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 Table of Contents  
Year : 2018  |  Volume : 1  |  Issue : 1  |  Page : 32-45

The spine clinics – Postoperative spinal infections - Clinical scenarios

1 Orthopaedic Spine Surgeon, Vitus Spine Care and Research, Bhagwan Mahaveer Jain Hospital, Bengaluru, Karnataka, India
2 Orthopaedic Spine Surgeon, Ganga Hospital, Coimbatore, Tamil Nadu, India
3 Orthopaedic Spine Surgeon, Sancheti Hospital, Pune, Maharashtra, India
4 Orthopaedic Spine Surgeon, Carolina Pines Regional Medical Center, Hartsville, SC, United States

Date of Web Publication17-Jan-2018

Correspondence Address:
Dr. Bidre Upendra
Vitus Spine Care and Research, Bhagwan Mahaveer Jain Hospital, Vasanth Nagar, Bengaluru - 560 052, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/isj.isj_38_17

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This section of the symposium brings four different clinical scenarios in patients presenting with postoperative surgical site infections (SSI) after spine surgery. The patients were managed in various medical centres having different infrastructures and different spine care professionals. The spine clinics aims at providing the reader with an overview of the difficult scenarios faced in the setting of postoperative spinal infection and the different lines of treatment chosen by the attending spine surgeons at their centres. The section ends with few literature supported guidelines in the management of surgical site infection (SSI) after spine surgery.

Keywords: Implant retention, postoperative infections,vacuum assisted closure

How to cite this article:
Upendra B, Kanna RM, Khurjekar K, Mahesh B, Badve SA. The spine clinics – Postoperative spinal infections - Clinical scenarios. Indian Spine J 2018;1:32-45

How to cite this URL:
Upendra B, Kanna RM, Khurjekar K, Mahesh B, Badve SA. The spine clinics – Postoperative spinal infections - Clinical scenarios. Indian Spine J [serial online] 2018 [cited 2023 Apr 1];1:32-45. Available from: https://www.isjonline.com/text.asp?2018/1/1/32/223446

  Introduction Top

With the ever-expanding knowledge, research, and literature available today, it seems that we ought to know the best line of management for any given clinical situation with evidence. However, when we are presented with clinical situations having many options, with no clarity on the best line of management, how do we take decisions? Do we trust our gut feelings, or rely on our best friend's opinion?

  Evidence Based Medicine Top

To minimize the wide variation in the line of management for a given clinical situation, the concept of evidence-based medicine evolved in the 1990s. Professor Archie Cochrane introduced and emphasized the concept of evidence based practice (1972).[1] McMaster University research group led by David Sackett and Gordon Guyatt established the evidence based practice methodologies, and the term “evidence based” was first used in 1990 by Eddy.[2] Evidence based medicine advocates decisions and policies to be based on scientific evidence and not just on individual experiences and beliefs of practitioners or experts. However, having the highest level of evidence (Level I – randomized controlled trials) is not always feasible in the field of spine surgery. The Spine Patient Outcomes Research Trial studies on lumbar canal stenosis,[3] degenerative spondylolisthesis,[4] and lumbar disc herniation [5] are one of the best available evidences in the field of spine surgery. Often, no credible evidence exists for choosing one procedure against another. Therefore, it may be safe to say that the practice of spine surgery involves a bit of “art” as a surgeon has to choose the best line of management not only from the best evidence available (or lack of it!) but also from his/her own experience, knowing what works best in his/her hands.

The section of spine clinics is being introduced to our readers to bring out the differences in the management with evidence from literature lacking clarity on the best line of management.

This edition of spine clinics brings to you few clinical situations in patients having postoperative spinal infections, where the surgeon chose a particular path of management in the best interest of the patient. The gists of four cases are presented in [Table 1]. Readers can go through any of the cases in detail, presented as clinical case situations by the authors.
Table 1: Clinical case scenarios in postoperative spinal infections – An overview

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  Clinical Scenario 1 Top

A postmenopausal 74-year-old female patient presented with chronic back pain following a trivial fall at home 10 months ago. The pain was progressively increasing in intensity and disabling her from sitting, turning in bed, or standing and walking to the restroom. She had difficulty in holding the bladder and had one or two episodes of nocturnal enuresis. She was on medications for hypertension, ischemic heart disease, and hyperthyroidism for the last 20 years.

On examination, the patient was moderately obese with thoracolumbar rounded kyphosis and focal tenderness at the thoracolumbar junction. She had no neurological deficit. She had osteoarthritis of both knee joints with no other organ system affection.


