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Review
. 2023 Mar 13;3(3):CD005431.
doi: 10.1002/14651858.CD005431.pub5.

Medical interventions for traumatic hyphema

Fasika A Woreta  1 , Kristina B Lindsley  2 , Almutez Gharaibeh  3 , Sueko M Ng  4 , Roberta W Scherer  5 , Morton F Goldberg  1
Affiliations
Review

Medical interventions for traumatic hyphema

Fasika A Woreta et al. Cochrane Database Syst Rev. .

Abstract

Background: 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: To assess the effectiveness of various medical interventions in the management of traumatic hyphema.

Search methods: 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.

PubMed Disclaimer

Conflict of interest statement

FW: none known

KL: none known

AG: none known

SN: none known

RS: none known

MG was an investigator for some of the trials included in this review and was a paid consultant for Panoptic Inc (not related to hyphema) and a non‐paid board member for Eyetech Inc (not related to hyphema).

Figures

1
1
Study flow diagram.
2
2
Methodologic quality summary: review authors' judgements about each methodologic quality item for each included study. Green: low risk of bias; red: high risk of bias; yellow: unclear risk of bias.
1.1
1.1. Analysis
Comparison 1: Systemic aminocaproic acid versus placebo, Outcome 1: Short‐term visual acuity from 20/20 to 20/40
1.2
1.2. Analysis
Comparison 1: Systemic aminocaproic acid versus placebo, Outcome 2: Long‐term visual acuity between 20/20 and 20/40
1.3
1.3. Analysis
Comparison 1: Systemic aminocaproic acid versus placebo, Outcome 3: Final visual acuity between 20/20 and 20/40
1.5
1.5. Analysis
Comparison 1: Systemic aminocaproic acid versus placebo, Outcome 5: Risk of secondary hemorrhage
1.7
1.7. Analysis
Comparison 1: Systemic aminocaproic acid versus placebo, Outcome 7: Risk of corneal blood stain
1.9
1.9. Analysis
Comparison 1: Systemic aminocaproic acid versus placebo, Outcome 9: Risk of glaucoma or elevated IOP
1.10
1.10. Analysis
Comparison 1: Systemic aminocaproic acid versus placebo, Outcome 10: Risk of optic atrophy
1.11
1.11. Analysis
Comparison 1: Systemic aminocaproic acid versus placebo, Outcome 11: Adverse effects: nausea or vomiting
2.1
2.1. Analysis
Comparison 2: Topical aminocaproic acid versus placebo, Outcome 1: Short‐term visual acuity from 20/20 to 20/40
2.3
2.3. Analysis
Comparison 2: Topical aminocaproic acid versus placebo, Outcome 3: Risk of secondary hemorrhage
2.5
2.5. Analysis
Comparison 2: Topical aminocaproic acid versus placebo, Outcome 5: Risk of glaucoma or elevated IOP
3.1
3.1. Analysis
Comparison 3: Low‐dose versus standard‐dose aminocaproic acid, Outcome 1: Unspecified time for visual acuity between 20/20 and 20/40
3.2
3.2. Analysis
Comparison 3: Low‐dose versus standard‐dose aminocaproic acid, Outcome 2: Time to resolution of primary hemorrhage (days)
3.3
3.3. Analysis
Comparison 3: Low‐dose versus standard‐dose aminocaproic acid, Outcome 3: Risk of secondary hemorrhage
3.5
3.5. Analysis
Comparison 3: Low‐dose versus standard‐dose aminocaproic acid, Outcome 5: Risk of glaucoma or elevated IOP
3.6
3.6. Analysis
Comparison 3: Low‐dose versus standard‐dose aminocaproic acid, Outcome 6: Adverse effects
3.7
3.7. Analysis
Comparison 3: Low‐dose versus standard‐dose aminocaproic acid, Outcome 7: Duration of hospitalization (days)
4.1
4.1. Analysis
Comparison 4: Systemic versus topical aminocaproic acid, Outcome 1: Short‐term visual acuity from 20/20 to 20/40
4.2
4.2. Analysis
Comparison 4: Systemic versus topical aminocaproic acid, Outcome 2: Risk of secondary hemorrhage
4.3
4.3. Analysis
Comparison 4: Systemic versus topical aminocaproic acid, Outcome 3: Adverse effects
5.1
5.1. Analysis
Comparison 5: Systemic tranexamic acid versus control, Outcome 1: Short‐term visual acuity from 20/20 to 20/40
5.3
5.3. Analysis
Comparison 5: Systemic tranexamic acid versus control, Outcome 3: Risk of secondary hemorrhage
5.5
5.5. Analysis
Comparison 5: Systemic tranexamic acid versus control, Outcome 5: Risk of corneal blood stain
5.6
5.6. Analysis
Comparison 5: Systemic tranexamic acid versus control, Outcome 6: Risk of glaucoma or elevated IOP
5.7
5.7. Analysis
Comparison 5: Systemic tranexamic acid versus control, Outcome 7: Adverse effects: nausea or vomiting
