Artificial intelligence for the vascular surgeon.

In recent years, artificial intelligence (AI) has permeated different aspects of vascular surgery to solve challenges in clinical practice. Although AI in vascular surgery is still in its early stages, there have been promising developments in its applications to vascular diagnosis, risk stratification, and outcome prediction. By establishing a baseline knowledge of AI, vascular surgeons are better equipped to use and interpret the data from these types of projects. This review aims to provide an overview of the fundamentals of AI and highlight its role in helping vascular surgeons overcome the challenges of clinical practice. In addition, we discuss the limitations of AI and how they affect AI applications.

Midline-Sparing Interapophysealaminar Decompression Technique for Management of Lumbar Stenosis in Pediatric Achondroplasia.

INTRODUCTION: Achondroplasia is the most common form of short-limb dwarfism in humans, with an incidence of 1 in 25,000-40,000 live births. About one-third of achondroplasia patients will require operative intervention for lumbar spinal stenosis, generally presenting with progressive neurogenic claudication. The anatomy of the achondroplastic lumbar spine, with shortened pedicles, hypertrophic zygapophyseal joints, and thickened laminae frequently results in the development of multilevel interapophyseolaminar stenosis, while stenosis is usually absent at the mid-laminar levels secondary to pseudo-scalloping of the vertebral bodies. Treatment remains controversial, as disrupting the posterior tension band with complete laminectomies in the pediatric population puts patients at risk of developing post-laminectomy kyphosis. CASE PRESENTATION: A 15-year-old girl with achondroplasia presented to clinic with debilitating neurogenic claudication in the setting of multilevel lumbar interapophyseolaminar stenosis. We present a technical case report of her successful surgical treatment using a midline posterior tension band sparing modification to the interapophyseolaminar decompression technique proposed by Thomeer et al. [J Neurosurg. 2002;96(3 Suppl l):292-7]. CONCLUSION: We demonstrate that an adequate interapophyseolaminar decompression can be achieved through the performance of bilateral laminotomies, bilateral medial facetectomies, and undercutting of the ventral spinous process while preserving supraspinous and interspinous ligament attachments. Given the generally multilevel nature of lumbar stenosis and longer life expectancies of pediatric achondroplasia patients, decompressive surgical interventions must aspire to minimize disruption of spine biomechanics if fusion surgery is to be avoided.

Lipid Deposition Profiles Influence Foreign Body Responses.

Fibrosis remains a significant cause of failure in implanted biomedical devices and early absorption of proteins on implant surfaces has been shown to be a key instigating factor. However, lipids can also regulate immune activity and their presence may also contribute to biomaterial-induced foreign body responses (FBR) and fibrosis. Here it is demonstrated that the surface presentation of lipids on implant affects FBR by influencing reactions of immune cells to materials as well as their resultant inflammatory/suppressive polarization. Time-of-flight secondary ion mass spectroscopy (ToF-SIMS) is employed to characterize lipid deposition on implants that are surface-modified chemically with immunomodulatory small molecules. Multiple immunosuppressive phospholipids (phosphatidylcholine, phosphatidylinositol, phosphatidylethanolamine, and sphingomyelin) are all found to deposit preferentially on implants with anti-FBR surface modifications in mice. Significantly, a set of 11 fatty acids is enriched on unmodified implanted devices that failed in both mice and humans, highlighting relevance across species. Phospholipid deposition is also found to upregulate the transcription of anti-inflammatory genes in murine macrophages, while fatty acid deposition stimulated the expression of pro-inflammatory genes. These results provide further insights into how to improve the design of biomaterials and medical devices to mitigate biomaterial material-induced FBR and fibrosis.