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Traumatic Hyphema in Children
Risk Factors for Complications
James C. Lai, MD;
Sharon Fekrat, MD;
Yolanda Barrón, MS;
Morton F. Goldberg, MD
Arch Ophthalmol. 2001;119:64-70.
ABSTRACT
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Objective To identify risk factors associated with higher rates of ocular complications
in children with traumatic hyphema.
Methods Consecutive inpatient records from July 1990 through December 1997 were
retrospectively reviewed for all children (aged  18 years) who were admitted
to the Wilmer Ophthalmological Institute, Baltimore, Md, within 48 hours of
a closed-globe injury leading to hyphema. Data obtained included age, sex,
race, sickle cell status, initial and final visual acuities, hyphema size
and intraocular pressure at presentation, the occurrence of a secondary hemorrhage,
subsequent intraocular pressure elevations, and therapeutic interventions.
Results Forty children fulfilled the inclusion criteria: 20 African American,
1 Asian American, and 19 white. Five of the 20 African American children had
sickle cell trait, and 1 had sickle cell anemia. The rate of secondary hemorrhage
was statistically higher in the African American population (P = .05), but no statistical difference existed between the rate of
secondary hemorrhage in patients with and without sickle cell hemoglobinopathy.
Sickle cell hemoglobinopathy was associated with a higher intraocular pressure
at presentation (P = .03) and during inpatient follow-up
(P = .02).
Conclusions In the setting of traumatic hyphema, African American children appear
to be at greater risk for developing a secondary hemorrhage. In our patients,
sickle cell hemoglobinopathy increased the risk of intraocular pressure elevation,
but did not seem to increase the risk of rebleeding beyond that associated
with race. Larger studies are needed to validate these observations.
INTRODUCTION
IN EYES WITH traumatic hyphema following closed-globe injury, a secondary
hemorrhage is associated with a worse visual outcome.1-2
Recurrent bleeding increases the risk of vision-threatening complications,
including corneal blood staining, secondary glaucoma, and optic atrophy. It
is, therefore, generally accepted that a major goal in the treatment of traumatic
hyphema is to prevent secondary hemorrhage and its associated sequelae. However,
the large variability in the reported rates of recurrent hemorrhage (3%-38%)
and associated ocular complications3-10
has led to controversy over the optimal management of traumatic hyphema.7-18
Numerous studies5-7,19-22
have attempted to identify risk factors for recurrent bleeding and associated
ocular complications in eyes with traumatic hyphema, which would guide medical
and surgical interventions. The influence of race on these issues has not
been fully explored.4, 8, 23
Patients with sickle cell hemoglobinopathy require special attention, because
they are at higher risk for developing ocular complications.24-26
As a result of the mechanical obstruction of the trabecular meshwork by sickled
erythrocytes, eyes of these patients are more likely to develop intraocular
pressure (IOP) elevations. Furthermore, these eyes are more likely to develop
central artery occlusion and optic nerve damage, with only marginal increases
in the IOP.24 It is unclear, however, whether
the presence of sickle cell hemoglobinopathy actually increases the risk of
secondary hemorrhage in these patients. The goals of this study were to determine
which factors, including but not limited to race and sickle cell hemoglobinopathies,
were associated with an increased risk of secondary hemorrhage and related
ocular complications.
MATERIALS AND METHODS
Consecutive inpatient records from July 1990 through December 1997 were
retrospectively reviewed for children (aged 18 years) admitted to the
Wilmer Ophthalmological Institute at The Johns Hopkins Hospital, Baltimore,
Md, within 48 hours after a closed-globe injury leading to hyphema. Patients
were excluded if they had a microhyphema (ie, visible only with a slitlamp
as dispersed, nonsettled erythrocytes), associated open-globe injury, preexisting
eye pathological features, or prior intraocular surgery. Aspirin, unlike other
nonsteroidal anti-inflammatory drugs, irreversibly inhibits the platelet enzyme
responsible for aggregation.27 Hemostasis is
impaired for at least 5 to 7 days following the administration of a single
dose of aspirin. Therefore, patients with a history of aspirin use within
2 weeks of presentation were excluded, while those with documented use of
other nonsteroidal anti-inflammatory drugs were not. Patients referred by
outside ophthalmologists for management were excluded to prevent any referral
bias to the study population. The following information was collected: age,
sex, race, sickle cell status, mechanism of injury, initial and final visual
acuities, hyphema size and IOP at presentation, subsequent IOP elevation during
hospitalization, the occurrence of a secondary hemorrhage, and medical or
surgical interventions. Because this was a retrospective review of clinical
outcomes, and not a prospective clinical trial, informed consent was not obtained
for inclusion in this study.