6.1
6.1. Analysis
Comparison 6: Aminomethylbenzoic acid versus placebo, Outcome 1: Risk of secondary hemorrhage
7.1
7.1. Analysis
Comparison 7: Corticosteroids versus control, Outcome 1: Short‐term (5 to 14 days) visual acuity from 20/20 to 20/40, systemic corticosteroids
7.2
7.2. Analysis
Comparison 7: Corticosteroids versus control, Outcome 2: Visual acuity between 20/20 and 20/50 at resolution of hyphema, systemic corticosteroids
7.3
7.3. Analysis
Comparison 7: Corticosteroids versus control, Outcome 3: Short‐term (5 to 14 days) visual acuity from 20/20 to 20/40, topical corticosteroids
7.4
7.4. Analysis
Comparison 7: Corticosteroids versus control, Outcome 4: Final visual acuity between 20/20 and 20/25, topical corticosteroids
7.7
7.7. Analysis
Comparison 7: Corticosteroids versus control, Outcome 7: Risk of secondary hemorrhage, systemic corticosteroids
7.8
7.8. Analysis
Comparison 7: Corticosteroids versus control, Outcome 8: Risk of secondary hemorrhage, topical corticosteroids
7.10
7.10. Analysis
Comparison 7: Corticosteroids versus control, Outcome 10: Risk of corneal blood stain, systemic corticosteroids
7.11
7.11. Analysis
Comparison 7: Corticosteroids versus control, Outcome 11: Risk of corneal blood stain, topical corticosteroids
7.12
7.12. Analysis
Comparison 7: Corticosteroids versus control, Outcome 12: Risk of peripheral anterior synechiae, systemic corticosteroids
7.13
7.13. Analysis
Comparison 7: Corticosteroids versus control, Outcome 13: Risk of glaucoma or elevated IOP, systemic corticosteroids
7.14
7.14. Analysis
Comparison 7: Corticosteroids versus control, Outcome 14: Risk of glaucoma or elevated IOP, topical corticosteroids
7.15
7.15. Analysis
Comparison 7: Corticosteroids versus control, Outcome 15: Risk of optic atrophy, topical corticosteroids
7.16
7.16. Analysis
Comparison 7: Corticosteroids versus control, Outcome 16: Duration of hospitalization (days), systemic corticosteroids
8.1
8.1. Analysis
Comparison 8: Aminocaproic acid versus prednisone, Outcome 1: Short‐term (5 to 14 days) visual acuity from 20/20 to 20/40
8.2
8.2. Analysis
Comparison 8: Aminocaproic acid versus prednisone, Outcome 2: Risk of secondary hemorrhage
8.3
8.3. Analysis
Comparison 8: Aminocaproic acid versus prednisone, Outcome 3: Adverse effect: any adverse event
9.1
9.1. Analysis
Comparison 9: Topical tranexamic acid versus prednisone, Outcome 1: Short‐term visual acuity from 20/20 to 20/40
9.3
9.3. Analysis
Comparison 9: Topical tranexamic acid versus prednisone, Outcome 3: Risk of secondary hemorrhage
10.1
10.1. Analysis
Comparison 10: Conjugated estrogen versus placebo, Outcome 1: Risk of secondary hemorrhage
10.2
10.2. Analysis
Comparison 10: Conjugated estrogen versus placebo, Outcome 2: Risk of corneal blood stain
11.1
11.1. Analysis
Comparison 11: Cycloplegics versus miotics, Outcome 1: Short‐term visual acuity
11.2
11.2. Analysis
Comparison 11: Cycloplegics versus miotics, Outcome 2: Time to resolution of primary hemorrhage (days)
11.3
11.3. Analysis
Comparison 11: Cycloplegics versus miotics, Outcome 3: Risk of secondary hemorrhage
12.1
12.1. Analysis
Comparison 12: Aspirin versus observation, Outcome 1: Risk of secondary hemorrhage
13.1
13.1. Analysis
Comparison 13: Monocular versus binocular patching, Outcome 1: Short‐term visual acuity
13.2
13.2. Analysis
Comparison 13: Monocular versus binocular patching, Outcome 2: Variable time length 'final' visual acuity
13.3
13.3. Analysis
Comparison 13: Monocular versus binocular patching, Outcome 3: Risk of secondary hemorrhage
13.5
13.5. Analysis
Comparison 13: Monocular versus binocular patching, Outcome 5: Risk of corneal blood stain
13.6
13.6. Analysis
Comparison 13: Monocular versus binocular patching, Outcome 6: Risk of glaucoma or elevated IOP
14.1
14.1. Analysis
Comparison 14: Ambulatory versus conservative treatment, Outcome 1: Short‐term visual acuity
14.3
14.3. Analysis
Comparison 14: Ambulatory versus conservative treatment, Outcome 3: Risk of secondary hemorrhage
14.4
14.4. Analysis
Comparison 14: Ambulatory versus conservative treatment, Outcome 4: Risk of corneal blood stain
14.5
14.5. Analysis
Comparison 14: Ambulatory versus conservative treatment, Outcome 5: Risk of glaucoma or elevated IOP
See this image and copyright information in PMC

