Controversies in The Pathophysiology and Management of Hyphema
Controversies in The Pathophysiology and Management of Hyphema
Controversies in The Pathophysiology and Management of Hyphema
ScienceDirect
Major review
Article history: Traumatic hyphemas present dilemmas to physicians. There are numerous controversies
Received 9 May 2015 pertaining to the optimal approach to traumatic hyphema and no standardized guidelines
Received in revised form 12 for its management. We address some of these controversies and present a pragmatic
November 2015 approach. We discuss various medical agents and surgical techniques available for treat-
Accepted 23 November 2015 ment, along with the indications for their use. We address the complications associated
Available online 26 November 2015 with hyphema and how to diagnose and manage them and consider the management of
hyphema in special situations such as in children and sickle-cell anemia and in rare
Keywords: clinical syndromes such as recurrent hyphema after placement of anterior chamber
hyphema intraocular lenses.
traumatic glaucoma ª 2016 Elsevier Inc. All rights reserved.
surgical drainage
angle recession
* Corresponding author: Rupesh Agrawal, MMed, FRCS (Glasg), FAMS, DNB, DO, National Healthcare Group Eye Institute, Tan Tock
Seng Hospital, Singapore 308433.
E-mail address: rupesh_agrawal@ttsh.com.sg (R. Agrawal).
0039-6257/$ e see front matter ª 2016 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.survophthal.2015.11.005
298 s u r v e y o f o p h t h a l m o l o g y 6 1 ( 2 0 1 6 ) 2 9 7 e3 0 8
options include bed rest, head elevation, an eye shield, and the Delayed hyphema after intraocular surgery may be the
use of pharmacologic agents (topical or systemic steroids, result of granulation tissue at the wound margin or caused by
antifibrinolytics, cycloplegics, miotics, aspirin, traditional Chi- damaged uveal vessels (e.g. from surgical trauma or from
nese medicine, and conjugated estrogen).34 Aside from the use intraocular lens-induced uveal trauma).63,94 This mechanism
of antifibrinolytics to prevent secondary hemorrhage, however, should be considered in patients with a history of ocular
there is no evidence of benefit from the use of these conser- surgery who present with spontaneous hyphema.
vative measures.34 Furthermore, there is a lack of consensus In the pediatric age group (less than 18 years of age)
regarding a treatment and follow-up strategy targeted at pre- hyphemas in the absence of predisposing ocular or systemic
venting delayed visual loss from complications of hyphema, as disease or medication should arouse the suspicion of non-
well as the management of certain special situations such as accidental injury.59 A significant but rare cause of sponta-
concurrent sickle-cell anemia. neous hyphema in children is juvenile xanthogranuloma.
We aim to address the controversies in the pathophysi- Juvenile xanthogranuloma is a predominantly dermatological
ology, evaluation, and management of hyphema. Because disorder most commonly presenting in children less than
trauma is the commonest cause, we focus our discussion on 2 years old characterized by a raised, orange skin lesions
closed-globe traumatic hyphema; however, we also analyze occurring either singly or in crops that will regress sponta-
special situations such as uveitis, pediatric hyphema, cataract neously. The most common ocular finding is diffuse or
surgery, refractive surgery, and hyphema in patients with discrete iris nodules that are often quite vascular and may
sickle-cell anemia. bleed spontaneously. Occasionally, the lesions may present in
other areas such as ciliary body, anterior choroid, cornea, lids,
and orbit.47 Complications include uveitis and glaucoma, with
resulting visual loss and phthisis. Biopsy of skin lesions helps
2. Pathophysiology of hyphema to confirm the diagnosis. The lesions classically contain an
infiltrate of lipid-laden histiocytes, lymphocytes, eosinophils,
The mean annual incidence rate of traumatic hyphema is and Touton giant cells.
estimated as 17/100,000 population in individuals less than Histologic examination of hyphemas reveals an erythro-
18 years of age1 and 20.7/100,000 population in individuals less cyte aggregate enveloped by a pseudocapsule of fibrin-plated
than 20 years of age.50 Direct orbital injury resulting in trau- coagulum.47 Clot absorption takes place by breakdown of
matic hyphema usually consists of a high-energy blow to the fibrin by fibrinolytic agents and escape of red blood cells
orbit (61%e66%), impact from a projectile (30.2%e36%), or through the trabecular meshwork and Schlemm canal.47
injury secondary to an explosion (2.4%e3%).50,97 Athletic in- Agents that open the trabecular meshwork thus accelerate
juries have become a major cause of traumatic hyphema, clot absorption.
