We strongly support the article by Lai et al1
in which the authors found African American children to be at higher risk
for developing a rebleed following a traumatic hyphema. They also found that
sickle cell hemoglobinopathy increased the risk of intraocular pressure elevation
but did not appear to increase the risk of secondary hemorrhage.
We have made similar observations at the University of Illinois Eye
and Ear Infirmary (Chicago). Even in the absence of hemoglobinopathies, the
course of hyphemas is prolonged and the incidence of rebleeding is higher
in African American patients. We hypothesized that this susceptibility might
be partly related to the release of melanin into the anterior chamber during
ocular trauma. This hypothesis was supported by our study in which we examined
the effects of melanin in a rabbit model of laser-induced hyphema.2 We demonstrated that the placement of melanin in
the anterior chamber resulted in a significantly prolonged course of hyphema.
During a histologic examination, a greater inflammatory response was observed
in the anterior chamber and trabecular meshwork in the melanin-treated eyes
than in the control eyes. Occlusion of the trabecular meshwork by melanin-laden
macrophages and other inflammatory cells was proposed as one of the mechanisms
responsible for the prolonged course of hyphema.
Lai WW, Edward DP, Tessler HH, Bhavnani VD. Risk Factors for Complications Following Traumatic Hyphema. Arch Ophthalmol. 2001;119(11):1732. doi: