What is optic atrophy caused by hyphema?

Updated: Jan 18, 2019
  • Author: David L Nash, MD; Chief Editor: Andrew A Dahl, MD, FACS  more...
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Answer

 

Optic atrophy may result from either acute, transiently elevated intraocular pressure or chronically elevated intraocular pressure; each occurrence was studied in a series of patients with hyphema in an attempt to identify predisposing factors. [11, 27]

Nonglaucomatous optic atrophy in patients with hyphema may be due to either the initial trauma or the transient periods of markedly elevated intraocular pressure. Diffuse optic pallor (and not glaucomatous cupping) is the result of transient periods of markedly elevated intraocular pressure. Pallor occurs with constant pressure of 50 mm Hg or higher for 5 days or 35 mm Hg or higher for 7 days. [6, 11]

The authors have observed numerous patients with sickle cell trait who developed a nonglaucomatous optic atrophy with relatively low elevations of intraocular pressure of 35-39 mm Hg for 2-4 days. [6] In spite of maximum medical therapy, final visual acuity was less than 20/400 in all patients. The authors continue to observe optic atrophy in patients with sickle cell trait who are referred to their institution and who have not had vigorous control of intraocular pressure and/or delay in paracentesis. Other studies indicate that patients with sickle cell hemoglobinopathies and anterior chamber hyphemas have more sickled erythrocytes in their anterior chambers than in their circulating venous blood. [28] The sickled erythrocytes obstruct the trabecular meshwork more profoundly than healthy red blood cells, and a consequent elevation of intraocular pressure occurs with lesser amounts of hyphema.

Systemic ocular hypotensive agents, such as acetazolamide and methazolamide, may not always be successful in reducing the intraocular pressure. In fact, they may be contraindicated in high or repeated dose regimens because of their possible contribution to intravascular hemoconcentration and increased microvascular sludging, both of which are detrimental in sickle cell hemoglobinopathy.

The increased intraocular pressure may not be tolerated well in these patients because of the increased susceptibility to impaired vascular perfusion within the optic nerve and the retina. Indeed, moderate elevation of intraocular pressure in patients with sickle cell hemoglobinopathy may produce rapid deterioration of visual function because of profound reduction of central retinal artery and posterior ciliary artery perfusion. [29, 30] For African American patients, the prevention of secondary hemorrhage is an especially critical factor.

Other complications associated with hyphema involve disruption of the posterior segment. These complications include, but are not limited to, choroidal rupture, macular scarring, retinal detachment, vitreous hemorrhage, and zonular dialysis. Even a case of sympathetic ophthalmia following hyphema has been reported. [31]


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