David J. Salvetti, Zachary J. Tempel, Ezequiel Goldschmidt, Nicole A. Colwell, Federico Angriman, David M. Panczykowski, Nitin Agarwal, Adam S. Kanter and David O. Okonkwo
Nutritional deficiency negatively affects outcomes in many health conditions. In spine surgery, evidence linking preoperative nutritional deficiency to postoperative surgical site infection (SSI) has been limited to small retrospective studies. Authors of the current study analyzed a large consecutive cohort of patients who had undergone elective spine surgery to determine the relationship between a serum biomarker of nutritional status (preoperative prealbumin levels) and SSI.
The authors conducted a retrospective review of the electronic medical charts of patients who had undergone posterior spinal surgeries and whose preoperative prealbumin level was available. Additional data pertinent to the risk of SSI were also collected. Patients who developed a postoperative SSI were identified, and risk factors for postoperative SSI were analyzed. Nutritional deficiency was defined as a preoperative serum prealbumin level ≤ 20 mg/dl.
Among a consecutive series of 387 patients who met the study criteria for inclusion, the infection rate for those with preoperative prealbumin ≤ 20 mg/dl was 17.8% (13/73), versus 4.8% (15/314) for those with preoperative prealbumin > 20 mg/dl. On univariate and multivariate analysis a low preoperative prealbumin level was a risk factor for postoperative SSI with a crude OR of 4.29 (p < 0.01) and an adjusted OR of 3.28 (p = 0.02). In addition, several previously known risk factors for infection, including diabetes, spinal fusion, and number of operative levels, were significant for the development of an SSI.
In this consecutive series, preoperative prealbumin levels, a serum biomarker of nutritional status, correlated with the risk of SSI in elective spine surgery. Prehabilitation before spine surgery, including strategies to improve nutritional status in patients with nutritional deficiencies, may increase value and improve spine care.
Presented at the 2016 AANS/CNS Joint Section on Disorders of the Spine and Peripheral Nerves
Ezequiel Goldschmidt, Jorge Rasmussen, Joseph D. Chabot, Gurpreet Gandhoke, Emilia Luzzi, Lina Merlotti, Romina Proni, Mónica Loresi, D. Kojo Hamilton, David O. Okonkwo, Adam S. Kanter and Peter C. Gerszten
Surgical site infections (SSIs) are a major source of morbidity after spinal surgery. Several recent studies have described the finding that applying vancomycin powder to the surgical bed may reduce the incidence of SSI. However, applying vancomycin in high concentrations has been shown in vitro to inhibit osteoblast proliferation and to induce cell death. Vancomycin may have a deleterious effect on dural healing after repair of an intentional or unintentional durotomy. This study was therefore undertaken to assess the effect of different concentrations of vancomycin on a human dura mater cell culture.
Human dura intended for disposal after decompressive craniectomy was harvested. Explant primary cultures and subcultures were subsequently performed. Cells were characterized through common staining and immunohistochemistry. A growth curve was performed to assess the effect of different concentrations of vancomycin (40, 400, and 4000 μg/ml) on cell count. The effect of vancomycin on cellular shape, intercellular arrangement, and viability was also evaluated.
All dural tissue samples successfully developed into fusiform cells, demonstrating pseudopod projections and spindle formation. The cells demonstrated vimentin positivity and also had typical features of fibroblasts. When applied to the cultures, the highest dose of vancomycin induced generalized cell death within 24 hours. The mean (± SD) cell counts for control, 40, 400, and 4000 μg/ml were 38.72 ± 15.93, 36.28 ± 22.87, 19.48 ± 6.53, and 4.07 ± 9.66, respectively (p < 0.0001, ANOVA). Compared with controls, vancomycin-exposed cells histologically demonstrated a smaller cytoplasm and decreased pseudopodia formation resulting in the inhibition of normal spindle intercellular arrangement.
When vancomycin powder is applied locally, dural cells are exposed to a concentration several times greater than when delivered systemically. In this in vitro model, vancomycin induced dural cell death, inhibited growth, and altered cellular morphology in a concentration-dependent fashion. Defining a safe vancomycin concentration that is both bactericidal and also does not inhibit normal dural healing is necessary.
Presented at the 2019 AANS/CNS Joint Section on Disorders of the Spine and Peripheral Nerves
Nitin Agarwal, Federico Angriman, Ezequiel Goldschmidt, James Zhou, Adam S. Kanter, David O. Okonkwo, Peter G. Passias, Themistocles Protopsaltis, Virginie Lafage, Renaud Lafage, Frank Schwab, Shay Bess, Christopher Ames, Justin S. Smith, Christopher I. Shaffrey, Douglas Burton, D. Kojo Hamilton and the International Spine Study Group
Obesity, a condition that is increasing in prevalence in the United States, has previously been associated with poorer outcomes following deformity surgery, including higher rates of perioperative complications such as deep and superficial infections. To date, however, no study has examined the relationship between preoperative BMI and outcomes of deformity surgery as measured by spine parameters such as the sagittal vertical axis (SVA), as well as health-related quality of life (HRQoL) measures such as the Oswestry Disability Index (ODI) and Scoliosis Research Society–22 patient questionnaire (SRS-22). To this end, the authors sought to clarify the relationship between BMI and postoperative change in SVA as well as HRQoL outcomes.
The authors performed a retrospective review of a prospectively managed multicenter adult spinal deformity database collected and maintained by the International Spine Study Group (ISSG) between 2009 and 2014. The primary independent variable considered was preoperative BMI. The primary outcome was the change in SVA at 1 year after deformity surgery. Postoperative ODI and SRS-22 outcome measures were evaluated as secondary outcomes. Generalized linear models were used to model the primary and secondary outcomes at 1 year as a function of BMI at baseline, while adjusting for potential measured confounders.
Increasing BMI (compared to BMI < 18) was not associated with change of SVA at 1 year postsurgery. However, BMIs in the obese range of 30 to 34.9 kg/m2, compared to BMI < 18 at baseline, were associated with poorer outcomes as measured by the SRS-22 score (estimated change −0.47, 95% CI −0.93 to −0.01, p = 0.04). While BMIs > 30 appeared to be associated with poorer outcomes as determined by the ODI, this correlation did not reach statistical significance.
Baseline BMI did not affect the achievable SVA at 1 year postsurgery. Further studies should evaluate whether even in the absence of a change in SVA, baseline BMIs in the obese range are associated with worsened HRQoL outcomes after spinal surgery.