All patients were admitted to the Wilmer Ophthalmological Institute
inpatient unit for bed rest. The affected eye was covered with a metal shield,
and cycloplegic eyedrops were administered. All patients were treated with
oral aminocaproic acid (Amicar) (37 of 40 patients) or oral prednisone (3
of 40 patients) at the discretion of the admitting physician. All affected
eyes were treated with topical corticosteroids. Eyes with an IOP greater than
21 mm Hg were also treated with a combination of either of the following:
levobunolol hydrochloride, apraclonidine hydrochloride, dorzolamide hydrochloride,
methazolamide, or acetazolamide. All African American children were screened
for sickle cell hemoglobinopathy, using a sickle hemoglobin solubility test
at The Johns Hopkins Hospital.28 Hemoglobin
electrophoresis was then used to differentiate between sickle cell trait and
other sickle cell hemoglobinopathies.
The hyphema size was graded according to the percentage of the anterior
chamber filled with blood.1 A grade 1 hyphema
occupied less than one third of the anterior chamber; grade 2, greater than
one third but less than one half of the anterior chamber; and grade 3, one
half or more of the anterior chamber. A grade 4 hyphema was a complete blood
clot ("8-ball hyphema") in the anterior chamber. A secondary
hemorrhage was defined as an increase in the measured quantity of layered
blood in the anterior chamber on slitlamp examination during follow-up. In
the setting of a grade 4 hyphema, a secondary hemorrhage was defined as the
appearance of fresh blood over old clots in the anterior chamber. An IOP elevation was defined as an IOP greater than 21 mm
Hg that developed during inpatient follow-up and resulted in the addition
of pressure-lowering agents to the preexisting medical regimen.
Associations between the incidence of a secondary hemorrhage and potential
risk factors were examined using  2, Fisher exact, and t tests, where appropriate. P.05
was considered to be statistically significant. Separate multivariate logistic
regressions were used to explore the risk factors for secondary hemorrhage
and for IOP elevation. Odds ratios and 95% confidence intervals were calculated.
The results of 3 separate sets of analyses are reported. In the first set,
all patients with sickle cell hemoglobinopathy (sickle cell trait or disease)
were compared with those with a normal hemoglobin level. Because there was
only 1 patient in the study with sickle cell disease, a second set of analyses
was then performed in which this patient was excluded. The third set of analyses
was restricted solely to African American patients, and those with sickle
cell hemoglobinopathy were compared with those with a normal hemoglobin level.
RESULTS
Sixty-two consecutive inpatient records coded for hyphema were reviewed
for the period between July 1990 and December 1997. Seven patients with delayed
presentation to the hospital, 6 with open-globe injuries, 5 with preexisting
pathological features in the affected eye, 2 referred by outside ophthalmologists
for management, and 1 with a microhyphema were excluded. Only 1 patient had
documented use of aspirin within 2 weeks of admission and was excluded from
the study. A total of 40 patients fulfilled the inclusion criteria: 20 (50%)
were African American; 1 (2%), Asian American; and 19 (47%), white. Of the
20 African American children, 5 (25%) had sickle cell trait and 1 (5%) had
sickle cell disease (Figure 1).
There were 36 male and 4 female patients (mean age, 10.6 years; range, 2.5-18.0
years). Thirty-one patients were admitted within 24 hours of sustaining injury
to the eye, and 9 (6 African Americans and 3 whites) were admitted more than
24 hours after the initial injury.