Plain radiographs revealed generalized osteoporosis, spondylotic changes in the lumbar spine, calcified aorta, and osteoporotic fractures at D12 and L1 vertebrae with thoracolumbar kyphosis [Figure 1]. Computed tomography (CT) [Figure 2] showed the presence of osteoporotic fractures at D12 and L1. Magnetic resonance imaging (MRI) [Figure 3] showed global hypointense signal changes with a linear dark signal in T1 sagittal images at L1 vertebra, indicative of pseudoarthrosis. The D12 vertebra was isointense with other vertebrae signifying a healed fracture. Although there were no cord signal changes, the retropulsed posterosuperior D12 vertebral body corner was indenting the conus medullaris. Bone mineral density studies showed a T-score of −3.94.
Figure 1: Anteroposterior (a) and lateral stress radiographs (b and c) of the thoracolumbar spine showing generalized osteoporosis, extensive spondylotic changes in the lumbar spine, calcified aorta, osteoporotic fractures at D12 and L1 vertebrae with L1 pseudoarthrosis, and thoracolumbar kyphosis

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Figure 2: Sagittal (a), coronal (b), and axial computed tomography images showing the presence of osteoporotic fractures at D12 and L1 vertebrae. The fracture at D12 appears healed with sclerosis while areas of gas shadows within the L1 vertebra and the adjacent disc spaces are present indicative of pseudoarthrosis, (c and d) show axial sections of D12 & L1 respectively

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Figure 3: Whole spine sagittal T2 images (a) showing the presence of osteoporotic fractures at D12, L1. Sagittal T1 image (b) showing global hypointense signal changes with a linear dark signal at L1 vertebra indicative of pseudoarthrosis. The retropulsed posterosuperior vertebral body D12 corner is seen indenting the conus medullaris in the axial image (c)

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The patient was counseled about pseudoarthrosis, progressive disabling pain, and impending cord compression, and a posterior surgery with open L1 vertebroplasty and pedicle screw-based stabilization and fusion was performed [Figure 4]. She had an uneventful postoperative course. Her pain improved significantly and she regained good ambulatory status within a week of surgery. She was started on antiosteoporotic medications (Vitamin D 60k weekly for 3 months and received injection teriparatide 20 μg subcutaneous daily for 18 months) and discharged home.
Figure 4: Postoperative anteroposterior and lateral radiographs (a and b) showing good implant position and L1 vertebroplasty

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Clinical presentation

At 6 weeks postoperatively, the patient reported back with worsening thoracolumbar junctional pain, unrelieved by rest, exacerbated by movements, and affecting her sleep. There were no motor or sensory deficits. She had episodes of fever and rigors in the last 2 weeks associated with dysuria. Radiographs, MRI, CT scan, and urine and blood analysis were performed. The white cell counts (WBC) were elevated (18,000/cumm) with relative neutrophilia, and the erythrocyte sedimentation rate (ESR – 131 mm/h) and C-reactive protein levels (CRP – 125 mg/dl) were increased. The lateral radiographs showed destruction of the D10 vertebral body with peri-implant vertebral lucencies [Figure 5].
Figure 5: Radiographs at 6 weeks (a and b) showing destruction of the D10 vertebral body with peri-implant vertebral lucencies (white arrow)

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CT and MRI of the spine showed D8–D10 ill-defined permeative vertebral destruction with secondary loosening of bilateral pedicle screws. There was diffuse vertebral body and disc edema, evident by hypointense signals in T1 sequences and hyperintense signals in T2 sequences in D9 and D10 vertebrae. Posterior epidural soft tissue thickening was present at D9 level causing canal narrowing and cord indentation, but cord signal changes were absent [Figure 6]. All these features were suggestive of D9–D10 infective spondylodiscitis with cavitation at T10 level.
Figure 6: (a and b) Postoperative sagittal magnetic resonance images of the spine showing diffuse vertebral body and disc edema, evident by hypointense signals in T1 sequences (white arrow) and hyperintense signals in T2 sequences in D9 and D10 vertebrae (white arrow). (c) Sagittal computed tomography image showing D8–D10 ill-defined permeative vertebral destruction involving D10 vertebral body with secondary loosening of bilateral pedicle screws (white arrow)

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Options for management

  • Debridement with implant removal and bed rest with antibiotics
  • Debridement with implant retention and antibiotics
  • Debridement with extension of posterior instrumentation proximally and revision of loose implants
  • Anterior debridement with cage and posterior revision instrumentation.

