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Complications of Hyphema

Complications of traumatic hyphema may be directly attributed to the retention of blood in


the anterior chamber. In addition to glaucoma, the four most significant complications
include posterior synechiae, peripheral anterior synechiae, corneal bloodstaining, and optic
atrophy. [11, 26]

Posterior synechiae

Posterior synechiae may form in patients with traumatic hyphema. This complication is
secondary to iritis or iridocyclitis. However, they are relatively rare complications in patients
who are medically treated. Posterior synechiae occur more frequently in patients who have
had surgical evacuation of the hyphema.

Peripheral anterior synechiae

Peripheral anterior synechiae occur frequently in medically treated patients in whom the
hyphema has remained in the anterior chamber for a prolonged period, typically 9 or more
days. The pathogenesis of peripheral anterior synechiae may be due to a prolonged iritis
associated with the initial trauma and/or chemical iritis resulting from blood in the anterior
chamber. Alternately, the clot in the chamber angle may subsequently organize, producing
trabecular meshwork fibrosis that closes the angle. Both mechanisms are likely to be
involved. [6, 11]

Corneal bloodstaining

Corneal bloodstaining primarily occurs in patients with a total hyphema and associated
elevation of intraocular pressure. The following factors may increase the likelihood of
corneal bloodstaining; all of these factors affect endothelial integrity:

 Initial state of the corneal endothelium; decreased viability resulting from trauma or
advanced age (eg, cornea guttata)
 Surgical trauma to the endothelium
 Large amount of formed clot in contact with the endothelium
 Prolonged elevation of intraocular pressure

Corneal bloodstaining may occur with low or normal intraocular pressure; rarely, it may also
occur in less than total hyphemas. However, these latter 2 instances probably can be
anticipated only in eyes with a severely damaged or compromised endothelium. Corneal
bloodstaining is more likely to occur in patients who have a total hyphema that remains for at
least 6 days with concomitant, continuous intraocular pressures of greater than 25 mm Hg. [6]
Clearing of the corneal bloodstains may require several or many months. Generally, the
corneal bloodstains form centrally and then spread to the periphery of the corneal
endothelium. During resolution, corneal bloodstaining clears peripherally and then centrally,
reversing the sequence of the initial staining process.
Optic atrophy

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 effectively than healthy 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 a 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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