From the Hospital Universitari de Bellvitge L’Hospitalet de Llobregat. Barcelona, Spain.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Silvia Sanz, Hospital Universitari de Bellvitge, Servei d’Oftalmologia planta 18, C. Feixa Llarga s/n, 08907 L’Hospitalet de Llobregat, Barcelona, Spain.
Decompression retinopathy is a rare complication that can occur after a sudden and marked reduction of intraocular pressure. The first description of this condition was done by Fechtner1 after a glaucoma filtering surgery. Recently, it has been reported after other ophthalmological procedures such as laser iridotomy,2,3 iridoplasty4 or 25 gauge transconjunctival sutureless vitrectomy5 in patients with previous high intraocular pressure (IOP) and even after medical resolution of an episode of acute angle closure glaucoma.6 The clinical appearance is characterized by vascular tortuosity and multiple intrarretinal and subhyaloid haemorraghes depending on the severity. In most cases, it resolves spontaneously without any visual sequelae.
We describe the case of a patient who developed an unilateral decompression retinopathy in her right eye after a Nd:YAG laser iridotomy for the treatment of an acute episode of angle closure glaucoma in both eyes and we also review the literature regarding this complication.
A 67-year-old woman came to our emergency department with a 24-hour-time history of ocular pain, red eye and blurred vision in both eyes. She also referred sick feeling with vomit. She had a past medical history of bronchial asthma treated with inhaled salbutamol. She had no evidence of hypertension or vascular disorders. She was not taking aspirin or anticoagulants. Visual acuity with correction was 2/20 (34º × −2, +3.75) in her right eye and counting fingers at 50 cm (175º × −0.75, +3.50) in her left eye. Biomicroscopy showed a microcystic corneal edema with unreactive and mild-dilated pupils and moderate cataracts in both eyes. IOP was 75 mm Hg in her right eye and 68 mm Hg in her left eye. A diagnosis of bilateral acute angle closure glaucoma was made. Intravenous medical treatment with a 20% mannitol solution was started to decrease intraocular pressure. Topical treatment with pilocarpine 2%, topical brimonidine and topical dexametasone was also started in both eyes. Two hours later IOP was lowered to 18 mm Hg in the right eye and 22 mm Hg in the left eye and after that a laser peripheral iriditomy was performed as a definitive treatment.
One week after the acute episode, visual acuity was 8/20 in the right eye and 4/20 in the left eye. The patient complained about blurred vision in her right eye. Fundus examination revealed diffuse deep retinal hemorrhages in the peripheral retina with macular involvement, and an extensive subhyaloid hemorrhage along the inferotemporal vascular arcade and the superior peripapillary area in the right eye (Fig. 1A). Left fundoscopy showed a 8/10 cup-to-disc ratio (Fig. 1b). One-month later, the hemorrhages had partially resolved in the right eye (Fig. 2). After a complete resolution of the hemorrhages, a phacoemulsification with intraocular lens implantation was performed in both eyes. Visual acuity improved to 20/20 (63º × −0.50, +0.25) in the right eye and to 8/20 (154º × −0.75, +0.50) in the left eye. After the surgery, an asymptomatic epiretinal membrane was observed in her right eye (Fig. 3).
Figure 1. (A) Right Fundus Examination Revealed Diffuse Deep Retinal Hemorrhages in the Peripheral Retina with Macular Involvement, and an Extensive Subhyaloid Hemorrhage Along the Inferotemporal Vascular Arcade and the Superior Peripapillary Area. (B) Left Fundoscopy Showed a 8/10 Cup-To-Disc Ratio Without Vascular Disorders.
Figure 2. Right Fundus Examination One Month Later the Iridotomy, with Great Resolution of Intraretinal Hemorraghes but with Subhyaloid Still Present.
Figure 3. Right Fundus Examination After Phacoemulsification Showing an Asymptomatic Epiretinal Membrane.
Decompression retinopathy is a rare ocular complication that was first reported by Fechtner1 after a trabeculectomy in a patient with an open angle glaucoma. The most frequent clinical appearance are scattered superficial and deep intraretinal hemorrhages beyond the vascular arcades. In some cases, we may also find tortuosity of retinal veins with or without optic disc edema resembling a central retinal vein occlusion but without any disturbance of retinal circulation or hemorrhages in the subhyloid space as we describe in our patient.
Fechtner1 suggested that acute lowering of IOP reduced the resistance to blood flow. When the increased blood flow is excessive, autoregulation of retinal vessels cannot tolerate the volume, which may overhelm the capacitance of the capillary bed and retinal veins, resulting in rare retinal bleeding. Defects in vascular autoregulatory mechanisms in patients with glaucoma may contribute to the intraretinal hemorrhages.8
On the other hand, retinal hemorrhages resembling central retinal vein occlusion may be explained by an anterior shift of the lamina cribosa that produces an acute blockage of the axonal transport. This abrupt packing of intra-axonal material may produce a compression of the central retinal vein resulting in vascular tortuosity and disc edema in some cases. This observation can be seen more frequently in patients with mild to moderate excavations and rarely in advanced glaucomatous damage. In our case, the patient present neither retinal vein tortuosity nor disc edema. In spite of showing a mild to moderate glaucoma with a cup-to-disc ratio of 4/10, she did not experimented a compartimental syndrome.
