Traumatic hyphema occurs most commonly in young men, as this demographic experiences more ocular trauma than any other. Trauma causes posterior displacement of the lens–iris interface with equatorial scleral expansion. The increase in equatorial diameter stretches the major iris arterial circle, arterial branches of the ciliary body, and/or recurrent choroidal arteries and veins. The hyphema results from injury to the vessels of the peripheral iris, iris sphincter, or anterior ciliary body (Fig 14-18). The bleeding may be so subtle that it can be detected only as a few circulating red blood cells on slit-lamp examination (microscopic hyphema; Fig 14-19), or it may form a clot in the anterior chamber (layered hyphema; Fig 14-20). Alternatively, the bleeding may be severe enough to fill the anterior chamber completely. The prognosis for traumatic hyphema is generally good and is independent of the size of the hyphema, as long as no additional complications are present. Even total, or eight-ball, hyphemas (Fig 14-21) can resolve without sequelae. Traumatic hyphema is frequently associated with corneal abrasion, anterior uveitis, and mydriasis, as well as with simultaneous injuries to the angle structures, lens, posterior segment, and orbit.
Figure 14-17 Ultrasound biomicroscopy of cyclodialysis.
(Courtesy of David Rootman, MD.)
Figure 14-18 Mechanism of hyphema and blunt force injury to the eye. Blunt force applied to the eye displaces the aqueous volume peripherally, causing an increase in hydraulic pressure at the lens, iris root, and trabecular meshwork. If this “wedge of pressure” exceeds the tensile strength of ocular structures, the vessels in the peripheral iris and the anterior ciliary body may rupture, leading to hyphema. The force may cause scleral ruptures, typically at the limbus and posterior to the muscle insertions, where the sclera is thinner and unsupported by the orbital bones. Severe trauma leads to lens subluxation, retinal dialysis, optic nerve avulsion, and/or vitreous hemorrhage.
(Illustration by Cyndie C.H. Wooley.)
Figure 14-19 Microscopic hyphema with blood on the endothelial surface following blunt trauma.
(Courtesy of Woodford S. Van Meter, MD.)
Figure 14-20 Layered hyphema from blunt trauma.
Spontaneous hyphema (ie, a hyphema that occurs without any history of trauma) is much less common and should alert the examiner to the possibility of rubeosis iridis (mainly central retinal vein obstruction and diabetic retinopathy), clotting abnormalities, herpetic disease, or intraocular lens (IOL) problems. Juvenile xanthogranuloma, retinoblastoma, iris vascular hamartomas, and leukemia are associated with spontaneous hyphema in children.
Figure 14-21 Total, or “eight-ball,” hyphema.
The major concern after a traumatic hyphema is rebleeding, which is seen in less than 5% of cases. Rebleeding usually occurs between 3 and 7 days after injury as a result of clot lysis and retraction. A complication associated with rebleeding is elevated IOP (seen in 50% of patients), which can potentially lead to glaucoma and optic atrophy.
The combination of elevated IOP, corneal endothelial damage, and blood in the anterior chamber can result in corneal blood staining (Fig 14-22A). Red blood cells within the anterior chamber release hemoglobin that penetrates the posterior corneal stroma, where it is absorbed by keratocytes. Within the keratocytes, breakdown of the hemoglobin into hemosiderin can result in the death of the keratocytes. It may be difficult to detect when blood is in apposition to the endothelium on slit-lamp examination; however, close observation reveals early blood staining as yellow granular changes and reduced fibrillar definition in the posterior corneal stroma. Blood staining can lead to a reduction in corneal transparency that may be permanent. Histologically, red blood cells and their breakdown products can be seen within the corneal stroma. Corneal blood staining often clears slowly, starting in the periphery (Fig 14-22B).
Medical management of traumatic hyphema
The treatment plan for traumatic hyphema should be directed at minimizing the possibility of secondary hemorrhage, controlling inflammation, and mitigating elevated IOP. It is essential that the patient wear a protective shield over the injured eye; restrict physical activity; elevate the head of the bed; and be observed closely, with daily observation initially. To reduce the risk of rebleeding, nonaspirin analgesics should be used for pain relief; however, even nonsteroidal anti-inflammatory medications can increase the risk of rebleeding. Most patients can be managed on an outpatient basis, but if satisfactory home care and outpatient observation cannot be ensured, admission to the hospital may be required.
