A Case Report of Disseminated Pott’s Disease (Spinal Tuberculosis) Complicated by Abscess and Near Complete Destruction of Cervical Spine (C5, C6)

Special Article – Tuberculosis

Austin Med Sci. 2020; 5(1): 1040.

A Case Report of Disseminated Pott’s Disease (Spinal Tuberculosis) Complicated by Abscess and Near Complete Destruction of Cervical Spine (C5, C6)

Satti HMA1* and Mohamed FAA2

¹Internal Medicine Resident Registrar, Sudan Medical Specialization Board, Sudan

²Emergency Medicine Resident, Ribat University Hospital, Sudan

*Corresponding author: Hassan Mohammed Abdelraheem Satti, Internal Medicine Resident Registrar, Sudan Medical Specialization Board, Sudan

Received: January 14, 2020; Accepted: February 24, 2020; Published: March 02, 2020

Abstract

Potts disease (PD) or spinal tuberculosis is a rare infectious disease, which is commonly spread from extra-spinal infection. It commonly involves the anterior aspect of multiple vertebrae. The most common affected site is the lower thoracic vertebrae, with the cervical vertebrae the least common site but has the most serious complication. Back pain is the earliest and most common symptom, along with other constitutional symptoms like fever, night sweating and weight loss. Other presentations depend on the stage of disease and the occurrence of complication. The most sensitive diagnostic modality is Magnetic resonance imaging (MRI) which demonstrates features of spondylodiscitis, disc collapse and disc destruction, cold abscess, vertebral wedging, vertebral collapse and spinal deformities. Histopathological analysis can be done by Ultrasound and computed tomographic (CT) guided needle aspiration or biopsy. Treatment is by combination Anti-Tuberculosis and surgery (debridement, decompression, fusion and bone auto-graft) in case of complication. A 55 years old man presented complain of dull back pain that started three weeks prior to admission along with fever and night sweating, one week later he started to develop neurological complication in form of lower limb weakness, his condition deteriorated gradually to the level of complete paraplegia and he also had urine retention. Diagnosis of pott’s disease was confirm based on MRI imaging and microscopically analysis of a needle aspiration sample. Patient was treated with a combination Anti-Tuberculosis and underwent surgery (decompression and fixation).

Keywords: Pott’s disease; Tuberculosis; Abscess; Neurological deficit; MRI

Introduction

Tuberculosis (TB) is considered a disease most prevalent among people with low socioeconomic status and so found mostly in underdeveloped countries. TB may involve any part of the body like; skin, lungs, brain, bones and intestines. Spinal TB is commonest type of tuberculosis involving the bony element, and it is called pott’s disease (PD). It may spread to the spine from the lungs and abdomen or it may manifest as primary disease [1]. The clinical presentation of PD depends on the Stage of disease, the affected site and the Presence of complications such as neurologic deficits, abscesses, or sinus tracts [2]. Diagnosis depends on the presence of characteristic clinical manifestations and neuroimaging findings. Etiological confirmation requires the demonstration of acid-fast bacilli on microscopy or culture of material obtained from the lesion.

Case Presentation

55 years old male farmer from El Gezira (middle Sudan) known to have diabetes mellitus type two for 10 years on insulin, presented complain of low grade fever that started 25 days prior to admission, fever was mainly at night and associated with sweating. Two days later he started to have dull back pain, mainly at cervical and lumbar region. Then after seven days, he started to develop lower limb weakness that deteriorated gradually to the level of complete paraplegia. In addition, the patient began to have urine retention in the last two days prior to admission. Patient had no history of cough or shortness of breath; also, he had no history of close contact with a patient with tuberculosis or chronic cough. Regarding other systemic review he has no complains. Patient is not smoker or alcohol consumer.

Examination at the date of admission showed the followings; patient was very ill, pale, not jaundice, not dyspneic, oriented in time place and person, blood pressure 117/55. Pulse rate 110/min (regular, large volume, synchronize, no radio-femoral delay), respiratory rate 18/min, spo2: 100%, temperature: 38C, jugular venous pressure (JVP) not raised. Pulmonary examination: normal air entry bilaterally, normal vesicular breathing, no crepitation or wheezing. Cardiac examination: normal S1 and S2 no added sound. Abdominal examination: no abnormalities detected. Back examination: tenderness in lumbar and cervical regions, no deformities. Neurological examination: Glasgow coma scale (GCS) was 15/15, cranial nerves examination were intact, upper limbs examination (power grade five, normal tone and reflexes, sensation was intact), Bilateral lower limbs examination (power grade zero, hypo-tonia and hypo-reflexes, sensation was diminished) (Table 1).

