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Bacterial Spectrum Analysis of Pediatric Septic Arthritis in Sanglah General Hospital (2019-2021): A Case Series

Journal of Clinical Orthopaedics | Vol 9 | Issue 1 |  January-June 2024 | page: 61-69 | Ida Bagus Anom Krishna Caitanya, Made Agus Maharjana, Nyoman Gede Grenata Nanda Ustriyana

DOI: https://doi.org/10.13107/jcorth.2024.v09i01.638


Author: Ida Bagus Anom Krishna Caitanya [1], Made Agus Maharjana [1], Nyoman Gede Grenata Nanda Ustriyana [1]

[1] Department of Orthopaedics and Traumatology, Faculty of Medicine Udayana University, Prof Ngoerah General Hospital, Denpasar, Indonesia

Address of Correspondence

Dr. Ida Bagus Anom Krishna Caitanya,
Department of Orthopaedics and Traumatology, Faculty of Medicine Udayana University, Prof Ngoerah General Hospital, Denpasar, Indonesia.
E-mail: borthopaedi@gmail.com


Abstract

This case series presents five pediatric patients diagnosed with septic arthritis in Sanglah General Hospital from 2019 to 2021. The most common infecting organism was Staphylococcus aureus, comprising 66.7% of all infections. Other organisms described in literatures are Salmonella, Staphylococcus epidermidis, Enterobacter cloacae, and Mycobacterium tuberculosis. Antibiotic treatment should be started as soon as the diagnosis is suspected and modified once the organism isolated from the synovial fluid (SF) has been characterized. Unfortunately, in many cases, despite a high clinical suspicion of SA, the diagnosis cannot be confirmed because the SF is sterile on bacterial culture. This may lead to difficulties in patient management. The case series also analyzed the possible causes of negative culture results. The data showed three cases with no pathogen organism detected, which can be turned to false negative that ruled out the infection cause of the arthritis. The study suggests that in the future, other techniques might prove useful in increasing the sensitivity of the detection of bacterial infection, such as Polymerase chain reaction and detection of antibodies against the teichoic acid staphylococcal cell wall component. The detection and identification of Kingela kingae in synovial fluid have improved significantly since the development of PCR. The specificity of these assays relies on the ability of the PCR to generate only the expected amplification product. The duration of the laboratory to process is also a factor that affects the result. The study concludes that early diagnosis and prompt treatment are crucial in achieving good functional outcomes in pediatric septic arthritis.
Keywords: septic arthritis, pediatric patients, bacterial spectrum, diagnosis, culture methods


References

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2. Erkilinc M, Gilmore A, Weber M, Mistovich RJ. Current concepts in pediatric septic arthritis. J Am Acad Orthop Surg 2021;29:196-206.
3. Hoswell RL, Johns BP, Loewenthal MR, Dewar DC. Outcomes of paediatric septic arthritis of the hip and knee at 1-20 years in an Australian urban centre. ANZ J Surg 2019;89:562-66.
4. Montgomery NI, Rosenfeld S. Pediatric osteoarticular infection update. J Pediatr Orthop 2015;35:74-81.
5. Castellazzi L, Mantero M, Esposito S. Update on the management of pediatric acute osteomyelitis and septic arthritis. Int J Mol Sci 2016;17:855.
6. Whiting ZG, Doerre T. Diagnosis of culture-negative septic arthritis with polymerase chain reaction in an immunosuppressed patient: A case report. JBJS Case Connect 2020;10:e20.00057.
7. Williams N, Cooper C, Cundy P. Kingella kingae septic arthritis in children: Recognising an elusive pathogen. J Child Orthop 2014;8:91-5.
8. Slinger R, Moldovan I, Bowes J, Chan F. Polymerase chain reaction detection of Kingella kingae in children with culture-negative septic arthritis in eastern Ontario. Paediatr Child Health 2016;21:79-82.
9. Spyridakis E, Gerber JS, Schriver E, Grundmeier RW, Porsch EA, St Geme JW, et al. Clinical Features and outcomes of children with culture-negative septic arthritis. J Pediatric Infect Dis Soc 2019;8:228-34.
10. Anino-Fernández J, Ramírez-Huaranga MA, Mínguez-Sanchez MD. False negatives of synovial fluid in septic arthritis. Reumatol Clin 2016;12:114-5.
11. Hujazi I, Oni D, Arora A, Muniz G, Khanduja V. The fate of acutely inflamed joints with a negative synovial fluid culture. Int Orthop 2012;36:1487-92.
12. Chan MM, Tse TS, Wan YC, Wah Hung Y, Fan JC. A rare and uncommon complication after use of hydrogen peroxide (H2O2): A review of use of H2O2 in orthopaedics. J Orthop Trauma Rehabil 2020;27:247-51.

How to Cite this article: Caitanya IBAK, Maharjana MA, Ustriyana NGGN. Bacterial Spectrum Analysis of Pediatric Septic Arthritis in Sanglah General Hospital (2019-2021): A Case Series. Journal of Clinical Orthopaedics 2024;January-June:9(1):61-69.

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The Role of Serum Procalcitonin in Establishing Diagnosis of Bone and Joint Infections

Journal of Clinical Orthopaedics | Vol 5 | Issue 1 |  Jan-Jun 2020   | page: 3-7 | John Nolan, Putu Feryawan Meregawa


Author: John Nolan [1], Putu Feryawan Meregawa [2]

[1] Faculty of Medicine, Udayana University, Denpasar.
[2] Departement of Orthopaedic and Traumatology, Medical Faculty, Udayana University-Sanglah General Hospital Denpasar, Indonesia.

Address of Correspondence
John Nolan,
Faculty of Medicine, Udayana University, Denpasar
E-mail: johnnolan@student.unud.ac.id


Abstract

Background: Acute bone and joint infection such as septic arthritis and osteomyelitis diagnostic are still considered as a pitfall especially in the emergency department. Some laboratory markers, such as total Count (TC), Erythrocyte Sedimentation Rate (ESR) and C – Reactive Protein (CRP) assessed regularly whereas those are not specific. Serum PCT has a role as a sensitive and specific marker in supporting the diagnosis of bone and joint infections.
Method: Literature review is done by searching journals with “serum procalcitonin”, “bone infections”, “diagnosis”, and “joint infections” on the search engines. From 37 journals that were reviewed, 34 were found suitable as reference for this paper.
Outcome: High level of serum PCT indicate the activation of immune system, specifically the innate immune system due to microbial infections. One of the most different aspect with CRP is serum PCT infrequently elevates in response to viral infection, which means PCT is useful in differentiating bacterial and viral infections Serum PCT concentration elevates following the endotoxin or cytokines release such as interleukin (IL)- 6, tumor necrosis factor (TNF)-alpha, and IL-1b which usually appears in bone and joint infections. Although its benefits, there are some limitation interfering the usage and levels of serum PCT.
Conclusion: Serum PCT has a role as a sensitive and specific marker in supporting the diagnosis of bone and joint infections due to its sensitivity following endotoxins release. Further researches and studies are required to identify the appropriate usage, interfering factors, and clinical application of serum PCT in establishing the diagnosis of bone and joint infections.
Keywords: Procalcitonin, Bone infections, joint infections, Diagnosis.


