The Circulasome: A Unifying Theory of Flap Vascularity

Summary:

Despite the critical roles of nondominant perforators, choke vessels, and direct and indirect linking vessels in flap vascularity, current models of flap perfusion focus on a primary large caliber perforators. The delay phenomenon, microvascularization, neovascularization, and vascular evolution, which depend on smaller caliber vessels, remain unaccounted for. We propose that the “circulasome” consists of the sum of the entire vascular components of a given region, such that the region is supplied by a primary supplying vessel. The circulasome represents one of the indices of flap supply and is proportional to the angiogenic potential of the region and the vascular substrate capable of promoting growth of vascular networks. By accounting for both the primary flap supplying vessel and secondary vascular structures, the circulasome provides a unifying explanation for neovascularization, delay phenomenon, angiosome and perforasome theories, and vascular evolution in flaps.

Takeaways

Question: Nondominant perforators, choke vessels, and direct and indirect linking vessels are critical in flap vascularity, yet current models of flap perfusion focus on primary large caliber perforators. The delay phenomenon, neovascularization, and vascular evolution, which depend on smaller caliber vessels, remain unaccounted for.

Findings: The “circulasome” is the sum of the entire vascular components of a region, such that the region is supplied by a primary supplying vessel. Higher vessel substrate promotes growth of vascular networks.

Meaning: The circulosome theory unifies the angiosome theory, perforasome theory, delay phenomenon, and contribution of nonprimary vascular supply to flap perfusion.

INTRODUCTION

The major consideration for pedicle or perforator flaps is a large caliber hemodynamically robust supplying vessel. This has been mainly justified by the Pouiselle law which states that flow is proportional to radius to the fourth power. These concepts derived from various mathematical formulae have been applied to quantitate flap circulation.^1,2

The “angiosome” concept suggested that source vessels supply a block of tissue and are bounded by reduced caliber choke vessels or nonreduced caliber true anastomoses.^3,4 The “perforasome” theory refined this concept and suggested each perforasome is linked to adjacent perforasomes by indirect and direct linking vessels which can be small or large caliber, such that there is collateral flow between perforators in events of vascular injury.⁵ Also, the perforasome theory stated that perforasomes are supplied preferentially by their source artery, and secondarily contributed to by perforators of adjacent source arteries, connected by linking vessels.⁵ The vasculosome theory suggested that a feeder vessel may perfuse a “vascular axis” consisting of adjacent perforators, connected by channels.⁶

Despite the crucial role of smaller caliber linking and choke vessels, flap design predominantly focuses on the primary supplying vessels. These secondary vascular structures, often considered intrinsic to the flap, minor, and less susceptible to surgical intervention, remain largely unaccounted for in models of flap vascularization. Furthermore, certain functional observations remain unaccounted for, suggesting the lack of a unifying explanation for flap vascularity.

First, random flaps and grafts depend on microvascular inosculatory growth for blood supply. Significant disruption of blood supply and direct flow occurs during surgery involving random flaps and grafts. Their success, despite lack of a central large caliber blood supply, suggests a substantial and nonnegligible contribution of microvascularization to tissue blood supply.

Second, during flap dissection, microvascular networks from vascular beds that are small and therefore nonamenable to surgical manipulation, are disrupted, leading to a generally unaccounted loss of blood supply and drainage to the flap. Although no studies have quantified this in pedicled flaps, it is plausible that total flap blood supply is decreased once a flap is dissected and maintained on the pedicle. The pedicle is sufficient, in most cases, to maintain most of the flap viability. However, expected rates of flap failure and edge necrosis suggest that single large caliber pedicles may not always be entirely sufficient.

Third, during the delay phenomenon, flap isolation on axial blood supply dilates and promotes vascular maturation of choke vessels into true anastomoses. On the molecular level, the delay procedure leads to hypoxia, which induces hypoxia-inducible factor 1-alpha that subsequently leads to the production of vascular endothelial growth factor, which depends on the vascular substrate present to drive vascularization,⁷ including choke zone vascularization.⁸ The modulation of choke vessels during delay occurs between 48 and 72 hours⁹ and represents the proangiogenic response. Therefore, the delay phenomenon, and its success in reducing flap failure, suggests that beyond the caliber of the supplying pedicle, microvascular growth and vascularization contribute significantly to flap vascularity.