Table 1: Laboratory results at admission.





  

    
Investigation 

    
Result 

    
Investigation 

    
Result 

  

  

    
C. Reactive Protein 

    
158mg/l 

    
Serum Urea 

    
46mg/dl 

  

  

    
ESR 

    
130mm/hrs 

    
Serum Creatinine 

    
0.4mg/dl 

  

  

    
TWBCS 

    
16.69x103 

    
Serum. Potassium 

    
3.7mg/dl 

  

  

    
Hemoglobin 

    
8.7 g/dl 

    
Serum. Sodium 

    
137mg/dl 

  

  

    
MCV 

    
76.7    f 

    
Urine General 

    
Pus Cell: Uncountable 

  

  

    
MCHC 

    
25 g/dl 

    
HbA1c 

    
10.40% 

  

  

    
Platelets 

    
519x103 

    
Thyroid Stimulating Hormones (TSH) 

    
2.8 (normal 0.27 to    4.2) 

  

  

    
ALT 

    
10 u/l (normal 7 to    55) 

    
FT4 

    
18.3 (normal 12 to    22) 

  

  

    
AST 

    
11.1 (normal 8 to 43) 

    
Prostate Specific Antigen (PSA) 

    
2.2 (normal <4) 

  

  

    
ALP 

    
89 (normal 45 to 115) 

    
F.PSA 

    
0.39 (normal <0.4) 

  

  

    
GGT

    
40 (normal 11 to 50) 

    
S. Alfa Fetoprotein    (AFP)

    
0.7 (normal <5.8) 

  

  

    
Serum Protein 

    
6.5 (normal 6.6 to    8.7) 

    
CA 19.9 

    
2.81 (normal 0 to 37) 

  

  

    
Serum Albumin 

    
2.3    (normal 3.4 to 4.8) 

    
CEA 

    
0.76 (normal <3.4) 

  

  

    
Total Bilirubin 

    
0.3mg/dl (normal <1.1) 

    
HIV 

    
Negative 

  

  

    
Direct Bilirubin 

    
0.1mg/dl (normal    <0.3) 

    
HBV 

    
Negative 

  

  

    
S.    Vitamin B12

    
307.6 (normal 211 to    946) 

    
HCV 

    
Negative 

  










Table 1: Laboratory results at admission.

Chest x-ray: normal findings. Abdominal ultrasound: bilateral hydro ureter and hydronephrosis. Cystogram -x ray: thick wall urinary bladder. Echocardiography: ischemic heart disease, mild diastolic dysfunction, depressed systolic function with EF: 35%. Oesophagogastro- duodenoscopy (OGD): in the esophagus there is extensive candidiasis. MRI whole spine with contrast: opinion features of disseminated pott’s disease (disseminated multilevel spondylodiscitis associated with multilevel cord myelopathy, left psoas abscess, near complete destruction of C5 and C6 (Figures 1-3).

Figure 1: MRI spine.

    

    
    

    

    Figure 1: MRI spine.

Figure 2: MRI spine.

    

    
    

    

    Figure 2: MRI spine.

Figure 3: MRI spine.

    

    
    

    

    Figure 3: MRI spine.

Therapeutic intervention

After stabilization, patient was admitted to the hospital and the following were done. Intravenous (IV) fluid (for one day then we encourage oral uptake), urinary catheter was inserted, input and output fluid chart, IV board spectrum antibiotics (after taking blood and urine sample for culture and sensitivity), insulin (long acting once at 7:00pm and three doses of short acting with meals), proton pump inhibitor (40mg iv once/day), enoxaparin subcutaneous prophylaxis dose (40mg once/day). Anti-tuberculosis tabs (FDC 4 tabs) once/day, pyridoxine (vitamin B6) 50mg tabs once/day. Blood transfusion (packed red blood cell 3 units), fluconazole 150mg IV once per day. After cardiologist consultation (Aspirin 100mg tabs once/day, Clopidogrel 75mg tabs once/day, Bisoprolol 2,5mg tabs once/day, Spironolactone 25mg tabs once/day, furosemide 20mg once/day) were added to his plan of management.

Steroid was started initially at presentation then stopped after diagnosis of PD was confirm and due to esophageal candidiasis. Neurosurgery and orthopedic consultation was done and they recommended spine fixation surgery. Do surgical intervention four days after admission (decompression and fixation). Surgery went without complication, post-surgery follow up patient did well, and his condition improved gradually. His follow up including examination and lab investigation is showed in (Table 2).

Table 2: Follow up (examination and laboratory investigation).





