What is the clinical presentation of elevated intraocular pressure in hyphema?

Updated: Jan 18, 2019
  • Author: David L Nash, MD; Chief Editor: Andrew A Dahl, MD, FACS  more...
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Increased intraocular pressures may accompany hyphemas of any size. Elevated intraocular pressures (>22 mm Hg) may be anticipated in approximately 32% of all patients with hyphemas at some time during their course. [11] Higher, more prolonged elevations of intraocular pressure are more commonly associated with near total or total hyphemas. Patients predisposed to glaucoma or with preexisting glaucoma and decreased facility of trabecular outflow are also more likely to develop glaucoma with a hyphema.

These highly elevated intraocular pressures occur during the acute phase of the hyphema and are separate from those related to angle recession. [16] In patients with pressure elevations, abnormal tonometric readings are frequently detected during the first 24 hours after injury. This initial period of elevated intraocular pressure is often followed by a period of normal or below normal pressure from the second day to the sixth day. Careful monitoring of the intraocular pressure is important and may determine the course of treatment. [17]

The early period of elevated intraocular pressure is probably the result of trabecular plugging by erythrocytes and fibrin. The following period of reduced pressure is most likely due to reduced aqueous production and uveitis, and hypotony may increase the chance of secondary hemorrhage. This period of reduced intraocular pressure is commonly followed by a subsequent rise in intraocular pressure, probably coincidental with the recovery of the ciliary body.

Elevated intraocular pressure then subsides with recovery of the trabecular meshwork and disappearance of the hyphema.

Exceptions include patients with a hyphema occupying greater than 75% of the anterior chamber and those with a total hyphema, in whom pressure elevation frequently has its onset simultaneously with the initial hyphema and remains continually elevated until the hyphema has had considerable resolution. When large segments of the anterior chamber angle are irreparably damaged and/or when organization of the fibrin or clot produces extensive peripheral anterior synechiae, the intraocular hypertension continues, becoming intractable chronic glaucoma.

Ghost cell glaucoma with hyphema, together with vitreous hemorrhage, may cause elevated intraocular pressure 2 weeks to 3 months after the initial injury. [18] Gradual clearing of the hyphema occurs, and erythrocytes in the vitreous cavity lose hemoglobin and become so-called ghost cells. The ghost cells then circulate forward into the anterior chamber, with resultant trabecular blockage due to the distorted, bulky configuration of the crenated red blood cell. Considerable delayed elevation of intraocular pressure may occur with ghost cell glaucoma, particularly in patients with poor facility of outflow.

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