References

1. Calhoun J, Manring M, Shirtliff M. Osteomyelitis of the Long Bones. Seminars in Plastic Surgery. 2009;23(02):059-072.
2. Goergens ED, McEvoy A, Watson M, Barrett IR. Acute osteomyelitis and septic arthritis in children. Journal of paediatrics and child health. 2005 Jan;41(1‐2):59-62.
3. Mathews CJ, Weston VC, Jones A, Field M, Coakley G. Bacterial septic arthritis in adults. The Lancet. 2010 Mar 6;375(9717):846-55.
4. Timsit S, Pannier S, Glorion C, Chéron G. Acute osteomyelitis and septic arthritis in children: one year experience. Archives de pediatrie: organe officiel de la Societe francaise de pediatrie. 2005 Jan;12(1):16-22.
5. Bonhoeffer J, Haeberle B, Schaad UB, Heininger U. Diagnosis of acute haematogenous osteomyelitis and septic arthritis: 20 years experience at the University Children’s Hospital Basel. Swiss medical weekly. 2001 Oct 6;131(39-40):575-81.
6. Kremers HM, Nwojo ME, Ransom JE, Wood-Wentz CM, Melton III LJ, Huddleston III PM. Trends in the epidemiology of osteomyelitis: a population-based study, 1969 to 2009. The Journal of bone and joint surgery. American volume. 2015 May 20;97(10):837.
7. Perron AD, Brady WJ, Miller MD. Orthopedic pitfalls in the ED: osteomyelitis. The American journal of emergency medicine. 2003 Jan 1;21(1):61-7.
8. Kolinsky DC, Liang SY. Musculoskeletal Infections in the Emergency Department. Emergency Medicine Clinics. 2018 Nov 1;36(4):751-66.
9. Shen CJ, Wu MS, Lin KH, Lin WL, Chen HC, Wu JY, Lee MH, Lee CC. The use of procalcitonin in the diagnosis of bone and joint infection: a systemic review and meta-analysis. European journal of clinical microbiology & infectious diseases. 2013 Jun 1;32(6):807-14.
10. Maharajan K, Patro DK, Menon J, Hariharan AP, Parija SC, Poduval M, Thimmaiah S. Serum Procalcitonin is a sensitive and specific marker in the diagnosis of septic arthritis and acute osteomyelitis. Journal of orthopaedic surgery and research. 2013 Dec 1;8(1):19.
11. Casado JF, Blanco AQ. Procalcitonin. A new marker for bacterial infection. Anales espanoles de pediatria. 2001 Jan;54(1):69-73.
12. Alkholi UM, Al-Monem NA, El-Azim AA, Sultan MH. Serum procalcitonin in viral and bacterial meningitis. Journal of global infectious diseases. 2011 Jan;3(1):14.
13. Wang C, Zhong DA, Liao Q, Kong L, Liu A, Xiao H. Procalcitonin levels in fresh serum and fresh synovial fluid for the differential diagnosis of knee septic arthritis from rheumatoid arthritis, osteoarthritis and gouty arthritis. Experimental and therapeutic medicine. 2014 Oct 1;8(4):1075-80.
14. Saeed K, Dryden M, Sitjar A, White G. Measuring synovial fluid procalcitonin levels in distinguishing cases of septic arthritis, including prosthetic joints, from other causes of arthritis and aseptic loosening. Infection. 2013 Aug 1;41(4):845-9.
15. Sigmund IK, McNally MA. Diagnosis of bone and joint infections. Orthopaedics and Trauma. 2019 Jun 1;33(3):144-52.\
16. Tsaras G, Maduka-Ezeh A, Inwards CY, Mabry T, Erwin PJ, Murad MH, Montori VM, West CP, Osmon DR, Berbari EF. Utility of intraoperative frozen section histopathology in the diagnosis of periprosthetic joint infection: a systematic review and meta-analysis. JBJS. 2012 Sep 19;94(18):1700-11.
17. Unkila-Kallio L, Kallio MJ, Peltola H, Eskola J. Serum C-reactive protein, erythrocyte sedimentation rate, and white blood cell count in acute hematogenous osteomyelitis of children. Pediatrics. 1994 Jan 1;93(1):59-62.
18. Gaigneux E, Cormier G, Varin S, Mérot O, Maugars Y, Le Goff B. Ultrasound abnormalities in septic arthritis are associated with functional outcomes. Joint Bone Spine. 2017 Oct 1;84(5):599-604.
19. Merlini L, Anooshiravani M, Ceroni D. Concomitant septic arthritis and osteomyelitis of the hip in young children; a new pathophysiological hypothesis suggested by MRI enhancement pattern. BMC medical imaging. 2015 Dec 1;15(1):17.
20. Fritz JM, McDonald JR. Osteomyelitis: approach to diagnosis and treatment. The Physician and sportsmedicine. 2008 Jan 1;36(1):50-4.
21. Wang S, Yin P, Quan C, Khan K, Wang G, Wang L, Cui L, Zhang L, Zhang L, Tang P. Evaluating the use of serum inflammatory markers for preoperative diagnosis of infection in patients with nonunions. BioMed research international. 2017;2017.
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24. Koramutla HK, Koyagura B, Ravindran B. Evaluation of serum procalcitonin as a significant marker in cases of septic arthritis and osteomyelitis: a two year study. International Journal of Research in Orthopaedics. 2018 Jul;4(4):601.
25. Ibrahim KA, Abdel-Wahab AA, Ibrahim AS. Diagnostic value of serum procalcitonin levels in children with meningitis: a comparison with blood leukocyte count and C-reactive protein. JPMA-Journal of the Pakistan Medical Association. 2011 Apr 1;61(4):346.
26. Chan T, Gu F. Early diagnosis of sepsis using serum biomarkers. Expert review of molecular diagnostics. 2011 Jun 1;11(5):487-96.
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28. Schuetz P, Christ-Crain M, Muller B. Procalcitonin and other biomarkers to improve assessment and antibiotic stewardship in infections–hope for hype?. Swiss medical weekly. 2009 Jun 13;139(23):318.
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How to Cite this article: Nolan J, Meregawa P.F. The Role of Serum Procalcitonin in Establishing Diagnosis of Bone and Joint Infections. Journal of Clinical Orthopaedics Jan-Jun 2020;5(1): 3-7.

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Surgical Site Infections in Orthopaedics: An Introduction

Journal of Clinical Orthopaedics | Vol 4 | Issue 2 |  July-Dec 2019 | page:5-6 |  Dr. Gautam Zaveri


Author: Dr. Gautam Zaveri [1]

[1] Department of Spine Surgery, Jaslok Hospital & Research Centre

Address of Correspondence
Dr. Gautam Zaveri,
Department of Spine Surgery, Jaslok Hospital & Research Centre
E-mail: gautamzaveri1969@gmail.com


Surgical Site Infections in Orthopaedics: An Introduction

Surgical site infections (SSIs) are defined as infections of tissues, organs or spaces exposed by surgeons during the performance of an invasive procedure, that occur within 30 days of surgery or within 1 year of surgery involving implants[1]. In the USA, SSIs are ranked third amongst all reported cases of inpatient nosocomial infections [2,3]. Approximately, 5,00,000 SSIs are reported in the USA every year (2.8 per 100 operations) [4], accounting for 16% of nosocomial infections in all hospitalized patients [5]. Between 30,000- 35,000 SSIs are reported annually in the USA following the performance of an orthopaedic invasive procedure[6]. In a developing nation such as India where surgeries are performed in operating theatres with varying standards and practice of asepsis, the incidence of SSIs is estimated to be many folds higher. As our horizons continue to expand, and we are called upon to perform more complex procedures on patients who are elderly, immuno-compromised and with multiple medical comorbidities, the incidence of SSIs is likely to rise further.
Orthopaedic surgeons have always dreaded SSIs. They compromise the outcome of an otherwise successful surgery resulting in increased suffering, disability, morbidity and mortality and may often compromise the eventual outcome. Besides SSIs result in more extended hospitalization, increased direct and indirect costs, loss of work hours and even job loss. Whitehouse et al. performed a case-controlled study to look at the outcomes following SSIs in orthopaedics [7]. They reported an increase in hospital stay by a median of 2 weeks per patient, approximately double rehospitalization rates and increased healthcare costs by more than 300%. They also found patients with SSIs to have substantially higher physical limitations and significant reductions in health-related quality of life.
Early detection of wound infection requires careful vigilance by the operating team. Pain that is out of proportion to the nature of surgery, fever and difficulty in moving the limb are early signs of infection that may appear even before the surgical site shows signs of infection such as local warmth, tenderness, redness, shininess, oedema, induration and discharge. Laboratory tests and x-rays are of limited use in diagnosing an early infection. In the immediate postoperative setting, an MRI scan is also of limited use because soft tissue hyperintensities and fluid collections are typically seen within the wound at this time. Obtaining a tissue sample to isolate an organism is vital in planning the subsequent treatment.
SSIs in orthopaedics is especially challenging because of the large muscle bulk, the problem of persistence of infection within the bone and the formation of biofilms on dead bone and implants. The treatment of an established SSI entails source control, coupled with targeted anti-biotics. Source control involves drainage of purulent material, physical debride-ment of dead and infected tissue including bone, and copious irrigation of the wound. Implants can be retained, removed or replaced based on the progress of bone healing, the formation of biofilms and the fixation of the implant within the bone. A variety of techniques can be used to obtain local control of infection including antibiotic-loaded cement beads, biocomposites like Stimulan coupled with antibiotics or application of silver nitrate solution. In severe infections, especially in the presence of implants, primary wound closure is avoided and negative pressure wound therapy is used to obtain a reduction in local infection, to promote granulation and healing of the wound. Occasionally, especially for extremity wounds, a flap may be required to cover exposed implant/ bone/ joints/ tendons / nerves. Antibiotics must be targeted to the organism isolated and administered for prolonged periods (8 to 12 weeks or even longer). Rifamycins are active against biofilms of staphylococci and fluoroquinolones against those of gram-negative bacilli.
The endpoint of stopping antibiotics and declaring complete eradication of infection has not yet been clearly outlined in the literature. No single investigation or clinical sign in isolation can help determine the healing of the infection. Clinical improvement wound healing, reduction in CRP, ESR and Total WBC count, MRI evidence of reduction in soft tissue hyperintensities, fluid collection and bone marrow oedema, fatty conversion of bone marrow with fusion, and a negative bone scan are some of the features of a healed infection.
In spite of considerable improvements in the operating room environment, surgical techniques and aseptic practices, SSIs continue to constitute a significant challenge for the medical team and healthcare institutions. A multipronged approach involving surveillance, antimicrobial prophylaxis, eradication of carrier status, infection control program-mes and education is vital to reduce the risk of SSI. The old adage, “An Ounce of Prevention is better than a Pound of Cure” is aptly suited to the problem of surgical site infections in orthopaedics.