whereas accidents at work have become relatively less
frequent. Kearns reported that athletic injuries accounted for
39.2% of 314 cases of traumatic hyphema, whereas accidents 3. Clinical features and examination
at work were responsible for 9.9% of the cases.49
The commonest source of blood in hyphema is a tear in The importance of a detailed history and a thorough ocular and
the anterior face of the ciliary body.107 A direct blow to the systemic evaluation cannot be stressed enough. The nature of
eye can rupture the blood vessels at the root of the iris. The the injury points to the likely type of damage sustained and
most frequently ruptured vessels are the major arterial therefore the prognosis. The priority in trauma is always to
circle of the iris and its branches, the recurrent choroidal stabilize airway, breathing, and circulation, and make an
arteries, and the veins crossing the suprachoroidal space assessment for threats to life. This is followed by an ophthalmic
between the ciliary body and episcleral venous plexus.95,107 evaluation that includes inspection for gross ocular injury,
Blunt injury is also associated with anteroposterior evaluation of the adnexae, visual acuity, pupillary function,
compression of the globe and simultaneous equatorial globe ocular motility, and the position of the globes.
expansion. Equatorial expansion induces stress on anterior Extensive conjunctival chemosis and hemorrhage may
chamber angle structures, which may lead to rupture of iris indicate an occult scleral rupture (Fig. 1). Proptosis may be
stromal and/or ciliary body vessels with subsequent hemor- secondary to a retrobulbar hematoma, and restriction in
rhage.22,95 Another possible source of initial hemorrhage is a ocular motility may suggest an orbital blowout fracture or a
rapid increase in intraocular pressure (IOP) immediately after contusive head injury. Every attempt should be made to
the contusive trauma. This eventually leads to rupture of the examine the adnexal region carefully and rule out any asso-
fragile vasculature of the iris from the pupillary sphincter ciated orbital or head trauma. Hyphema can be associated
and/or angle.22 with open-globe (Fig. 2A) or closed-globe injuries. In patients
Lacerating injury may be associated with direct damage to with open-globe injury, primary wound closure is the priority
blood vessels and hypotony, both of which can precipitate (Fig. 2B). One should not attempt surgical washout of
hyphema.107 There is no consensus regarding the predomi- hyphema in open-globe injuries as the blind approach could
nant source of bleeding (angle vessels or iris sphincter vessels) lead to adverse consequences. Surgical washout can be
and their respective risks of rebleeding; however, current considered in patients with nonresolving hyphema or sickle-
opinion is that fragile angle vessels have the higher risk of cell trait because of the higher risk of secondary glaucoma
bleeding as a result of their proximity to the major arterial and permanent visual loss.34 We shall focus on hyphema after
circle of the iris.22 closed-globe trauma.
s u r v e y o f o p h t h a l m o l o g y 6 1 ( 2 0 1 6 ) 2 9 7 e3 0 8 299
Microhyphema Circulating
RBC’s only
II 1/3e1/2 of AC
III >1/2 of AC
Fig. 3 e Different shades of red: E, B, and C: old traditional terminology is based on black (eigth) ball of snooker, however as
seen in panels B and C, D: there is presence of more bright red color and dull red color in panel D which closely resembles A:
Red (third or 11th) of snooker.
s u r v e y o f o p h t h a l m o l o g y 6 1 ( 2 0 1 6 ) 2 9 7 e3 0 8 301
by 50% after day 6.79 Corneal blood staining starts as central complications of anticoagulant medications has been re-
straw yellow discoloration of the deep stroma that spreads ported to be significantly greater than that of antiplatelet
peripherally. Blood staining causes endothelial decompensa- medications.86 Common indications for anticoagulation
tion by mechanical disruption of the endothelium and also by therapy include atrial fibrillation, prosthetic heart valves, and
photosensitization of the endothelium by hemoglobin- deep vein thrombosis. Antiplatelet therapy is commonly
derived porphyrins in the presence of light.39,40 The blood indicated for the prevention of acute cardiac and cerebro-
staining clears centripetally and may take anywhere from vascular events in at-risk patients.86 Therefore, the decision to
several months to 2 years to clear.15,19 In children, corneal stop these medications after the occurrence of hyphema must
blood staining may be further complicated by amblyopia.15 be made on a case-by-case basis in consultation with the pa-
tient’s primary care physician.
