P002: DEATH BY VITRECTOMY: AN IN-VIVO PORCINE MODEL OF VENOUS AIR EMBOLISM
Howard Palte, MD; University of Miami
Purpose: In recent years there have been a number of case reports of lethal venous air embolism during the fluid/air exchange (FAX) phase of pars plana vitrectomy (PPV) surgery. The proposed mechanism involves passage of air into the suprachoroidal space, dilation of the vortex veins and escape into the systemic venous circulation. This porcine model, the first in-vivo study of the theory, affirms the migration of infused air from the suprachoroidal zone through the vortex veins en route to the central circulation and heart.
Methods: Approval was obtained from the University Animal Care and Use Committee. Under general anesthesia, PPV was performed in three eyes of two pigs. End-tidal CO2, ECG, oral trans-mucosal oxygen saturation and carotid arterial pressure were measured in real-time. Additionally, trans-esophageal echocardiography (TEE) was used to detect intra-cardiac air. A 25-gauge three port PPV and lensectomy were performed in all eyes.
Results: In two eyes, attempted infusion into the suprachoroidal space was unsuccessful. However, in the third eye the suprachoroidal space was identified and an infusion of air at 30 mm Hg was began. This resulted in the development of a large choroidal detachment. The pressure was increased to 60 mm Hg. Within 30 seconds, intra-cardiac air was detected on TEE and EtCO2 levels fell. Blood pressure and ECG changes followed approximately three minutes later with oxygen saturation plummeting at the four minute mark. The interval between increasing the infusion pressure and death was six minutes.
At autopsy, the heart was opened under water. A profuse egression of air bubbles was observed.
Conclusions: This in vivo porcine model confirms that air infused into the suprachoroidal space via a malpositioned vitrectomy cannula can produce fatal venous air embolism.