Surgical intervention in patients with surgical site infection (SSI) typically would involve a combination of wound debridement (single or multiple), irrigation, negative suction application, implant revision, extension of instrumentation, and occasionally, additional anterior debridement and reconstruction.[6],[7] Depending on the extent of the infection and the patient's health status, an appropriate extent of surgical debridement is tailored for each patient. Debridement and irrigation are the keystones in the surgical treatment of peri-implant spine infections. The goal is to reduce the load of infective organisms while residual infection is tackled by antibiotics and host defense mechanisms.[8] Ideally, surgical debridement should be performed as early as possible which also may increase the likelihood of implant retention.[9]


The patient was planned for revision posterior instrumentation and debridement in view of extensive spondylodiscitis with instability. Anterior debridement and combined instrumentation were not undertaken in view of the morbidity involved. The surgical plan was to perform proximal screw revision, extension of instrumentation, and transpedicular vertebral debridement. Under general anesthesia and prone position, the surgical site was exposed through a standard posterior approach. There was no evidence of infection around the distal screws. Both the rods and the proximal four screws were removed. D9–D10 laminectomy was performed to decompress the cord. Thorough transpedicular debridement of the D10 vertebra was performed. The instrumentation was extended proximally to three segments. The anterior vertebral defect was packed with autologous bone grafts acquired during laminectomy. An appropriately contoured rod was placed and secured with nuts [Figure 7]. The debrided tissue was sent for histopathological examination and culture.
Figure 7: Immediate postoperative anteroposterior (a) and lateral radiographs (b) showing D9–D10 laminectomy and instrumentation extended proximally to three segments. The D10 anterior vertebral defect was packed with autologous bone grafts (white arrow)

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The patient was initiated on empirical antibiotics (cefuroxime 500 mg twice daily and amikacin 500 mg twice daily) based on antibiogram of the institution. Urine and tissue culture revealed growth of Pseudomonas aeruginosa which was sensitive to ciprofloxacin, levofloxacin, meropenem, azithromycin, piperacillin/tazobactam, polymyxin B, and colistin. She was treated with piperacillin and tazobactam (4.5 g QID) intravenously for 3 weeks, followed by another 3 months with oral levofloxacin (500 mg BD). She started showing improvement in her back pain from the 2nd week of antibiotic therapy. The blood parameters (total counts, ESR, and CRP) started normalizing and reached normal levels by the 3rd month.

Final outcome and follow-up

At 1-year follow up, the patient has remained symptom free since the last evaluation and is ambulatory. Plain X-rays showed good healing of the D10 lesion (sclerosis) with implants in the optimal position [Figure 8].
Figure 8: Final postoperative anteroposterior (a) and lateral radiographs (b) showing good healing of the D10 lesion (sclerosis) (white arrow) and implants in optimal position

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  Clinical Scenario 2 Top

A 37-year-old female was operated at another center for an L2 unstable burst fracture [Figure 9] with D12–L4 posterior pedicle screw-rod instrumentation and anterior column reconstruction using a cage [Figure 10].
Figure 9: Unstable L2 burst fracture with posterior facetal subluxation and kyphosis

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Figure 10: D12–L4 pedicle screw-rod stabilization with anterior column reconstruction using mesh cage

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The patient was mobilized on the 3rd postoperative day with improved pain. Her back pain started worsening again after 3 months. On repeat X-ray, implants were seen in situ with bone resorption around the cage [Figure 11]. The patient was given symptomatic treatment at the same center and was called for a followup after 3 months.
Figure 11: Three months postoperative radiographs showing a suboptimally placed cage with surrounding bone resorption

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At 7 months postoperatively, the patient developed a discharging sinus at the operative scar. Radiographs showed loosening and backing out of the implants with cage slipping posteriorly [Figure 12]. The patient was advised revision surgery in view of infection and implant failure, but the patient supposedly refused the revision surgery.
Figure 12: Seven months followup radiograph showing implant failure with backing out of the screws and migration of cage

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Clinical presentation

After 18 months of trauma, the patient presented to us on a wheelchair with progressive back pain and a persistent discharging sinus at operative scar for 10 months with inability to stand and walk without support for the last 2 weeks. On examination, she had grade 3 motor power in her hips and knees with grade 4 power in her ankle and toes. There were no sensory deficits, but the patient complained of straining to urinate for the past 2 weeks. Lower limb reflexes were diminished with plantars downgoing. She had no other comorbidities. Radiograph showed broken implants with proximal screw back-out, cage migration, and increased kyphosis [Figure 13].
Figure 13: Radiograph at 18 months followup showing broken pedicle screws with implant back out and kyphosis with posteriorly migrated cage

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Options for management

The authors considered the following issues while planning for further management: active discharging sinus; partial neurological deficit with early bladder involvement; internal gibbus compressing over conus; fibrosis due to earlier surgery; and complete resorption of L2 vertebra.

