The Journal of Bone and Joint Surgery (American). 2006;88:2252-2257.
doi:10.2106/JBJS.E.00348
© 2006 The Journal of Bone and Joint Surgery, Inc.
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Superior Mesenteric Artery Syndrome Following Spinal Deformity Correction

Stuart V. Braun, MD1, Douglas M. Hedden, MD, FRCSC2 and Andrew W. Howard, MD, MSc, FRCSC3

1 Stuart V. Braun, MD Department of Orthopaedics, Floating Hospital for Children, Tufts-New England Medical Center, 750 Washington Street, #206, Boston, MA 02111. E-mail address for S.V. Braun: sbraun{at}tufts-nemc.org
2 Douglas M. Hedden, MD, FRCSC Stollery Children's Hospital, 2C3.65, WCM Centre, 8440 112 Street, Edmonton, AB T6G 2B7, Canada
3 Andrew W. Howard, MD, MSc, FRCSC Division of Orthopaedic Surgery, The Hospital for Sick Children, S107-555 University Avenue, Toronto, ON M5G 1X8, Canada

Investigation performed at The Hospital for Sick Children, Toronto, Ontario, Canada

The authors did not receive grants or outside funding in support of their research for or preparation of this manuscript. They did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.


Background: Superior mesenteric artery syndrome is a known complication associated with the correction of spinal deformity. Recent investigations of this disorder have focused on patient height and weight. We are not aware of any published study examining the degree of deformity, type of curve, or magnitude of correction, and to our knowledge all of the reported literature on this syndrome lacks control data. The purpose of this study was to examine the relationship between the correction of spinal deformity and the development of superior mesenteric artery syndrome in patients with scoliosis. Our hypothesis was that greater correction of spinal deformity would increase the risk of the development of superior mesenteric artery syndrome.

Methods: A case-control study was performed over a five-year period. The primary outcome measure was the development of superior mesenteric artery syndrome. The predictor variables that were considered included demographic characteristics; preoperative height, weight, and body mass index; aspects of the deformity, including curve magnitude, Lenke curve classification, and correction; and operative factors, including surgical approach, estimated blood loss, and the presence of operative hypotension.

Results: A review of the records on 364 surgical procedures for scoliosis identified seventeen cases of superior mesenteric artery syndrome. Thirty-four subjects who had had surgery for scoliosis but no superior mesenteric artery syndrome were randomly selected as controls. Eight of the seventeen subjects with superior mesenteric artery syndrome had undergone a two-stage procedure (compared with one of the thirty-four controls, p < 0.001), nine of the seventeen had had combined anterior and posterior procedures (compared with two of the thirty-four controls, p < 0.001), and seven of the seventeen had had a thoracoplasty (compared with two of the thirty-four controls, p < 0.001). No significant differences were noted between the groups with regard to demographic factors. Compared with the controls, the patients in whom superior mesenteric artery syndrome developed were shorter (by a mean of 7.1 cm, p = 0.03), weighed less (by a mean of 11.5 kg, p = 0.001), had a lower body mass index (p = 0.003), had a greater minimal thoracic curve magnitude achieved by bending (a mean of 12° greater [45° for subjects with superior mesenteric artery syndrome and 33° for controls], p = 0.015), had a lower percent correction of the thoracic curve on bending (a mean of 11% lower, p = 0.025), and had more lumbar lateralization (88%, compared with 61% in the control group, had a Lenke lumbar modifier of B or C instead of A, p = 0.008). Multivariate logistic regression analysis identified a staged procedure (odds ratio, 31.0), the lumbar modifier (odds ratio, 9.06), body mass index (odds ratio, 7.75), and thoracic stiffness (odds ratio, 6.67) as the most predictive of the development of superior mesenteric artery syndrome.

Conclusions: Preoperative identification of the risk factors described above in conjunction with preoperative nutritional maximization should be considered in order to limit the prevalence of superior mesenteric artery syndrome in patients undergoing surgical correction of spinal deformity.

Level of Evidence: Therapeutic Level III. See Instructions to Authors for a complete description of levels of evidence.


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