References

1. Guideline for Prevention of Surgical Site Infection (2017). Centre for disease control and prevention. https://www.cdc.gov/infectioncontrol/guidelines/ssi/index.html accessed 15th March 2019
2. Haley RW, Culver DH, White JW, et al. The nation-wide nosocomial infection rate: a new need for vital statistics. Am J Epidemiology 1985; 121: 159- 167 Epidemiol 1985;121:159-167.
3. Horan TC, Culver DH, Gaynes RP, et al. Nosocomial infections in surgical patients in the United States, January 1986–June 1992. Infect Control Hosp Epidemiology 1993; 14:73-80
4. Jarvis WR. Selected aspects of the socioeconomic impact of nosocomial infections: morbidity, mortality, cost, and prevention. Infect Control Hosp Epidemiology 1996; 17:552- 557 Epidemiol 1996;17:552-557
5. Lee J, Singletary R, Schmader K, et al: Surgical site infection in the elderly following orthopaedic surgery. Risk factors and outcomes. J Bone Joint Surg Am 2006; 88:1705-1712
6. Greene LR: Guide to the elimination of Orthopaedic surgery surgical site infections: An executive summary of the Association for Professionals in Infection Control and Epidemiology elimination guide. Am J Infect Control 2012; 40:384-386
7. Whitehouse JD, Friedman D, Kirkland KB, et al. The impact of surgical site infections following orthopaedic surgery at a community hospital and a university hospital: Adverse quality of life, excess length of stay and extra costs. Inf Control & Hosp Epidemiology 2002; 23: 183- 189.


How to Cite this article: Zaveri G. Surgical Site Infections in Orthopaedics: An Introduction. Journal of Clinical Orthopaedics July-Dec 2019;4(2):5-6.

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Diagnosis of Surgical Site Infection

Journal of Clinical Orthopaedics | Vol 4 | Issue 2 |  July-Dec 2019 | page:12-16 | Dr. Manish Kothari


Author: Dr. Manish Kothari [1]

[1] Consultant Spine Surgeon, Jaslok Hospital & Research Centre, Mumbai

Address of Correspondence
Dr. Manish Kothari
Jaslok Hospital & Research Centre, Mumbai
E-mail: dr.manish.kothari@jaslokhospital.net


Abstract

Diagnosis of Surgical site infection is one of the most important factors that determines the further management of SSI. The diagnosis is based on various factors including clinical, laboratory investigations, Radiology, Bacteriology and molecular modalities. The current review summarises the salient features in all modalities.
Keywords: Surgical Site infection, Diagnosis.


References

1. Harrop JS, Styliaras JC, Ooi JC, Radcliff KE, Vaccaro AR, Wu C. Contributing factors to surgical site infections. J Am Acad Ortho Surg. 2012; 20(2):94-101.
2. WHO document on Global Guidelines For the Prevention of Surgical Site Infection. WHO Guidelines Development Group; Geneva, Switzerland; 2016;58-177
3. Guideline for Prevention of Surgical Site Infection (2017). Centre for disease control and prevention. https://www.cdc.gov/infectioncontrol/guidelines/ssi/index.html accessed 15th March 2019.
4. Simodynes, EE, Cochran, RM. Aeromonas hydrophila infection complicating an open tibial fracture. A case report. Clin OrthopRelat Res 1982; 171: 117–120
5. Levitsky KA, Hozack WJ, Balderston RA, et al. Evaluation of the painful prosthetic joint. Relative value of bone scan, sedimentation rate, and joint aspiration. J Arthroplasty. 1991;6:237–244.
6. Schinsky MF, Della Valle CJ, Sporer SM, et al. Perioperative testing for joint infection in patients undergoing revision total hip arthroplasty. J Bone Joint Surg Am. 2008;90:1869–1875. doi: 10.2106/JBJS.G.01255.
7. Spangehl MJ, Masri BA, O’Connell JX, et al. Prospective analysis of preoperative and intraoperative investigations for the diagnosis of infection at the sites of two hundred and two revision total hip arthroplasties. J Bone Joint Surg Am. 1999;81:672–683.
8. Bilgen O, Atici T, Durak K, et al. C-reactive protein values and erythrocyte sedimentation rates after total hip and total knee arthroplasty. J Int Med Res. 2001;29:7–12.
9. Park KK, Kim TK, Chang CB, et al. Normative temporal values of CRP and ESR in unilateral and staged bilateral TKA. Clin OrthopRelat Res. 2008;466:179–188. doi: 10.1007/s11999-007-0001-x. [PMC free article]
10. Forster IW, Crawford R. Sedimentation rate in infected and uninfected total hip arthroplasty. Clin OrthopRelat Res. 1982;168:48–52.
11. Lee Y, McKechnie T, Doumouras AG, Handler C, Eskicioglu C, Gmora S, Anvari M, Hong D. Diagnostic Value of C-Reactive Protein Levels in Postoperative Infectious Complications After Bariatric Surgery: a Systematic Review and Meta-Analysis. Obes Surg. 2019 Mar 21
12. Aljabi Y, Manca A, Ryan J, Elshawarby A. Value of procalcitonin as a marker of surgical site infection following spinal surgery. The Surgeon. 2019 Apr 1;17(2):97-101.
13. Cyteval, C, Hamm, V, Sarrabère, MP. Painful infection at the site of hip prosthesis: CT imaging. Radiology 2002; 224(2): 477–483
14. Kohan, AA, Rubbert, C, Vercher-Conejero, JL. The impact of orthopedic metal artifact reduction software on interreader variability when delineating areas of interest in the head and neck. PractRadiat Oncol 2015; 5(4): e309–e315.
15. Cyteval, C, Bourdon, A. Imaging orthopedic implant infections. Diagn Interv Imaging 2012; 93(6): 547–557
16. Plodkowski,A.J., Hayter,C.L., Miller,T.T., Nguyen,J.T., Potter,H.G. Lamellated hyperintense synovitis: potential MR imaging sign of an infected knee arthroplasty. 2013/1; 1: 256-260
17. Talbot BS, Weinberg EP. MR imaging with metal-suppression sequences for evaluation of total joint arthroplasty. Radiographics. 2015 Nov 20;36(1):209-25.
18. Glaudemans, AWJM, Signore, A. FDG-PET/CT in infections: the imaging method of choice? Eur J Nucl Med Mol Imaging 2010; 37(10): 1986–1991.
19. Basu, S, Kwee, TC, Saboury, B. FDG-PET for diagnosing infection in hip and knee prostheses: prospective study in 221 prostheses and subgroup comparison with combined (111)In-labeled leukocyte/(99)mTc-sulfur colloid bone marrow imaging in 88 prostheses. J Nucl Med 2014; 39(7): 609–615.
20. Schwotzer N, Wahl P, Fracheboud D, Gautier E, Chuard C. Optimal culture incubation time in orthopedic device-associated infections: a retrospective analysis of prolonged 14-day incubation. Journal of clinical microbiology. 2014 Jan 1;52(1):61-6.
21. Bémer, P.; Plouzeau, C.; Tande, D.; Léger, J.; Giraudeau, B.; Valentin, A.S.; Jolivet-Gougeon, A.; Vincent, P.; Corvec, S.; Gibaud, S.; et al. Evaluation of 16S rRNA gene PCR sensitivity and specificity for diagnosis of prosthetic joint infection: A prospective multicenter cross-sectional study. J. Clin. Microbiol. 2014, 52, 3583–3589.
22. Hartley, J.C.; Harris, K.A. Molecular techniques for diagnosing prosthetic joint infections. J. Antimicrob. Chemother. 2014, 69 (Suppl. 1), i21–i24.
23. Yano, M.H.; Klautau, G.B.; da Silva, C.B.; Nigro, S.; Avanzi, O.; Mercadante, M.T.; Salles, M.J.C. Improved diagnosis of infection associated with osteosynthesis by use of sonication of fracture fixation implants. J. Clin. Microbiol. 2014, 52, 4176–4182.
24. Yano, M.H.; Klautau, G.B.; da Silva, C.B.; Nigro, S.; Avanzi, O.; Mercadante, M.T.; Salles, M.J.C. Improved diagnosis of infection associated with osteosynthesis by use of sonication of fracture fixation implants. J. Clin. Microbiol. 2014, 52, 4176–4182.
25. Schinsky, M.F.; Della Valle, C.J.; Sporer, S.M.; Paprosky, W.G. Perioperative testing for joint infection in patients undergoing revision total hip arthroplasty. J. Bone Jt. Surg. Ser. A 2008, 90, 1869–1875.
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How to Cite this article: Kothari M. Diagnosis of surgical site infection. Journal of Clinical Orthopaedics July-Dec 2019;4(2):12-16.

