A Backstop for Failing Eyelid and Orbital Grafts — and What an 11-Patient Case Series Can Actually Prove

Extreme macro clinical photograph of a thin sheet of full-thickness skin graft held with fine forceps over a pale periocular surgical field under sterile cool-toned light

Reconstructive surgery around the eye works with almost no margin for error. The skin is thin, the blood supply is often already damaged by the scarring the operation is meant to repair, and a graft that fails to take does not simply mean a revision. It can mean an exposed orbital implant, a lid that no longer closes over the cornea, or a socket that will not hold a prosthesis.

That is the setting for a retrospective case series published in the October 2026 issue of International Ophthalmology. Ismail Uyanik and colleagues, working across eye departments in Diyarbakır, Bursa and Istanbul, describe eleven patients who underwent graft-based oculoplastic reconstruction and were judged to be at high risk of delayed healing or tissue loss — and who received hyperbaric oxygen therapy as an adjunct to their surgical repair.

Eleven patients, a very mixed cohort

The cohort was deliberately broad, because the patients who worry oculoplastic surgeons are rarely a tidy diagnostic group. Five had surgery to repair an exposed orbital implant sphere. The others were treated for cicatricial entropion, necrotizing scleritis, tissue loss after trauma, wound dehiscence and infection following lower-eyelid blepharoplasty, orbital cellulitis after endophthalmitis and evisceration, and delayed healing after dermolipoma excision.

All eleven had graft-supported repairs. Bacterial culture was positive in five. The authors compared patients who received ten hyperbaric sessions with those who received twenty, and reported that clinical stabilization and wound closure were achieved without the need for further major reconstructive surgery in most cases.

Then comes the finding that looks, at first glance, like an argument against the treatment. The twenty-session group took a mean of 82.6 days to recover; the ten-session group took 40.9 days. The difference was statistically significant at P = 0.032.

The authors do not read it as harm. Their interpretation is that the patients given the longer course were sicker to begin with — more severe baseline disease, more compromised tissue, more infection — and that the observation reflects that severity rather than a blunted effect of the extra sessions. That is a reasonable hypothesis. It is also unfalsifiable inside this dataset, which is the central limitation of the paper and the reason it should be read as a description of what a team did and how it went, not as evidence that more oxygen helps or hurts.

What the study cannot do

There is no control group. The treatment decisions were made by clinicians, not randomized, and the cohort is small enough that a handful of patients could move any number in either direction. The indications differ from one another so widely that pooling them into a single recovery-time comparison stretches the statistics thin.

The authors are unusually candid about this, writing that further studies are needed “to clarify patient selection criteria and define optimal HBOT protocols in oculoplastic reconstruction.” Anyone quoting the 40.9-day versus 82.6-day figure as proof that twenty sessions are wasteful — or that the therapy worked at all — is quoting a confounded retrospective.

The paper also sits inside a small existing literature rather than starting from nothing. A 2025 case series in the Journal Français d’Ophtalmologie examined the same question in oculoplastic surgery, and the idea traces back to a 1986 report in the Archives of Ophthalmology by Gonnering and colleagues on hyperbaric oxygen as an adjunct in periorbital reconstruction. What the new paper adds is a slightly larger, more contemporary cohort with a session-count comparison — not a new mechanism.

Why grafts around the eye are a plausible target

The rationale is anatomical. Grafts and flaps survive by being revascularized from their bed, and the periocular region is a place where perfusion is routinely marginal. In ischemic tissue, the failure cascade is not only hypoxia: reperfusion itself drives leukocyte adhesion and oxidative injury at the graft margin.

Stephen Thom’s review of hyperbaric oxygen mechanisms, published in Plastic and Reconstructive Surgery in 2011, lays out what pressure does that normobaric oxygen cannot — transiently inhibiting lipid peroxidation, impairing leukocyte adhesion to injured endothelium, and supporting fibroblast proliferation, collagen deposition and angiogenesis in poorly perfused tissue. Work from the early 1990s by Wayne Zamboni and colleagues used laser Doppler analysis to show improved reperfusion in ischemic axial skin flaps, one of the laboratory findings that helped move hyperbaric oxygen from diving medicine into reconstructive surgery.

A 2008 review of hyperbaric oxygen and the eye by Frank Butler and colleagues in Undersea and Hyperbaric Medicine catalogued both the ophthalmic applications and their limits, and a 2023 narrative review in the Journal of Clinical Medicine surveyed the modern ophthalmic evidence base. The recurring verdict is that the therapy is a supporting act, not a substitute for sound surgical technique and infection control.

The regulatory frame — and the counterweight

The FDA lists “preparation and preservation of compromised skin grafts and flaps” among the cleared indications for hyperbaric oxygen therapy. Devices are regulated as Class II, cleared through the 510(k) pathway under Product Code CBF. That cleared indication is what makes a series like this one clinically legitimate rather than experimental — but the FDA’s August 25, 2025 letter to health care providers is a blunt reminder of the stakes: the agency says it is aware of fires involving hyperbaric oxygen therapy devices that caused serious injuries and deaths, and it directs facilities to follow manufacturer instructions, maintain fire prevention and staff training, monitor patients, and control prohibited electrical and static-generating items. Those duties apply to every session.

Medicare’s National Coverage Determination 20.29 likewise treats the therapy as adjunctive, not primary, for compromised grafts and flaps — a coverage design that mirrors the clinical consensus that hyperbaric oxygen buys the surgeon a better environment rather than doing the surgeon’s work.

The ocular risk profile deserves its own mention, because the tissue being treated is the eye. A 2015 review by Charles McMonnies in Clinical and Experimental Optometry examined hyperbaric oxygen as a possible contributor to ocular complications and contraindications, and a 2000 survey of more than 3,300 treatment courses by Plafki and colleagues in Aviation, Space, and Environmental Medicine documented the more common adverse effects of therapy — ear and sinus barotrauma above all, but also transient visual changes and, rarely, pulmonary or central nervous system oxygen toxicity. Transient myopia after a course of treatment is well described; it is usually reversible, but it is not nothing for a patient whose vision is already fragile.

There is also a category error worth naming plainly. This case series describes 2.0-to-2.5 ATA clinical treatment in a medical facility, with a supervising physician and a chamber built to medical device standards. It has no relationship to the 1.3 ATA “wellness” lounge sessions sold for recovery and longevity, none of which the FDA has cleared for any purpose, and none of which would be a sensible way to manage a threatened eyelid graft.

What would actually settle the question

The honest summary is that eleven heterogeneous patients healed acceptably while receiving hyperbaric oxygen, and that this tells us almost nothing about whether the oxygen caused the healing. Grafts around the eye sometimes take, sometimes struggle, and sometimes fail, and a series without a comparison arm cannot separate the therapy’s contribution from good surgery, antibiotics and time.

The next step the authors themselves gesture toward is unglamorous but necessary: define which periocular grafts are truly at risk — by perfusion measurement, not by surgeon’s intuition — and then compare protocols in a prospective, ideally controlled design. Until that exists, hyperbaric oxygen in oculoplastic reconstruction remains what it has been since the 1980s: a defensible rescue option, offered case by case, documented carefully, and priced with the fire-safety and oxygen-toxicity risks of a Class II medical device in mind.

Sources

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