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Figure 1. Of the 20 African American children,
1 (5%) had sickle cell disease, 5 (25%) had sickle cell trait, and the remainder
(14 [70%]) had a normal hemoglobin level.
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Thirty-four (85%) of the eyes had a grade 1 hyphema; 1 (2.5%), grade
2; 1 (2.5%), grade 3; and 4 (10%), grade 4. The overall secondary hemorrhage
rate was 10.3% (4/39). One patient with sickle cell trait developed a secondary
hemorrhage 3 days following an anterior chamber washout for a grade 4 hyphema.
Because the surgical intervention may have contributed to the rebleed, this
patient was excluded from the analyses of the rate and risk factors for secondary
hemorrhage. Sex and age were not found to be statistically associated with
the incidence of rebleeding (P = .36 and P = .91, respectively). All of the rebleeds occurred in patients with
a grade 1 hyphema and within 5 days of the initial injury. Of the 3 patients
who were treated with oral corticosteroids, 1 developed a secondary hemorrhage.
This patient, who did not have sickle cell hemoglobinopathy, was switched
to treatment with aminocaproic acid after developing the rebleed on hospital
day 1, but subsequently developed another rebleed on hospital day 5. Of the
37 patients treated with aminocaproic acid, 4 developed a secondary hemorrhage.
The rate of secondary hemorrhage was statistically higher in the African
American population (4 [21%] of 19) compared with the non–African American
population (0 [0%] of 20) (P = .05) (Figure 2A). Of the 4 African American patients who rebled, 1 had
sickle cell disease and 3 did not have sickle cell hemoglobinopathy (Table 1). None of the 4 patients with sickle
cell trait developed a rebleed. The rate of secondary hemorrhage among patients
with sickle cell hemoglobinopathy (1 [20%] of 5) compared with all those without
sickle cell hemoglobinopathy (3 [9%] of 34) was not statistically significant
(P = .44) (Figure
2B). Furthermore, when the analysis was restricted to only African
American patients, there was no statistical difference between the rate of
secondary hemorrhage among African American patients with sickle cell hemoglobinopathy
(1 [20%] of 5) compared with those without it (3 [21%] of 14) (P>.99) (Figure 2C). Of the
14 African American children who were seen within 24 hours of sustaining injury
to the eye, 2 patients, 1 of whom had sickle cell disease, developed a secondary
hemorrhage. In comparison, 2 of the 6 African American patients who sought
medical attention more than 24 hours after their injury developed a secondary
hemorrhage. When excluding the 1 patient with sickle cell disease from analysis,
a delay of more than 24 hours to treatment did not result in a statistically
significant increase in the rate of rebleeding (2 [33%] of 6 vs 1 [8%] of
13; P = .11). Within the white population, no secondary
hemorrhages (0/3) developed in the group of patients who were seen more than
24 hours after the initial injury.
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Figure 2. A, The rate of secondary hemorrhage
was statistically higher in the African American (AA) population compared
with the non-AA population (4 [21%] of 19 vs 0 [0%] of 20; P=
.05). B, The rate of secondary hemorrhage among patients with sickle cell
hemoglobinopathy (AS + SS) compared with those without AS + SS was not statistically
significantly different (1 [20%] of 5 vs 3 [9%] of 34; P= .44).
C, When the analysis was restricted to only AA patients, the rate of secondary
hemorrhage among AA patients with AS + SS and without AS + SS was not statistically
significantly different (1 [20%] of 5 vs 3 [21%] of 14; P>.99).
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Table 1. Patients With Secondary Hemorrhage*
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The difference in mean (±SEM) IOP at presentation between patients
with sickle cell trait (43 ± 9 mm Hg) and patients without sickle cell
trait (20 ± 1 mm Hg) approached statistical significance (P = .06) (Figure 3A). When
the patient with sickle cell disease was included in the analysis, the mean
(±SEM) IOP of patients with sickle cell hemoglobinopathy on admission
remained 43 ± 7 mm Hg (Figure 3B).
With this additional patient, the IOP at presentation of patients with sickle
cell hemoglobinopathy was statistically higher than that of those without
it (P = .03). In the analysis restricted solely to
African American patients, those with sickle cell hemoglobinopathy had a statistically
higher IOP at presentation than African American patients with a normal hemoglobin
level (43 ± 7 vs 20 ± 2 mm Hg; P =
.03) (Figure 3C).
