Sports-related traumatic hyphema

Sports-related traumatic hyphema

John P. Difiori

Hyphema is the accumulation of blood in the anterior chamber of the eye. Traumatic hyphema, an injury frequently incurred in ball and racquet sports, is often first evaluated by a primary care physician. Recognition of this eye injury, skill in its initial management and an understanding of both long-term care and preventive measures will enable the physician to help patients retain good vision.

Epidemiology

Although the true incidence is not known, sports-related eye injuries are thought to account for nearly 25 percent of severe eye injuries.[1,2] Hyphema is among the most common sports-related eye injuries. The overall incidence of traumatic hyphema is 12.2 cases per 100,000 population, with approximately 37 percent of cases resulting from sports injury.[3]

In pediatric patients between 10 and 20 years of age, the majority of ocular injuries are sports-related, and hyphema is the most frequently encountered injury.[4] Sports that are most commonly associated with traumatic hyphema include baseball, softball and racquet sports (Table 1).[3,5] Traumatic hyphema in children less than 10 years of age is most often caused by a projectile object but may not be related to sports involvement[4] (Table 2).[3,6]

Etiology

Traumatic hyphema can be caused by either blunt or penetrating injury. Blunt trauma causes an increase in anterior chamber pressure, which produces a tear of the

TABLE 1

Sports Most Frequently Causing

Traumatic Hyphema

Percentage of cases

related to sport

Sport (Total cases = 127)

Baseball/softball 31

Racquetball 19

Hockey 18

Tennis 14

Basketball 3

Other 15

ciliary body or the iris and results in bleeding within the anterior chamber[7] (Figure 1). A penetrating injury can cause hyphema by directly damaging the ocular vasculature. The accumulated blood drains via the trabecular meshwork in the angle of the anterior chamber.

Classification

Hyphemas are classified according to the amount of blood in the anterior chamber (Table 3).[8,9] Approximately 70 percent of hyphemas are grade 1, in which blood fills less than one-third of the anterior chamber[9,10] (Figure 2). In grade 2 hyphema, blood fills between one-third and one-half of the anterior chamber. In grade 3 hyphema, blood fills one-half to somewhat less than the total anterior chamber space. Blood fills the entire anterior chamber in grade 4 hyphema (often referred to as “black-ball” or “eight-ball” hyphema).

Evaluation

The patient with traumatic hyphema should be evaluated carefully, since even TABLE 2

Causes of Traumatic Hyphema

Percentage of cases

related to cause

Cause (Total cases = 489)

Projectile

Ball 17.0

Rock/dirt 7.0

BB shot 3.9

Slingshot 2.9

Snowball 2.0

Wood chip 1.8

Hockey puck 1.2

Other 15.5

51.3

Blow

Fist/finger 11.2

Flexible object 8.2

Baseball bat 5.1

Stick 5.1

Fall 4.9

Other 10.8

45.3

Explosion

Battery 0.6

Firecrackers 0.6

Roll of caps 0.4

Other 0.8

2.4

Unknown 0.8

TABLE 3

Classification of Traumatic Hyphema

Percentage of cases

Amount of filling in each grade

Class in anterior chamber (Total cases = 371)

Grade 1 Less than one-third 72

Grade 2 One-third to one-half 20

Grade 3 More than one-half, but less 5

than total

Grade 4 Total 3

TABLE 4

Ocular Injuries Associated with Traumatic Hyphema

Percentage of cases

with injury

Injury (Total cases = 425)

Corneal abrasion 26

Secondary hemorrhage 19

Angle recession 17

Vitreous hemorrhage 16

Traumatic mydriasis 12

Macular edema 11

Peripheral edema 10

Increased intraocular 9

pressure

Eyelid laceration 8

Orbital fracture 7

Iris dialysis 7

Corneal blood stain 6

Traumatic cataract 4

Lens subluxation 2

Retinal detachment 2

Optic nerve neuropathy 2

No associated injury 17

a small amount of blood in the anterior chamber can signify severe intraocular damage. Particular attention should be given to signs of associated ocular injuries, which were present in 83 percent of patients in one study (Table 4).[6] The presence of other ocular injuries suggests more severe trauma and indicates a poorer prognosis.[11]

The time of the injury and its mechanism should be recorded. This information will help identify the period of greatest risk for rebleeding and may provide insight into the degree of ocular damage. Any previous history of ocular problems should be noted, since such problems could ultimately affect the visual acuity that is recovered. All medications being used by the patient should be recorded, particularly anticoagulants and antiplatelet agents.