4.4. Optic atrophy Evaluation of the patient’s suitability to stop or reduce
these medications involves consideration of the desired
In the setting of posttraumatic hyphema, optic atrophy may therapeutic international normalized ratio range for the pa-
develop secondary to traumatic nerve contusion or secondary tient’s medical condition, coexisting medical conditions
glaucoma. The risk of developing optic atrophy related to which may further affect clotting ability (e.g. chronic liver
elevated IOP is greater if the pressure is allowed to remain at disease, bone marrow suppression), and the time taken for
50 mm Hg or more for 5 days or 35 mm Hg or more for 7 days in normal clotting and coagulation to be restored after stopping
otherwise healthy individuals.80 Patients with sickle-cell dis- these medications.
ease or trait develop optic atrophy at lower IOPs.89
5.1. Medical management
(4) Microscopic corneal blood staining. up visits. Both hospitalization and follow up are governed by
(5) The hyphema fails to resolve to less than 50% of the the degree of hyphema and risk of rebleeding.3,90,109 Patients
anterior chamber volume by 8 days (to prevent peripheral with high-grade hyphema or high risk of rebleed (Table 2) may
anterior synechiae formation). be admitted for daily examination and close monitoring.
Other patients will benefit from close outpatient follow up on
There are varied surgical modalities for management of days 2 and 7 to allow early detection of rebleeding (which can
hyphema depending on the severity and density of hyphema. occur in up to one-third of patients) or indications for surgical
These will be elaborated on in the following section. intervention (as outlined in the previous section). Subse-
quently, once hyphema has resolved and the patient is no
5.2.1. Anterior chamber washout and clot removal longer on topical medication, physicians can safely opt for
The most common surgical approach used is the limbal par- quarterly follow up to monitor IOP.91 Based on the presence or
acentesis needle drainage. Surgeons may opt to do this as an absence of raised IOP, optic nerve damage, or angle recession,
outpatient procedure. A 27-gauge needle attached to a tuber- attending physicians can gradually lengthen follow-up
culin syringe may be used to aspirate the blood slowly. This intervals.
will only remove liquefied portions of the clot, but is often
sufficient to normalize the IOP and restore aqueous flow. 5.4. Screening for sickle-cell disease or trait in patients of
Anterior chamber washout using an irrigating Simcoe cannula African descent
can be done if the hyphema has not yet organized. When
managing organized hyphema, anterior chamber washout Patients with sickle-cell disease or trait have a higher inci-
using an automated anterior vitrectomy through limbal or dence of secondary hemorrhage, increased IOP, and optic at-
clear corneal incisions can be performed. Vitrectomy can rophy in the setting of traumatic hyphema compared to
debulk the clot without shearing the anatomic structures and nonesickle-cell patients.55,67,89,105 Hence, screening is war-
causing rebleed. Anterior chamber stability must be main- ranted in patients of African descent.89 Even low-grade
tained (by raising the height of the bottle and through use of hyphema can lead to significant impairment of aqueous
cohesive viscoelastic agents), and hypotony should be avoided outflow, intractable increase in IOP, and optic neuropathy in
to minimize subsequent bleeding. The infusion port is used to sickle-cell disease, posing a serious threat to vision.89
maintain a constant irrigation and the clot cut and aspirated
with the help of a vitrectomy cutter introduced through a clear
corneal incision. Care should be taken to avoid iatrogenic 6. Special situations
trauma to the lens, iris, or corneal endothelium. Visco-
dissection can be used to separate the adherent hyphema 6.1. Sickle-cell hemoglobinopathies
from underlying iris. In addition, the settings of the vitrector
should be on irrigate-cut-aspirate rather than irrigate- As outlined in the previous sections, patients with sickle-cell
aspirate-cut as the latter setting may result in rebleeding disease are at significantly elevated risk of developing com-
due to traction on the clot and blood vessels. An 8-ball plications of hyphema.
