Macular hemorrhage as a cause of acute angle closure

Abstract

Dear Editor, It has long been known that massive retinal hemorrhages associated with exudative age-related macular degeneration (ARMD) can lead to angle closure glaucoma[1,2] that is completely unresponsive to the usual antiglaucomatous treatments.[3] The mechanism of action here is thought to be related to physical pressure pushing the lens forward, closing the angle. Massive choroidal hemorrhage has also been noted to be a cause of angle closure.[4] A literature search however did not reveal any published cases of angle closure associated with smaller macular hemorrhages. A 72-year-old retired sailor presented to our department having suffered an acute coughing fit during the abysmal performance of the Welsh rugby team against England at this year's Six Nations Championships. This led to the vision in the right eye becoming increasingly blurred such that by the end of the game he was unable to see any detailed images. After a further hour he noticed increasing pain in his right eye and presented to our eye department; where it was noted that his intraocular pressure was 59 mmHg in the affected eye, being 16 mmHg in the left eye. Visual acuity was measured at hand movements, being 6/12 in the left eye, with the anterior segment demonstrating ciliary flush, a fixed mid dilated pupil and corneal edema. The patient was also very nauseous, but did not actually vomit. His blood pressure at initial presentation measured 170/95 mmHg. Gonioscopy revealed closed angles in the right eye in which no angle structures could be identified anywhere and narrow angles of Shaffer grade I-II in the contralateral eye, in which Schwalbe's line was the only angle structure visible in two quadrants with the trabecular meshwork being identifiable in a further two quadrants. A Volk 3-mirror lens was used for gonioscopy, but indentation was not performed. Fundoscopy of the left eye revealed nothing of note other than macular drusen. He had background history of chronic obstructive pulmonary disease and hypertension, with medications including a symbicort inhaler (budesonide/formoterol) and oral aspirin 75 mg. He was also taking candesartan 8 mg, simvastatin 40 mg, and using a salbutamol inhaler on a pro re nata (PRN) basis. He was also known to be hypermetropic, with his right eye refractive error measuring +3.5 diopters and his left eye +3.0 diopters. Axial length measurements taken at a later date measured the right eye at 21.75 mm and left eye at 22.15 mm. Our patient responded well to our standard treatment for angle closure glaucoma, which consists of intravenous acetazolamide 500 mg and topical pilocarpine (2%), and latanaprost (0.005%); and after 3 h the cornea had cleared enough for bilateral yttrium-aluminum-garnet (YAG) peripheral iridotomies to be undertaken. With these measures, the pressure fell to 12 mmHg, the anterior chamber deepened, and the angle opened to a similar status as the unaffected left eye; enabling a fundoscopic examination to be performed. During this examination it was noted that there was a fresh disciform macular hemorrhage at the back of the right eye. This intraretinal hemorrhage extended to the arcades but not beyond, involving the entire macular region [Fig. 1]. There was no evidence of a choroidal effusion seen in either eye. He did not require long term topical or systemic therapy once the episode of angle closure had subsided, but his vision unfortunately did not improve beyond counting fingers despite subsequent intravitreal treatment with ranibizumab. His cough was normally under control, but it was thought that the excessive stress of watching his national rugby team perform badly had caused an abnormally severe episode. Figure 1 This picture of the patient's right fundus demonstrates the size and extent of the macular hemorrhage We suggest that in patients with narrow angles small increases in posterior segment pressure, such that can be caused by a disciform macular hemorrhage, may be sufficient to cause angle closure by transmitting pressure to the lens via the vitreous, thus closing the angle. Hypertension and coughing are postulated to be factors that played a role in causing the neovascular membrane to bleed, thus triggering the cascade. It is possible that these two events occurred by coincidence and are not linked; but as the history is strongly suggestive and the theoretical mechanism plausible, it is an interesting hypothesis to consider and more reporting needs to be done by other clinicians who may be encountering the same but not linking the two events. It should be acknowledged that rapid reduction of intraocular pressure can lead to an exacerbation of any underlying hemorrhage, although the history here suggests that the hemorrhage preceded the rise in pressure. This has not been previously described and underlines the importance of fundoscopic examination in all angle closure cases.