Most ophthalmologists administer long-acting topical cycloplegic agents initially to control inflammation and improve patient comfort, facilitate posterior segment evaluation, and eliminate iris movement. Topical corticosteroids are beneficial in controlling anterior chamber inflammation and preventing synechiae formation, and they may play a role in preventing rebleeding. Oral corticosteroids are controversial in the treatment of hyphema but may be used to facilitate the resolution of severe inflammation and/or to prevent rebleeding.
A, Dense corneal blood staining after a traumatic hyphema. B, Clearing of central corneal blood staining.
(Courtesy of Robert W. Weisenthal, MD.)
Aggressive treatment of elevated IOP is important to reduce the risk of corneal blood staining and optic atrophy. Topical antihypertensive agents (β-blockers and α-agonists) are the mainstay of therapy, although intravenous or oral hyperosmotic agents may occasionally be required. If medical management fails to control IOP, surgical evacuation of the blood may be required in order to reduce the risk of permanent corneal blood staining.
Antifibrinolytic agents (eg, aminocaproic acid, tranexamic acid, prednisone) were previously thought to reduce the incidence of rebleeding, but studies have shown no statistical improvement in visual outcome. Because these agents can have significant adverse effects (eg, nausea, vomiting, postural hypotension, muscle cramps, conjunctival suffusion, nasal stuffiness, headache, rash, pruritus, dyspnea, toxic confusional states, and arrhythmias), they are rarely used today in the treatment of hyphema.
Gharaibeh A, Savage HI, Scherer RW, Goldberg MF, Lindsley K. Medical interventions for traumatic hyphema. Cochrane Database Syst Rev. 2013;(12):CD005431.
Surgical intervention in traumatic hyphema
Surgery should be performed at the earliest definitive detection of corneal blood staining. Some authors suggest that surgery is indicated when IOP is higher than 25 mm Hg on average for 5 days with a total hyphema or when IOP is higher than 60 mm Hg for 2 days. Patients with preexisting optic nerve damage or sickle cell hemoglobinopathies may require earlier intervention. Indications for surgical intervention are summarized in Table 14-4.
The simplest way to surgically treat a persistent anterior chamber clot is anterior chamber irrigation with balanced salt solution through a limbal paracentesis. The goal is to remove circulating red blood cells that may obstruct the trabecular meshwork; removal of the entire clot is neither necessary nor wise because of the risk of a secondary hemorrhage. The irrigation procedure can be repeated. If irrigation is not successful, the irrigation/aspiration handpiece, used in cataract surgery, may be effective. The use of a cutting instrument or intraocular diathermy may be necessary in severe cases. Iris damage, lens injury, endothelial cell trauma, and additional bleeding are potentially serious complications of surgical intervention.
Table 14-4 Indications for Surgical Intervention in Traumatic Hyphema
Sickle cell complications
When a traumatic hyphema develops in an African American patient, a sickle cell workup should be performed to investigate the possibility of sickle cell hemoglobinopathy. Patients with sickle cell disease and carriers of the sickle cell trait are predisposed to sickling of red blood cells in the anterior chamber. Because sickle cells have restricted outflow through the trabecular meshwork, they may raise IOP dramatically. In addition, the optic nerve seems to be at greater risk of damage in patients with sickle cell disease, even those with modest IOP elevation, presumably as a result of a decrease in blood flow to the optic nerve.
The clinician must make every effort to control elevated IOP in these patients. Carbonic anhydrase inhibitors and osmotic agents reduce aqueous pH and lead to hemo-concentration, both of which may exacerbate sickling of red blood cells. For this reason, carbonic anhydrase inhibitors should be avoided in sickle cell patients. Surgical intervention is recommended if average IOP remains 25 mm Hg or higher after the first 24 hours or if there are repeated, transient elevations, with IOP higher than 30 mm Hg for 2–4 days, despite medical intervention.
Bansal S, Gunasekeran DV, Ang B, et al. Controversies in the pathophysiology and management of hyphema. Surv Ophthalmol. 2015;61(3):297–308.
Campagna JA. Traumatic hyphema: current strategies. Focal Points: Clinical Modules for Ophthalmologists. San Francisco: American Academy of Ophthalmology; 2007, module 10.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.