Traumatic Hyphema

Prithvi S. Sankar, M.D.

Teresa C. Chen, M.D.
Cynthia L. Grosskreutz, M.D., Ph.D.
Louis R. Pasquale, M.D.

䡲 Definition

Hyphema is an accumulation of blood, mainly consisting of erythro-

cytes that disperse and layer within the anterior chamber. Normally, the
anterior chamber is devoid of cells of any kind. A microhyphema occurs
when erythrocytes are suspended in the anterior chamber but visible lay-
ering is not seen on slit-lamp examination.

䡲 Incidence and Etiology

Hyphemas most often are encountered with ocular injuries, including

penetrating trauma and blunt force injury. Hyphema may, however, be
present in non-trauma-related conditions, including iris neovasculariza-
tion, melanoma, blood clotting disturbances, medication-induced antico-
agulation, leukemia, and juvenile xanthogranuloma. There has even been
a case reported of retinoblastoma presenting as a hyphema.1 Although
hyphemas may occur from other causes, traumatic hyphemas are the main
focus of this chapter.

䡲 Pathophysiology

The pathophysiology of traumatic hyphemas is important to under-

stand. Initially, blunt trauma indents and stretches the globe, resulting in
distortion of the normal ocular architecture. This disruption elevates the
57
58 䡲 Sankar et al.

intraocular pressure and then causes a posterior displacement of the lens-

iris diaphragm. Bleeding then occurs from tearing and disrution of the
well-vascularized ciliary body and iris.2 These blunt force injuries mainly
affect the anterior face of the ciliary body, but iris tears, iridodialyses, and
cyclodialyses can occur. Bleeding eventually stops, owing to the increase in
the intraocular pressure, causing vasospasm of the bleeding vessels and
formation of a fibrin-platelet clot. The clot may actually extend from the
anterior chamber to the posterior chamber and occasionally into the
vitreous. The clot reaches its maximum stabilization in approximately 4 to
7 days. These clots do not show fibroblastic activity or neovascularization,
unlike clots in other parts of the body.3 Hyphemas break down and resolve
within the anterior chamber via the fibrinolytic system. Plasminogen is
converted to plasmin, which activates the fibrinolytic system that helps to
break down the clot. The blood and the breakdown products then clear
via the trabecular meshwork.4

䡲 Examination and Investigations

Most patients present with a history of trauma and decreased vision or

pain in the eye. When a person presents with a hyphema, it is imperative
to perform a complete eye examination, which includes intraocular pres-
sure measurement and dilated funduscopic assessment. A ruptured globe
must be ruled out. A ruptured globe might not be readily apparent,
particularly if there is significant subconjunctival hemorrhage. Signs of
occult rupture in the setting of a traumatic hyphema include poor vision,
low intraocular pressure, an abnormally deep anterior chamber, and pu-
pillary distortion.
As discussed, numerous causes of hyphema do not involve trauma.
However, trauma is still the most common etiology. Knowing the mecha-
nism of the injury is important and can aid in the treatment of the patient.
Also, abuse should always be considered, especially in children, when the
report of the circumstances leading to the hyphema is questionable.
Hyphemas are typically graded on the amount of blood within the
anterior chamber. Grade I is less than one-third filling of the anterior
chamber. Grade II is one-third to one-half of the anterior chamber, and
grade III is one-half to near total filling of the anterior chamber. Grade IV
is a complete, total hyphema, also known as an 8-ball hyphema.5 Grading
the hyphema is important to monitor the patient longitudinally. If this
grading system is not employed, the actual measurement of the hyphema
in millimeters can serve as a useful way to monitor its progress.
A history of sickle cell anemia must be sought out, and a sickle cell
preparation should be considered in every patient, especially those with
black ancestry. Also, a review of the patient’s medication list, with particu-
lar attention to anticoagulants, should be performed. Gonioscopy and
 Traumatic Hyphema 䡲 59

scleral depressed ophthalmoscope should probably be deferred in the

acute setting, as they may exacerbate bleeding into the anterior chamber.
Bleeding time, hemoglobin electrophoresis, platelet count, prothrombin
time, partial thromboplastin time, liver function, and blood urea nitrogen
and creatinine may be tested, depending on the patient’s history, on the
ocular examination, and on what treatment will be initiated. Vision, hy-
phema status, intraocular pressure, and evaluation for corneal blood stain-
ing should be determined every day for the first 4 days after the initial
injury.
Approximately 1 month after injury, careful gonioscopy should be
performed to evaluate for potential bleeding sites and to examine for the
presence of angle recession. A dilated retinal examination with scleral
depression should also be performed at 1 month to rule out retinal pa-
thology.