Black and Hispanic patients should be tested for sickle cell trait or disease, because these patients have a higher risk of complications such as increased intraocular pressure due to blockage of the trabecular meshwork by sickled erythrocytes. Patients with sickle cell trait or disease may also be more prone to optic nerve atrophy.[12] Finally, a history of bleeding disorders should be elicited.

Baseline visual acuity should always be recorded. If the vision of the injured eye is poor, color and light sensation should be tested, as well as pupillary response. An afferent pupillary defect (e.g., no response to direct light but consensual response maintained) suggests optic nerve or retinal damage; however, this finding may also be solely attributable to the hyphema.[13]

Lacerations and blow-out fractures sometimes accompany traumatic hyphema. The periorbital skin, lids and conjunctiva should be examined for lacerations. Excessive conjunctival edema can indicate scleral rupture. Enophthalmos or restricted extraocular movement suggests the presence of a blow-out fracture.

The cornea should be carefully examined, since any corneal injury increases the chance of blood staining. The examination should include a search for foreign bodies.

The size and shape of the hyphema should be recorded, preferably in a drawing. Clots or sites of active bleeding should be noted. The lens should be inspected for abnormalities, including traumatic cataract and dislocation. Pupillary size and shape should be noted.

The patient should be referred to an ophthalmologist for dilated examination of the fundus and intraocular pressure measurement. Gonioscopy should be performed by an ophthalmologist no earlier than one week after the injury in order to avoid inducing a rebleed.[14]

For unknown reasons, some patients with traumatic hyphema appear drowsy.[7,15] The mechanism of injury should be clearly defined, so that a head injury can be dealth with appropriately.

Complications

SECONDARY HEMORRHAGE

Secondary hemorrhage, a serious complication of traumatic hyphema, occurs in 4 to 38 percent of patients.[3,6,8,10,16-22] It is thought to be caused by clot lysis and retraction, and it usually occurs two to seven days after the injury.[20] Overall, secondary hemorrhage is a poor prognostic sign because the bleeding predisposes patients to elevated intraocular pressure, corneal blood staining and visual loss.[16,17,21]

Some studies suggest that patients with a grade 3 or grade 4 hyphema have a higher incidence of secondary hemorrhage.[3,9,19,20] Other studies report a high rate of rebleeding in small hyphemas.[5,23,24] Thus, both large and small hyphemas should be considered at risk for rebleeding.

Some studies have shown a higher incidence of rebleeding in black patients.[6] Other studies have noted a lower incidence of rebleeding in predominantly white populations.[25] Because of the variable populations in previous studies, this racial predilection may account for the wide range of secondary hemorrhage rates reported.

ELEVATED INTRAOCULAR PRESSURE

Elevated intraocular pressure can occur in hyphemas of any grade. Although increased intraocular pressure is thought to be more common in high-grade hyphemas, it develops in nearly one-third of all cases.[11] Elevated intraocular pressure can occur in the first hours after the injury or can develop weeks to months later. The initial increase in intraocular pressure is caused by obstruction and clogging of the trabecular meshwork by red blood cells, platelets and fibrin. Direct damage to the absorption network is also possible. Fibrosis of the trabecular meshwork or peripheral anterior synechiae (adhesions) can cause persistent glaucoma.[14,26]

CORNEAL BLOOD STAINING

Corneal blood staining can result when a large or persistent hyphema is accompanied by an elevation in intraocular pressure. It is thought that increased pressure causes infiltration of the corneal stroma by hemoglobin and hemosiderin.[27] Any damage to the corneal endothelium increases the likelihood of blood staining. Blood staining of the cornea can cause significant loss of vision and can produce occlusion amblyopia in children.[21,26]

OPTIC NERVE ATROPHY

Optic nerve atrophy results from either prolonged elevation in intraocular pressure or direct injury to the optic nerve. It can result in irreversible visual loss.