Further course of management was planned keeping all the above clinical issues in mind. The authors had the following dilemma while planning the revision surgery:

  1. Whether implant removal with debridement will exaggerate the deformity?
  2. Whether delaying the stabilization after debridement worsens the already deteriorating neurology?
  3. Whether and when to do a staged reinstrumentation procedure?
  4. Whether to go anterior? Or posterior? Or combined approach?
  5. How rigid and long should be the revision construct?

In literature, there have been proponents of both single-staged and multistage procedures.

Pull ter Gunne et al.[10] suggested aggressive wound and soft tissue debridement with retention of stable hardware, primary replacement of instrumentation if fixation had failed and primary closure. According to their study, 76% of deep infections were cured with single debridement. The studies by Weinstein et al.[11] and Ido et al.[12] also indicated that debridement and retention of stable implants to prevent gross instability give good results.

On the contrary, Hedequist et al.[13] stated that for complete eradication of infection, implants have to be removed as areas underneath rods and spinal anchor points leave pockets of infected tissue behind and increase the chance of reinfection. They had to revise and stabilize six patients who had loss of stability after implant removal. They recommend immediate implant removal in the first stage with debridement and revision surgery with instrumentation if necessary in the second stage. Hegde et al.[14] and Bose [15] also advised removal of the instrumentation, giving an interval for infection to settle with delayed revision instrumentation in their respective studies.


All options for the management were discussed in detail with the patient and relatives with pros and cons of each intervention. A two-staged procedure was planned after taking the patient and relatives into confidence.

Procedure one

Surgery was performed in the form of implant removal and thorough debridement [Figure 14]. Deep cultures taken during the debridement grew Staphylococcus aureus. The patient was given strict bed rest and intravenous (IV) antibiotics for 6 weeks. IV meropenem 1 g thrice a day was given for 2 weeks followed by injection linezolid 600 mg twice daily for 4 weeks since Staphylococcus in the culture was sensitive to both. Despite 6 weeks of antibiotic therapy, the patient had intermittent scanty discharge from the sinus. Fresh cultures showed no growth. The patient had persistent back pain but had no worsening of her neurology. Definitive surgery was planned at the end of 8 weeks.
Figure 14: Radiographs and magnetic resonance imaging after implant removal and conservative management showing significant sagittal malalignment and neural compression, despite strict bed rest

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Procedure two

Posterior instrumentation was done from D10 to L5 with pedicle screws, and L2 corpectomy was performed eliminating the internal gibbus with global decompression of the cord [Figure 15]. Cage filled with autologous bone graft was used for reconstruction of anterior column through posterolateral approach [Figure 16]. Sinus tract excision was performed and wound was closed in layers. Cultures showed no growth. Postoperatively, cefepime 2 g IV every 12 h was given for a week followed by oral cefixime 400 mg for another week. Sutures were removed on the 21st day keeping in the mind that it was the 3rd surgery at the same site.
Figure 15: Intraoperative picture showing global decompression of the spinal cord with kyphosis correction using posterior instrumentation and mesh cage

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Figure 16: Postoperative radiograph showing posterior long-segment stabilization, kyphosis correction, and anterior column reconstruction using cage

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Final outcome and followup

The patient gradually improved neurologically with supervised physiotherapy, regaining grade 4 power in both hip flexion and knee bilaterally at the end of 6 months. At the end of approximately 5 years since the 1st surgery and 3 years from the last definitive surgery [Figure 17], the patient is walking without support and doing all her household activities.
Figure 17: Postoperative radiograph at 3 years followup showing peri-implant lucency without any clinical consequences

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  Clinical Scenario Three Top

A 55-year old female underwent routine fenestration microdiscectomy for a L4–L5 disc prolapse at another center [Figure 18]. She developed postdiscectomy dural leak, and an attempt of dural closure had failed with persistent soakage from the wound. She was on regular dressing, but the wound leak continued for 1 month without any intervention.
Figure 18: Magnetic resonance imaging pictures of a 55-year-old female having L4–L5 left-sided posterolateral disc extrusion before undergoing microdiscectomy