hyphema can be removed with the conventional limbal clot These patients have been found to have enhanced fibri-
delivery method. nolysis which explains the predisposition to secondary hem-
orrhage.43 Furthermore, sickled erythrocytes face greater
5.2.2. Trabeculectomy and iridectomy resistance in passing through the outflow channels of the
Trabeculectomy and iridectomy are useful adjuncts in man- trabecular meshwork, as they are less pliable than normal
agement of clots associated with large hyphema. Trabecu- biconcave erythrocytes. Hence they slow the process of
lectomy modulated with either mitomycin C or 5-flurouracil hyphema resolution and lead to exaggerated increase in
can be combined with clot expression in patients with glau- IOP.37,38 Making matters worse, patients with sickle-cell dis-
coma not controlled by maximal medical therapy.41,106 Glau- ease are susceptible to vascular occlusion at relatively low
coma shunts as a primary procedure have shown promising IOPs or relatively brief durations of high pressures.75
results in such cases as well; however, this surgery may be Medical treatment of glaucoma poses a serious challenge
complicated by postoperative hypotony, choroidal effusion, in these patients as most commonly used systemic agents are
and secondary hemorrhage41 and is best reserved for patients contraindicated.36 Use of hyperosmotic or diuretic agents (e.g.,
with intractable glaucoma. glycerine, isosorbide, and mannitol) should be avoided, as
In summary, the various surgical methods are associated they may cause hemoconcentration and increased blood vis-
with significant risks, including damage to corneal endothe- cosity in the ocular microvasculature.31,36
lium, lens injury, prolapse of intraocular contents, and Systemic carbonic anhydrase inhibitors cause systemic
rebleeding.87 Hence, surgical management should be reserved acidosis in addition to the hemoconcentration, which in-
for carefully selected patients at high risk of developing sight creases erythrocyte sickling.31 ACA, a carbonic anhydrase in-
threatening complications. hibitor, increases the concentration of ascorbic acid in
aqueous humor and exacerbates the sickling process. This is
5.3. Hospitalization and follow-up postulated to be because it acts as a reducing agent.4
A literature search did not reveal any definitive evidence
There are no standardized guidelines for the admission of a for the risk of systemic acidosis and hemoconcentration from
patient with hyphema and similarly for frequency of follow- topical carbonic anhydrase inhibitors; however, their local
s u r v e y o f o p h t h a l m o l o g y 6 1 ( 2 0 1 6 ) 2 9 7 e3 0 8 305
efficacy may be less than that of their systemic counterparts.24 of hyphema. Some peculiar syndromes described with cata-
Methazolamide is the only systemic drug that can be used ract surgery and associated hyphema are as follows:
safely for increased IOP in hyphema with background sickle-
cell disease.20 6.3.1. Swan syndrome
In conclusion, we recommend treating hyphema aggres- Characterized by recurrent intraocular bleeds even months
sively in this subgroup of patients. The IOP should be kept low to years after cataract surgery involving a scleral incision.98
Swan syndrome usually presents with blurred vision with
by using a combination of topical drugs such as timolol,
associated mild-to-moderate degree of pain. On examina-
apraclonidine, or brimonidine. Systemic therapy with meth-
tion, there is hyphema or vitreous hemorrhage and neo-
azolamide can be considered in recalcitrant cases. Surgical
intervention should be instituted earlier and at lower IOP vascularisation of the angle that is best managed by either
thresholds to prevent optic nerve damage.26 focal argon laser photocoagulation or direct diathermy of the
new vessels or surgical excision of the vessels or scleral
wound resuturing. With clear corneal incision cataract sur-
6.2. Management of hyphema in children gery becoming more widely used, the incidence of this syn-
drome has reduced greatly; however, in developing countries
The management of hyphema in infants and children requires where manual small incision cataract surgery is still per-
special considerations. First, the possibility of nonaccidental formed, one may need to consider this entity in cases of
injury or abuse must be considered. Furthermore, non- recurrent hyphema seen post cataract surgery.
traumatic etiologies of hyphema such as retinoblastoma, ju-
venile xanthogranuloma of the iris, and bleeding diathesis
from blood dyscrasias such as leukemia should also be 6.4. Uveitis with hyphema
explored.
Hyphema is a common admitting diagnosis in children Anterior uveitis has been described to be associated with
sustaining ocular trauma.25 Injury with toys (balls, stones, hyphema in cases of Reiter syndrome, juvenile chronic
projectiles) is the predominant etiology.22 The rate of arthritis, ankylosing spondylitis, idiopathic anterior uveitis,
rebleeding of hyphema in children is similar to that in and Herpes simplex. In these cases, hyphema has been found
adults.15,22,52 In the past, hospitalization had been recom- to be associated with increased inflammation. Conservative
mended for the first few days after the injury15,22,28,52,68; management with topical steroids is the treatment of choice.
however, few ophthalmologists would advocate hospitali- Bleeding in the anterior chamber (Amsler sign) following
zation for hyphema today. Instead, patients can be dis- paracentesis has been described in Fuchs heterochromic
charged with emphasis and advice on strict avoidance of iridocyclitis29 and is also seen in other uveitic cases
physical activity. Children younger than 5 years of age are following anterior chamber decompression. Although not
more likely to develop long term visual impairment second- pathognomonic, Amsler sign often occurs in Fuchs hetero-
ary to amblyopia from visual deprivation by media opacity chromic iridocyclitis from rupturing of the fine rubeotic
(hyphema, traumatic cataract, or corneal blood staining).11 vessels crossing the trabecular meshwork. These fragile
Minimizing the interval between the injury and the restora- vessels may also lead to hyphema secondary to pressure
tion of media clarity is hence a priority in these patients. from gonioscopy or applanation tonometry.
Monocular occlusion after injury to protect against further
mechanical injury should be minimized, as the expected
benefit must be weighed against the risk of inducing ambly-
7. Outcome measures
opia in young children.
