Traumatic
hyphema is the entry of blood into the anterior chamber, the space between the cornea and iris, following significant injury to the eye.
Hyphema may be associated with significant complications that uncommonly cause permanent vision loss. Complications include elevated intraocular pressure, corneal blood staining, anterior and posterior synechiae, and optic nerve
atrophy. People with
sickle cell trait or disease may be particularly susceptible to increases in intraocular pressure and
optic atrophy. Rebleeding is associated with an increase in the rate and severity of complications.
OBJECTIVES: We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (which contains the Cochrane Eyes and Vision Trials Register) (2022, Issue 3); MEDLINE Ovid; Embase.com; PubMed (1948 to March 2022); the ISRCTN registry; ClinicalTrials.gov; and the World Health Organization (WHO) International Clinical Trials Registry Platform (ICTRP). The last date of the search was 22 March 2022.
SELECTION CRITERIA: Two review authors independently assessed the titles and abstracts of all reports identified by the electronic and manual searches. We included randomized and quasi-randomized trials that compared various medical (non-surgical) interventions versus other medical interventions or control groups for the treatment of traumatic
hyphema following closed-globe
trauma. We applied no restrictions on age, gender, severity of the closed-globe
trauma, or level of visual acuity at time of enrollment.
DATA COLLECTION AND ANALYSIS: We used standard methodological procedures expected by Cochrane and assessed the certainty of evidence using GRADE.
MAIN RESULTS: We included 23 randomized and seven quasi-randomized studies with a total of 2969 participants. Interventions included
antifibrinolytic agents (systemic and topical
aminocaproic acid,
tranexamic acid, and aminomethylbenzoic
acid),
corticosteroids (systemic and topical),
cycloplegics,
miotics,
aspirin,
conjugated estrogens,
traditional Chinese medicine, monocular versus bilateral patching, elevation of the head, and
bed rest. We found no evidence of an effect on visual acuity for any intervention, whether measured within two weeks (short term) or for longer periods. In a meta-analysis of two trials, we found no evidence of an effect of
aminocaproic acid on long-term visual acuity (RR 1.03, 95% confidence interval (CI) 0.82 to 1.29) or final visual acuity measured up to three years after the
hyphema (RR 1.05, 95% CI 0.93 to 1.18). Oral
tranexamic acid appeared to provide little to no benefit on visual acuity in four trials (RR 1.12, 95% CI 1.00 to 1.25). The remaining trials evaluated the effects of various interventions on short-term visual acuity; none of these interventions was measured in more than one trial. No intervention showed a statistically significant effect (RRs ranged from 0.75 to 1.10). Similarly, visual acuity measured for longer periods in four trials evaluating different interventions was also not statistically significant (RRs ranged from 0.82 to 1.02). The evidence supporting these findings was of low or very low certainty. Systemic
aminocaproic acid reduced the rate of recurrent
hemorrhage (RR 0.28, 95% CI 0.13 to 0.60), as assessed in six trials with 330 participants. A sensitivity analysis omitting two studies not using an intention-to-treat analysis reduced the strength of the evidence (RR 0.43, 95% CI 0.17 to 1.08). We obtained similar results for topical
aminocaproic acid (RR 0.48, 95% CI 0.20 to 1.10) in two trials with 131 participants. We assessed the certainty of the evidence as low. Systemic
tranexamic acid had a significant effect in reducing the rate of secondary
hemorrhage (RR 0.33, 95% CI 0.21 to 0.53) in seven trials with 754 participants, as did aminomethylbenzoic
acid (RR 0.10, 95% CI 0.02 to 0.41), as reported in one study. Evidence to support an associated reduction in risk of complications from secondary
hemorrhage (i.e. corneal blood staining, peripheral anterior synechiae, elevated intraocular pressure, and development of
optic atrophy) by
antifibrinolytics was limited by the small number of these events. Use of
aminocaproic acid was associated with increased
nausea,
vomiting, and other adverse events compared with placebo. We found no evidence of an effect on the number of adverse events with the use of systemic versus topical
aminocaproic acid or with standard versus lower
drug dose. The number of days for the primary
hyphema to resolve appeared to be longer with the use of systemic
aminocaproic acid compared with no use, but this outcome was not altered by any other intervention. The available evidence on usage of systemic or topical
corticosteroids,
cycloplegics, or
aspirin in traumatic
hyphema was limited due to the small numbers of participants and events in the trials. We found no evidence of an effect between a single versus
binocular patch on the risk of secondary
hemorrhage or time to rebleed. We also found no evidence of an effect on the risk of secondary
hemorrhage between ambulation and complete
bed rest.
AUTHORS' CONCLUSIONS: We found no evidence of an effect on visual acuity of any of the interventions evaluated in this review. Although the evidence was limited, people with traumatic
hyphema who receive
aminocaproic acid or
tranexamic acid are less likely to experience secondary
hemorrhage. However,
hyphema took longer to clear in people treated with systemic
aminocaproic acid. There is no good evidence to support the use of
antifibrinolytic agents in the management of traumatic
hyphema, other than possibly to reduce the rate of secondary
hemorrhage. The potentially long-term deleterious effects of secondary
hemorrhage are unknown. Similarly, there is no evidence to support the use of
corticosteroids,
cycloplegics, or non-
drug interventions (such as patching,
bed rest, or head elevation) in the management of traumatic
hyphema. As these multiple interventions are rarely used in isolation, further research to assess the additive effect of these interventions might be of value.