Ocular venous air embolism (OVAE) is an intraoperative complication during vitrectomy in which pressurized air enters the suprachoroidal space due to slippage of the infusion cannula and then enters the systemic venous circulation via the vortex veins. It is also recently referred to as Presumed Air by Vitrectomy Embolisation (PAVE)1).
The air eventually reaches the right ventricular outflow tract. This impairs gas exchange in the lungs, leading to cardiovascular collapse. A sudden drop in EtCO₂ is the first sign and can be fatal within minutes.
Thirteen cases have been reported in the literature. Of these, 9 (69%) were fatal1). Among the 9 fatal cases, 5 died in the operating room, 3 died on the day of the event, and 1 died of multi-organ failure 4 weeks later. In the 4 survivors, air infusion was promptly stopped when a drop in EtCO₂ was noted.
A survey found that only 20% of vitreous surgeons are aware of this condition 1). This low awareness is thought to contribute to its high mortality rate.
Only 13 cases have been reported in the literature, indicating an extremely low incidence. However, 69% (9/13) of reported cases were fatal, potentially making it the most lethal of all iatrogenic venous air embolisms 1).
OVAE occurs under general anesthesia, so patients do not experience symptoms themselves. The surgical team recognizes it through changes in anesthesia monitors.
Signs appear in the following order.
In the case by Helal Birjandi et al. (2026), during air-fluid exchange, the infusion cannula slipped secondarily, causing EtCO₂ to drop sharply from 47 to 14 mmHg, SpO₂ to decrease from 97% to 73%, mean arterial pressure to fall to 58 mmHg, and heart rate to rise from 66 to 101 bpm1).
Postoperative echocardiography revealed acute right heart strain with right ventricular dilation and flattening of the interventricular septum (D-sign)1). CT angiography ruled out pulmonary embolism and showed pulmonary edema1). Cardiac enzyme levels (CK, troponin T) were mildly elevated1).
The root cause of OVAE is the entry of pressurized air from the eye into the suprachoroidal space, reaching the systemic circulation via the vortex veins. The situations leading to this are described below.
In reported cases, during the use of 23-gauge transconjunctival sutureless trocar cannulas, subconjunctival fluid accumulation and conjunctival edema progressed, causing all three trocars to loosen. After reinsertion, secondary slippage occurred, leading to air injection into the suprachoroidal space 1).
Air-fluid exchange during transconjunctival sutureless vitrectomy carries the highest risk. Because the cannula is not suture-fixed, it can easily slip, and pressurized air may enter the suprachoroidal space 1). It can also occur in trauma repair and choroidal tumor resection.
The diagnosis of OVAE is primarily a clinical diagnosis based on intraoperative anesthesia monitoring findings. Postoperatively, it is confirmed by imaging tests and blood tests.
The following examinations are performed after surgery to check for the effects of air embolism.
| Examination | Findings |
|---|---|
| Echocardiography | Right ventricular dilation, D-sign |
| CT angiography | Rule out pulmonary embolism, pulmonary edema |
| Cardiac enzymes | Mild elevation of CK and troponin |
In reported cases, postoperative echocardiography confirmed acute right heart strain with right ventricular dilation and ventricular septal flattening (D-sign). CT angiography ruled out pulmonary embolism and revealed pulmonary edema1).
If sudden changes in hemodynamics occur during surgery, differentiate the following.
If OVAE is suspected, immediate action within seconds is required.
Immediate Response
Immediate cessation of gas insufflation: Stop air or gas injection immediately when OVAE is suspected.
100% oxygen administration: Increase FiO₂ to 100% to maximize oxygenation.
Trendelenburg position: Place the patient head-down to trap air in the ventricles and reduce migration to the pulmonary circulation.
Circulatory Support and Resuscitation
Vasopressor administration: Use vasoconstrictors for hypotension.
Closed-chest cardiac massage: Compress the lower sternum to expel air from the pulmonary outflow tract and improve blood flow.
Cardiopulmonary resuscitation: Initiate promptly if cardiac arrest occurs.
ECMO: If indicated, transfer to a facility equipped with extracorporeal membrane oxygenation.
In reported cases, in addition to stopping air injection, stabilization of intraocular pressure with viscoelastic injection, drainage of air and fluid from the suprachoroidal space via two posterior sclerotomies, placement of an anterior chamber maintainer, and exchange to a suture-fixed long cannula were performed. Hemodynamics stabilized within 10 minutes1).
The surgery was switched to cryocoagulation, perfluorocarbon injection, subretinal fluid drainage, and silicone oil tamponade and completed1). The patient was managed in the postoperative ICU and discharged on the second postoperative day. Visual acuity was 20/160, intraocular pressure was 14 mmHg, and the retina was attached under silicone oil1).
Immediately stop gas infusion, increase FiO₂ to 100%, and place the patient in Trendelenburg position (head-down tilt). Performing these initial steps within seconds is directly linked to survival. Administer vasopressors and cardiopulmonary resuscitation as needed, and consider transfer to a facility capable of ECMO.
The mechanism of OVAE is understood as a process in which pressurized air flows from the intraocular space into the suprachoroidal space and reaches the systemic venous circulation.
If the infusion cannula is positioned outside the vitreous cavity (in the suprachoroidal space), pressurized air is directly injected into the suprachoroidal space. This causes the vortex veins to tear, and air is transmitted to the systemic circulation via the following route.
Vortex veins → Ophthalmic vein → Cavernous sinus → Jugular vein → Right atrium → Right ventricle
Air reaching the right ventricle obstructs the right ventricular outflow tract. This impairs gas exchange in the lungs, leading to the following cascade:
Because air is injected under pressure and the eye is anatomically close to the heart, OVAE may be the most lethal of all iatrogenic venous air embolisms.
A related complication is perfluorocarbon syndrome. Perfluorocarbon liquid (PFCL) used during vitrectomy can leak into the systemic circulation through disrupted choroidal vessels and, at body temperature, transition to a gas, causing delayed pulmonary embolism.
The vapor pressure of PFCL varies by type. Perfluoro-n-octane (PFO) has a vapor pressure of 50–55 mmHg at 37°C, while perfluorodecalin (PFD) has a lower vapor pressure of 13.6 mmHg at 37°C. Unlike OVAE, it often develops several hours after surgery, with dyspnea as the initial symptom. Four cases have been reported in the literature; two who received ECMO survived, but the other two died.