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Surgical Site Infections in Orthopaedics: Epidemiology & Microbiology

Journal of Clinical Orthopaedics | Vol 4 | Issue 2 |  July-Dec 2019 | page:7-11 | Dr. Kedar Deogaonkar, Aditya Menon, Gautam Zaveri


Author: Dr. Kedar Deogaonkar [1], Aditya Menon [2], Gautam Zaveri [3]

[1] Department of Spine Surgery, Jaslok Hospital & Research Centre.

Address of Correspondence
Dr. Gautam Zaveri,
Department of Spine Surgery, Jaslok Hospital & Research Centre
E-mail: gautamzaveri1969@gmail.com


Abstract

Surgical site infections are one of the most common nosocomial infections. understanding epidemiology and microbiology of SSI will help in defining the problem and developing stratergies for prevention and management
Keywords: Surgical Site infection, Diagnosis.


References

1. Harrop JS, Styliaras JC, Ooi JC, et al. Contributing factors to surgical site infections. J AAOS. 2012; 20(2):94-101
2. National Nosocomial Infections Surveillance (NNIS) System Report, data summary from January 1992 through June 2004, Am J Infect Control. 2004; 32:470- 85
3. Ercole FF, Chianca TCM. Infecção de sítiocirúrgico empacientes submetidos à artroplastia de quadril. Revista Latino-Am. Enfermagem. 2002; 10(2):157-65
4. Lima ALLM, Zumiotti AV, Uip DE, Silva JS. Fatorespreditivos de infecçãoempacientes com fraturasexpostasnos membros inferiores. Acta Ortop Bras. 2004; 12(1):23-39
5. Maksimovic J. Incidence of surgical site infections in the departments of orthopedics and traumatology. Vojnosanit Pregl. 2006; 63(8):725-9
6. Maksimovic J, Markovíc-Denic L, Bumbasrevic M, et al. Surgical site infections in orthopedics patients: prospective cohort study. Croat Med J. 2008; 49(1):58-65
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22. Khan MS, Rehman S, Ali MA, et al. Infection in orthopedic implant surgery, its risk factors and outcome. J Ayub Med Coll Abbottabad, 2008; 20(1):23-5
23. Wassef MA, Hussein A, Abdul Rahman EM, El-Sherif RH. A Prospective Surveillance of Surgical Site Infections: Study for Efficacy of Preoperative Antibiotics Prophylaxis. Afr. J. Microbiol. Res. 2012; 6(12):3072-8
24. Singh R. Prevalence and Antibiotic Sensitivity Pattern of Bacteria Isolated from Nosocomial Infections in Orthopaedic Patients. J. Orthopaedics. 2010; 7(2):153-159
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26. Anderson DJ, Sexton DJ, Kanafani ZA, et al. Severe surgical site infection in community hospitals epidemiology, key procedures and the changing prevelance of methicillin resistant Staphyloccocus aureus. Infect control hospl epidemiol. 2007; 28(9):1047-1053
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34. Hansen S, Schwab F, Asensio A, et al. Methicillin resistant Staphylococcus Aureus in Europe which infection control measures are taken? Infection, 2010, 38(3)
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How to Cite this article: Deogaonkar K, Menon A, Zaveri G. Surgical Site Infections in Orthopaedics: Epidemiology & Microbiology. Journal of Clinical Orthopaedics July-Dec 2019;4(2):7-11.

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Management of Infected Non – Unions

Vol 2 | Issue 2 |  July – Dec 2017 | Page 25-31 | John Mukhopadhaya


Authors: John Mukhopadhaya [1]

[1]Department of Orthopaedics and Joint Replacement, Paras HMRI Hospital, Patna, Bihar, India.

Address of Correspondence
Dr. John Mukhopadhaya
Department of Orthopaedics and Joint Replacement,
Paras HMRI Hospital, Patna, Bihar, India.
Email: mukhoj@gmail.com


Abstract

Infected nonunions are difficult problems to tackle. The treatment is often multistaged and involves high expenses and has major impact on both patient as well as surgeons. Understanding of the basics of infected non-union including etiopathology, diagnostic criteria and management algorithms is helpful in successfully managing this complication. This article provides a basic overview of infected nonunions along with new methods of management including Masquelet technique and techniques of managing bone gaps
Keywords: infected non-union, diagnosis, management


References

1. Brinker MR, Hanus BD, Sen M, O’Connor DP. The devastating effects of tibial nonunion on health-related quality of life. J Bone Joint Surg Am. 2013 Dec 18;95(24):2170-6.
2. Struijs PA, Poolman RW, Bhandari M. Infected nonunion of the long bones. J Orthop Trauma. 2007 Aug;21(7):507-11.
3. Chaudhary MM. Infected nonunion of tibia. Indian J Orthop. 2017 May-Jun;51(3):256-268.
4. Tetsworth K, Cierny G 3rd. Osteomyelitis debridement techniques. Clin Orthop Relat Res. 1999 Mar;(360):87-96.
5. Shyam AK, Sancheti PK, Patel SK, Rocha S, Pradhan C, Patil A. Use of antibiotic cement-impregnated intramedullary nail in treatment of infected non-union of long bones. Indian J Orthop. 2009 Oct;43(4):396-402.
6. Bhatia C, Tiwari AK, Sharma SB, Thalanki S, Rai A. Role of Antibiotic Cement Coated Nailing in Infected Nonunion of Tibia. Malays Orthop J. 2017 Mar;11(1):6-11.
7. Pradhan C, Patil A, Puram C, Attarde D, Sancheti P, Shyam A. Can antibiotic impregnated cement nail achieve both infection control and bony union in infected diaphyseal femoral non-unions? Injury. 2017 Aug;48 Suppl 2:S66-S71.
8. Putnis S, Khan WS, Wong JM. Negative pressure wound therapy – a review of its uses in orthopaedic trauma. Open Orthop J. 2014 Jun 27;8:142-7.
9. Giannoudis PV, Faour O, Goff T, Kanakaris N, Dimitriou R. Masquelet technique for the treatment of bone defects: tips-tricks and future directions. Injury. 2011 Jun;42(6):591-8.
10. Patwardhan S, Shyam AK, Mody RA, Sancheti PK, Mehta R, Agrawat H. Reconstruction of bone defects after osteomyelitis with nonvascularized fibular graft: a retrospective study in twenty-six children. J Bone Joint Surg Am. 2013 May 1;95(9):e56, S1.
11. Yin P, Ji Q, Li T, Li J, Li Z, Liu J, Wang G, Wang S, Zhang L, Mao Z, Tang P. A Systematic Review and Meta-Analysis of Ilizarov Methods in the Treatment of Infected Nonunion of Tibia and Femur. PLoS One. 2015 Nov 3;10(11):e0141973
12. Mukhopadhaya J, Raj M. Distraction osteogenesis using combined locking plate and Ilizarov fixator in the treatment of bone defect: A report of 2 cases. Indian J Orthop. 2017 Mar-Apr;51(2):222-228.
13. Dhillon MS, Rajasekharan S, Sancheti P. Status of road safety and injury burden: India. J Orthop Trauma. 2014;28 Suppl 1:S43-4.


