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Visual field defects after vitrectomy with fluid-air exchange
  1. Division of Ophthalmology, Department of Surgery, University of Hawaii School of Medicine, Honolulu, Hawaii and The Retina Center at Pali Momi, Kapi'olani Health, Aiea, Hawaii
  1. The Retina Center at Pali Momi, 98–1079 Moanalua Road, Suite 470, Aiea, Hawaii 96701, USA retinahi{at}

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Editor,—The paper by Cullinane and Cleary presents an excellent prospective study of peripheral visual field loss in patients undergoing macular hole surgery. The authors compared vitrectomy with complete posterior cortical vitreous peeling to limited vitrectomy with removal of cortical vitreous off the macula, but not off the optic nerve head or the peripheral retina. The authors showed a statistically significant decrease in peripheral visual field defects with the limited vitrectomy technique (0%, 0/22 patients) compared with the complete vitrectomy group (22%, 18/82 patients).

The authors postulated that this difference is due to the avoidance of traction on the optic nerve head during peeling of the posterior hyaloid, thus limiting damage to the peripapillary nerve fibre layer, which they believed would be most severe nasally because of firmer vitreopapillary attachments nasally. This explanation does not take into account the variable position of visual field defects found in other studies based on the position of the infusion cannula. If the infusion cannula is superiorly located, visual field defects occur superiorly, implicating inferior retinal damage. If the infusion cannula is inferonasal, visual field defects occur inferonasally and not inferotemporally. The inferotemporal location of field defects noted in most studies is based on the conventional placement of the infusion cannula inferotemporally in three port vitrectomy, which results in infused air directed towards the superonasal mid-peripheral retina.

Animal studies show damage to the inner limiting membrane, nerve fibre layer, and ganglion cells of the retina in the path of the pressurised air flow from the infusion cannula. This inner retinal damage could be caused by desiccation of the retina or by direct mechanical damage by the pressurised air flow. However, humidification of air did not prevent inner retinal damage in animal models, and the sharp demarcation between damaged and undamaged retina on electron microscopic studies supports the theory of direct mechanical damage to the inner retina. In addition, decreasing the infusion air pressure also decreased the risk of inner retinal damage. What I think this work by Cullinane and Gleary shows is that leaving the peripheral vitreous in place is another way of protecting the peripheral retina from mechanical damage by pressurised air flow. However, I would be concerned about the potential risk of increased postoperative retinal detachment, which was 10% in the limited vitrectomy group and 4% in the complete vitrectomy group, but was not statistically significant because of small sample size. However, this increased risk of retinal detachment was also a concern in a previous study utilising similar surgical techniques (Brian Conway, Western Association for Vitreoretinal Education Meeting, Maui, Hawaii, 1996).

Because of the studies on retinal damage by pressurised air infusion and the significance of high infusion air pressure, it would be important to know the usual infusion air pressure utilised during fluid-air exchange by the authors, and if the infusion air pressure varied at any point during the period of the study or between the two vitrectomy groups. Currently, in order to minimise retinal damage induced by pressurised air infusion during vitrectomy for any surgical indication requiring fluid-air exchange, I would recommend simply using a low infusion air pressure.


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