Ligation of the anterior humeral circumflex artery ablates blood flow to the lesser tuberosity osteotomy in a cadaveric model

Abstract: Introduction A lesser tuberosity osteotomy (LTO) is commonly utilized during shoulder arthroplasty and has associated nonunion rates as high as 13%. The role of the anterior humeral circumflex artery (AHCA) in lesser tuberosity perfusion is unknown, and the purpose of this study is to better define its contribution and subsequently the effect of its ligation on perfusion to the lesser tuberosity. It was hypothesized that AHCA ligation would compromise LTO perfusion in a cadaveric model. Methods Ten cadaveric shoulders were prepared via a standard deltopectoral approach. The axillary artery was isolated and cannulated for dye injection. With the AHCA intact, 20cc of a radiopaque contrast agent was injected to visualize vasculature under fluoroscopy, this served as the specimen's evaluation of baseline vasculature. After flushing with 20 cc of normal saline, an LTO was performed, followed by 20 cc blue-dye injection to assess bleeding at the osteotomy site and 20 cc of contrast dye agent to assess radiographic pooling. The specimen was flushed again with 20 cc of normal saline and the ACHA was then ligated, followed by repeat blue dye and contrast agent injections. The outcome variables were presence of vascular perfusion of the lesser tuberosity demonstrated on fluoroscopy using the iodinated contrast dye and pooling of blue dye at the lesser tuberosity osteotomy bed pre and post ACHA ligation. Each specimen was used as its own internal control comparing the ACHA intact state and the ACHA ligated state. Results The AHCA, posterior humeral circumflex artery (PHCA), and ascending branches were visible via fluoroscopy in all control specimens. Contrast pooling at the LTO was observed with the AHCA intact in all specimens. All specimens had contrast pooling from the inferior LTO from the periosteum, and 3 (30%) also had osseous bleeding from the inferior half of the osteotomy. Following ligation of the AHCA, zero specimens had contrast pooling at the osteotomy bed (p<0.001, CI [0.0-0.28]), and zero had any flow to the lesser tuberosity from the PHCA or other contributing vessels. In all specimens, ligation of the AHCA led to disappearance of the ascending vessels seen on fluoroscopy. Discussion/Conclusion In this cadaveric model, AHCA ligation during a standard deltopectoral approach eliminated macroscopic blood flow to the LTO. Future research with advanced imaging and clinical studies are needed to assess the risk of LTO nonunion with AHCA ligation.