471 Risk Factors for Surgical Site Infections (SSIs) after Spine Operations (SOs)

Sunday, April 3, 2011
Trinity Ballroom (Hilton Anatole)
Andrew Behan, MS , University of Iowa College Public Health and Trinity Regional Medical Center, Rock Island, IL
Jean Pottinger, MA , CQSPI, University of Iowa Hospitals and Clinics, Iowa City, IA
Hsiu-yin Chiang , University of Iowa College of Medicine and College of Public Health, Iowa City, IA
Ravindhar Vodela, MBBS , The University of Iowa College of Medicine and Metro Infectious Disease Consultants, L.L.C., Hinsdale, IL
Loreen Herwaldt, MD , The University of Iowa College of Medicine, College of Public Health, and Hospitals and Clinics, Iowa City, IA
Background: SSIs after SOs cause morbidity and increase cost. Few studies have assessed risk factors for SSIs after SOs and outcomes of these SSIs.

Objective: To identify risk factors for SSIs after SOs done at the University of Iowa Hospitals and Clinics (UIHC) and outcomes of these SSIs.

Methods: We performed a case-control study with 55 cases and 220 controls that had SOs (laminectomy [lami] or spinal fusion [SF]) from 01/07 to 06/09 at the UIHC. A case was any patient who met the National Healthcare Safety Network’s definition of SSI. Controls were randomly selected from patients who had SOs but did not acquire SSIs. Data on demographic characteristics, underlying diseases, medications, operations, hospitalizations, postop clinic visits, and readmissions were abstracted from medical records. The Fisher’s exact test and t-test were used for univariable analyses and stepwise logistic regression was used for multivariable analyses.

Results: Of 55 SSIs, 80% were deep incisional or organ space; S. aureus caused 55%. Cases and controls were similar with respect to: age, smoking, diabetes, wound class, preop skin prep, incontinence, pre- and postop glucose, preop medications, and lowest intraop temperature. After controlling for the Charlson comorbidity index, insurance coverage, and the preop hemoglobin, factors independently associated with SSI after SOs were: the lowest intraop temperature (OR = 2.2; 95% confidence interval [CI]1.1, 4.2; P = .02), procedure done by a neurosurgeon (NS; OR = 3.7; 95% CI 1.6, 8.9; P = .003), posterior approach (OR = 7.1; 95% CI 2.3, 22.1; P = .0007), SF of 4-8 vertebrae (OR = 5.3; 95% CI 2.1, 13.2; P = .0004), and postop transfusion (OR = 4.2; 95% CI 1.5, 12.0; P = .008). Factors independently associated with SSIs after SF were: lower preop hemoglobin (OR = 1.7; 95% CI 1.1, 2.5; P = .008), procedure done by a NS (OR = 7.1; 95% CI 1.7, 29.8; P = .007); posterior approach (OR = 6.9; 95% CI 1.1, 42.9; P = .04), no graft done (OR = 11.2; 95% CI 1.4, 90.8; P = .02); postop transfusion (OR = 6.6; 95% CI 1.3, 32.3; P = .02); SF of 4-8 vertebrae (OR = 30.5; 95% CI 3.0, 309.8; P = .004). Lack of private insurance was the only factor independently associated with SSIs after lami (OR = 3.7; 95% CI 1.1, 12.8; P = .04). NSs were more likely than orthopedic surgeons to do SF 4-8 vertebrae (P = .005). After adjusting the overall model for SF of 4-8 vertebrae, procedures done by NSs were still associated with an increased risk of SSI but the P-value increased from .003 to .02. Compared with controls, patients with SSIs had longer postop lengths of stay (4 vs 6 days; P = .001) and were more likely to be readmitted within 30 days postop (P < .0001) and to receive antimicrobials during readmissions (P < .0001). 

Conclusions: SSIs after SOs increase healthcare use significantly. Few risk factors for SSI are easily remedied. Screening for S. aureus carriers and implementing interventions to decrease S. aureus skin contamination might reduce SSIs in patients undergoing SOs.