Some authors report the use of systemic steroids with or
Proposed primary outcome measures that can be evaluated in
without topical steroids, instead of ACA, in managing children
the management of hyphema are visual acuity and stage of
with traumatic hyphema. This was done with the rationale to
hyphema. Secondary outcome measures include the inci-
control inflammation and reduce the risk of secondary hem-
dence of complications such as corneal blood staining, ocular
orrhage85; however, because of the potential for systemic
hypertension requiring surgical intervention, optic atrophy,
steroids to interfere with growth, we do not recommend this.
and rebleeding.
Final visual outcome and prognosis of hyphema in children
Poor visual outcome after resolution of hyphema is often
remain similar to adult patients.15,22,25
attributed to associated injuries from blunt trauma and is less
commonly directly from hyphema.14,49,68,70,76,96,104 Visual
6.3. Hyphema associated with cataract and refractive outcomes after total hyphema are generally poorer than
surgery subtotal hyphema.11,78,80
Varying incidence of glaucoma has been reported in pa-
Cataract surgery may also be associated with various degrees tients with and without rebleeding, with a significantly higher
of hyphema from either surgical trauma or erosion by the risk in patients with rebleeding.16,23,42,45,51,59,61,88,100 Read and
haptic of the intraocular lens into the iris.63,94 With manual Goldberg found optic atrophy without glaucomatous damage
small incision cataract surgery, there may be hypotony from in 6% of eyes in a series of 135 cases.80 Corneal blood staining
poor approximation of the wound on the first postoperative occurs in 2%e11% of cases of traumatic hyphemas.11,17,80,87
day associated with a complete hyphema. With anterior Reported incidence of secondary hemorrhage varies from 2%
chamber implantable lenses, there is an increase in incidence to 37%5,13,20,21,30,50,54e56,57,67,71,76,80,82,87,92,99
306 s u r v e y o f o p h t h a l m o l o g y 6 1 ( 2 0 1 6 ) 2 9 7 e3 0 8
15. Cohen SB, Fletcher ME, Goldberg MF, Jednock NJ. Diagnosis erythrocytes out of the anterior chamber of the human and
and management of ocular complications of sickle monkey eye: light and electron microscopic studies.
hemoglobinopathies: Part V. Ophthalmic Surg. Ophthalmic Surg. 1979;10:89e123
1986;17:369e74 39. Gottsch JD, Graham CR Jr, Hairston RJ, et al. Protoporphyrin
16. Cole JG, Byron HM. Evaluation of 100 eyes with traumatic IX photosensitization of corneal endothelium. Arch
hyphema: intravenous urea. Arch Ophthalmol. Ophthalmol. 1989;107:1497e500
1964;71:35e43 40. Gottsch JD, Messner EP, McNair DS, et al. Corneal blood
17. Coles WH. Traumatic hyphema: an analysis of 235 cases. staining: an animal model. Ophthalmology. 1986;93:797
South Med J. 1968;61:813e6 41. Graul TA, Ruttum MS, Lloyd MA, et al. Trabeculectomy for
18. Crawford JS, Lewandowski RL, Chan W. The effect of aspirin traumatic hyphema with increased intraocular pressure.
on rebleeding in traumatic hyphema. Am J Ophthalmol. Am J Ophthalmol. 1994;117:155e9
1975;80:543e5 42. Gregersen E. Traumatic hyphema I and II. Acta Ophthalmol
19. Crouch ER Jr, Crouch ER. Management of traumatic (Copenh). 1962;40:192e201
hyphema: therapeutic options. J Pediatr Ophthalmol 43. Hagger D, Wolff S, Owen J, Samson D. Changes in
Strabismus. 1999;36:238 coagulation and fibrinolysis in patients with sickle cell
20. Crouch ER Jr, Frenkel M. Aminocaproic acid in the disease compared with healthy black controls. Blood Coagul
treatment of traumatic hyphema. Am J Ophthalmol. Fibrinolysis. 1995;6:93e9
1976;81:355e60 44. Hallet C, Willoughby C, Shafiq A, et al. Pitfalls in the
21. Crouch ER Jr, Williams PB, Gray MK, et al. Topical management of a child with mild haemophilia A and a
aminocaproic acid in the treatment of traumatic hyphema. traumatic hyphema. Haemophilia. 2000;6:118
Arch Ophthalmol. 1997;115:1106e12 45. Henry MM. Nonperforating eye injuries with hyphema. Am J
22. Crouch ER, Williams PB. Trauma: ruptures and bleeding, in Ophthalmol. 1960;49:1298e300
Tasmani W, Jager EM (eds) Duane’s Clinical Ophthalmology. 46. Howard GM, Hutchinson BT, Fredrick AR Jr. Hyphema
Philadelphia, PA, Lippincott; 1993, pp 1e18 resulting from blunt traumadgonioscopic, tonographic, and
23. Darr JL, Passmore JW. Management of traumatic hyphema. ophthalmoscopic observation following resolution of the
Am J Ophthalmol. 1967;63:134e6 hemorrhage. Trans Am Acad Ophthalmol Otolaryngol.