Update of

References

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References to studies excluded from this review

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Krasnov 1971b {published data only}
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Latinovic 1981 {published data only}
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Li 1997 {published data only}
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Logai 1974 {published data only}
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Mathis 1987 {published data only}
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Missotten 1977 {published data only}
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Mortensen 1978 {published data only}
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Munoz Negrete 1989 {published data only}
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Murzin 1966 {published data only}
    1. Murzin AA. Experiences with the use of fibrinolysin and trypsin in intraocular hemorrhages [Opyt primeneniia fibrinolizina i tripsina pri vnutriglaznykh krovoizliianiiakh]. Vestnik Oftalmologii 1966;79(3):19-21. - PubMed
Ohrstrom 1972 {published data only}
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Oksala 1967 {published data only}
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Pierse 1964 {published data only}
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Pogorel'skii 1966 {published data only}
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Polychronakos 1967 {published data only}
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Rakusin 1971 {published data only}
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Roberts 2006 {published data only}
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Romano 1986 {published data only}
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Romashchenko 1985 {published data only}
    1. Romashchenko AD, Makarova VP. Experience in treating intraocular hemorrhage using immobilized streptokinase [Opyt lecheniia vnutrioglaznogo krovoizliianiia s pomoshch'iu immobilizovannoi streptokinazy]. Oftalmologicheskii Zhurnal 1985;3:148-51. - PubMed
Rouher 1966 {published data only}
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Spoor 1990 {published data only}
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Stepanov 2002 {published data only}
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Surel 1987 {published data only}
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Tartakovskaia 1972 {published data only}
    1. Tartakovskaia AI, Mikhailova NA. Pathogenetic role of fibrinolysis in recurring intra-ocular hemorrhages and their treatment with sigma-aminocapronic acid [Patogeneticheskaia rol' fibrinoliza pri retsidiviruiushchikh vnutriglaznykh krovoizliianiikah i ikh terapiia sigma-aminokapronovoi kislotoi]. Vestnik Oftalmologii 1972;1:41-5. - PubMed
Travkin 1997 {published data only}
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Uusitalo 1988 {published data only}
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Volpe 1991 {published data only}
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Wang 2010 {published data only}
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Watkins 1974 {published data only}
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Williamson 1973 {published data only}
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Yasuna 1974 {published data only}
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Zhang 2013 {published data only}
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Zhang 2014 {published data only}
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Zhou 1982 {published data only}
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References to other published versions of this review

Gharaibeh 2011
    1. Gharaibeh A, Savage HI, Scherer RW, Goldberg MF, Lindsley K. Medical interventions for traumatic hyphema. Cochrane Database of Systematic Reviews 2011, Issue 1. Art. No: CD005431. [DOI: 10.1002/14651858.CD005431.pub2] - DOI - PMC - PubMed
Gharaibeh 2013
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Gharaibeh 2019
    1. Gharaibeh A, Savage HI, Scherer RW, Goldberg MF, Lindsley K. Medical interventions for traumatic hyphema. Cochrane Database of Systematic Reviews 2019, Issue 1. Art. No: CD005431. [DOI: 10.1002/14651858.CD005431.pub4] - DOI - PMC - PubMed
Savage 2005
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