Treatment

The primary goal of treatment is to prevent rebleeding, because of its association with the development of increased intraocular pressure and corneal blood staining. The first step is proper positioning of the patient. The patient should be initially maintained in a supine position with the head elevated 30 to 45 degrees. This position promotes layering and absorption of the hemorrhage and aids in classification of the hyphema. Layering of the hyphema inferiorly also improves visual acuity and allows an earlier evaluation of the retina and optic nerve.[11,26] The patient should avoid bending forward or lowering the head, which may delay layering and absorption. Reading and other near-viewing activities (e.g., playing hand-held video games) should be avoided, because rapid eye movements may increase the risk of rebleeding.[26]

An opthalmologic consultation should be obtained when the examination is complete. Prior to this evaluation, the patient should receive nothing orally, except medication. Pain management may be necessary, but aspirin and nonsteroidal anti-inflammatory drugs should be avoided because of their potential to incite a rebleed. Sedation may be used as needed.

Topical medications, including miotics and cycloplegics, have not been shown to be effective in preventing rebleeding.[3,9,18,21] However, cycloplegics are commonly used as a supportive measure. Corneal abrasions may be treated with a topical antibiotic. Finally, the injured eye should be protected with a shield (Figures 3 and 4). It is important to tape the shield in such a way as to ensure bony support. This may be accomplished by extending the tape onto the forehead and the maxilla.

Some ophthalmologists choose not to hospitalize patients with small or uncomplicated hyphemas. These patients should receive daily ophthalmologic examinations, including slit-lamp biomicroscopic evaluation and measurement of intraocular pressure. Complete bed rest is not necessary. Hospitalization is advised in patients with large hyphemas and in patients with sickle cell disease, since these patients are more likely to have complications. Patients who are unable to cooperate with daily outpatient examinations should also be hospitalized.

Elevated intraocular pressure can be treated with topical beta blockers or oral acetazolamide (Diamox), glycerol or mannitol (Osmitrol). Increased intraocular pressure in patients with sickle cell trait or disease should not be treated with acetazolamide, because this agent can lower pH and increase sickling. In these patients, methazolamide (Neptazane), which raises pH, is the preferred drug.[12,14] In pediatric patients, glycerol and mannitol should be avoided because of the risk of inducing dehydration.[27]

The prevention of secondary hemorrhage through the use of antifibrinolytic agents is controversial. Both aminocaproic acid (Amicar) and tranexamic acid (Cyklokapron) competitively inhibit clot lysis. Several studies have demonstrated that these agents lower the incidence of secondary hemorrhage.[5,10,23,24,28] However, one recent study[25] found no improvement in rebleeding rates with aminocaproic acid administration. In addition, because of adverse reactions, such as nausea, vomiting and hypotension, neither aminocaproic acid nor tranexamic acid is widely used.[9,24] Topical antifibrinolytics are presently being studied in the hope that they will reduce systemic complications.[29] Antifibrinolytic agents are contraindicated in pregnant women and in patients with renal insufficiency or clotting disorders.

Other research has supported the use of systemic steroids to prevent secondary hemorrhage. An early study evaluating the use of prednisone[30] demonstrated a trend toward reduction of the incidence of rebleeding, but the reduction was not considered statistically significant. A recently published study[31] showed that patients treated with prednisone had an incidence of secondary hemorrhage equal to that of patients treated with aminocaproic acid. The mechanism of action of prednisone is not known, but it may be the result of its anti-inflammatory effect on damaged blood vessels.

Most patients with traumatic hyphema do not require surgical intervention. Indications for surgery are not well defined but, in general, include uncontrolled elevation of intraocular pressure, corneal blood staining, and high-grade or total hyphema that persists for several days.[11] Surgical techniques include paracentesis, irrigation and aspiration, and automated vitrectomy. Patients with sickle cell disease may need early surgical intervention because of their increased risk of complications.[12,20]

Prognosis

The usual duration of an uncomplicated hyphema is four to six days.[26] Complications such as glaucoma can persist for weeks to months. Although patients with small hyphemas can have poor results, large hyphemas generally carry a worse prognosis.[8,11,18] Good visual acuity (i.e., 20/40) is achieved in approximately 80 percent of patients with a grade 1 hyphema, compared with only 35 percent of patients with a grade 4 hyphema.[11] In large part, this difference is due to the higher incidence of rebleeding and other complications associated with high-grade hyphemas.[3,16,17,21] Associated ocular injuries also worsen the prognosis.[11]

Prevention

Traumatic hyphema and other sports-related eye injuries can be prevented through the use of protective eye guards. Eye guards made of polycarbonate or other impact-resistant materials dissipate forces into soft tissue and bone, thus preventing damage to the eye.