How to Cite this article:  Mukhopadhaya J. Management of Infected Non-unions. Journal of Clinical Orthopaedics July-Dec 2017; 2(2):25-31

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Spinal tuberculosis – an Update

Vol 2 | Issue 1 |  Jan – June 2017 | Page 31-42 | Kshitij Chaudhary, Arjun Dhawale, Ram Chaddha, Vinod Laheri


Authors: Kshitij Chaudhary [1], Arjun Dhawale [1], Ram Chaddha [2], Vinod Laheri [2].

[1] Sir HN Reliance Foundation Hospital, Department of Orthopaedics and Spine Surgery; Mumbai, India
[2] Apollo Hospital, Navi Mumbai, Maharashtra. India

Address of Correspondence
Dr. Kshitij Chaudhary
Sir HN Reliance Foundation Hospital, Department of Orthopaedics and Spine Surgery; Mumbai, India
Email: chaudhary.kc@gmail.com


Abstract

Musculoskeletal tuberculosis, especially spinal tuberculosis is a challenging scenario. The disease presentation varies and profile of the organism is changing rapidly with rise of antibiotic resistance. The management protocols need to be revisited in light of new information and current review is aimed at achieving this goal. This review article is a summary of the symposium conducted by Bombay Orthopaedic Society at KEM Hospital in November 2016. The focus of this discussion was primarily on nonoperative management of spinal tuberculosis including focus on diagnostic protocol and medical management controversies. Surgical aspect of the disease is also covered with recent advances in the spine surgical protocols mentioned in brief.
Keywords: Spinal Tuberculosis, diagnosis, antibiotic resistance, surgery.


1. Introduction

Spinal tuberculosis is the most common infection affecting the skeletal system in our country, and if incorrectly treated, can have devastating and permanent sequelae. The emergence of drug-resistant tuberculosis and HIV has turned this age old infection into a deadly and terrifying disease. Poor socioeconomic conditions and an unhygienic living environment contribute to the persistence of the infection in our society. Poor access to quality healthcare and indiscriminate and unscientific use of second-line antibiotics has stoked the fire as we stand and stare helplessly at the impending epidemiological disaster. It behooves us as representatives of the medical community to educate ourselves and others regarding this problem and practice recommended treatment guidelines.

2. Clinical Features

The most common presenting symptom of spinal tuberculosis is back pain or neck pain. Most patients seek consultation after weeks or months of pain as the onset is usually insidious and progression is slow. Frequently it is mistaken as benign low back pain, and treated with painkillers as the early radiographs are often normal. Patients may experience constitutional symptoms (reported incidence varies between 17-54%), however, compared to pyogenic spondylodiscitis fever, anorexia, fatigue are less common. Therefore, the clinician should maintain a high degree of suspicion, especially in patients who complain of ongoing pain for more than a month, have rest pain, or if associated constitutional symptoms are present. In addition, as tuberculosis affects the anterior column primarily, a knuckle deformity, i.e. prominence of a single spinous process might be one of the early signs of tuberculous spondylodiscitis. Some patient can also present with a cold abscess in remote locations like the posterior triangle of the neck (cervical spine TB), along the ribs (thoracic spine TB), or in the inguinal region (lumbar spine TB). The clinician should also maintain a high degree of suspicion in immunocompromised patients, especially HIV infections, and should also be wary of patients with a history of tuberculosis, or those who have come in contact with tuberculosis patients.Unfortunately, in our country, many patients are diagnosed late and present with complications that may require surgical intervention. There are two main complications of spinal tuberculosis – spinal deformity and neurological deficit. The spinal deformity that typically develops as a consequence of anterior spinal column destruction is kyphosis. The kyphosis is usually of an angular variety that can cause long-term consequences if severe. The most grave among them is late-onset myelopathy due to a stretch of the spinal cord over an internal gibbus. In children, kyphosis can continue to progress after healing. The children who are more likely to have progressive deformity are identified using the “spine at risk” signs as described by Rajasekaran. These radiographic signs are seen when the posterior elements become incompetent, thus resulting in progressive deformity.Neurological deficits are mainly seen in cervical and thoracic tuberculosis. The cause of neurological deficit can be “soft” or “hard” compression (described in detail in the section on radiological features). Another rare cause of neurological deficit is inflammatory vascular thrombosis of spinal arteries resulting in spinal infarct. There are no diagnostic imaging findings to diagnose a spinal infarct, and this is usually a diagnosis of exclusion.

Radiographic Features

3.1.  Radiographs

Standard radiographs, anteroposterior and lateral views, are used commonly as the first line of investigation; however, they suffer from several disadvantages. Radiographic changes are usually not apparent until more than 50% of the vertebral body is destroyed, thus delaying the diagnosis. Junctional areas and posterior elements are difficult to visualize. Disc space narrowing with endplate erosions (paradiscal lesions) are early radiographic signs. With progressing and destruction of the spinal column, the radiographs may show varying degree of focal kyphosis due to vertebral body collapse. A paraspinal abscess may cast soft tissue shadow, which in the thoracic spine may be difficult to differentiate from the descending aorta. Abscess in cervical spine will show up as an increase in retropharyngeal space and those in the lumbar spine may result in asymmetry or bulging of the psoas outline. In chronic cases, calcifications in abscess wall are pathognomonic of tuberculosis. Calcifications are formed because, unlike pyogenic bacteria, MTB lacks proteolytic enzymes. Progression of kyphosis or vertebral body destruction early in the course of chemotherapy (first three months) should not be considered as a sign of treatment failure.

3.2.  MRI

MRI is the imaging modality of choice for spinal TB and can detect infection early in its course. Paradiscal involvement is the most common type of lesion. Central body, subligamentous, posterior element tuberculosis can also sometimes be encountered. The entire spine should be screened as noncontiguous lesion are seen in 16-71% of patients. The recommended protocol for imaging is presented in Table 1.

In many parts of the country, the diagnosis of spinal TB rests on imaging findings on MRI. In an endemic country like ours, the clinician usually is right because the odds are in his favor. However, there are no pathognomonic imaging features of spinal TB that can reliably differentiate it from other spinal infection or tumors. Hence, tissue diagnosis is mandatory and recommended. Table 2 enumerates the radiological differences between spinal TB and pyogenic infection; however, it is important to remember that these have a poor predictive value.


Brucellosis frequently affects the lumbar spine. Anterior osteophytes (parrot beak) is a typical radiological feature on radiographs. Intradiscal air is identified in about one-third cases. Fungal osteomyelitis is difficult to differentiate from spinal TB on imaging. Metastasis or spinal tumors frequently affect the pedicle and spare the disc. The paravertebral soft tissue involved in lymphomas demonstrates a low signal on T2 MRI. However, noncaseating or granular varieties of spinal TB may look similar. Early infection and type 1 Modic type degenerative changes may look similar, although a high signal in the disc should raise the suspicion of infective spondylodiscitis.MRI is useful for another purpose – to diagnose the type, extent, and severity of epidural spinal cord compression (Figure 1).

“Soft” compression should be differentiated from “hard” compressions as this has implications for the management of the patient. Abscess (diffuse hyperintense T2 signal and hypointense T1 signal) and caseous granulation tissue (heterogeneous hyperintense to isointense T2 signal) are “soft” compressions. Bony sequestrum and retropulsed disc (hypointense T1 and T2 signal) are “hard” compressions (Figure 1). Translations and internal gibbous causing spinal cord compression is another example of “hard” compression. “Hard” compressions that cause neurological deficit cannot be treated with chemotherapy alone and usually require surgical decompression. Rarely, non-compressive lesions, such as vascular infarct or meningeal inflammation) are the cause of neurological deficit. It is extremely difficult to prove these as the cause of spinal cord dysfunction, especially in patients with epidural spinal cord compression.

3.3.  CT scan

CT scan is primarily used to assess the extent of osseous destruction accurately before surgical intervention, especially in extensive infection. In some situations, it may help differentiate “hard” from “soft” epidural compression.

