Intraoperative management of suspected ocular venous air embolism (OVAE) during vitrectomy for retinal detachment

Sep 28, 2026

Rare ocular venous air embolism (OVAE) can occur during pars plana vitrectomy for retinal detachment and may be fatal. A 57-year-old patient undergoing 23-gauge vitrectomy developed abrupt hemodynamic instability during air-fluid exchange, with falling end-tidal CO2 and oxygen saturation suggesting air embolism, likely from suprachoroidal air entry after trocar displacement. Immediate cessation of air infusion, internal tamponade, cardiovascular support, and surgical revision stabilized hemodynamics. Postoperative imaging supported right heart strain, while retinal detachment was treated successfully without long-term systemic or ocular complications.

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CategoryHealthcare

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American Journal of Ophthalmology Case Reports 41 (2026) 102485 Contents lists available at ScienceDirect American Journal of Ophthalmology Case Reports journal [homepage:](homepage: www.ajocasereports.com/)[ www.ajocasereports.com/](homepage: www.ajocasereports.com/) Intraoperative management of suspected ocular venous air embolism (OVAE) during vitrectomy for retinal detachment Alireza Helal Birjandia,* , Ermioni Panidou-Marschelkea, Lisa-Marie Horn b, Kilian Arltb, Carsten Frammea, Jan Todea a Universit¨atsklinik für Augenheilkunde, Medizinische Hochschule Hannover (MHH), Germany b Klinik für An¨asthesiologie und Intensivmedizin, Medizinische Hochschule Hannover (MHH), Germany | A B S T R A C T | | --- | | Objective: report a rare case of ocular venous air embolism (OVAE) occurring during pars plana vitrectomy for retinal detachment and to highlight key intraoperative management steps that led to a successful outcome.
Observations: A 57-year-old patient undergoing 23-gauge vitrectomy developed abrupt hemodynamic instability during air-fluid exchange. Intraoperative signs—including sudden drops in end-tidal CO2 and oxygen saturation—prompted suspicion of air embolism, likely due to suprachoroidal air infusion via a dislodged trocar. Immediate cessation of air infusion, internal tamponade, cardiovascular support, and surgical revision of the infusion system stabilized the patient. Postoperative imaging supported right heart strain consistent with venous air entry. The retinal detachment was successfully treated, and the patient recovered without long-term systemic or ocular complications.
Conclusion: This case underscores the potentially fatal risk of OVAE during vitrectomy and the importance of early recognition, prompt intervention, and secure cannula placement. Increased awareness and surgical vigilance are critical for prevention and management of this underreported complication. | 1. Case presentation A 57-year-old male presented with a macula-off rhegmatogenous retinal detachment from 8:00 to 3:30 and, with a horseshoe tear at 2:00, two weeks of progressive symptoms, acute central vision loss since the previous day, and an incipient cataract. Best-corrected visual acuity was hand motion in the right eye. Intraocular pressure (IOP) was normal. Combined phacoemulsification, intraocular lens implantation, and 23G vitrectomy under general anesthesia were scheduled. Vitrectomy was performed via pars plana using three transconjunctival, unsutured trocar cannulas. During peripheral vitrectomy, subconjunctival fluid was observed, indicating initial cannula displacement. We assume that this fluid tracked through the unsutured sclerotomies, creating a positive-feedback loop that led to massive conjunctival edema. The resulting edema progressively loosened all three trocars, including the infusion line (Fig. 1). To evacuate the accumulated fluid, a temporal conjunctival incision was made. After trocar reimplantation, vitrectomy was completed into the far periphery. Shortly thereafter, a dome-shaped 360-degree non-hemorrhagic choroidal effusion developed (Fig. 2), with anterior chambershallowing. To stabilize the posterior segment, an air-fluid exchange was initiated. Intraoperative assessment revealed secondary displacement of the correctly reimplanted infusion cannula. Immediately, mean arterial pressure dropped to 58 mmHg, end-tidal CO2 fell from 47 to 14 mmHg, SpO2 decreased from 97 % to 73 %, and heart rate rose from 66 to 101 bpm, indicating systemic air embolism likely caused by suprachoroidalair entry via the displaced cannula. Air infusion was stopped, viscoelastic injected, FiO2 increased to 100 %, and vasopressors administered. An attempted intraoperative Echocardiography was inconclusive due to obesity and surgical position. Intraoperative inspection revealed infusion cannula displacement with presumed suprachoroidal air infusion. To decompress intraocular pressure, two posterior scle

FAQs

What triggered suspicion of ocular venous air embolism during surgery?

During air-fluid exchange, abrupt hemodynamic instability occurred alongside sudden drops in end-tidal CO2 and oxygen saturation, prompting suspicion of air embolism likely from suprachoroidal air infusion via a displaced cannula.

How was the intraoperative air embolism managed to stabilize the patient?

Air infusion was stopped, viscoelastic was injected, FiO2 increased to 100%, and vasopressors were administered. The infusion cannula was revised with a longer, sutured cannula and intraocular decompression was performed via posterior sclerotomies with air and fluid egress.

What postoperative findings supported venous air entry and what was the clinical outcome?

Echocardiography showed acute right heart strain with right ventricular dilation and septal flattening (D-sign). CT angiography excluded pulmonary embolism, and the retina remained attached under silicone oil; the patient was discharged in stable condition without long-term systemic or ocular complications.

Sep 28, 2026

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