Although intraretinal hemorrhages and vascular tortuosity are the two vascular disorders mostly described in the literature, our patient presented an extensive hemorrhage in the subhyaloid space. Obana et al.7 suggested an hypothesis that could explain the cause of the bleeding found in our patient. In the acute phase of an angle closure glaucoma with a pupillary block, aqueous humour volume increases markedly in the posterior chamber and vitreous gel is pushed back to the posterior pole. The medical management with administration of hyperosmotic agents or carbonic anhydrase inhibitors remove fluid from the vitreous contracting it. Following iridotomy, aqueous humour flows inmediatelly from the posterior to the anterior chamber allowing the previously displaced vitreous to move forward. These two mechanisms induce a fast posterior vitreous detachment that disrupts small vessels on the surface of the retina and cause the subhyaloid hemorrhages.
It is difficult to determine common risk factors in ocular decompression retinopathy. In previous cases reported, after the resolution of an acute episode of angle closure glaucoma, patients were females belonging to the 50 to 70 years age group as our patient was. Older people have more cataract that may contribute to develop angle closure glaucoma and, moreover, acute angle closure glaucoma is more frequent in women. However, these two factors may not be true risk factors to develop a decompression retinopathy. Some vascular problems have been described in some patients such as high blood pressure2,4,7, migraine4 or even α-thalassaemia4 and, in general, aged people have more vascular fragility. Another possible risk factor is the severity of glaucomatous nerve damage. Most of the cases reported in the literature had a severe cupped disc. In contrast, our patient with a bilateral acute angle closure glaucoma only developed a decompression retinopathy in the right eye; that eye showed a mild to moderate optic neuropathy whereas the left eye had a severe glaucoma.
In most of the cases, the course of the disease was benign with spontaneous recovering and with good visual prognosis.2–4 In our patient, the hemorrhages resolved spontaneously in 4 months with good visual recovery in spite of having observed an asymptomatic epiretinal membrane in her right eye after phacoemulsification surgery.
In conclusion, decompression retinopathy is a rare complication that can occur after any procedure that produces a quick and significant reduction of IOP.1–7 As a consequence, we should employ preventive manoeuvers to achieve IOP reduction as slow as possible. Even though, our patient and other reported cases in the literature presented the decompression retinopathy after lowering IOP with medical treatment before performing a laser iridotomy. After the resolution of an acute angle closure glaucoma, we suggest to explore the posterior pole, as soon as possible, to detect this complication that can be misdiagnosed if the patient does not complain about poor vision.
- Fechtner RD, Minckler D, Weinreb RN, et al. Complications of glaucoma surgery: ocular decompression retinopathy. Arch Ophthalmol. 1992;110:965–968.
- Nah G, Aung T, Yip CC. Ocular decompression retinopathy after resolution of acute primary angle closure glaucoma. Clin Exp Ophthalmol. 2000;28:319–320. doi:10.1046/j.1442-9071.2000.00325.x [CrossRef]
- Landers J, Craig J. Decompression retinopathy and corneal oedema following Nd:YAG laser peripheral iridotomy. Clin Exp Ophthalmol. 2006;34:182–193. doi:10.1111/j.1442-9071.2006.01180.x [CrossRef]
- Lai JS, Lee VY, Leung DY, et al. Decompression retinopathy following laser peripheral iridoplasty for acute primary angle closure. Eye2005;19:1345–1347. doi:10.1038/sj.eye.6701774 [CrossRef]
- Rezende FA, Regis LG, Kickinger M, et al. Decompression retinopathy after 25-gauges transconjunctival sutureless vitrectomy: report of 2 cases. Arch Ophthalmol. 2007;125:699–700. doi:10.1001/archopht.125.5.699 [CrossRef]
- Alwitry A, Khan K, Rotchford A, et al. Severe decompression retinopathy after medical treatment of acute primary angle closure. Br J Ophthalmol. 2007;91:121. doi:10.1136/bjo.2006.100479 [CrossRef]
- Obana A, Gotho Y, Ueda N, et al. Retinal and subhyaloid hemorrhage as a complication of laser iridectomy for primary angle-closure glaucoma. Arch Ophthalmol. 2000;118:1449–1451.
- Grunwald JE, Riva CE, Stone RA, et al. Retinal autoregulation in open-angle glaucoma. Ophthalmology. 1984;91:1690–1694.