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The patient developed intermittent fever which progressed to frank meningitis with rapidly deteriorating Glasgow coma scale (GCS) requiring ventilator support. The patient was shifted to our center on ventilator support. She was given grave prognosis due to septicemia, thrombocytopenia, and high-grade fever with low GCS.[16] On examination, the patient had yellowish thick purulent discharge from the operative site. Neurological examination could not be performed as the patient was sedated and ventilated with two ionotropes. No imaging was done at this time due to the grave condition of the patient. She underwent emergency debridement after counseling the relatives about the risk for life without the procedure, and the only way to reduce the microbial burden was by surgical debridement and drainage of the abscess.[10] Intraoperatively, copious thick abscess was found which was drained and sent for culture and sensitivity. On probing the dural defect, pockets of abscess drained from within the thecal sac. Roots were found to be clumped and no attempt was made to suture the dural defect. The wound was thoroughly debrided and washed with saline lavage and local vancomycin was instilled before closure. A closed drain was put without any negative suction for 5 days postoperatively. Culture grew S. aureus[17] sensitive to vancomycin, teicoplanin, linezolid, clindamycin. IV teicoplanin 400 mg twice a day and linezolid 600 mg twice daily were given for 2 weeks. She gradually showed signs of recovery and fever spikes decreased, had good urine output, and was extubated on the 3rd postoperative day. On regaining normal GCS, she had left partial foot drop with no other motor deficits. She was shifted out of the Intensive Care Unit after 10 days with no further discharge from the operative site. After the completion of IV antibiotics for 2 weeks, the patient was discharged with oral linezolid 600 mg twice daily and clindamycin 300 mg twice daily for 1 month. The patient recovered well from the episode with gradual supported walking, and sutures were removed at 14 days with good skin healing and no signs of local infection. Her neurology ankle dorsiflexion also improved gradually.

Clinical presentation

At 6 weeks postdebridement, the patient came to us with progressive difficulty in walking with significant back and leg pains for the past 1–2 weeks. The surgical wound showed no signs of infection. Her ESR and CRP which had decreased postdebridement showed an elevated level in comparison to the previous values.[18],[19] Her CT scans [Figure 19] showed L4–L5 partial endplate destruction and MRI showed enhancing soft tissue on contrast study [Figure 20] in the interbody region. Her left ankle weakness had deteriorated in the past week (2/5 from 3/5).
Figure 19: Computed tomography scans of the patient showing destruction of the endplates of L4 and L5 at 6 weeks postdebridement

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Figure 20: Magnetic resonance imaging pictures at 6 weeks showing interbody region with enhancing soft tissue on contrast study with epidural and paraspinal tracking

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Options for management [11],[14]

  1. Repeat debridement and antibiotics with brace
  2. Repeat debridement with posterior instrumentation and antibiotics
  3. Repeat debridement with posterior instrumentation + interbody cage [20] and antibiotics
  4. Anterior approach with debridement and cage + posterior instrumentation.

There had been reluctance for the use of implants in the setting of an active infection two decades ago. However, with studies supporting the beneficial results of use of instrumentation in active tuberculosis and then in nontubercular spinal infections, there has been a wider acceptance for single-stage stabilization and debridement in the setting of bony destruction and instability with active infective focus.[21]


The patient and relatives were explained about the residual infection along with bony destruction contributing to instability. She underwent surgery with pedicle screws at L3, L4, and S1 bilaterally. L5 instrumentation was attempted but was given up once we found that the screw had no hold due to destruction of L5 upper half. The interbody region was thoroughly debrided and calcium sulfate pellets mixed with vancomycin 1 g powder were packed in the interbody region to give anterior column support and also act as antibiotic carriers [Figure 21]. Culture again grew S. aureus sensitive to gentamicin, amikacin, vancomycin, clindamycin, and rifampicin.
Figure 21: Postoperative radiographs showing posterior instrumentation and interbody region filled with calcium sulfate pellets mixed with vancomycin

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She was put on IV amikacin 500 mg twice daily and linezolid 600 mg twice daily for 2 weeks with monitoring of renal functions and blood counts, and then the plan was to continue on oral clindamycin and linezolid for 4–6 weeks. The patient developed fever spikes 2 weeks postoperatively and was found to have a large gluteal abscess and very minimal discharge from the surgical site. The gluteal abscess was drained, and a repeat lavage of the surgical wound was carried out. The implants were found to be securely fixed and were not removed.[8],[9] The culture again grew S. aureus sensitive to amikacin, linezolid, rifampicin, and clindamycin. She was continued on IV linezolid 600 mg twice daily and clindamycin 300 mg twice daily for 2 weeks. Her wound healed with no further signs of infection locally or in blood parameters with no further bony destruction or implant loosening on radiographs [Figure 22]. She was discharged after suture removal with oral linezolid 600 mg twice a day for 6 weeks and then followed with oral rifampicin 600 mg once a day for 3 months.
Figure 22: Postoperative radiographs at 4 weeks poststabilization showing partial lucency in the calcium sulfate granules and minimal radiolucency around S1 screws

