Abstract

Category: Ankle Introduction/Purpose: Injuries to the deltoid ligament complex on the medial aspect of the ankle account for 10-15% of ankle sprains. Chronic deltoid insufficiency can lead to medial or multidirectional ankle instability, necessitating operative stabilization. Many studies have examined the anatomy of the deltoid ligament complex, with a focus on characterizing the various bands that comprise its structure. To our knowledge the vascular supply to the deltoid ligament has not been previously studied. This information may have implications in the progression of deltoid injuries to chronic insufficiency, and is an important consideration when performing operative reconstruction of the deltoid ligament. The purpose of our study was to describe the vascular supply to the deltoid ligament utilizing a method of chemical debridement with cadaveric specimens. Methods: Twenty-seven matched pairs of adult cadaver legs, fifty-four legs total, were studied. Specimens with any signs of prior trauma or surgical treatment were excluded. The legs were amputated below the knee and injected with India Ink, followed by Ward Blue Latex, in the anterior tibial, posterior tibial and peroneal arteries. Specimens were chemically debrided utilizing 6.0% sodium hypochlorite, leaving vascular casts, ligaments and bones. The vascular supply to the deltoid ligament was evaluated, photographed, and recorded. Results: The vascular supply to the deltoid ligament complex was clearly visualized in 50 of the specimens. The deltoid ligament in all 50 specimens was supplied by arterial branches from the dorsalis pedis, specifically the medial tarsal arteries. Thirty-two of the specimens (64.0%) had an additional contribution from the anterior tibial artery, while the medial tarsal arteries were the only anterior vascular supply in the remaining eighteen specimens (36.0%). Thirty-nine specimens (78.0%) had additional arterial supply to the deltoid ligament from the posterior tibial artery. In thirteen (30.0%) of these specimens, the posterior tibial artery provided the dominant arterial supply, as determined by vessel diameter. Conclusion: Deltoid injuries can become chronic, leading to recurrent ankle instability. Our study shows that the deltoid ligament complex receives a consistent arterial supply from the dorsalis pedis and anterior tibial arteries, and that this anterior vasculature is the dominant supply in the majority of specimens. A large portion of our specimens also had additional arterial supply from the posterior tibial artery. Knowledge of the arterial anatomy of the deltoid ligament complex is valuable when planning operative treatment of medial ankle, and may also provide information for future studies examining the progression of medial ankle sprains to chronic deltoid insufficiency.

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