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Figure 3. A, The difference in mean (±SEM)
intraocular pressure (IOP) at presentation between patients with sickle cell
trait (AS) and without AS approached statistical significance (43 ±
9 vs 20 ± 1 mm Hg; P= .06) (the patient with sickle cell
disease was excluded from this analysis). B, When the patient with sickle
cell disease was included in the analysis, the difference in mean IOP at presentation
between patients with sickle cell hemoglobinopathy (AS + SS) and without AS
+ SS was statistically significant (43 ± 7 vs 20 ± 1 mm Hg; P= .03). C, In the analysis restricted solely to African American patients,
those with AS + SS had a statistically higher IOP at presentation than those
with a normal hemoglobin level (43 ± 7 vs 20 ± 2 mm Hg; P= .03).
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An initially higher IOP at presentation was not, however, found to be
associated with a higher rate of secondary hemorrhage in the analysis comparing
patients with and without sickle cell hemoglobinopathy (P = .13). Similarly, when the analysis was restricted to only African
American patients, there was still no statistically increased risk for secondary
hemorrhage in patients who were initially seen with a higher IOP (P = .40).
The rate of IOP elevation in the eyes of subjects with sickle cell trait
(4 [80%] of 5) was significantly higher than that in eyes of patients without
sickle cell trait (5 [15%] of 34) (P = .006) (Figure 4A). The 1 patient with sickle cell
disease had an elevated IOP on admission but did not develop further episodes
of IOP elevation during hospitalization. When this patient was included in
the analysis, the rate of IOP elevation for patients with sickle cell hemoglobinopathy
decreased to 67% (4/6) (Figure 4B).
The association between sickle cell hemoglobinopathy and IOP elevation remained
significant (P = .02). When the analysis was restricted
to African American patients, the difference in the rate of IOP elevation
between patients with and without sickle cell hemoglobinopathy approached
statistical significance (4 [67%] of 6 vs 3 [21%] of 14; P = .05) (Figure 4C).
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Figure 4. A, The rate of intraocular pressure
(IOP) elevation in subjects with sickle cell trait (AS) was significantly
higher than that in subjects without AS (4 [80%] of 5 vs 5 [15%] of 34; P= .006). B, The rate of IOP elevation for patients with sickle cell
hemoglobinopathy (AS + SS) was significantly higher than that for patients
with a normal hemoglobin level (4 [67%] of 6 vs 5 [15%] of 34; P=
.02). C, When the analysis was restricted to African American patients, the
difference in the rate of IOP elevation between patients with and without
AS + SS approached statistical significance 4 [67%] of 6 vs 3 [21%] of 14; P= .05).
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Using a multivariate logistic regression analysis, the association between
sickle cell hemoglobinopathy and secondary hemorrhage was not found to be
statistically significant (P>.05). Patients with
sickle cell hemoglobinopathy, however, were approximately 8 times more likely
to have developed an IOP elevation (odds ratio, 8.33; 95% confidence interval,
1.03-66.67), even after controlling for the development of secondary hemorrhage.
However, when the analysis was restricted to African American patients, this
association was no longer statistically significant (P>.05)
(odds ratio, 6.21; 95% confidence interval, 0.62-62.50).
Three patients, all with a sickle cell hemoglobinopathy, required surgical
intervention. Two patients, 1 with sickle cell disease and the other with
sickle cell trait, underwent an anterior chamber washout following the development
of a secondary hemorrhage. The third subject with sickle cell trait underwent
an anterior chamber washout for a grade 4 hyphema and an elevated IOP. This
patient subsequently developed a secondary hemorrhage 3 days following the
procedure. The association between sickle cell hemoglobinopathy and surgical
intervention approached statistical significance (P
= .05). Race, initial hyphema size, initial visual acuity, initial IOP, and
subsequent elevation of IOP were not associated with an increased risk of
surgical intervention (P = .23, P = .39, P = .20, P
= .31, and P = .12, respectively).
