Vascular Damage Caused by Internal Fixation Implants

Kenneth A. Johnson, MVSc, PhD, FACVSc, DACVS, DECVS

The four principles of surgical fracture treatment formulated by the AO (Arbeitsgemeinschaft fűr Osteosynthesefragen) in Switzerland in 1962 proved to be a revolutionary, pivotal change in our philosophy and approach to fracture treatment. These four principles were aimed at returning the fractured limb to proper shape and function. They espoused the need for (1) anatomical reduction, (2) stable internal fixation, (3) preservation of blood supply, and (4) early pain-free mobilization.[1] With the early development of a range of new fracture fixation implants for internal fixation—primarily compression plates and screws—surgeons initially were obsessed with seeing perfectly reconstructed fractures on the postoperative radiographs, and healing without callus formation. Realistically, this could only be achieved by completely ignoring the third AO principle, namely, “Preservation of the blood supply to soft tissues and bone by careful handling and gentle reduction techniques.”

Over the last 60 years, there have been only minor changes in the wording of the four AO principles. However, what changed was the realization that when the third AO principle was ignored, complications like delayed fracture healing, wound breakdown, and infection frequently ensued. Surgeons learned that the preservation of blood supply to soft tissues and bone could only be achieved by bridging fixation of nonreducible long bone fractures, instead of struggling to obtain a perfect anatomical reduction during the surgery. This transition was made possible by new technologies including locking implants, minimally invasive osteosynthesis, and computer-aided navigation.

Apart from surgeon-inflicted damage, the insertion of internal fixation implants per se can also cause inadvertent vascular damage to soft tissues and bone.[2] Recent clinical studies of canine tarsal arthrodesis found a 15% rate of plantar necrosis with this surgery.[3] It has been suggested that this complication is due to damage to the principal blood supply to the plantar region coming from the dorsal pedal artery. The study by Holroyd and colleagues published in this issue of the journal investigated this proposal.[3] The aim of their study was to define landmarks of the intermetatarsal channel of the dorsal pedal artery and to assess whether damage to the dorsal pedal artery during metatarsal screw placement in dogs undergoing tarsal arthrodesis could be a mechanism in the development of plantar necrosis. Findings of their study suggested that screws placed in the proximal 25% of the metatarsus could be violating the third AO principle, by disrupting the blood supply to soft tissues and bone in this region.[3] Further prospective studies are needed to establish if careful planning of screw insertion sites in the metatarsus can reduce the risk of this complication.

Publication History

Article published online:
11 September 2023

• References

• 1 Johnson AL, Houlton JEF, Vannini R. eds. AO Principles of Fracture Management in the Dog and Cat. Davos Platz, Switzerland: AO Publishing; 2005
• 2 Field JR. The evolving concept of indirect fracture fixation. In: Sumner-Smith G. ed. Bone in Clinical Orthopedics. 2nd ed.. Dubendorf, Switzerland: AO Publishing; 2002: 447-467
• 3 Holroyd KL, Meeson RL, Pead MJ, Mukherjee L, Ferguson JF, Kulendra E. Risk factors associated with plantar necrosis following tarsal arthrodesis in dogs. Vet Comp Ortho Traumatol 2023; 36 (05) 257-265