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Final outcome and followup

She has been under regular followup and her last followup at 3 years postoperatively showed good consolidation and fusion of the L4–L5 interbody region with no implant loosening [Figure 23]. She had regained her ankle dorsiflexion with power of 4/5 and was able to walk 2–3 km without support at the time of her final followup.
Figure 23: Three years followup radiograph showing consolidation of the calcium sulfate granules and good L4-5 interbody fusion with implant in situ

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  Clinical Scenario 4 Top

A 73-year-old male presented with back pain and progressive difficulty in standing, sitting, or walking, all worsening over the past 2 months. On examination, she had tenderness with gibbus at thoracolumbar junction. On neurological evaluation, the motor power in the lower extremities was 4/5 with minimal sensory disturbances.

The patient had a history of squamous cell carcinoma involving the lower one-third of the esophagus, treated with multiple cycles of radiation therapy a year back. The laboratory and radiology workup for the metastatic screening including 18-F-fluoro-2-deoxyglucose (FDG) positron emission tomography/CT (FDG PET CT) scan had been negative.


MRI with contrast and CT scan [Figure 24] revealed vertebral fractures at D12 and L1 levels, with retropulsion of the bone fragments causing significant spinal canal compromise. A presumptive diagnosis of D12 and L1 vertebral insufficiency fracture was made in view of complete absence of activity on a FDG PET CT scan.
Figure 24: Computed tomography and magnetic resonance imaging images showing vertebral fractures at T12 and L1 levels, with retropulsion of the bone fragments causing spinal canal compromise

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The patient was initially reluctant for any interventional treatment and was being treated with thoracolumbosacral orthosis. However, as the pain and lower extremity neurological function worsened, the patient consented for a surgical intervention after detailed counseling. Before the surgical intervention, the motor power in the lower extremities worsened to 2/5 with evidence of diffuse hypoesthesia below the T12 dermatome.

The surgical procedure involved D8–L4 posterior spinal fusion using cannulated-fenestrated pedicle screw fixation with PMMA cement augmentation [Figure 25]. The spinal cord decompression was achieved using right-sided hemilaminectomy and costotransversectomy to complete the D12 and L1 corpectomy. The corpectomy defect was filled in with a 40-mm mesh cage packed with allograft (A decision to use the allograft was made to avoid additional blood loss related to autograft harvest with the background of the preexisting anemia. In addition, local autograft could not be used due to the concern for a possible metastasis from the esophageal malignancy). Thus, adequate neural decompression could be performed simultaneously maintaining the integrity of the midline structures in addition to the left-sided lamina, facets, and the ligamentous structures. The surgical blood loss was 600 ml. The histopathological analysis of the tissue from D12 and L1 corpectomy was suggestive of an insufficiency fracture secondary to vertebral osteonecrosis and osteoporosis. The possible cause of osteonecrosis was attributed to prior radiation therapy focused on the lower third of the esophagus and the esophagogastric junction. The postoperative course was uneventful. The lower extremity neurology demonstrated steady improvement and the patient could be mobilized with walker by 2 weeks.
Figure 25: Postoperative radiographs showing cement-augmented pedicle screws with decompression and anterior column reconstruction with titanium mesh cage

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Clinical presentation

The surgical incision showed signs of delayed healing, and by 3 weeks, wound gaping was evident with the presence of infected granulation and seropurulent discharge [Figure 26]. The WBC, ESR, and the quantitative CRP levels were elevated.[19] The cultures from the wound indicated infection with methicillin-resistant S. aureus (MRSA). The patient and the family were counseled concerning the occurrence of SSI in association with wound dehiscence and delayed healing partially related to prior radiation. There was no evidence of implant failure or loosening on radiographs. Clinically, the patient had mild increase in pain without any worsening of neurology.
Figure 26: At 3 weeks, wound gaping was evident with the presence of infected granulation and seropurulent discharge

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Options for management

The treatment options included the use of systemic antibiotics, irrigation and debridement with retention of implants, use of myocutaneous flaps, promoting wound healing by secondary intention, and/or negative suction therapy.[20],[22],[23],[24] Implant removal in the absence of peri-implant bone resorption or screw back out is usually not recommended as it would make the spine unstable.[12] The management of a postoperative wound infection mandates use of a multipronged strategy. In addition to the spine surgeon, involvement of infectious disease, plastic surgeon, and the wound care team is helpful.[25],[26]