On admission, African American patients had a visual acuity of 20/40
or better in 9 (45%) of 20 patients compared with 8 (40%) of 20 non–African
American patients. Of the African American patients with sickle cell hemoglobinopathy,
2 (33%) of 6 had a visual acuity of 20/40 or better compared with 7 (50%)
of 14 African American patients without sickle cell hemoglobinopathy. On discharge
from the hospital, the visual acuity was 20/40 or better in 13 (65%) of 20
patients in the African American and the non–African American groups.
Of African American patients with sickle cell hemoglobinopathy, 3 (50%) of
6 had a visual acuity of 20/40 or better compared with 10 (71%) of 14 African
American patients without sickle cell hemoglobinopathy. Because many patients
were lost to follow-up (15 at the 1-week follow-up and 27 at the 4-week follow-up),
no meaningful analysis of long-term visual acuity could be performed. However,
no cases of corneal blood staining, optic atrophy, or vascular occlusions
developed during the follow-up that was recorded.
COMMENT
The presence of a sickle cell hemoglobinopathy in a patient with traumatic
hyphema is associated with an increased risk of ocular complications.24-26 Within the stagnant
environment of a hyphema, the erythrocytes in these eyes are predisposed to
sickling and to clogging the trabecular outflow tract. The resultant IOP elevation
leads to hypoperfusion and hypoxia of the anterior and posterior segments
of the eye, thereby perpetuating a cycle in which further sickling and sludging
of erythrocytes occur. The end result is that these patients are more likely
to develop central retinal artery occlusion or optic nerve damage at only
modest elevations in IOP compared with patients with normal erythrocytes.
Relatively few studies8, 12, 19, 21, 29
have examined the risk of secondary hemorrhage in patients with traumatic
hyphema and sickle cell hemoglobinopathy. Reported rates of secondary hemorrhage
in patients with sickle cell hemoglobinopathy range from 0% to 80% (Table 2). It remains unclear whether the
presence of a sickle cell hemoglobinopathy increases the likelihood of secondary
hemorrhage.
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Table 2. Rate of Secondary Hemorrhage in African American Patients
With Sickle Cell Hemoglobinopathy*
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Our study retrospectively reviewed the inpatient records of all children
admitted to the Wilmer Ophthalmological Institute from July 1990 through December
1997. This 7 -year period was chosen because the department's databases
were computerized beginning in 1990, and because pediatric patients with traumatic
hyphema were routinely admitted for treatment during this period. Our study
population consisted of an equal distribution of African American and non–African
American patients. The overall rate of secondary hemorrhage in our study was
10.3%. The rate of rebleeding in African Americans in our study was significantly
higher than that of non–African Americans (21% vs 0%); (P = .047). This finding is consistent with other reports4, 7-8,21, 23, 29
that have found a higher rate of rebleeding in the African American population
(Table 3). It is unclear what
accounts for this racial difference in the rate of secondary hemorrhage. One
hypothesis is that confounding socioeconomic issues, such as increased severity
of disease or delay in seeking medical attention, may increase the likelihood
of recurrent bleeding in the African American population.4, 8, 23
Other reports4, 23 have postulated
that there may simply be a predisposition of unknown type, possibly enhanced
uveal inflammation and vascular congestion, for African American individuals
to develop a rebleed.
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Table 3. Increased Rate of Secondary Hemorrhage in African American
Patients
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Whether the increased frequency of sickle cell hemoglobinopathy in African
American individuals contributes to their propensity for developing a secondary
hemorrhage has been unclear. Our data suggest that sickle cell hemoglobinopathy
may not increase the risk of secondary hemorrhage. In this study, the rate
of rebleeding among patients with sickle cell hemoglobinopathy was 20% (1/5)
and the rate of rebleeding in those without sickle cell hemoglobinopathy was
9% (3/34). This was not a significant difference (P
= .44). Furthermore, when the analysis was restricted to African American
patients, those with sickle cell hemoglobinopathy (1 [20%] of 5) did not have
a statistically higher rate of rebleeding compared with those with a normal
hemoglobin level (3 [21%] of 14) (P>.99). The lack
of a significant association may have been the result of the sample size not
being statistically powerful enough to detect small differences among groups
of patients (power = 9% when the patient with sickle cell disease was excluded,
and power = 25% when the patient with sickle cell disease was included). Additional
studies with larger sample sizes may clarify the possible relation between
sickle cell hemoglobinopathy and the development of secondary hemorrhage.