24. Gupta D. Glaucoma due to ocular injury, in Gupta D (ed) 1965;69:294e306
Glaucoma diagnosis and management. Philadelphia, 47. Karcioglu ZA, Mullaney PB. Diagnosis and management of
Lippincott; 2005, p 157 iris juvenile xanthogranuloma. J Paediatr Ophthalmol
25. DeRespinis PA, Caputo AR, Fiore PM, Wagner RS. A survey of Strabismus. 1997;34(1):44e51
severe eye injuries in children. Am J Dis Child. 48. Katz J, Feldman MA, Bass EB, et al, Study of Medical Testing
1989;143:711e6 for Cataract Surgery Team. Risks and benefits of
26. Deutsch TA, Weinreb RN, Goldberg MF. Indications for anticoagulant and antiplatelet medication use before
surgical management of hyphema in patients with sickle cataract surgery. Ophthalmology. 2003;110(9):1784e8
cell trait. Arch Ophthalmol. 1984;102:566e9 49. Kearns P. Traumatic Hyphema: a retrospective study of 314
27. Dunn AS, Turpie AG. Perioperative management of patients cases. Br J Ophthalmol. 1991;75(3):137e41
receiving oral anticoagulants: a systematic review. Arch 50. Kennedy RH, Brubaker RF. Traumatic hyphema in a defined
Intern Med. 2003;163(8):901e8 population. Am J Ophthalmol. 1988;106:123
28. Edwards WC, Layden WE. Traumatic hyphema. A report of 51. Kitazawa Y. Management of traumatic hyphema with
184 consecutive cases. Am J Ophthalmol. 1973;75:110e6 glaucoma. Int Ophthalmol Clin. 1981;21:167e81
29. Ellingson FT. The uveitis-glaucoma-hyphema syndrome 52. Kraft SP, Christianson MD, Crawford JS, et al. Traumatic
associated with the Mark VIII anterior chamber lens hyphema in children. Treatment with epsilon-aminocaproic
implant. J Am Intraocul Implant Soc. 1978;4(2):50e3 acid. Ophthalmology. 1987;94:1232e7
30. Farber MD, Fiscella R, Goldberg MF. Aminocaproic acid 53. Kurz GH, Zimmerman LE. Spontaneous hyphema and acute
versus prednisone for the treatment of traumatic hyphema. glaucoma as initial signs of recurrent iris melanoma. Arch
Ophthalmology. 1991;98:279 Ophthalmol. 1963;69:581e2
31. Finch CA. Pathophysiologic aspects of sickle cell anemia. Am 54. Kushner AG. Traumatic hyphema. Surv Ophthalmol.
J Med. 1972;53:1e6 1959;4:2e10
32. Fong LP. Secondary hemorrhage in traumatic 55. Kutner B, Fourman S, Brein K, et al. Aminocaproic acid
hyphemadpredictive factors for selective prophylaxis. reduces the risk of secondary hemorrhage in patients
Ophthalmology. 1994;101:1583 with traumatic hyphema. Arch Ophthalmol.
33. Ghafari AB, Siamian H, Aligolbandi K, Vahedi M. Hyphema 1987;105:206e8
caused by trauma. Med Arch. 2013;67(5):354e6 56. Lai JC, Fekrat S, Barron Y, Goldberg MF. Traumatic hyphema
34. Gharaibeh A, Savage HI, Scherer RW, Goldberg MF, in children: risk factors for complications. Arch Ophthalmol.
Lindsley K. Medical interventions for traumatic hyphema. 2001;119:64e70
Cochrane Database Syst Rev. 2011;(1):CD005431 57. Laughlin RC. Anterior chamber hemorrhage in
35. Gilbert HD, Jensen AD. Atropine in the treatment of nonperforating injuries. Trans Pac Coast Otoophthalmol Soc
traumatic hyphema. Ann Ophthalmol. 1973;5:1297e300 Annu Meet. 1948;29:133e40
36. Goldberg MF. The diagnosis and treatment of secondary 58. Lawrence T, Wilison D, Harvey J. The incidence of secondary
glaucoma after hyphema in sickle cell patients. Am J hemorrhage after traumatic hyphema. Ann Ophthalmol.