  

    
    
Day 0 

    
Day one 

    
Day two 

    
Day five 

    
Day ten 

    
Third week 

  

  

    
Vital signs 

    
Stable 

    
Stable 

    
Stable 

    
Stable 

    
Stable 

    
Stable 

  

  

    
Lower limb power 

    
Grade zero 

    
Grade zero 

    
Grade zero 

    
Grade zero 

    
Grade one 

    
Grade two 

  

  

    
TWBCS 

    
16.69x103 

    
    
15.09x103 

    
9.9x103 

    
5.3x103 

    
4.2x103 

  

  

    
CRP 

    
158 

    
152 

    
138 

    
51 

    
40 

    
20 

  

  

    
Hemoglobin 

    
8.7 g/dl 

    
    
9.1 g/dl 

    
10 g/dl 

    
10.4 g/dl 

    
11 g/dl 

  

  

    
Urine general 

    
Pus cell: Uncountable 

    
    
    
Clear 

    
    
Clear 

  










Table 2: Follow up (examination and laboratory investigation).

Discussion

Tuberculosis (TB) is one of the ancient infectious disease, it still posing a major health, social and economic burden at a global level and especially in low and middle income countries [3]. Sudan has low health expenditure (6.2% of GDP) and has an estimated TB incident rate of 117 per 100,000 individuals [4].

Pathogenesis

TB is caused by members of the specie Mycobacterium tuberculosis complex (MTBC), among which Mycobacterium tuberculosis (MTB) is the most important etiologic agent of TB in humans [5]. MTB infection acquire by breathing contaminated air droplets with tubercilli bacilli that were coughed or sneezed by a nearby person who has active Tuberculosis. Then it reach alveoli where it is likely to be kill by professional alveolar macrophage [6]. If the bacilli can survive this frst line of defense, it starts actively replicating and diffuses to nearby cells, reaching in few weeks of exponential growth a high bacterial burden [7]. Spread to other organs through lymphatics or haematogenous dissemination occurs during these early steps of infection [8].

Diagnosis of TB

Definitive diagnosis requires the detection of MTB by using at least one of the following microbiological techniques: microscopically analysis, isolation in culture or molecular methods [9]. Specimens such as sputum and Broncho-alveolar lavage are used for the diagnosis of pulmonary TB, and it shows high sensitivity and specificity [10]. On the other hand, there is lower sensitivity of the microbiological assays in the non-pulmonary specimens probably due to lower bacterial concentration, and this make the diagnosis of non- pulmonary TB more difficult.

Immunological diagnosis by the Mantoux test or tuberculin skin test (TST) and by the interferon- gamma release assays (IGRAs) only detect MTB infection without distinguishing between Latent and active TB patients [11].

Presentation

Patients with Potts disease may have history of pulmonary tuberculosis or concomitant disease. Constitutional symptoms of Potts disease are fever, night sweating and weight loss [12]. Back pain is the earliest and most common symptom of Potts disease, with patients usually experiencing this problem for weeks before seeking treatment. Neurologic abnormalities include spinal cord compression with paraplegia, paresis, impaired sensation and nerve root pain occurs in half of cases. Cervical spine is a less common affected site but it is more serious because severe neurologic complications are more likely. Spinal tuberculosis seems to be more common in persons infected with HIV than HIV negative, but the clinical presentation is similar in both [13].

Treatment

Early diagnosis and proper treatment will prevent further neurologic complications of pott’s disease. The principle of treatment is conservative treatment with a combination of anti-TB drugs. The standard medical treatment protocol includes isoniazid, rifampicin, Ethambutol, and Pyrazinamide, with duration of six months, which may be prolonged to 9–12 months in complicated cases [14,15]. Early surgical intervention, if surgery is indicated, is recommended to avoid further instability and neurologic complications. Indications for surgical intervention include neurological deficit, spinal deformity, resistant to medical therapy, large paravertebral abscess, and indefinite diagnosis [16-18].

In our patient although the onset of symptoms was acute and without past medical history of TB, chronic cough or contact with a patient having TB, but still spinal tuberculosis (PD) was on the top of our differential diagnosis, because the patient presented with features highly suggestive of pott’s disease and came from a region with a high incidence of tuberculosis. So we targeted the workup to confirm the diagnosis and to exclude other possibilities as early as possible, because early diagnosis and intervention is a corner stone in management of spinal tuberculosis especially if it presents with complications like cord compression and destruction of vertebrae. Involving multiple departments and teamwork help us reaching provisional diagnosis more easily and rapidly, this lead to good outcome and prevention of permanent complications.