However, because the difference in the rate of secondary hemorrhage between
African American patients with and without sickle cell hemoglobinopathy is
so small, it is unlikely that a clinically significant difference in the rates
would exist even with larger sample sizes.
Our study did confirm the finding in previous reports24-26
that patients with a sickle cell hemoglobinopathy were at a higher risk for
developing an elevation in IOP. The mean IOP at initial examination of patients
with sickle cell hemoglobinopathy was significantly higher than that of patients
without hemoglobinopathy (43 ± 7 vs 20 ± 1 mm Hg; P = .03). Furthermore, the subsequent rate of IOP elevation during
hospitalization was significantly higher in patients with a sickle cell hemoglobinopathy
(66% vs 15%; P = .02). Of 5 patients with sickle
cell trait, 4 developed an IOP elevation during hospitalization. The 1 patient
with sickle cell disease initially had an IOP of 40 mm Hg and was immediately
prescribed an aggressive pressure-lowering regimen, which probably prevented
any subsequent IOP elevation. The increased risk for the development of an
IOP elevation in patients with sickle cell hemoglobinopathy is likely due
to the clogging of the trabecular meshwork by sickled erythrocytes.24-25 Unlike other studies,6, 22
however, a higher IOP at presentation was not associated with an increased
risk of secondary hemorrhage in our study.
The identification of patient characteristics predictive for secondary
hemorrhage may assist in guiding management decisions in the treatment of
patients with traumatic hyphema. In this study, we found that African American
patients are at a higher risk of developing a rebleed. These patients may
deserve closer clinical scrutiny than non–African American patients.
Based on evidence that non–African American patients are less likely
to rebleed and, therefore, less likely to benefit from aminocaproic acid treatment,
other studies15, 17, 30
have recommended that aminocaproic acid treatment be reserved only for patients
at greater risk for secondary hemorrhage. In our study, the decision to initiate
oral aminocaproic acid treatment was not influenced by the patient's race.
However, based on the results of this and previous studies,15, 17, 30
we recommend that aminocaproic acid treatment be based on individual patient
characteristics, including race.
We have also found that patients with sickle cell hemoglobinopathy are
more likely to have a higher IOP and to develop subsequent elevations in IOP.
It is unclear whether this translates into an increased risk of secondary
hemorrhage, but our data do not support this relation. Until this question
is resolved, we recommend that patients with sickle cell hemoglobinopathy
who have traumatic hyphema continue to receive aggressive management to lower
their IOP, because they are at greater risk for developing other associated
ocular complications such as IOP elevations, central retinal artery occlusions,
and optic neuropathies, as demonstrated by this and previous studies.24-26
AUTHOR INFORMATION
Accepted for publication May 25, 2000.
This study was supported in part by core grant EY 01765 from the National
Institutes of Health, Bethesda, Md; an unrestricted research grant from Research
to Prevent Blindness Inc, New York, NY; and a travel fellowship grant from
the National Eye Institute, Bethesda, and the Association for Research in
Vision and Ophthalmology, Rockville, Md.
Presented in part at the Association for Research in Vision and Ophthalmology
Meeting, Fort Lauderdale, Fla, March 15, 1998.
Reprints: Morton F. Goldberg, MD, Wilmer Ophthalmological Institute,
The Johns Hopkins Medical Institutions, 727 Maumenee Bldg, 600 N Wolfe St,
Baltimore, MD 21287-9278 (e-mail: mgoldbrg{at}jhmi.edu).
From the Wilmer Ophthalmological Institute, The Johns Hopkins Medical
Institutions, Baltimore, Md.
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Risk Factors for Complications Following Traumatic Hyphema
Lai et al.
Arch Ophthalmol 2001;119:1732-1732.
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