Ophthalmol. 1979;87:43e9 1990;22:276
37. Goldberg MF, Dizon R, Raichand M, Goldbaum M. Sickled 59. Leone CR Jr. Traumatic hyphema in children. J Pediatr
erythrocytes, hyphema and secondary glaucoma: III. Ophthalmol. 1966;3:7e13
Effects of sickle cell and normal human blood samples in 60. Lifschitz T, Yermiahu T, Biedner B, Yassur Y. Traumatic total
rabbit anterior chambers. Ophthalmic Surg. hyphema in a patient with severe hemophilia. J Pediatr
1979;10:52e61 Ophthalmol Strabismus. 1986;23:80e1
38. Goldberg MF, Tso MO. Sickled erythrocytes, hyphema, and 61. Loring MJ. Traumatic hyphema. Am J Ophthalmol.
secondary glaucoma: VII. The passage of sickled 1958;45:873e80
308 s u r v e y o f o p h t h a l m o l o g y 6 1 ( 2 0 1 6 ) 2 9 7 e3 0 8
62. Luksza L, Homziuk M, Nowakowska-Klimek M, Glasner L, 84. Romano PE, Robinson JA. Traumatic hyphema: a
Iwaszkiewicz-Bilikiewicz B. Traumatic Hyphema caused by comprehensive review of the past half century. Binocul Vis
eye injuries. Klin Oczna. 2005;107(4-6):250e1 Strabismus Q. 2000;15:175
63. Magargal LE, Goldberg RE, Uram M, et al. Recurrent 85. Rynne MV, Romano PE. Systemic corticosteroids in the
microhyphema in the pseudophakic eye. Ophthalmology. treatment of traumatic hyphema. J Pediatr Ophthalmol
1983;90:1231e4 Strabismus. 1980;17:141e3
64. McDonald CJ, Raafat A, Mills MJ, Rumble JA. Medical and 86. Saxena R, Koudstaal P. Anticoagulant versus antiplatelet
surgical management of spontaneous hyphaema secondary therapy for preventing stroke in patients with nonrheumatic
to immune thrombocytopenia. Br J Ophthalmol. atrial fibrillation and a history of stroke or transient ischemic
1989;73:922e5 attack. Cochrane Database Syst Rev. 2004;(4):CD000187
65. McGetrick JJ, Jampol LM, Goldberg MF, et al. Aminocaproic 87. Shammas HF, Matta CS. Outcome of traumatic hyphema.
acid decreases secondary hemorrhage after traumatic Ann Ophthalmol. 1975;7:701
hyphema. Arch Ophthalmol. 1983;101:1031e3 88. Shea M. Traumatic hyphema in children. Can Med Assoc J.
66. Mooney D. Angle recession and secondary glaucoma. Br J 1957;76:466e9
Ophthalmol. 1973;57(8):608e12 89. Shingleton BJ, Hersh PS. Traumatic hyphema, in Shingleton
67. Nasrullah A, Kerr NC. Sickle cell trait as a risk factor for BJ, Hersh PS, Kenyon KR (eds) Eye Trauma. St Louis, MO,
secondary hemorrhage in children with traumatic hyphema. Mosby; 1991, pp 104e16
Am J Ophthalmol. 1997;123:783 90. Shiuey Y, Lucarelli MJ. Traumatic hyphema: outcomes of
68. Ng CS, Strong NP, Sparrow JM, Rosenthal AR. Factors related outpatient management. Ophthalmology. 1998;105(5):851e5
to the incidence of secondary haemorrhage in 462 patients 91. Shiuey Y, Lucarelli MJ. Traumatic hyphema: outcomes of
with traumatic hyphema. Eye. 1992;6:308e12 outpatient management. Ophthalmology. 1998;105:851
69. Ng DS, Ching RH, Chan CW. Angle-recession glaucoma: 92. Skalka HW. Recurrent hemorrhage in traumatic hyphema.
long-term clinical outcomes over a 10-year period in Ann Ophthalmol. 1978;10:1153e7
traumatic microhyphema. Int Ophthalmol. 93. Smith B, Regan WF Jr. Blow-out fracture of the orbit;
2015;35(1):107e13 mechanism and correction of internal orbital fracture. Am J
70. Ohrstrom A. Treatment of traumatic hyphaema with Ophthalmol. 1957;44(6):733e9
corticosteroids and mydriatics. Acta Ophthalmol (Copenh). 94. Speakman JS. Recurrent hyphema after surgery. Can J
1972;50:549e55 Ophthalmol. 1975;10:299e304
71. Palmer DJ, Goldberg MF, Frenkel M, et al. A comparison of 95. Spoor TC. Anterior segment injuries: blunt ocular
two dose regimens of epsilon aminocaproic acid in the traumadwhat happens when the eye is struck by a blunt
prevention and management of secondary traumatic object? in Spoor TC (ed) An Atlas of Ophthalmic Trauma.