4. Biopsy

As we have seen, there are no pathognomonic imaging signs that can reliably differentiate spinal tuberculosis from other spinal infections or tumors. Hence, a biopsy to obtain tissue for histopathological and microbiological diagnosis is mandatory to confirm the diagnosis of spinal tuberculosis. Besides, the mounting incidence of multi-drug resistant tuberculosis has made biopsy unavoidable. The yield of spinal biopsy is variable and depends not only on the expertise of the surgeon or radiologist doing the biopsy but also on the availability of specialized, well-equipped laboratories and microbiologists. Access to such facilities is non-existent in resource-poor regions of our country. However, there is a particular subset of spinal tuberculosis patients in whom biopsy is mandatory as in these patients the probability of encountering drug resistance is high (Table 3).


In patients with uncomplicated spinal TB (i.e. patients who are not planned for surgical intervention), a closed core biopsy is indicated. CT-guided core biopsy is ideal to acquire a representative sample safely, however, when unavailable, a fluoroscopy-guided biopsy can work as well, especially if the target area is easily accessible. Core biopsy (10-14G bone biopsy needle) is preferred to fine needle aspiration cytology or FNAC (18-22G needles) as the diagnostic yield of the latter is poorer. In any case, aspiration biopsy if required can always be performed via a core biopsy needle. Higher microbiological yield is obtained if paraspinal or prevertebral abscesses are targeted for pus sample rather than bone cores. If the patient has multiple sites of spinal TB, a more easily accessible and safer area is chosen. The biopsy can be performed via a transpedicular or extrapedicular approach, and the choice depends on the target area of biopsy. Anterolateral approach is required in cases of cervical spine TB. The neuromuscular bundle can be displaced manually, and the needle can be placed under CT image guidance. This technique requires considerable expertise and a confident radiologist. Biopsy for craniovertebral tuberculosis can be performed either transorally or via a posterolateral approach. Microbiological samples are collected in sterile containers in saline (2-3ml is enough for the purpose is only to keep the tissue hydrated; if a large quantity of saline is used the lab has to centrifuge to isolate the tissue) and sent immediately to the lab. Histopathological samples are collected in 10% formalin. The following tests should be ordered on the samples (Table 4).

4.1.  MGIT Cultures and Drug sensitivity testing

Definitive diagnosis of Mycobacterium tuberculosis infection rests on positive microbiological culture from the tissue sample. The traditional method of culture using Lowenstein-Jensen solid medium has been replaced with BACTEC™ MGIT™ liquid cultures. MGIT cultures are more sensitive (50 to 60% in osteoarticular tuberculosis) and can give faster results. Results are available in a few weeks (maximum 45 days) (Figure 2).

Prior treatment with chemotherapy can lower the yield and hence when possible it is better to perform a biopsy before initiating chemotherapy. It is not recommended to stop chemotherapy if the patient is on antitubercular medications only for the purpose of biopsy. If the results are positive, one should ask for phenotypic drug sensitivity testing (DST) for first-line drugs. In addition, phenotypic DST can be done for second-line drugs if one suspects MDR tuberculosis. The approximate cost of BACTEC™ MGIT™ liquid cultures is Rs. 1000-1500. First-line DST costs about Rs. 4000-5000 and second-line DST costs about Rs. 5000-6000.Most labs will also perform direct smear and AFB staining before putting the sample in for culture. The sensitivity of direct smears is poor (less than 10%) in osteoarticular TB cannot be relied on to make a diagnosis.

4.2.  Histopathological examination (HPE)

Histopathological diagnosis is usually obtained in about 60% of spinal TB patients. The classical histopathological features are caseating necrosis, epitheliod cell granuloma, lymphocytic infiltrate, and Langhans giant cells. It is important to remember that granulomas can be detected in other infections and inflammatory disorders as well. Therefore a positive HPE diagnosis can only suggest a probable diagnosis of mycobacterial infection. AFB staining of HPE samples can sometimes detect mycobacteria (not necessarily Mycobacterium tuberculosis), but as with direct smear, the sensitivity is quite low.

4.3.  Other cultures

It is a good custom to always ask for pyogenic bacterial cultures as well. This practice may detect a primary pyogenic infection or rarely secondary bacterial infection in addition to tuberculosis. It is also important to consider the possibility of fungal infections in susceptible and at-risk patients.

4.4.  GeneXpert

GeneXpert is a new molecular test that detects the presence of Mycobacterium tuberculosis DNA. The main advantage is its rapid turnaround time. Results are usually available within 6 hours. It can detect Rifampicin resistance as well and thus aid in starting MDR treatment early in the course of therapy. As it is a DNA-based test, the specificity is 100%. However, the sensitivity is quite low of osteoarticular tuberculosis (about 60 to 70%). Therefore a negative GeneXpert cannot be used to rule out tuberculosis infection. The test is not widely available, especially in remote areas of the country. However, wherever feasible, it can be a useful adjunct to the above tests. The approximate cost is about Rs. 1500-2000 and in many centers, it is available free of charge through public-private partnerships under the DOTS program.

4.5.  Line Probe Assay

Line probe assay or LPA is another DNA PCR-based molecular test that is specifically used for detecting drug resistance. The first-line kit detects Isoniazid and Rifampicin resistance and aids in the diagnosis of MDR-TB. The second-line kit detects Ethambutol, cyclopeptides (Capreomycin, Kanamycin, Amikacin and Viomycin) and fluoroquinolone resistance and aids in the diagnosis of XDR-TB. WHO recommends its use for smear-positive respiratory samples only. However, this test can be used as an alternative to phenotypic DST after MGIT cultures are positive. The results are available within 48 hrs (compared to phenotypic DST which requires about 3 weeks) and a diagnosis of MDR or XDR can be established (Figure 2). The information provided by this test can streamline MDR or XDR therapy earlier in the course of therapy. It is not recommended to rely only on LPA results as monoresistance to drugs not included in the kit can be missed. Therefore, phenotypic DST is always required to complete drug sensitivity testing. If the patient has a low risk for drug resistance, then phenotypic DST is adequate. If the patient has a high risk for drug resistance, then LPA followed by phenotypic DST is advocated if the clinician wants to establish the diagnosis of MDR or XDR to guide therapy. The main disadvantage is the cost. First-line kits cost Rs 2000-3000 and second-line kits cost about Rs. 5000-60005.

Other investigations

Other investigationsCBC, ESR, CRP are a measure of disease activity and are frequently used to monitor therapeutic response to chemotherapy. They are more likely to be markedly abnormal in pyogenic infection compared to tuberculosis. Xray Chest should be done, as up to 67% patients may have either active focus or healed sequelae of pulmonary tuberculosis. Tests to detect HIV should be performed in high-risk patients or patients presenting with extensive or atypical spinal TB. Serological tests (IgM, IgG titers) and interferon release assays (Quantiferon TB Gold, TB-SPOT test) cannot differentiate latent from active infection and are not recommend by WHO. Mantoux test is of limited value in an endemic country like India. LFT and RFT are ordered as a baseline before starting chemotherapy and later to monitor side-effects.

6.  First line chemotherapy

As with pulmonary tuberculosis, multidrug chemotherapy is the mainstay of treatment for spinal tuberculosis. Empirical treatment is usually started after biopsy before confirmation of mycobacterial infection. It is advisable to involve a chest physician or infectious disease specialist early in the course of therapy. The drugs that comprise first-line chemotherapy are Isoniazid (H), Rifampicin (R), Pyrazinamide (Z), and Ethambutol (E). The WHO recommends two months of intensive chemotherapy comprising of HRZE followed by a continuation phase of HR. The doses are weight-dependent (Table 6)

and hence fixed dose combinations should be avoided (e.g. Tab AKT 4 kit has 450mg Rifampicin that is inadequate for more than 60kg individual). There is no evidence to show that corticosteroids improve or enhance treatment effect of antibiotic and may be detrimental. However, it is a common practice (although not evidence-based) to start a short course of steroids for patients presenting with an acute neurological deficit.

6.1.  Duration of multi-drug chemotherapy

There is a lack of consensus regarding the ideal duration of multidrug chemotherapy for spinal TB. WHO recommends nine months of treatment for TB of bones and joints (2HREZ + 7 HR) because of the serious risk of disability in addition to difficulties in assessing treatment response. British Thoracic Society (BTS) recommends six months (2HREZ + 4 HR) of chemotherapy. American Thoracic Society (ATS) recommends six months of chemotherapy in adults and 12 months in children for spinal TB. Inadequate or unessential, prolonged duration of treatment should be avoided.

