A 38-year-old man with longstanding low intraocular pressure (IOP) in his right aphakic eye presented with severe pain and high IOP (35 mm Hg). On examination, visual acuity was light perception. The central and peripheral portions of the iris were directly opposed to the posterior corneal surface and synechial closure of the pupil margin. B-scan ultrasonography showed posterior vitreous detachment. The patient was treated with topical cycloplegics, a topical beta-blocker, and a systemic hyperosmotic agent. After 1 week, the anterior chamber was deep centrally, with peripheral synechiae between the iris and the cornea. The IOP of the right eye was 4 mm Hg. This case is an unusual spontaneous malignant glaucoma occurring in a longstanding hypotonous eye.
From the Department of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju, South Korea.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Sang Woo Park, MD, Department of Ophthalmology, Chonnam National University Medical School and Hospital. 8 Hakdong, Donggu, Gwangju 501-757, South Korea. E-mail: email@example.com
Posted Online: October 01, 2012
Spontaneous Malignant Glaucoma in a Longstanding Hypotonous Eye
Malignant glaucoma was first introduced by von Graefe1 and is a rare condition characterized by an axially shallow or flat anterior chamber, high intraocular pressure (IOP), and eye pain not relieved by peripheral iridotomy. It can occur after a variety of ophthalmic procedures and less commonly in aphakia.2–5 This report describes a case of malignant glaucoma that occurred spontaneously in an aphakic longstanding hypotonous eye. To our knowledge, spontaneous malignant glaucoma has not been reported in a longstanding hypotonous eye.
A 38-year-old man presented with severe pain in his right aphakic eye for 3 days. His medical history was significant for longstanding low IOP in the right eye, ranging from 4 to 6 mm Hg, and light perception visual acuity following lens removal secondary to ocular trauma, which had happened 10 years previously. On examination, visual acuity was light perception in the right eye and 20/20 in the left eye. IOP was 35 mm Hg in the right eye and 13 mm Hg in the left eye. The anterior chamber was flat, and the central and peripheral portions of the iris were directly opposed to the posterior corneal surface. Fundus examination could not be performed due to synechial closure of the pupil margin (Figure 1A). B-scan ultrasonography showed posterior vitreous detachment. However, there was no choroidal detachment or hemorrhage (Figure 1B). Ultrasound biomicroscopy revealed anterior chamber flattening and forward movement of the ciliary process and the iris (Figures 1C and D).
Figure 1. (A) Pretreatment photograph of anterior segment shows flat anterior chamber and synechial closure of the pupil margin. (B) B-scan ultrasonography shows pooling of aqueous humor behind a posterior vitreous detachment and there is no choroidal detachment or hemorrhage. (C and D) Pretreatment ultrasound biomicroscopy shows a flat anterior chamber and forward movement of the ciliary processes. (E) Posttreatment photograph of anterior segment shows a centrally deep anterior chamber and peripheral anterior synechiae. (F) Posttreatment ultrasound biomicroscopy shows a centrally deep anterior chamber. C = cornea; I = iris; CP = ciliary process.
We suspected malignant glaucoma as a cause of the abrupt IOP elevation owing to the flattening of the central and peripheral chamber and fluid accumulation behind a posterior vitreous detachment. The patient was treated with topical cycloplegics (atropine sulfate 0.5% three times daily), a topical beta-blocker (timolol maleate 0.5% twice daily), and a hyperosmotic agent (15% mannitol) intravenously to reduce aqueous production and break a ciliary block. After 1 week, the anterior chamber was deep centrally, with peripheral synechiae between the iris and the cornea (Figure 1E). The IOP of the right eye was 4 mm Hg. Ultrasound biomicroscopy showed that the anterior chamber was deep centrally (Figure 1F). The patient continued to receive topical cycloplegics three times daily and a topical beta-blocker twice daily for several weeks, after which they were withdrawn gradually. On the last follow-up visit, the ocular pain had subsided, the anterior chamber was well maintained, and the IOP was maintained at 4 to 6 mm Hg.
When normal aqueous flow is impeded by apposition of the ciliary processes against the equator of the lens or anterior hyaloid, aqueous misdirection to the vitreous cavity leads to increased vitreous volume, forward displacement of the iris–lens or iris–vitreous diaphragm, anterior chamber shallowing, and increased IOP.1,2,6 We believe our patient had impeded normal aqueous flow due to longstanding ciliovitreal block and synechial closure of the pupil margin. In addition, the posterior vitreous detachment, seen in our case, can induce vitreous condensation. Anterior vitreous condensation precipitates vitreous impermeability, resulting in the trapping of aqueous humor in the vitreous cavity, as shown by B-scan ultrasonography. This process has been suggested by other investigators.6 In our case, it seems likely that the longstanding impairment of aqueous production prevented the manifestation of malignant glaucoma. Although medical treatment was successful in our case, surgical procedures such as laser photodisruption and pars plana vitrectomy are needed to disrupt the barrier to anterior aqueous flow in a medically unresponsive or recurred case. Our case shows that spontaneous malignant glaucoma can occur in a longstanding hypotonous eye if there are anatomical risk factors.
- von Graefe A. Beitrage zur pathologie und therapie des glaucoms. Arch Fur Ophthalmol. 1869;15:108. doi:10.1007/BF02721215 [CrossRef]
- Scheie HG, Ewing MQ. Aphakic glaucoma. Trans Ophthalmol Soc U K. 1978;98:111–117.
- Cashwell LF, Martin TJ. Malignant glaucoma after laser iridotomy. Ophthalmology. 1992;99:651–658.
- Kodjikian L, Gain P, Donate D, Rouberol F, Burillon C. Malignant glaucoma induced by a phakic posterior chamber intraocular lens for myopia. J Cataract Refract Surg. 2002;28:2217–2221. doi:10.1016/S0886-3350(02)01213-0 [CrossRef]
- Tomey KF, Senft SH, Antonious SR, Shammas IV, Shihab ZM, Traverso CE. Aqueous misdirection and flat anterior chamber after posterior chamber implant with and without trabeculectomy. Arch Ophthalmol. 1987;105:770–773. doi:10.1001/archopht.1987.01060060056032 [CrossRef]
- Quigley HA, Friedman DS, Congdon NG. Possible mechanism of primary angle-closure and malignant glaucoma. J Glaucoma. 2003;12:167–180. doi:10.1097/00061198-200304000-00013 [CrossRef]