Furthermore, there is significant vascular evolution, maturation, and adaptation that occur within flaps beyond the primary supplying vessel. The mathematical models thus far focus on the dimensions of the primary supplying vessel and exclude such biological phenomenon.

IDEA

We propose that in addition to the primary supplying vessel, secondary vascular structures, inclusive of nondominant perforators, the choke system, and linking vessels, are critical in flap adaption and vascular evolution. This theory proposes the following principles.

The first principle is that the circulasome consists of the sum of the entire vascular components of a given region, such that the region is supplied by a primary supplying vessel. The circulasome represents one of the indices of flap supply and is proportional to the angiogenic potential of the region and the vascular substrate capable of promoting growth of vascular networks.

The second principle is that circulasomes with higher vascular density, as measured, estimated, or calculated by vessel surface area or volume, have the highest angiogenic potential and available vascular substrate, and will facilitate the conversion of choke systems to true anastomoses. Additionally, the increased vascular substrate enables neovascularization. Vessel surface area $[\mathrm{\Sigma }(2\pi r\times l)]$ and vessel volume [$\mathrm{\Sigma }(\pi r^2\times l)$] both remain proportional to radius to the fourth power. Therefore, according to the circulasome principle, the largest caliber perforator or pedicle is the primary supplying vessel for a flap, consistent with previous models.

Practically, the flap intrinsic vascularity is difficult to measure by computed tomography angiography. Formal arteriography is likely too invasive and impractical routinely. However, power Doppler ultrasound can delineate networks (Fig. 1). Figure 1A, B demonstrates evaluation of functional vascular density of a circulasome. Figure 1C, D demonstrates functional flow between two circulasome territories connected by large caliber anastomoses distally and small caliber vessel linking vessels proximally.

Fig. 1.

Use of power Doppler ultrasound to delineate circulasomes in a sample deep inferior epigastric perforator. Power Doppler demonstrates functional vascular density (A) of a circulasome [ellipse in (B)]. Power Doppler demonstrates functional flow (C) between two circulasome territories with perforators connected by large caliber anastomoses distally [vertical ellipses in (D)] and small caliber vessel linking vessels proximally [horizontal ellipse in (D)].

The third principle is that inclusion of nondominant perforators in the flap may add increased vessel substrate for additional linking vessels to form between perforasome circulations, thus establishing more robust circulasomes and enabling increased neovascularization. Figure 2 demonstrates potential neovascularization occurring between proximal regions of dominant and nondominant perforators, and distal indirect and direct linking vessels. Practically, by cutting the nondominant perforator farthest from the flap, and fixing the ligated vessel under the flap, higher density of vascular substrate may be retained in the flap, contributing to neovascularization via interperforator networks and collateral to distal networks.

Fig. 2.

Potential neovascularization occurring between vascular structures. The dominant perforator (A), nondominant perforators (B), and choke vessels (C) are depicted. Neovascularization may form between proximal regions of dominant and nondominant perforators (D), and distal indirect and direct linking vessels (E). Figure created with BioRender.com.

DISCUSSION

The circulasome theory unifies the angiosome theory, perforasome theory, vasculosome theory delay phenomenon, and contribution of nonprimary vascular supply to flap perfusion. The circulasome theory posits that the entire sum of vascular components of a region determines angiogenic potential. A higher choke vessel density logically leads to larger interperforasome or interangiosome perfusion. A larger vascular density also increases the potential and substrate for neovascularization.

The circulasome theory addresses flap vascular evolution, by accounting for both choke vessel dynamics and neovascularization while maintaining the principle of a large hemodynamically robust perforator as the primary flap supply. The use of power Doppler is innovative and consistent with the growing use of technologies in plastic surgery.¹⁰ Further clinical and radiologic studies are required to demonstrate the circulasome theory, particularly in raised flaps.

DISCLOSURE

The authors have no financial interest to declare in relation to the content of this article.