Re: “Evaluation of the Microvascular Blood Flow, Oxygenation, and Survival of Tarsoconjunctival Flaps Following the Modified Hughes Procedure”
Memarzadeh et al.1 measure blood flow and oxygenation of the tarsoconjunctival flap immediately after it is sutured into place, after verapamil, and 12 hours postoperatively. Their data suggest that the blood flow and oxygenation at these time points is essentially zero. We commend the authors for an elegant design and meticulous measurements; however, we suggest that this experimental design neglects the primary mechanism that enables the survival of the full-thickness skin graft that is placed anterior to the tarsoconjunctival flap. The full-thickness skin graft completes the anterior lamellar reconstruction of a modified Hughes procedure and relies on the nutrition from the recipient tissue to survive. Initially, the skin graft is dependent upon passively absorbing nutrients from the wound bed via plasmatic imbibition.2–5 During this time, the skin graft may be ischemic for up to 48 hours, which is then followed by inosculation and capillary ingrowth.6 Many theories exist to explain revascularization, and despite the controversies, all agree that capillary perfusion and vascular ingrowth requires far more than 12 hours and typically is not present until the sixth or seventh postoperative day. We submit that if the tarsoconjunctival flap was truly avascular as indicated by this study, the full-thickness skin graft would not be capable of surviving by these known mechanisms. In our experience, we have not seen necrosis of the skin graft following a modified Hughes procedure.
We would be interested to see data regarding blood flow and oxygenation at least 2 weeks postoperatively, as at this time point, the graft survival is more likely to be dependent on capillary blood flow originating from the tarsoconjunctival flap itself, as opposed to imbibition. Indeed, when the tarsoconjunctival flap is divided several weeks later, we often note significant bleeding, which, again, would not be possible if the flap was not perfused following its transposition into the lower eyelid. The authors’ data essentially proves the aforementioned physiology of graft survival; namely, the initial perfusion of the tarsoconjunctival flap does not occur via microvascular anastomosis, but rather, the flap is initially ischemic but surviving via plasmatic imbibition.
The authors also describe the maintenance of lower eyelid vertical height when performing modified Hughes procedures. We whole-heartedly agree with this point and believe that the tarsoconjunctival flap performs a similar role to a tarsorrhaphy in providing upward pull of the lower eyelid in opposition to the natural tendency toward retraction. We have performed autogenous-free tarsconjunctival grafts similar to those described by Hawes,7 and although the grafts themselves have survived, we have observed retraction and vertical shortening of the eyelid as compared with those eyelids reconstructed with a modified Hughes flap (unpublished data). This is in contrast to the outcomes presented by Hawes et al.8 in which they found similar rates of lower eyelid retraction using free tarsoconjunctival grafts and modified Hughes flaps. In our opinion, the fact that a Hughes flap retains a direct connection to the blood supply from the upper eyelid allows for more robust healing with less atrophy of the grafted tissue.