䡲 Medical Management

Once the diagnosis of hyphema is made, the practitioner should com-

municate the serious nature of the injury to the patient and stress the
possibility of vision-threatening complications in the days, weeks, months,
and even years after the injury.

Inpatient Versus Outpatient Management

In the past, patients with hyphemas were almost uniformly admitted to
the hospital. This was meant better to enforce strict bed rest, to enable use
of intravenous fluids and medications, and to facilitate early surgical in-
terventions.2
Recently, however, there has been a move to treat hyphemas on an
outpatient basis. In addition to cost-effectiveness, outcomes appear to be
similar. Noncontrolled clinical trials6,7 have reported no difference in the
incidence of hyphema complications between patients treated in the hos-
pital and those treated at home. In a retrospective review, 154 patients at
the Massachusetts Eye and Ear Infirmary were treated at home, and their
results were compared to a historical cohort who were treated in the
hospital. The rebleed rate of the outpatients (4.5%) compared favorably
to that of the inpatients (5.0%).8 Inpatient hospitalization should be con-
sidered for those patients who may have an increased risk of rebleeding,
have uncontrolled glaucoma, or are unable to make frequent office visits.

Bed Rest
Most authors have found no significant difference between moderate
activity and strict bed rest.9 However, most practitioners still encourage
60 䡲 Sankar et al.

limited activity. The head of the bed should be elevated to encourage the
hyphema to gravitate to the inferior angle and away from the visual axis.
Hyphemas that layer over the pupillary axis may impede visual recovery
and may cause pupillary block glaucoma.

Shield
Protection of the injured eye takes on special importance after one
suffers from a hyphema. Further injury to the eye is possible, especially
considering the already compromised vision. A shield or protective eye-
wear should be worn at all times, including nighttime, until the hyphema
clears.

Aspirin
The discontinuation of aspirin has been somewhat controversial. Nu-
merous authors10,11 have suggested the deleterious effect of aspirin in
rebleeding; however, others12 have not implicated aspirin in rebleeding.
Even though there is controversy regarding this topic, most practitioners
still discontinue aspirin and nonsteroidal antiinflammatory agents in the
face of a hyphema.

Cycloplegia
Another controversial topic in hyphema is the use of cycloplegia.
Cycloplegia dilates the pupil and helps to relax the ciliary body, thereby
decreasing inflammation and improving the patient’s comfort. Dilating
the pupil may also compress iris vessels and prevent stress to the vessels
from the constantly moving pupil, allowing these vessels to heal. Although
most ophthalmologists continue the use of cycloplegia for those reasons,
at least one study13 suggested that cycloplegia has no effect on secondary
hemorrhage.

Topical Steroids
Most hyphemas also have a component of uveitis because the blood-
aqueous barrier has been disrupted. Therefore, topical steroids have been
used to decrease the inflammation and to improve the patient’s comfort.
Regimens vary and are often titrated according to the amount of inflam-
mation present within the anterior chamber. As the inflammation im-
proves, the steroid is tapered. Caution should be exercised if steroids are
used for a prolonged period of time. The development of cataracts or
glaucoma14,15 from steroid use can cause unwanted complications.

Oral Steroids
There has been recent controversy regard oral steroids in the treat-
ment of hyphema. In his correspondence, Pollard16 related that he ob-
 Traumatic Hyphema 䡲 61

tained no rebleeds in 250 cases treated using the regimen of 40 mg/day

in divided doses proposed by Yasuna.17 Although another study also
showed beneficial role of systemic steroids,18 still another study showed no
substantial benefit.19 The potential side effects of steroid medication
should not be overlooked.

