexia as this case, clinicians should have high suspicion for spinal tuberculosis, especially in regions with a high prevalence. The main focus of investigations needs to be lungs and spine asking chest X-rays, MRI or CT-scan chest, spine, and brain if warranted as in this female patient with recent intractable seizures. Sudden deteriorating epileptic control in a known epileptic or new onset of seizures in a patient suspected of disseminated multifocal tuberculosis raises the possibility of brain involvement as proved in our case. Therefore MRI or CT-brain needs to be included in the list of investigations because it has diagnostic, therapeutic and prognostic value in terms of adjuvant steroid therapy, which on one hand helps to preserve vital organ function and on the other hand guards against the anticipated paradoxical reaction which is common in cases of disseminated tuberculosis [15]. Early appropriate surgical referrals should be ensured because surgical intervention is a diagnostic and therapeutic priority in such patients with GATA class-III spinal tuberculosis as in our case.

  Acknowledgments Top

I express my gratitude to my house physician Dr. Hatem Al-Farra for arranging figures and my daughter Sidra Chaudhry 4th year MBBS student of Shifa College of Medicine, Islamabad, Pakistan, for revising and computing the whole manuscript on an urgent basis, sparing time from her busy schedules, which made its timely submission possible.

  References Top

M. Turgut, Spinal tuberculosis (Pott's disease): Its clinical presentation, surgical management, and outcomes. A survey study on 694 patients, Neurosurg. Rev. 24 (1) (2001) 8–13.  Back to cited text no. 1
C.Y.Weng, C.Y. Chi, P.J. Shih, et al, Spinal tuberculosis in non- HIV infected patients: 10-Year experience of a medical centre in central Taiwan, J. Microbiol. Immunol. Infect. 43 (6) (2010) 464–469.  Back to cited text no. 2
F. Gelal, D. Sabah, R. Doğan, A. Avci, Case report: Multifocal skeletal tuberculosis involving the lumbar spine and a sacroiliac joint, Diagn. Interv. Radiol. 12 (2006) 139–141.  Back to cited text no. 3
S.L. Moore, M. Rafii, Imaging of musculoskeletal and spinal tuberculosis, Radiol. Clin. North Am. 39 (2001) 329–342.  Back to cited text no. 4
L. Comican, R. Hammal, J. Messenger, et al, Current difficulties in the diagnosis and management of spinal tuberculosis, Postgrad. Med. J. 82 (963) (2006) 46–51.  Back to cited text no. 5
S. Nakao, A. Takeda, H. Matsumoto, et al, A case of pulmonary tuberculosis complicated with multiple bone and joint tuberculosis, Kekkaku 75 (2000) 429–434.  Back to cited text no. 6
L.J. Rowe, T.R. Yochum, Essentials of Skeletal Radiology, Lippincott, Williams and Wilkins, Philadelphia, 2005. pp. 1373–1426.  Back to cited text no. 7
M.D. Iseman (Ed.), Tuberculosis down through the centuries, A Clinician's Guide to Tuberculosis, Lippincott, Williams & Wilkins, Philadelphia, 2000, pp. 1–19 (From 2004).  Back to cited text no. 8
T. Dormandy, A History of Tuberculosis, New York University Press, New York, 2000.  Back to cited text no. 9
S.H. Ferebee, Controlled chemoprophylaxis trials in tuberculosis: A general review, Adv. Tuberc. Res. 17 (1970) 28–106.  Back to cited text no. 10
R.F. MacLain, C. Isada, Spinal tuberculosis deserves a place on the radar screen, Cleve. Clin. J. Med. 71 (7) (2004) 534–549.  Back to cited text no. 11
L.A. Chaudhry, Ba Essa Ebtesam, Al-Sulaiman Shehab, A case of milliary tuberculosis manifested an unusual paradoxical reaction at 3 weeks of antiTB treatment, JCPS 22 (2012) 43–45.  Back to cited text no. 12
E. Oguz, A. Shehirlioglu, M. Altinmakas, et al, A new classification and guide for surgical treatment of spinal tuberculosis, Int. Orthop. J. 32 (1) (2008) 127–133.  Back to cited text no. 13
P.S. Issak, O. Boachie-Adjei, Surgical correction of kyphotic deformity n spinal tuberculosis, Int. Orthop. (2011). doi: 10.10.1007/s00264-011-1292-9.  Back to cited text no. 14
S.L. Cheng, H.C.Wang, P.C. Yang, Paradoxical response during anti-tuberculosis treatment in HIV-negative patients with pulmonary tuberculosis, Int. J. Tuberc. Lung Dis. 11 (2007) 1290–1295.  Back to cited text no. 15


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]


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