6.2.  Role of DOTS (directly observed therapy short course)

Under the newer regime (National TB program), DOTS is no longer supportive of alternate day therapy, and daily treatment is recommended.

6.3.  Adverse effects of First-line anti-TB drugs

The common adverse effects are nausea, vomiting, hepatitis (HRZ), peripheral neuropathy (H), discolored body fluids (R), color/night blindness (E), joint pains (Z). It is best to consult the treating physician if the patient develops adverse effects as the drugs may need to be modified or discontinued.

6.4.  TB and HIV co-infection

The risk of developing tuberculosis (TB) is estimated to be between 26 and 31 times greater in people living with HIV (PLHIV) than among those without HIV infection. HIV-positive patients are more likely than HIV-negative patients to have extrapulmonary TB or smear-negative pulmonary TB. HIV testing is recommended in patients who were diagnosed with TB. The preferred recommendation for many TB-HIV patients is to start and complete TB treatment, and then start ART (antiretroviral therapy). However, if the patient’s clinical status is poor (other signs of HIV clinical stage 3 or 4 or CD4 count is less than 350/mm3), it may be necessary to refer the patient for ART treatment sooner. If patient is not on ART, start TB treatment immediately, or if already started, continue TB treatment.

6.5.  Judging treatment response to multidrug chemotherapy

The treatment response is mainly monitored using clinical and radiological evidence. Biochemical markers such as CBC, ESR, and CRP are not reliable markers to assess healing. Clinical response to healing is judged by resolution of constitutional symptoms, weight gain, improved appetite, reduction in spinal pain, and progressive increase in activity. Radiographs may show initial deterioration, however eventually healing is seen as remineralization of bone and sclerosis of vertebral bodies. The end result of healing may be spontaneous fusion or a stiff fibrous ankylosis. Routine interval MRIs on follow-up are not recommended, especially in the initial few months of antibiotic treatment. A paradoxical worsening of MRI findings can be noted up to 3 months, and this is believed to be secondary to an immunological response to the dying bacilli. MRI is indicated if there are reasons to suspect drug resistant or poor response to antibiotics. MRI findings of healing are a resolution of marrow edema with or without its conversion to a fatty marrow. An abscess may get walled off, and sterile collections may be encountered on MRI for years following the termination of treatment. Hence, by itself, abscess on MRI at the end of treatment is not taken as a sign of persistence of infection.If the clinical and radiological response is poor or inadequate, the surgeon must consider these possible scenarios: 1) drug resistance, 2) late responder, 3) mechanical or instability related pain, or 4) incorrect diagnosis of spinal TB. This may require a repeat biopsy or assessment of spinal column stability using dynamic or weight bearing radiographs. If the diagnosis is in doubt, in spite of following this protocol and the patient continues to deteriorate, a surgical debridement and column reconstruction may be indicated.

7.  Management of MDR TBMDR-

TB is defined as resistance to at least both Isoniazid and Rifampicin. Extensively drug-resistant tuberculosis or XDR-TB is defined as resistance to any fluoroquinolone and at least one injectable second-line antibiotic in addition to Isoniazid and Rifampicin resistance. One of the primary reasons for the emergence of MDR strains, apart from the rise of HIV co-infection, is the indiscriminate and unscientific use of multi-drug chemotherapy by clinicians, making it one of the most dangerous iatrogenic creations. In addition to the high morbidity and mortality risk, the drug therapy for MDR-TB is potentially toxic and can have permanent sequelae (Table 6). India ranks second amongst the high-burden MDR-TB countries. A very high percentage of MDR strains (51%) have been reported in an urban center in Mumbai compared to 2% in a rural center. A 30% primary drug resistance in pediatric spinal TB patients has been reported at tertiary referral center in Mumbai. Following are the principles of management of MDR-TB:1.  Early detection of MDR and prompt initiation of effective treatment are important for successful outcomes 2.  A biopsy is a must, and all efforts must me made to culture the organism to obtain drug sensitivity testing. 3.  A lab competent in microbiological testing should be chosen. 4.  It is imperative to involve a chest physician or an infectious disease specialist for treatment. 5.  Never add a single drug to a failing regimen 6. MDR-TB regimen should be composed of at least five drugs likely to be effective, including four second-line anti-TB drugs that are likely to be effective plus pyrazinamide 7. One chosen from group A, one from Group B and at least two from Group C 8. Agents from Group D1 are added if they are considered to add benefit. 9. The total number of anti-TB drugs to include in the regimen needs to balance expected benefit with the risk of harms and  nonadherence when the pill burden is high. 10. In the treatment of MDR-TB, an intensive phase of 8 months is suggested for most patients, and the duration may be modified according to the patient’s response to therapy. 11. In the treatment of patients newly diagnosed with MDR-TB, a total duration of 20 months is suggested for most patients, and the duration may be modified according to the patient’s response to therapy.

General principles

12. Social support is an essential component of care and treatment delivery13. Any adverse effects of drugs should be managed immediately and adequately to relieve suffering, minimise the risk of treatment interruptions, and prevent morbidity and mortality due to serious adverse effects14. Antiretroviral therapy (ART) is recommended for all patients with HIV and drug-resistant TB, irrespective of CD4 cell-count, as early as possible (within the first eight weeks) following initiation of the anti-TB treatment15. Extra-pulmonary drug-resistant TB is treated with the same strategy and duration as pulmonary drug-resistant TB16. Immunomodulators have the potential to improve outcomes of all TB including M/XDR-TB

8.  Surgical Management

Spinal tuberculosis is a medical disease, and surgery is reserved for its complications, the most common being neurological deficit and spinal deformity. The decision for surgical intervention is also dependent on the age, primarily because of the risk of progression of deformity in children during the active infection as well as after healing.With the advent of multi-drug resistant tuberculosis, the middle-path regimen described by Tuli needs to be revisited. A biopsy and MGIT culture to determine sensitivity are mandatory and should be sent for all surgical cases. The suggested algorithm is presented in Figure 3.

8.1.  Indications for surgery

8.1.1.  Neurological deficitThe decision to operate a patient with weakness primarily depends on the cause of epidural spinal cord compression. As we have seen, “soft” or “hard” spinal cord compression can cause a neurological deficit. In general, patients who present with spinal cord       dysfunction due to “hard” spinal cord compression are not amenable to medical management. These patients are best treated with surgical decompression.     Patients with who present with deficits due to “soft” spinal cord compression (abscess and granulation tissue) are more likely to respond to medical treatment if the deficits are mild. In these patients, the indication for surgery are the following:17. Severe neurological deficit (inability to walk across the room) at presentation18. Worsening neurology on chemotherapy19. No improvement in neurological deficit with at least six weeks of chemotherapy20. New onset neurological deficit on chemotherapy.

8.1.2.  Spinal deformity

Another consequence or complication of the tuberculous destruction of the spine is a spinal deformity, which is typically an angular kyphosis. It is well known that the final angle of kyphosis shows a strong positive correlation with the initial degree of vertebral body loss. Patients that are anticipated to have a large kyphotic deformity are best treated early in the active phase of the disease. Rajasekaran et. al. have reported that about one vertebral body loss in the thoracic spine and 1.5 vertebral loss in lumber spine corresponds to about 30 to 35º of focal kyphosis and this, they recommend, is a relative indication for early surgery. The MRC trials, which were randomized controlled trials comparing conservative versus surgical treatment in patients with mild to moderate disease (less than 3 vertebral body loss and those that could walk across the room) found that the conservative group had an average 25º increase in kyphosis over 15 years. About 5% of these patients presented with an alarming increase in kyphosis up to 70º. No case of late onset myelopathy was reported in 15 years. However, the Hong Kong group questioned whether 15 years of MRC trial was enough to claim with certainty that there are no long-term consequences of such deformities. In a review of 60 patients that were conservatively treated at the Hong Kong center, they found 25 patients developing late onset myelopathy with over 65% presented more than 20 years later. Hence it is important for the surgeon to keep in mind that patients presenting with intact neurology who are treated conservatively can potentially develop grave consequences due to angular kyphosis especially in the thoracic spine. Thus, following are the indications for surgery in patients who do not present with a neurological deficit:21. Extensive destruction of spinal column (more than 2 to 3 vertebral body destruction)22. Circumferential destruction (translation or dislocation)23. Progressive kyphosis beyond 30º or severe kyphosis are presentation