Antifibrinolytic Agents
The theory behind the use of antifibrinolytic agents is that these
agents aid in clot stabilization. Lysis of the hyphema clot is mediated by
the fibrinolytic system. If the clot stabilizes, there would be more time for
the injured vessels to heal and thereby prevent a rebleed. Aminocaproic
acid inhibits the conversion of plasminogen to plasmin, which therefore
decreases the amount of plasmin available for the fibrinolysis. It may also
have a lesser effect on antiplasmin activity.20 These activities would theo-
retically help to promote clot stabilization and to prevent further bleed-
ing.
Aminocaproic acid was initially studied by Crouch and Frenkel21 and
then by others,22,23 who have found that its use decreases the incidence of
secondary hemorrhage. The current recommended dose is 50 mg/kg
orally every 4 hours, up to 30 gm/day for 5 days.3 Treatment is usually
started in the hospital, owing to the side effects. The side effect profile
includes nausea, muscle weakness (elevated creatinine phosphokinase),
abdominal cramps, bradycardia, and hypotension. Aminocaproic acid is
cleared by the kidneys, and special attention should be paid to those who
have a history of hematuria or renal insufficiency.20 Often, these side
effects can be severe enough to lead to discontinuation of the medication,
which may result in rebleeding.21 Recently, topical aminocaproic acid has
been investigated for use in traumatic hyphema, which could decrease or
eliminate much of the systemic side effects.24
Tranexamic acid also competitively inhibits activation of plasminogen
to plasmin. Its use has also been studied in the use of traumatic hy-
phema.25 This antifibrinolytic agent is more potent than is aminocaproic
acid and has fewer side effects.26 Recently, Rahmani and Jahadi27 com-
pared the use of tranexamic acid and oral prednisolone and placebo in
238 patients. In their randomized clinical trial, the rate of rebleed was
10% in the tranexamic acid group, 18% in the oral steroid group, and
26% in the placebo group. Although they noted a higher-than-expected
rate of rebleed in all subgroups, these authors did note a statistical dif-
ference between the tranexamic group and the placebo group.

Newer Modalities
Tissue plasminogen activator is a newer modality that may serve as an
adjuvant to known therapies. Kim and coworkers28 used intracameral tis-
62 䡲 Sankar et al.

sue plasminogen activator to treat 3 eyes with persistent total hyphemas

and elevated intraocular pressure. All had resolution within 24 to 48
hours, although 1 had a vitreous hemorrhage.
Transcorneal oxygen therapy has also been tried in those with hy-
phema and sickle cell trait. Benner29 studied 3 patients with glaucoma
caused by sickle cell hyphema and treated them with transcorneal oxygen
therapy. All 3 patients in this case series had reduction of intraocular
pressure within a few hours after treatment. The premise of using this
therapy is to increase the partial pressure of oxygen and to prevent the
rigid sickle cells from forming and clogging the trabecular meshwork.

䡲 Special Considerations

Sickle Cell Anemia

As mentioned, it is important to keep in mind the possibility of sickle
cell disease or trait in patients with hyphemas. This hereditary condition
causes normal erythrocytes to become deformed and rigid with a slightly
decreased oxygen concentration. These sickled cells, when present in the
anterior chamber, clog the trabecular meshwork and impede the outflow
of aqueous. As the intraocular pressure rises, further hypoxia develops,
and further sickling occurs. This set of circumstances may then lead to
refractory glaucoma. Therefore, the condition in these patients needs to
be managed with a great deal of care.
Not only are those with sickle cell disease at risk; those with the trait
are too. Sickle cell trait encompasses approximately 10% of the black
population, and this trait should be screened in all black patients. Nas-
rullah and Kerr30 described 99 children with hyphema, 13 of whom had
sickle cell trait. Eleven of the sickle cell patients had elevated intraocular
pressure, and 6 eventually required surgical washout to control the intra-
ocular pressure. Sickle cell disease patients are also at risk for vasoocclu-
sive disease due to the sickling, even at mildly elevated intraocular pres-
sure, which poses a great risk to the optic nerve.
The management of patients with sickle cell hyphemas differs from
that of other patients. As described, strict adherence to medical manage-
ment should be maintained. The intraocular pressure should be kept as
low as possible to prevent further hypoxia and further sickling. Hospital-
ization may be required. Caution should be applied to the choice of
intraocular pressure–lowering agents. Beta-adrenergic antagonists are still
the preferred medication. Miotics tend to increase inflammation, whereas
carbonic anhydrase inhibitors, both oral and topical, may cause systemic
acidosis that may cause more sickling and precipitate a sickle cell crisis.
Hyperosmotic agents can cause hemoconcentration and should be
avoided. There has to be a balance between lowering the intraocular
pressure and using agents that cause sickling. Usually, attempts are made
 Traumatic Hyphema 䡲 63

to keep the intraocular pressure below 25 mm Hg; otherwise, surgical

options may be needed. Newer therapies, including transcorneal oxygen-
ation, may have a role in future therapies.