The availability of negative suction sponge therapy has added a new dimension to the treatment of complex wound infections.[27],[28] The technique uses a polyurethane foam sponge to occupy the entire wound cavity after a thorough debridement. The wound with the sponge is sealed with an adhesive film, and the suction tubing is attached to an aperture in the film. A suction of 125 mmHg is applied either continuously or in a cyclical fashion. The vacuum sponge dressing is changed every 3–4 days under sterile conditions. The negative suction therapy works by draining the infectious exudates, improving microcirculation, and promoting the growth of healthy granulation and debridement of the necrotic tissue along with bacterial clearance.[29],[30]

In wound infections following spine surgery, negative suction therapy in combination with other measures can help eradicate the infection, salvage the instrumentation and the bone graft, and achieve a sound wound healing.[26],[31] Once the infection has been eradicated, either a secondary closure could be achieved or the wound may be allowed to heal by secondary intention with extended use of negative suction therapy. Certain situations may demand a more complex management strategies including plastic surgical intervention.[32],[33]


Irrigation and debridement of the wound were carried out under general anesthesia with retention of the implants as there were no signs of implant loosening. Based on the plastic surgeon's inputs, wound vacuum therapy was chosen as a primary method of wound management leaving the surgical wound open [Figure 27]. The fascia was closed over a deep drain. The subcutaneous layer and the skin were not sutured as the approximation was under tension. The vacuum sponge was placed over the fascia with vacuum-assisted closure (VAC) dressing [Figure 28].
Figure 27: The surgical wound was left open with few stay sutures on the skin to facilitate primary application of vacuum-assisted closure dressing with no attempt made for closure of skin and subcutaneous tissues

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Figure 28: Vacuum-assisted closure dressing in situ over the wound

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IV antibiotics were initiated as per the sensitivity. IV vancomycin was administered in the dose of 20 mg/kg body weight intravenously every 12 h for 3 weeks. Complete blood count, quantitative CRP, and ESR were sequentially monitored. Appropriate dietary adjustments were made to improve the nutrition and the protein intake. Vacuum dressing changes were carried out every 3–4 days in the dressing room. Cultures were obtained every week were found to be negative by the end of 3 weeks. The patient was shifted on oral antibiotics for another 3 weeks. Oral clindamycin was administered in the dose of 300 mg every 6 h for 3 weeks. The total duration of the antibiotics was 6 weeks based on infectious disease specialist recommendations. No further antibiotics were deemed necessary as the wound cultures were negative for any pathogenic organisms.

Over a period of 3 months, the wound gradually had signs of healing with secondary intention. The wound decreased in size with the use of repeat vacuum dressings and local debridement. The wound eventually shrunk in size, and a secondary suturing was performed to complete the closure. A satisfactory wound healing was achieved approximately at the end of 5 months [Figure 29].
Figure 29: Healed surgical wound with vacuum-assisted closure and secondary closure at 5 months postoperatively

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Final outcome and followup

The patient did not experience any problems related to the wound or the spinal fixation construct during the course of the follow-up. He developed a right inter-trochanteric fracture that needed fixation at 6 months after the spinal fixation. At 1-year postspinal fixation, the patient had radiological findings of asymptomatic mild proximal junctional kyphosis due to a stable D6 vertebral compression fracture secondary to the osteoporosis [Figure 30]. At 18 months follow-up, he continued to be mobile with no spinal or wound complaints.
Figure 30: One-year followup radiographs showing proximal junctional kyphosis with D6 compression fracture

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  Editorial Comments Top

The case scenarios discussed above follow the broad principles of management in the setting of postoperative spinal infections. However, there are a few variations depending on the clinical status of the patient and the surgeon's preference.

  • All authors favored early thorough debridement with specimen for culture and sensitivity
  • Cases 1, 2, and 4 had implants in situ when the postoperative infection set in. Authors of Case 4 retained the implants as it had good bony hold with no loosening, whereas in Case 1, the authors partially removed the loosened implants and extended the instrumentation proximally even with active infection
  • On the contrary, authors in Case 2 preferred to remove the loosened implants and deferred immediate spinal stabilization, to facilitate infection control. Spinal stabilization was later performed during a subsequent staged surgery
  • Case 3 had no implants in situ at the time of active SSI, and only debridement was done during the first stage for infection control. Spinal stabilization was done at a later stage when secondary instability and bone erosions were noted
  • Although culture-specific antibiotics were used for treatment in all the case scenarios, the antibiotic regimens used by the authors was not for a uniform duration.