8.1.2.1.  Childhood Spine Tuberculosis

Childhood spinal tuberculosis deserves a special mention here. Tuberculosis infection in a child can result in a malignant progression kyphosis. In children too, the severity of deformity is related to the degree of vertebral body loss. Rajasekaran et al. reported that 88% children who had more than two vertebral body loss had progressive deformity (Type 1 progression). Besides, the deformity continued to evolve as the child got older even after healing of the infection (Type 2 progression). Children, especially less than 5-year-olds, tend to present with a more extensive disease compared to adults. This is probably because of delayed diagnosis and relatively more cartilaginous nature of the spinal column.It is important to anticipate deformity in childhood tuberculosis to prevent severe kyphosis as the child grows. Rajasekaran’s ‘spine-at-risk’ signs can help to identify such patients. These signs are essentially indicative of posterior spinal column failure. The signs are based on radiographs and include retropulsion, separation of facets, toppling and lateral translation. The presence of 2 or more signs is an indication for early surgery even in the absence of neurological deficit. It is also important to remember that the child who has a stable spine (<2 spine-at-risk signs) at presentation can develop instability in the course of treatment even if the infection is under control.Reconstruction of the spine in children is challenging especially in the young (<8-year-olds) and in those that present with extensive spinal column destruction. The posterior elements are small, and instrumentation can be technically challenging. The surgeon may have to use a combination of strategies to stabilize the pediatric spinal column, including pedicle screws instrumentation, augmentation using tapes (Mersilene) or wires, anterior column reconstruction and postoperative bracing or casting. It is important to be aggressive regarding spinal column reconstruction in children.

8.1.3.  Disease (Poor response to medical treatment)

It is important to review and consider various clinical scenarios that could be responsible for a poor response to medical treatment. Involving the physician in the decision-making process is imperative.8.1.3.1.  Mechanical or instability related painIn adults, spinal instability may manifest as mechanical back pain not improving with chemotherapy. Worsening of pain and mechanical instability after a conservative trial of bracing and chemotherapy is a relative indication for surgery.

8.1.3.2.  Drug resistance

If the clinical and radiological response to chemotherapy is poor (progressive of infection with new lesions), a biopsy for culture and DST is indicated. If conclusive evidence of drug resistance cannot be obtained, debridement and spinal column reconstruction may be indicated. MDR-TB not responding to chemotherapy, especially XDR TB may need surgery to decrease disease burden.

8.1.3.3.  Diagnosis in doubt

Lastly, it is important to entertain the possibility of non-tuberculous diagnosis in a patient who does not show a response to chemotherapy. Again, biopsy or surgery may be indicated to establish the diagnosis.

8.1.4.  Rare indications for surgery

24. Large paraspinal abscess causing column destruction25. Prevertebral abscess causing respiratory distress or dysphagia26. Spinal tumor syndrome

8.2.  Surgical approach

The decision making to chose a particular surgical approach depends on the age, region of involvement, number of levels involved, posterior column integrity, severity of kyphosis, location and direction of epidural spinal cord compression, medical co-morbidities, surgeon preference or expertise, and finally infrastructure capability. No single approach can best treat the entire spectrum of possible situations. Any surgeon who offers only one procedure is not providing the highest level of care. Hence, it is important to individualize the surgical approach to achieve the following goals of the surgery:27. Effective spinal cord decompression28. Reliable spinal column reconstruction (graft or cage from good bone to good bone, adequate instrumentation adhering to biomechanics principles)

8.2.1.  Standalone anterior spinal cord decompression and reconstruction

As tuberculosis affects the anterior spinal column, anterior debridement and fusion has long been the gold standard of treatment. It has several advantages, which include direct access to pathology, safe and effective decompression without handling of the spinal cord and optimal reconstruction of the anterior column without damaging intact posterior elements. It is ideal for treating one or two level involvement, especially in the mid thoracic spine in an otherwise young and healthy individual. Patients with comorbidities, especially osteoporosis or preexisting pulmonary pathology are not ideal candidates. Anterior approach to the cervicothoracic and lumbosacral area is difficult due to regional anatomy. In patients with extensive spinal destruction (more than 2 VB loss in the thoracic spine and more than 1 VB loss in thoracolumbar and lumbar spine) or severe kyphosis, standalone anterior spinal instrumentation is biomechanically inferior to posterior pedicle screw construct. Furthermore, in the past few decades, surgeons have gained expertise in accessing the anterior column via the posterior approach, and the indications for a standalone anterior surgery are dwindling. In the cervical spine and anteriorly accessible regions of the cervicothoracic spine, anterior approach and fusion remain the gold standard.

8.2.2.  Posterior instrumentation without anterior column reconstruction

Rarely, tuberculosis presents as posterior element disease with spinal cord compression. In these patients, a standalone posterior approach is an obvious choice. In patients with less severe anterior column destruction, a posterior approach to decompress the spinal cord via transfacetal or transpedicular approach may be successful. As the antibiotics heal the anterior column and restore its integrity, the posterior instrumentation helps to maintain spinal alignment. However, frequently the technique of spinal cord decompression via a posterior approach may involve excision of anterior column sufficient enough to warrant grafting of anterior column. It is important not to compromise spinal cord decompression in an attempt to avoid anterior column reconstruction.

8.2.3.  Posterior approach with anterior column reconstruction

This approach is most popular to treat spinal tuberculosis of the thoracic and lumbar area. The posterior approach is the workhorse of a spinal surgeon, and most surgeons are far more comfortable with it compared to the anterior approach. As per necessity, a progressive sacrifice of the posterior elements can provide increasing access to the anterior column. (Transfacetal, transpedicular, extracavitary lateral approach). Anterior reconstruction is challenging when a cage of graft needs to be implanted, especially if it spans multiple levels. In the lumbar region, this is even more challenging as the lumbar nerve roots have to be protected while approaching the anterior column. The approach also may involve spinal cord handling if one is not careful, and frequently a less experienced surgeon may end up doing a suboptimal job fearing injuring to the neural structures.

8.2.4.  Anterior and posterior approach

Extensive anterior column destruction (3 or more vertebral bodies in thoracic spine or more than 1 vertebral body in the lumbar spine) with or without severe kyphosis, warrants a global access to take advantages of both anterior and posterior approach (Figure 4). Usually, posterior approach is performed first to correct the alignment and stabilize the spine followed by anterior spinal cord decompression and reconstruction using a structural graft or cage. A global approach can be morbid and potentially could be staged to avoid complications.

9.  Take home message

29. Clinical features can be subtle, and the clinician needs to have a high degree of suspicion for spinal tuberculosis to be able to diagnose this infection early.

30. There are no radiological features that are pathognomonic for spinal tuberculosis

31. A biopsy is recommended not only for diagnosis but also to treat it with effective antibiotics.

32. New diagnostic tests, such as GeneXpert and LPA, can be used to diagnose MDR-TB early in the course of treatment

33. Surgeons who treat spinal tuberculosis should follow recommended guidelines when prescribing multi-drug chemotherapy

34. It is advisable to involve a chest physician or an infection disease specialist early in the course of treatment.

35. Management of MDR-TB is complex and potentially morbid, and all efforts should be taken not to generate iatrogenic cases of MDR-TB by prescribing irrational and unscientific chemotherapy

36. Surgical management is reserved for complications of spinal tuberculosis.

37. Childhood spinal TB can have a malignant progression of deformity, in spite of effective medical management and these should be identified early.

38. The treating physician or orthopedic surgeon should be cognisant of the indications for surgery and make an appropriate referral to a spine surgeon, especially in children.

10.  Acknowledgment

This review article is a summary of the symposium conducted by Bombay Orthopaedic Society at KEM Hospital in November 2016. The focus of this discussion was primarily on nonoperative management of spinal tuberculosis. We would like to thank and acknowledge Dr. Abhay Nene, Dr. Mihir Bapat, Dr. Amit Sharma, Dr. Vishal Kundnani, and Dr. Samir Dalvie for their participation in this symposium. We would like to especially thank our guest speakers Dr. Vikas Punamiya (Chest Physician, Breach Candy Hospital) and Dr. Shashikala Shivaprakash (Head of Microbiology at Sir HN Reliance Foundation Hospital) for sharing their expertise and knowledge regarding this topic with the members of the Bombay Orthopedic Society.


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How to Cite this article: Chaudhary K, Dhawale A, Chaddha R, Laheri V. Spinal Tuberculosis – an Update. Journal of Clinical Orthopaedics Jan – June 2017; 2(1):31-42.

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