Children
The approach to traumatic hyphema in children is different from that
for adults. A child may not be as compliant or as cooperative as an adult
with treatment. Therefore, evaluation of a child and the parent’s ability to
take care of the child is important. One must also not forget to consider
child abuse in all children with traumatic hyphemas, as this may be the
initial presenting sign. If abuse is suspected, prompt consultation with the
pediatrician and social agencies is required.
Affected children should be examined as thoroughly as possible, and
medical measures as described should be implemented. Although the
long-term effects of most glaucoma medications have not been established
in children, most clinicians use these medications in an effort to lower the
intraocular pressure during the acute phase. The regimen for topical
medications is similar to the adult regimen. Oral acetazolamide (20
mg/kg/day in four divided doses), methazolamide (10 mg/kg/day in
four divided doses), and even mannitol (1.5 gm/kg of the 10% solution
intravenously) may be given.
The question of whether children should be treated as inpatients or as
outpatients has been raised. Admission to the hospital used to be advo-
cated in all cases wherein traumatic hyphemas occurred in children. How-
ever over the last few years, children have been treated on an outpatient
basis without significant differences in final visual acuity as compared to
that in inpatients.31 If children are treated as outpatients, daily visits must
be performed, with special attention paid to the cornea and the intraoc-
ular pressure.
Deciding between inpatient and outpatient treatment can be difficult.
Indications to admit include penetrating ocular trauma, secondary hem-
orrhage, suspected child abuse, hyphemas greater than 50%, or risk of a
noncompliant patient or family or both.31 Again, those with sickle cell
hemoglobinopathy are at higher risk for developing an intraocular pres-
sure rise, and admission may be warranted.32

䡲 Surgical Management

In approximately 5% of patients with hyphemas, medical therapy fails,

necessitating surgical intervention.5 Newer modalities of treating patients
medically may lower the incidence of patients needing surgery. Indica-
tions for surgery include refractory elevated intraocular pressure, pres-
ence of corneal blood staining, and persistence of the clot.3 It has been
64 䡲 Sankar et al.

proposed that intraocular pressure elevation of 50 mm Hg for 5 days or 35

mm Hg for 7 days requires surgical intervention. Sickle cell patients
should have early intervention if their pressures are not controlled within
the first 24 hours. There are several different techniques for removal of
the clot.
Manual irrigation and aspiration of the blood is a common technique.
Using either a manual irrigation-aspiration system or just an irrigation
cannula, a washout of suspending debris may occur through a one- or
two-cornea incision approach.3 Removal of all the blood is not necessary.
This technique is relatively easy to perform and spares the conjunctiva if
a future filtering procedure is necessary.
Evacuation of the hyphema sometimes requires the use of vitrectomy
instrumentation, owing to clot retention.33 Care should be taken not to
damage the corneal endothelium, lens capsule, or iris during the proce-
dure. Two clear cornea entry sites are made. One site is used as an infu-
sion port, usually a 20-gauge needle or cannula connected to balanced salt
solution. The vitrectomy instrument, working through the second site,
may be used to facilitate removal of the clot with light cutting action and
aspiration. Initially, the vacuum is set at 200 mm Hg, with a cutting rate of
200 cycles per minute. The bottle height should be fairly high so as to
keep the intraocular pressure from becoming too low. Should a secondary
hemorrhage occur, the bottle height should be raised as high as possible
to elevate the intraocular pressure and to tamponade the bleeding. Vis-
coelastics may also be used after evacuation of the initial clot, if the bleed-
ing persists. Diathermy may be used if the site of bleeding is localized.31
Limbal clot delivery has become less frequently used. Its disadvantages
include the large limbal wound, formation of conjunctival scarring that
may prevent future filtering surgery, and inadvertent delivery of uveal and
other intraocular tissue along with the clot.3 Generally, if this procedure
is performed, it is better to wait until day 4, by which time maximal clot
formation and retraction has occurred.
Trabeculectomy with anterior chamber washout and peripheral iri-
dectomy is generally reserved for those in whom medical and prior sur-
gical management have failed. This approach was first suggested by Weiss
and associates34 and has been used by others35 to control the intraocular
pressure while the remaining blood is cleared.