What does literature say?

The following are a few literature-supported guidelines in the management of postoperative SSIs – a take home from the spine clinics section:

  • Clinical features of SSI are constant and severe surgical site pain, unrelieved by rest, along with swelling, redness or discharge at the operative site [14]
  • Laboratory tests: ESR is a good marker of inflammatory process; however, CRP is the most sensitive indicator of postoperative infection.[34] The CRP usually peaks on the 3rd postoperative day and returns normal within 2 weeks after the procedure [19]
  • A raising trend of CRP and to a lesser extent of ESR is a strong indication of postoperative infection in the presence of physical signs and symptoms [14],[19],[34]
  • Imaging – MRI with gadolinium contrast gives further valuable information on the site of infection, abscess formation, and endplate or bony involvement, which in turn helps in planning the management [35]
  • Identifying type of infection (MRI for anatomical extent) is important in planning SSI management (CDC guidelines on SSI [36])

    • Superficial SSI (above fascial layer) may respond to culture-specific IV antibiotics alone [10]
    • Deep SSI (involves muscles below fascial layers, and or disc/bones) rarely responds to antibiotics alone [10],[14],[36]
    • Organ/space SSI (involves any part of the anatomy opened during an operation) rarely responds to antibiotics alone.[10],[14],[36]

  • In Noninstrumented spine-isolation of the causative organism with a CT-guided or image-guided biopsy/aspiration from the infective area [14],[37] is recommended
  • Nonoperative management requires immobilization or bracing along with organism-specific antibiotic therapy [37]
  • Postoperative discitis without vertebral involvement: Percutaneous transforaminal endoscopic debridement is an effective minimally invasive option [38]
  • If percutaneous needle culture is negative, open biopsy should be considered – empirical antibiotics are not advised except in patients with sepsis, neutropenia, or neurological deficits,[39] where surgical debridement and/or stabilization with empirical antibiotics is advised. A local, institution-specific antibiotic sensitivity/resistance pattern may be helpful in deciding on the antibiotics to be used as empirical treatment
  • Indications for surgical debridement and/or stabilization

    • Absence of clinical improvement and raising acute phase reactants (ESR, CRP) even after initiation of culture-specific antibiotics and immobilization
    • Increasing discharge or dehiscence of the incision, clinical sepsis, neurological deficits, epidural abscess, and instability from bone destruction – all favour surgical debridement and stabilization.[9],[10],[14]

Is it proper to retain or remove implants in the postoperative spinal infections?

  • Loose bone graft material, loose pedicle screws, and nonessential spinal instrumentation need to be removed [40]
  • Essential instrumentation required to maintain structural stability of the spine should be retained, and if found loose, augmentation with fresh instrumentation may be required to preserve spinal integrity [41],[42],[43]
  • Several authors have reported complete resolution of infection with retention or augmentation of spinal instrumentation, essential for maintaining structural stability, even in active spinal infections [44],[45],[46],[47]
  • In case of late infection with spinal instrumentation and solid fusion, instrumentation can be removed.[48] However, there have been instances of progression of spinal deformity after implant removal for late infections of the spine.[49]

Are there any antibiotic protocols useful in the setting of postoperative spinal infections?

  • Infectious Diseases Society of America (IDSA)[50] recommends a duration of 6 weeks of parenteral or highly bioavailable oral antimicrobial therapy for vertebral osteomyelitis in adults
  • Recent recommendations advise 8 weeks of IV antibiotic therapy for patients with resistant organisms such as MRSA.[51] IV antibiotics are chosen based on the type of causative organism and its sensitivity profile
  • There is no consensus on how long the antibiotics need to be given intravenously before switching over to oral substitutes
  • As a general guideline, it is recommended that all attempts should be made to switch over from IV to appropriate oral antibiotic therapy as soon as clinical improvement makes it possible.[52] A working knowledge of the oral bioavailability of the specific culture-sensitive antibiotic would facilitate the early switchover (advice from institutional infection control board is recommended)
  • For example, linezolid has >90% oral bioavailability and clindamycin has 60%–90% oral bioavailability and can be switched to oral forms once patient is able to take orally [53] (advice from institutional infection control board is recommended).

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18], [Figure 19], [Figure 20], [Figure 21], [Figure 22], [Figure 23], [Figure 24], [Figure 25], [Figure 26], [Figure 27], [Figure 28], [Figure 29], [Figure 30]

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