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Hyphema with traumatic iritis and increased IOP: The patient has a hyphema with traumatic iritis and an acute increase in IOP. Postinjury accumulation of blood in the anterior chamber can be a sign of major intraocular trauma with associated damage to vascular and other intraocular tissues. Blunt trauma to the globe results in tears to the ciliary body, iris, and other anterior segment structures. These tears cause shearing of blood vessels, including those that make up the major arterial circle of the anterior segment and are responsible for hyphema formation. The potential for secondary hemorrhage and persistent elevations in IOP can result in poor final visual result.
Symptoms of hyphema include pain and photophobia. The patient's visual acuity can be affected as a result of obstructing cells and blood. Initially, the IOP can markedly rise, as in this case, because of the disruption of the normal egress of aqueous humor into the trabecular meshwork from clogging by red blood cells and their byproducts or from direct trauma to the meshwork itself from the initial trauma.
Regarding the management of acute traumatic hyphema, first assess for concomitant injuries (eg, globe rupture, intraocular foreign body) that require emergency consultation with an ophthalmologist. If no emergency associated injuries exist, the goal of acute management is minimizing the risk of rebleeding and decreasing any pathologic increase in IOP. Rebleeding can occur with any activity that places additional shear forces on the affected blood vessels. Patients should avoid activities such as reading, tasks requiring excessive eye movements, or moving between different lighting conditions, which may cause papillary play (ie, the normal constriction and dilation of the iris in response to light). A long-acting cycloplegic agent, such as atropine or cyclopentolate (ophthalmic) can eliminate accommodation and dilate the pupil to desired effect. Topical steroids can help with associated iritis.
IOP above 24-30 mm Hg should be treated. The hyphema should be allowed to layer. Pharmacologic therapy with a topical beta-blocker (which decreases the production of aqueous humor) should be initiated. Use of carbonic anhydrase inhibitor agent, which rapidly decreases the production of aqueous humor, should be considered in patients who do not have sickle cell disease, as should an osmotic diuretic agent, such as intravenous mannitol or oral glycerol. Activities that increase IOP (eg, coughing, vomiting) should be avoided.
This patient was treated by ordering bed rest, elevating the head of the bed, and administering a topical beta-blocker and a carbonic anhydrase inhibitor. The hyphema decreased in volume and became layered by gravity (bottom image). In addition, his posttherapeutic IOP was 19 mm Hg, which made surgical washout of the anterior chamber unnecessary. A hard eye patch was placed, and follow-up with an ophthalmologist was arranged for the next morning.
Hyphema or glaucoma does not usually result in an APD unless the optic nerve is damaged as a result of persistent or marked elevations in IOP. Reducing this pressure on an emergency basis can help preserve the vision of patients with a hyphema and associated elevations in IOP.
For more information about hyphema, see the eMedicine articles Hyphema and Glaucoma, Hyphema (within the Ophthalmology specialty) and Eye Injuries (within the Consumer Health specialty).
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