hyphemas. Ophthalmology. 1986;93:102e8 London, Mosby; 1997, pp 35e49
72. Pilger IS. Medical treatment of traumatic hyphema. Surv 96. Spoor TC, Hammer M, Belloso H. Traumatic hyphema.
Ophthalmol. 1967;20:28 Failure of steroids to alter its course: a double-blind
73. Pollard ZF. Two hundred more traumatic hyphema cases with prospective study. Arch Ophthalmol. 1980;98:116e9
no rebleeds on the Yasuna Oral Steroids No Touch Protocol. 97. Spoor TC, Kwitko GM, O’Grady JM, et al. Traumatic hyphema
Correspondence Binocul Vis Strabismus Q. 2000;15:250 in an urban population. Am J Ophthalmol. 1990;109:23
74. Rad AS, Kheradvar A. Juvenile xanthogranuloma: concurrent 98. Swan KC. Hyphema due to wound vascularization after
involvement of skin and eye. Cornea. 2001;20(7):760e2 cataract extraction. Arch Ophthalmol. 1973;89:87e90
75. Radius RL, Finkelstein D. Central retinal artery occlusion 99. Thomas MA, Parrish RK 2nd, Feuer WJ. Rebleeding after
(reversible in sickle trait) with glaucoma. Br J Ophthalmol. traumatic hyphema. Arch Ophthalmol. 1986;104:206e10
1976;60:428e30 100. Thygeson P, Beard C. Observations in traumatic hyphema.
76. Rahmani B, Jahadi HR. Comparison of tranexamic acid Am J Ophthalmol. 1952;35:977e85
and prednisolone in the treatment of traumatic 101. Tonjum AM. Gonioscopy in traumatic hyphema. Acta
hyphema. A randomized clinical trial. Ophthalmology. Ophthalmol (Copenh). 1966;44:650e64
1999;106:375e9 102. Tonjum AM. Intraocular pressure and facility of outflow late
77. Rahmani B, Jahadi HR, Rajaeefard A. An analysis of risk for after ocular contusion. Acta Ophthalmol (Copenh).
secondary hemorrhage in traumatic hyphema. 1968;46:886e908
Ophthalmology. 1999;106:380e5 103. Turkcu FM, Yuksel H, Sahin A, Caca l. Demographic and
78. Rakusin W. Traumatic hyphema. Am J Ophthalmol. etiological characteristics of children with traumatic
1972;74:284e92 serious hyphema. Ulus Travma Acil Cerrahi Derg.
79. Read J. Traumatic hyphema: surgical vs medical 2013;19(4):357e62
management. Ann Ophthalmol. 1975;7:659e62 104. Volpe NJ, Larrison WI, Hersh PS, et al. Secondary
80. Read J, Goldberg MF. Comparison of medical treatment for hemorrhage in traumatic hyphema. Am J Ophthalmol.
traumatic hyphema. Trans Am Acad Ophthalmol 1991;112:507e13
Otolaryngol. 1974;78:799 105. Wax MB, Ridley ME, Magargal LE. Reversal of retinal and
81. Romano PE. Management of traumatic hyphema. Perspect optic disc ischemia in a patient with sickle cell trait and
Ophthalmol. 1981;5:33e8 glaucoma secondary to traumatic hyphema.
82. Romano PE, Hope GM. The effect of age and ethnic Ophthalmology. 1982;89:845e51
background on the natural rebleed rate in untreated 106. Weiss JS, Parrish RK, Anderson DR. Surgical therapy of
traumatic hyphema in children. Metab Pediatr Syst traumatic hyphema. Ophthalmic Surg. 1983;14:343e5
Ophthalmol. 1990;13:26e31 107. Wilson FM II. Traumatic hyphema: pathogenesis and
83. Romano PE, Phillips PJ. Traumatic hyphema: a critical review management. Ophthalmology. 1980;87:910
of the scientifically catastrophic history of steroid treatment 108. Wilson TW, Jeffers JB, Nelson LB. Aminocaproic acid
thereof, and a report of 24 additional cases with no prophylaxis in traumatic hyphema. Ophthalmic Surg.
rebleeding after treatment with the Yasuna Systemic 1990;21:807e9
Steroid, No Touch PLUS protocol. Binocle Vis Strabismus Q. 109. Wilson TW, Nelson LB, Jeffers JB, et al. Outpatient management
2000;15:187 of traumatic hyphemas. Ann Ophthalmol. 1990;22:366