Conclusion

The case described in this report is of a man with no history of TB, close contact with TB patient or chronic cough. Who presented with back pain, paraplegia and urine retention. The patient was diagnosed as having disseminated pott’s disease complicated by epidural abscess, psoas abscess and near completed destruction of cervical spine (C5, C6). Treated by combination Anti-Tuberculosis and underwent surgery (decompression and fixation). Patient condition was improved gradually and discharge after three weeks from admission date on good condition.

References

  1. Schirmer P, RIenault CA, Holodniy M. Is spinal tuberculosis contagious? Int J nfect Dis. 2010; 14: 659-666.
  2. Ferrer MF, Torres LG, RIamírez OA, Zarzuelo MR, Del Prado González N. Tuberculosis of the spine. A systematic review of case series. Int Orthop. 2012; 36: 221-231.
  3. World Health Organization. Global Tuberculosis report. 2012.
  4. Adam MA, Ali HM, Khalil EA. First-line drug resistance patterns of Mycobacterium tuberculosis complex isolates from re-treatment patents from Sudan. J Tuberc Res. 2016; 4: 98-104.
  5. Cole ST, Brosch RI, Parkhill J, Garnier T, Churcher C, Harris D, et al. deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence. Nature. 1998; 393: 537-544.
  6. Urdahl KB, Shafiani S, Ernst JD. Imitation and regulation of T-cell responses in tuberculosis. Mucosal Immunol. 2011; 4: 288-293.
  7. Wolf AJ, Desvignes L, Linas B, Banaiee N, Tamura T, Takatsu K, et al. Imitation of the adaptive immune response to Mycobacterium tuberculosis depends on antgen production in the local lymph node, not the lungs. J Exp Med. 2008; 205: 105-115.
  8. Balasubramanian V, Pavelka MS, Jr, Bardarov SS, Martn J, Weisbrod TR, McAdam RA, et al. Allelic exchange in Mycobacterium tuberculosis with long linear recombination substrates. J Bacteriol. 1996; 178: 273-279.
  9. Delogu G, Herrmann JL. Mycobacterium species. In: Cornaglia G, Courcol RI, Herrmann JL, Kahlmeter G, Peigue-Lafeuille H, Vila J, editors. European Manual of Clinical Microbiology. ESCMID. 297-307.
  10. Drouillon V, Delogu G, Detori G, Lagrange PH, Benecchi M, Houriez F, et al. Multicenter evaluation of a transcription-reverse transcription concerted assay for rapid detection of Mycobacterium tuberculosis complex in clinical specimens. J Clin Microbiol. 47: 3461-3465.
  11. Golet D, Carrara S, Butera O, Amicosante M, Ernst M, Sauzullo I, et al. Accuracy of immunodiagnostic tests for active tuberculosis using single and combined results: a multicenter TBNET-Study. PLoS. ONE. 2008; 3: e3417.
  12. Pertuiset E, Beaudreuil J, Liote F, Horusitzky A, Kemiche F, Richette P, et al. Spinal tuberculosis in adults. 1999; 78; 309-320.
  13. Jellis JE. Human immunodeficiency virus and osteoartcular tuberculosis. 2002; 27-31.
  14. Johansen IS, Nielsen SL, Hove M, Kehrer M, Shakar S, Wøyen AV, et al. Characteristic’s and clinical outcome of bone and joint tuberculosis from 1994 to 2011: A retrospective register-based study in Denmark. Clin Infect Dis. 2015; 61: 554-562.
  15. Thwaites G, Fisher M, Hemingway C, Scott G, Solomon T, Innes J, et al. British Infection Society guidelines for the diagnosis and treatment of tuberculosis of the central nervous system in adults. 2009; 59: 167-187.
  16. Turgut M. Spinal tuberculosis (Potts disease): Its clinical presentation, surgical management, and outcome. A survey study on 694 patents. Neurosurg Rev. 2001; 24: 8-13.
  17. Rezai ARI, Lee M, Cooper PRI. Modern management of spinal tuberculosis. Neurosurgery. 1995; 36: 87-97.
  18. Oguz E, Sehirlioglu A, Altnmakas M, Ozturk C, Komurcu M, Solakoglu C, et al. A new classification and guide for surgical treatment of spinal tuberculosis. Int Orthop. 2008; 32: 127-133.

Citation: Satti HMA and Mohamed FAA. A Case Report of Disseminated Pott’s Disease (Spinal Tuberculosis) Complicated by Abscess and Near Complete Destruction of Cervical Spine (C5, C6). Austin Med Sci. 2020; 5(1): 1040.