PURPOSE: To investigate the long-term histological changes in rabbit retina damaged by infusion air during vitrectomy. METHODS: Fourteen eyes of 14 rabbits were used. A standard three-port vitrectomy with artificial posterior vitreous detachment followed by fluid-air exchange was performed. After the fluid-air exchange, one side port was kept open for 30 s to freely introduce the air into the vitreous cavity under a pressure of 40 mmHg. Four weeks after surgery, indocyanine green angiography and histological examination were performed. RESULTS: At the air-infused area, indocyanine green angiography revealed the filling delay of the choroidal circulation in the early phase. The retinal surface was smooth and the internal limiting membrane was revealed to be intact by scanning electron microscopy. Light microscopy documented the thinning of the photoreceptor layer in the air-infused area. Transmission electron microscopy showed the disarrangement of the retinal pigment epithelium and loss of choriocapillaries. CONCLUSION: Infusion air during vitrectomy causes long-term outer retinal damage after surgery. Thinning of the photoreceptor cells, disarrangement of the retinal pigment epithelium and loss of choriocapillaries reflect the findings that we have observed previously in clinical cases. Visual field defect is a complication of vitreous surgery using fluid-air exchange. Although the visual field defects were observed just after surgery, abnormal fundus lesions continued to appear over time after the surgical procedure.
PURPOSE: To investigate the long-term histological changes in rabbit retina damaged by infusion air during vitrectomy. METHODS: Fourteen eyes of 14 rabbits were used. A standard three-port vitrectomy with artificial posterior vitreous detachment followed by fluid-air exchange was performed. After the fluid-air exchange, one side port was kept open for 30 s to freely introduce the air into the vitreous cavity under a pressure of 40 mmHg. Four weeks after surgery, indocyanine green angiography and histological examination were performed. RESULTS: At the air-infused area, indocyanine green angiography revealed the filling delay of the choroidal circulation in the early phase. The retinal surface was smooth and the internal limiting membrane was revealed to be intact by scanning electron microscopy. Light microscopy documented the thinning of the photoreceptor layer in the air-infused area. Transmission electron microscopy showed the disarrangement of the retinal pigment epithelium and loss of choriocapillaries. CONCLUSION: Infusion air during vitrectomy causes long-term outer retinal damage after surgery. Thinning of the photoreceptor cells, disarrangement of the retinal pigment epithelium and loss of choriocapillaries reflect the findings that we have observed previously in clinical cases. Visual field defect is a complication of vitreous surgery using fluid-air exchange. Although the visual field defects were observed just after surgery, abnormal fundus lesions continued to appear over time after the surgical procedure.