The Canadian Standards Association (CSA) and the American Standard of Testing and Materials (ASTM) have set specifications for eye guards. Eye guards meeting these standards should be considered mandatory in all racquet sports. In other sports, such as football, ice hockey and lacrosse, protection of the eye should be part of general head protection.[32] The effectiveness of eyeguards is illustrated by a 1988 review,[33] in which no significant eye injuries were reported in squash or racquetball players wearing eye guards that met 1985 or 1986 CSA or ASTM standards.

REFERENCES

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[10.] Uusitalo RJ, Ranta-Kemppainen L, Tarkkanen A. Management of traumatic hyphemia in children. An analysis of 340 cases. Arch Ophthalmol 1988;106:1207-9.

[11.] Read JE, Crouch ER. Trauma: ruptures and bleeding. In: Tasman W, Jaeger EA, eds. Duane’s Clinical ophthalmology. Vol. 4. Philadelphia: Lippincott, 1991:1-18.

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[13.] Striph GG, Halperin LS, Stevens JL, Chu FC. Afferent pupillary defect caused by hyphema. Am J Ophthalmol 1988;106:352-3.

[14.] Gottsch JD. Hyphema: diagnosis and management. Retina 1990;10(Suppl 1):S65-71.

[15.] Cohn JN, Scagliotti D, Deutsch TA. Bradycardia with traumatic hyphema in children. J Pediatr Ophthalmol Strabismus 1987;24(6): 315-7.

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[20.] Crouch ER Jr, Frenkel M. Aminocaproic acid in the treatment of traumatic hyphema. Am J Ophthalmol 1976;81:355-60.

[21.] Agapitos PJ, Noel LP, Clarke WN. Traumatic hyphema in children. Ophthalmology 1987; 94:1238-41.

[22.] Lawrence T, Wilson D, Harvey J. The incidence of secondary hemorrhage after traumatic hyphema. Ann Ophthalmol 1990;22: 276-8.

[23.] McGetrick JJ, Jampol LM, Goldberg MF, Frenkel M, Fiscella RG. Aminocaproic acid decreases secondary hemorrhage after traumatic hyphema. Arch Ophthalmol 1983;101:1031-3.

[24.] Kutner B, Fourman S, Brein K, et al. Aminocaproic acid reduces the risk of secondary hemorrhage in patients with traumatic hyphema. Arch Ophthalmol 1987;105:206-8.

[25.] Volpe NJ, Larrison WI, Hersh PS, Kim T, Shingleton BJ. Secondary hemorrhage in traumatic hyphema. Am J Ophthalmol 1991;112: 507-13.

[26.] Bloom JN. Traumatic hyphema in children. Pediatr Ann 1990;19:368-71,375.

[27.] Gottsch JD, Messmer EP, McNair DS, Font RL. Corneal blood staining. An animal model. Ophthamology 1986;93:797-802.

[28.] Loewy DM, Williams PB, Crouch ER Jr, Cooke WJ. Systemic aminocaproic acid reduces fibrinolysis in aqueous humor. Arch Ophthalmol 1987;105:272-6.

[29.] Allingham RR, Crouch ER Jr, Williams PB, Catlin JC, Loewy DM, Jacobson J. Topical aminocaproic acid significantly reduces the incidence of secondary hemorrhage in traumatic hyphema in the rabbit model. Arch Ophthalmol 1988;106:1436-8.

[30.] Spoor TC, Hammer M, Belloso H. Traumatic hyphema. Failure of steroids to alter its course: a double-blind prospective study. Arch Ophthalmol 1980;98:116-9.

[31.] Farber MD, Fiscella R, Goldberg MF. Aminocaproic acid versus prednisone for the treatment of traumatic hyphema. Ophthalmology 1991;98:279-86.

[32.] Diamond GR, Quinn GE, Pashby TJ, Easterbrook M. Ophthalmologic injuries. Clin Sports Med 1982;1:469-82.

[33.] Easterbrook M. Eye protection in racquet sports. Clin Sports Med 1988;7:253-66.

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