䡲 Complications

Rebleeding
Rebleeding is the most common complication of traumatic hyphema
and may eventually lead to other complications. In fact, most of the thera-
pies are employed to prevent rebleeding. The rebleeding rate varies from
3.5 to 38%.3 Again, the most common time is 2 to 5 days after injury, when
 Traumatic Hyphema 䡲 65

the initial clot begins to retract and lyse, causing the injured vessels to
bleed again. Some studies suggest that there is a higher rate of surgery in
those patients who have suffered a rebleed.36 Those at higher risk of
rebleeding include those with a 50% hyphema,5 those who are black,37
and those who initially have high intraocular pressure and poor vision.38
Rebleeding tends to cause more complications, such as glaucoma, corneal
blood staining, and posterior synechiae. The final visual acuity of those
with rebleed have been reported as no worse than those without rebleed
in some studies39 but not in others.38

Corneal Blood Staining

Corneal blood staining most often occurs in those who have large
hyphemas and sustained elevation of intraocular pressure. Other factors
that contribute include prolonged clot duration and corneal endothelial
dysfunction. Hemosiderin and breakdown products of erythrocytes are
found within the keratocytes. Clinically, these areas take on a yellow
granular appearance that may be difficult to notice in its initial stages.
Once noted, however, the clot should be evacuated, and care should be
taken to control the intraocular pressure. Clearing may take several
months to years and usually starts first at the peripheral cornea. Penetrat-
ing keratoplasty should be considered in children who have significant
corneal changes and who are in the amblyopic age range.3

Glaucoma
Management of intraocular pressure is important in the management
of any hyphema. As mentioned, elevated intraocular pressure may lead to
a number of complications, including optic atrophy and corneal blood
staining. The main cause of elevated pressure is thought to be due to the
obstruction of the trabecular meshwork with erythrocytes and inflamma-
tory debris. Direct trauma to the angle may also play a role. The general
occurrence of elevated intraocular pressure in these patients is roughly
25%.3 Several factors do influence the rise in pressure. Sickle cell hemo-
globinopathy (as mentioned) influences intraocular pressure. Lai and
colleagues32 reported that those children who have the hemoglobinopa-
thy have a statistically higher pressure than those who did not. Also influ-
encing pressure is clot size. Larger clots have a higher and more pro-
longed pressure rise than do smaller clots.31 As a clot retracts, one must
also be aware that a component of pupillary block may occur if the clot sits
along the pupil and prevents flow of aqueous to the anterior chamber and
the drainage channels.
The treatment of elevated pressure is chiefly medical. Topical ␤-ad-
renergic antagonists are usually the first line of therapy. Topical ␣-adren-
ergic agonists, topical and oral carbonic anhydrase inhibitors, and other
66 䡲 Sankar et al.

oral agents may be used. Owing to the increase in the inflammatory re-
sponse, miotics should not be used. Prostaglandin analogs may also cause
an inflammatory response, and caution should be exercised in using
them. Special consideration should be given to those with sickle cell dis-
ease or trait. If sustained lowering of the intraocular pressure is not
achieved, one must consider surgical therapy.

Other Complications
Other complications of traumatic hyphema include peripheral ante-
rior synechiae, posterior synechiae, cataract formation, optic atrophy, and
angle recession glaucoma. Optic atrophy may be the most significant
complication of traumatic hyphema, and it is usually secondary to an
elevated intraocular pressure. In the setting of traumatic hyphema, there
may be optic nerve pallor out of proportion to cupping. The optic atrophy
may also be secondary to the actual injury that caused a traumatic optic
neuropathy. Again, sickle cell patients are at higher risk for developing
optic atrophy.

䡲 Prognosis

It is important to recognize and treat hyphemas correctly. Treatment

should be aimed at lowering intraocular pressure, preventing rebleeds,
and reducing the risk of optic atrophy and corneal blood staining. Ap-
proximately 75% of patients will achieve a final visual acuity of 20/50 or
better.5,31 Severity of the trauma also affects final visual acuity. Traumatic
optic neuropathy, choroidal rupture, retinal detachment-dialysis, vitreous
hemorrhage, lens opacities, lens subluxation, and corneal scarring may all
limit final visual acuity.
In conclusion, with appropriate diagnosis and management of a hy-
phema and of its complications, preservation of vision can be achieved.

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